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1. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, Vol. 1, 2005 , , ,

Transcranial colour-coded duplex sonography is a relatively new non-invasive method for imaging both the intracranial circulation and the parenchymal structures of the brain.
Transcranial colour-coded duplex sonography is a relatively new non-invasive method for imaging both the intracranial circulation and the parenchymal structures of the brain. It allows multiple investigation, follow up and evaluation of the therapeutic efficacy in patients with various brain diseases cerebral infarctions, intracerebral haematomas, cerebral oedema, stenoses and aneurysms of the basal cerebral arteries, arterio-venous malformations, thrombosis of cerebral veins, brain tumors and some neurodegenerative diseases. The article summarises the update knowledge concerning the clinical application of this method in neurology.
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It allows multiple investigation, follow up and evaluation of the therapeutic efficacy in patients with various brain diseases cerebral infarctions, intracerebral haematomas, cerebral oedema, stenoses and aneurysms of the basal cerebral arteries, arterio-venous malformations, thrombosis of cerebral veins, brain tumors and some neurodegenerative diseases.
Transcranial colour-coded duplex sonography is a relatively new non-invasive method for imaging both the intracranial circulation and the parenchymal structures of the brain. It allows multiple investigation, follow up and evaluation of the therapeutic efficacy in patients with various brain diseases cerebral infarctions, intracerebral haematomas, cerebral oedema, stenoses and aneurysms of the basal cerebral arteries, arterio-venous malformations, thrombosis of cerebral veins, brain tumors and some neurodegenerative diseases. The article summarises the update knowledge concerning the clinical application of this method in neurology.
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Contrast-enhanced transcranial colour \-coded sonography in acute hemispheric brain infarction.
Postert T, Braun B, Meves et al. Contrast-enhanced transcranial colour \-coded sonography in acute hemispheric brain infarction.
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CA and VMR are impaired in patients with carotid stenoses and occlusions, in recent and subcortical cerebral infarctions, arteriovenous malformations, subarachnoid hemorhages, traumatic brain injuries, in orthostatic intolerance.
CA and VMR are impaired in patients with carotid stenoses and occlusions, in recent and subcortical cerebral infarctions, arteriovenous malformations, subarachnoid hemorhages, traumatic brain injuries, in orthostatic intolerance. The CA impairment is associated with increased risk of stroke in carotid occlusions and with poor prognosis in cerebral infarctions and subarachnoid hemorhages.The autoregulation of the cerebral arteries is improved after carotid endarterectomy or stenting.
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Age, intracranial pressure, autoregulation, and outcome after brain trauma.
6, Czosnyka M, Balesteri M, Steiner L, Smielewski P, Hutchinson PJ, Matta, B, Pickard JD. Age, intracranial pressure, autoregulation, and outcome after brain trauma.
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Tissue oxygen reactivity and cerebral autoregulation after severe traumatic brain Injury.
Lang EW, Czosnyka M, Mehdorn HM. Tissue oxygen reactivity and cerebral autoregulation after severe traumatic brain Injury.
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Noninvasive cerebrovascular autoregulation assessment in traumatic brain injury: Validation and utility.
Lang EW, Lagopoulos J, Griffith J, Yip K, Mudaliar Y, Mehdorn M, Dorsch NW. Noninvasive cerebrovascular autoregulation assessment in traumatic brain injury: Validation and utility.
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Brain
Brain
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Dynamic cerebral autoregulation during brain activation paradigms.
Panerai R, Moody M, Eams P, Potter J. Dynamic cerebral autoregulation during brain activation paradigms.
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Cerebrovasc Brain Metab Rev
Cerebrovasc Brain Metab Rev
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Flodmark O., Imaging of the neonatal brain, In: Levene MI, Litford RJ (eds), Fetal and Neonatal Neurology and neurosurgery, 2 ed Churchill Livingstone, Edinburgh 1995, 105 – 128
Flodmark O., Imaging of the neonatal brain, In: Levene MI, Litford RJ (eds), Fetal and Neonatal Neurology and neurosurgery, 2 ed Churchill Livingstone, Edinburgh 1995, 105 – 128
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Ultrasounds in non vascular brain diseases, hyperbaric medicine, imaging brain parenchyma and cerebral venous system were another innovative topics along with arterial wall imaging including intima-media tichkness (IMT) and distensibility studies.
The 10th Meeting of the European Society of Neurosonology and Cerebral Hemodynamics (ESNCH) focused the attention in different topics. Specific sessions were devoted to emerging problems as the role of the ultrasounds in stroke units (perfusion imaging and sonothrombolysis) is known to be very important. Ultrasounds in non vascular brain diseases, hyperbaric medicine, imaging brain parenchyma and cerebral venous system were another innovative topics along with arterial wall imaging including intima-media tichkness (IMT) and distensibility studies. Classical topics such as carotid plaque characterization, emboli detection monitoring, ultrasound contrast imaging, ultrasound diagnosis of foramen ovale, ultrasound application during carotid surgery and functional assessment of cerebral hemodynamics were also presented. The advance in neurosonology, connected with echo-contrast bolus traking for analysis of cerebral circulation time, the assessment of the global cerebral blood volume and ultrasound evaluation of movement disorders, was discussed in a separate session. Proper time was dedicated to training and certification in Neurosonology in the European community.
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2. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 1, 2005, No. 2 , , ,

Cerebrovascular Risk Factors and Brain Microembolism
Cerebrovascular Risk Factors and Brain Microembolism
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It accounts for about 20% of cases of brain infarction and has the highest recurrent stoke risk compared to all other subtypes of stroke [2, 3].
An important cause of transient ischemic attack (TIA) and stroke is atherosclerotic carotid artery stenosis. It accounts for about 20% of cases of brain infarction and has the highest recurrent stoke risk compared to all other subtypes of stroke [2, 3]. Therefore, rapid intervention in this patient group is needed and they should be managed efficiently to minimize the incidence of stroke.
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Emboli protection devices (EBPs) have also been designed to protect the brain from embolisation during stenting.
A stent is a small tube made of nickel-titanium, a bendable metal that springs back after being bent, and is in today’s practice selfexpendable after placement. Emboli protection devices (EBPs) have also been designed to protect the brain from embolisation during stenting. It is used to catch the small particles that may be dislodged from the plaque into the brain circulation, which may help reduce the incidence of stroke during the procedure. To improve the safety of endovasular treatment, new designs of stents (like drug-eluted stents), delivery systems, and EBP are constantly designed.
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It is used to catch the small particles that may be dislodged from the plaque into the brain circulation, which may help reduce the incidence of stroke during the procedure.
A stent is a small tube made of nickel-titanium, a bendable metal that springs back after being bent, and is in today’s practice selfexpendable after placement. Emboli protection devices (EBPs) have also been designed to protect the brain from embolisation during stenting. It is used to catch the small particles that may be dislodged from the plaque into the brain circulation, which may help reduce the incidence of stroke during the procedure. To improve the safety of endovasular treatment, new designs of stents (like drug-eluted stents), delivery systems, and EBP are constantly designed.
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Comparison of phenytoin with noncompetitive N-methyl-D-aspartate anatagonists in a model of focal brain ischemia in the rat.
Boxer PA, Cordon JJ, Mann ME, Rodolosi LC, Vartanian MG, Rock DM, Taylor CP, Marcoux FW. Comparison of phenytoin with noncompetitive N-methyl-D-aspartate anatagonists in a model of focal brain ischemia in the rat.
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Supratentorial brain infarcts in adult-onset seizures: the Maastricht epilepsy case register.
Heuts-van Raak EP, Boellaard A, De Krom MC et al. Supratentorial brain infarcts in adult-onset seizures: the Maastricht epilepsy case register.
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Late seizures following a first symptomatic brain infarct are related to large infarcts involving the posterior area around the lateral sulcus.
Heuts-van Raak L, Lodder J, Kessels F. Late seizures following a first symptomatic brain infarct are related to large infarcts involving the posterior area around the lateral sulcus.
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Brain Res Rev
Brain Res Rev
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traumatic parenchymal brain hemorrhages.
traumatic parenchymal brain hemorrhages.
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Optico-cerebral syndrome: Simultaneous hemodynamic infarction of optic nerve and brain.
Bogousslavsky J, Regli F, Zografos L, et al. Optico-cerebral syndrome: Simultaneous hemodynamic infarction of optic nerve and brain.
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Cerebrovascular Risk Factors and Brain Microembolism in Patients with Carotid Obstructions
Cerebrovascular Risk Factors and Brain Microembolism in Patients with Carotid Obstructions
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Risk factors and brain microembolism
Risk factors and brain microembolism
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Risk factors and brain microembolism
Risk factors and brain microembolism
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Clinical diagnosis of brain embolism.
Caplan LR. Clinical diagnosis of brain embolism.
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with brain tumours.
with brain tumours.
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Prof. Vantov was a regular participant in the working sessions of the group “Intermozg” (Berlin) that deals with brain structure and functioning.
Prof. Vantov was a regular participant in the working sessions of the group “Intermozg” (Berlin) that deals with brain structure and functioning. Prominent scholars such as Schreiber (Warsaw), Kasil (Moscow), Schtempeny (Warsaw), Petrescu (Bucharest) write chapters in monographs edited by him.
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Working Group „Intracranial Pressure, Brain Edema and Brain Circulation“ of the German Society of Neurosurgery.
Working Group „Intracranial Pressure, Brain Edema and Brain Circulation“ of the German Society of Neurosurgery.
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3. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 2, 2006, No. 1 , , ,

recovery via plastic reorganization in the adult brain
recovery via plastic reorganization in the adult brain
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human brain, neurorehabilitation,
human brain, neurorehabilitation,
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via Plastic Reorganization in the Adult Brain
via Plastic Reorganization in the Adult Brain
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Brain Research and Rehabilitation Center “Neuron” – Kuopio, Finland
Brain Research and Rehabilitation Center “Neuron” – Kuopio, Finland
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Contrary to what was previously held as a fact, recent research advances have demonstrated that the adult human brain has a certain capacity for plastic reorganization and self-repair after a stroke.
Recovery of function after cerebrovascular stroke is attributable to a number of factors, including events (such as reabsorption of perilesional edema and tissue reperfusion) in the first few days after the incident. Yet the recovery after the stroke and consistent reorganization in the neural tissue takes many weeks and even many months. Recovery from strokes with identical initial clinical manifestations may vary greatly and our understanding of the recovery processes, though exponentially increased during last 10 years, is still very limited. Contrary to what was previously held as a fact, recent research advances have demonstrated that the adult human brain has a certain capacity for plastic reorganization and self-repair after a stroke. The mechanisms responsible for post-stroke recovery are complex and they operate at different levels, from signal transduction and gene transcription to synaptic and neural network level reorganization. The integrated use of functional neuroimaging techniques, at the same time trying to overcome the limitations of each specific methodology, is likely to shed much light on brain plasticity mechanisms. Neuroanatomical and neurophysiological changes likely underlie reorganization of the central nervous system and these changes are, in part, possible to characterize experimentally using imaging methods to evidence the post-stroke plasticity. Better understanding of these mechanisms can provide neurorehabilitation with powerful tools to help in designing and implementing new therapeutic approaches to stroke patients both in the acute and the chronic stages after a
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The integrated use of functional neuroimaging techniques, at the same time trying to overcome the limitations of each specific methodology, is likely to shed much light on brain plasticity mechanisms.
Recovery of function after cerebrovascular stroke is attributable to a number of factors, including events (such as reabsorption of perilesional edema and tissue reperfusion) in the first few days after the incident. Yet the recovery after the stroke and consistent reorganization in the neural tissue takes many weeks and even many months. Recovery from strokes with identical initial clinical manifestations may vary greatly and our understanding of the recovery processes, though exponentially increased during last 10 years, is still very limited. Contrary to what was previously held as a fact, recent research advances have demonstrated that the adult human brain has a certain capacity for plastic reorganization and self-repair after a stroke. The mechanisms responsible for post-stroke recovery are complex and they operate at different levels, from signal transduction and gene transcription to synaptic and neural network level reorganization. The integrated use of functional neuroimaging techniques, at the same time trying to overcome the limitations of each specific methodology, is likely to shed much light on brain plasticity mechanisms. Neuroanatomical and neurophysiological changes likely underlie reorganization of the central nervous system and these changes are, in part, possible to characterize experimentally using imaging methods to evidence the post-stroke plasticity. Better understanding of these mechanisms can provide neurorehabilitation with powerful tools to help in designing and implementing new therapeutic approaches to stroke patients both in the acute and the chronic stages after a
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brain tissue lesion has occurred and stabilized.
brain tissue lesion has occurred and stabilized. During last couple of years new biological re-
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The brain areas with increased perfusion are known to receive and integrate the information from different sensory systems and plan the movement execution.
For analysis, data of those patients whose affected hemisphere was the left one, were mirrored. After mirroring, all lesions were in the same hemisphere and they could be realigned into the same position and analyzed. The specific areas with an increase in perfusion in the affected hemisphere were in the precentral gyrus, premotor cortex (Brodmann’s area 6 (BA6), frontal cortex, and superior frontal gyrus (BA10). In the nonaffected hemisphere, perfusion was increased in the superior frontal gyrus (BA6) and cingulate gyrus (BA31). In the cerebellum increased perfusion was seen bilaterally. The brain areas with increased perfusion are known to receive and integrate the information from different sensory systems and plan the movement execution. The motor behavior of the affected hand of these patients improved significantly after the two weeks of therapy. Additionally, regional cerebral perfusion decreased in the lingual gyrus (BA18) in the affected hemisphere. In the nonaffected frontal cortex, two areas with decreased perfusion were also found in the middle frontal gyrus (BA8/10). Also, the fusiform gyrus (BA20) and inferior temporal gyrus (BA37) in the nonaffected hemisphere showed decreased perfusion.
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Neurorehabilitation and Plastic Reorganization in the Adult Brain
Neurorehabilitation and Plastic Reorganization in the Adult Brain
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Brain Research and Rehabilitation Center “Neuron” Kortejoki, FIN-71130 Kuopio
Brain Research and Rehabilitation Center “Neuron” Kortejoki, FIN-71130 Kuopio
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In: Donaghy M (ed) Brain’s diseases of the nervous system.
Warlow C. Stroke, transient ischemic attacks, and intracranial venous thrombosis. In: Donaghy M (ed) Brain’s diseases of the nervous system. Oxford University Press, 2001:775-896.
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degree with the topic “Studies on the protein components of liquor and blood plasma and secretion of Cortisol, CTH and Insulin in acute covered brain traumas”.
In 1963 prof. Karakanev was acknowledged a specialty in neurology. In 1976 he acquired the Ph.D. degree with the topic “Studies on the protein components of liquor and blood plasma and secretion of Cortisol, CTH and Insulin in acute covered brain traumas”. He was assigned for Associate Professor in 1977 and for Professor of Neurology– in 1990.
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Brain Research and
Brain Research and
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Brain Research and Rehabilitation
Brain Research and Rehabilitation
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4. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 2, 2006, No. 2 , , ,

It is a reliable, noninvasive technique for measuring BFV in the major arteries at the base of the brain and with portable, relatively inexpensive equipment.
In 1982 R. Aaslid et al. [1] introduced a pulsed transcranial Doppler system (TCD) using a low frequency (2 MHz) transducer that enabled recordings of the blood flow velocities (BFV) from intracranial arteries through selected cranial foramina and thin regions of the skull (ultrasonic windows). TCD, like extracranial Doppler, is based on the principle that ultrasonic signals reflected off moving objects (erythrocytes) demonstrate a change of frequency, which is shifted in direct proportion to the velocity of the moving object [2]. It is a reliable, noninvasive technique for measuring BFV in the major arteries at the base of the brain and with portable, relatively inexpensive equipment. TCD has now become one of the most important tools for the evaluation of the cerebral vasculature.
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) on the cerebral circulation are mostly demonstrated in resistance brain arterioles and play an important role in cerebral autoregulation that enables relatively constant cerebral blood flow (CBF) during variations of cerebral perfusion pressure.
) on the cerebral circulation are mostly demonstrated in resistance brain arterioles and play an important role in cerebral autoregulation that enables relatively constant cerebral blood flow (CBF) during variations of cerebral perfusion pressure. Thus, the differences between CBF at rest and after the induction of hypercapnia reflect the state of cerebral vasomotor reactivity (VMR) and, hence cerebrovascular reserve capacity. VMR is defined as the vasodilation capacity of cerebral arterioles to external stimuli, such as increasing extracellular pCO
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ischemic brain events;
ischemic brain events;
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Brain
Brain
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Early improvement of brain circulation in the acute stroke, complete recanalization and dramatic clinical recovery are feasible goals of the future STL.
) has better mechanical TL efficacy but potentially more side effects compared to diagnostic US technique that is more safe. Accelerated clot dissolution with the help of diagnostic US could be a practical alternative for the patients who are unsuitable for t-PA treatment. Early improvement of brain circulation in the acute stroke, complete recanalization and dramatic clinical recovery are feasible goals of the future STL. The benefit of STL development concerns therapeutic window above 3 hours, quick revascularization of the affected cerebral zones, smaller amounts of t-PA with reduced risk of symptomatic hemorrhage, simple noninvasive application in many patients, improvement of neurologic deficit and final stroke outcome.
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Demchuk и съавтори (от същия колектив) публикуват новаторската ТДС система за оценка и класификация на кръвотока в мозъчните съдове при оклузия и реканализация – TIBI (Thrombolysis In Brain Ischemia) [17].
11, 12, 17, 27, 39]. През 2001 г. Demchuk и съавтори (от същия колектив) публикуват новаторската ТДС система за оценка и класификация на кръвотока в мозъчните съдове при оклузия и реканализация – TIBI (Thrombolysis In Brain Ischemia) [17]. Тя е аналогична на кардиологичната система при миокарден инфаркт – TIMI (ангиографска класификация за измерване на резидуалния коронарен кръвоток и реканализация при болните с МИ) [11].
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Терапевтичният УЗ с нискочестотна (КHz) система е изпитван в проучването Transcranial LowFrequency Ultrasound-Medicated Thrombolysis in Brain Ischemia – TRUMBI [16].
71.4 KHz (с 7% до общ ТЛ ефект от 60%) [10]. Терапевтичният УЗ с нискочестотна (КHz) система е изпитван в проучването Transcranial LowFrequency Ultrasound-Medicated Thrombolysis in Brain Ischemia – TRUMBI [16]. Това е първото мултицентрово клинично проучване от 6 германски университетски центъра за оценка на безопасността на t-PA, плюс нискочестотен УЗ (300 kHz), при лечение на ИМИ [16]. Изследването е било преустановено, след като при 5 от 26 пациенти в целевата група (36%) са регистрирани симптоматични хеморагии чрез ЯМР, без ефективна ранна реканализация или клинична разлика в изхода на 3-я месец [16]. Това изследване демонстрира биоефектите на средно-килохерцните УЗ емисии за индуциране на симптоматични кръвоизливи, включително в зони, които не са били засегнати от исхемия.
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(Combined Lysis of Thrombus in Brain Ischemia using transcranial Ultrasound and Systematic TPA) [5, 10] е изследване, в което са рандомизирани 126 пациенти с ИМИ.
(Combined Lysis of Thrombus in Brain Ischemia using transcranial Ultrasound and Systematic TPA) [5, 10] е изследване, в което са рандомизирани 126 пациенти с ИМИ. То доказа, че продължителното ТДС мониториране (общо 2 часа) чрез 2-МHz диагностична сонда, с мощност 750 mW, постоянни ъгъл и местоположение на инсонация, при дълбочина – мястото с найлош остатъчен ток по TIBI скалата, има положителен ефект върху първичните крайни цели. Не установява повишаване на честотата на хеморагичните мозъчни усложнения при ТЛ на болни с ИМИ и демонстрира тенденция за подобро възстановяване след ИМИ спрямо болните с плацебо [5]. Резултатите от изследването на Alexandrov и сътр. показват, че 2-часовото ТДС мониториране на СМА при болни с ИМИ е без сериозни странични ефекти и усилва индуцираната от t-PA реканализиция (на 2-я час
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Transcranial Low-Frequency Ultrasound-Mediated Thrombolysis in Brain Ischemia: Increased Risk of Hemorrhage With Combined Ultrasound and Tissue Plasminogen Activator: Results of a Phase II Clinical Trial.
Daffertshofer M, Gass A, Ringleb P, Sitzer M, Sliwka U, Els T, Sedlaczek O, Koroshetz WJ, Hennerici MG. Transcranial Low-Frequency Ultrasound-Mediated Thrombolysis in Brain Ischemia: Increased Risk of Hemorrhage With Combined Ultrasound and Tissue Plasminogen Activator: Results of a Phase II Clinical Trial.
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Thrombolysis in Brain Ischemia (TIBI) Transcranial Doppler Flow Grades Predict Clinical Severity, Early Recovery, and Mortality in Patients Treated With Intravenous Tissue Plasminogen Activator.
Demchuk AM, Burgin WS, Christou I, Felberg RA, Barber PA, Hill MA, Alexandrov AV. Thrombolysis in Brain Ischemia (TIBI) Transcranial Doppler Flow Grades Predict Clinical Severity, Early Recovery, and Mortality in Patients Treated With Intravenous Tissue Plasminogen Activator.
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Does LowEnergy Ultrasound, Known to Enhance Thrombolysis, Affect the Size of Ischemic Brain Damage?
G, Olsson SB. Does LowEnergy Ultrasound, Known to Enhance Thrombolysis, Affect the Size of Ischemic Brain Damage?
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Ultrasound contrast agents for brain perfusion imaging and ischemic stroke therapy.
Martina AD, Meyer-Wiethe K, Allemann E et al. Ultrasound contrast agents for brain perfusion imaging and ischemic stroke therapy.
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Good final results of treatment, without any changes in sinus thrombosis is due to rapid compensation of venous blood flow by anastomoses, “intracranial decompression” by CSF and cerebral detritus leakage, surgical and therapeutical control of the brain edema, despite of lack of effect of anticoagulant therapy in one of the patients.
Good final results of treatment, without any changes in sinus thrombosis is due to rapid compensation of venous blood flow by anastomoses, “intracranial decompression” by CSF and cerebral detritus leakage, surgical and therapeutical control of the brain edema, despite of lack of effect of anticoagulant therapy in one of the patients.
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Interventional treatment of brain artery obstructions
Interventional treatment of brain artery obstructions
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Neurological management of brain artery aneurysms
Neurological management of brain artery aneurysms
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5. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 3, 2007, No. 1 , , ,

It has been suggested that the blockade of the angiotensin-renin system may protect the brain aganst ischemia.
channel modulators, inhibitors of NOmediated neurotoxicity and drugs, which modes of action are not quite clear. Some free-radical scavengers and antiinflammatory drugs could also exert neuroprotective action. However, until now the clinical trials, using the available neuroprotective drugs, are disappointing, although these agents have been found to reduce infarct size in animal stroke models. Combinations of neuroprotective drugs targeted at different stages of the ischemic cascade may be more useful. It has been suggested that the blockade of the angiotensin-renin system may protect the brain aganst ischemia. Statins also exhibit neuroprotective effects. Probably, transplanted stem cells may possess neuroprotective properties. It seems, the modification of the acute gene expression, induced by cerebral ischemia, and the apoptotic gene program could become promising treatment approach. Special attention should be given to the brain white matter lessions and cerebral small vessel disease. Further well designed preclinical and clinical studies are needed to evaluate the efficacy of neuroprotection in cerebral ischemia.
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Special attention should be given to the brain white matter lessions and cerebral small vessel disease.
Combinations of neuroprotective drugs targeted at different stages of the ischemic cascade may be more useful. It has been suggested that the blockade of the angiotensin-renin system may protect the brain aganst ischemia. Statins also exhibit neuroprotective effects. Probably, transplanted stem cells may possess neuroprotective properties. It seems, the modification of the acute gene expression, induced by cerebral ischemia, and the apoptotic gene program could become promising treatment approach. Special attention should be given to the brain white matter lessions and cerebral small vessel disease. Further well designed preclinical and clinical studies are needed to evaluate the efficacy of neuroprotection in cerebral ischemia.
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Brain Res
Brain Res
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lez RG: Imaging-guided acute ischemic stroke therapy: From “time is brain” to “physiology is brain”.
lez RG: Imaging-guided acute ischemic stroke therapy: From “time is brain” to “physiology is brain”.
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Can inhibition of apoptosis rescue ischemic brain?
Silverstein FS. Can inhibition of apoptosis rescue ischemic brain?
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Wintermark M: Brain perfusion-CT in acute stroke patients.
Wintermark M: Brain perfusion-CT in acute stroke patients.
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A local cerebral circulation unit is the territory of a blood vessel, supplying a functional part of the brain.
A local cerebral circulation unit is the territory of a blood vessel, supplying a functional part of the brain. This is in the same time a “nutritional unit” reacting adequately on the metabolic processes and needs of this particular brain part. This unit is a subsystem of the cerebral circulation system, which one in turn is part of the whole body circulation system.
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This is in the same time a “nutritional unit” reacting adequately on the metabolic processes and needs of this particular brain part.
A local cerebral circulation unit is the territory of a blood vessel, supplying a functional part of the brain. This is in the same time a “nutritional unit” reacting adequately on the metabolic processes and needs of this particular brain part. This unit is a subsystem of the cerebral circulation system, which one in turn is part of the whole body circulation system.
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and adenosine increase, consequent of brain activity, results in widening of blood vessel lumen, decrease of the resistance and increase of the blood circulation.
and adenosine increase, consequent of brain activity, results in widening of blood vessel lumen, decrease of the resistance and increase of the blood circulation. This is a metabolic control (again in forth power!), without participation of neuronal meditation, as a parallel positive autoregulation mechanism of mill clack type. This is the normal way of work at the “nutrition unit” level.
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It is enabling the adequate local changes to provide O2 for the brain metabolism,
This mechanisms and there feedback, superimposed over the aforementioned ones, make the system multistable (in the meaning of Ashby WR, 1960) [1]. It is working reliable in changing conditions of heart output and blood pressure. It is enabling the adequate local changes to provide O2 for the brain metabolism,
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Minciotti et al (1991) support the opinion that is no direct correlation between carotid lesions and brain hemodynamic alterations, since less than half of the patients examined showed TCD signs of CBF reduction.
Minciotti et al (1991) support the opinion that is no direct correlation between carotid lesions and brain hemodynamic alterations, since less than half of the patients examined showed TCD signs of CBF reduction. The explanation is given with the modeling the system.
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Intracranial pressure (ICP) when raised, results in a consequent rise of the blood pressure (the experiment of Dubois Raymond), which is a defensive reflex, ensuring the income of blood into the brain arterial system (if ICP≥ABP no circulation is possible).
Now, it is clear why lowering the blood pressure too mush, in cases with subarachnoid hemorrhage, is not the proper thing to do. Intracranial pressure (ICP) when raised, results in a consequent rise of the blood pressure (the experiment of Dubois Raymond), which is a defensive reflex, ensuring the income of blood into the brain arterial system (if ICP≥ABP no circulation is possible).
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syndrome”. It may be also the capillary 0-point displacement and increased ischemia of the brain tissue.
syndrome”. It may be also the capillary 0-point displacement and increased ischemia of the brain tissue. The genesis of the hyperperfusion syndrome is better understood in the light of this presentation, as well as are TIA.
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Desingn for a brain.
Ashby WR. Desingn for a brain. The origin of adaptive behavior. Chapman& Hall Ltd., London, 1960.
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Brain Dev
Brain Dev
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Brain Dev
Brain Dev
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brain reorganization, motor control, stroke
brain reorganization, motor control, stroke
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It may be based on: (1) brain repair (restitution, i.e.
The functional recovery from stroke is a complex process, the mechanisms of which are mostly unknown. It may be based on: (1) brain repair (restitution, i.e. the biological recovery of the damage area itself); (2) adaptive reorganization (recruitment of new additional neural networks that can activate the same final pathways) and/or
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At present, there are strong indications that all these mechanisms are potentially involved in the process of recovery after brain injury, however, the ability of human adult brain to reorganize itself remains more or less restricted.
(3) compensatory strategy (behavioral substitution, i.e. patients learn to compensate for their deficit). At present, there are strong indications that all these mechanisms are potentially involved in the process of recovery after brain injury, however, the ability of human adult brain to reorganize itself remains more or less restricted. Irrespective of the type and the amount of applied therapy certain biological processes, characterized as “spontaneous neurological recovery”, are supposedly responsible for the final functional outcome after stroke. The final outcome has been shown to be determined within a limited time window during the acute phase of brain injury if recovery is seen early after stroke onset, better outcomes may be expected six months later although motor recovery may continue over a period of years in some individuals with appropriate rehabilitation. The present review summarizes the recent theories and hypotheses for brain reorganization of motor control after unilateral stroke.
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The final outcome has been shown to be determined within a limited time window during the acute phase of brain injury if recovery is seen early after stroke onset, better outcomes may be expected six months later although motor recovery may continue over a period of years in some individuals with appropriate rehabilitation.
(3) compensatory strategy (behavioral substitution, i.e. patients learn to compensate for their deficit). At present, there are strong indications that all these mechanisms are potentially involved in the process of recovery after brain injury, however, the ability of human adult brain to reorganize itself remains more or less restricted. Irrespective of the type and the amount of applied therapy certain biological processes, characterized as “spontaneous neurological recovery”, are supposedly responsible for the final functional outcome after stroke. The final outcome has been shown to be determined within a limited time window during the acute phase of brain injury if recovery is seen early after stroke onset, better outcomes may be expected six months later although motor recovery may continue over a period of years in some individuals with appropriate rehabilitation. The present review summarizes the recent theories and hypotheses for brain reorganization of motor control after unilateral stroke.
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The present review summarizes the recent theories and hypotheses for brain reorganization of motor control after unilateral stroke.
(3) compensatory strategy (behavioral substitution, i.e. patients learn to compensate for their deficit). At present, there are strong indications that all these mechanisms are potentially involved in the process of recovery after brain injury, however, the ability of human adult brain to reorganize itself remains more or less restricted. Irrespective of the type and the amount of applied therapy certain biological processes, characterized as “spontaneous neurological recovery”, are supposedly responsible for the final functional outcome after stroke. The final outcome has been shown to be determined within a limited time window during the acute phase of brain injury if recovery is seen early after stroke onset, better outcomes may be expected six months later although motor recovery may continue over a period of years in some individuals with appropriate rehabilitation. The present review summarizes the recent theories and hypotheses for brain reorganization of motor control after unilateral stroke.
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Theoretical basis for brain plasticity after TBI.
Bach-Y-Rita, P. Theoretical basis for brain plasticity after TBI.
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Brain Injury
Brain Injury
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Brain
Brain
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Brain
Brain
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Brain
Brain
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Functional and cellular effects of enviromental enrichment after experimental brain infarcts.
Johansson BB. Functional and cellular effects of enviromental enrichment after experimental brain infarcts.
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Brain
Brain
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Behavioral and Brain Sciences
Behavioral and Brain Sciences
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Restoration of function after brain injury.
Luria AR. Restoration of function after brain injury. Pergamon Press Ltd, Oxford, England, 1963.
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Brain
Brain
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Non-invasive imaging of brain functions and brain recovery:applying lessions from cognitive neuroscience to neurorehabilitation.
Matthews PM, Johansen-Berg H, Reddy H. Non-invasive imaging of brain functions and brain recovery:applying lessions from cognitive neuroscience to neurorehabilitation.
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Brain
Brain
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Morphological and functional brain alterations.
Pantano P, Formisano R, Ricci M, Di Piero V, Sabatini U, Di Pofi B, Rossi R, Bozzao L, Lenzi LG. Motor recovery after stroke. Morphological and functional brain alterations.
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Brain
Brain
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Purification of a pluripotent neural stem cell from the adult mouse brain.
Rietze RL, Valcanis H, Brooker GF, Thomas T, Voss AK, Bartlett PF. Purification of a pluripotent neural stem cell from the adult mouse brain.
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Reorganisation of cerebral circuits in human ischemic brain disease.
Seitz RJ,Butefisch CM, Kleiser R, Homberg V. Reorganisation of cerebral circuits in human ischemic brain disease.
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Brain
Brain
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Brain
Brain
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Functional reorganization of the brain in recovery from striocapsular infarction in man.
Weiller C, Chollet F, Friston KJ, Wise RJS, Frachowiak RSJ. Functional reorganization of the brain in recovery from striocapsular infarction in man.
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1987: Introduced functional transcranial Doppler for study and quantification of evoked flow responses and the dynamic relationship between brain function and blood flow.
1987: Introduced functional transcranial Doppler for study and quantification of evoked flow responses and the dynamic relationship between brain function and blood flow.
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Неговият метод за количествена оценка на мозъчния кръвен ток с импедансна техника, известен в чуждестранната литература като “метод на Хаджиев” е публикуван в “Progress in Brain Research”.
Неговите научни интереси са в областта на мозъчносъдовите заболявания, главоболието и невропротекцията. Автор е на 28 монографии и на 470 статии, 67 от които са публикувани в международни списания или книги и са широко цитирани, повече от 800 цитирания. Неговият метод за количествена оценка на мозъчния кръвен ток с импедансна техника, известен в чуждестранната литература като “метод на Хаджиев” е публикуван в “Progress in Brain Research”. Той разработва коцепцията за асимптомните исхемични мозъчносъдови заболявания, публикувана в книги и статии, включително в чуждестранни списания. От патофизиологична гледна точка дефинира транзиторната исхемична атака (ТИА) като исхемична пенамбра с различна продължителност, която може да прерастне в мозъчен инфаркт или да премине в доброкачествена олигемия и посочва, че ТИА е идеалния обект за бърза реваскуларизация и невропротекция. Автор е на указания за първична и вторична профилактика на исхемичните инсулти. Редактор е на учебници и ръководства по неврология. Чел е лекции по мозъчносъдови заболявания и главоболие в Австрия, Хърватска и Турция.
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His method for quantitative evaluation of cerebral blood flow by impedance technique, known as “method of Hadjiev” in the international literature, has been published in “Progress in Brain Research” He introduces the concept of asymptomatic ischemic cerebrovacular disorders, published in books and papers, including in foreign journals.
67 of which are printed in international journals or books and are widely cited, more than 800 citations. His method for quantitative evaluation of cerebral blood flow by impedance technique, known as “method of Hadjiev” in the international literature, has been published in “Progress in Brain Research” He introduces the concept of asymptomatic ischemic cerebrovacular disorders, published in books and papers, including in foreign journals. From pathophysiological viewpoint he defines the TIA as a ischemic penumbra with different duration, which could proceed to cerebral infarct or reduce to benign oligemia and pointed out that TIA is an ideal target for rapid reperfusion and neuroprotection. Author of guidelines for primary and secondary prevention of ischemic stroke. He is an Editor of textbooks and manuals of Neurology. Prof. D. Hadjiev has delivered lectures on cerebrovascular diseases and headache in Austria, Croatia and Turkey.
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7th World Congress on Brain Injury
7th World Congress on Brain Injury
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6. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 3, 2007, No. 2 , , ,

