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24 results of 12 texts with exact phrase : 'subarachnoid hemorrhage'.

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

Cerebral autoregulation testing after aneurysmal subarachnoid hemorrhage: the Phase relationship between arterial blood pressure and cerebral
Lang EW, Diehl RR, Mehdorn M. Cerebral autoregulation testing after aneurysmal subarachnoid hemorrhage: the Phase relationship between arterial blood pressure and cerebral
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2. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 1, 2005, No. 2 , , ,

Predictors and Clinical Impact of Epilepsy after Subarachnoid Hemorrhage.
Claassen J, Peery S, Kreiter KT et al. Predictors and Clinical Impact of Epilepsy after Subarachnoid Hemorrhage.
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Epileptic seizures after subarachnoid hemorrhage.
Hasan D, Schonk RSM, Avezaar CJJ et al. Epileptic seizures after subarachnoid hemorrhage.
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Neurological and psychosocial outcome 4 to 7 years after subarachnoid hemorrhage.
Ogden JA, Utley T, Mee EW. Neurological and psychosocial outcome 4 to 7 years after subarachnoid hemorrhage.
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3. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 3, 2007, No. 1 , , ,

Now, it is clear why lowering the blood pressure too mush, in cases with subarachnoid hemorrhage, is not the proper thing to do.
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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4. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 4, 2008, No. 2 , , ,

Diagnosis and monitoring of subarachnoid hemorrhage by transcranial color-coded realtime sonography. Neurosurgery
Becker G, Greiner K, Kaune B, Winkler J, Brawanski A, Warmuth-Metz M, Bogdahn U. Diagnosis and monitoring of subarachnoid hemorrhage by transcranial color-coded realtime sonography. Neurosurgery
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5. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 4, 2008, No. 2 , , ,

U. Cerebral venous flow velocity predicts poor outcome in subarachnoid hemorrhage.
U. Cerebral venous flow velocity predicts poor outcome in subarachnoid hemorrhage.
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6. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 7, 2011, No. 2 , , ,

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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7. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 9, 2013, No. 2 , , ,

Microembolic Signals Detection during Routine Transcranial Doppler after Acute Subarachnoid Hemorrhage.
Microembolic Signals Detection during Routine Transcranial Doppler after Acute Subarachnoid Hemorrhage.
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It has been frequently employed for the clinical evaluation of cerebral vasospasm following subarachnoid hemorrhage (SAH).
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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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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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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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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MICROEMBOLIC SIGNALS DETECTION DURING ROUTINE TRANSCRANIAL DOPPLER AFTER ACUTE SUBARACHNOID HEMORRHAGE
MICROEMBOLIC SIGNALS DETECTION DURING ROUTINE TRANSCRANIAL DOPPLER AFTER ACUTE SUBARACHNOID HEMORRHAGE
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The cerebral vasospasm is considered one of the most common and serious complications of Subarachnoid hemorrhage (SAH) can be a cause of neurological ischemic transient or permanent, and contributes to increased rates of morbidity and mortality of patients.
The cerebral vasospasm is considered one of the most common and serious complications of Subarachnoid hemorrhage (SAH) can be a cause of neurological ischemic transient or permanent, and contributes to increased rates of morbidity and mortality of patients. Previous studies suggested that intracranial aneurysms can act as sources of distal embolization. Spontaneous thrombus can be observed within the aneurysmal sac, presumably because of turbulence and slow flow. The aim of this study was to describe the detection of some MES during routine vasospasm monitoring by transcranial Doppler (TCD).
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brain vasospasm, microembolic signals, subarachnoid hemorrhage, transcranial Doppler.
brain vasospasm, microembolic signals, subarachnoid hemorrhage, transcranial Doppler.
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8. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 10, 2014, No. 2 , , ,

A study in patients with subarachnoid hemorrhage shows that the abnormal VMR after СО
It is found that the measurement of the VMR could be used for evaluation of the therapeutic interventions in patients with carotid disease. Improvement of the investigated with BOLD –MRI impaired VMR in patients with high-grade stenoses after carotid endarterectomy is reported [10]. In similar patients the subgroup with reduced VMR in the MCA is the only independent risk factor for new ischemic accident after carotid stenting [18]. A study in patients with subarachnoid hemorrhage shows that the abnormal VMR after СО
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Cerebrovascular Carbon Dioxide Reactivity and Delayed Cerebral Ischemia After Subarachnoid Hemorrhage.
Carrera E, Kurtz P, Badjatia N, Fernandez L, Claassen J, K Lee K, Schmidt JM, Connolly ES,Marshall RS, Mayer SA. Cerebrovascular Carbon Dioxide Reactivity and Delayed Cerebral Ischemia After Subarachnoid Hemorrhage.
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9. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 12, 2016, No. 2 , , ,

