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238 results of 27 texts with exact phrase : 'thrombosis'.

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

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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Assessment of intracranial venous hemodynamics in normal individuals and patients with cerebral venous thrombosis.
Stolz E, Kaps M, Dorndorf W. Assessment of intracranial venous hemodynamics in normal individuals and patients with cerebral venous thrombosis.
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Konus O., Ilgit E., Ozdemir A., Onal B.: Spontaneous thrombosis of a vein of Galen aneurismal malformation: possible effects of contrast media.
Konus O., Ilgit E., Ozdemir A., Onal B.: Spontaneous thrombosis of a vein of Galen aneurismal malformation: possible effects of contrast media.
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2. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 1, 2005, No. 2 , , ,

Various ophthalmologic disorders as an isolated independent manifestation or in combination with concomitant neurologic symptomatology can be observed in patients with carotid occlusive disease (carotid stenosis or thrombosis).
Various ophthalmologic disorders as an isolated independent manifestation or in combination with concomitant neurologic symptomatology can be observed in patients with carotid occlusive disease (carotid stenosis or thrombosis). Some of these symptoms are transient like amaurosis fugax (transient monocular blindness), which is very frequent predictor of the carotid occlusive disease. Other are a result of definite choroidal, retinal, optic nerve, visual sensory pathways damage, to wit: central retinal artery or branch central retinal artery occlusion, ischemic optic neuropathy, unilateral venous-stasis retinopathy, ischemic ocular syndrome, contralateral homonymous hemianopias and quadrantanopias. Their exact interpretation, especially of the transient ophthalmologic symptoms, supports the early diagnosis of carotid pathology and prevents the late definite neurologic and ophthalmologic complications.
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7 symptomatic), in 3 patients with moderate grade stenosis (1 asymptomatic and 2 symptomatic) and in 1 patient with asymptomatic carotid artery thrombosis.
7 symptomatic), in 3 patients with moderate grade stenosis (1 asymptomatic and 2 symptomatic) and in 1 patient with asymptomatic carotid artery thrombosis. No relationship was found between MES, age and sex of the patients and any of the studied cerebrovascular risk factors individually or in combination.
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3. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 2, 2006, No. 1 , , ,

in Young Patient with Thrombosis of Middle Cerebral Artery
in Young Patient with Thrombosis of Middle Cerebral Artery
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Arteriosclerosis, Thrombosis, and Vascular Biology
Arteriosclerosis, Thrombosis, and Vascular Biology
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Arteriosclerosis, Thrombosis, and Vascular Biology
Arteriosclerosis, Thrombosis, and Vascular Biology
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Comparative Clinical, Neurosonographic and Neuroimaging Investigations in Young Patient with Thrombosis
Comparative Clinical, Neurosonographic and Neuroimaging Investigations in Young Patient with Thrombosis
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MCA thrombosis, transcranial Doppler sonography
MCA thrombosis, transcranial Doppler sonography
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The case report represents a 43-year-old man with acute ischemic cerebral stroke in the right middle cerebral artery (MCA) territory related to arterial hypertension, thrombosis of the origine of the right MCA and long-lasting risk factors-smoking, alcohol abuse and stress.
The case report represents a 43-year-old man with acute ischemic cerebral stroke in the right middle cerebral artery (MCA) territory related to arterial hypertension, thrombosis of the origine of the right MCA and long-lasting risk factors-smoking, alcohol abuse and stress. The clinical examination reveals a mild left-sided hemiparesis, left facial palsy and left hemihypesthesia, which undergo improvement and complete recovery one year after the incident. In the acute stage of stroke a subcortical lacunar infarction in the right hemisphere (motor region) is proved by a CT scan. The magnetic resonance imaging registers ischemic zones in the right cerebral hemisphere and transcranial Doppler sonography (TCD) reveals thrombosis of the sphenoid part of the right MCA, confirmed by magnetic resonance angiography (MRA). On the 17th day from the stroke onset some initial recanalization of the MCA is detected by TCD and one year later a complete racanalization is observed.
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The magnetic resonance imaging registers ischemic zones in the right cerebral hemisphere and transcranial Doppler sonography (TCD) reveals thrombosis of the sphenoid part of the right MCA, confirmed by magnetic resonance angiography (MRA).
The case report represents a 43-year-old man with acute ischemic cerebral stroke in the right middle cerebral artery (MCA) territory related to arterial hypertension, thrombosis of the origine of the right MCA and long-lasting risk factors-smoking, alcohol abuse and stress. The clinical examination reveals a mild left-sided hemiparesis, left facial palsy and left hemihypesthesia, which undergo improvement and complete recovery one year after the incident. In the acute stage of stroke a subcortical lacunar infarction in the right hemisphere (motor region) is proved by a CT scan. The magnetic resonance imaging registers ischemic zones in the right cerebral hemisphere and transcranial Doppler sonography (TCD) reveals thrombosis of the sphenoid part of the right MCA, confirmed by magnetic resonance angiography (MRA). On the 17th day from the stroke onset some initial recanalization of the MCA is detected by TCD and one year later a complete racanalization is observed.
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Patient with Thrombosis of Middle Cerebral Artery in the Young
Patient with Thrombosis of Middle Cerebral Artery in the Young
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Patient with Thrombosis of Middle Cerebral Artery in the Young
Patient with Thrombosis of Middle Cerebral Artery in the Young
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Stroke, transient ischemic attacks, and intracranial venous thrombosis.
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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4. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 2, 2006, No. 2 , , ,