Premotor and Motor Brain Cortex Responses to Transcranial Magnetic Stimulation in Hemiparetic Patients Assessed by Motor Threshold
Premotor and Motor Brain Cortex Responses to Transcranial Magnetic Stimulation in Hemiparetic Patients Assessed by Motor Threshold
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Brain Research and Rehabilitation Center “Neuron”, Kuopio, Finland
Brain Research and Rehabilitation Center “Neuron”, Kuopio, Finland
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The regimen used in ESPS2 trial [7] (ASA 25 mg x 2/d + DP 200 mg x 2/d) diminished the risk of brain infarct 21.3% when compared with treatment with ASA alone without increasing the risk of bleeding (absolute risk reduction 3.0% dur-
Patients with stroke are prone to a recurrent stroke [4]. Therefore, the best possible antithrombotictherapyforsecondaryprevention should be selected according to the individual needs,especiallytolerabilityinsymptomatic patients with carotid artery stenosis, antithrombotic therapy should be initiated as soon as the diagnosis of a TIA or cerebral infarction has been made [5]. Alternative choices are acetylsalicylic acid (ASA) [6], a combination of ASA and extended release dipyridamole (DP) [7, 8], or clopidogrel [9]. At present, the first choice is the combination of ASA + extended release DP. The regimen used in ESPS2 trial [7] (ASA 25 mg x 2/d + DP 200 mg x 2/d) diminished the risk of brain infarct 21.3% when compared with treatment with ASA alone without increasing the risk of bleeding (absolute risk reduction 3.0% dur-
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f the reason for TIA or brain infarction is atherosclerosis, antiplatelet therapy should be continued permanently, if there are no contraindications (e.g.
f the reason for TIA or brain infarction is atherosclerosis, antiplatelet therapy should be continued permanently, if there are no contraindications (e.g. ulcer, thrombocytopenia, therapy resistant elevated BP). Otherwise, therapy continues until the risk factor inducing symptoms disappeares.
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There is no scientific evidence for the secondary alternative for patients who experience new TIAs or a brain infarction while being treated with Aspirin + DP, Aspirin, or Clopidogrel.
There is no scientific evidence for the secondary alternative for patients who experience new TIAs or a brain infarction while being treated with Aspirin + DP, Aspirin, or Clopidogrel. If a patient is on Aspirin, it may be possible to intensify the therapy by adding DP or by changing Aspirin to Clopidogrel. In this case, the therapeutic decisions must be taken with careful consideration according to each individual patient.
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Prof. Juhani Sivenius, MD Brain Research and Department of Neurology Rehabilitation Center “Neuron” Kuopio University Hospital 71130 Kuopio
Prof. Juhani Sivenius, MD Brain Research and Department of Neurology Rehabilitation Center “Neuron” Kuopio University Hospital 71130 Kuopio
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Homocysteine and brain atrophy on MRI of non-demented eldery.
Heijer T, Vermeer SE, Clarke R et al. Homocysteine and brain atrophy on MRI of non-demented eldery.
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Brain
Brain
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To study the bioelectrical brain activity and to evaluate the blood flow velocity (BFV) changes of the middle cerebral artery (MCA) during a Simulating Air Combat Maneuvers (SACM) in human centrifuge.
To study the bioelectrical brain activity and to evaluate the blood flow velocity (BFV) changes of the middle cerebral artery (MCA) during a Simulating Air Combat Maneuvers (SACM) in human centrifuge.
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Simultaneously the bioelectrical brain activity was registered using 8-chanel Holter-electroencephalography (EEG).
The study was performed in 15 pilots, tested by the method of SACM with maximal +Gz-8G load. The cardiac reactivity was assessed using 3chanels electrocardiography (ECG). A parallel infra-red pletismography at the level of the right temporal artery was applied and the delayed pulse wave (measured in milliseconds between R wave of the ECG and the peak of the pletismography) was estimated. By means of transcranial Doppler sonography the BFV of the right MCA at a depth of 50–55 mm was monitored. Simultaneously the bioelectrical brain activity was registered using 8-chanel Holter-electroencephalography (EEG). A visual and
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The usage of an antigravity suit and antigravity straining maneuvers prevented the severe reduction of brain circulation.
In overloading up to 3G an increase in the quantity of the fast wave activity within the range of 12–14 Hz was observed. The subsequent increase in the acceleration in the range of 4,5 – 5G resulted in a common delay of the EEG activity with shifting to 6-8 Hz teta frequency maximums. In some of the pilots an appearance of delta activity (2-4 Hz) was found during the 7-8 G hypergravitational stress. A decrease in the MCA BFV was preceded by the appearance of a “blackout” period. The usage of an antigravity suit and antigravity straining maneuvers prevented the severe reduction of brain circulation.
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The study shows typical gradual changes of electrophysiological brain activity and cerebral hemodynamics, which can be used as objective criteria for adaptation to the hypergravitational stress.
The study shows typical gradual changes of electrophysiological brain activity and cerebral hemodynamics, which can be used as objective criteria for adaptation to the hypergravitational stress. The maximums in the EEG delta range can predict the appearance of “blackout” periods and the subsequent loss of consciousness (e.g. G-LOG).
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Premotor and Motor Brain Cortex Responses to Transcranial Magnetic Stimulation
Premotor and Motor Brain Cortex Responses to Transcranial Magnetic Stimulation
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To assess the excitability and the function of premotor and primary motor brain cortex by determination of the motor threshold (MT) of gaining arms and legs motor responses using transcranial magnetic stimulation (TMS).
To assess the excitability and the function of premotor and primary motor brain cortex by determination of the motor threshold (MT) of gaining arms and legs motor responses using transcranial magnetic stimulation (TMS).
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Premotor brain cortex motor response to TMS, 2007 (personal communication).
Baykushev S, Struppler A, Gozmanov G, Mavrov R. Premotor brain cortex motor response to TMS, 2007 (personal communication).
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Caramia M, Cicinelli P, Paradiso C et al: Excitability changes of muscular responses to magnetic brain stimulation in patients with central motor disorders.
Caramia M, Cicinelli P, Paradiso C et al: Excitability changes of muscular responses to magnetic brain stimulation in patients with central motor disorders.
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Brain
Brain
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Epilepsy and the Functional Anatomy of the Human Brain.
Penfield W, Jasper H. Epilepsy and the Functional Anatomy of the Human Brain. Boston: Little & Brown, 1954.
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7. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 4, 2008, No. 1 , , ,

in Brain Death Confirmation
in Brain Death Confirmation
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The Role of Transcranial Doppler in Brain Death Confirmation
The Role of Transcranial Doppler in Brain Death Confirmation
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brain death, confirmatory test, transcranial
brain death, confirmatory test, transcranial
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The definition of brain death is the irreversible loss of all brain functions, including the brainstem.
The definition of brain death is the irreversible loss of all brain functions, including the brainstem. Since the diagnosis of brain death allows organ donation or withdrawal of support, the exact criteria for diagnose must be determined. Repeated neurological examination must confirm loss of brainstem reflexes, followed by the usage of con
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Since the diagnosis of brain death allows organ donation or withdrawal of support, the exact criteria for diagnose must be determined.
The definition of brain death is the irreversible loss of all brain functions, including the brainstem. Since the diagnosis of brain death allows organ donation or withdrawal of support, the exact criteria for diagnose must be determined. Repeated neurological examination must confirm loss of brainstem reflexes, followed by the usage of con
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sation of brain or brainstem activity or confirming the cerebral circulatory arrest.
sation of brain or brainstem activity or confirming the cerebral circulatory arrest. The neurosonological tests are preferred, allowing bedside evaluation in highly unstable patients, reducing the risk for residual organs function. The evaluation of extraand intracranial cerebral hemodynamic exhibits high resistance pattern parallel with the increase of intracranial pressure, finally leading to cerebral circulatory arrest. Trained personal and strict protocols are required.
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Diagnosis of brain death
Diagnosis of brain death
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Brain death is a clinical diagnosis, first time defined in 1968 [1].
Brain death is a clinical diagnosis, first time defined in 1968 [1]. In 1995. American Academy of Neurology (AAN) defined practice parameters that should serve as guidelines in management of patients with brain death [2, 3]. A survey on brain death criteria [4] throughout the world revealed
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American Academy of Neurology (AAN) defined practice parameters that should serve as guidelines in management of patients with brain death [2, 3].
Brain death is a clinical diagnosis, first time defined in 1968 [1]. In 1995. American Academy of Neurology (AAN) defined practice parameters that should serve as guidelines in management of patients with brain death [2, 3]. A survey on brain death criteria [4] throughout the world revealed
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A survey on brain death criteria [4] throughout the world revealed
Brain death is a clinical diagnosis, first time defined in 1968 [1]. In 1995. American Academy of Neurology (AAN) defined practice parameters that should serve as guidelines in management of patients with brain death [2, 3]. A survey on brain death criteria [4] throughout the world revealed
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Major differences between countries were present between presence of legal standards on organ transplantation, presence of practice guidelines for brain death for adults, number of physicians required to declare brain death, observational period or presence of required expertise of examining physicians.
uniform agreement on the neurological examination with exception of apnea test. Major differences between countries were present between presence of legal standards on organ transplantation, presence of practice guidelines for brain death for adults, number of physicians required to declare brain death, observational period or presence of required expertise of examining physicians. Only 40% of national practice guidelines require confirmatory testing.Accepted tests are conventional or multislice computerized tomography (MSCT) angiography, electroencephalography, evoked potentials, transcranial Doppler sonography (TCD), isotope angiography, Technetium-99m hexamethylpropylene-amineoxime brain scan (99mTc-HMPAO) [5]. After confirming the clinical diagnosis with one of the tests, the examined brain death person is declared dead.
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Only 40% of national practice guidelines require confirmatory testing.Accepted tests are conventional or multislice computerized tomography (MSCT) angiography, electroencephalography, evoked potentials, transcranial Doppler sonography (TCD), isotope angiography, Technetium-99m hexamethylpropylene-amineoxime brain scan (99mTc-HMPAO) [5].
uniform agreement on the neurological examination with exception of apnea test. Major differences between countries were present between presence of legal standards on organ transplantation, presence of practice guidelines for brain death for adults, number of physicians required to declare brain death, observational period or presence of required expertise of examining physicians. Only 40% of national practice guidelines require confirmatory testing.Accepted tests are conventional or multislice computerized tomography (MSCT) angiography, electroencephalography, evoked potentials, transcranial Doppler sonography (TCD), isotope angiography, Technetium-99m hexamethylpropylene-amineoxime brain scan (99mTc-HMPAO) [5]. After confirming the clinical diagnosis with one of the tests, the examined brain death person is declared dead.
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After confirming the clinical diagnosis with one of the tests, the examined brain death person is declared dead.
uniform agreement on the neurological examination with exception of apnea test. Major differences between countries were present between presence of legal standards on organ transplantation, presence of practice guidelines for brain death for adults, number of physicians required to declare brain death, observational period or presence of required expertise of examining physicians. Only 40% of national practice guidelines require confirmatory testing.Accepted tests are conventional or multislice computerized tomography (MSCT) angiography, electroencephalography, evoked potentials, transcranial Doppler sonography (TCD), isotope angiography, Technetium-99m hexamethylpropylene-amineoxime brain scan (99mTc-HMPAO) [5]. After confirming the clinical diagnosis with one of the tests, the examined brain death person is declared dead.
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Some of the tests are more convenient to use due to technical reasons like bedside evaluation of unstable brain death patients [5].
Some of the tests are more convenient to use due to technical reasons like bedside evaluation of unstable brain death patients [5]. Therefore TCD and electroencephalographic tests are preferable, although technical or patient contraindications may present a problem. Angiography or radionuclear cerebral flow studies require special settings that are not available in all hospitals. Application of contrast medium in angiography is potentially harmful for the residual organ functions, so noninvasive tests are preferred.
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Neurosonological tests in brain death
Neurosonological tests in brain death
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The Neurosonology Research Group (NSRG) of the World Federation of Neurology (WFN) created guidelines for the use of TCD in determination of cerebral circulatory arrest in brain death confirmation [6], and may be adopted and endorsed by national societies [5, 7].
The Neurosonology Research Group (NSRG) of the World Federation of Neurology (WFN) created guidelines for the use of TCD in determination of cerebral circulatory arrest in brain death confirmation [6], and may be adopted and endorsed by national societies [5, 7]. Due to noninvasiveness and bedside evaluation, these tests entered the clinical practice. American Academy of Neurology assessed TCD as a useful adjunct test for the evaluation of cerebral circulatory arrest associated with brain death (Type A, Class II evidence) [8].
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American Academy of Neurology assessed TCD as a useful adjunct test for the evaluation of cerebral circulatory arrest associated with brain death (Type A, Class II evidence) [8].
The Neurosonology Research Group (NSRG) of the World Federation of Neurology (WFN) created guidelines for the use of TCD in determination of cerebral circulatory arrest in brain death confirmation [6], and may be adopted and endorsed by national societies [5, 7]. Due to noninvasiveness and bedside evaluation, these tests entered the clinical practice. American Academy of Neurology assessed TCD as a useful adjunct test for the evaluation of cerebral circulatory arrest associated with brain death (Type A, Class II evidence) [8].
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Extensive death of brain tissue causes extreme increase of intracranial pressure (ICP).
Extensive death of brain tissue causes extreme increase of intracranial pressure (ICP). When the ICP equals the diastolic arterial pressure, brain perfusion in present only during systole and with further increase of ICP over the systolic arterial pressure, cerebral perfusion will cease [7]. Due to elasticity of the arterial wall and the compliance of the vasculature distal to the recording site, such cerebral circulatory arrest is associated with Doppler evidence of oscillatory movement of blood in the large arteries at the base of the brain. However the net forward flow volume is zero. With time the oscillations become low amplitude spectral spikes until no pulsations are
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When the ICP equals the diastolic arterial pressure, brain perfusion in present only during systole and with further increase of ICP over the systolic arterial pressure, cerebral perfusion will cease [7].
Extensive death of brain tissue causes extreme increase of intracranial pressure (ICP). When the ICP equals the diastolic arterial pressure, brain perfusion in present only during systole and with further increase of ICP over the systolic arterial pressure, cerebral perfusion will cease [7]. Due to elasticity of the arterial wall and the compliance of the vasculature distal to the recording site, such cerebral circulatory arrest is associated with Doppler evidence of oscillatory movement of blood in the large arteries at the base of the brain. However the net forward flow volume is zero. With time the oscillations become low amplitude spectral spikes until no pulsations are
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Due to elasticity of the arterial wall and the compliance of the vasculature distal to the recording site, such cerebral circulatory arrest is associated with Doppler evidence of oscillatory movement of blood in the large arteries at the base of the brain.
Extensive death of brain tissue causes extreme increase of intracranial pressure (ICP). When the ICP equals the diastolic arterial pressure, brain perfusion in present only during systole and with further increase of ICP over the systolic arterial pressure, cerebral perfusion will cease [7]. Due to elasticity of the arterial wall and the compliance of the vasculature distal to the recording site, such cerebral circulatory arrest is associated with Doppler evidence of oscillatory movement of blood in the large arteries at the base of the brain. However the net forward flow volume is zero. With time the oscillations become low amplitude spectral spikes until no pulsations are
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Transcranial Doppler in Brain Death Confirmation
Transcranial Doppler in Brain Death Confirmation
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The cause of coma must be established and must be sufficient to account for a permanent loss of brain function.
Certain prerequisites must be fulfilled before using Doppler sonography to confirm cerebral circulatory arrest [5, 6, 7]. The cause of coma must be established and must be sufficient to account for a permanent loss of brain function. Other conditions such as intoxication, hypothermia, severe arterial hypotension, metabolic disorders and others have been excluded. Clinical evaluation by two experienced examiners must show no evidence of cerebral or brainstem functions. Cerebral circulatory arrest can be confirmed if certain extraand intracranial Doppler sonographic findings have been recorded and documented bilaterally on two examinations at an interval of at least 30 min. These findings are systolic spikes or oscillating flow in any cerebral artery which can be recorded by bilateral transcranial insonation for anterior circulation, or any intracranial vertebral or basilar artery which can be recorded by suboccipital insonation for the posterior circulation. The diagnosis established by the intracranial examination must be confirmed by the extracranial bilateral recording of the common carotid arteries, internal carotid arteries and vertebral arteries.
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Value of TCD in brain death confirmation
Value of TCD in brain death confirmation
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Most TCD findings are based on the assessment of blood flow in the middle cerebral arteries, or diagnose of brain dead was made on clinical grounds alone, without apnea test.
Most of the articles evaluating the sensitivity of the neurosonological test were analyzed in the recently published meta-analysis [9]. Among searched literature, only two high-qualities [10, 11] and eight low-quality studies were included [12-17]. Other didn’t meet the validation criteria for further analysis. Most TCD findings are based on the assessment of blood flow in the middle cerebral arteries, or diagnose of brain dead was made on clinical grounds alone, without apnea test. Some are comparing TCD with other diagnostic tests, although validity of reference tests can be compromised. Meta-analysis [9] of the two high-quality studies showed a sensitivity of 95% (95% CI 92-97%) and a specificity of 99% (95% CI 97-100%) to detect brain death. Metaanalysis of all ten studies showed a sensitivity of 89% and a specificity of 99%. All studies investigators performing TCD were not blinded to clinical, electroencephalographic or radiographic results. This meta-analysis showed that TCD is
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Meta-analysis [9] of the two high-quality studies showed a sensitivity of 95% (95% CI 92-97%) and a specificity of 99% (95% CI 97-100%) to detect brain death.
Most of the articles evaluating the sensitivity of the neurosonological test were analyzed in the recently published meta-analysis [9]. Among searched literature, only two high-qualities [10, 11] and eight low-quality studies were included [12-17]. Other didn’t meet the validation criteria for further analysis. Most TCD findings are based on the assessment of blood flow in the middle cerebral arteries, or diagnose of brain dead was made on clinical grounds alone, without apnea test. Some are comparing TCD with other diagnostic tests, although validity of reference tests can be compromised. Meta-analysis [9] of the two high-quality studies showed a sensitivity of 95% (95% CI 92-97%) and a specificity of 99% (95% CI 97-100%) to detect brain death. Metaanalysis of all ten studies showed a sensitivity of 89% and a specificity of 99%. All studies investigators performing TCD were not blinded to clinical, electroencephalographic or radiographic results. This meta-analysis showed that TCD is
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a reliable test that can extend clinical criteria in the assessment of the diagnosis brain death.
a reliable test that can extend clinical criteria in the assessment of the diagnosis brain death. Sensitivity and specificity for a positive pattern of oscillating flow and systolic spikes, indicating cerebral circulatory arrest were high in selected patient population. Few false-positive cases were reported in the literature, but only two instances [10, 17] were defined as false positive according to predefined criteria in this meta-analysis. In one patient [10] with TCD criteria of cerebral circulatory arrest, weak respiration was recorded after TCD examination. In the other report [17], a clinically brain-dead patient with cerebral circulatory arrest on TCD and angiography, EEG examination became isoelectric only several hours later. Both these patients became brain dead shortly after the false-positive TCD examination.
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In the other report [17], a clinically brain-dead patient with cerebral circulatory arrest on TCD and angiography, EEG examination became isoelectric only several hours later.
a reliable test that can extend clinical criteria in the assessment of the diagnosis brain death. Sensitivity and specificity for a positive pattern of oscillating flow and systolic spikes, indicating cerebral circulatory arrest were high in selected patient population. Few false-positive cases were reported in the literature, but only two instances [10, 17] were defined as false positive according to predefined criteria in this meta-analysis. In one patient [10] with TCD criteria of cerebral circulatory arrest, weak respiration was recorded after TCD examination. In the other report [17], a clinically brain-dead patient with cerebral circulatory arrest on TCD and angiography, EEG examination became isoelectric only several hours later. Both these patients became brain dead shortly after the false-positive TCD examination. Large opening of the scull may result in false negative results. After evaluating validity of TCD diagnosed brain death depending on the time lapse between clinical diagnosis and the performance of TCD, a specificity of 100% 24 hours after the clinical diagnosis was obtained [13].
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Both these patients became brain dead shortly after the false-positive TCD examination.
a reliable test that can extend clinical criteria in the assessment of the diagnosis brain death. Sensitivity and specificity for a positive pattern of oscillating flow and systolic spikes, indicating cerebral circulatory arrest were high in selected patient population. Few false-positive cases were reported in the literature, but only two instances [10, 17] were defined as false positive according to predefined criteria in this meta-analysis. In one patient [10] with TCD criteria of cerebral circulatory arrest, weak respiration was recorded after TCD examination. In the other report [17], a clinically brain-dead patient with cerebral circulatory arrest on TCD and angiography, EEG examination became isoelectric only several hours later. Both these patients became brain dead shortly after the false-positive TCD examination. Large opening of the scull may result in false negative results. After evaluating validity of TCD diagnosed brain death depending on the time lapse between clinical diagnosis and the performance of TCD, a specificity of 100% 24 hours after the clinical diagnosis was obtained [13].
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After evaluating validity of TCD diagnosed brain death depending on the time lapse between clinical diagnosis and the performance of TCD, a specificity of 100% 24 hours after the clinical diagnosis was obtained [13].
Few false-positive cases were reported in the literature, but only two instances [10, 17] were defined as false positive according to predefined criteria in this meta-analysis. In one patient [10] with TCD criteria of cerebral circulatory arrest, weak respiration was recorded after TCD examination. In the other report [17], a clinically brain-dead patient with cerebral circulatory arrest on TCD and angiography, EEG examination became isoelectric only several hours later. Both these patients became brain dead shortly after the false-positive TCD examination. Large opening of the scull may result in false negative results. After evaluating validity of TCD diagnosed brain death depending on the time lapse between clinical diagnosis and the performance of TCD, a specificity of 100% 24 hours after the clinical diagnosis was obtained [13].
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It can be applied as a confirmatory test in brain death confirmation only after fulfilling the prerequisites.
Characteristic hemodynamic spectra obtained in insonating arteries by means of TCD according to the protocol may serve as a useful test in cerebral circulatory arrest confirmation. It can be applied as a confirmatory test in brain death confirmation only after fulfilling the prerequisites. Clinical evaluation by two experienced examiners must show no evidence of cerebral or brainstem functions, the cause of coma is known and sufficient to account for a permanent loss of brain function and other conditions are excluded.
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Clinical evaluation by two experienced examiners must show no evidence of cerebral or brainstem functions, the cause of coma is known and sufficient to account for a permanent loss of brain function and other conditions are excluded.
Characteristic hemodynamic spectra obtained in insonating arteries by means of TCD according to the protocol may serve as a useful test in cerebral circulatory arrest confirmation. It can be applied as a confirmatory test in brain death confirmation only after fulfilling the prerequisites. Clinical evaluation by two experienced examiners must show no evidence of cerebral or brainstem functions, the cause of coma is known and sufficient to account for a permanent loss of brain function and other conditions are excluded.
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Report of the Ad Hoc Committee of the Harvard Medical School to Examine the Definition of Brain Death.
Report of the Ad Hoc Committee of the Harvard Medical School to Examine the Definition of Brain Death. A definition of irreversible coma.
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Determining brain death in adults.
Wijdicks EFM. Determining brain death in adults.
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Practice parameters for determining brain death in adults (Summary statement).
can Academy of Neurology. Practice parameters for determining brain death in adults (Summary statement).
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Brain death worldwide.
Wijdicks EFM. Brain death worldwide. Accepted fact but no global consensus in diagnostic criteria.
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Transcranial Doppler in Brain Death Confirmation
Transcranial Doppler in Brain Death Confirmation
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Consensus opinion on diagnosing brain death – guidelines for use of confirmatory tests.
Demarin V, Lovrencic-Huzjan A, Vargek-Solter V, Vukovic V, Miskov S, Mikula I, Peric M, Gopcevic A, Kusic Z, Balenovic A, Klanfar Z, Busic M. Consensus opinion on diagnosing brain death – guidelines for use of confirmatory tests. Report of Croatian Neurovascular Society and University Department of Neurology, Sestre milosrdnice University Hospital, Reference Center for Neurovascular Disorders and the Ministry of Health of Republic of Croatia.
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Transcranial Doppler as a confirmatory test in brain death.
Lovrencic-Huzjan A, Vukovic V, Jergovic K, Demarin V. Transcranial Doppler as a confirmatory test in brain death.
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Transcranial Doppler ultrasonography to confirm brain death: a meta-analysis.
Monteiro LM, Bollen CW, van Huffelen AC, Ackerstaff RG, Jansen NJ, van Vught AJ. Transcranial Doppler ultrasonography to confirm brain death: a meta-analysis.
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diagnosis of brain death.
diagnosis of brain death.
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Transcranial Doppler ultrasound in brain death: experience in 140 patients.
Zurynski Y, Dorsch N, Pearson I, Chong R. Transcranial Doppler ultrasound in brain death: experience in 140 patients.
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Brain death and transcranial Doppler: experience in 130 cases of brain dead patients.
Ducrocq X, Braun M, Debouverie M, Junges C, Hummer M, Vespignani H. Brain death and transcranial Doppler: experience in 130 cases of brain dead patients.
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Time dependent validity in the diagnosis of brain death using transcranial Doppler sonography.
Kuo JR, Chen CF, Chio CC, Chang CH, Wang CC, Yang CM, Lin KC. Time dependent validity in the diagnosis of brain death using transcranial Doppler sonography.
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Utility of transcranial Doppler ultrasonography for confirmatory diagnosis of brain death: two sides of the coin.
Dosemeci L, Dora B, Yilmaz M, Cengiz M, Balkan S, Ramazanoglu A. Utility of transcranial Doppler ultrasonography for confirmatory diagnosis of brain death: two sides of the coin.
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Sensitivity of transcranial Doppler for confirming brain death: a prospective study of 270 cases.
de Freitas AG, Andre C. Sensitivity of transcranial Doppler for confirming brain death: a prospective study of 270 cases.
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Comparison between transcranial color Doppler ultrasonography and angiography in the confirmation of brain death.
Poularas J, Karakitsos D, Kouraklis G, Kostakis A, De Groot E, Kalogeromitros A, Bilalis D, Boletis J, Karabinis A. Comparison between transcranial color Doppler ultrasonography and angiography in the confirmation of brain death.
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Diagnosis of brain death.
Van Velthoven, Calliauw L. Diagnosis of brain death. Transcranial Doppler sonography as an additional method.
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Nitric oxide linking space and time in the brain.
Edelman GM., Gally JA. Nitric oxide linking space and time in the brain.
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She was Head of Department of Clinical Neurology and Center for Neurological Sciences and Brain at Sestre milosrdnice University Hospital.
She was Head of Department of Clinical Neurology and Center for Neurological Sciences and Brain at Sestre milosrdnice University Hospital. In 1991 she became a professor of neurology at University of Zagreb. Since 1994 she has been Head of University Department of Neurology, Sestre milosrdnice University Hospital. Under her leadership the Department became a Reference Center for Neurovascular Disorders of Ministry of Health of Republic of Croatia in 1997.
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From 1973 to 1982 he worked in the Central Laboratory for Brain Studies, part of Bulgarian Academy of Sciences.
He graduated from the Higher Medical Institute of Sofia in 1952 with honors for academic excellence. He started work in the Ministry of Interior and leaded the Central Military Medical Commission until 1955. At that time he specialized in Neurology. In 1970 Dr. Haralanov became an Associate Professor. From 1973 to 1982 he worked in the Central Laboratory for Brain Studies, part of Bulgarian Academy of Sciences. In 1982 he moved to the Department of Neurology in Medical Academy – Sofia. In 1985 he was elected for Professor in Neurology. From 1985 to 1989 when Prof. Haralanov retired, he was the Head of the Chair of Neurology of the Scientific Institute of Neurology and Psychiatry in Medical Academy – Sofia.
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These monographs along with his PhD thesis “Problems of the brain circulation” (1981), show his main direction of interest: investigation of the brain circulation and more specific – the main cerebral vessels. Prof.
Prof. Haralanov’s scientific activity contains more than 200 publications, including coauthorship in 3 Neurology books and 2 monographs – “Pathology of carotid circulation” (1970) and “Insufficiency of basal circulation” (1974). These monographs along with his PhD thesis “Problems of the brain circulation” (1981), show his main direction of interest: investigation of the brain circulation and more specific – the main cerebral vessels. Prof. Haralanov presents his personal conception concerning some vascular
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variants and anomalies with related disturbances in the brain haemodynamics.
variants and anomalies with related disturbances in the brain haemodynamics. Extraand intracranial vascular anastomoses are also studied in his works. Collateral circulation as a compensatory mechanism is another point of his topics.
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The exploration of the local vascular brain damage lead Prof.
The exploration of the local vascular brain damage lead Prof. Haralanov to important conclusions in the field of Neuropsychology, as well as in the clinical presentation of Wallenberg – Zaharchenko syndrome.
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8. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 4, 2008, No. 2 , , ,

How Do the Brain Neurons Work – Localy or Globaly?
How Do the Brain Neurons Work – Localy or Globaly?
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Ultrasound Pattern of the Brain Death
Ultrasound Pattern of the Brain Death
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cognitive brain functions, equipotentialism, localisationism
cognitive brain functions, equipotentialism, localisationism
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How Do the Brain Neurons Work – Localy or Globaly?
How Do the Brain Neurons Work – Localy or Globaly?
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The knowledge about the cognitive brain functions is marked by the struggle between two conceptions – localisationism and holism (globalism) and its most extreme manifestation equipotentialism.
The knowledge about the cognitive brain functions is marked by the struggle between two conceptions – localisationism and holism (globalism) and its most extreme manifestation equipotentialism. In 19th and 20th centuries many remarkable scientists and clinicians adduced arguments supporting the one or the other opinion. The development of neurologic science and practice in the last years and the introduction of modern neuroimaging methods (Positron Emission Tomography, functional Magnetic Resonance Imaging) proved that some specific, but elementary operations are really completed by precise neurons in exactly localized brain areas. However, each cognitive function is related to many operations, located in different (sometimes very distant) cerebral zones, forming unite functional system. The modern method for understanding the cognitive functions is called connectionism and is based on revealing and computerized simulation of these relations.
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The development of neurologic science and practice in the last years and the introduction of modern neuroimaging methods (Positron Emission Tomography, functional Magnetic Resonance Imaging) proved that some specific, but elementary operations are really completed by precise neurons in exactly localized brain areas.
The knowledge about the cognitive brain functions is marked by the struggle between two conceptions – localisationism and holism (globalism) and its most extreme manifestation equipotentialism. In 19th and 20th centuries many remarkable scientists and clinicians adduced arguments supporting the one or the other opinion. The development of neurologic science and practice in the last years and the introduction of modern neuroimaging methods (Positron Emission Tomography, functional Magnetic Resonance Imaging) proved that some specific, but elementary operations are really completed by precise neurons in exactly localized brain areas. However, each cognitive function is related to many operations, located in different (sometimes very distant) cerebral zones, forming unite functional system. The modern method for understanding the cognitive functions is called connectionism and is based on revealing and computerized simulation of these relations.
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How do the brain neurons work
How do the brain neurons work
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brain death, neurosonology, circulatory arrest
brain death, neurosonology, circulatory arrest
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Ultrasound Pattern of the Brain Death
Ultrasound Pattern of the Brain Death
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To demonstrate the ability of neurosonology in brain death confirmation.
To demonstrate the ability of neurosonology in brain death confirmation.
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А 17 years old men with clinical diagnosis of brain death is described – by repeated examination the loss of brainstem reflexes was confirmed.
А 17 years old men with clinical diagnosis of brain death is described – by repeated examination the loss of brainstem reflexes was confirmed. Brain computer tomography (CT), digital subtraction angiography (DSA) and multirange Doppler sonography monitoring of the blood flow velocity in carotid and basal
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Brain computer tomography (CT), digital subtraction angiography (DSA) and multirange Doppler sonography monitoring of the blood flow velocity in carotid and basal
А 17 years old men with clinical diagnosis of brain death is described – by repeated examination the loss of brainstem reflexes was confirmed. Brain computer tomography (CT), digital subtraction angiography (DSA) and multirange Doppler sonography monitoring of the blood flow velocity in carotid and basal
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Brain CT showed massive cerebral hemorrhage with blood within the ventricle system after rupture of aneurysm of the anterior communicating artery, proved by CT angiography.
Brain CT showed massive cerebral hemorrhage with blood within the ventricle system after rupture of aneurysm of the anterior communicating artery, proved by CT angiography. DSA demonstrated stop of the blood flow at the carotid siphons. The extracranial and transcranial Doppler sonography confirmed the existence of a cerebral circulatory arrest – systolic spikes or oscillating blood flow were recorded bilaterally from the internal and middle cerebral arteries at an interval of 30 min, while the blood circulation within the external carotid artery was preserved.
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Ultrasound monitoring of the cerebral hemodynamics is an easy and informative non-invasive method for evalustion of cerebral circulatory arrest in brain death.
Ultrasound monitoring of the cerebral hemodynamics is an easy and informative non-invasive method for evalustion of cerebral circulatory arrest in brain death.
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Ultrasound Pattern of the Brain Death
Ultrasound Pattern of the Brain Death
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Ultrasound Pattern of the Brain Death
Ultrasound Pattern of the Brain Death
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Utility of transcranial Doppler ultrasonography for confirmatory diagnosis of brain death: two sides of the coin.
Dosemeci L, Dora B, Yilmaz M, Cengiz M, Balkan S, Ramazanoglu A. Utility of transcranial Doppler ultrasonography for confirmatory diagnosis of brain death: two sides of the coin.
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Sensitivity of transcranial Doppler for confirming brain death: a prospective study of 270 cases.
de Freitas AG, Andre C. Sensitivity of transcranial Doppler for confirming brain death: a prospective study of 270 cases.
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Application of transcranial Doppler ultrasonography for the diagnosis of brain death.
Hadani M, Bruk B, Ram Z, Knoller N, Spiegelmann R, Segal E. Application of transcranial Doppler ultrasonography for the diagnosis of brain death.
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Time dependent validity in the diagnosis of brain death using transcranial Doppler sonography.
Kuo JR, Chen CF, Chio CC, Chang CH, Wang CC, Yang CM, Lin KC. Time dependent validity in the diagnosis of brain death using transcranial Doppler sonography.
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Transcranial Doppler ultrasonography to confirm brain death: a meta-analysis.
Jansen NJ, van Vught AJ. Transcranial Doppler ultrasonography to confirm brain death: a meta-analysis.
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Comparison between transcranial color Doppler ultrasonography and angiography in the confirmation of brain death.
Poularas J, Karakitsos D, Kouraklis G, Kostakis A, De Groot E, Kalogeromitros A, Bilalis D, Boletis J, Karabinis A. Comparison between transcranial color Doppler ultrasonography and angiography in the confirmation of brain death.
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Report of the Ad Hoc Committee of the Harvard Medical School to Examine the Definition of Brain Death.
Report of the Ad Hoc Committee of the Harvard Medical School to Examine the Definition of Brain Death. A definition of irreversible coma.
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Practice parameters for determining brain death in adults (Summary statement).
Report of the Quality Standards Subcommittee of the American Academy of Neurology. Practice parameters for determining brain death in adults (Summary statement).
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Brain death worldwide.
Wijdicks EFM. Brain death worldwide. Accepted fact but no global consensus in diagnostic criteria.
read the entire text >>