It has been frequently employed for the clinical evaluation of cerebral vasospasm following subarachnoid hemorrhage (SAH).
Transcranial Doppler (TCD) is a relatively new, non-invasive tool, allowing for bedside monitoring to determine flow velocities indicative of changes in vascular caliber. 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. TCD is a suitable bedside method for daily assessment of the changes of intracranial pressure (ICP) by continuous monitoring of the changes of blood flow velocities and pulsatility index (PI), reflecting decreases in cerebral perfusion pressure due to increases in ICP. Growing body of literature demonstrates the usefulness of transbulbar B-mode sonography of the optic nerve for detecting increased ICP in patients requiring neurocritical care. 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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10. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 13, 2017, No. 1 , , ,

Nowadays, induced hypertension has been abandoned as a treatment for ischemic stroke due to the perceived risk of hemorrhage and edema, but interestingly similar therapy has become the gold standard for management of cerebral vasospasm after subarachnoid hemorrhage (triple H therapy) [10].
mind that vasopressor agents may cause edema or hemorrhage if they are administered after the stroke has already occurred. That is why Wise et al. suggest that it is probably better to discontinue vasopressor therapy in patients who do not have any clinical improvement after several hours of treatment [9]. Nowadays, induced hypertension has been abandoned as a treatment for ischemic stroke due to the perceived risk of hemorrhage and edema, but interestingly similar therapy has become the gold standard for management of cerebral vasospasm after subarachnoid hemorrhage (triple H therapy) [10]. Rordorf and colleagues have conducted a retrospective study on 63 patients admitted to the neurological intensive care unit with a diagnosis of ischemic stroke. Thirty-three were not given a pressor agent, while 30 were treated with phenylephrine in an attempt to improve cerebral perfusion. The results of this study suggest that careful use of phenylephrineinduced hypertension is not associated with an increase in morbidity or mortality in AIS and that a subset of patients, particularly those with multiple stenoses of cerebral arteries, may improve neurologically upon elevation of the blood pressure [11]. A few years later the same author and his colleagues conducted a pilot study of druginduced hypertension for the treatment of acute stroke. They concluded that induced hypertension in acute stroke is feasible and probably safe, and can improve the neurological examination in some patients [12].
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11. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 13, 2017, No. 2 , , ,

Shunt-dependent hydrocephalus after aneurysmal subarachnoid hemorrhage: incidence, predictors, and revision rates.
O'Kelly CJ, Kulkarni AV, Austin PC, Urbach D, Wallace MC. Shunt-dependent hydrocephalus after aneurysmal subarachnoid hemorrhage: incidence, predictors, and revision rates. Clinical article.
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12. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 14, 2018, No. 1 , , ,

Other risk factors were included in the analysis: trauma during the preceding month, infection during the preceding month, fibromuscular dysplasia based on the vascular imaging finding, remote head or neck surgery, anemia, thrombophilia, presence of Factor V Leiden, MTHFRC677T genotype, psoriasis, thyroid abnormalities, increased circulation IgG and IgM complex, atrial fibrillation, familial occurrence of subarachnoid hemorrhage.
>7 mmol/l during non-acute phase, or use of antidiabetic therapy), smoking status, body mass index, and migraine [4]. Other risk factors were included in the analysis: trauma during the preceding month, infection during the preceding month, fibromuscular dysplasia based on the vascular imaging finding, remote head or neck surgery, anemia, thrombophilia, presence of Factor V Leiden, MTHFRC677T genotype, psoriasis, thyroid abnormalities, increased circulation IgG and IgM complex, atrial fibrillation, familial occurrence of subarachnoid hemorrhage. Data of the functional outcome after 3 months using the modified Rankin Scale (mRS) were used. A moderate-to-severe handicap was defined by a mRS ≥3. The record of major complications within the first 3 months was retrieved from the
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Familial subarachnoid hemorrhage/Фамилен субарахноиден кръвоизлив
Familial subarachnoid hemorrhage/Фамилен субарахноиден кръвоизлив
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