Venous Sinuses Damage and Thrombosis after
Venous Sinuses Damage and Thrombosis after
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Using transcranial Doppler US it is possible to identify the signals of disturbed circulation and by mechanical action of US to increase the surface of t-PA action over the thrombosis.
Based on numerous studies in the last three decades, research in improvement of the acute stroke thrombolysis (TL) efficacy has been directed in the way of natural fusion of diagnostic and therapeutic ultrasound (US). Using transcranial Doppler US it is possible to identify the signals of disturbed circulation and by mechanical action of US to increase the surface of t-PA action over the thrombosis. US energy could be applied for pure mechanical TL as well as for enhancing enzyme-mediated TL. Sonothrombolysis (STL) is more effective if combined with contrast agents. Microbubble agents accelerate drug pharmacodynamics at the site and improve mechanical dissolution of a thrombus. Low frequency and high intensity intracranial US insonation (between 20 KHz and 1 МHz; 1-35 W/сm
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Venous Sinuses Damage and Thrombosis after Craniocerebral Gunshot Injuries
Venous Sinuses Damage and Thrombosis after Craniocerebral Gunshot Injuries
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gunshot injury, preudotumour cerebri, venous sinus thrombosis
gunshot injury, preudotumour cerebri, venous sinus thrombosis
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Two patients who underwent craniocerebral gunshot injuries with direct damage of venous sinuses and venous sinuses thrombosis with good outcome are presented.
Two patients who underwent craniocerebral gunshot injuries with direct damage of venous sinuses and venous sinuses thrombosis with good outcome are presented. CT angiography is of great value for diagnosis of CVO and estimation of the cerebral venous system as far as for evolution of effectiveness of the anticoagulant 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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Gunshot venous sinuses damage and thrombosis
Gunshot venous sinuses damage and thrombosis
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Gunshot venous sinuses damage and thrombosis
Gunshot venous sinuses damage and thrombosis
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Cerebral venous thrombosis a review of 38 Cases.
Bosser Mg, Chiras J, Bories J, Castaigne P. Cerebral venous thrombosis a review of 38 Cases.
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Heparin Urokinasae treatment in aseptic dural sinus thrombosis.
Di Rocco C, Janne Lli A, Leone G, Moschini M, Valori VM. Heparin Urokinasae treatment in aseptic dural sinus thrombosis.
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Superior sagittal sinus thrombosis.
Gttelfinger DM, Kokemen E. Superior sagittal sinus thrombosis.
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Hanley DF, Feldman E, Borel CO, Rosenbaum AE, Goldberg AL.Treatment of sagittal sinus thrombosis associated with cerebral hemorrhage and intracranial hypertension.
Hanley DF, Feldman E, Borel CO, Rosenbaum AE, Goldberg AL.Treatment of sagittal sinus thrombosis associated with cerebral hemorrhage and intracranial hypertension.
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5. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 3, 2007, No. 2 , , ,

Further recommendations are provided for the prevention of recurrent stroke in a variety of other specific circumstances, including arterial dissections, patent foramen ovale, hyperhomocysteinemia, hypercoagulable states, sickle cell disease, cerebral venous sinus thrombosis, stroke among women, particularly with regard to pregnancy and the use of postmenopausal hormones, the use of anticoagulation after cerebral hemorrhage, and special approaches for the implementation of guidelines and their use in high-risk populations. [
A comprehensive review of the published guidelines and recommendations on the prevention of ischemic stroke among survivors of ischemic stroke or transient ischemic attack is presented. Evidence-based recommendations are included for the control of risk factors, interventional approaches for atherosclerotic disease, antithrombotic treatments for cardioembolism, and the use of antiplatelet agents for noncardioembolic stroke. Further recommendations are provided for the prevention of recurrent stroke in a variety of other specific circumstances, including arterial dissections, patent foramen ovale, hyperhomocysteinemia, hypercoagulable states, sickle cell disease, cerebral venous sinus thrombosis, stroke among women, particularly with regard to pregnancy and the use of postmenopausal hormones, the use of anticoagulation after cerebral hemorrhage, and special approaches for the implementation of guidelines and their use in high-risk populations. [
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6. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 4, 2008, No. 1 , , ,