Diagnosis of brain death.
Van Velthoven, Calliauw L. Diagnosis of brain death. Transcranial Doppler sonography as an additional method.
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Brain computer tomography (CT), TCCDS and DSA were applied in all patients.
The study was performed in 25 patients (7 men and 18women, mean age 54±13 years). Brain computer tomography (CT), TCCDS and DSA were applied in all patients.
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Brain
Brain
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Through transcranial Doppler sonography (TCD) a slight reduction in the brain blood circulation on the side of the stenosis was pre-operatively ascertained.
101 patients (85 men and 16 women, mean age 63.2 years) with ACS were screened. The average degree of the stenosis ascertained was 81.9%. Through transcranial Doppler sonography (TCD) a slight reduction in the brain blood circulation on the side of the stenosis was pre-operatively ascertained. In all patients CE of a. carotis interna was carried out with shunt. In 99 patients (98%) successful CE was carried out. By means of CCDS and TCD significant improvement of the regional carotid haemodynamics and the haemodynamic of the intracranial arteries on the side of the operation was ascertained. In 1 patient (0.99%) stroke developed as a result of thrombosis of internal carotid artery.
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The method can be successfully applied in the prophylaxis of the ischemic brain stroke in case of patients with critical carotid stenosis.
CEA in ACS is an efficacious method of removal of the carotid pathology with a minimum per cent of blood vessel complications. The method can be successfully applied in the prophylaxis of the ischemic brain stroke in case of patients with critical carotid stenosis.
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To evaluate the motor threshold of excitability during transcranial magnetic stimulation (TMS) of the premotor brain cortex in patients with focal secondary generalized epilepsy.
To evaluate the motor threshold of excitability during transcranial magnetic stimulation (TMS) of the premotor brain cortex in patients with focal secondary generalized epilepsy.
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The premotor and motor brain cortex threshold excitability of 10 patients with secondary generalized epilepsy was assessed by TMS. C
The premotor and motor brain cortex threshold excitability of 10 patients with secondary generalized epilepsy was assessed by TMS. C
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Caramia M, Cicinelli P, Paradiso C et al: Excitability changes of muscular responses to magnetic brain stimulation in patients with central motor disorders.
Caramia M, Cicinelli P, Paradiso C et al: Excitability changes of muscular responses to magnetic brain stimulation in patients with central motor disorders.
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Epilepsy and the Functional Anatomy of the Human Brain.
Penfield W, Jasper H. Epilepsy and the Functional Anatomy of the Human Brain. Boston: Little, Brown, 1954
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The aim of the review is to introduce two new imaging methods – diffusion and perfusion tests for detection of morphological and functional changes in vascular and other diseases of the brain and other human organs and systems.
The aim of the review is to introduce two new imaging methods – diffusion and perfusion tests for detection of morphological and functional changes in vascular and other diseases of the brain and other human organs and systems. The diffusion test is performed by magnetic resonance imaging (MRI), and the perfusion test – using multidetectional computer tomography (CT). Both methods are applied for early diagnosis of various (mainly vascular) disorders of the central nervous system and other human systems by imaging of the vessel’s network (arteries, veins and capillaries) of the pathology process, as well as for control of the treatment and prognosis of the disease.
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The advantage of high relaxivity contrast agents in brain perfusion.
Cotton F, Hernier M. The advantage of high relaxivity contrast agents in brain perfusion.
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Perfusion imaging with computed tomography – brain and beyond.
Miles KA. Perfusion imaging with computed tomography – brain and beyond.
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Разбира се, неговите научни приноси се цитират многократно в най-авторитетни списания, сред които можем да посочим: “Brain”, “Neuropsychologia”, “Brain and Language”, “Revue Neurologique”, “Neurosurgery”, “Neurosci-
Разбира се, неговите научни приноси се цитират многократно в най-авторитетни списания, сред които можем да посочим: “Brain”, “Neuropsychologia”, “Brain and Language”, “Revue Neurologique”, “Neurosurgery”, “Neurosci-
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ence reports”, “European Journal of Neurology”, “Cognitive Brain Research”, “Cognitive Neuropsychology”, “Behavioral Neurology”, “Cortex”, “Experimental Brain Research”, “Journal of Neuroscience”, “Neuroscience and Behavioral Physiology”, “Neurocase” и много други.
ence reports”, “European Journal of Neurology”, “Cognitive Brain Research”, “Cognitive Neuropsychology”, “Behavioral Neurology”, “Cortex”, “Experimental Brain Research”, “Journal of Neuroscience”, “Neuroscience and Behavioral Physiology”, “Neurocase” и много други.
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His publications have been cited many times in competent journals on many languages, such as “Brain and language”, “European Journal of Neurology”, “Cognitive Neuropsychology”, and in main neuropsycological monographs –
His publications have been cited many times in competent journals on many languages, such as “Brain and language”, “European Journal of Neurology”, “Cognitive Neuropsychology”, and in main neuropsycological monographs –
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Brain
Brain
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Brain reorganization after stroke.
Brain reorganization after stroke.
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Brain reorganization after stroke.
Brain reorganization after stroke.
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in brain aneurysms.
in brain aneurysms.
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Brain anoxia,
Brain anoxia,
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9. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 5, 2009, No. 1 , , ,

in an occlusive disease of an artery supplying the brain.
scattered signal from the blood vessels in the case of reduced blood flow velocities in pathological situations e.g. in an occlusive disease of an artery supplying the brain. In transcranial examination, contrast agents help to improve the insonation conditions, especially in the case of an insufficient temporal bone window. Recently, based on experience from myocardial perfusion imaging, several reports were published on the imaging of cerebral perfusion. Suitable for imaging cerebral perfusion are the secondgeneration contrast media such as SonoVue™.
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in an occlusive disease of an artery supplying the brain).
In neurosonology, ultrasound contrast agents can be used to improve the insonation conditions (e.g. in the case of an insufficient temporal bone window in transcranial imaging) and/or to enhance the backscattered signal from the blood vessels in the case of reduced blood flow velocities in pathological situations (e.g. in an occlusive disease of an artery supplying the brain).
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Contrast-enhanced evaluation of the extracranial brain supplying arteries
Contrast-enhanced evaluation of the extracranial brain supplying arteries
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In the contrast-enhanced sonographic evaluation of the extracranial brain-supplying arteries, it is possible to obtain more detailed information about the anatomical course of the cerebral vessels and about the pathological conditions, especially if the native scanning is insufficient.
In the contrast-enhanced sonographic evaluation of the extracranial brain-supplying arteries, it is possible to obtain more detailed information about the anatomical course of the cerebral vessels and about the pathological conditions, especially if the native scanning is insufficient.
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Contrast-enhanced evaluation of the intracranial arteries supplying the brain
Contrast-enhanced evaluation of the intracranial arteries supplying the brain
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The use of echo contrast agents in the colorcoded examination of the extraand intracranial brain-supplying arteries has already become part of the clinical routine in the diagnosis of cere-
The use of echo contrast agents in the colorcoded examination of the extraand intracranial brain-supplying arteries has already become part of the clinical routine in the diagnosis of cere-
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At present, further clinical research is focused on the imaging of blood flow in the capillaries of brain parenchyma and on the evaluation of cerebral perfusion with the aim of imaging the cerebral perfusion deficit in stroke patients.
brovascular disease. At present, further clinical research is focused on the imaging of blood flow in the capillaries of brain parenchyma and on the evaluation of cerebral perfusion with the aim of imaging the cerebral perfusion deficit in stroke patients. Based on experience from myocardial perfusion imaging, several reports have recently been published on the imaging of cerebral perfusion [12, 13].
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in imaging of very low blood flow velocities in the capillaries of the brain parenchyma, the low mechanical index (MI) imaging modality is a preferred approach.
With increasing transmission power, the bubbles show an increasingly nonlinear response (ie, the backscattered signal contains frequencies that differ from the insonating frequency and the returned signal is thus distorted). The nonlinear signals contain overtones or harmonic and subharmonic signals at multiples and fractions of the insonating frequency. The second harmonic signal, which occurs at twice the incidence frequency, is used in a new ultrasound technique known as second harmonic imaging [16, 17]. When the energy of the insonating beam is further increased to mechanical indexes greater than approximately 0.3, there is a corresponding rise in the destruction of the microbubbles. In the applications where the microbubbles need to be preserved – e.g. in imaging of very low blood flow velocities in the capillaries of the brain parenchyma, the low mechanical index (MI) imaging modality is a preferred approach. Different techniques such as pulse inversion harmonic imaging, power modulation, harmonic power Doppler imaging, and contrast pulse sequencing are described to evaluate perfusion in microcirculation [18]. For quantification of brain tissue perfusion, bolus injection kinetics, refill injection kinetics or diminution kinetics are currently being explored. After a bolus injection of the contrast agent, time intensity curves with wash-in and wash-out phases can be analyzed. Postert and Seidel were able to measure time-intensity curves through the intact skull with transcranial sonography using the bubble response from the contrast agents Levovist™ and Optison™ respectively [19]. They showed that the examination is feasible, not only in young adults with a good acoustic temporal bone window.
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For quantification of brain tissue perfusion, bolus injection kinetics, refill injection kinetics or diminution kinetics are currently being explored.
The second harmonic signal, which occurs at twice the incidence frequency, is used in a new ultrasound technique known as second harmonic imaging [16, 17]. When the energy of the insonating beam is further increased to mechanical indexes greater than approximately 0.3, there is a corresponding rise in the destruction of the microbubbles. In the applications where the microbubbles need to be preserved – e.g. in imaging of very low blood flow velocities in the capillaries of the brain parenchyma, the low mechanical index (MI) imaging modality is a preferred approach. Different techniques such as pulse inversion harmonic imaging, power modulation, harmonic power Doppler imaging, and contrast pulse sequencing are described to evaluate perfusion in microcirculation [18]. For quantification of brain tissue perfusion, bolus injection kinetics, refill injection kinetics or diminution kinetics are currently being explored. After a bolus injection of the contrast agent, time intensity curves with wash-in and wash-out phases can be analyzed. Postert and Seidel were able to measure time-intensity curves through the intact skull with transcranial sonography using the bubble response from the contrast agents Levovist™ and Optison™ respectively [19]. They showed that the examination is feasible, not only in young adults with a good acoustic temporal bone window. The value of this diagnostic method could also be demonstrated in pathological conditions, e.g. in patients with acute hemispheric stroke [20, 21].
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lower mechanical index was used, demonstrated the capability of the contrast agent SonoVue™ to image cerebral perfusion and the less perfused areas of the brain.
lower mechanical index was used, demonstrated the capability of the contrast agent SonoVue™ to image cerebral perfusion and the less perfused areas of the brain.
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Transient response harmonic imaging: An ultrasound technique related to brain perfusion.
ttner T. Transient response harmonic imaging: An ultrasound technique related to brain perfusion.
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Harmonic grey scale imaging of the human brain.
Seidel G, Greis C, Sonne J, Kaps M. Harmonic grey scale imaging of the human brain.
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mann E, Seidel G: Ultrasound contrast agents for brain perfusion imaging and ischemic stroke therapy.
mann E, Seidel G: Ultrasound contrast agents for brain perfusion imaging and ischemic stroke therapy.
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Harmonic imaging of the human brain.
Seidel G, Algermissen C, Christoph A, Claassen L, Vidal-Langwasser M, Katzer T. Harmonic imaging of the human brain. Visualization of brain perfusion with ultrasound.
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Visualization of brain perfusion with ultrasound.
Seidel G, Algermissen C, Christoph A, Claassen L, Vidal-Langwasser M, Katzer T. Harmonic imaging of the human brain. Visualization of brain perfusion with ultrasound.
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Ultrasound perfusion imaging of the human brain.
Wiesmann M, Seidel G. Ultrasound perfusion imaging of the human brain.
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Comparison of transcranial brain tissue perfusion images between ultraharmonic, second harmonic, and power harmonic imaging.
Shiogai T, Takayasu N, Mizuno T, Nakagawa M, Furuhata H. Comparison of transcranial brain tissue perfusion images between ultraharmonic, second harmonic, and power harmonic imaging.
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Raiha I, Tarvonen S, Kutki T, Sourander L, Relationship between vascular factors and White matte low attenuation of the brain.
Raiha I, Tarvonen S, Kutki T, Sourander L, Relationship between vascular factors and White matte low attenuation of the brain.
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Managing depression in brain injuri rehabilitation: the use of an integrated care pathway and preliminary report of response to sertraline.
Turner – Stokes L., Hassan N., Pierce K., Clegg F. Managing depression in brain injuri rehabilitation: the use of an integrated care pathway and preliminary report of response to sertraline.
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white brain matter
white brain matter
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To define what is normal or abnormal in the aging brain is a difficult task.
To define what is normal or abnormal in the aging brain is a difficult task. To define the normal and abnormal changes in white brain matter is even harder. Age – associated brain changes progressing with time, could become symptomatic (for example development of memory disturbances) after passing a given threshold. The subthreshold changes are related to normal aging but these above – threshold are abnormal and represent different severity stages of the same pathophysiological process.
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To define the normal and abnormal changes in white brain matter is even harder.
To define what is normal or abnormal in the aging brain is a difficult task. To define the normal and abnormal changes in white brain matter is even harder. Age – associated brain changes progressing with time, could become symptomatic (for example development of memory disturbances) after passing a given threshold. The subthreshold changes are related to normal aging but these above – threshold are abnormal and represent different severity stages of the same pathophysiological process.
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Age – associated brain changes progressing with time, could become symptomatic (for example development of memory disturbances) after passing a given threshold.
To define what is normal or abnormal in the aging brain is a difficult task. To define the normal and abnormal changes in white brain matter is even harder. Age – associated brain changes progressing with time, could become symptomatic (for example development of memory disturbances) after passing a given threshold. The subthreshold changes are related to normal aging but these above – threshold are abnormal and represent different severity stages of the same pathophysiological process.
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Boon A, Lodder J, Heuts-van Raak, Kessel F, Silent brain infarcts in 755 consecutive patients with a first-ever supratentorial ischemic stroke: relationship with index-stroke subtype, vascular risk factors, and mortality.
Boon A, Lodder J, Heuts-van Raak, Kessel F, Silent brain infarcts in 755 consecutive patients with a first-ever supratentorial ischemic stroke: relationship with index-stroke subtype, vascular risk factors, and mortality.
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blood pressure and brain atrophy in the healthy elderly.
blood pressure and brain atrophy in the healthy elderly.
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Brain volumes in healthy adults aged 40 years and over: a voxel based morphometry study.
Riello R, Sabattoli F, Beltramello A, Bonetti M, Bono G, Falini A, Magnani G, Minonzio G, Piovan E, Alaimo G, Ettori M, Galluzzi S, Locatelli E, Noiszewska M, Testa C, Frisoni GB. Brain volumes in healthy adults aged 40 years and over: a voxel based morphometry study.
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Brain magnetic resonance imaging and neuropsy¬chologic evaluation of patients with idiopathic dilated car-diomyopathy.
Schmidt R, Fazekas F, Offenbacher H, Dusleag J, Lechner H. Brain magnetic resonance imaging and neuropsy¬chologic evaluation of patients with idiopathic dilated car-diomyopathy.
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Brain volume changes on longitudinal magnetic resonance imaging in normal older people.
Tang Y, Whitman GT, Lopez I, Baloh RW. Brain volume changes on longitudinal magnetic resonance imaging in normal older people.
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Brain
Brain
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He has introduced for the first time in the country some new EMG methodic, introduced, also, the somatosensory evoked potential taken off from the brain cortex for diagnostic purpose.
He helped ten new EMG laboratories to be opened in other cities of Bulgaria. He has introduced for the first time in the country some new EMG methodic, introduced, also, the somatosensory evoked potential taken off from the brain cortex for diagnostic purpose. He has been consultant of EMG laboratories of the Institute of Medical Specialization, Bulgarian Academy of Sciences and Military Medical Academy, Sofia. The first courses on EMG have been organized by prof. Baykushev (1970, 1971). He has been tutor and consultant of many dissertations for scientific degrees MD and DSc.
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The differences in the characteristics of primary motor and premotor brain cortex in healthy volunteers have been shown.
Prof. Baykushev introduced in Bulgaria for the first time the transcranial magnetic stimulation (TMS) for therapeutic application in neurology and psychiatry. In a recent work with prof. Struppler and ass.prof.Gozmanov, motor thresholds have been used for functional diagnostics. The differences in the characteristics of primary motor and premotor brain cortex in healthy volunteers have been shown. This has created a new way for magnetic stimulation particularly in epilepsy (2008).
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IXth International Conference on Quantification of Brain Function with PET
IXth International Conference on Quantification of Brain Function with PET
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www.kenes.com/brain
www.kenes.com/brain
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10. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 5, 2009, No. 1 , , ,

How does the blood leave the brain?
nster T, Rademacher J, Klingebiel R, Valdueza JM. How does the blood leave the brain? A systematic ultrasound analysis of cerebral venous
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Intracranial venous hemodynamics in patients with midline dislocation due to postischemic brain edema.
Stolz E, Gerriets T, Babacan SS, Jauss M, Kraus J, Kaps M. Intracranial venous hemodynamics in patients with midline dislocation due to postischemic brain edema.
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to perform comparative clinical, neurosonological, neurophysiological and neuroimaging examinations in chronic bilateral carotid thrombosis and to assess the brain abilities for compensation of the circulation deficit.
to perform comparative clinical, neurosonological, neurophysiological and neuroimaging examinations in chronic bilateral carotid thrombosis and to assess the brain abilities for compensation of the circulation deficit.
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Routine electroencephalography was applied for evaluation of the brain electric activity.
the main head and the basal cerebral arteries is described. The cerebral parenchyma was assessed by magnetic resonance imaging (MRI) and the vascular system – by digital subtracted angiography and magnetic resonance angiography. Routine electroencephalography was applied for evaluation of the brain electric activity.
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The combination of neurosonological, neurophysiological and neuroimaging methods enables to assess the complex relation between the severity, location and predilection of vascular pathology, the efficacy of collateral circulation, morphological brain changes and individual human abilities for brain reorganization in presence of chronic circulation deficit, caused by bilateral carotid thrombosis.
The combination of neurosonological, neurophysiological and neuroimaging methods enables to assess the complex relation between the severity, location and predilection of vascular pathology, the efficacy of collateral circulation, morphological brain changes and individual human abilities for brain reorganization in presence of chronic circulation deficit, caused by bilateral carotid thrombosis.
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Viable brain with bilateral internal carotid occlusion, a case report.
Basiri K, Ghadiri F, Saadatnia M. Viable brain with bilateral internal carotid occlusion, a case report.
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Transorbital sonographic monitoring of optic nerve diameter in patients with severe brain injury.
Transorbital sonographic monitoring of optic nerve diameter in patients with severe brain injury.
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Optic nerve sonography in the diagnostic evaluation of adult brain injury.
Soldatos Т, Karakitsos D, Chatzimichail K, Papathanasiou M, Gouliamos A, Karabinis A. Optic nerve sonography in the diagnostic evaluation of adult brain injury.
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Never treatment of epilepsy-brain pacemakers and transcranial magnetic stimulation.
Akamatsu N. Never treatment of epilepsy-brain pacemakers and transcranial magnetic stimulation.
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rTMS of the brain.Oral presentation at the International Esperanto Medical Conference, 11-16 юли 2005, Plovdiv, 6-7 (Abstracts).
Baykushev S, Gozmanov G, Baykouchev K. rTMS of the brain.Oral presentation at the International Esperanto Medical Conference, 11-16 юли 2005, Plovdiv, 6-7 (Abstracts).
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Fauth C, Meyer BU, Prosiegel M, Zihl, Conrad B: Seizure induction and magnetic brain stimulation after stroke. (Letter)
Fauth C, Meyer BU, Prosiegel M, Zihl, Conrad B: Seizure induction and magnetic brain stimulation after stroke. (Letter)
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Technology insight: noninvasive brain stimulation in neurology-perspectives on the therapeutic potential of rTMS and tDCS.
Fregni F, Pascual-Leone A. Technology insight: noninvasive brain stimulation in neurology-perspectives on the therapeutic potential of rTMS and tDCS.
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New methods of minimally invasive brain modulation as therapies in psychiatry: TMS, MST, VNS and DBS.
George MS. New methods of minimally invasive brain modulation as therapies in psychiatry: TMS, MST, VNS and DBS.
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Repetitive transcranial magnetic stimulation activates specific regions in rat brain.
Ji R, Schlaepfer T, Aizenman C, Epstein C, Qui D, Huang J, Rupp F. Repetitive transcranial magnetic stimulation activates specific regions in rat brain.
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Epilepsy and the Functional Anatomy of the Human Brain.
Penfield W, Jasper H. Epilepsy and the Functional Anatomy of the Human Brain. Boston: Little, Brown, 1954.
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11. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 6, 2010, No. 1 , , ,

One patient suffered from brain hemorrhage.
In 7 patients a reversal of the neurological symptoms was observed. One patient suffered from brain hemorrhage. One patient died despite the successful racanalization of the culprit vessel. There were no local complications.
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от Brain Attack Coalition [4, 5].
Първите препоръки за създаване на специализиран първичен център за лечение на ИМИ в САЩ са публикувани през 2001 г. от Brain Attack Coalition [4, 5]. Предложени са 11 критерии, които могат да се обобщят в две групи:
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Recommendations for establishment of primary stroke centres (PSCs) in the USA were published in 2001 by the Brain Attack Coalition [4, 5].
Recommendations for establishment of primary stroke centres (PSCs) in the USA were published in 2001 by the Brain Attack Coalition [4, 5]. There are 11 criteria for establishing PSC, which can be divided into two main groups:
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Another factor that limits the wider application of TL in AIS in EU and US is the concern that brain haemorrhage may harm the patient.
Another factor that limits the wider application of TL in AIS in EU and US is the concern that brain haemorrhage may harm the patient. The rate of large space occupying haematoma was found to be 1-1.1% in the placebo group and 4-5.9% in the rt-PA group [30, 68]. Despite this 4-5.4-fold risk, rt-PA significantly increased the overall chance of not being disabled or dead after stroke. This indicates that not all of these haemorrhages were symptomatic. Many of them occur in the ischemic area, but other in the remote zones. Accordingly, the definition of SICH should be: “Clinical deterioration by >4 points NIHSS (or equivalent) combined with brain haemorrhage without other pathology or clinical
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Accordingly, the definition of SICH should be: “Clinical deterioration by >4 points NIHSS (or equivalent) combined with brain haemorrhage without other pathology or clinical
Another factor that limits the wider application of TL in AIS in EU and US is the concern that brain haemorrhage may harm the patient. The rate of large space occupying haematoma was found to be 1-1.1% in the placebo group and 4-5.9% in the rt-PA group [30, 68]. Despite this 4-5.4-fold risk, rt-PA significantly increased the overall chance of not being disabled or dead after stroke. This indicates that not all of these haemorrhages were symptomatic. Many of them occur in the ischemic area, but other in the remote zones. Accordingly, the definition of SICH should be: “Clinical deterioration by >4 points NIHSS (or equivalent) combined with brain haemorrhage without other pathology or clinical
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advanced imaging approach with CT (ASPECTS); MRI (a digital atlas using the ASPECTS scoring – measures the stroke severity in an automated fashion and facilitates more objective, sensitive, and potentially more complex scoring); MRI diffusion and perfusion may reveal brain tissue at risk that can be salvaged with TL in individual patients within a 3-hour time window and possibly even longer (grade C evidence) [21, 23, 41, 47, 54, 57];
advanced imaging approach with CT (ASPECTS); MRI (a digital atlas using the ASPECTS scoring – measures the stroke severity in an automated fashion and facilitates more objective, sensitive, and potentially more complex scoring); MRI diffusion and perfusion may reveal brain tissue at risk that can be salvaged with TL in individual patients within a 3-hour time window and possibly even longer (grade C evidence) [21, 23, 41, 47, 54, 57];
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Walker; for the Brain Attack Coalition.
Marler, MR. Mayberg, RD. Starke, HW. Todd; KM. Viste, M Girgus, T Shephard, RN; M Emr; P Shwayder, MD. Walker; for the Brain Attack Coalition. Recommendations for the Establishment of Primary Stroke Centers.
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RD, Croft JB, Magnis E, Mulligan D, Jagoda A, O’Connor R, Cawley CM, Connors JJ, Rose-DeRenzy JA, Emr M, Warren M, Walker MD; Brain Attack Coalition.
RD, Croft JB, Magnis E, Mulligan D, Jagoda A, O’Connor R, Cawley CM, Connors JJ, Rose-DeRenzy JA, Emr M, Warren M, Walker MD; Brain Attack Coalition. Recommendations for comprehensive stroke centers: a consensus statement from the Brain Attack Coalition.
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Recommendations for comprehensive stroke centers: a consensus statement from the Brain Attack Coalition.
RD, Croft JB, Magnis E, Mulligan D, Jagoda A, O’Connor R, Cawley CM, Connors JJ, Rose-DeRenzy JA, Emr M, Warren M, Walker MD; Brain Attack Coalition. Recommendations for comprehensive stroke centers: a consensus statement from the Brain Attack Coalition.
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Brain Nerve
Brain Nerve
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12. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 6, 2010, No. 2 , , ,

basal ganglia, brain, MRT, thalamus
basal ganglia, brain, MRT, thalamus
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Etiological diagnosis based on brain imaging may be difficult.
Several diseases may cause non specific MRT abnormalities of the bilateral basal ganglia and thalami. Etiological diagnosis based on brain imaging may be difficult. This review summarises diagnostic values of brain MRI and clinical data in different diseases causing bilateral basal ganglia and thalami MRI lesions: toxic, metabolic, vascular, infectious, inflammatory diseases and tumors.
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This review summarises diagnostic values of brain MRI and clinical data in different diseases causing bilateral basal ganglia and thalami MRI lesions: toxic, metabolic, vascular, infectious, inflammatory diseases and tumors.
Several diseases may cause non specific MRT abnormalities of the bilateral basal ganglia and thalami. Etiological diagnosis based on brain imaging may be difficult. This review summarises diagnostic values of brain MRI and clinical data in different diseases causing bilateral basal ganglia and thalami MRI lesions: toxic, metabolic, vascular, infectious, inflammatory diseases and tumors.
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Diffusion-weighted imaging patterns of brain damage associated with cerebral venous thrombosis.
Ducreux D, Oppenheim C, Vandamme X, Dormont D, Samson Y, Rancurel G. Diffusion-weighted imaging patterns of brain damage associated with cerebral venous thrombosis.
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MRI of the brain in Wilson disease: T2 signal loss under therapy.
Engelbrecht V, Schlaug G, Hefter H, Kahn T, Modder U. MRI of the brain in Wilson disease: T2 signal loss under therapy.
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Initial and follow-up brain MRI findings and correlation with the clinical course in Wilson's disease.
Roh K, Lee T, Wie A, Lee B, Park S, Chang K. Initial and follow-up brain MRI findings and correlation with the clinical course in Wilson's disease.
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Brain Dev
Brain Dev
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Brain MRI of chronic alcoholism.
Vargas M, Lenz V, Bin J, Bogorin A, Eid M. Brain MRI of chronic alcoholism.
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Structured Assessment of Depression in Brain Damage (SADBD).
Structured Assessment of Depression in Brain Damage (SADBD).
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Domains and determinants of quality of life after stroke caused by brain infarction.
Kauhanen ML, Korpelainen JT, Hiltunen P, Nieminen P, Sotaniemi KA, Myllylä VV. Domains and determinants of quality of life after stroke caused by brain infarction.
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The structured assessment of depression in brain-damaged individuals: translation and validation study of the Italian version.
Monaco F, Mazzini L, Marchetti C, Torta R, Cicolin A, Mantegazza P, Pastore I, Ruggerone S, Mula M. The structured assessment of depression in brain-damaged individuals: translation and validation study of the Italian version.
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Protective effect of Curcumin, the active principle of turmeric (Curcuma longa) in haloperidol-induced orofacial dyskinesia and associated behavioural, biochemical and neurochemical changes in rat brain.
Bishnoi M, Chopra K, Kulkarni S. Protective effect of Curcumin, the active principle of turmeric (Curcuma longa) in haloperidol-induced orofacial dyskinesia and associated behavioural, biochemical and neurochemical changes in rat brain.
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Long-term effects of pallidal deep brain stimulation in tardive dystonia.
Gruber D, Trottenberg T, Kivi A, Schoenecker T. Long-term effects of pallidal deep brain stimulation in tardive dystonia.
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Decreased plasma brain-derived neurotrophic factor levels in schizophrenic patients with tardive dyskinesia: association with dyskinetic movements.
Tan Y, Zhou D, Zhang X. Decreased plasma brain-derived neurotrophic factor levels in schizophrenic patients with tardive dyskinesia: association with dyskinetic movements.
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Intern J Stroke Brain Res
Intern J Stroke Brain Res
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Aging and aging brain.
Aging and aging brain.
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13. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 7, 2011, No. 1 , , ,

This perspective has now been expanded clearly into the direction of new application methods like the B-mode imaging of the brain parenchyma and peripheral nerves.
Recent developments in Neurosonology suggest an extraordinary potential for clinical application.A few years ago, ultrasound as for the field of Neurology was mainly associated with finding evidence of stenosis within the framework of cerebro-vascular questions. This perspective has now been expanded clearly into the direction of new application methods like the B-mode imaging of the brain parenchyma and peripheral nerves.
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Computed tomography of head showed small hypodense areas in the parenchyma of the left temporoparietal part of the brain.
Neurologic examination revealed right central hemiparesis, and motor aphasia. Laboratory tests revealed dyslipidemia. Echocardiography excluded the presence of thrombotic masses in the cardiac chambers. Color-coded duplex sonography showed a bifurcation thrombus with a distal-shaped tail creating highgraded stenosis, lying free in the lumen of the internal carotid artery with a total thrombus length – about 4 cm (fig. 1A). CTA of supraaortal arteries confirmed the presence of a free floating thrombus in the initial part of the left ICA (fig. 1B). Computed tomography of head showed small hypodense areas in the parenchyma of the left temporoparietal part of the brain. We began therapy with two antiplatelets (Aspirin, Clopidogrel), low molecular weight Heparin, statin and medications helping protection of the brain parenchyma.An urgent endarterectomy of the left CCA and left ICA with patch plastic was done.
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We began therapy with two antiplatelets (Aspirin, Clopidogrel), low molecular weight Heparin, statin and medications helping protection of the brain parenchyma.An urgent endarterectomy of the left CCA and left ICA with patch plastic was done.
Laboratory tests revealed dyslipidemia. Echocardiography excluded the presence of thrombotic masses in the cardiac chambers. Color-coded duplex sonography showed a bifurcation thrombus with a distal-shaped tail creating highgraded stenosis, lying free in the lumen of the internal carotid artery with a total thrombus length – about 4 cm (fig. 1A). CTA of supraaortal arteries confirmed the presence of a free floating thrombus in the initial part of the left ICA (fig. 1B). Computed tomography of head showed small hypodense areas in the parenchyma of the left temporoparietal part of the brain. We began therapy with two antiplatelets (Aspirin, Clopidogrel), low molecular weight Heparin, statin and medications helping protection of the brain parenchyma.An urgent endarterectomy of the left CCA and left ICA with patch plastic was done.
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CTA of supraaortal brain arteries confirmed the presence of a free floating thrombus in
53-year-old male presented at the hospital with repeating IS in the area of the right MCA with light left-sided hemiparesis. He had been treated with antiplatelet, statin, and antihypertensive drugs, which achieved good control of blood pressure and lipid profile. CCDS detected a thrombus in the bifurcation of the right CCA, covering the initial part of the right ICA, leading to about 70-80% stenosis (fig. 2A). CTA of supraaortal brain arteries confirmed the presence of a free floating thrombus in
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Snoring and the risk of ischemic brain infarction. Stroke
Palomaki H. Snoring and the risk of ischemic brain infarction. Stroke
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PET with 18F-fluorodeoxyglucose (FDG-PET) assesses regional glucose metabolism in the brain.
Though consensus statements and guidelines recommend structural imaging methods such as computed tomography (CT) and magnetic resonance imaging (MRI) as standard techniques in dementia, more attention is currently being paid to functional imaging methods, including positron emission tomography (PET). In recent years PET is increasingly used in clinical neurology to understand disease pathogenesis, to aid diagnosis, and to monitor disease progression and response to treatment [27]. PET with 18F-fluorodeoxyglucose (FDG-PET) assesses regional glucose metabolism in the brain. Applied in subjects with cognitive impairment, it assures increased diagnostic accuracy, helps to establish the diagnosis in preclinical stages and to solve difficult cases [17].
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CT and MRI, known as structural imaging methods, are invaluable when structural brain lesions exist.
CT and MRI, known as structural imaging methods, are invaluable when structural brain lesions exist. However, they often provide normal or non-specific results when pathological alterations are only at a functional level, which is the case of most neurodegenerative diseases, especially in the early stages [24]. Such alterations can be detected by functional methods as PET and single photon emission tomography (SPECT) [2, 12]. These methods use either non-specific markers for metabolism/perfusion, or specific receptor and molecule markers. The latter are attractive for their specificity, but expensive, often hard to obtain, and not all are approved for clinical use. Because of the better resolution, PET tends to outperform perfusion SPECT in the workup of cognitive impairment and dementia [11].
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found decreased entorhinal cortex glucose metabolism at baseline to be the most accurate regional predictor of clinical change, as well as of further neocortical temporal lobe and hippocampal involvement, suggesting an “entorhinal cortex” stage of brain pathology that can be detected in normal elderly [18].
cognitive impairment or even AD [7]. Mosconi et al. found decreased entorhinal cortex glucose metabolism at baseline to be the most accurate regional predictor of clinical change, as well as of further neocortical temporal lobe and hippocampal involvement, suggesting an “entorhinal cortex” stage of brain pathology that can be detected in normal elderly [18]. Such findings suggest that FDG-PET may be useful in prevention studies for individuals at risk for dementia in the preclinical stage of Alzheimer’s disease [4]. The identification of asymptomatic individuals at risk could be even more important should an effective neuroprotective agent that can delay or prevent progression to AD become available in the future [7].
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Registration of brain FDG-PET can be done using PET or PET/CT, either in 2D or 3D mode, though the addition of CT is not as important as in oncology.
Registration of brain FDG-PET can be done using PET or PET/CT, either in 2D or 3D mode, though the addition of CT is not as important as in oncology. The attenuation correction technique is of great importance as using correction models from different vendors could lead to statistical differences between images. It is therefore appropriate to compare only images obtained by the same correction method. CT correction is often preferred as being the fastest and unsusceptible to emission photons from the patient [14, 10, 23].
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Patient preparation is of great importance for obtaining reliable results for FDG brain metabolism.
Patient preparation is of great importance for obtaining reliable results for FDG brain metabolism. Attention should be paid to blood glucose level, especially in diabetic patients. Hyperglycemia leads to decreased accumulation of FDG in the brain due to competition with blood glucose, resulting in deteriorated image quality. Patients should be at rest, in a quiet and darkened room, avoiding all activities, e.g. reading or talking. It is advisable to discontinue psychotropic drugs temporarily on the day of assessment [5].
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Hyperglycemia leads to decreased accumulation of FDG in the brain due to competition with blood glucose, resulting in deteriorated image quality.
Patient preparation is of great importance for obtaining reliable results for FDG brain metabolism. Attention should be paid to blood glucose level, especially in diabetic patients. Hyperglycemia leads to decreased accumulation of FDG in the brain due to competition with blood glucose, resulting in deteriorated image quality. Patients should be at rest, in a quiet and darkened room, avoiding all activities, e.g. reading or talking. It is advisable to discontinue psychotropic drugs temporarily on the day of assessment [5].
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In our study we used a Philips Gemini TF (Time Of Flight) PET/CT, 16 slice CT, LYSO crystal (PET) with a brain PET/CT – low dose
In our study we used a Philips Gemini TF (Time Of Flight) PET/CT, 16 slice CT, LYSO crystal (PET) with a brain PET/CT – low dose
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ползвахме: апарат Philips Gemini TF (Time Of Flight) PET/CT, 16 slice CT, LYSO crystal (PET); протокол: Вrain PET/CT – Low dose CT/3Dmode PET, single frame 10 min/frame; корекция на атенюацията: Low dose CT; реконструкция: Iterrative, Brain CTAC; инжектирана активност: 185mBq (възрастни); време на фиксация:
ползвахме: апарат Philips Gemini TF (Time Of Flight) PET/CT, 16 slice CT, LYSO crystal (PET); протокол: Вrain PET/CT – Low dose CT/3Dmode PET, single frame 10 min/frame; корекция на атенюацията: Low dose CT; реконструкция: Iterrative, Brain CTAC; инжектирана активност: 185mBq (възрастни); време на фиксация:
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Reconstruction: Iterrative, Brain CTAC.
CT/3D-mode PET, single frame 10 min/frame protocol. Attenuation correction: Low dose CT. Reconstruction: Iterrative, Brain CTAC. Injected activity: 185mBq (adults). Fixation time: ~60 min. Analysis: visual assessment, MIP, quantification with NeuroQ (v.3.0).
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Brain MRI (fig.
Clinical examination was normal. Neurological examination showed no focal signs. Neuropsychological assessment revealed moderate dementia: MMSE: 15/30, BNT short version: 10/15; 10 words list recall (3 trials): 0/10, 2/10, 4/10; constructional praxis: 8/11; 10 word delayed recall: 1/10, with 2 intrusions; word recognition: not applicable (patient unable to understand task); literal verbal fluency for 1 min (letter М): 0; The four instrumental activities of daily living score (4-IADL): 4/4 points, marked impairment. CERAD depression scale: 0 points, no depression. Brain MRI (fig. 1А) demonstrated cortical atrophy which was prominent in the left temporal lobe. PET/СТ with FDG (fig. 1B) provided evidence for temporal and parietal hypometabolism, more pronounced on the left, suggestive of Alzheimer’s disease.
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Brain MRI (fig.
depression scale: 0 points, no depression. Brain MRI (fig. 2А) demonstrated cortical atrophy. PET/СТ with FDG (fig. 2B) provided evidence for hypometabolism affecting the temporal and parietal lobes bilaterally, on both visual assessment and neuroquantification. An area of minor hypometabolism was found in the posterior cingulum. The findings were described as typical of Alzheimer’s disease.
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FDG-PET assessment of brain glucose metabolism is renowned in neurology, experimental and clinical dementology.
FDG-PET assessment of brain glucose metabolism is renowned in neurology, experimental and clinical dementology. The described cases of patients with AD and MCI illustrate its characteristics and potential for the first time in Bulgaria. Regardless of its high cost and yet limited clinical application, the method stands out with good tolerability, high sensitivity and specificity. It helps resolving difficult or atypical clinical cases. As demonstrated by the literature review, FDG-PET has a wide spectrum of applications. It contributes significantly to the progress of cognitive neuroscience and clinical practice for identifying preclinical and early stages of dementia and for evaluation of progression.
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Normal brain aging clinical, immunological, neuropsychological, and neuroimaging features.
Caserta MT, Bannon Y, Fernandez F, Giunta B, Schoenberg MR, Tan J. Normal brain aging clinical, immunological, neuropsychological, and neuroimaging features.
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Brain Imaging.
Fontaine S, Nordberg A. Brain Imaging. In: Gauthier S. (ed). Clinical Diagnosis and Management of Alzheimer‘s Disease. Martin Dunitz. London, 1996, 83-106.
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Automated PET/CT brain registration for accurate attenuation correction.
Khurshid K, Berger KL, McGough RJ. Automated PET/CT brain registration for accurate attenuation correction. Conf Proc IEEE Eng Med Biol Soc 2009:5805-5808.
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FDG-PET changes in brain glucose metabolism from normal cognition to pathologically verified Alzheimer‘s disease.
Mosconi L, Mistur R, Switalski R, Tsui WH, Glodzik L, Li Y, Pirraglia E, De SS, Reisberg B, Wisniewski T, de Leon MJ. FDG-PET changes in brain glucose metabolism from normal cognition to pathologically verified Alzheimer‘s disease.
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Brain 18F-FDG PET in the diagnosis of neurodegenerative dementias: comparison with perfusion SPECT and with clinical evaluations lacking nuclear imaging.
Silverman DH. Brain 18F-FDG PET in the diagnosis of neurodegenerative dementias: comparison with perfusion SPECT and with clinical evaluations lacking nuclear imaging.
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EANM procedure guidelines for PET brain imaging using [(18)F]FDG, version 2.
Varrone A, Asenbaum S, Vander BT, Booij J, Nobili F, Nagren K, Darcourt J, Kapucu OL, Tatsch K, Bartenstein P, Van LK. EANM procedure guidelines for PET brain imaging using [(18)F]FDG, version 2.
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www.kenes.com/brain
www.kenes.com/brain
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International Conference on Heart & Brain
International Conference on Heart & Brain
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www.kenes.com/heart-brain
www.kenes.com/heart-brain
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They are the basis of the recent progress in clarifying the structural and functional brain correlates of normal language functions.
The application of functional neuroimaging methods for assessment of language functions is an important step in the progress of theoretical and practical neuroscience towards overcoming the limitations of structural imaging. Providing information about the state and dynamics of general and local perfusion, metabolism, or cerebral activity, they are widely applied for evaluation of cognitive and more specifically, language functions. They are the basis of the recent progress in clarifying the structural and functional brain correlates of normal language functions. They are largely applied in diagnostics and follow-up of disorders leading to language disturbances. Understanding the specific values of every functional neuroimaging method (single photon emission tomography, positron emission tomography, functional magnetic resonance tomography, ultrasound neuroimaging and functional transcranial Doppler ultrasound) enables the creation of adequate diagnostic patterns for specific clinical cases.
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“Looking at how the brain works is not the same thing as looking at how the mind works”
“Looking at how the brain works is not the same thing as looking at how the mind works”
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They are the basis of the recent progress in clarifying the structural and functional brain correlates of normal language functions.
The application of functional neuroimaging methods (FNM) for assessment of language functions is an important step in the progress of theoretical and practical neuroscience for overcoming the limitations of structural imaging. Providing information about the state and dynamics of general and local perfusion, metabolism, or cerebral activity, they are widely applied in evaluation of cognitive and, more specifically, language functions. They are the basis of the recent progress in clarifying the structural and functional brain correlates of normal language functions. They are largely applied in the diagnostics and follow-up of disorders leading to language disturbances. Conforming to established traditions, aphasic speech phenomena in vascular cerebral lesions are subject to routine assessment but attention toward language pathology in other brain disorders (degenerative, demyelinating, neoplastic, etc.) is increasing. The spectrum of degenerative and cerebrovascular diseases nowadays tends to broaden its boundaries including disorders which have not been characterized by language or other cognitive pathology so far [1, 2, 14, 15, 24, 26, 29, 39, 45,
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Conforming to established traditions, aphasic speech phenomena in vascular cerebral lesions are subject to routine assessment but attention toward language pathology in other brain disorders (degenerative, demyelinating, neoplastic, etc.) is increasing.
The application of functional neuroimaging methods (FNM) for assessment of language functions is an important step in the progress of theoretical and practical neuroscience for overcoming the limitations of structural imaging. Providing information about the state and dynamics of general and local perfusion, metabolism, or cerebral activity, they are widely applied in evaluation of cognitive and, more specifically, language functions. They are the basis of the recent progress in clarifying the structural and functional brain correlates of normal language functions. They are largely applied in the diagnostics and follow-up of disorders leading to language disturbances. Conforming to established traditions, aphasic speech phenomena in vascular cerebral lesions are subject to routine assessment but attention toward language pathology in other brain disorders (degenerative, demyelinating, neoplastic, etc.) is increasing. The spectrum of degenerative and cerebrovascular diseases nowadays tends to broaden its boundaries including disorders which have not been characterized by language or other cognitive pathology so far [1, 2, 14, 15, 24, 26, 29, 39, 45,
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Neuroimaging studies of cognitive control in patients with focal brain lesions contribute to the understanding of brain cognitive systems functioning.
Data obtained by functional neuroimaging confirm and elucidate in detail the conception of stages, loci and mechanisms taking part in the production and perception of normal, variant, deviant, and mainly pathological speech. Morphological analysis of word forms from spontaneous or provoked speech of patients remains an important component of studies. Neurolinguistic analysis is also realized on the basis of lexical production of patients from different nosological groups. Such complex approach allows the knowledge of anatomic-functional correlates of the processes and subprocesses of lexical production to be expanded by the data obtained from event-related potentials and other neurophysiological methods [34, 35, 36, 40, 41, 70]. Neuroimaging studies of cognitive control in patients with focal brain lesions contribute to the understanding of brain cognitive systems functioning. Two distinct networks with dissociable resting state connectivity patterns have been identified. The independence of the network due to a double dissociation of lesion location in two different measures of network integrity can be demonstrated in patients with heterogeneous impairment of the networks: one, of functional correlations among the nods of the network, and the other, of within-node qualities of the network. It is thus becoming clear that the influence of anatomical impairment spreads out of the lesion field but remains within the existing network
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Technically and practically admissible brain activation has been registered in standard neuropsychological conditions in healthy individuals [5].
is one of the earliest FNM put into practice. It is used not only to document static images of hypoperfusion in hypofunction or atrophy of specific areas, but also to demonstrate blood flow changes as a result of provoked neuronal activity. Technically and practically admissible brain activation has been registered in standard neuropsychological conditions in healthy individuals [5]. Characteristic areas of hypoperfusion have been described in different dementias. The level of frontotemporal hypoperfusion on SPECT has recently been used as a reference for the assessment of dementia severity and feasibility of the modified clinical dementia rating scale for fronto-temporal lobar degeneration by the Consortium of Mayo Clinic and University of California FTLD-centers [10]. SPECT has been applied for studying primary progressive aphasia (PPA) together with neuropsychological assessment and MRI [71]. In cases of frontotemporal dementia (FTD) presenting with aphasia with neologisms and semantic memory impairment, and amyotrophic lateral sclerosis, developed 2 to 3 years later, SPECT would show bilateral frontal and sometimes anterior temporal hypoperfusion [68, 81].
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Single photon emission tomography plays a role in clarifying the mechanisms of cognitive pathology seen in brain atrophy, infarction in the territory of the superior cerebellar artery or posterior fossa neoplasms.
Single photon emission tomography plays a role in clarifying the mechanisms of cognitive pathology seen in brain atrophy, infarction in the territory of the superior cerebellar artery or posterior fossa neoplasms. Hypoperfusion is noted not only in the cerebellar hemispheres, but in the contralateral frontal lobe as well. A functional interruption of cerebello-cerebral tracts connecting the cerebellum with the frontal areas handling attention and planning processes is suspected. Hypoperfusion in specific areas, detected through SPECT, supports the hypothesis for a crossed cerebellocerebral diaschisis [23, 54, 59].
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allows the structural and functional brain correlates of different stages and processes of word finding to be determined.
allows the structural and functional brain correlates of different stages and processes of word finding to be determined. It is assumed that local changes are indicative of local synaptic activity. Word finding is related to the dorsolateral and medial parts of the left frontal lobe, and lexical processing, to the posterior part of the left temporal lobe around the Sylvian fissure. The lower lateral areas of the temporal cortex and lower-posterior parietal lobe also take part in the process of reaching the semantic areas. Cerebellar lesions are believed to influence phonemic aspects of word finding strategies while semantic mechanisms are spared [51, 83].
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allows assessment of cortical activity in nonlesioned brain areas associated with speech errors in aphasia.
allows assessment of cortical activity in nonlesioned brain areas associated with speech errors in aphasia. Specific speech errors are connected a spread cortical activity in aphasia of different type and severity. The production of phonemic errors is attributed to the left posterior perilesional, occipital and temporal areas, while similar activity in the right hemisphere is related to semantic errors [30]. Perfusion MRI areas depicts of hypoperfusion due to a specific dysfunction. The character and origin of speech errors related to interruption of access to semantics or lexical representations can thus be clarified. Relationship exists between the semantic deficit and the dysfunction or stroke of Broadmann area (BA) 22, as well as between semantic errors due to lexical access deficit and hypoperfusion or stroke in the left inferior temporal gyrus, BA 37 [14].
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Many questions concerning the dynamics of language processes in aphasia have been answered thanks to the intensive use of fMRI in studies of brain reorganization developed for Bulgaria to the impaired language functioning.
Many questions concerning the dynamics of language processes in aphasia have been answered thanks to the intensive use of fMRI in studies of brain reorganization developed for Bulgaria to the impaired language functioning. When lesions are small, recovery is usually good and supported by mechanisms of the left hemisphere. When much language eloquent cortex is damaged, structures of the right hemisphere take part in the recovery [16].
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Functional magnetic resonance imaging could also contribute to the study of brain plasticity after stoke by mapping the dynamics of brain reorganization.
Functional magnetic resonance imaging could also contribute to the study of brain plasticity after stoke by mapping the dynamics of brain reorganization. The illustration of brain activity in the process of recovery of some cognitive functions facilitates the clarification of brain function modifications [3].
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The illustration of brain activity in the process of recovery of some cognitive functions facilitates the clarification of brain function modifications [3].
Functional magnetic resonance imaging could also contribute to the study of brain plasticity after stoke by mapping the dynamics of brain reorganization. The illustration of brain activity in the process of recovery of some cognitive functions facilitates the clarification of brain function modifications [3].
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Brain areas have been identified where specific functional language loci and the main components of the lexical semantic system are situated (automatic activation of semantic representations, their strategic attainment and inhibition of competitors), the corresponding areas of activation being pointed out by functional magnetic resonance imaging [17, 33].
Brain areas have been identified where specific functional language loci and the main components of the lexical semantic system are situated (automatic activation of semantic representations, their strategic attainment and inhibition of competitors), the corresponding areas of activation being pointed out by functional magnetic resonance imaging [17, 33].
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New evidences of the thesis that naming is supported by a network of brain regions have been found through discriminant and linear regression analysis of diffusion and perfusion MRI showing varying degrees of hypoperfusion in specific target areas.
New evidences of the thesis that naming is supported by a network of brain regions have been found through discriminant and linear regression analysis of diffusion and perfusion MRI showing varying degrees of hypoperfusion in specific target areas. Different components of this network are required for different cognitive processes and representations of complex tasks [24].
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The assessment of brain perfusion in order
The assessment of brain perfusion in order
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The possibility of precise localization of brain areas responsible for language functions is especially important when a precise identification of the neoplasm site is needed or when it affects strategic language areas and treatment should be extremely conservative.
Neuro-oncological practice is not only a motivator out also a recipient of the attainments of language function assessment through FNM. fMRI is a renowned non-invasive technique for preoperative mapping of language areas. The possibility of precise localization of brain areas responsible for language functions is especially important when a precise identification of the neoplasm site is needed or when it affects strategic language areas and treatment should be extremely conservative. Two paradigms have been tested for estimation of speech lateralization and for visualization of cortical areas: naming a verb, appropriate to a given noun, and generation of words containing a given letter. These conditions provide results visualizing frontal and temporal speech areas, determining the dominant hemisphere [4, 27,
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Preoperative fMRI is optimal for localizing specific brain functions controlling the motor, sensory and language spheres [48].
Preoperative fMRI is optimal for localizing specific brain functions controlling the motor, sensory and language spheres [48]. Such assessment of language areas and functions alone, without direct brain mapping is though not recommended if important surgical decisions are to be made [67, 76].
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Such assessment of language areas and functions alone, without direct brain mapping is though not recommended if important surgical decisions are to be made [67, 76].
Preoperative fMRI is optimal for localizing specific brain functions controlling the motor, sensory and language spheres [48]. Such assessment of language areas and functions alone, without direct brain mapping is though not recommended if important surgical decisions are to be made [67, 76].
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From another point of view, brain autoregulation can be normal in patients with AD, but relatively insufficient, due to exreme fluctuations of blod pressure.
From another point of view, brain autoregulation can be normal in patients with AD, but relatively insufficient, due to exreme fluctuations of blod pressure. The variability of
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As an event-related neuroimaging method monitoring blood flow changes in middle cerebral arteries it has been applied for determining the brain lateralization of language and other cognitive functions.
Functional transcranial Doppler ultrasound (fTDU) with application of different tests is a complementary neuroimaging tool evaluating changes of blood perfusion caused by neuronal activation during cognitive assessment. Like other neuroimaging methods, sensitive to perfusion, such as PET and fMRI, fTDU is based on the close relationship between changes of cerebral blood flow and neuronal activity. This method assures much better temporal resolution compared to other neuroimaging techniques. Other advantages include low dependence on motion artifacts, easy application even in children and in uncooperative patients, and noninvasiveness. As an event-related neuroimaging method monitoring blood flow changes in middle cerebral arteries it has been applied for determining the brain lateralization of language and other cognitive functions. A significant increase in velocity has been registered in the dominant hemisphere during a cognitive task [8, 42]. At the same time, fTDU spectroscopy assures a more understandable picture of changes related to the influence of a given mental stimulus [25, 52].
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Changes in the reactivity of brain blood vessels may be important for reduction of cognitive capacity related to the hemisphere ipsilateral to carotid stenosis.
Changes in the reactivity of brain blood vessels may be important for reduction of cognitive capacity related to the hemisphere ipsilateral to carotid stenosis. Indications for surgical treatment of asymptomatic carotid stenosis should therefore be specified more precisely [72, 78].
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Neuroimaging in brain tumors.
Arbizu J, Dominguez P, Diez-Valle R, Vigil C, Garcia-Eulate R, Zubieta JL, Richter JA. Neuroimaging in brain tumors.
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Verbal fluency as a prefrontal activation probe: a validation study using 99mTc-ECD brain SPET.
Audenaert K, Brans B, Van LK, Lahorte P, Versijpt J van HK, Dierckx R. Verbal fluency as a prefrontal activation probe: a validation study using 99mTc-ECD brain SPET.
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Brain Lang
Brain Lang
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The FTLD-modified Clinical Dementia Rating scale is a reliable tool for defining disease severity in frontotemporal lobar degeneration: evidence from a brain SPECT study.
Borroni B, Agosti C, Premi E, Cerini C, Cosseddu M, Paghera B, Bellelli G, Padovani A. The FTLD-modified Clinical Dementia Rating scale is a reliable tool for defining disease severity in frontotemporal lobar degeneration: evidence from a brain SPECT study.
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Where (in the brain) do semantic errors come from?
Cloutman L, Gottesman R, Chaudhry P, Davis C, Kleinman JT, Pawlak M, Herskovits EH, Kannan V, Lee A, Newhart M, Heidler-Gary J, Hillis AE. Where (in the brain) do semantic errors come from?
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Brain
Brain
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Brain Lang
Brain Lang
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Brain
Brain
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Brain Res
Brain Res
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[Functional imaging for brain tumors (perfusion, DTI and MR spectroscopy)].
Essig M, Giesel F, Stieltjes B, Weber MA. [Functional imaging for brain tumors (perfusion, DTI and MR spectroscopy)].
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Hum Brain Mapp
Hum Brain Mapp
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Gonzalez-Darder JM, Gonzalez-Lopez P, Talamantes F, Quilis V, Cortes V, Garcia-March G, Roldan P Multimodal navigation in the functional microsurgical resection of intrinsic brain tumors located in eloquent motor areas: role of tractography.
Gonzalez-Darder JM, Gonzalez-Lopez P, Talamantes F, Quilis V, Cortes V, Garcia-March G, Roldan P Multimodal navigation in the functional microsurgical resection of intrinsic brain tumors located in eloquent motor areas: role of tractography.
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Brain Lang
Brain Lang
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Kozub J, Urbanik A, Chrzan R, Karcz P [Presurgical functional brain examination MR (fMRI)].
Kozub J, Urbanik A, Chrzan R, Karcz P [Presurgical functional brain examination MR (fMRI)].
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Frontal Assessment Battery and brain perfusion images in amnestic mild cognitive impairment.
Sakurai H, Iwamoto T. Frontal Assessment Battery and brain perfusion images in amnestic mild cognitive impairment.
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[Brain functional imaging of frontotemporal lobar degeneration].
Nakano S, Matsuda H. [Brain functional imaging of frontotemporal lobar degeneration].
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Brain Nerve
Brain Nerve
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Nomura EM, Gratton C, Visser RM, Kayser A, Perez F, D‘Esposito M Double dissociation of two cognitive control networks in patients with focal brain lesions.
Nomura EM, Gratton C, Visser RM, Kayser A, Perez F, D‘Esposito M Double dissociation of two cognitive control networks in patients with focal brain lesions.
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Recent advances in imaging of brain tumors.
Sanghvi DA. Recent advances in imaging of brain tumors.
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Brain
Brain
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Preoperative and intraoperative brain mapping for the resection of
Spena G, Nava A, Cassini F, Pepoli A, Bruno M, D‘Agata F, Cauda F, Sacco K, Duca S, Barletta L, Versari P. Preoperative and intraoperative brain mapping for the resection of
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Brain
Brain
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Hum Brain Mapp 2010, epub.
Wilke M, Pieper T, Lindner K, Dushe T, Staudt M, Grodd W, Holthausen H, Krageloh-Mann I. Clinical functional MRI of the language domain in children with epilepsy. Hum Brain Mapp 2010, epub.
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Protecting the brain from gaseous and solid micro-emboli during coronary artery bypass grafting: a randomized controlled trial.
nburg M. Protecting the brain from gaseous and solid micro-emboli during coronary artery bypass grafting: a randomized controlled trial.
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degree with the topic “Studies on the protein components of liquor and blood plasma and secretion of Cortisol, CTH and Insulin in acute covered brain traumas”.
In 1963 prof. Karakanev was acknowledged a specialty in neurology. In 1976 he acquired the Ph.D. degree with the topic “Studies on the protein components of liquor and blood plasma and secretion of Cortisol, CTH and Insulin in acute covered brain traumas”. He was assigned for Associate Professor in 1977 and for Professor of Neurology – in 1990.
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14. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 7, 2011, No. 2 , , ,

Hemineglect, Hemianopsia and Signs of Gerstmann Syndrome in Brain Lobar Parenchymal Hemorrhage –
Hemineglect, Hemianopsia and Signs of Gerstmann Syndrome in Brain Lobar Parenchymal Hemorrhage –
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Cerebral vasospasm is a dreaded complication of subarachnoid hemorrhage that can lead to brain infarction and in severe cases, death.
Cerebral vasospasm is a dreaded complication of subarachnoid hemorrhage that can lead to brain infarction and in severe cases, death. Angiography was at that time practically the only modality to diagnose the arterial narrowing caused by vasospasm. In Bern we were lucky to have a neuroradiologist, Prof. Peter Huber, who was an expert in this field and who had developed a technique to accurately measure the diameter of the intracranial arteries. A clear inverse relationship between the degree of angiographic spasm and the TCD velocities was found, and monitoring of cerebral vasospasm remains one of the most useful and widespread applications of the technique.
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Brain
Brain
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Hemineglect, Hemianopsia and Signs of Gerstmann Syndrome in Brain Lobar Parenchymal Hemorrhage –
Hemineglect, Hemianopsia and Signs of Gerstmann Syndrome in Brain Lobar Parenchymal Hemorrhage –
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brain hemorrhage, Gerstmann syndrome, hemianopsia, hemineglect
brain hemorrhage, Gerstmann syndrome, hemianopsia, hemineglect
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to follow up and differentiate neurological and neuropsychological symptoms in a patient with parenchymal brain hemorrhage, involving primary and associative visual cortex.
to follow up and differentiate neurological and neuropsychological symptoms in a patient with parenchymal brain hemorrhage, involving primary and associative visual cortex.
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Dynamics of neurological status, brain computer tomography scans, perimetry and neuropsychological testing were reported.
We present a case of a 63 years old woman suffered from lobar intracerebral hemorrhage with left-occipital localization, who experienced recent stenting of right coronary artery. The patient was prospectively followed up at first and sixth month of the stroke onset. Dynamics of neurological status, brain computer tomography scans, perimetry and neuropsychological testing were reported. Specialized neuropsychological battery of tests was used.
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Research on healthy volunteers and patients suggests that the right brain hemisphere is dominant for activation of spatial attention, therefore the hemineglect is more frequent and more severe in right hemisphere impairment, but it also occurs in left hemispherical damage [1, 10].
Unilateral neglect syndrome is a result of a broad neuronal cognitive net dysfunction, with cortical epicenter localized in the posterior parietal cortex, frontal visual fields and cingulate gyrus. This net coordinates the aspects of spatial attention, regardless of the input or output modality [10]. Research on healthy volunteers and patients suggests that the right brain hemisphere is dominant for activation of spatial attention, therefore the hemineglect is more frequent and more severe in right hemisphere impairment, but it also occurs in left hemispherical damage [1, 10]. Injury of left hemisphere is manifested mainly with executive and motivation deficits leading to unilateral neglect. Investigations about primary damage of subcortical structures or their secondary involvement due to hypometabolism of associated cortical zones are still ongoing [1].
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The objective of this study is to follow up and differentiate neurological and neuropsychological symptoms in a patient with parenchymal brain hemorrhage involving the primary and associative visual cortex.
The objective of this study is to follow up and differentiate neurological and neuropsychological symptoms in a patient with parenchymal brain hemorrhage involving the primary and associative visual cortex.
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Visual-spatial disorders in brain parenchymal hemorrhage
Visual-spatial disorders in brain parenchymal hemorrhage
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The patient was prospectively followed up on first and sixth month of the brain hemorrhage onset.
The patient was prospectively followed up on first and sixth month of the brain hemorrhage onset. Dynamics of neurological status, brain computed tomography (CT) findings, perimetry and results of neuropsychological testing were reported. A specialized neuropsychological battery based on Goodglass and Kaplan-Boston-1983 test for assessment of gnosis, praxis, language functions, memory and attention was used [4]. The test was adapted and validated for use in Bulgaria in 1995 by B. Alexandrova, M. Terzieva, I.
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Dynamics of neurological status, brain computed tomography (CT) findings, perimetry and results of neuropsychological testing were reported.
The patient was prospectively followed up on first and sixth month of the brain hemorrhage onset. Dynamics of neurological status, brain computed tomography (CT) findings, perimetry and results of neuropsychological testing were reported. A specialized neuropsychological battery based on Goodglass and Kaplan-Boston-1983 test for assessment of gnosis, praxis, language functions, memory and attention was used [4]. The test was adapted and validated for use in Bulgaria in 1995 by B. Alexandrova, M. Terzieva, I. Turnev and L. Mavlov.
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Brain CT scan visualized intracerebral hemorrhage in the left parietooccipital region with compression to occipital horn and corpus of left lateral ventricle with size 3/4/6 cm (fig. 1A).
Blood tests showed hypertriglyceridemia. Coagulation parameters were normal. ADP test for Clopidogrel sensitivity revealed slightly inhibited platelet aggregation. A chest X-ray found left ventricular extended arc, thickened and enlarged aorta. Brain CT scan visualized intracerebral hemorrhage in the left parietooccipital region with compression to occipital horn and corpus of left lateral ventricle with size 3/4/6 cm (fig. 1A).
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Brain CT scan:
Brain CT scan:
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and month after brain hemorrhage
and month after brain hemorrhage
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Line bisection in the acute period of brain hemorrhage with right spatial neglect
Line bisection in the acute period of brain hemorrhage with right spatial neglect
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Visual-spatial disorders in brain parenchymal hemorrhage
Visual-spatial disorders in brain parenchymal hemorrhage
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We observed the rare combination of hemineglect and hemianopsia, as well as Gerstmann syndrome due to brain hemorrhage in the left parietooccipital lobe.
The presented case is interesting because of its complex combination and difficult differentiation of simultaneously occurring visual and visual-spatial disturbances. We observed the rare combination of hemineglect and hemianopsia, as well as Gerstmann syndrome due to brain hemorrhage in the left parietooccipital lobe. Similar results are revealed by other authors [3, 5, 7, 10].
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Application of neuroimaging methods contributes to objectify the location, severity and type of damage in the brain parenchyma and its evolution.
The study shows that the diagnosis of enlarged Gerstmann syndrome with hemianopsia and hemineglect requires a multidisciplinary approach and is supported by the combined use of clinical, neuropsychological, neurophysiologic and ophthalmological examinations. The prospective monitoring is important. Application of neuroimaging methods contributes to objectify the location, severity and type of damage in the brain parenchyma and its evolution.
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Visual-spatial disorders in brain parenchymal hemorrhage
Visual-spatial disorders in brain parenchymal hemorrhage
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Brain
Brain
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Exp Brain Res
Exp Brain Res
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Brain
Brain
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Brain
Brain
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Two large, phase 3 trials – TRANSFORMS and FREEDOMS demonstrated that fingolimod improved the clinical outcome for MS patients – reduced the annualized relapse rate, decreased the risk of confirmed disability progression and reduced the number and volume of brain lesions on MRI images.
(fingolimod), is the first oral drug licensed by the European Medicines Agency as a single disease modifying therapy in highly active relapsing remitting multiple sclerosis (MS). Fingolimod mediates its therapeutic effects through the immune system and directly on the central nervous system (CNS). Fingolimod reduces the recirculation of auto-reactive central memory Tcells and their infiltration in the CNS, where they would cause neurodegeneration. Peripheral lymphocyte count reduction is reversible and reflects the reversible retention of circulating lymphocytes in lymph nodes, but not their depletion. Two large, phase 3 trials – TRANSFORMS and FREEDOMS demonstrated that fingolimod improved the clinical outcome for MS patients – reduced the annualized relapse rate, decreased the risk of confirmed disability progression and reduced the number and volume of brain lesions on MRI images.
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Fingolimod can cross the blood–brain barrier into CNS where S1PRs are expressed, and is present in CNS following oral administration [11].
Fingolimod can cross the blood–brain barrier into CNS where S1PRs are expressed, and is present in CNS following oral administration [11]. S1PR modulation by fingolimod is highly effective in numerous experimental autoimmune encephalomyelitis (EAE) models of MS in any stage of the disease [12]. The results show that fingolimod improves neuronal electrophysiological function, reduces motor impairment, decreases demyelination in CNS and restores the integrity of the blood–brain barrier [3]. In MS animal models fingolimod reduces demyelination and microglia activation in CNS in intact blood–brain barrier, indicating effects independent of lymphocyte infiltration [2]. Consistent with EAE models, S1PR modulation by fingolimod in patients with relapsing remitting MS has been shown to reduce disease progression, relapse activity and rate of brain atrophy compared to placebo or approved interferon β-1a therapy [9, 14].
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The results show that fingolimod improves neuronal electrophysiological function, reduces motor impairment, decreases demyelination in CNS and restores the integrity of the blood–brain barrier [3].
Fingolimod can cross the blood–brain barrier into CNS where S1PRs are expressed, and is present in CNS following oral administration [11]. S1PR modulation by fingolimod is highly effective in numerous experimental autoimmune encephalomyelitis (EAE) models of MS in any stage of the disease [12]. The results show that fingolimod improves neuronal electrophysiological function, reduces motor impairment, decreases demyelination in CNS and restores the integrity of the blood–brain barrier [3]. In MS animal models fingolimod reduces demyelination and microglia activation in CNS in intact blood–brain barrier, indicating effects independent of lymphocyte infiltration [2]. Consistent with EAE models, S1PR modulation by fingolimod in patients with relapsing remitting MS has been shown to reduce disease progression, relapse activity and rate of brain atrophy compared to placebo or approved interferon β-1a therapy [9, 14].
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In MS animal models fingolimod reduces demyelination and microglia activation in CNS in intact blood–brain barrier, indicating effects independent of lymphocyte infiltration [2].
Fingolimod can cross the blood–brain barrier into CNS where S1PRs are expressed, and is present in CNS following oral administration [11]. S1PR modulation by fingolimod is highly effective in numerous experimental autoimmune encephalomyelitis (EAE) models of MS in any stage of the disease [12]. The results show that fingolimod improves neuronal electrophysiological function, reduces motor impairment, decreases demyelination in CNS and restores the integrity of the blood–brain barrier [3]. In MS animal models fingolimod reduces demyelination and microglia activation in CNS in intact blood–brain barrier, indicating effects independent of lymphocyte infiltration [2]. Consistent with EAE models, S1PR modulation by fingolimod in patients with relapsing remitting MS has been shown to reduce disease progression, relapse activity and rate of brain atrophy compared to placebo or approved interferon β-1a therapy [9, 14].
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Consistent with EAE models, S1PR modulation by fingolimod in patients with relapsing remitting MS has been shown to reduce disease progression, relapse activity and rate of brain atrophy compared to placebo or approved interferon β-1a therapy [9, 14].
Fingolimod can cross the blood–brain barrier into CNS where S1PRs are expressed, and is present in CNS following oral administration [11]. S1PR modulation by fingolimod is highly effective in numerous experimental autoimmune encephalomyelitis (EAE) models of MS in any stage of the disease [12]. The results show that fingolimod improves neuronal electrophysiological function, reduces motor impairment, decreases demyelination in CNS and restores the integrity of the blood–brain barrier [3]. In MS animal models fingolimod reduces demyelination and microglia activation in CNS in intact blood–brain barrier, indicating effects independent of lymphocyte infiltration [2]. Consistent with EAE models, S1PR modulation by fingolimod in patients with relapsing remitting MS has been shown to reduce disease progression, relapse activity and rate of brain atrophy compared to placebo or approved interferon β-1a therapy [9, 14].
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International Conference on Heart & Brain
International Conference on Heart & Brain
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www.kenes.com/heart-brain
www.kenes.com/heart-brain
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15. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 8, 2012, No. 1 , , ,