The complications were associated with the removed unstable plaques of type I, the existence of a high degree ICA stenosis (> 90%), a recent cerebral stroke (less then 1 month prior to CEA), the presence of a counterlateral ICA thrombosis or existance of MFA.
Before the carotid surgery a slight reduction in the blood circulation on the side of stenosis was found in all patients’ groups. In 201 patients (98%) the CEA was successfully performed. The preoperative diagnosis was confirmed in 100% by the intraoperative finding. Using color Duplex sonography and TCD a significant improvement of the regional and cerebral hemodynamics on the side of CEA was established. In 4 patients (1.95%) a perioperative stroke was developed. The complications were associated with the removed unstable plaques of type I, the existence of a high degree ICA stenosis (> 90%), a recent cerebral stroke (less then 1 month prior to CEA), the presence of a counterlateral ICA thrombosis or existance of MFA. As a second step after the successful CEA in the patients with MFA a vascular reconstruction or aorto-coronary bypass was performed.
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Carotid stenoses exceeding 70% are indicative for CEA Stenosis more than 60% can be operated in the case of a concurrent counterlateral ICA thrombosis or the existance of MFA when the postoperative complications are below 3%.
Color duplex sonography and TCD are methods of choice for both the screening of carotid pathology and the preoperative and postoperative diagnostics in CEA. The CEA in patients with asymptomatic and symptomatic carotid stenosis and a concurrent MFA is an effective treatment method for removing the carotid pathology with a minimum percentage of vascular complications. Carotid stenoses exceeding 70% are indicative for CEA Stenosis more than 60% can be operated in the case of a concurrent counterlateral ICA thrombosis or the existance of MFA when the postoperative complications are below 3%.
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7. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 4, 2008, No. 2 , , ,

In 1 patient (0.99%) stroke developed as a result of thrombosis of internal carotid artery.
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. In another patient transitory amaurosis fugas was developed. In both cases the complications were attributed to unstable plaques
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8. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 4, 2008, No. 2 , , ,