Thrombosis of the false lumen occurs often in case of blind ending of dissection, which is a potential source of emboli to the brain.
it can cause acute arterial obstruction, ranging from stenosis to thrombosis, late aneurysm or embolic events. Thrombosis of the false lumen occurs often in case of blind ending of dissection, which is a potential source of emboli to the brain. In re-rupture of the flap a fenestra (communication between the two lumens) is formed, through which blood flow returns to the true lumen. In a small diameter fenestra, the increased pressure in the false lumen causes narrowing or occlusion of the "true lumen" [10]. Large traumatic lesions of the tunica intima (6-8 mm) are a common cause of extensive intramural thrombus, which can cause obstruction of the arterial lumen or spontaneous recanalization. In 60% of acute dissections an intramural pseudolumen is detected by angiography.
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The brain computed tomography was negative.
In the first postoperative day the patient had labile blood pressure with hypertensive crisis to 240/160 mm Hg, accompanied by severe headache and photophobia. The brain computed tomography was negative. In the following weeks he complained of pain in the left neck, associated with increasing blood pressure. The patient was instructed to perform a regular sonographic examination on the 30
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Dissection can be completely asymptomatic in case with good collateral circulation or complicated with atherothrombosis, which is a potential source of emboli to the brain.
carotid dissection causes ischemic stroke without preceding symptoms and/or symptoms of cerebral edema. The Initial thrombosis can quickly pass into arterial stenosis or spontaneous improvement. Dissection can be completely asymptomatic in case with good collateral circulation or complicated with atherothrombosis, which is a potential source of emboli to the brain. In 60% of cases with acute carotid dissections the neuroimaging methods detect ischemic changes in the brain parenchyma.
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In 60% of cases with acute carotid dissections the neuroimaging methods detect ischemic changes in the brain parenchyma.
carotid dissection causes ischemic stroke without preceding symptoms and/or symptoms of cerebral edema. The Initial thrombosis can quickly pass into arterial stenosis or spontaneous improvement. Dissection can be completely asymptomatic in case with good collateral circulation or complicated with atherothrombosis, which is a potential source of emboli to the brain. In 60% of cases with acute carotid dissections the neuroimaging methods detect ischemic changes in the brain parenchyma.
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Transcranial magnetic stimulation is a noninvasive neurophysiologic method for stimulation of brain motor cortex based on electromagnetic induction.
Transcranial magnetic stimulation is a noninvasive neurophysiologic method for stimulation of brain motor cortex based on electromagnetic induction. It is subdivided on transcranial and peripheral in dependence of tаrget anatomical structures. The method gives information about corticospinal conductivity, promotes topical diagnosis, determination of its severity and prognostic value about recovery. The method is applicable in the diagnosis and treatment of different diseases in Neurology, Psychiatry and Neurosurgery.
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Brain cortex, nerve roots, plexuses, cranial and peripheral nerves stimulation by rapidly changing magnetic field leads to depolarization and hyperpolarization of neurons and induces well detectable weak electric currents.
Magnetic stimulation (MS) is a noninvasive neurophysiologic method of studying the functions and relations in nervous system using electromagnetic induction. It is divided on transcranial (TMS) and peripheral (PMS) depending on target anatomical structures. Brain cortex, nerve roots, plexuses, cranial and peripheral nerves stimulation by rapidly changing magnetic field leads to depolarization and hyperpolarization of neurons and induces well detectable weak electric currents. Since its introduction in 1985 this method has undergone a large development and has given new perspectives in pathophysiology, diagnostics and therapy of different diseases in Neurology, Psychiatry and Neurosurgery.
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field reaches the brain and induces oppositely directed secondary ion currents in tissues.
field reaches the brain and induces oppositely directed secondary ion currents in tissues. For this reason TMS is called a “non-electrode” electrical stimulation and the magnetic field is the mediator between the two electrical currents (in the coil and in the brain). This manipulation is painless and does not require analgesics or anesthesia. Rarely, patients complain of mild headache or discomfort at stimulation side. So called “impact-effect” is produced when the coil is placed on the primary motor cortex. A single intensive impulse causes a non-voluntary motor reaction in contralateral muscles.
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For this reason TMS is called a “non-electrode” electrical stimulation and the magnetic field is the mediator between the two electrical currents (in the coil and in the brain).
field reaches the brain and induces oppositely directed secondary ion currents in tissues. For this reason TMS is called a “non-electrode” electrical stimulation and the magnetic field is the mediator between the two electrical currents (in the coil and in the brain). This manipulation is painless and does not require analgesics or anesthesia. Rarely, patients complain of mild headache or discomfort at stimulation side. So called “impact-effect” is produced when the coil is placed on the primary motor cortex. A single intensive impulse causes a non-voluntary motor reaction in contralateral muscles. The minimal stimulus (percentile of 2T) needed to cause a non-voluntary movement in a given muscle group or an EMG response bigger than 20 µV is called a “motor threshold” and has large individual physiologic variations [43].
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The stimulation of any part of brain cortex provokes different effects according to the functional activity of stimulated area [41, 15].
– leads to depolarization of underlying neurons and induces an action potential. The stimulation of primary motor cortex causes muscular activity – a motor evoked potential, recorded by EMG. The stimulation of any part of brain cortex provokes different effects according to the functional activity of stimulated area [41, 15].
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They cause long-lasting changes in brain cortex activity (lasting from minutes to hours).
– repetitive impulses are applied. They cause long-lasting changes in brain cortex activity (lasting from minutes to hours). The effect may be inhibitory or excitatory. Low rate stimulation (1 Hz) decreases while this with 5 Hz increases temporarily brain cortex activity. It is accepted that the physiologic mechanism is close to long-lasting facilitation and inhibition [16].
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Low rate stimulation (1 Hz) decreases while this with 5 Hz increases temporarily brain cortex activity.
– repetitive impulses are applied. They cause long-lasting changes in brain cortex activity (lasting from minutes to hours). The effect may be inhibitory or excitatory. Low rate stimulation (1 Hz) decreases while this with 5 Hz increases temporarily brain cortex activity. It is accepted that the physiologic mechanism is close to long-lasting facilitation and inhibition [16].
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Magnetic field stimulates brain cortex neurons and generates series of descending corticospinal impulses.
Magnetic field stimulates brain cortex neurons and generates series of descending corticospinal impulses. Summarized temporal and spatial activity convenes to the spinal motor neurons and leads to MEP generation. The MEP consists of a direct D-wave (probably generated by the axonal hill of cortical neurons) and several indirect I-waves with 10 ms duration (on intervals of 1.5-2.0 ms) [18, 48]. Their origin is not well understood. It is supposed that they are a result
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brain cortex silent period
brain cortex silent period
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estimation of conduction time from brain cortex to spinal motor neurons in anterior corn
estimation of conduction time from brain cortex to spinal motor neurons in anterior corn
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It is the conduction time from brain cortex to anterior corn spinal motor neurons.
It is the conduction time from brain cortex to anterior corn spinal motor neurons. MEP latency from the stimulus to the start of response is measured first. Peripheral motor conduction time (motor root
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Brain strokes.
Brain strokes.
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MEP changes show the loss of rapidly propagating corticospinal neurons and prolonged CMCT – slowed conductivity in brain lesion due to big myelinated axons damage.
In mild paresis there is a prolongation of CMCT and reduction of MEP amplitude at the motor disturbance side. In severe paresis MEP is not registered [5, 12]. Cortical strokes change CMCT and MEP according to the number and type of preserved corticospinal relations capable of generating response. MEP changes show the loss of rapidly propagating corticospinal neurons and prolonged CMCT – slowed conductivity in brain lesion due to big myelinated axons damage. The MEP amplitude has a prognostic value for recovery – the higher amplitude correlates with the better prognosis [11, 21, 52]. The motor threshold in the damaged hemisphere is higher and in the healthy hemisphere – lower than normal, probably due to the lack of inhibitory influence from injured areas. A lower motor threshold and higher MEP amplitude in the healthy hemisphere indicates a more severe damage of the other hemisphere [10]. In the recovery phase of stroke the “silent period” could be estimated – its shortage correlates with the level of spasticity [56]. This period is shortened only in strokes of primary motor cortex.
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All patients had cortical defects on brain convexity [27].
In experimental conditions, low frequency rTMS (0.5 Hz) reduces the incidence of epileptic status and prolongs the latency of pentilentetrazol-induced seizures in rats. The results from the application of low frequency rTMS in clinical conditions range from optimistic (reduction in seizure frequency by 36.2%) in uncontrolled studies to moderate and not very reliable in controlled randomized trials [2, 27]. In a controlled blind study on 24 patients with focal epilepsy (temporal and extratemporal) and a coil located on the epileptogenic focus, a statistically significant change in relapse frequency was not found. A better effect was observed in neocortical than in mesiotemporal focuses [50]. A randomized, controlled clinical trial with simulated rTMS found a statistically significant reduction in EEG epileptiform activity and improvement in some aspects of cognitive activity lasting about 2 months after stimulation. All patients had cortical defects on brain convexity [27]. The response of surface and neocortical temporal foci correlates with the modern capabilities of TMS – the intensity of the induced electric field decreases rapidly in depth. The introduction of a new design of the stimulating coil, called H-coil would improve the stimulation of deep epileptogenic foci (distance of 5 cm from the scalp). It was found that rTMS is well tolerated by patients and side effects are mild (17.1%). The most frequent complication is headache. Repetitive TMS poses little risk of inducing seizures in strict compliance with approved work instructions [5].
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This allowed precise localization of areas subject to stimulation and evaluation of TMS-induced anatomical and functional effects on the brain.
Recently, in scientific practice combined functional MRI (fMRT) and neuronavigated TMS were introduced. This allowed precise localization of areas subject to stimulation and evaluation of TMS-induced anatomical and functional effects on the brain. TMS-induced metabolic changes can be measured using PET and changes in blood oxygen saturation – with fMRT. Both methods have short-term effectiveness: seconds for fMRT and up to five minutes for PET, so that brain responses in the first 10 ms after the stimulus are ignored. Promising prospects for solving this problem is the simultaneous application of TMS and EEG, offering high resolution in time and evaluation of cortical reactivity and connections [45]. Induced by TMS EEG responses are with specific latency and high spatial and temporal resolution. This allows evaluation of impulse spreading through intra-and interhemispheric corticocortical fibers.
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Both methods have short-term effectiveness: seconds for fMRT and up to five minutes for PET, so that brain responses in the first 10 ms after the stimulus are ignored.
Recently, in scientific practice combined functional MRI (fMRT) and neuronavigated TMS were introduced. This allowed precise localization of areas subject to stimulation and evaluation of TMS-induced anatomical and functional effects on the brain. TMS-induced metabolic changes can be measured using PET and changes in blood oxygen saturation – with fMRT. Both methods have short-term effectiveness: seconds for fMRT and up to five minutes for PET, so that brain responses in the first 10 ms after the stimulus are ignored. Promising prospects for solving this problem is the simultaneous application of TMS and EEG, offering high resolution in time and evaluation of cortical reactivity and connections [45]. Induced by TMS EEG responses are with specific latency and high spatial and temporal resolution. This allows evaluation of impulse spreading through intra-and interhemispheric corticocortical fibers. The introduction of new simulation techniques and equipment, and the identification of optimal simulation parameters would lead to more pronounced and long lasting therapeutic effects.
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In recent decades it has been shown that the adult human brain has some capacity for plastic reorganization and functional recovery after injury.
In recent decades it has been shown that the adult human brain has some capacity for plastic reorganization and functional recovery after injury. TMS is one of modern methods for noninvasive somatotopic cortical localization of motor functions and study of the functional reorganization of affected motor areas. Together with other neuroimaging techniques, it helps for a more detailed study of these processes and tracks the results of the therapy and rehabilitation. The future of TMS is to modify and streamline
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the process of brain reorganization and control the development of complex rehabilitation programs.
the process of brain reorganization and control the development of complex rehabilitation programs.
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Brain
Brain
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Brain
Brain
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Brain
Brain
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Transcranial magnetic stimulation and the human brain.
Hallett M. Transcranial magnetic stimulation and the human brain.
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Brain
Brain
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Magnetic brain stimulation: central motor conduction studies in multiple sclerosis.
Hess CW, Mills KR, Murray NMF, Schriefer TN. Magnetic brain stimulation: central motor conduction studies in multiple sclerosis.
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Brain
Brain
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Brain
Brain
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Brain and Language
Brain and Language
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Transcranial magnetic stimulation: studying the brain-behaviour relationship by induction of ‘virtual lesions’.
Pascual-Leone A, Bartrés-Faz D, Keenan JP. Transcranial magnetic stimulation: studying the brain-behaviour relationship by induction of ‘virtual lesions’.
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Pharmacological changes in the silent period after transcranial brain stimulation in normal subjects, patients with Parkinson`s disease and drug-induced parkinsonism.
Pharmacological changes in the silent period after transcranial brain stimulation in normal subjects, patients with Parkinson`s disease and drug-induced parkinsonism.
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Brain
Brain
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Brain stimulation for epilepsy.
Theodore WH, Fisher RS. Brain stimulation for epilepsy.
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Brain
Brain
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Inhibitory actions of motor cortex following unilateral brain lesions as studied by magnetic brain stimulation.
Von Giesen HJ, Roick H, Benecke R. Inhibitory actions of motor cortex following unilateral brain lesions as studied by magnetic brain stimulation.
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Exp Brain Res
Exp Brain Res
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It could provoke hemodynamic impairment which in turn could lead to a critical decrease cardiac output and brain perfusion [2].
The most common reason for cardiac syncope is arrhythmia. It could provoke hemodynamic impairment which in turn could lead to a critical decrease cardiac output and brain perfusion [2]. In sick-sinus syndrome, due to
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It has been proved that liquor investigation, Doppler-sonography of carotid arteries, cerebral angiography, brain computed tomography and electroencephalography do not contribute to the diagnostic work-up in the absence of clinical signs of a neurological disease.
syncope includes a thorough anamnesis, physical examination and some basic laboratory parameters. Cardio-vascular system evaluation is of paramount importance for the further diagnostic and therapeutic work-up, as well as for prognosis, and includes: 12-lead ECG, continuous ECG monitoring – in-hospital or ambulatory with Holter ECG, implantable loop-event recorders, telemonitoring, electrophysiological study, signal-averaged ECG, carotid sinus massage, echocardiography, stress ECG test, tilt-table test. It has been proved that liquor investigation, Doppler-sonography of carotid arteries, cerebral angiography, brain computed tomography and electroencephalography do not contribute to the diagnostic work-up in the absence of clinical signs of a neurological disease. Nevertheless neurological examination is warranted in case of a clinical suspicion of neurological disease, as well as when traumatic brain damage could not be ruled out. Psychiatric patients’ evaluation is appropriate in cases of multifold recurrent episodes of loss of consciousness in young adults and other co-existing nonspecific complaints.
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Nevertheless neurological examination is warranted in case of a clinical suspicion of neurological disease, as well as when traumatic brain damage could not be ruled out.
syncope includes a thorough anamnesis, physical examination and some basic laboratory parameters. Cardio-vascular system evaluation is of paramount importance for the further diagnostic and therapeutic work-up, as well as for prognosis, and includes: 12-lead ECG, continuous ECG monitoring – in-hospital or ambulatory with Holter ECG, implantable loop-event recorders, telemonitoring, electrophysiological study, signal-averaged ECG, carotid sinus massage, echocardiography, stress ECG test, tilt-table test. It has been proved that liquor investigation, Doppler-sonography of carotid arteries, cerebral angiography, brain computed tomography and electroencephalography do not contribute to the diagnostic work-up in the absence of clinical signs of a neurological disease. Nevertheless neurological examination is warranted in case of a clinical suspicion of neurological disease, as well as when traumatic brain damage could not be ruled out. Psychiatric patients’ evaluation is appropriate in cases of multifold recurrent episodes of loss of consciousness in young adults and other co-existing nonspecific complaints.
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brain injury, brain plasticity,
brain injury, brain plasticity,
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brain reorganization, neurorehabilitation
brain reorganization, neurorehabilitation
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Numerous surveys reveal that even limited, the ability of the human brain to reorganize itself continues throughout life which is associated with brain plasticity on two functional levels: sensorimotor cortex (cortex plasticity) and neural network (neural plasticity).
The traditional concept that the central nervous system (CNS) does not regenerate after injury evolved over the last 15 years. Numerous surveys reveal that even limited, the ability of the human brain to reorganize itself continues throughout life which is associated with brain plasticity on two functional levels: sensorimotor cortex (cortex plasticity) and neural network (neural plasticity). Drug and non-drug effects of treatment model the brain plasticity and facilitate the process of structural and functional brain reorganization which determines the ability of continuous functional recovery following brain injury [32]. The recovery potential increases when combining motor retraining, pharmacotherapy, stimulating techniques and cell therapy [20]. The changes in brain activity can be objectified by appropriate functional neuroimaging and electrophysiological methods [13].
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Drug and non-drug effects of treatment model the brain plasticity and facilitate the process of structural and functional brain reorganization which determines the ability of continuous functional recovery following brain injury [32].
The traditional concept that the central nervous system (CNS) does not regenerate after injury evolved over the last 15 years. Numerous surveys reveal that even limited, the ability of the human brain to reorganize itself continues throughout life which is associated with brain plasticity on two functional levels: sensorimotor cortex (cortex plasticity) and neural network (neural plasticity). Drug and non-drug effects of treatment model the brain plasticity and facilitate the process of structural and functional brain reorganization which determines the ability of continuous functional recovery following brain injury [32]. The recovery potential increases when combining motor retraining, pharmacotherapy, stimulating techniques and cell therapy [20]. The changes in brain activity can be objectified by appropriate functional neuroimaging and electrophysiological methods [13].
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The changes in brain activity can be objectified by appropriate functional neuroimaging and electrophysiological methods [13].
The traditional concept that the central nervous system (CNS) does not regenerate after injury evolved over the last 15 years. Numerous surveys reveal that even limited, the ability of the human brain to reorganize itself continues throughout life which is associated with brain plasticity on two functional levels: sensorimotor cortex (cortex plasticity) and neural network (neural plasticity). Drug and non-drug effects of treatment model the brain plasticity and facilitate the process of structural and functional brain reorganization which determines the ability of continuous functional recovery following brain injury [32]. The recovery potential increases when combining motor retraining, pharmacotherapy, stimulating techniques and cell therapy [20]. The changes in brain activity can be objectified by appropriate functional neuroimaging and electrophysiological methods [13].
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Cognitive disorders, behavioral and emotional changes arising directly or as a result of injury may hamper rehabilitation and brain recovery [9].
Cognitive disorders, behavioral and emotional changes arising directly or as a result of injury may hamper rehabilitation and brain recovery [9]. Impairments of concentration of attention and memory and occurrence of depression limit patient’s independence and have an adverse effect on his rehabilitation if not diagnosed and treated properly [31]. Selective inhibitors of serotonin, mirtazapine and tetracyclic antidepressants are used to treat depression in combination with psychotherapy [19]. In cases of frontal lobe syndromes beta blockers, dopamine agonists, more recent atypical antipsychotics and stimulating techniques are used [12]. In children and young people with diffuse brain injuries and increased risk of psychiatric complications and slow cognitive development, drug treatment is supported by adapted educational programs.
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In children and young people with diffuse brain injuries and increased risk of psychiatric complications and slow cognitive development, drug treatment is supported by adapted educational programs.
Cognitive disorders, behavioral and emotional changes arising directly or as a result of injury may hamper rehabilitation and brain recovery [9]. Impairments of concentration of attention and memory and occurrence of depression limit patient’s independence and have an adverse effect on his rehabilitation if not diagnosed and treated properly [31]. Selective inhibitors of serotonin, mirtazapine and tetracyclic antidepressants are used to treat depression in combination with psychotherapy [19]. In cases of frontal lobe syndromes beta blockers, dopamine agonists, more recent atypical antipsychotics and stimulating techniques are used [12]. In children and young people with diffuse brain injuries and increased risk of psychiatric complications and slow cognitive development, drug treatment is supported by adapted educational programs.
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Dysphagia and cortical impairments are frequent symptoms in brain injuries caused by stroke, traumas and other etiological factors.
Speech disorders combined with cognitive deficit hamper considerably patients’ communication. Diagnosing aphasia is sometimes impossible when there is a slight defect, apraxia and agnosia [28]. Dysphagia and cortical impairments are frequent symptoms in brain injuries caused by stroke, traumas and other etiological factors.
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New technology is available to promote supportive activities and reduce isolation following brain injury [14].
The clinician assists the patient in answering the question, "What can you actively do to ensure that your deficits interfere as little as possible with what you want to do? " [35]. Involvement, support and carry over provided by the individual's support system are integral parts of the treatment plan. New technology is available to promote supportive activities and reduce isolation following brain injury [14].
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Modifications of constraint-induced movement therapy are becoming standards of care for brain injury patients after the "plateau" phase (fig.
Over the last decade a lot of new methods have been used to achieve a better function in affected limb – classical and new dynamic ortheses with electric stimulation, spring and robotic mechanisms, visual stimulation, etc. (fig. 1) [29]. Modifications of constraint-induced movement therapy are becoming standards of care for brain injury patients after the "plateau" phase (fig. 2) [15]. For the purposes of aesthetics and easy movement, however, a light material is used which makes the product more expensive and hardly affordable for common use [39].
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Occurrence of any syncope incidents, heart arrhythmia or ischemia, pulmonary embolism and faints are kept under observation.Antihypertensive medications for optimal mean arterial pressure and adequate brain perfusion are used [41].
Occurrence of any syncope incidents, heart arrhythmia or ischemia, pulmonary embolism and faints are kept under observation.Antihypertensive medications for optimal mean arterial pressure and adequate brain perfusion are used [41].
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The technological progress in Medicine and Neurorehabilitation allows introduction of new approaches for stimulation of the processes of regeneration, brain plasticity and reorganization.
The technological progress in Medicine and Neurorehabilitation allows introduction of new approaches for stimulation of the processes of regeneration, brain plasticity and reorganization. Applying hypothermia in acute period of brain injury enhances the clinical outcome. Amphetamine may improve recovery after stroke when
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Applying hypothermia in acute period of brain injury enhances the clinical outcome.
The technological progress in Medicine and Neurorehabilitation allows introduction of new approaches for stimulation of the processes of regeneration, brain plasticity and reorganization. Applying hypothermia in acute period of brain injury enhances the clinical outcome. Amphetamine may improve recovery after stroke when
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Benzodiazepines and antipsychotics appear to slow recovery after traumatic brain injury and stroke.
combined with a therapy program. Dopaminergic and acetylcholinesterase inhibitors improve memory. Benzodiazepines and antipsychotics appear to slow recovery after traumatic brain injury and stroke. Modern neuroimaging technologies allow monitoring of neurophysiologic changes and expand the knowledge about the factors affecting the rehabilitation processes [4].
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It has been shown that reduced activation of the ipsilateral hemisphere improves motor function in both healthy individuals and those with traumatic brain injury or stroke.
It has been shown that reduced activation of the ipsilateral hemisphere improves motor function in both healthy individuals and those with traumatic brain injury or stroke. The combined use of transcranial magnetic stimulation improves cortical activation and may be a useful therapy adjunct [27]. Robot-assisted practice may be helpful by implementation of repetitive training tasks; body weight-supported treadmill training promotes gait improvement after traumatic brain injury, stroke or partial spinal cord injury (fig. 3). An important fact is that general aerobic exercise programs stimulate CNS plasticity. Functional electrical stimulation enhances somatosensory input to the brain. Continued activity and training after formal therapy is necessary to preserve functional gains [17].
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Robot-assisted practice may be helpful by implementation of repetitive training tasks; body weight-supported treadmill training promotes gait improvement after traumatic brain injury, stroke or partial spinal cord injury (fig. 3).
It has been shown that reduced activation of the ipsilateral hemisphere improves motor function in both healthy individuals and those with traumatic brain injury or stroke. The combined use of transcranial magnetic stimulation improves cortical activation and may be a useful therapy adjunct [27]. Robot-assisted practice may be helpful by implementation of repetitive training tasks; body weight-supported treadmill training promotes gait improvement after traumatic brain injury, stroke or partial spinal cord injury (fig. 3). An important fact is that general aerobic exercise programs stimulate CNS plasticity. Functional electrical stimulation enhances somatosensory input to the brain. Continued activity and training after formal therapy is necessary to preserve functional gains [17].
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Functional electrical stimulation enhances somatosensory input to the brain.
It has been shown that reduced activation of the ipsilateral hemisphere improves motor function in both healthy individuals and those with traumatic brain injury or stroke. The combined use of transcranial magnetic stimulation improves cortical activation and may be a useful therapy adjunct [27]. Robot-assisted practice may be helpful by implementation of repetitive training tasks; body weight-supported treadmill training promotes gait improvement after traumatic brain injury, stroke or partial spinal cord injury (fig. 3). An important fact is that general aerobic exercise programs stimulate CNS plasticity. Functional electrical stimulation enhances somatosensory input to the brain. Continued activity and training after formal therapy is necessary to preserve functional gains [17].
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Traumatic brain injuries.
Traumatic brain injuries.
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Treatment is directed towards reduction of complications following traumatic brain injury (TBI).
Treatment is directed towards reduction of complications following traumatic brain injury (TBI). The recovery prognosis correlates with the duration of posttraumatic amnesia [43]. Cognitive and behavioral changes and disorders of executive functions are common in traumatic injuries of the frontal lobe [37], which may cause mental retardation in children. Impaired social functions of patients worsen the long-term family relations. Cognitive and behavioral deficits prevent returning to school or work environment. Even though the sequence of recovery after TBI follows a certain model, it is a heterogeneous disorder and rehabilitation programs must be adapted to patient’s individual needs – change of environment, training of relatives.
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Pharmacotherapy plays a considerable role in long-term prognosis in traumatic and vascular brain injuries [10].
The recovery prognosis correlates with the duration of posttraumatic amnesia [43]. Cognitive and behavioral changes and disorders of executive functions are common in traumatic injuries of the frontal lobe [37], which may cause mental retardation in children. Impaired social functions of patients worsen the long-term family relations. Cognitive and behavioral deficits prevent returning to school or work environment. Even though the sequence of recovery after TBI follows a certain model, it is a heterogeneous disorder and rehabilitation programs must be adapted to patient’s individual needs – change of environment, training of relatives. Pharmacotherapy plays a considerable role in long-term prognosis in traumatic and vascular brain injuries [10].
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Recovery depends on the location, severity and type of the spinal cord injury, genetic possibilities for brain reorganization, adequacy of provided intensive care and neuroprotection, degree of spinal cord regeneration and possibilities of cell transplantation.
Clinical trials of animal models suggest that only a small number (5% to 10%) of surviving axons are needed to support functional recovery. Recovery depends on the location, severity and type of the spinal cord injury, genetic possibilities for brain reorganization, adequacy of provided intensive care and neuroprotection, degree of spinal cord regeneration and possibilities of cell transplantation. Gray matter hypoperfusion and axonal demyelization areas are influenced [16].
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It is assumed that functional recovery may be due to (1) biological brain regeneration (restitution); (2) adaptive reorganization by engagement of new neural networks that affect the final executive paths for implementation of the affected function and/or
The mechanisms of functional recovery following CNS injury remain unclear. It is assumed that functional recovery may be due to (1) biological brain regeneration (restitution); (2) adaptive reorganization by engagement of new neural networks that affect the final executive paths for implementation of the affected function and/or
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Complete morphological recovery following brain injury may never be achieved, but the possibility of functional motor recovery by stimulation of brain plasticity through a long specific-oriented and intensive Neurorehabilitation gives optimism in cases of disability [18].
Complete morphological recovery following brain injury may never be achieved, but the possibility of functional motor recovery by stimulation of brain plasticity through a long specific-oriented and intensive Neurorehabilitation gives optimism in cases of disability [18]. A hope is reposed in the triad: neurotransplantation of stem cells, use of neurotrophic factors and special neurorehabilitation program using new technological transfer and biorobots.
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Neurobehavioral management of traumatic brain injury in the critical care setting.
Arciniegas DB, McAllister TW. Neurobehavioral management of traumatic brain injury in the critical care setting.
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Medication in the treatment of the behavioural sequelae of traumatic brain injury.
Bates G. Medication in the treatment of the behavioural sequelae of traumatic brain injury.
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Relation of executive functioning to pragmatic outcome following severe traumatic brain injury.
Douglas JM. Relation of executive functioning to pragmatic outcome following severe traumatic brain injury.
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Neurologic examination of the patient with traumatic brain injury.
Gelber DA, Callahan CD. Neurologic examination of the patient with traumatic brain injury. In: Ashley MJ, editor. Traumatic brain injury: rehabilitation, treatment, and case management. 3rd ed. Boca Raton, FL, CRC Press, 2010, 3-27.
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Traumatic brain injury: rehabilitation, treatment, and case management.
Gelber DA, Callahan CD. Neurologic examination of the patient with traumatic brain injury. In: Ashley MJ, editor. Traumatic brain injury: rehabilitation, treatment, and case management. 3rd ed. Boca Raton, FL, CRC Press, 2010, 3-27.
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Splinting the hand in the functional position after brain impairment: a randomized, controlled trial.
Lannin NA, HorsleySA, Herbert R. Splinting the hand in the functional position after brain impairment: a randomized, controlled trial.
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Aging with traumatic brain injury: cross-sectional follow-up of people receiving inpatient rehabilitation over more than 3 decades.
Sendroy-Terrill M, Whiteneck GG, Brooks CA. Aging with traumatic brain injury: cross-sectional follow-up of people receiving inpatient rehabilitation over more than 3 decades.
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Traumatic brain injury in the United States: assessing outcomes in children,
Traumatic brain injury in the United States: assessing outcomes in children,
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Its clinical interests included epilepsy, vascular brain diseases, Neurorehabilitation and Parkinsonism.
Prof. Stoyan Baykushev was born in 1929 in Varna. He graduated from the Higher Medical Institute in Plovdiv in 1953. In 1960 he acquired a specialty in Nervous diseases. Since 1977 he was a Doctor of Medical Sciences and Professor of Neurology. His scientific work includes over 220 publications and 16 books at home and abroad. Its clinical interests included epilepsy, vascular brain diseases, Neurorehabilitation and Parkinsonism.
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From 1973 to 1982 he worked in the Central Laboratory for Brain Studies of the Bulgarian Academy of Sciences.
Prof. Haralan Haralanov was born in Novi Pazar on 30 September 1923. He graduated from the Higher Medical Institute of Sofia in 1952 with honors for academic excellence. He started work in the Ministry of Interior and leaded the Central Military Medical Commission until 1955. In 1970 Dr. Haralanov became an Associate Professor. From 1973 to 1982 he worked in the Central Laboratory for Brain Studies of the Bulgarian Academy of Sciences. In 1982 he moved to the Department Neurology in Medical Academy – Sofia. In 1985 he was elected for Professor in Neurology. From 1985 to 1989 when Prof. Haralanov retired, he was the Head of the Chair of Neurology of the Scientific Institute of Neurology and Psychiatry in Medical Academy – Sofia.
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These monographs along with his PhD thesis “Problems of the brain circulation” (1981), show his main direction of interest: investigation of the brain circulation and more specific – the main cerebral vessels.
(1960), Clinical Neurophysiology in Burdenko Institute of Neurosurgery (Moscow, 1960-61), Clinical and Experimental Otoneurology with Prof. Bourgeat (Paris) who at that time was the President of the European Association of Space Medicine (1970). Prof. Haralanov’s scientific activity contains more than 200 publications, including coauthorship in 3 Neurology books and 2 monographs – “Pathology of carotid circulation” (1970 and “Insufficiency of basal circulation” (1974). These monographs along with his PhD thesis “Problems of the brain circulation” (1981), show his main direction of interest: investigation of the brain circulation and more specific – the main cerebral vessels.
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16. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 2, 2012, No. 2 , , ,

beside the descriptions of plaque morphology and risk factors, grading of carotid stenosis, microemboli detection, acute stroke managment, brain tissue imaging and cerebral autoregulation.
beside the descriptions of plaque morphology and risk factors, grading of carotid stenosis, microemboli detection, acute stroke managment, brain tissue imaging and cerebral autoregulation. The technical development of the US equipment demonstrates further improvements of the image quality and fast processing leading to increased spacial and temporal resolution, improved contrast imaging, elasthography and easy to use application to support the application of the US technology even in the daily routine with high quality. Ultrasound application in other than neurological indication extended more and more the diagnostic field in competition to CT/MRI e.g. analysis of tumour tissue using ultrasound contrast agents, searching for lymph node pathology and future aspects of local drug application by loaded microbubbles and treatment via sonovaporation [14].
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It is known that although limited, the ability of the human brain to reorganize continues throughout life which is associated with brain plasticity on two functional levels: sensorimotor cortex (cortical plasticity) and neuronal network (neuronal plasticity).
It is known that although limited, the ability of the human brain to reorganize continues throughout life which is associated with brain plasticity on two functional levels: sensorimotor cortex (cortical plasticity) and neuronal network (neuronal plasticity). Changes in the central nervous system can be objectified with different functional neuroimaging and electrophysiological methods [1, 7, 15]. Recently, similar studies have established bilateral changes in motor control after stroke in which the participation of non-paretic side is proportional to the severity of brain injury [2, 3, 7, 14] and is associated with functional and
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Recently, similar studies have established bilateral changes in motor control after stroke in which the participation of non-paretic side is proportional to the severity of brain injury [2, 3, 7, 14] and is associated with functional and
It is known that although limited, the ability of the human brain to reorganize continues throughout life which is associated with brain plasticity on two functional levels: sensorimotor cortex (cortical plasticity) and neuronal network (neuronal plasticity). Changes in the central nervous system can be objectified with different functional neuroimaging and electrophysiological methods [1, 7, 15]. Recently, similar studies have established bilateral changes in motor control after stroke in which the participation of non-paretic side is proportional to the severity of brain injury [2, 3, 7, 14] and is associated with functional and
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Brain reorganization after stroke.
Green JB. Brain reorganization after stroke.
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Neuroimaging examination of the brain was conducted by 1.5 Tesla MRI (GE HTX SigmaUSA).
Neuroimaging examination of the brain was conducted by 1.5 Tesla MRI (GE HTX SigmaUSA).
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In differential diagnosis we can discuss brain metastases, abscesses, arterio-venous malformations and others [3].
The presentation of this case, based on clinical data (anamnesis, symptoms, progress) and changes in neuroimaging examinations (types of signal abnormalities, localization of changes and association with other abnormalities) demonstrates the differential diagnostic problems [20]. Firstly it is necessary to differentiate thrombosis from thrombophlebitis, in which the cause and primary localization need to be identified. In differential diagnosis we can discuss brain metastases, abscesses, arterio-venous malformations and others [3].
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The neuroprotective effect of mild hypothermia was demonstrated in animal studies and in humans with brain ischemia and traumatic brain injuries.
Baron Dominique Jean Larrey – a French surgeon in Napoleon’s army recorded an interesting observation – injured soldiers in a status of hypothermia who were moved closer to the fire died more rapidly than those who remained hypothermic. The first article which focused on the effect of hypothermia in patients after severe head injuries was published in 1945. The first medical application of hypothermia was in 1950s. The method was used in intracranial aneurysm surgery for reaching of bloodless operational field. The early investigations were mostly focused on deep hypothermia leading to serious adverse events which limited its wide application. The neuroprotective effect of mild hypothermia was demonstrated in animal studies and in humans with brain ischemia and traumatic brain injuries. The positive effect of mild hypothermia for increasing survival of patients after cardiac arrest and newborns with birth asphyxia for lowering the risk of brain damage was proved in controlled clinical trials and meta-analyses [21, 22].
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The positive effect of mild hypothermia for increasing survival of patients after cardiac arrest and newborns with birth asphyxia for lowering the risk of brain damage was proved in controlled clinical trials and meta-analyses [21, 22].
The first article which focused on the effect of hypothermia in patients after severe head injuries was published in 1945. The first medical application of hypothermia was in 1950s. The method was used in intracranial aneurysm surgery for reaching of bloodless operational field. The early investigations were mostly focused on deep hypothermia leading to serious adverse events which limited its wide application. The neuroprotective effect of mild hypothermia was demonstrated in animal studies and in humans with brain ischemia and traumatic brain injuries. The positive effect of mild hypothermia for increasing survival of patients after cardiac arrest and newborns with birth asphyxia for lowering the risk of brain damage was proved in controlled clinical trials and meta-analyses [21, 22].
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Stabilization of blood-brain barrier (BBB);
Stabilization of blood-brain barrier (BBB);
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This effect was shown most clearly for post-anoxic brain injury but could be also applicable to other organs such as heart and kidneys.
The initial observations were based on the deep hypothermia and on the hypothesis that there was a close relationship between the therapeutic effect and the level of temperature decline [19]. Further investigations suggested that even mild hypothermia in the first hours after an ischemic event had a preventive effect for avoiding or diminishing permanent injuries. This effect was shown most clearly for post-anoxic brain injury but could be also applicable to other organs such as heart and kidneys. The collected evidences for cells’ protection as well as the additive and supportive effect to the standard therapy justified the application of TH in guidelines. For example, in 2003 the American Heart Association (AHA) and the International Liaison Committee on Resuscitation (ILCOR) included the hypothermia as a treatment option added to the standard care of patients following cardiac arrest [5, 16].
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Cooling is widely used for preserving organs for transplantation, the induced hypothermia is used as a treatment in neonatal encephalopathy, cardiac arrest, myocardial infarction, ischemic stroke, traumatic brain or spinal cord injury without fever and neurogenic fever after stroke or brain trauma [22].
Cooling is widely used for preserving organs for transplantation, the induced hypothermia is used as a treatment in neonatal encephalopathy, cardiac arrest, myocardial infarction, ischemic stroke, traumatic brain or spinal cord injury without fever and neurogenic fever after stroke or brain trauma [22]. An overview of these treatment options in different conditions is provided below:
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The benefit of TH in patients after a cardiac arrest is neuroprotection since the brain is at risk of ischemia during the incident [3, 4, 5].
The benefit of TH in patients after a cardiac arrest is neuroprotection since the brain is at risk of ischemia during the incident [3, 4, 5]. The interpretation of results after completion of two landmark studies in patients after sudden cardiac arrest who were in coma (the first one in Europe and the second one – in Australia, both completed almost simultaneously with the results published in New England Journal of Medicine in 2002) showed the positive effect of mild TH on the short-term neurologic recovery and survival [3, 17]. The patients were cooled 3-4 hours after the incident to the target temperature of 32–34°C and then rewarmed
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Hypothermic therapy for neonatal encephalopathy is proven to reduce brain damages and increase survival of newborns with birth asphyxia [10, 23].
Hypothermic therapy for neonatal encephalopathy is proven to reduce brain damages and increase survival of newborns with birth asphyxia [10, 23]. Therapeutic hypothermia decreases brain tissue injury in infants with hypoxic–ischemic encephalopathy. Data from randomized controlled trials (CoolCap, NICHD, TOBY) and meta-analyses prove the benefits of hypothermia for survival of infants without neurologic deficit for 18 months and reduction of brain development impairment. The objective of another trial – ICE determines the effectiveness and safety of moderate whole-body hypothermia in newborns with hypoxic-ischemic encephalopathy born in hospitals with and without newborn intensive care facilities or complex hypothermia equipment. The study main conclusion is that the whole-body hypothermia is effective and appears to be safe when started within 6 hours after birth at hospital for term or near-term newborns with hypoxic-ischemic encephalopathy [12]. Additional evidences for persistence of ben-
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Therapeutic hypothermia decreases brain tissue injury in infants with hypoxic–ischemic encephalopathy.
Hypothermic therapy for neonatal encephalopathy is proven to reduce brain damages and increase survival of newborns with birth asphyxia [10, 23]. Therapeutic hypothermia decreases brain tissue injury in infants with hypoxic–ischemic encephalopathy. Data from randomized controlled trials (CoolCap, NICHD, TOBY) and meta-analyses prove the benefits of hypothermia for survival of infants without neurologic deficit for 18 months and reduction of brain development impairment. The objective of another trial – ICE determines the effectiveness and safety of moderate whole-body hypothermia in newborns with hypoxic-ischemic encephalopathy born in hospitals with and without newborn intensive care facilities or complex hypothermia equipment. The study main conclusion is that the whole-body hypothermia is effective and appears to be safe when started within 6 hours after birth at hospital for term or near-term newborns with hypoxic-ischemic encephalopathy [12]. Additional evidences for persistence of ben-
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Data from randomized controlled trials (CoolCap, NICHD, TOBY) and meta-analyses prove the benefits of hypothermia for survival of infants without neurologic deficit for 18 months and reduction of brain development impairment.
Hypothermic therapy for neonatal encephalopathy is proven to reduce brain damages and increase survival of newborns with birth asphyxia [10, 23]. Therapeutic hypothermia decreases brain tissue injury in infants with hypoxic–ischemic encephalopathy. Data from randomized controlled trials (CoolCap, NICHD, TOBY) and meta-analyses prove the benefits of hypothermia for survival of infants without neurologic deficit for 18 months and reduction of brain development impairment. The objective of another trial – ICE determines the effectiveness and safety of moderate whole-body hypothermia in newborns with hypoxic-ischemic encephalopathy born in hospitals with and without newborn intensive care facilities or complex hypothermia equipment. The study main conclusion is that the whole-body hypothermia is effective and appears to be safe when started within 6 hours after birth at hospital for term or near-term newborns with hypoxic-ischemic encephalopathy [12]. Additional evidences for persistence of ben-
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Traumatic injuries of the brain and spinal cord
Traumatic injuries of the brain and spinal cord
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The aim of the treatment of brain and/or spinal cord injuries is the recovering of adequate perfusion; surgical evacuation of hematomas (if necessary) and oedema prophylaxis.
The aim of the treatment of brain and/or spinal cord injuries is the recovering of adequate perfusion; surgical evacuation of hematomas (if necessary) and oedema prophylaxis. Animal studies show the positive effect of hypothermia in central nervous system injuries. Basic science evidence also suggests that cooling affects many secondary biochemical cascades that are activated after acute injury. The potential benefit of this non-specific therapy is based on the observation that hypothermia reduces brain metabolism and energy consumption which might be feasible for improving the outcome of the injury [2, 19]. Comparing with the pharmacologic treatment which acts to a single neurochemical process, hypothermia interferes and inhibits multiple pathological processes simultaneously acting non-specifically. The results from the studies in humans are quite controversial and inconsistent.
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The potential benefit of this non-specific therapy is based on the observation that hypothermia reduces brain metabolism and energy consumption which might be feasible for improving the outcome of the injury [2, 19].
The aim of the treatment of brain and/or spinal cord injuries is the recovering of adequate perfusion; surgical evacuation of hematomas (if necessary) and oedema prophylaxis. Animal studies show the positive effect of hypothermia in central nervous system injuries. Basic science evidence also suggests that cooling affects many secondary biochemical cascades that are activated after acute injury. The potential benefit of this non-specific therapy is based on the observation that hypothermia reduces brain metabolism and energy consumption which might be feasible for improving the outcome of the injury [2, 19]. Comparing with the pharmacologic treatment which acts to a single neurochemical process, hypothermia interferes and inhibits multiple pathological processes simultaneously acting non-specifically. The results from the studies in humans are quite controversial and inconsistent. The results are difficult to interpret due to the limited number of patients, lack of controls, concomitant surgical procedures or concomitant use of drugs etc. [2, 6, 19]. So far, there are no sufficient data from controlled studies in humans about the benefits of hypothermia in treatment of brain injuries in term to improve outcome and reduce mortality.
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So far, there are no sufficient data from controlled studies in humans about the benefits of hypothermia in treatment of brain injuries in term to improve outcome and reduce mortality.
The potential benefit of this non-specific therapy is based on the observation that hypothermia reduces brain metabolism and energy consumption which might be feasible for improving the outcome of the injury [2, 19]. Comparing with the pharmacologic treatment which acts to a single neurochemical process, hypothermia interferes and inhibits multiple pathological processes simultaneously acting non-specifically. The results from the studies in humans are quite controversial and inconsistent. The results are difficult to interpret due to the limited number of patients, lack of controls, concomitant surgical procedures or concomitant use of drugs etc. [2, 6, 19]. So far, there are no sufficient data from controlled studies in humans about the benefits of hypothermia in treatment of brain injuries in term to improve outcome and reduce mortality.
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There is a correlation related to body temperature of patients with ischemic stroke or brain trauma, measured at admission to the Intensive Care Unit (ICU) – patients with normal body temperature after the incident have a better prognosis than the others with febrility regardles the time of occurrence.
There is a correlation related to body temperature of patients with ischemic stroke or brain trauma, measured at admission to the Intensive Care Unit (ICU) – patients with normal body temperature after the incident have a better prognosis than the others with febrility regardles the time of occurrence. The body temperature at admission is considered to be an independent predictor of the short-term outcome and long-term mortality after stroke [9, 13]. Many studies show that elevated temperature is associated with a worse outcome in patients with acute ischemic stroke [9]. Clinical trials in patients with severe closed head injury demonstrate the benefits of moderateTH. Hypothermic therapy in early stages after the incident when body temperature is kept low for a longer period could be a long-lasting neuroprotective measure but the hypothesis should be proved in further controlled clinical trials [9, 13].
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Review Article of the Use of Early Hypothermia in the Treatment of Traumatic Brain Injuries.
Arcure J, Harrison E. Review Article of the Use of Early Hypothermia in the Treatment of Traumatic Brain Injuries.
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The method is well established as neuroprotective in treatment of acute ischemic brain injuries such as anoxic encephalopathy after cardiac arrest and perinatal asphyxia.
Therapeutic hypothermia (TH) is one of the most promising treatment strategies for acute ischemic stroke. The method is well established as neuroprotective in treatment of acute ischemic brain injuries such as anoxic encephalopathy after cardiac arrest and perinatal asphyxia. Animal studies strongly demonstrate the benefit of hypothermia after focal cerebral ischemia, without indicating critical publication bias. TH has only been rudimentarily studied in stroke patients. The present article summarizes the place of hypothermia in the management of acute ischemic stroke.
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since the ancient time however its clinical application is limited – it is mainly applied for patients with cardiac arrest and of newborns with birth asphyxia for lowering the risk of brain damages [3, 8, 24].
since the ancient time however its clinical application is limited – it is mainly applied for patients with cardiac arrest and of newborns with birth asphyxia for lowering the risk of brain damages [3, 8, 24]. As of the current moment, clinical data about hypothermia and its application in patients after an acute ischemic stroke showed good results [12, 14, 19, 25].
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Minimal decrease of body temperature is known to be well tolerated leading to a significant reduction of pathologic pathways in the brain as well as to improvement of the nervous system functions [14, 20, 25] while febrility and subfebrility in the first days after the stroke are associated with untoward clinical outcomes [20].
Therapeutic hypothermia (TH) is one of the most investigated neuroprotective method which prevents the neurons from cell’s death in a status of cerebral ischemia [22]. Minimal decrease of body temperature is known to be well tolerated leading to a significant reduction of pathologic pathways in the brain as well as to improvement of the nervous system functions [14, 20, 25] while febrility and subfebrility in the first days after the stroke are associated with untoward clinical outcomes [20]. It is presumed that the therapeutic hypothermia exerts its effect by influencing of metabolic processes in a neuron – a decrease of body temperature to 35°–30°C is leading to a reduction of oxygen consumption and CO
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The modern approach of treatment of ischemic stroke in the first hours of occurrence of the event refers to an early recanalization of thrombotic artery occlusion; avoiding the formation of infarction zone or limitation the process by recovering the brain perfusion in the area of the ischemic penumbra [1, 4, 6, 15].
The modern approach of treatment of ischemic stroke in the first hours of occurrence of the event refers to an early recanalization of thrombotic artery occlusion; avoiding the formation of infarction zone or limitation the process by recovering the brain perfusion in the area of the ischemic penumbra [1, 4, 6, 15]. Nowadays this target is achieved by intravenous or intra-arterial trombolysis with recombinant tissue plasminogen activator (rt-PA) within 3-4.5 hours of the stroke occurrence [1]. Hypothermia is not conventionally used method although it is known to reduce the infarct size by >40% when body temperature decreases to 34°C or below.
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As it is shown in a model of intracerebral hemorrhage with no application of autologous blood or collagenases that hypothermia reduces the brain edema and stabilizes blood-brain barrier with no significant effect on the outcome of the disease.
The effect of hypothermia for treatment of hemorrhagic stroke is less investigated. As it is shown in a model of intracerebral hemorrhage with no application of autologous blood or collagenases that hypothermia reduces the brain edema and stabilizes blood-brain barrier with no significant effect on the outcome of the disease. The early cooling is associated with worsening of the patient’s condition however the reason for that is still not well investigated [10, 14, 25].
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Hypotermia therapy after traumatic brain injury in children.
Hutchison E, Ward R, Lacroix J, Hebert P, Barnes M, bohn D, Dorks P. Hypotermia therapy after traumatic brain injury in children.
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Neuronal death in brain infarcts in man.
Love S, Barber R, Wilcock G. Neuronal death in brain infarcts in man.
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Physiological effects and brain protection by hypothermia and cerebrolysin after moderate forebrain ischemia in rats.
Schwab M,Bauer R, Zwiener U. Physiological effects and brain protection by hypothermia and cerebrolysin after moderate forebrain ischemia in rats.
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Moderate hypothermia and brain temperature in patients with severe middle cerebral artery infarction.
Schwab M, Schwarz S, Aschoff A, Keller E, Hacke W. Moderate hypothermia and brain temperature in patients with severe middle cerebral artery infarction.
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17. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 9, 2013, No. 1 , , ,

Subsequently, they reported improvement in the Multiple Sclerosis Functional Composite (MSFC) in relapsing remitting MS and a reduction of Gadolinium enhancing lesions on brain MRI during a mean follow-up of 18 months in a small monocentric open angioplastic intervention study [66].
ported a correlation of the clinical course of MS with specific patterns of venous obstructions [9]. Subsequently, they reported improvement in the Multiple Sclerosis Functional Composite (MSFC) in relapsing remitting MS and a reduction of Gadolinium enhancing lesions on brain MRI during a mean follow-up of 18 months in a small monocentric open angioplastic intervention study [66]. “CCSVI” and its presumed efficacious therapeutic approach termed “liberation treatment” caused enormous interest in the scientific community, amongst patient support groups and in the media. Several clinical trials on angioplasty have started since, and numerous desperate MS patients seek relief from their incurable disease through questionable medical procedures. However, in the meantime the number of publications that refute the “CCSVI” hypothesis has far exceeded that of its supporters. This review aims to analyse and critically comment on methodical aspects of “CCSVI” in the context of (patho-)physiological plausibility, which refers mainly to color-coded duplex ultrasonography (US), which is the only method according to Zamboni to define “CCSVI”.
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of damaged brain tissue [48].
of damaged brain tissue [48].
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The anatomy of collateral venous flow from the brain and its value in aetiological interpretation of intracranial pathology.
Andeweg J. The anatomy of collateral venous flow from the brain and its value in aetiological interpretation of intracranial pathology.
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How does the blood leave the brain?
nster T, Rademacher J, Klingebiel R, Valdueza JM. How does the blood leave the brain? A systematic ultrasound analysis of cerebral venous drainage patterns.
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Patients with brain hemorrhage, dementia, concomitant liver, kidney and cancerous diseases, and previous surgery were excluded from the study.
We studied 47 (26 males and 21 females) ischemic stroke patients (mean age 63 years), who were admitted to the Neurology Clinic of University Hospital, Pleven (2008) within 24 hours of onset. Patients with brain hemorrhage, dementia, concomitant liver, kidney and cancerous diseases, and previous surgery were excluded from the study. A detailed questionnaire on the medical history and physical state of the patients was filled in by an experienced neurologist. Data regarding demographics, vascular risk factors, and concomitant treatment were also collected. CT scan of the brain was performed on admission to the clinic. An informed consent was obtained from the patients. The study was approved by the Ethics Committee of the Medical University Pleven.
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CT scan of the brain was performed on admission to the clinic.
We studied 47 (26 males and 21 females) ischemic stroke patients (mean age 63 years), who were admitted to the Neurology Clinic of University Hospital, Pleven (2008) within 24 hours of onset. Patients with brain hemorrhage, dementia, concomitant liver, kidney and cancerous diseases, and previous surgery were excluded from the study. A detailed questionnaire on the medical history and physical state of the patients was filled in by an experienced neurologist. Data regarding demographics, vascular risk factors, and concomitant treatment were also collected. CT scan of the brain was performed on admission to the clinic. An informed consent was obtained from the patients. The study was approved by the Ethics Committee of the Medical University Pleven.
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Стволова/Brain stem
Стволова/Brain stem
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Ultrasound, Stroke, Cerebral venous and sinus thrombosis, Brain Tumours, Migraine
Ultrasound, Stroke, Cerebral venous and sinus thrombosis, Brain Tumours, Migraine
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Imaging of brain parenchyma
Imaging of brain parenchyma
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Neuro-Cardio-Sonology (Heart & Brain)
Neuro-Cardio-Sonology (Heart & Brain)
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18. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 9, 2013, No. 2 , , ,

“Heart and Brain”
“Heart and Brain”
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Satellite Symposium of Actavis “Heart and Brain”
Satellite Symposium of Actavis “Heart and Brain”
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Arterial Blood Pressure – When Becomes a Foe of the Brain?
Arterial Blood Pressure – When Becomes a Foe of the Brain?
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Anatomy of Brain Supplying Vessels.
Anatomy of Brain Supplying Vessels.
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Specific TCD Clinical Applications for Patients with Traumatic Brain Injury.
Specific TCD Clinical Applications for Patients with Traumatic Brain Injury.
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Monitoring the Brain During Invasive Cardiovascular Examinations and Surgery.
Monitoring the Brain During Invasive Cardiovascular Examinations and Surgery.
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Intraoperative Ultrasound to Control Resection of Brain Metastases.
Intraoperative Ultrasound to Control Resection of Brain Metastases.
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Transcranial Doppler for Brain Death in Infants.
Transcranial Doppler for Brain Death in Infants. The Role of the Fontanelles.
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Transcranial Doppler and Oximetry Tissue Catheter Monitoring in Diffuse Brain Vasospasm.
Transcranial Doppler and Oximetry Tissue Catheter Monitoring in Diffuse Brain Vasospasm.
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Brain Hemodynamic Improvement after Retrograde Ventriculo-Sinus Shunt in Hydrocephalus Patients.
Brain Hemodynamic Improvement after Retrograde Ventriculo-Sinus Shunt in Hydrocephalus Patients.
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Safety Evaluation of Mid-Frequency Sonothrombolysis: Animal Brain Experiment.
Safety Evaluation of Mid-Frequency Sonothrombolysis: Animal Brain Experiment.
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Ultrasonic Evaluation of Acetazolamide Vasoreactivity in Brain Tissue and Major Cerebral Arteries.
Ultrasonic Evaluation of Acetazolamide Vasoreactivity in Brain Tissue and Major Cerebral Arteries.
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Our Experience with Endovascular Treatment of Brain Aneurysms and AVMs.
Our Experience with Endovascular Treatment of Brain Aneurysms and AVMs.
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Clinical Studies of the Effects of Artificial Technogenic Electromagnetic Radiation when Registering Brain Activity with an EEG.
Clinical Studies of the Effects of Artificial Technogenic Electromagnetic Radiation when Registering Brain Activity with an EEG.
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Ultrasound safety with midfrequency transcranial sonothrombolysis: preliminary study on normal macaca monkey brain.
Shimizu J, Fukuda T, Abe T, Ogihara M, Kubota J, Sasaki A, Azuma T, Sasaki K, Shimizu K, Oishi T, Umemura S, Furuhata H. Ultrasound safety with midfrequency transcranial sonothrombolysis: preliminary study on normal macaca monkey brain.
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Thus, a better interpretation of the findings raised by Doppler sonography of the brain supplying arteries should be possible.
The introduction to the hemodynamic principles should lead to a basic understanding of parameters that determine the cerebral blood flow velocity. Thus, a better interpretation of the findings raised by Doppler sonography of the brain supplying arteries should be possible.
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ANATOMY OF BRAIN SUPPLYING VESSELS
ANATOMY OF BRAIN SUPPLYING VESSELS
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This tutorial will cover the basic knowledge of the arterial blood supply of the brain.
This tutorial will cover the basic knowledge of the arterial blood supply of the brain. The extracranial anterior and posterior system, i.e. the carotid and the vertebral arteries will be discussed as well as the intracranial arteries. Special attention will be paid to the concept of endarteries versus collateral blood supply. The latter comprises of course the circle of Willis. Also, there will be a short reflection on the anatomical properties of the vessel wall, which are the prerequisite for their functional behaviour.
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So, the participant will be able to learn the essential facts of the arteries that take care of the blood supply of the brain.
So, the participant will be able to learn the essential facts of the arteries that take care of the blood supply of the brain. The tutorial will focus on practically relevant aspects which are needed for the understanding of the physiology of the arterial cerebral circulation and the examination of both the extraand intracranial vessels by means of ultrasound.
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To a lesser degree, TCD has also been used to evaluate cerebral autoregulatory capacity, monitor cerebral circulation during cardiopulmonary bypass and carotid endarterectomy, to diagnose brain death and for monitoring of cerebral hemodynamics in neurotrauma.
It has been frequently employed for the clinical evaluation of cerebral vasospasm following subarachnoid hemorrhage (SAH). To a lesser degree, TCD has also been used to evaluate cerebral autoregulatory capacity, monitor cerebral circulation during cardiopulmonary bypass and carotid endarterectomy, to diagnose brain death and for monitoring of cerebral hemodynamics in neurotrauma.
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TCD findings compatible with the diagnosis of brain death include systolic spikes without diastolic flow or with diastolic reversed flow, and no demonstrable flow in a patient in who flow had been clearly documented on a previous examination.
TCD findings compatible with the diagnosis of brain death include systolic spikes without diastolic flow or with diastolic reversed flow, and no demonstrable flow in a patient in who flow had been clearly documented on a previous examination. Assessment of cerebral autoregulation using TCD blood flow velocity has been previously validated to be predictive of outcome following traumatic brain injury.
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Assessment of cerebral autoregulation using TCD blood flow velocity has been previously validated to be predictive of outcome following traumatic brain injury.
TCD findings compatible with the diagnosis of brain death include systolic spikes without diastolic flow or with diastolic reversed flow, and no demonstrable flow in a patient in who flow had been clearly documented on a previous examination. Assessment of cerebral autoregulation using TCD blood flow velocity has been previously validated to be predictive of outcome following traumatic brain injury.
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They will undergo to blood tests, ECG, brain CT, carotid US, TCCD or TCD.
This is a multicenter, interventional, controlled, randomized study. Patients older than 18 years will be enrolled if presenting with acute IS within 4.5 of symptom onset. They will undergo to blood tests, ECG, brain CT, carotid US, TCCD or TCD. Patients should have an occlusion of the middle cerebral artery documented by TCD, TCCD or CTA. Exclusion criteria will be: cerebral hemorrhage on CT and dramatic spontaneous neurologic improvement. Informed consent will be obtained from all patients or their next of kin. Patients will be randomized to receive either tPA alone or tPA
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SPECIFIC TCD CLINICAL APPLICATIONS FOR PATIENTS WITH TRAUMATIC BRAIN INJURY
SPECIFIC TCD CLINICAL APPLICATIONS FOR PATIENTS WITH TRAUMATIC BRAIN INJURY
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Critical care management of patients with traumatic brain injury (TBI) has undergone tremendous advances.
Critical care management of patients with traumatic brain injury (TBI) has undergone tremendous advances. Neurosurgeons, neurologists and neurointensivists, including military, have a large armamentarium of invasive monitoring modalities available to detect secondary brain injury and guide therapy. The primary goal monitoring is to prevent secondary insults to the brain, primarily cerebral ischemia due to the posttraumatic vasospasm (PTV), and intracranial hypertension (ICH). This lecture summarizes the advantages and the specific roles of transcranial Doppler (TCD) ultrasound to establish and monitor the presence of PTV and ICH.
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Neurosurgeons, neurologists and neurointensivists, including military, have a large armamentarium of invasive monitoring modalities available to detect secondary brain injury and guide therapy.
Critical care management of patients with traumatic brain injury (TBI) has undergone tremendous advances. Neurosurgeons, neurologists and neurointensivists, including military, have a large armamentarium of invasive monitoring modalities available to detect secondary brain injury and guide therapy. The primary goal monitoring is to prevent secondary insults to the brain, primarily cerebral ischemia due to the posttraumatic vasospasm (PTV), and intracranial hypertension (ICH). This lecture summarizes the advantages and the specific roles of transcranial Doppler (TCD) ultrasound to establish and monitor the presence of PTV and ICH.
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The primary goal monitoring is to prevent secondary insults to the brain, primarily cerebral ischemia due to the posttraumatic vasospasm (PTV), and intracranial hypertension (ICH).
Critical care management of patients with traumatic brain injury (TBI) has undergone tremendous advances. Neurosurgeons, neurologists and neurointensivists, including military, have a large armamentarium of invasive monitoring modalities available to detect secondary brain injury and guide therapy. The primary goal monitoring is to prevent secondary insults to the brain, primarily cerebral ischemia due to the posttraumatic vasospasm (PTV), and intracranial hypertension (ICH). This lecture summarizes the advantages and the specific roles of transcranial Doppler (TCD) ultrasound to establish and monitor the presence of PTV and ICH.
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intracranial hypertension, posttraumatic vasospasm, transcranial Doppler ultrasound, traumatic brain injury.
intracranial hypertension, posttraumatic vasospasm, transcranial Doppler ultrasound, traumatic brain injury.
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MONITORING THE BRAIN DURING INVASIVE CARDIOVASCULAR EXAMINATIONS AND SURGERY
MONITORING THE BRAIN DURING INVASIVE CARDIOVASCULAR EXAMINATIONS AND SURGERY
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In the brain, such ultrasensitive Doppler paves the way for fUltrasound (functional ultrasound imaging) of brain activity with unprecedented spatial and temporal resolution compared to fMRI.
precision characterization of complex vascular and cardiac flows. It also gives ultrasound the ability to detect very subtle blood flow in very small vessels. In the brain, such ultrasensitive Doppler paves the way for fUltrasound (functional ultrasound imaging) of brain activity with unprecedented spatial and temporal resolution compared to fMRI. Examples such as the functional imaging of cerebral blood volume during epileptic seizures will be presented and ill emphasize the potential of this new imaging modality.
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We will also emphasize how fUS combined with ultrasonic neurostimulation could lead to first extracorporeal brain machine interfaces.
in cognitive science. Beyond clinical application, it will be a fantastic tool for people in neuroscience working on small animals. This technology should help them answer unsolved questions. We will also emphasize how fUS combined with ultrasonic neurostimulation could lead to first extracorporeal brain machine interfaces.
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Cerebrovascular diseases (CVD) represent conditions which occur as a result of changes in blood vessels of the brain, as well as the vessels supplying the brain.
Cerebrovascular diseases (CVD) represent conditions which occur as a result of changes in blood vessels of the brain, as well as the vessels supplying the brain. The most common types of CVDs are ischemic stroke, transient ischemic attack, hemorrhagic stroke and vascular dementia. CVDs affect millions of people worldwide, regardless of age, and represent a group of very important medical and social problems. Therefore, their prevention is becoming an imperative. Risk factors, such as age, gender, genetic factors, hypertension, diabetes mellitus, hypercholsterolemia, atrial fibrillation, orlifestyle,are causing changes of vessel walls which lead to CVD. Early changes of the blood vessel wall can be detected by early ultrasound screening methods which allow us to detect changes before the disease becomes clinically evident.
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An elegant application of TCS is the intraand postoperative localization of deep brain stimulation electrodes in patients with movement disorders.
basal ganglia changes also in other movement disorders such as lenticular nucleus hyperechogenicity in idiopathic dystonia and Wilson's disease and caudate nucleus hyperechogenicity in Huntington's disease. Reduced echogenicity of midbrain raphe is frequent in depressive disorders and was found to correlate with responsivity to serotonin reuptake inhibitors. An elegant application of TCS is the intraand postoperative localization of deep brain stimulation electrodes in patients with movement disorders. The detection of changes of deep brain structures on TCS in multiple sclerosis patients was found to have a predictive value for further disease progression.
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The detection of changes of deep brain structures on TCS in multiple sclerosis patients was found to have a predictive value for further disease progression.
basal ganglia changes also in other movement disorders such as lenticular nucleus hyperechogenicity in idiopathic dystonia and Wilson's disease and caudate nucleus hyperechogenicity in Huntington's disease. Reduced echogenicity of midbrain raphe is frequent in depressive disorders and was found to correlate with responsivity to serotonin reuptake inhibitors. An elegant application of TCS is the intraand postoperative localization of deep brain stimulation electrodes in patients with movement disorders. The detection of changes of deep brain structures on TCS in multiple sclerosis patients was found to have a predictive value for further disease progression.
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deep brain stimulation, movement disorders, substania nigra, transcranial sonography.
deep brain stimulation, movement disorders, substania nigra, transcranial sonography.
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brain venous system, clinical implications, neurosonography.
brain venous system, clinical implications, neurosonography.
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Thirty-three patients with acute atherothrombotic brain infarction (group ATBI), 33 cardiogenic cerebral embolism (group CE) and 31 normal controls (group NC) were enrolled.
Thirty-three patients with acute atherothrombotic brain infarction (group ATBI), 33 cardiogenic cerebral embolism (group CE) and 31 normal controls (group NC) were enrolled. BAD and CAD at the end-diastolic phase were measured in each group by ultrasonography. KruskalWallis test followed by Scheffe’s post-hoc test was used to compare differences among three groups.
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Carotid artery sonography was performed in 140 consecutive patients with atherothrombotic brain infarction to evaluate extracranial ICA stenosis.
Carotid artery sonography was performed in 140 consecutive patients with atherothrombotic brain infarction to evaluate extracranial ICA stenosis. The AcT ratio
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These findings are in favor of an independent influence of obstructive sleep apnea on carotid artery atherosclerosis and asymtomatic changes of the brain in performet MRI.
These findings are in favor of an independent influence of obstructive sleep apnea on carotid artery atherosclerosis and asymtomatic changes of the brain in performet MRI.
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The intracranial hypertension is an important clinical condition and represents high risk to patients with acute brain injury.
The image of the real-time ultrasound combined with pulsed Doppler system is a noninvasive and bedside method that allows the cerebral blood flow velocity and evaluation and flow resistance measurement in intracranial hypertension patients. The intracranial hypertension is an important clinical condition and represents high risk to patients with acute brain injury. In this study, we describe in an experimental model, application of cerebral duplex to evaluate changes in pre and post-intracranial hypertension.
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In our model was possible to perform the evaluation of brain hemodynamic changes with TCD without problems in all tested animals.
In our model was possible to perform the evaluation of brain hemodynamic changes with TCD without problems in all tested animals.
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TRANSCRANIAL DOPPLER AND OXIMETRY TISSUE CATHETER MONITORING IN DIFFUSE BRAIN VASOSPASM
TRANSCRANIAL DOPPLER AND OXIMETRY TISSUE CATHETER MONITORING IN DIFFUSE BRAIN VASOSPASM
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Intracranial vasospasm is an important cause of brain ischemia when associated to subarachnoid hemorrhage.
Intracranial vasospasm is an important cause of brain ischemia when associated to subarachnoid hemorrhage. Multimodal monitoring can detect brain flow decrease and patients with high risk to develop brain ischemic lesions. TCD can detect and measure vasospasm intensity in the large intracranial arteries. Usually the oximetry catheter is implanted in the area most likely to occur vasospasm, which is near of brain bleeding. It can measure brain tissue oxygen (PtiO2) in areas with oligoemia associated to vasospasm. They give support to plane treatment to improve brain blood flow in patients suffering brain vasospasm.
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Multimodal monitoring can detect brain flow decrease and patients with high risk to develop brain ischemic lesions.
Intracranial vasospasm is an important cause of brain ischemia when associated to subarachnoid hemorrhage. Multimodal monitoring can detect brain flow decrease and patients with high risk to develop brain ischemic lesions. TCD can detect and measure vasospasm intensity in the large intracranial arteries. Usually the oximetry catheter is implanted in the area most likely to occur vasospasm, which is near of brain bleeding. It can measure brain tissue oxygen (PtiO2) in areas with oligoemia associated to vasospasm. They give support to plane treatment to improve brain blood flow in patients suffering brain vasospasm.
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Usually the oximetry catheter is implanted in the area most likely to occur vasospasm, which is near of brain bleeding.
Intracranial vasospasm is an important cause of brain ischemia when associated to subarachnoid hemorrhage. Multimodal monitoring can detect brain flow decrease and patients with high risk to develop brain ischemic lesions. TCD can detect and measure vasospasm intensity in the large intracranial arteries. Usually the oximetry catheter is implanted in the area most likely to occur vasospasm, which is near of brain bleeding. It can measure brain tissue oxygen (PtiO2) in areas with oligoemia associated to vasospasm. They give support to plane treatment to improve brain blood flow in patients suffering brain vasospasm.
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It can measure brain tissue oxygen (PtiO2) in areas with oligoemia associated to vasospasm.
Intracranial vasospasm is an important cause of brain ischemia when associated to subarachnoid hemorrhage. Multimodal monitoring can detect brain flow decrease and patients with high risk to develop brain ischemic lesions. TCD can detect and measure vasospasm intensity in the large intracranial arteries. Usually the oximetry catheter is implanted in the area most likely to occur vasospasm, which is near of brain bleeding. It can measure brain tissue oxygen (PtiO2) in areas with oligoemia associated to vasospasm. They give support to plane treatment to improve brain blood flow in patients suffering brain vasospasm.
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They give support to plane treatment to improve brain blood flow in patients suffering brain vasospasm.
Intracranial vasospasm is an important cause of brain ischemia when associated to subarachnoid hemorrhage. Multimodal monitoring can detect brain flow decrease and patients with high risk to develop brain ischemic lesions. TCD can detect and measure vasospasm intensity in the large intracranial arteries. Usually the oximetry catheter is implanted in the area most likely to occur vasospasm, which is near of brain bleeding. It can measure brain tissue oxygen (PtiO2) in areas with oligoemia associated to vasospasm. They give support to plane treatment to improve brain blood flow in patients suffering brain vasospasm.
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A 48 years old woman with subarachnoid hemorrhage (Hess IV) and intracranial brain hemorrhage at right side in cranial tomography (CT)(Fisher IV).
A 48 years old woman with subarachnoid hemorrhage (Hess IV) and intracranial brain hemorrhage at right side in cranial tomography (CT)(Fisher IV). She was underwent a middle cerebral artery aneurism clipping, intracranial pressure (ICP) catheter implantation and catheter to measure brain parenchyma PtiO
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She was underwent a middle cerebral artery aneurism clipping, intracranial pressure (ICP) catheter implantation and catheter to measure brain parenchyma PtiO
A 48 years old woman with subarachnoid hemorrhage (Hess IV) and intracranial brain hemorrhage at right side in cranial tomography (CT)(Fisher IV). She was underwent a middle cerebral artery aneurism clipping, intracranial pressure (ICP) catheter implantation and catheter to measure brain parenchyma PtiO
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area. Serial TCD exams disclosed diffuse brain vasospasm,
area. Serial TCD exams disclosed diffuse brain vasospasm,
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Despite treatment with 3H therapy, we noted ischemic areas in brain CT at opposite side of bleeding (left side), when PtiO
which were more intense at left side. Despite treatment with 3H therapy, we noted ischemic areas in brain CT at opposite side of bleeding (left side), when PtiO
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Brain vasospasm can be focal or diffuse.
Brain vasospasm can be focal or diffuse. In this case TCD suggested more intensity vasospasm at opposite side of bleeding; ischemic areas were disclosed by CT exam in this side, confirming TCD findings. Brain oxymetry catheter can monitor a small area of brain tissue so it is not reliable as a isolated monitor method in patients with subarachnoid hemorrhage and diffuse vasospasm.
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Brain oxymetry catheter can monitor a small area of brain tissue so it is not reliable as a isolated monitor method in patients with subarachnoid hemorrhage and diffuse vasospasm.
Brain vasospasm can be focal or diffuse. In this case TCD suggested more intensity vasospasm at opposite side of bleeding; ischemic areas were disclosed by CT exam in this side, confirming TCD findings. Brain oxymetry catheter can monitor a small area of brain tissue so it is not reliable as a isolated monitor method in patients with subarachnoid hemorrhage and diffuse vasospasm.
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brain ischemia, brain oximetry, diffuse vasospasm, subarachnoid hemorrhage.
brain ischemia, brain oximetry, diffuse vasospasm, subarachnoid hemorrhage.
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brain vasospasm, microembolic signals, subarachnoid hemorrhage, transcranial Doppler.
brain vasospasm, microembolic signals, subarachnoid hemorrhage, transcranial Doppler.
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In cases with pure autonomic failure the cerebral autoregulation seemed to be preserved if the MBP was maintained within the limit for brain autoregulation.
The pattern of orthostatic adjustment of the cerebral and systemic hemodynamics depended on the topic of the lesion, the type (“passive” or “active”) of the orthostatic challenge and the antigravity efficacy of the peripheral muscle pump. A paradoxical cerebral vasoconstriction due to hyperventilation was found in patients with postural tachycardia syndrome. In cases with pure autonomic failure the cerebral autoregulation seemed to be preserved if the MBP was maintained within the limit for brain autoregulation. During the induced neurally mediated syncope the selective loss of diastolic BFV and the increase in Pulsatility index were typically observed.
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brain vascular autoregulation, fulminant hepatic failure, transcranial Doppler.
brain vascular autoregulation, fulminant hepatic failure, transcranial Doppler.
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BRAIN HEMODYNAMIC IMPROVEMENT AFTER RETROGRADE VENTRICULO-SINUS SHUNT IN HYDROCEPHALUS PATIENTS
BRAIN HEMODYNAMIC IMPROVEMENT AFTER RETROGRADE VENTRICULO-SINUS SHUNT IN HYDROCEPHALUS PATIENTS
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Transcranial Doppler can evaluate intracranial hypertension relief after this surgical procedure measuring brain blood flow velocities, pulsatility and resistivity index.
shunt (RVSS) is proposed in order to solve the question of ventricular catheterization complications related to siphoning. Transcranial Doppler can evaluate intracranial hypertension relief after this surgical procedure measuring brain blood flow velocities, pulsatility and resistivity index.
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Therefore, this method may be a useful tool for assessing the pre post operative brain hemodynamic in patients with hydrocephalus.
Although still preliminary, improved hemodynamic encephalic demonstrated by transcranial Doppler was compatible with the clinical improvement of patients. Therefore, this method may be a useful tool for assessing the pre post operative brain hemodynamic in patients with hydrocephalus.
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brain artery velocities, hydrocephalus, transcranial Doppler, ventricle sinus shunt.
brain artery velocities, hydrocephalus, transcranial Doppler, ventricle sinus shunt.
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The risk of transient ischemic attack and stroke following transfemoral aortic valve implantation (TAVI) is 2-10% and is even higher considering silent ischemic brain injury.
The risk of transient ischemic attack and stroke following transfemoral aortic valve implantation (TAVI) is 2-10% and is even higher considering silent ischemic brain injury. Periprocedural microembolic signals (MES) and hemodynamic changes (HC) may be considered physiopathological markers of such events. We show neurosonological and neuroradiological data about a patient submitted to TAVI.
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Moreover, patient underwent brain magnetic resonance with diffusion-weighted sequences (MRDWI) before and after TAVI.
cerebral artery was performed by transcranial Doppler (TCD), in order to reveal MES and HC (left acoustical temporal bone window was inadequate). Moreover, patient underwent brain magnetic resonance with diffusion-weighted sequences (MRDWI) before and after TAVI.
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Post-procedural brain MR-DWI detected two recent-onset signal abnormalities in the right emisphere.
1103 MES were detected: 116 (10.5%) during the crossing of the native valve by guidewire and pigtail catheter, 50 (4.5%) during valve predilatation with balloon, 29 (2.6%) related to passage of device (CoreValve) in the aortic arch and its positioning in the valve, 693 (62.9%) during release of the prosthesis, 215 (19.5%) in the phase of catheter removal. As for HC, peak systolic velocity reduction (from 82 cm/s to 38 cm/s) and heart rate increase (from 66 to 156 beats per minute) were observed in a period of 8 seconds during predilation. Post-procedural brain MR-DWI detected two recent-onset signal abnormalities in the right emisphere. Patient remained asymptomatic during hospital stay.
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TCD monitoring may provide useful and real-time data on the physiopathological mechanisms underlying the risk of ischemic brain injury during TAVI, identifying phases at higher risk.
TCD monitoring may provide useful and real-time data on the physiopathological mechanisms underlying the risk of ischemic brain injury during TAVI, identifying phases at higher risk. Further research is needed to validate these findings.
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aortic valve implantation, ischemic brain lesion, transcranial Doppler.
aortic valve implantation, ischemic brain lesion, transcranial Doppler.
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SAFETY EVALUATION OF MID-FREQUENCY SONOTHROMBOLYSIS: ANIMAL BRAIN EXPERIMENT
SAFETY EVALUATION OF MID-FREQUENCY SONOTHROMBOLYSIS: ANIMAL BRAIN EXPERIMENT
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1.We applied a developed probe to Macaca monkey brain via sonication of the MCA through a temporal window.
1.We applied a developed probe to Macaca monkey brain via sonication of the MCA through a temporal window. Each three cynomolgus monkeys were maintained for 1 day and 7 days after sonication. And more two elder rhesus monkeys were sonicated under the alteplase (0.9 mg/kg) i.v., and maintained for 7 days. An automatic switching circuit operated a therapeutic US (T-beam) generator for thrombolysis (490 kHz; CW-US, Ispta 0.72 W/cm2) and diagnostic TC-CFI (D-beam; 2.5 MHz; Ispta 0.20 W/cm2). A 15-min protocol, comprising 4 repeats of a sequence of 120s T-beam followed by 30-s D-beam and then 5-min T-beam deactivation monitoring with D-beam, was repeated 4 times.
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There was no brain damage in monkey brain by developed probe at eMI=0.42.
One of the hemorrhagic causes in the TRUMBI trial is high effective mechanical index (eMI) over 2.0. There was no brain damage in monkey brain by developed probe at eMI=0.42. According to McDannold, the eMI threshold of the disruption in rabbit BBB by BW-US is 1.38. In our rabbit study, the similar traumatic change appeared at the eMI=1.56 by BWUS. It suggests that high eMI at brain induce traumatic damage.
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It suggests that high eMI at brain induce traumatic damage.
One of the hemorrhagic causes in the TRUMBI trial is high effective mechanical index (eMI) over 2.0. There was no brain damage in monkey brain by developed probe at eMI=0.42. According to McDannold, the eMI threshold of the disruption in rabbit BBB by BW-US is 1.38. In our rabbit study, the similar traumatic change appeared at the eMI=1.56 by BWUS. It suggests that high eMI at brain induce traumatic damage.
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ULTRASONIC EVALUATION OF ACETAZOLAMIDE VASOREACTIVITY IN BRAIN TISSUE AND MAJOR CEREBRAL ARTERIES
ULTRASONIC EVALUATION OF ACETAZOLAMIDE VASOREACTIVITY IN BRAIN TISSUE AND MAJOR CEREBRAL ARTERIES
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In order to evaluate cerebrovascular reserve capacity in the brain tissue, acetazolamide (ACZ) cerebrovascular reactivity (CVR) has been measured in major cerebral arteries by transcranial Doppler sonography.
In order to evaluate cerebrovascular reserve capacity in the brain tissue, acetazolamide (ACZ) cerebrovascular reactivity (CVR) has been measured in major cerebral arteries by transcranial Doppler sonography. This has shown some correlation with CVR in the brain tissue, as measured by neuroradiological modalities.
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This has shown some correlation with CVR in the brain tissue, as measured by neuroradiological modalities.
In order to evaluate cerebrovascular reserve capacity in the brain tissue, acetazolamide (ACZ) cerebrovascular reactivity (CVR) has been measured in major cerebral arteries by transcranial Doppler sonography. This has shown some correlation with CVR in the brain tissue, as measured by neuroradiological modalities.
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We have evaluated ACZ CVR in the brain tissue by transcranial power modulation imaging (PMI) and correlated with transcranial color duplex sonography (TCDS) observed CVR in the major arteries.
We have evaluated ACZ CVR in the brain tissue by transcranial power modulation imaging (PMI) and correlated with transcranial color duplex sonography (TCDS) observed CVR in the major arteries.
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1) Regardless of the use of timeor intensitydependant parameters or a transducer holder, the tendency of close ACZ relationships between brain tissue perfusion and velocity changes in the major arteries remains unchanged.
1) Regardless of the use of timeor intensitydependant parameters or a transducer holder, the tendency of close ACZ relationships between brain tissue perfusion and velocity changes in the major arteries remains unchanged. 2) Easily disrupted CVR in the brain tissue due to intraparenchymal lesions resulted in poor correlation with CVR in the major arteries.
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2) Easily disrupted CVR in the brain tissue due to intraparenchymal lesions resulted in poor correlation with CVR in the major arteries.
1) Regardless of the use of timeor intensitydependant parameters or a transducer holder, the tendency of close ACZ relationships between brain tissue perfusion and velocity changes in the major arteries remains unchanged. 2) Easily disrupted CVR in the brain tissue due to intraparenchymal lesions resulted in poor correlation with CVR in the major arteries.
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brain ultrasound Dupplex, Machado Joseph
brain ultrasound Dupplex, Machado Joseph
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OUR EXPERIENCE WITH ENDOVASCULAR TREATMENT OF BRAIN ANEURYSMS AND AVMS
OUR EXPERIENCE WITH ENDOVASCULAR TREATMENT OF BRAIN ANEURYSMS AND AVMS
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Endovascular treatment of brain aneurysm and AVM’s is
Endovascular treatment of brain aneurysm and AVM’s is
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The last 15 years endovascular technics shown significant progress and development in treatment of brain vascular malformations.
The last 15 years endovascular technics shown significant progress and development in treatment of brain vascular malformations.
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Neonate’s brain has high plasticity after birth and great opportunities for recovery.
Neonate’s brain has high plasticity after birth and great opportunities for recovery. Thanks to this fact premature neonates with hypoxic impairments of the CNS and at risk of developing motor disorders have better motor outcomes if they have EPI that started within the first days after birth.
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Initial questions accentuate on the dopamine deficiency as the major pathobiochemical symptom and on the causes for neurons degeneration in substantia nigra and other brain areas.
Initial questions accentuate on the dopamine deficiency as the major pathobiochemical symptom and on the causes for neurons degeneration in substantia nigra and other brain areas. Knowledge of the synthesis and degradation of dopamine is necessary to understand the mechanisms of neuroprotection and delaying the disease progression via treatment with anticholinergic agents or dopamine precursors in combination of inhibitors of the peripheral DOPA decarboxylase. The program allows the students to understand and learn about the action of MAO and COMT
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ELECTROMAGNETIC RADIATION WHEN REGISTERING BRAIN ACTIVITY WITH AN EEG
ELECTROMAGNETIC RADIATION WHEN REGISTERING BRAIN ACTIVITY WITH AN EEG
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The influence of artificial electromagnetic radiation (EMR) is actual for the quality of recording brain activity.
At present portable EEG-devices are widely used. The influence of artificial electromagnetic radiation (EMR) is actual for the quality of recording brain activity. A lot of artifacts are considered non-physiological artifacts that are caused by a wide range of electromagnetic radiation: from 3 to 3000 MHz. Considering the above, the identification, description and making a list of these artifacts is a priority now. It will make it possible to create a software filter for EEGsystems.
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19. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 10, 2014, No. 1 , , ,