Bilateral thrombosis of the carotid arteries – clinical, neurosonological, neurophysiological and neuroimaging examinations
Bilateral thrombosis of the carotid arteries – clinical, neurosonological, neurophysiological and neuroimaging examinations
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cerebral sinuses, cerebral veins, cerebral venous thrombosis,
cerebral sinuses, cerebral veins, cerebral venous thrombosis,
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Cerebral venous sinus thrombosis.
Allroggen H, Abbott RJ. Cerebral venous sinus thrombosis.
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Cerebral venous thrombosis.
Ameri A, Bousser MG. Cerebral venous thrombosis.
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Cerebral venous thrombosis: diagnosis and management.
Bousser MG. Cerebral venous thrombosis: diagnosis and management.
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Cerebral venous thrombosis.
Breteau G. Cerebral venous thrombosis. 3-year clinical outcome in 55 consecutive patients.
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acute dural sinus thrombosis.
acute dural sinus thrombosis.
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Magnetic resonance imaging of cerebral venous sinus thrombosis.
Connor SE, Jarosz JM. Magnetic resonance imaging of cerebral venous sinus thrombosis.
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Cerebral venous thrombosis in adults.
Daif A, Awada A, al-Rajeh S Abduljabbar M, Al Tahan AR, Obeid T, Malibary T. Cerebral venous thrombosis in adults. A study of 40 cases from Saudi Arabia.
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Clinical features and prognostic factors of cerebral venous sinus thrombosis in a prospective series of 59 patients.
de Bruin S, de Haan R, Stam J. Clinical features and prognostic factors of cerebral venous sinus thrombosis in a prospective series of 59 patients.
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Effect of echo-contrast media on the visualization of transverse sinus thrombosis with transcranial 3-D duplex sonography.
Delcker A, Hаussermann P, Weimar C. Effect of echo-contrast media on the visualization of transverse sinus thrombosis with transcranial 3-D duplex sonography.
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Coagulation studies, factor V Leiden and anticardiolipin antibodies in 40 cases of cerebral venous sinus thrombosis.
Deschiens M, Conard J, Horellou M, Ameri A, Preter M, Chedu F. Coagulation studies, factor V Leiden and anticardiolipin antibodies in 40 cases of cerebral venous sinus thrombosis.
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Cerebral venous and sinus thrombosis: an update.
upl KM, Masuhr F. Cerebral venous and sinus thrombosis: an update.
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Safety of anticoagulation for cerebral venous thrombosis associated with intracerebral Hematoma.
Fink JN, McAuley DL. Safety of anticoagulation for cerebral venous thrombosis associated with intracerebral Hematoma.
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Cerebral Venous Thrombosis.
Frey JL, Muro GJ, McDougall CG, Dean BL, Jahnke HK. Cerebral Venous Thrombosis. Combined Intrathrombus rtPA and Intravenous Heparin.
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MRI of clot in cerebral venous thrombosis: high diagnostic value of susceptibility-weighted images.
Idbaih A, Boukobza M, Crassard I, Porcher R, Bousser MG, Chabriat H. MRI of clot in cerebral venous thrombosis: high diagnostic value of susceptibility-weighted images.
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Cerebral venous sinus thrombosis.
Kimber J. Cerebral venous sinus thrombosis.
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Imaging of Cerebral Venous Thrombosis: Current Techniques, Spectrum of Findings, and Diagnostic. Pitfalls.
Leach JL, Fortuna RB, Jones BV, Gaskill-Shipley MF. Imaging of Cerebral Venous Thrombosis: Current Techniques, Spectrum of Findings, and Diagnostic. Pitfalls.
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Cerebral Venous Thrombosis. Emedicine.
McElveen WA, Gonzalez RF, Keegan AP. Cerebral Venous Thrombosis. Emedicine. Updated: Nov 5, 2008 www.emedicine.medscape.com/article/1162804-print
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Cerebral venous thrombosis: developments in imaging and treatment.
Perkin GD. Cerebral venous thrombosis: developments in imaging and treatment.
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Echocontrastenhanced transcranial color-coded sonography for the diagnosis of transverse sinus thrombosis.
Ries S, Steinke W, Neff KW, Hennerici M. Echocontrastenhanced transcranial color-coded sonography for the diagnosis of transverse sinus thrombosis.
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Еndovascular Thrombectomy and Thrombolysis for Severe Cerebral Sinus Thrombosis: A Prospective Study.
Stam J, Majoie C. B.L.M, van Delden OM, van Lienden KP, Reekers JA. Еndovascular Thrombectomy and Thrombolysis for Severe Cerebral Sinus Thrombosis: A Prospective Study.
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Intracranial venous hemodynamics is a factor related to a favorable outcome in cerebral venous thrombosis.
Stolz E, Gerriets T, Budeker RH, Hьgens-Penzel M, Kaps M. Intracranial venous hemodynamics is a factor related to a favorable outcome in cerebral venous thrombosis.
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Assessment of intracranial venous hemodynamics in normals and patients with cerebral venous thrombosis.
Stolz E, Kaps M, Dorndorf W. Assessment of intracranial venous hemodynamics in normals and patients with cerebral venous thrombosis.
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Influence of recanalization on outcome in dural sinus thrombosis: A prospective study.
Stolz E, Trittmacher S, Rahimi A, Gerriets T, Ruttger C, Siekmann R, Kaps M. Influence of recanalization on outcome in dural sinus thrombosis: A prospective study.
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The syndrome of latent cerebral venous thrombosis: its frequency and relation to age and congestive heart failure.
Towbin A. The syndrome of latent cerebral venous thrombosis: its frequency and relation to age and congestive heart failure.
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Monitoring of venous hemodynamics in patients with cerebral venous thrombosis by transcranial Doppler ultrasound.
Valdueza JM, Hoffmann O, Weih M, Mehraein S, Einhоupl KM. Monitoring of venous hemodynamics in patients with cerebral venous thrombosis by transcranial Doppler ultrasound.
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R. Dural sinus thrombosis: value of venous MRA for diagnosis and follow up.
R. Dural sinus thrombosis: value of venous MRA for diagnosis and follow up.
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Anticoagulation in Cerebral Venous Sinus Thrombosis: Are We Treating Ourselves?
Wasay M, Kamal AK. Anticoagulation in Cerebral Venous Sinus Thrombosis: Are We Treating Ourselves?
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Bilateral thrombosis of the carotid arteries – clinical, neurosonological, neurophysiological and neuroimaging examinations
Bilateral thrombosis of the carotid arteries – clinical, neurosonological, neurophysiological and neuroimaging examinations
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bilateral carotid thrombosis,
bilateral carotid thrombosis,
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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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A case of 62-year-old woman with bilateral thrombosis of the common and internal carotid arteries determined by color-coded duplex scan of
A case of 62-year-old woman with bilateral thrombosis of the common and internal carotid arteries determined by color-coded duplex scan of
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Chronic thrombosis of the common and internal carotid arteries caused by confluent heterogenic plaques and collateral circulation through the external carotid arteries, the vertebral arteries and the posterior part of the circle of Willis were demonstrated by color-coded duplex scan.
Non-specific features and mild neurological and cognitive impairment were found by clinical examination. Modifiable risk factors for cerebrovascular diseases (arterial hypertension, hyperlipidemia and regular smoking) were registered. Hypertonic angiopathy with cholesterol emboli in the retinal vessels were seen by ophtalmoscopy. Chronic thrombosis of the common and internal carotid arteries caused by confluent heterogenic plaques and collateral circulation through the external carotid arteries, the vertebral arteries and the posterior part of the circle of Willis were demonstrated by color-coded duplex scan. A good correlation between the neurosonographic and angiographic findings was established. Focal leucoencephalopathy and ventriculomegaly were detected by MRI. Irregular alpha rhythm from the parietooccipital regions and mild intraocular asymmetry with relatively prolonged P 100 latency on the right side were registered electrophysiologically.
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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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Correlative studies in bilateral carotid thrombosis
Correlative studies in bilateral carotid thrombosis
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Correlative studies in bilateral carotid thrombosis
Correlative studies in bilateral carotid thrombosis
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Carotid thrombosis.
Chandaburi KS. Carotid thrombosis. An evaluation and followup study of 65 cases
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Delayed bilateral internal carotid artery thrombosis following accidental strangulation.
Kiani SH, Simes DC. Delayed bilateral internal carotid artery thrombosis following accidental strangulation.
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Bilateral top of carotid occlusion presenting as basilar thrombosis.
Liberato B, Harel NY, Krakauer JW. Bilateral top of carotid occlusion presenting as basilar thrombosis.
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9. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 6, 2010, No. 1 , , ,

Monitoring for complications such as, secondary haemorrhage, space-occupying oedema, seizures, infections, decubital ulcers, deep venous thrombosis, pulmonary embolism, etc.
The location for such a unit in Austria follows a maximum of 90-min isochrones (transport time) to the hospital. In such a unit, a rapid diagnosis is made, confirmed by neuroimaging, followed by early treatment and minimizing residual disability. In addition, prevention, early recognition as well as treatment of complications arising from the stroke are an important domain of SUs. Even within the acute phase, rehabilitation is initiated to be followed by seamless further treatment and neurorehabilitation outside the SU [11-14]. In the SUs it is essential to watch out for: cardiac arrhythmia, dehydration/ fluid overload, electrolyte disturbances, systemic diseases, metabolic management, BP control, intracranial pressure, aspiration pneumonia, body temperature, progression of symptoms. Monitoring for complications such as, secondary haemorrhage, space-occupying oedema, seizures, infections, decubital ulcers, deep venous thrombosis, pulmonary embolism, etc. is made.
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10. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 6, 2010, No. 2 , , ,

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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11. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 7, 2011, No. 1 , , ,

the initial part of the right ICA and established thrombosis of the right ICA to the siphon level and of right MCA (fig. 2B).
the initial part of the right ICA and established thrombosis of the right ICA to the siphon level and of right MCA (fig. 2B). Computed tomography of head showed an extensive ischemic area of the right MCA. Because of recurrent IS and high risk of embolization of the right ophthalmic artery it was decided an endarterectomy of the right CCA and right ICA and patch plastic to be done.
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99%) and thrombosis (100%) [3].
99%) and thrombosis (100%) [3]. According to their structure the plaques are determined as homogeneous, heterogeneous, mixed and calcified. Their surface is evaluated as smooth (regular), rugged (irregular) or having cavities (more than 2 mm concaves and ulcers). Clinically the plaques are characterized as stable (homogeneous, smooth and fibrose cover) and non stable (heterogeneous, with inner hemorrhages and cholesterol spots) [1].
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12. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 7, 2011, No. 2 , , ,

Are known polymorphisms in the platelet receptors that mediate platelet aggregation and increased tendency to thrombosis in carriers.
Platelets play key role of spontaneous hemostasis. The change in platelet count or activity of their receptors for aggregation and adhesion are pare of the reason that together with the processes leading to direct damage to the endothelium, may create for the formation of abnormally blood clot – a condition known as thrombophilia. Are known polymorphisms in the platelet receptors that mediate platelet aggregation and increased tendency to thrombosis in carriers. Carrier testing and detection of genetically individuals allows the development of personalized therapy and preventive measures by avoiding provoking risk factors.
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The main exogenous cause of arterial thrombosis is damage to the vascular endothelium due to sudden changes in blood pressure (ie.
The main exogenous cause of arterial thrombosis is damage to the vascular endothelium due to sudden changes in blood pressure (ie. High shear stress). Congenital defects in platelet increase this risk [15, 41]. According to some studies, platelet aggregation and adhesion are determinant by the type, number and activity of glycoproteins on platelet membrane. Their function varies among individuals and depends on polymorphisms in genes of the membrane receptor [18, 21].
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5% of the total population down rare genetic variants associated with thrombosis, and another
5% of the total population down rare genetic variants associated with thrombosis, and another
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Polymorphisms are associated with plasma levels of coagulation factors and the risk of thrombosis.
part is a genetic polymorphism. Polymorphisms are associated with plasma levels of coagulation factors and the risk of thrombosis. Their importance is discussed in both homozygous and the heterozygous carriers of alleles.
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C1565T polymorphism (A1/A2) in the glycoprotein IIb/IIIa is associated with increased ability of platelets to bind fibrinogen, which mediates plateletaggregationandincreasedsusceptibilityto thrombosis in his presence [2, 4, 25, 35].
C1565T polymorphism (A1/A2) in the glycoprotein IIb/IIIa is associated with increased ability of platelets to bind fibrinogen, which mediates plateletaggregationandincreasedsusceptibilityto thrombosis in his presence [2, 4, 25, 35]. This type platelets are activated at lower threshold concentration of adrenalin administered in vitro (serving as an activator of platelets). Threshold concentration for heterozygous carriers of allotype A2 is about 19% lower than that of allotype A1 and homozygous carriers of the A2 allotype have about 35% lower activation threshold concentration adrenaline to the media allotype A1, which explains the increased tendency to aggregation of platelets in carriers of A1/A2 polymorphism [16]. High percentage of patients with early onset of coronary heart disease and those who developed ischemic stroke before the age of 60 are carriers of haplotype A2. It has been shown that the A2 allele is a risk factor for stroke in the large vessels [39, 43]. A2 haplotype is found more often in healthy relatives of patients with CVD [19].
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Genetic variants C807T and G873A in the gene for the synthesis of glycoprotein Ia determine structural changes and increased expression of the receptor on platelet membranes [8, 13, 49] – platelets in these polymorphisms have an increased adhesive ability and tendency to thrombosis.
Genetic variants C807T and G873A in the gene for the synthesis of glycoprotein Ia determine structural changes and increased expression of the receptor on platelet membranes [8, 13, 49] – platelets in these polymorphisms have an increased adhesive ability and tendency to thrombosis. C807T polymorphism is an indepen-
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Von Willebrand factor expressed on the activated platelet surface glycoprotein Іb and thus initiate thrombosis.
Another independent risk factor for ischemic stroke is polymorphism Kozak T/C of the glycoprotein Ib alpha, which is associated with an increase in its expression on the surface of platelets [23, 26, 47]. Von Willebrand factor expressed on the activated platelet surface glycoprotein Іb and thus initiate thrombosis.
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Hemostasis and Thrombosis: Basic Principles and Clinical Practice.
Colman R, Clowes A, George J, Goldhaber S, Marder V. Hemostasis and Thrombosis: Basic Principles and Clinical Practice. 5th Edition, 2006.
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Common risk factors for both arterial and venous thrombosis.
Gordon D. O. Lowe. Common risk factors for both arterial and venous thrombosis.
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PIA1/A2 polymorphism of platelet glycoprotein IIIa and risks of myocardial infarction, stroke, and venous thrombosis.
Ridker PM, Hennekens CH, Schmitz C, Stampfer MJ, Lindpaintner K. PIA1/A2 polymorphism of platelet glycoprotein IIIa and risks of myocardial infarction, stroke, and venous thrombosis.
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13. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 8, 2012, No. 1 , , ,