The Year of the Brain
The Year of the Brain
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Година на мозъка The Year of the Brain
Година на мозъка The Year of the Brain
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The European Brain Council (EBC) has launched the Year of the Brain project.
The European Brain Council (EBC) has launched the Year of the Brain project. Jt is beginning now and will run through into 2015. The Year of the Brain (YotB) has three key aims or "pillars
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The Year of the Brain (YotB) has three key aims or "pillars
The European Brain Council (EBC) has launched the Year of the Brain project. Jt is beginning now and will run through into 2015. The Year of the Brain (YotB) has three key aims or "pillars
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To educate society about how to nurture and protect the brain and prevent brain disease;
To educate society about how to nurture and protect the brain and prevent brain disease;
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To improve care and treatment access for those affected by brain disease;
To improve care and treatment access for those affected by brain disease;
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To increase investment in brain-related Research and Development (R&D) for the benefit of future generations.
To increase investment in brain-related Research and Development (R&D) for the benefit of future generations.
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The organisation of YotB is being led by Dr Mary Baker MBE, President of the Year of the Brain.
The organisation of YotB is being led by Dr Mary Baker MBE, President of the Year of the Brain. The EBC encourages potential partners to brand brain-related activities with the YotB logo, provided these activities are non-promotional in nature. These may be regular events or events organised especially for YotB.
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The EBC encourages potential partners to brand brain-related activities with the YotB logo, provided these activities are non-promotional in nature.
The organisation of YotB is being led by Dr Mary Baker MBE, President of the Year of the Brain. The EBC encourages potential partners to brand brain-related activities with the YotB logo, provided these activities are non-promotional in nature. These may be regular events or events organised especially for YotB.
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Recent examinations via functional Magnetic Resonance Imaging (fMRI) of the brain try to explain their pathogenesis but it still remains insufficient [4].
The hallucinations vary from simple (photopsias, scotoms, simple colored objects), to more complex (different pictures, faces) [6]. The causes of their occurrence are numerous from different psychoses, deliria, dementias to conditions with unknown etiology as the Charles-Bonnet Syndrome [2, 5, 13]. Recent examinations via functional Magnetic Resonance Imaging (fMRI) of the brain try to explain their pathogenesis but it still remains insufficient [4].
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The results were compared with those obtained from brain
ln 2008 and 2009 experimental implantation of "Alloplant" was made in Russia with controversial subjective effect. Since then the patient has color hallucinations known as Charles Bonnet Syndrome. Parallel clinical and neuro-ophthalmological examinations for evaluation of his neurological and visual impairments were performed. The multimodal neuro-ophthalmo-sonography 2D/3D/4D was usеd for visualizing the structures: the vitreous bodies, the ophthalmic nerves and the ophthalmic papillae. The blood vessels of the eyes including the ophthalmic arteries and veins were evaluated by B-flow imaging. The results were compared with those obtained from brain
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ln order to evaluate the functional activity of the brain cortex classical electroencephalography was performed with quantitive Fast Fourier Transformation (FFT).
ln order to evaluate the functional activity of the brain cortex classical electroencephalography was performed with quantitive Fast Fourier Transformation (FFT). The alpha power temporooccipitally was evaluated and analyzed after flash photostimulation at 9 Нz for both eyes and for each eye separately (while the other eye was covered with a patch). Thirty-second intervals of the conventional EEG record were analyzed. Pattern reversal evoked patentials were performed using standart parameters of the medical equipment.
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Magnetic Resonance lmaging of the brain
Magnetic Resonance lmaging of the brain
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showed normal brain parenchyma, cortex and ocular muscles.
showed normal brain parenchyma, cortex and ocular muscles. Bilateral atrophy of the ophthalmic nerves, left eye deformities and silicone filled right ocular bulb were observed (fig. 3).
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FFT before the photostimulation showed nonsignificant asymmetry in the alpha power, which is higher in the right brain hemisphere.
revealed frequency peak in 8.8 Hz. FFT before the photostimulation showed nonsignificant asymmetry in the alpha power, which is higher in the right brain hemisphere. During the bilateral intermittent photostimulation (9 Hz) significant reduction of the alpha power temporooccipitally was registered. The changes were more prominent on the left cortex while stimulating the right eye. The examination was associated with simple visual hallucinations (colored circles) at the end of the photostimulation and lasting a couple of minutes after ceasing the stimuli (fig. 4).
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Normal brain parenchyma, ocular muscles and occipital cortex (
Вrain MRI. Normal brain parenchyma, ocular muscles and occipital cortex (
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Most authors consider them as being a result of deafferentation caused by absent visual impulses ascending toward the brain cortex.
lt is known that the hallucinations in the Charles Bonnet syndrome can greatly vary from simple, repeating colored spots to complex colorful images of people and objects. The patients understand that these images are not real and can describe them very detailed in shape and localization. Most authors consider them as being a result of deafferentation caused by absent visual impulses ascending toward the brain cortex. This hypothesis is supported by experimental research showing the appearance of such hallucinations in healthy sighted individuals deprived from light [1О]. The functional MRl examinations within people with Charles Bonnet syndrome demonstrate presence of reorganized neuron network with high activity in the ventral visual cortex during and in the absence of hallucinations [5, 11]. According to Santhouse et all. [12] using fMRl it's possible to make mapping of the hallucinations they assume that the complex hallucinations correspond to damage of the front-temporal cortex, the activation of gyrus fusiformis is associated with images of different faces, the ventral occipital cortex hallucinations of objects and scenes and the parietal lob paliopsias and perseverational images. The simple hallucinations (in a form of lines, dots, circles of light etc.) are associated with bilateral damage of the visual pathways from the retina to the primary visual cortex and very seldom appear after damaged associational visual fields [З, 5].
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Brain
Brain
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The brain parenchyma, cranial bones and soft tissues were evaluated by native and contrast СT of the head and neck.
The patient underwent a complex clinical examination searching for tumor formations in other locations. The brain parenchyma, cranial bones and soft tissues were evaluated by native and contrast СT of the head and neck. The major basal cerebral and facial arteries and veins were examined preoperatively with multimodal 2D/3D/4D neurosonography with B-flow imaging of the blood stream and 4-dimensional imaging of the tumor.
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scan of the head and neck performed preoperatively established normal brain parenchyma and cranial bones.
scan of the head and neck performed preoperatively established normal brain parenchyma and cranial bones. А large heterogeneous tumor formation in the left facial area was displayed. lt had hourglass shape above and below the zygomatic arch and was initially interpreted as lymphangioma. Аt the level of the lower jaw the tumor had solid structure with poor vascularization. No changes in the neighboring structures were detected. ln the occipito-parietal area along the sagittal plane a second 35 mm in size formation was found.
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Laboratory tests, a double CТ scan of the brain
From 2009 to 2013 on the territory of the Second Clinic of Neurology with ICU at the University Hospital "St. Marina" Varna 166 (3.1%) thrombolyses from a total of 5353 patients with AIS were conducted, classified by the etiopathogenic classification ТОASТ. Тhe neurological status of each patient was examined and estimated by NIHSS. Laboratory tests, a double CТ scan of the brain
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(after hospitalization and within 24 hours after the trombolysis) and Dupplex scanning of the main brain vessels in the first 24 hours after the onset of symptoms were performed.
(after hospitalization and within 24 hours after the trombolysis) and Dupplex scanning of the main brain vessels in the first 24 hours after the onset of symptoms were performed. Evaluation of the functional status of the patients was performed twice with modified Rankin Scale (mRS) before hospital discharge and 3 months after the incident.
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Laboratory tests, a double СT scan of the brain (after hospitalization and within 24 hours after the thrombolysis) and Dupplex scanning of the brain vessels in the first 24 hours after the onset of the symptoms are performed.
The severity of the neurological deficit in each patient is estimated with NIHSS. Laboratory tests, a double СT scan of the brain (after hospitalization and within 24 hours after the thrombolysis) and Dupplex scanning of the brain vessels in the first 24 hours after the onset of the symptoms are performed. The evaluation of the patients' functional status is twice performed with modified Rankin Scale (mRS) after hospital discharge and 3 months after the incident.
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ln the other cases the reason is lack of recanalization, malignant brain edema, fallowed by herniation, cerebrovascular pathology and severe comorbidity, leading to death.
lization 19.27% (32/166) of the patients died, as the intracerebral hemorrhage was cause for death in 8 of them. ln the other cases the reason is lack of recanalization, malignant brain edema, fallowed by herniation, cerebrovascular pathology and severe comorbidity, leading to death.
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Results from CT Scan of the Brain by Hospitalization and 24 Hours after TL.
Results from CT Scan of the Brain by Hospitalization and 24 Hours after TL.
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Резултати от КТ на глава/ ResuЫts from СТ Scan of the Brain
Резултати от КТ на глава/ ResuЫts from СТ Scan of the Brain
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A decompressive craniectomy is performed because of loss of consciousness, persisting severe motor deficit in the first 24 hours after the thrombolysis and МRl evidence of extensive brain edema.
A decompressive craniectomy is performed because of loss of consciousness, persisting severe motor deficit in the first 24 hours after the thrombolysis and МRl evidence of extensive brain edema. Postoperatively a complete restoration of consciousness and partial regression of focal neurological signs are observed.
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The presentation of this clinical case supports the necessity of decompressive craniectomy in patients with acute ischemic stroke and massive brain edema after thrombolysis.
The presentation of this clinical case supports the necessity of decompressive craniectomy in patients with acute ischemic stroke and massive brain edema after thrombolysis. The indications for this potential life-saving procedure are still debated.
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Neuroimaging examination of the brain was conducted by 1.5 Tesla МRl (GE HTХ Sigma
There were many risk factors for cerebrovascular disease: arterial hypertension, dyslipidemia, obesity. А pointed laboratory examination of complete blood count, biochemistry and coagulation status was performed. Мain head arteries were examined with Sonix SP (Сanada) by color coded duplex scanning using 7.5 Hz transducer. The thickness of the carotid artery intima-media complex was measured by B-mode imaging in real-time using a standard program for automatic averaging of values. With pulse Doppler sonography speed parameters of blood flow were measured. Neuroimaging examination of the brain was conducted by 1.5 Tesla МRl (GE HTХ Sigma
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USА). Аn ischemic stroke in the territory of the МСА was diagnosed and confirmed by СT scan of the brain.
USА). Аn ischemic stroke in the territory of the МСА was diagnosed and confirmed by СT scan of the brain. Аll criteria of the National Health lnsurance Fund for thrombolytic therapy
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The optimal treatment of brain edema includes osmotherapy with mannitol, blood pressure control, head elevation to 30°, maintenance of normothermia, normoglycemia and normovolemia.
Malignant cerebral ischemia occurs in a significant number of patients with acute cerebrovascular incidents. The mortality rate in those patients is very high due to progressive, severe cerebral edema. ln these patients decompressive craniectomy is indicated and is applied after an exact clinical and neuroimaging evaluation. The optimal treatment of brain edema includes osmotherapy with mannitol, blood pressure control, head elevation to 30°, maintenance of normothermia, normoglycemia and normovolemia. lt's considered that the early decompressive craniectomy leads to better
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MRI of the brain – ischemic stroke in MCA territory with hemorrhagic transformation
MRI of the brain – ischemic stroke in MCA territory with hemorrhagic transformation
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Quality of life after hemicraniectomy for traumatic brain injury in adults.
Danish SF, Barone D, Lega BC, Stein SC. Quality of life after hemicraniectomy for traumatic brain injury in adults. A review of the literature.
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Sinking skin flaps, paradoxical herniation, and external brain tamponade: a review of decompressive craniectomy management.
Akins PT, Guppy KH. Sinking skin flaps, paradoxical herniation, and external brain tamponade: a review of decompressive craniectomy management.
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Predictors of fatal brain edema in massive hemispheric ischemic stroke.
Kasner SE, Demchuk AM, Berrouschot J, Schmutzhard E, Harms L, Verro P, Chalela JA, Abbur R, McGrade H, Christou I, Krieger DW. Predictors of fatal brain edema in massive hemispheric ischemic stroke.
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Early clinical and radiological predictors of fatal brain swelling in ischemic stroke.
Krieger DW, Demchuk AM, Kasner SE, Jauss M, Hantson L. Early clinical and radiological predictors of fatal brain swelling in ischemic stroke.
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is a complex of diagnostic and therapeutic procedures in emergency setting after CA for restoring of circulation and providing of oxygenated blood to brain.
is a complex of diagnostic and therapeutic procedures in emergency setting after CA for restoring of circulation and providing of oxygenated blood to brain. Weisfeldt et al. defined three consecutive phases after СА according to ischemia progression: electrical phase (0-4 min) following by circulatory phase (4-10 min) and metabolic phase (more than 10 min) [29].
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CNS symptoms coma, seizures, myoclonus, cognitive dysfunction and brain death.
CNS symptoms coma, seizures, myoclonus, cognitive dysfunction and brain death. Seizures after ROSC are observed in 5-15% of adults and in up to 40% of patients in coma (generalized, non-generalized, myoclonuses,
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etc.). They increase the brain metabolism three times leading to additional brain damage.
etc.). They increase the brain metabolism three times leading to additional brain damage.
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Symptoms of brain damage might deepen by impaired microcirculation, impaired autoregulation, hypercarbia, hyperoxia, pyrexia, hyperglycemia and seizures.
The severity of lRS varies depending on the continuation and the cause of the cardiac arrest. ln case of short term CА, the lRS might not be displayed. Symptoms of brain damage might deepen by impaired microcirculation, impaired autoregulation, hypercarbia, hyperoxia, pyrexia, hyperglycemia and seizures. Significant MD is often observed after СА and usually recovers in 2-3 days. Neurologic complications are a cause of death in 2/3 of patients after СА before being admitted to an lntensive Care Unit and in 1/4 of hospitalized patients [22].
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are classified based on the time after the begining of CА and unsuccessful CPR, as follows: 0-5 min clinical death (CD); 5-10 min CD without neurological deficiency; 10-15 min CD with neurological deficiency; 1520 min cortical death; and over 20 min brain and biologic death.
are classified based on the time after the begining of CА and unsuccessful CPR, as follows: 0-5 min clinical death (CD); 5-10 min CD without neurological deficiency; 10-15 min CD with neurological deficiency; 1520 min cortical death; and over 20 min brain and biologic death.
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is a result of discontinuation of the effective brain circulation demonstrated with reversible and temporary failure of brain functions.
is a result of discontinuation of the effective brain circulation demonstrated with reversible and temporary failure of brain functions. СА is identified with the clinical death. Аfter 2-3 minutes the alveolar anoxia leads to clinical death due to oxygen depletion of body reserves [30]. lt might be a result of removal of the technical support of circulation and respiration.
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is a result of severe destruction of the brain cortex and a loss of its functional connections with the other brain structures (apallic syndrome, chronic vegetative status).
is a result of severe destruction of the brain cortex and a loss of its functional connections with the other brain structures (apallic syndrome, chronic vegetative status). The patient is in bed and all living systems might operate for a long period of time [30].
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Brain Death
Brain Death
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is a result of stopping of brain circulation and irreversible changes of brain functions and brain stem presenting with three main events: coma, absence of stem reflexes and apnea [2, 13, 30].
is a result of stopping of brain circulation and irreversible changes of brain functions and brain stem presenting with three main events: coma, absence of stem reflexes and apnea [2, 13, 30]. Аs of the current moment in medical regulation (Regulation No.14/ 15.04.2004) and in term of transplantation, the locally accepted definition of this condition is: "irreversible and permanent cessation of all functions of the brain in the presence of heartbeat".
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Аs of the current moment in medical regulation (Regulation No.14/ 15.04.2004) and in term of transplantation, the locally accepted definition of this condition is: "irreversible and permanent cessation of all functions of the brain in the presence of heartbeat".
is a result of stopping of brain circulation and irreversible changes of brain functions and brain stem presenting with three main events: coma, absence of stem reflexes and apnea [2, 13, 30]. Аs of the current moment in medical regulation (Regulation No.14/ 15.04.2004) and in term of transplantation, the locally accepted definition of this condition is: "irreversible and permanent cessation of all functions of the brain in the presence of heartbeat".
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Mild therapeutic hypothermia improves survival after СА providing brain neuroprotection.
The rhythm of pulseless СА in children usually progresses from bradyarrhythmia to asystole or PЕА and rarely to VF [21]. The first documented rhythm of СА in the age group above 75 y/a is VF or PVT in 36% of hospitalized and in 24% of ambulatory patients. VF or PVT is registered in 25% during the reanimation stages or after the first documented rhythm of asystole or PЕА [22]. Relation is observed between VF and PVT as well as between PЕА and asystole in case identical risk factors are present. For example, acute myocardial infarction is associated with firstly documented VF or PVT; the acute respiratory failure and hypotension correlate with PЕА and asystole [20]. Mild therapeutic hypothermia improves survival after СА providing brain neuroprotection. The up-to-date guidelines
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; sonography for cerebral circulatory arrest; Computed Tomography; CT angiography; digital subtraction angiography; isotope angiography and isotope scanning of brain [2, 22, 27].
; sonography for cerebral circulatory arrest; Computed Tomography; CT angiography; digital subtraction angiography; isotope angiography and isotope scanning of brain [2, 22, 27]. A reliable prognosis could not be done based on only clinical signs, electrophysiological tests and biomarkers. Cerebral Performance Categories and Glasgow Outcome Scoring System are scales developed for assessment of neurologycal functions after CA, however they are not applicable in the first hours/ days after SCA [22, 27].
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The diagnosis of brain death.
Goila А, Pawar М. The diagnosis of brain death.
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Evidencebased guideline update: Determining brain death in adults: Report of the Quality Standards Subcommittee of the Аmerican Аcademy of Neurology.
Wijdicks E, Varelas P, Gary S, Gronseth D, Greer D. Evidencebased guideline update: Determining brain death in adults: Report of the Quality Standards Subcommittee of the Аmerican Аcademy of Neurology.
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Aging brain, Stroke and Dementia
Aging brain, Stroke and Dementia
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20. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 10, 2014, No. 2 , , ,

Brain Imaging in Neurorehabilitation
Brain Imaging in Neurorehabilitation
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Ultrasound Imaging of Brain Parenchyma,
Ultrasound Imaging of Brain Parenchyma,
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Supporting the initiative "Year of the Brain" of the European Council on Brain and designating with its logo all the BSNCH events which will be held till the end of 2015.
Supporting the initiative "Year of the Brain" of the European Council on Brain and designating with its logo all the BSNCH events which will be held till the end of 2015.
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Leading European specialists in the field of Neurology will present current problems on the topics of the aging brain, stroke and dementia, and new technologies applied in Neurorehabilitation and Neurosonology.
Leading European specialists in the field of Neurology will present current problems on the topics of the aging brain, stroke and dementia, and new technologies applied in Neurorehabilitation and Neurosonology.
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AGING BRAIN,
AGING BRAIN,
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AGING BRAIN, STROKE AND DEMENTIA
AGING BRAIN, STROKE AND DEMENTIA
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Silent Brain Infarction.
Silent Brain Infarction.
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Brain Imaging in Neurorehabilitation.
Brain Imaging in Neurorehabilitation.
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Brain Imaging in Neurorehabilitation.
Brain Imaging in Neurorehabilitation.
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Ultrasound Imaging of Brain Parenchyma, Temporal Arteries and Orbita.
Ultrasound Imaging of Brain Parenchyma, Temporal Arteries and Orbita.
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She was Head of Department of Clinical Neurology and Centre for Neurological Sciences and Brain Research in University Hospital Centre “Sestre Milosrdnice” from May 1994.
She was Head of Department of Clinical Neurology and Centre for Neurological Sciences and Brain Research in University Hospital Centre “Sestre Milosrdnice” from May 1994. until November 2011. Under her leadership the Department became Reference Centre for Neurovascular Disorders and Reference Centre for Headaches of Ministry of Health of Republic of Croatia. From November 2011 until September 2012, she was Counselor for International Collaboration in the same institution. She was appointed Medical director of Medical Centre Aviva in September 2012.
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She is member of the Executive Board of the Academy of Medical Sciences of Croatia, Fellow of American Academy of Neurology, Fellow of American Heart Association, Fellow of European Stroke Organization and member of World Stroke Organization Board of Directors, member of International Headache Society, Subspecialty Scientific Panel for Stroke, Subspecialty Scientific Panel for Headache and Subspecialty Scientific Panel on Higher Cortical Functions of European Academy of Neurology (EAN), Vice President of Croatian Brain Council, and more.
Member of many Croatian and international professional societies, president of Kuratorium of International Neuropsychiatric Pula Congresses, president of Central and Eastern European Stroke Society and the Secretary General of the WFN Applied Research Group on Organization and Delivery of Care. She is member of the Executive Board of the Academy of Medical Sciences of Croatia, Fellow of American Academy of Neurology, Fellow of American Heart Association, Fellow of European Stroke Organization and member of World Stroke Organization Board of Directors, member of International Headache Society, Subspecialty Scientific Panel for Stroke, Subspecialty Scientific Panel for Headache and Subspecialty Scientific Panel on Higher Cortical Functions of European Academy of Neurology (EAN), Vice President of Croatian Brain Council, and more.
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She was two terms president of Croatian Neurological Society, founder and the first president of Croatian Society for Neurovascular Disorders and Croatian Stroke Society, whose workgroup published national Recommendations for Stroke Management 2001 and 2006, as well as Evidence based Guidelines for Management of Primary Headaches 2005 and 2008, Consensus Opinion on Brain Death Diagnosing 2005, and Recommendations for the Management of Patients with Carotid Stenosis 2010.
She was two terms president of Croatian Neurological Society, founder and the first president of Croatian Society for Neurovascular Disorders and Croatian Stroke Society, whose workgroup published national Recommendations for Stroke Management 2001 and 2006, as well as Evidence based Guidelines for Management of Primary Headaches 2005 and 2008, Consensus Opinion on Brain Death Diagnosing 2005, and Recommendations for the Management of Patients with Carotid Stenosis 2010. She initiated national program of stroke management, organization of stroke unit network and thrombolysis therapy in Croatia.
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Cross-disciplinary research into the development, application and user perspectives of novel technologies (Functional Electrical Stimulation, Non-Invasive Brain Stimulation, Rehabilitation Robotics, Constraint induced Movement Therapy, and Movement Sensors) for upper limb and trunk neurorehabilitation.
Cross-disciplinary research into the development, application and user perspectives of novel technologies (Functional Electrical Stimulation, Non-Invasive Brain Stimulation, Rehabilitation Robotics, Constraint induced Movement Therapy, and Movement Sensors) for upper limb and trunk neurorehabilitation.
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Neuropsychological and behavioral examination and evaluation, Neurosonology (Extracranial/Transcranial ultrasound, Temporal arteries sonography, Orbita ultrasonography), Ultrasound examination of the brain parenchyma (basal ganglia), Stroke management (including thrombolytic therapy and sonothombolysis).
Neuropsychological and behavioral examination and evaluation, Neurosonology (Extracranial/Transcranial ultrasound, Temporal arteries sonography, Orbita ultrasonography), Ultrasound examination of the brain parenchyma (basal ganglia), Stroke management (including thrombolytic therapy and sonothombolysis).
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Cerebrovascular Disorders (genetics, path-physiology of arteriosclerosisespecially the role of insulin resistance in atherogenesis, asymptomatic carotid artery stenosis and vascular dementia, rare causes of stroke especially in young adults), Ultrasound Techniques in Neurology (Power Triplex Color Doppler, Transcranial Doppler, detection of the circulating micro emboli and cerebral vasomotor reactivity testing, sonothrombolysis), chronic headaches (co-morbidity of migraine, chronic tension type of headache, rare headaches-SUNCT, cluster headache, paroxysmal hemicranias), Neuropsychology and Dementia, Movement Disorders (neuroimaging techniques, brain parenchyma sonography).
Cerebrovascular Disorders (genetics, path-physiology of arteriosclerosisespecially the role of insulin resistance in atherogenesis, asymptomatic carotid artery stenosis and vascular dementia, rare causes of stroke especially in young adults), Ultrasound Techniques in Neurology (Power Triplex Color Doppler, Transcranial Doppler, detection of the circulating micro emboli and cerebral vasomotor reactivity testing, sonothrombolysis), chronic headaches (co-morbidity of migraine, chronic tension type of headache, rare headaches-SUNCT, cluster headache, paroxysmal hemicranias), Neuropsychology and Dementia, Movement Disorders (neuroimaging techniques, brain parenchyma sonography).
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Dr. Tarkka received her PhD at the University of Jyväskylä 1986, did many years of neuroscience research in USA and Germany and then served as Director of Research at the Brain Research and Rehabilitation Center Neuron, Kuopio.
Dr. Tarkka received her PhD at the University of Jyväskylä 1986, did many years of neuroscience research in USA and Germany and then served as Director of Research at the Brain Research and Rehabilitation Center Neuron, Kuopio. She is Adjunct Professor in Cognitive Neuroscience and Researcher in the Department of Health Sciences, University of Jyväskylä, Jyväskylä, Finland.
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AF conveys a strong risk of cumulative brain injury and cognitive morbidity, which can be prevented with pharmacological treatment [5].
The vascular cognitive impairment (VCI) concept intends to emphasize the need to prevent the development of dementia. The high prevalence of VCI and the necessity of prevention strategies targeting vascular risk factors highlight its importance in AF. AF conveys a strong risk of cumulative brain injury and cognitive morbidity, which can be prevented with pharmacological treatment [5].
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Clinical manifestation of stroke is rapidly developing loss of brain function due to disturbance in the blood supply to the brain.
Stroke is one of the leading causes of mortality and disability in modern countries. Clinical manifestation of stroke is rapidly developing loss of brain function due to disturbance in the blood supply to the brain. Challenging the brain with different tasks creates new neural connections and intensive exercise leads to improvement in neuroplasticity.
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Challenging the brain with different tasks creates new neural connections and intensive exercise leads to improvement in neuroplasticity.
Stroke is one of the leading causes of mortality and disability in modern countries. Clinical manifestation of stroke is rapidly developing loss of brain function due to disturbance in the blood supply to the brain. Challenging the brain with different tasks creates new neural connections and intensive exercise leads to improvement in neuroplasticity.
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Neuroplasticity can be defined as brain’s ability to change, remodel and reorganize for purpose of better ability to adapt to new situations.
Neuroplasticity can be defined as brain’s ability to change, remodel and reorganize for purpose of better ability to adapt to new situations. The concept of neuroplasticity is quite new, and it is one of the most important discoveries in neuroscience. The fact is that neural networks are not fixed, but occurring and disappearing dynamically throughout our whole life, depending on experiences. While we repeatedly practice one activity such as a sequence of movements or a mathematical problem, neuronal circuits are being formed, leading to better ability to perform the practiced task with less waste of energy. Once we stop practicing a certain activity, the brain will redirect these neuronal circuits by a much known ‘use it or lose it’ principle. Neuroplasticity leads to many different occurrences, such as habituation, sensitization to a certain position, medication tolerance, even recovery following brain injury.
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Once we stop practicing a certain activity, the brain will redirect these neuronal circuits by a much known ‘use it or lose it’ principle.
Neuroplasticity can be defined as brain’s ability to change, remodel and reorganize for purpose of better ability to adapt to new situations. The concept of neuroplasticity is quite new, and it is one of the most important discoveries in neuroscience. The fact is that neural networks are not fixed, but occurring and disappearing dynamically throughout our whole life, depending on experiences. While we repeatedly practice one activity such as a sequence of movements or a mathematical problem, neuronal circuits are being formed, leading to better ability to perform the practiced task with less waste of energy. Once we stop practicing a certain activity, the brain will redirect these neuronal circuits by a much known ‘use it or lose it’ principle. Neuroplasticity leads to many different occurrences, such as habituation, sensitization to a certain position, medication tolerance, even recovery following brain injury.
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Neuroplasticity leads to many different occurrences, such as habituation, sensitization to a certain position, medication tolerance, even recovery following brain injury.
Neuroplasticity can be defined as brain’s ability to change, remodel and reorganize for purpose of better ability to adapt to new situations. The concept of neuroplasticity is quite new, and it is one of the most important discoveries in neuroscience. The fact is that neural networks are not fixed, but occurring and disappearing dynamically throughout our whole life, depending on experiences. While we repeatedly practice one activity such as a sequence of movements or a mathematical problem, neuronal circuits are being formed, leading to better ability to perform the practiced task with less waste of energy. Once we stop practicing a certain activity, the brain will redirect these neuronal circuits by a much known ‘use it or lose it’ principle. Neuroplasticity leads to many different occurrences, such as habituation, sensitization to a certain position, medication tolerance, even recovery following brain injury.
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The brain damage caused by a stroke may result in the loss of cerebral function.
The brain damage caused by a stroke may result in the loss of cerebral function. However, the brain can use neuroplasticity to adjust itself functionally, by reorganizing the cortical maps, which contributes to the stroke recovery. The changes in the cortex organization include an increase in the number and density of dendrites, synapses and neurotrophic factors synthesis which results in two ways: unmasking of existing neuronal circuits and establishing of new neuronal circuits. Term neuroplasticity comes from Greek word "plastos" which means pliable; it means that neurochemical, synaptic, receptor and functional reorganization in brain results in new functional possibilities. After damage of the motor cortex, changes of activation in other motor areas are observed. These changes occur in homologue areas of the nonaffected hemisphere which can substitute for the lost functions or in the intact cortex adjacent to the damage.
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However, the brain can use neuroplasticity to adjust itself functionally, by reorganizing the cortical maps, which contributes to the stroke recovery.
The brain damage caused by a stroke may result in the loss of cerebral function. However, the brain can use neuroplasticity to adjust itself functionally, by reorganizing the cortical maps, which contributes to the stroke recovery. The changes in the cortex organization include an increase in the number and density of dendrites, synapses and neurotrophic factors synthesis which results in two ways: unmasking of existing neuronal circuits and establishing of new neuronal circuits. Term neuroplasticity comes from Greek word "plastos" which means pliable; it means that neurochemical, synaptic, receptor and functional reorganization in brain results in new functional possibilities. After damage of the motor cortex, changes of activation in other motor areas are observed. These changes occur in homologue areas of the nonaffected hemisphere which can substitute for the lost functions or in the intact cortex adjacent to the damage. Due to these cortical reorganizations, which begin from one to two days after the stroke, and can be extended for months, the patients can recover, at least in part, their lost abilities.
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Term neuroplasticity comes from Greek word "plastos" which means pliable; it means that neurochemical, synaptic, receptor and functional reorganization in brain results in new functional possibilities.
The brain damage caused by a stroke may result in the loss of cerebral function. However, the brain can use neuroplasticity to adjust itself functionally, by reorganizing the cortical maps, which contributes to the stroke recovery. The changes in the cortex organization include an increase in the number and density of dendrites, synapses and neurotrophic factors synthesis which results in two ways: unmasking of existing neuronal circuits and establishing of new neuronal circuits. Term neuroplasticity comes from Greek word "plastos" which means pliable; it means that neurochemical, synaptic, receptor and functional reorganization in brain results in new functional possibilities. After damage of the motor cortex, changes of activation in other motor areas are observed. These changes occur in homologue areas of the nonaffected hemisphere which can substitute for the lost functions or in the intact cortex adjacent to the damage. Due to these cortical reorganizations, which begin from one to two days after the stroke, and can be extended for months, the patients can recover, at least in part, their lost abilities. The recovery of functions of the limbs which is promoted by plasticity is more difficult to occur, due to a
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With the loss of a brain area’s function, the body part that was linked to this area is also affected and its mobility power is lost too.
phenomenon known as "learned non use". With the loss of a brain area’s function, the body part that was linked to this area is also affected and its mobility power is lost too. As the patient can not move his most affected limb, he compensates this using the other limb. Thus, after a certain period, when the damage effects aren’t present anymore and brain adaptations happen, the movements could be recovered, but the patient has already 'learned" that the limb is no longer functional [1]. Cognitive abilities like processing speed, memory and reasoning start to decline in our late twenties. Normal aging process and many different neurological disorders like stroke, dementia, Alzheimer’s and Parkinson’s disease, Huntington disease, multiple sclerosis and acquired brain trauma contribute to the decline of our cognitive abilities.
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Thus, after a certain period, when the damage effects aren’t present anymore and brain adaptations happen, the movements could be recovered, but the patient has already 'learned" that the limb is no longer functional [1].
phenomenon known as "learned non use". With the loss of a brain area’s function, the body part that was linked to this area is also affected and its mobility power is lost too. As the patient can not move his most affected limb, he compensates this using the other limb. Thus, after a certain period, when the damage effects aren’t present anymore and brain adaptations happen, the movements could be recovered, but the patient has already 'learned" that the limb is no longer functional [1]. Cognitive abilities like processing speed, memory and reasoning start to decline in our late twenties. Normal aging process and many different neurological disorders like stroke, dementia, Alzheimer’s and Parkinson’s disease, Huntington disease, multiple sclerosis and acquired brain trauma contribute to the decline of our cognitive abilities.
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Normal aging process and many different neurological disorders like stroke, dementia, Alzheimer’s and Parkinson’s disease, Huntington disease, multiple sclerosis and acquired brain trauma contribute to the decline of our cognitive abilities.
phenomenon known as "learned non use". With the loss of a brain area’s function, the body part that was linked to this area is also affected and its mobility power is lost too. As the patient can not move his most affected limb, he compensates this using the other limb. Thus, after a certain period, when the damage effects aren’t present anymore and brain adaptations happen, the movements could be recovered, but the patient has already 'learned" that the limb is no longer functional [1]. Cognitive abilities like processing speed, memory and reasoning start to decline in our late twenties. Normal aging process and many different neurological disorders like stroke, dementia, Alzheimer’s and Parkinson’s disease, Huntington disease, multiple sclerosis and acquired brain trauma contribute to the decline of our cognitive abilities.
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He suggested that human brain is capable for continuous functional changes.
About 120 years ago, William James was the first to suggest the theory of neuroplasticity in his work Principles of Psychology [2]. He suggested that human brain is capable for continuous functional changes. Polish neuroscientist Jerzy Konorski was the first to define the term ‘neuroplasticity’ in 1948. Konorski suggested a theory by which neurons which have been activated by closeness of an active neural circuit, change and incorporate themselves into that circuit [З]. Donald Нebb, a Canadian psychologist established a Нebb's rule, defined also as pre-post coincidence, implying that changes of biochemical processes in one neuron can stimulate neighboring simultaneously activated synapses, this being the basic principle of synaptic plasticity [4]. Paul Bach-y-Rita is the pioneer in demonstrating neuroplasticity on actual cases, claiming
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that healthy regions of the brain can take over the functions of injured parts of the brain.
that healthy regions of the brain can take over the functions of injured parts of the brain. This was the basis of his treatment for people who suffered vestibular damage. He patented an appliance which when connected to one’s tongue, stimulates receptors by vibrations in a frequency and amplitude in correlation with pixel analysis from the surroundings [5, 6, 7]. Edward Taub supported research and developed first real and applicable treatments for patients. He proved, first using rhesus monkeys, then on humans, that tying up of healthy half of the body in case of hemiplegia, “forces” the damaged part of the brain to faster rehabilitation [8, 9, 10]. Michael Merzenich is yet another neuroscientist who left his mark in the field of neuroplasticity.
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He proved, first using rhesus monkeys, then on humans, that tying up of healthy half of the body in case of hemiplegia, “forces” the damaged part of the brain to faster rehabilitation [8, 9, 10].
that healthy regions of the brain can take over the functions of injured parts of the brain. This was the basis of his treatment for people who suffered vestibular damage. He patented an appliance which when connected to one’s tongue, stimulates receptors by vibrations in a frequency and amplitude in correlation with pixel analysis from the surroundings [5, 6, 7]. Edward Taub supported research and developed first real and applicable treatments for patients. He proved, first using rhesus monkeys, then on humans, that tying up of healthy half of the body in case of hemiplegia, “forces” the damaged part of the brain to faster rehabilitation [8, 9, 10]. Michael Merzenich is yet another neuroscientist who left his mark in the field of neuroplasticity. He designed software for in order to help people with learning difficulties [11, 12].
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All these scientists had to fight against an academic dogma which disapproved the existence of adult brain neuroplasticity, except during developmental phase.
All these scientists had to fight against an academic dogma which disapproved the existence of adult brain neuroplasticity, except during developmental phase. Until the Decade of the brain (1990-2000), the word ‘neuroplasticity’ itself, lead to articles not being published in prestigious journals. When asked, Eric Kandel, a Nobel Prize winner in medicine, said that neuroplasticitiy is what marked the Decade of the brain.
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Until the Decade of the brain (1990-2000), the word ‘neuroplasticity’ itself, lead to articles not being published in prestigious journals.
All these scientists had to fight against an academic dogma which disapproved the existence of adult brain neuroplasticity, except during developmental phase. Until the Decade of the brain (1990-2000), the word ‘neuroplasticity’ itself, lead to articles not being published in prestigious journals. When asked, Eric Kandel, a Nobel Prize winner in medicine, said that neuroplasticitiy is what marked the Decade of the brain.
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When asked, Eric Kandel, a Nobel Prize winner in medicine, said that neuroplasticitiy is what marked the Decade of the brain.
All these scientists had to fight against an academic dogma which disapproved the existence of adult brain neuroplasticity, except during developmental phase. Until the Decade of the brain (1990-2000), the word ‘neuroplasticity’ itself, lead to articles not being published in prestigious journals. When asked, Eric Kandel, a Nobel Prize winner in medicine, said that neuroplasticitiy is what marked the Decade of the brain.
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Neuroplasticity is a general term, defining the fact that the brain changes, recognizing the need for further definition of the term.
Neuroplasticity is a general term, defining the fact that the brain changes, recognizing the need for further definition of the term. We distinguish structural from functional neuroplasticity.
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Structural neuroplasticity: synaptic plasticity refers to changes in the strength between neurons (synapses), chemical or electric meeting points between brain cells.
Structural neuroplasticity: synaptic plasticity refers to changes in the strength between neurons (synapses), chemical or electric meeting points between brain cells. Synaptic plasticity is a general term, and the name itself has no meaning other that something changed within the synapse, but can include many specific processes such as long-term changes in the number of receptors for certain neurotransmitters, or changes where some proteins are being synthetized more within the cell.
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Structural plasticity is a normal marking of fetal neurons during brain development and is called developmental plasticity, including neurogenesis and neuronal migration.
Synaptogenesis refers to formation and fitting of synapse or group of synapses into a neural circuit [1З]. Structural plasticity is a normal marking of fetal neurons during brain development and is called developmental plasticity, including neurogenesis and neuronal migration. Neuronal migration is a process in which neurons travel from their ‘place of birth’ in fetal ventricular or subventricular zone, towards their final position in the cortex.
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During development, brain areas become specialized for certain tasks such as processing signals form the surrounding areas through sensory receptors.
During development, brain areas become specialized for certain tasks such as processing signals form the surrounding areas through sensory receptors. For example, in occipital brain area, the fourth layer of cortex hypertrophies in order to receive signals from the visual pathway [14].
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For example, in occipital brain area, the fourth layer of cortex hypertrophies in order to receive signals from the visual pathway [14].
During development, brain areas become specialized for certain tasks such as processing signals form the surrounding areas through sensory receptors. For example, in occipital brain area, the fourth layer of cortex hypertrophies in order to receive signals from the visual pathway [14].
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It is a process which mainly takes place during brain
Neurogenesis is formation of new neurons. It is a process which mainly takes place during brain
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development, even though in the last decade neurogenesis was found in adult brain as well.
development, even though in the last decade neurogenesis was found in adult brain as well. On the other hand, neuronal death occurs throughout life, due to brain damage or programmed cell death. Other forms of structural neuroplasticity include changes in white or gray matter density which can be visualized by magnetic resonance.
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On the other hand, neuronal death occurs throughout life, due to brain damage or programmed cell death.
development, even though in the last decade neurogenesis was found in adult brain as well. On the other hand, neuronal death occurs throughout life, due to brain damage or programmed cell death. Other forms of structural neuroplasticity include changes in white or gray matter density which can be visualized by magnetic resonance.
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After establishing the fact that brain has a possibility of remodeling its own neural maps, the main question for neurorehabilation medicine is how to direct this neuroplasticity to regain lost functions caused by a neurologic deficit.
After establishing the fact that brain has a possibility of remodeling its own neural maps, the main question for neurorehabilation medicine is how to direct this neuroplasticity to regain lost functions caused by a neurologic deficit. This emphasizes the need to neuroanatomically define every neurologic lesion. When we know which neural pathway is damaged, we can start looking for bypasses.
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Movement rehabilitation: when we learn complex movements, the brain firstly recognizes basic motoric movements, and divides them and stores them into a given model which is then remembered.
Movement rehabilitation: when we learn complex movements, the brain firstly recognizes basic motoric movements, and divides them and stores them into a given model which is then remembered. The same network of neurons will activate every time we observe, think, or make a certain movement, or hear sounds which remind us of that movement. If we focus on repetitive movements, it is important to understand the purpose of the movement. For example, for a patient practicing hand pronation, the movement itself is not the purpose; the purpose is for him to be able to open the door again. This way we can stimulate other neuronal circuits which can lead to execution of this
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If the experience is changing dramatically or parts of the brain are damaged, parts of the brain can change their function without structural changes.
Neuronal processing of different signals: in 1821, a French soldier named Charles Barbier, visited a Royal institution “night writing”, in Paris, presenting his invention, a code of 12 dots which offer possibilities to soldiers to communicate and share information on the battle field, without the need for speech. Usage of the code showed to be too difficult for soldiers, but not for a blind boy from that institution, Louis Braille. Braille lowered the number of dots from 12 to 6, and published the first Braille book in 1829. In 1839 he added mathematical and music symbols [19]. How can a blind person process and translate position of the dots so fast? If the experience is changing dramatically or parts of the brain are damaged, parts of the brain can change their function without structural changes. From this example, visual cortex in a blind person, if it’s not receiving information from the visual pathway, it can process the sense of touch. 150 years later, Uhl and his coworkers proved that tactile reading in blind subject activates the occipital, visual part of the cortex [20]. Remodeling of brain maps after brain damage is a revolutionary term which opened a pathway for new understanding of neurorehabilitation [21]. After accepting the fact, the future of neurorehabilitation lies in defining neural pathways and ways we can regain lost function by using bypass pathways in the brain [22].
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Remodeling of brain maps after brain damage is a revolutionary term which opened a pathway for new understanding of neurorehabilitation [21].
In 1839 he added mathematical and music symbols [19]. How can a blind person process and translate position of the dots so fast? If the experience is changing dramatically or parts of the brain are damaged, parts of the brain can change their function without structural changes. From this example, visual cortex in a blind person, if it’s not receiving information from the visual pathway, it can process the sense of touch. 150 years later, Uhl and his coworkers proved that tactile reading in blind subject activates the occipital, visual part of the cortex [20]. Remodeling of brain maps after brain damage is a revolutionary term which opened a pathway for new understanding of neurorehabilitation [21]. After accepting the fact, the future of neurorehabilitation lies in defining neural pathways and ways we can regain lost function by using bypass pathways in the brain [22].
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After accepting the fact, the future of neurorehabilitation lies in defining neural pathways and ways we can regain lost function by using bypass pathways in the brain [22].
How can a blind person process and translate position of the dots so fast? If the experience is changing dramatically or parts of the brain are damaged, parts of the brain can change their function without structural changes. From this example, visual cortex in a blind person, if it’s not receiving information from the visual pathway, it can process the sense of touch. 150 years later, Uhl and his coworkers proved that tactile reading in blind subject activates the occipital, visual part of the cortex [20]. Remodeling of brain maps after brain damage is a revolutionary term which opened a pathway for new understanding of neurorehabilitation [21]. After accepting the fact, the future of neurorehabilitation lies in defining neural pathways and ways we can regain lost function by using bypass pathways in the brain [22].
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Our brain is constantly changing during lifetime.
Our brain is constantly changing during lifetime. During fetal development structural changes are dominant, such as neurogenesis and migration of neurons, while in adult brain the dominant type of neuroplasticity is functional, allowing the
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During fetal development structural changes are dominant, such as neurogenesis and migration of neurons, while in adult brain the dominant type of neuroplasticity is functional, allowing the
Our brain is constantly changing during lifetime. During fetal development structural changes are dominant, such as neurogenesis and migration of neurons, while in adult brain the dominant type of neuroplasticity is functional, allowing the
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Age-related changes in topological organization of structural brain networks in healthy individuals.
Wu K, Taki Y, Sato K, Kinomura S, Goto R, Okada K, Kawashima R, He Y, Evans AC, Fukuda H. Age-related changes in topological organization of structural brain networks in healthy individuals.
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Hum Brain Mapp
Hum Brain Mapp
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Brain mechanisms in sensory substitution.
Bach-Y-Rita P. Brain mechanisms in sensory substitution. New York: Academic Press, 1972.
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The plastic human brain cortex.
Pascual-Leone A, Amedi A, Fregni F. The plastic human brain cortex.
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brain to constantly adapt to environment and in
brain to constantly adapt to environment and in
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Although relatively easy to define, VaD has proved difficult to diagnose because of the wide variability in mechanisms, brain changes, syndromes, and course.
Although relatively easy to define, VaD has proved difficult to diagnose because of the wide variability in mechanisms, brain changes, syndromes, and course. At present, the current criteria for VaD such as the DSM-IV, select an heterogeneous group and may have biased findings in research studies and clinical trials. In 1993, the NINDS-AIREN International Work Group [20] proposed diagnostic criteria for VaD focusing on the delineation of the clinical subtypes of VaD, consistent with the heterogeneity of dementia syndrome from CVD. Accordingly, the main subcategories of ischaemic VaD include multi-infarct dementia, strategic single-infarct dementia, and small-vessel disease with dementia.
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This proposition provides a sharper delineation of the clinical and the brain imaging features of patients with subcortical VaD.
To further refine the criteria for subcortical VaD, Erkintunti et al. [11] have proposed a modification of the NINDS-AIREN criteria as a new research criteria for subcortical VaD. This proposition provides a sharper delineation of the clinical and the brain imaging features of patients with subcortical VaD. For example, according to
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Brain’s high metabolic demand requires that cerebral blood vessels have a fine tune regulation of vascular resistance, controlling blood flow distribution.
Brain’s high metabolic demand requires that cerebral blood vessels have a fine tune regulation of vascular resistance, controlling blood flow distribution. Two fast regulating principles of cerebral perfusion are well accepted: cerebral autoregulation maintains a stable cerebral blood flow for a wide range of systemic blood pressure variation, and cerebral neurovascular coupling adapts local cerebral blood flow to the metabolic needs and activity of the underlying cortex.
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A better understanding of the relationship between cerebral hemodynamics and structural changes in the aging brain is an essential step towards identifying preventive and therapeutic strategies for age related cerebrovascular disease.
Interesting findings seem to show that cerebral blood flow regulation may reflect the neurological dysfunction caused by cerebral microvascular disease, namely associated with slow gait speed and risk of falls. A better understanding of the relationship between cerebral hemodynamics and structural changes in the aging brain is an essential step towards identifying preventive and therapeutic strategies for age related cerebrovascular disease.
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The relatively small human brain, which represents around 2% of the body weight, consumes 20% of total body oxygen and claims 15% of the cardiac output, in order to maintain the necessary levels of metabolic activity of 3.5 ml.100 g brain-1.min-1 [1].
The relatively small human brain, which represents around 2% of the body weight, consumes 20% of total body oxygen and claims 15% of the cardiac output, in order to maintain the necessary levels of metabolic activity of 3.5 ml.100 g brain-1.min-1 [1].
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Furthermore, the brain has no energetic reserve, thus requiring a continuous blood flow during the whole cardiac cycle.
Furthermore, the brain has no energetic reserve, thus requiring a continuous blood flow during the whole cardiac cycle. A proof of this statement is the fact that a pathologic condition involving an intracranial pressure high enough to
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prevent blood from entering the skull during diastole results in brain death [3].
prevent blood from entering the skull during diastole results in brain death [3].
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Another important issue is that the brain is surrounded by bone, and therefore the intracranial volume must be kept rather constant, with equilibrium of brain parenchyma, blood and cerebrospinal fluid volumes [25].
Another important issue is that the brain is surrounded by bone, and therefore the intracranial volume must be kept rather constant, with equilibrium of brain parenchyma, blood and cerebrospinal fluid volumes [25].
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Brain’s high metabolic demand and these volume-balance requirements imply that cerebral blood vessels have a fine tune regulation of vascular resistance, controlling blood flow distribution.
Brain’s high metabolic demand and these volume-balance requirements imply that cerebral blood vessels have a fine tune regulation of vascular resistance, controlling blood flow distribution.
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How does brain regulate vasoreactivity?
How does brain regulate vasoreactivity?
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Brain circulatory physiology is not yet fully understood and competing theories about the modulating role of myogenic, neurogenic and metabolic mechanisms still exist.
Brain circulatory physiology is not yet fully understood and competing theories about the modulating role of myogenic, neurogenic and metabolic mechanisms still exist.
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Functional brain imaging may assist in the selection of rehabilitation methods that best foster recovery [24].
Looking at the performance of cerebral autoregulation in acute stroke can be very helpful if this allows adjusting the blood pressure, and investigations are ongoing on this topic [7, 14]. This adaptation can potentially reduce the risk of further ischemia when BP decreases or help preventing edema and hemorrhage when BP increases. The analysis of the cerebral evoked flow to cortical activation is important to evaluate the performance of the neurovascular coupling unit, both for neuronal and endothelial dysfunction, and also allows localizing some cortical functions, as in the laterality studies [10]. It can be useful for predicting stroke risk [4], and after stroke it might help in assessing changes in motor organization with rehabilitation. Functional brain imaging may assist in the selection of rehabilitation methods that best foster recovery [24].
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A mismatch between the demand and supply would result in relative hypoperfusion and brain dysfunction.
Neurovascular coupling (NVC) ensures that blood flow is increased to meet the increased metabolic demands of the activated neurons. A mismatch between the demand and supply would result in relative hypoperfusion and brain dysfunction.
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A better understanding of the relationship between cerebral hemodynamics and structural changes in the aging brain is an essential step towards identifying preventive and therapeutic strategies
As cerebrovascular disease is known to progress asymptomatically in the early stages of Fabry disease, a cohort of patients from families with the classical phenotype were studied with functional transcranial Doppler. The authors concluded that Fabry disease patients of both genders, without prior history of stroke or transient ischemic attack, may have disturbed neurovascular coupling in the visual cortex, as well as decreased resting posterior cerebral artery BFV. These findings support the role of functional TCD, along with duplex ultrasound and MR techniques, in the evaluation of these patients, since early stages of disease [4]. Finally, interesting findings seem to show that cerebral blood flow regulation may reflect the neurological dysfunction caused by cerebral microvascular disease [22, 23]. Data from the MOBILIZE Boston study shows that changes in CBF velocity responses to an N-Back task to study the NVC was significantly associated with gait speed and that subjects with higher NVC were able to suppress the negative relationship between white matter hyperintensities and gait speed [23]. A better understanding of the relationship between cerebral hemodynamics and structural changes in the aging brain is an essential step towards identifying preventive and therapeutic strategies
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Transcranial Doppler and brain death.
Azevedo E, Teixeira J, Neves JC, Vaz R. Transcranial Doppler and brain death.
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Aging gracefully: compensatory brain activity in high-performing older adults.
Cabeza R, Anderson ND, Locantore JK, McIntosh AR. Aging gracefully: compensatory brain activity in high-performing older adults.
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Motor recovery after stroke: lessons from functional brain imaging.
Thirumala P, Hier DB, Patel P. Motor recovery after stroke: lessons from functional brain imaging.
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Mediators of vascular and parenchymal mechanisms in secondary brain damage.
Wahl M, Schilling L, Unterberg A, Baethmann A. Mediators of vascular and parenchymal mechanisms in secondary brain damage.
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Although Alzheimer's disease is the most common cause of cognitive decline in the aged population, independant causes of cognitive dysfunction such as vascular disease, subclinical brain injury, silent brain infarction, and clinically overt stroke are important causes and contributors to cognitive dysfunction [1].
The global aging of the population has lead to greater numbers of older people, owing to factors such as an increasing life expectancy and a decreasing birth rate. Aging is usually associated with cognitive changes, which may range from mild changes in cognitive function to more severe impairment causing dementia. The growth in the number of patients suffering from dementia is becoming a burden of constantly increasing importance to society. Although Alzheimer's disease is the most common cause of cognitive decline in the aged population, independant causes of cognitive dysfunction such as vascular disease, subclinical brain injury, silent brain infarction, and clinically overt stroke are important causes and contributors to cognitive dysfunction [1]. The overall prevalence of dementia in wealthy countries is 5% to 10% in populations aged >65 years. The prevalence of Alzheimer's disease (AD) doubles every 4.3 years, whereas the prevalence of vascular dementia (VaD) doubles every 5.3 years. Vascular cognitive impairment is strongly associated with age. In low-to-middle-income countries, the prevalence of dementia is lower than in wealthy countries but is still related to age. Incidence rates are variable, but age-related [1, 2].
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VCI is a syndrome with evidence of clinical stroke or subclinical vascular brain injury, and cognitive impairment affecting at least one cognitive domain.
vascular disease can cause mild cognitive deficits that affect multiple cognitive functions, the term 'vascular' mild cognitive impairment (VaMCI) was proposed [5, 6]. Patients diagnosed with VaMCI are in transition towards Alzheimer's disease. [7] Vascular cognitive impairment (VCI) encompasses all cognitive disorders associated with cerebrovascular disease, from developed mild cognitive deficits to dementia. VCI is a syndrome with evidence of clinical stroke or subclinical vascular brain injury, and cognitive impairment affecting at least one cognitive domain. The most severe form of VCI is VaD (Table 1) [1].
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Identification of early stages of microangiopathicatherosclerotic changes of the small brain blood vessels can be assessed by means of neuro-
The initial diagnostic approach to cognitive changes with age includes a clinical assessment and a neuropsychological evaluation [18]. Neuroradiological procedures may be of benefit in assessing early morphological changes and are usually based on computed tomography (CT) and magnetic resonance imaging (MRI) findings. Identification of early stages of microangiopathicatherosclerotic changes of the small brain blood vessels can be assessed by means of neuro-
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Novel neurosonological methods utilizing sophisticated software, may also have a place in the assessment of cognitive impairment, with findings potentially appearing prior to structural and morphological changes in the brain.
imaging techniques such as positron emission tomography (PET) and single photon emission CT (SPECT) of cerebral blood flow (CBF) are also useful, but often have limited clinical availability [19, 20, 21, 22]. Novel neurosonological methods utilizing sophisticated software, may also have a place in the assessment of cognitive impairment, with findings potentially appearing prior to structural and morphological changes in the brain.
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Useful in assessment of cerebral lateralization during major brain functions (i.e.
Useful in assessment of cerebral lateralization during major brain functions (i.e. language, facial processing, etc.).
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Intracranial haemodynamics of the aging brain can sucesfully be assessed using TCD, functional TCD assessing the response to various stressors, and the TCD detection of cerebral emboli, while extracranial neurosonological methods involve the measurement of intima-media thickness (IMT), plaque formation and composition, and alterations in arterial mechanisms based on B mode ultrasound imaging, such as pulse pressure wave or flow-mediated dilation.
Both intracranial and extracranial neurosonological methods are convenient, relatively widely available, and generally inexpensive diagnostic tools. Intracranial haemodynamics of the aging brain can sucesfully be assessed using TCD, functional TCD assessing the response to various stressors, and the TCD detection of cerebral emboli, while extracranial neurosonological methods involve the measurement of intima-media thickness (IMT), plaque formation and composition, and alterations in arterial mechanisms based on B mode ultrasound imaging, such as pulse pressure wave or flow-mediated dilation.
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Brain
Brain
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In addition, neuronal aggregates adjacent to a lesion in the brain areas may take over the function previously played by the damaged neurons.
New insights in the effect of stroke lesions and therapeutic methods have changed traditional clinical rehabilitation and more evidence based therapies are provided. The rehabilitation process is divided in regeneration, neuroplasticity and adaption. Learning and repetitive exercises are the most important aspect for the rehabilitation success. In addition, neuronal aggregates adjacent to a lesion in the brain areas may take over the function previously played by the damaged neurons. Such reorganization modifies the interhemispheric networking in organization of the cortices. This reorganization may be responsible for clinical recovery of motor performances and sensorimotor integration after a stroke.
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The application of mirror is done to pretend the brain with a normalized illusion of motion of the paretic arm and hand.
of learned nonuse in that the preference for the less affected arm is learned as a result of unsuccessful repeated attempts in using the affected arm. The constraint-induced therapy (CIT) protocol, which was proved in animal experimental settings, which forces the use of the affected limb by restraining the use of the less affected limb, has been specifically developed to reverse learned nonuse. CIT has been shown to be effective in the recovery of arm and hand functions after stroke in multisite randomized clinical trials. Other therapeutic strategies with circle training containing multiple functionalities are promising. The application of mirror is done to pretend the brain with a normalized illusion of motion of the paretic arm and hand. This supports the hypothesis of reconnecting brain areas.
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This supports the hypothesis of reconnecting brain areas.
of learned nonuse in that the preference for the less affected arm is learned as a result of unsuccessful repeated attempts in using the affected arm. The constraint-induced therapy (CIT) protocol, which was proved in animal experimental settings, which forces the use of the affected limb by restraining the use of the less affected limb, has been specifically developed to reverse learned nonuse. CIT has been shown to be effective in the recovery of arm and hand functions after stroke in multisite randomized clinical trials. Other therapeutic strategies with circle training containing multiple functionalities are promising. The application of mirror is done to pretend the brain with a normalized illusion of motion of the paretic arm and hand. This supports the hypothesis of reconnecting brain areas.
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In recent years, efforts have focused on investigating the neurophysiological changes that occur in the brain after stroke, and on developing novel strategies such as additional brain stimulation to enhance sensorimotor and cognitive recovery.
In recent years, efforts have focused on investigating the neurophysiological changes that occur in the brain after stroke, and on developing novel strategies such as additional brain stimulation to enhance sensorimotor and cognitive recovery. Repetitive transcranial magnetic stimulation (rTMS) was introduced as a therapeutic tool for improving the efficacy of rehabilitation for recovery after stroke. The current hypothesis is that disturbances of interhemispheric activities after stroke result in a pathological hyperactivity of the intact hemisphere. The rationale of using rTMS as a complementary therapy is mainly to decrease the cortical excitability in regions that are presumed to hinder optimal recovery by lowfrequency rTMS delivered to the unaffected hemi-
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Altogether, in combination with conventional therapeutic approaches, rTMS has a potential to become a complementary strategy to enhance stroke recovery by modulating the excitability of targeted brain areas.
sphere, while high-frequency rTMS delivered to the affected hemisphere facilitates cortical excitability. There is a growing body of research in stroke patients investigating the effect of rTMS on facilitating recovery by modifying cortical and subcortical networks. Altogether, in combination with conventional therapeutic approaches, rTMS has a potential to become a complementary strategy to enhance stroke recovery by modulating the excitability of targeted brain areas. Today it is not clear which parameters (frequency, burst pattern, stimulation time etc) are optimizing the beneficial effects of rTMS on stroke recovery. Similar discussion are held in the literature about the effects of transcranial direct current stimulation (tDCS).
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Brain Imaging in Neurorehabilitation
Brain Imaging in Neurorehabilitation
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This syllabus discusses the usefulness of navigated transcranial magnetic stimulation (TMS) as a brain imaging tool in stroke patients.
This syllabus discusses the usefulness of navigated transcranial magnetic stimulation (TMS) as a brain imaging tool in stroke patients. TMS assessment of the motor tract function and walking ability over time in stroke patients with poor or non-existent initial gait is in the focus. Main data is derived from twenty-seven patients, first assessed one week post-stroke, and followed up for six months. Outcome measure in these patients was walking ability. Motor evoked potentials (MEP) in lower limbs early on predicted better physical functioning at 3 weeks and at 6 months in all patients (p
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Financial support for this work was provided by Brain Research and Rehabilitation Center Neuron and Kuopio University Hospital, Kuopio, Finland.
nen, PhD, and physiotherapists Pirjo Huuskonen and Dorota Musialowicz for their help. Financial support for this work was provided by Brain Research and Rehabilitation Center Neuron and Kuopio University Hospital, Kuopio, Finland.
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Brain lesion size and location: effects on motor recovery and functional outcome in stroke patients.
Chen CL, Tang FT, Chen HC, Chung CY, Wong MK. Brain lesion size and location: effects on motor recovery and functional outcome in stroke patients.
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Brain
Brain
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Recent concepts emphasize on optimal stimulation of brain plasticity using relevant task-oriented and high-intensity training in better motivated and moving patients who have preserved cognition and receive family support.
The restoration of gait after stroke is a primary and long-term goal of neurorehabilitation. This article focuses on the update scientific theories for the influence of neurorehabilitation on restoration of hemiparetic gait due to unilateral supratentorial stroke. At presence it is accepted that stroke patients have an optimal time window for fast recovery within the rehabilitation. A significant motor improvement can be achieved in the first 6 months after stoke following by a plateau, although some functional recovery may be observed many years after stroke. Gait restoration in chronic hemiparesis is mainly associated with the use of optimal behavior strategies for compensation the existed motor deficit where the non-affected, clinically healthy side is more involved. Recent concepts emphasize on optimal stimulation of brain plasticity using relevant task-oriented and high-intensity training in better motivated and moving patients who have preserved cognition and receive family support.
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brain regions, including cerebral motor cortex, cerebellum, and brain stem.
brain regions, including cerebral motor cortex, cerebellum, and brain stem. Peripheral sensory information and descending inputs from motor cortex modulate continuously the CPGs function, the drive for locomotion and the coordination to negotiate a complex environment [13, 23].
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Motor outcome after unilateral supratentorial stroke is known to depend on the location of the brain lesion and the total number of residual descending fibers in the cerebral peduncles [48].
Motor outcome after unilateral supratentorial stroke is known to depend on the location of the brain lesion and the total number of residual descending fibers in the cerebral peduncles [48]. Bilateral impairments and different diaschisis phenomena are observed in unilateral hemispheric lesions while the common course of restoration of motor function consists of a regular sequence following a general pattern of reflex changes and ability for voluntary movement [46]. A complex functional reorganization involving more or less clinically "healthy" side is related to motor recovery after stroke utilizing those residual descending motor pathways, which are unaffected by the lesion and are bilaterally organized [19, 33].
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These findings suggest that motor behavior of chronic stroke patients reflects the complex relationship between morphological lesion at the onset of stroke and associated structural and functional brain reorganization that may result in a newly and bilaterally organized control of ambulation in the presence of motor deficit.
These findings suggest that motor behavior of chronic stroke patients reflects the complex relationship between morphological lesion at the onset of stroke and associated structural and functional brain reorganization that may result in a newly and bilaterally organized control of ambulation in the presence of motor deficit. The final motor output is generated from one side – by the preserved CPGs in the spinal cord, which are programmed to operate in a stereotyped manner under supraspinal motor control mechanisms, and from other side – reflect some newly and
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The neurobiological basis of recovery after stroke is based on the theory of brain plasticity [4, 27].
The neurobiological basis of recovery after stroke is based on the theory of brain plasticity [4, 27]. It remains not completely understood although many evidences have been accumulated that after stroke the brain can reorganize itself [10, 28]. Several mechanisms for functional recovery are assumed: (1) brain repair (restitution, i.e. the biological recovery of the damage area itself); (2) adaptive reorganization (recruitment of new additional neural networks that can activate the same final pathways) and/or (3) compensatory strategy (behavioral substitution, i.e. patients learn to compensate for their deficit).
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It remains not completely understood although many evidences have been accumulated that after stroke the brain can reorganize itself [10, 28].
The neurobiological basis of recovery after stroke is based on the theory of brain plasticity [4, 27]. It remains not completely understood although many evidences have been accumulated that after stroke the brain can reorganize itself [10, 28]. Several mechanisms for functional recovery are assumed: (1) brain repair (restitution, i.e. the biological recovery of the damage area itself); (2) adaptive reorganization (recruitment of new additional neural networks that can activate the same final pathways) and/or (3) compensatory strategy (behavioral substitution, i.e. patients learn to compensate for their deficit).
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Several mechanisms for functional recovery are assumed: (1) brain repair (restitution, i.e.
The neurobiological basis of recovery after stroke is based on the theory of brain plasticity [4, 27]. It remains not completely understood although many evidences have been accumulated that after stroke the brain can reorganize itself [10, 28]. Several mechanisms for functional recovery are assumed: (1) brain repair (restitution, i.e. the biological recovery of the damage area itself); (2) adaptive reorganization (recruitment of new additional neural networks that can activate the same final pathways) and/or (3) compensatory strategy (behavioral substitution, i.e. patients learn to compensate for their deficit).
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At present there are strong indications that all these mechanisms are potentially involved in the recovery process after brain injury, however the ability of human adult brain to reorganize itself remains more or less restricted.
At present there are strong indications that all these mechanisms are potentially involved in the recovery process after brain injury, however the ability of human adult brain to reorganize itself remains more or less restricted. Irrespective of the type and the amount of applied therapy certain biological processes, characterized as the “spontaneous neurological recovery”, are supposedly responsible for the functional outcome after stroke. The final outcome has been shown to be determined within a limited time window during the acute phase of brain injury – if recovery is seen early after stroke onset, better outcomes may be expected six months later although motor recovery may continue over a period of years in some individuals with appropriate rehabilitation [17].
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The final outcome has been shown to be determined within a limited time window during the acute phase of brain injury – if recovery is seen early after stroke onset, better outcomes may be expected six months later although motor recovery may continue over a period of years in some individuals with appropriate rehabilitation [17].
At present there are strong indications that all these mechanisms are potentially involved in the recovery process after brain injury, however the ability of human adult brain to reorganize itself remains more or less restricted. Irrespective of the type and the amount of applied therapy certain biological processes, characterized as the “spontaneous neurological recovery”, are supposedly responsible for the functional outcome after stroke. The final outcome has been shown to be determined within a limited time window during the acute phase of brain injury – if recovery is seen early after stroke onset, better outcomes may be expected six months later although motor recovery may continue over a period of years in some individuals with appropriate rehabilitation [17].
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It has been demonstrated that behavioral experience is the most potent modulator of brain plasticity.
Knowledge for post-stroke neuroplasticity has been grown recently gleaned from both animal models and human populations. It has been demonstrated that behavioral experience is the most potent modulator of brain plasticity. Based on the quantity and quality of motor experience, the brain can be reshaped after injury in either adaptive or maladaptive ways. Many studies have demonstrated the neurophysiological and neuroanatomical changes triggered by motor experience, injury and interaction of these processes. Using new techniques novel perspectives take place in the injured brain, providing a real-time window into post-injury plasticity. These new approaches are likely to accelerate the pace of basic research, and provide a wealth of opportunities to translate basic principles into therapeutic methodologies [28].
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Based on the quantity and quality of motor experience, the brain can be reshaped after injury in either adaptive or maladaptive ways.
Knowledge for post-stroke neuroplasticity has been grown recently gleaned from both animal models and human populations. It has been demonstrated that behavioral experience is the most potent modulator of brain plasticity. Based on the quantity and quality of motor experience, the brain can be reshaped after injury in either adaptive or maladaptive ways. Many studies have demonstrated the neurophysiological and neuroanatomical changes triggered by motor experience, injury and interaction of these processes. Using new techniques novel perspectives take place in the injured brain, providing a real-time window into post-injury plasticity. These new approaches are likely to accelerate the pace of basic research, and provide a wealth of opportunities to translate basic principles into therapeutic methodologies [28].
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Using new techniques novel perspectives take place in the injured brain, providing a real-time window into post-injury plasticity.
Knowledge for post-stroke neuroplasticity has been grown recently gleaned from both animal models and human populations. It has been demonstrated that behavioral experience is the most potent modulator of brain plasticity. Based on the quantity and quality of motor experience, the brain can be reshaped after injury in either adaptive or maladaptive ways. Many studies have demonstrated the neurophysiological and neuroanatomical changes triggered by motor experience, injury and interaction of these processes. Using new techniques novel perspectives take place in the injured brain, providing a real-time window into post-injury plasticity. These new approaches are likely to accelerate the pace of basic research, and provide a wealth of opportunities to translate basic principles into therapeutic methodologies [28].
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These findings confirm that the gait alterations after stroke affect both legs and the motor system contralateral to the brain lesion appear to be relatively disinhibited with co-activation significantly elicited during swing phase on the AS.
The patients with chronic hemiparesis use different strategies of reciprocal muscle activation and types of ankle movements depending on the severity of leg muscle paresis, the degree of gait recovery and the use of orthotic devices. A larch variability of EMG patterns during walking have been described by several studies – based on abnormal leg muscle activation [20], synergy exhibited by the NS [37], primitive patterns of mass extension and flexion [30], reciprocal ankle (TA/ TS) muscle inhibition [40] and co-activation [22] – fig. 6 B, C, D. These findings confirm that the gait alterations after stroke affect both legs and the motor system contralateral to the brain lesion appear to be relatively disinhibited with co-activation significantly elicited during swing phase on the AS. Thus even in present of motor deficit both legs act in a co-operative manner, each limb affecting muscle activation and temporal behaviour of the other. Orthotic devices are common in cases with reduced distal motor outcome with severe peroneal muscle deficit where the ankle on the AS needs to be stabilized. However, in presence of motor deficit the relationship between gait performance and plantar flexor strength appered to be more complex and secondary to the brain reorganisation following stroke.
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However, in presence of motor deficit the relationship between gait performance and plantar flexor strength appered to be more complex and secondary to the brain reorganisation following stroke.
A larch variability of EMG patterns during walking have been described by several studies – based on abnormal leg muscle activation [20], synergy exhibited by the NS [37], primitive patterns of mass extension and flexion [30], reciprocal ankle (TA/ TS) muscle inhibition [40] and co-activation [22] – fig. 6 B, C, D. These findings confirm that the gait alterations after stroke affect both legs and the motor system contralateral to the brain lesion appear to be relatively disinhibited with co-activation significantly elicited during swing phase on the AS. Thus even in present of motor deficit both legs act in a co-operative manner, each limb affecting muscle activation and temporal behaviour of the other. Orthotic devices are common in cases with reduced distal motor outcome with severe peroneal muscle deficit where the ankle on the AS needs to be stabilized. However, in presence of motor deficit the relationship between gait performance and plantar flexor strength appered to be more complex and secondary to the brain reorganisation following stroke.
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(based on the state of the brain after stroke).
(based on the state of the brain after stroke). There are general agreement that the combination of different rehabilitation strategies seems to be more effective than overground gait training alone [6]. However, the neurophysiological and motor learning techniques are not specifically focused on the gait rehabilitation. Compared to conventional therapy the use of robotic devices (including systems for BWSTT and FES) seems to be more effective for stroke gait recovery [6], but needs further evaluation.
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– it is based on central pattern generator theories for postural and gait control and aims to activate the “innate”, stored movement patterns in children with birth related brain damage and adult stroke patients [47].
– it is based on central pattern generator theories for postural and gait control and aims to activate the “innate”, stored movement patterns in children with birth related brain damage and adult stroke patients [47].
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Repetitive Transcranial Magnetic Stimulation (rTMS) is applied to enhance motor recovery by a non-invasive deep brain stimulation of motor cortex.
Both robotic devices and FES can be controlled or triggered by biological signals recorded from the patient. Such positive feedback loop can enhance learning. The new approaches as braincomputer interfacing (BCI) and Functional near infrared spectroscopy-based BCIs are under investigations [6]. Repetitive Transcranial Magnetic Stimulation (rTMS) is applied to enhance motor recovery by a non-invasive deep brain stimulation of motor cortex.
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