it can cause acute arterial obstruction, ranging from stenosis to thrombosis, late aneurysm or embolic events.
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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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 study was conducted in a 62-year-old man with multifocal atherosclerosis, caused ischemic heart disease, chronic arterial insufficiency of lower extremities as a result of chronic thrombosis of the deep femoral artery and transient motor aphasia 1 month before hospitalization.
The study was conducted in a 62-year-old man with multifocal atherosclerosis, caused ischemic heart disease, chronic arterial insufficiency of lower extremities as a result of chronic thrombosis of the deep femoral artery and transient motor aphasia 1 month before hospitalization. There is a combination of several cardiovascular risk factors longstanding hypertension, dyslipidemia, degenerative aortic valve stenosis, chronic thrombosis of the right ICA and severe stenosis (75%) of the left ICA (proved by ultrasound methods Fig. 1), followed by CEA patch plastic without shunt in 2011.
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There is a combination of several cardiovascular risk factors longstanding hypertension, dyslipidemia, degenerative aortic valve stenosis, chronic thrombosis of the right ICA and severe stenosis (75%) of the left ICA (proved by ultrasound methods Fig.
The study was conducted in a 62-year-old man with multifocal atherosclerosis, caused ischemic heart disease, chronic arterial insufficiency of lower extremities as a result of chronic thrombosis of the deep femoral artery and transient motor aphasia 1 month before hospitalization. There is a combination of several cardiovascular risk factors longstanding hypertension, dyslipidemia, degenerative aortic valve stenosis, chronic thrombosis of the right ICA and severe stenosis (75%) of the left ICA (proved by ultrasound methods Fig. 1), followed by CEA patch plastic without shunt in 2011.
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Sonographic examination revealed persistent chronic thrombosis of the right ICA, intact patch of the left ICA and a spiral dissection of the left CCA beginning from the bifurcation and covering the two thirds of the CCA.
Sonographic examination revealed persistent chronic thrombosis of the right ICA, intact patch of the left ICA and a spiral dissection of the left CCA beginning from the bifurcation and covering the two thirds of the CCA. Ultrasound angiography showed blood flow by crossing true and false lumen in the form of the loop. A 3-dimensional ultrasound mapping visualized a small fenestra through which the blood flow returned to the true lumen. The dissection caused approximately 50% local lumen CCA stenosis without hemodynamic changes in the distal blood flow (Fig. 2).
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The Initial thrombosis can quickly pass into arterial stenosis or spontaneous improvement.
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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The false lumen thrombosis has longer, winding and variable diameter along the artery, narrowing the true lumen to total occlusion [2].
from anechoic in the acute stage to isoechoic or heterogeneous in the chronic dissections. The false lumen thrombosis has longer, winding and variable diameter along the artery, narrowing the true lumen to total occlusion [2].
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In patients with ischemic stroke, prophylaxis with unfractionated heparin has shown almost 80% reduction of deep venous thrombosis incidence [36].
Preventive measures against decubitus ulcers are: avoidance of continuous immobilization, daily inspection and drying of the skin with a special attention to the buttocks, coccyx and heels. Timely evaluation and treatment of dysphagia prevents pneumonia, dehydration and malnutrition. In patients with ischemic stroke, prophylaxis with unfractionated heparin has shown almost 80% reduction of deep venous thrombosis incidence [36]. Sexual dysfunction may be affected by treatment of depression and sexual counseling [38]. It is important to evaluate the risk of falls and to create prevention strategies [11].
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Elastic compression stockings for prevention of deep vein thrombosis.
Sachdeva A, Dalton M, Amaragiri SV, LeesT. Elastic compression stockings for prevention of deep vein thrombosis.
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14. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 2, 2012, No. 2 , , ,

Cerebral Venous Thrombosis of Straight Sinus and Right Transverse Sinus –
Cerebral Venous Thrombosis of Straight Sinus and Right Transverse Sinus –
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The cause was thrombosis of the left internal carotid artery.
A 54-year-old patient with right-sided spastic hemiparesis 1 year and 8 months after ischemic stroke in the left middle cerebral artery was studied. The cause was thrombosis of the left internal carotid artery. The severity of paresis was evaluated by manual muscle testing (MMT).
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Cerebral Venous Thrombosis of Straight Sinus and Right Transverse Sinus – a Case Report
Cerebral Venous Thrombosis of Straight Sinus and Right Transverse Sinus – a Case Report
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multiple hemorrhages, thrombosis of dural sinuses
multiple hemorrhages, thrombosis of dural sinuses
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On MRI and MRI venography multifocal subcortical hemorrhages from cerebral venous thrombosis of sinus sagittalis superior and right sinus transversus were seen.
On MRI and MRI venography multifocal subcortical hemorrhages from cerebral venous thrombosis of sinus sagittalis superior and right sinus transversus were seen.
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The application of neurosonography in cases with thrombosis of intracranial veins and dural sinuses is difficult and requires high class medical equipments and good preparation of the neurosonologists [1, 5, 6, 7].
The application of neurosonography in cases with thrombosis of intracranial veins and dural sinuses is difficult and requires high class medical equipments and good preparation of the neurosonologists [1, 5, 6, 7]. The diagnostic value of the different methods is presented in a clinical case with intracranial venous pathology.
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Cerebral venous thrombosis of straight sinus and right transverse sinus
Cerebral venous thrombosis of straight sinus and right transverse sinus
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On post contrast flair images central defects in the filling of sinus sagittalis superior, right sinus transversus and sinus sigmoideus due to thrombosis were visualized (fig.
On post contrast flair images central defects in the filling of sinus sagittalis superior, right sinus transversus and sinus sigmoideus due to thrombosis were visualized (fig. 1 and fig. 2).
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Firstly it is necessary to differentiate thrombosis from thrombophlebitis, in which the cause and primary localization need to be identified.
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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Klisurski [2] the criteria for ultrasound diagnosis of cerebral venous thrombosis are pointed out as follows:
term prognosis. Based on a publication of E. Titianova and M. Klisurski [2] the criteria for ultrasound diagnosis of cerebral venous thrombosis are pointed out as follows:
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In 70 % of the cases, the thrombosis is in sinus sagittalis superior and sinus transversus, in 30 % the involvement is combined – sinuses, cortical and cerebellar veins.
Thromboses of cerebral veins and dural sinuses are very rare comparing to arterial lesions. In 70 % of the cases, the thrombosis is in sinus sagittalis superior and sinus transversus, in 30 % the involvement is combined – sinuses, cortical and cerebellar veins.
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Cerebral venous thrombosis of straight sinus and right transverse sinus
Cerebral venous thrombosis of straight sinus and right transverse sinus
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Effect of echo-contrast media on the visualization of transverse sinus thrombosis with transcranial 3-D duplex sonography.
Delker A, Haussermann P, Weimar C. Effect of echo-contrast media on the visualization of transverse sinus thrombosis with transcranial 3-D duplex sonography.
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Coagulation studies, factor leiden a and anticardiolipin antibodies in 40 cases of cerebral venous sinus thrombosis.
Deschiens M, Conard J, Horellow M, Ameri A, Peter M. Coagulation studies, factor leiden a and anticardiolipin antibodies in 40 cases of cerebral venous sinus thrombosis.
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Cerebral venous thrombosis& developments in imaging and treatment.
Perkin GD. Cerebral venous thrombosis& developments in imaging and treatment.
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Echocontrast enhancedtranskranial color-coded sonography for the diagnosis of transverse sinus thrombosis.
Ries S, Steinke W, Neff KW, Hennerici M. Echocontrast enhancedtranskranial color-coded sonography for the diagnosis of transverse sinus thrombosis.
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J. Endovascular thrombectomy and thrombolysis for severe cerebral sinus thrombosis: a prospective study.
J. Endovascular thrombectomy and thrombolysis for severe cerebral sinus thrombosis: a prospective study.
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assessment of intracranial venous hemodynamics in normal and patients with cerebral venous thrombosis.
Stolz E, Kaps M, Dorndorf W. assessment of intracranial venous hemodynamics in normal and patients with cerebral venous thrombosis.
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Influence of recanalization on outcome in dural sinus thrombosis: A prospective study.
Stolz E, trittmacher S, Rahimi A, Geriets t, Ruttger C, Siekmann R, kaps M. Influence of recanalization on outcome in dural sinus thrombosis: A prospective study.
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R. Dural sinus thrombosis: value of venous MRA for diagnosis and follow up.
R. Dural sinus thrombosis: value of venous MRA for diagnosis and follow up.
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anticoagulation in cerebral venous sinus thrombosis: are we treating ourselves?
Wasay m, Kamal A. anticoagulation in cerebral venous sinus thrombosis: are we treating ourselves?
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15. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 9, 2013, No. 1 , , ,

In 1947, Putnam, believing that thrombosis of the cerebral veins was a common finding in MS patients published preliminary results of treatment using dicoumarin in MS patients after experiments using induced sinus thrombosis in primates [50].
He coined the term “CCSVI” (chronic cerebrospinal venous insufficiency) in analogy to perivenous inflammation in chronic venous insufficiency of the legs. While Zamboni’s approach does not challenge the commonly accepted understanding of MS immunopathology [37], it does relegate it to the final stage in the disease cascade. According to the “CCSVI” concept, MS pathology starts with intracranial venous stasis based on a proximal obstruction of the main cervical and/or thoracic veins. This leads to perivenous diapedesis of erythrocytes in the white matter with subsequent release of iron, the actual catalyst of the widely known and accepted immune cascade [37]. The theory of venous outflow changes reaches back to the times of Charcot, who in 1868 provided an early histopathological description of perivenous inflammation in MS [16]. In 1947, Putnam, believing that thrombosis of the cerebral veins was a common finding in MS patients published preliminary results of treatment using dicoumarin in MS patients after experiments using induced sinus thrombosis in primates [50]. However, his findings have not been validated or revisited since this time. In 1986, Schelling posed the hypothesis that venous intracranial or intraspinal reflux plays a significant role in the development of MS [53]. Subsequently, Zamboni and colleagues published several studies which were meant to support the “CCSVI” hypothesis [67,69,70]. They applied catheter angiographies in order to demonstrate various extracranial venous outflow obstructions in the internal jugular veins (IJVs) or azygos veins (AVs) [66], and re-
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In the field of neurology, research begun to focus in the mid-nineties of the past century primarily on impaired venous drainage in primarily venous disorders like cerebral venous and sinus thrombosis [12, 55].
Currently, US is one popular technique for imaging the venous system. In the field of neurology, research begun to focus in the mid-nineties of the past century primarily on impaired venous drainage in primarily venous disorders like cerebral venous and sinus thrombosis [12, 55]. Subsequently, primarily non-venous disease entities were studied. In transient global amnesia (TGA) an increased prevalence of IJV valve insufficiency (IJVVI) was seen which occurs in 20-30% of the normal population, but in up to 70% of TGA patients [1, 52, 54]. A significantly increased prevalence of IJVVI was recently also shown for transient monocular blindness [30], leucoaraiosis [15], primary exertional headache [23], primary intracranial hypertension [40] and chronic obstructive pulmonary disease [19]. More recent research data suggest that the venous system may play a considerable role in arterial stroke. Yu and co-workers found that an impaired ipsilateral venous drainage due to a hypoplastic or aplastic lateral sinus (transversus and sigmoid sinus) was accompanied by pronounced infarction leading to higher morbidity and mortality [65].
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As a side note, a retrograde flow signal in the BVR can also be present in cerebral venous thrombosis [12, 56] and tumour-induced obstructions of the SS [5, 44], as well as in arterio-venous angioma [61].
in its middle and distal sections. In comparison, the other DCVs are more difficult to investigate using transcranial US. This especially applies to the ICVs, showing a detection rate of approximately 10 to 20% [111, 56]. As the anatomy of the BVR is extremely stable and forms part of the internal venous system, a flow towards the probe in the distal BVR can definitely be regarded as a pathological finding. However, an image of a retrograde flow in the BVR was never shown by Zamboni. As a side note, a retrograde flow signal in the BVR can also be present in cerebral venous thrombosis [12, 56] and tumour-induced obstructions of the SS [5, 44], as well as in arterio-venous angioma [61].
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Assessment of intracranial venous hemodynamics in normal individuals and patients with cerebral venous thrombosis.
Stolz E, Kaps M, Dorndorf W. Assessment of intracranial venous hemodynamics in normal individuals and patients with cerebral venous thrombosis.
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Monitoring of venous hemodynamics in patients with cerebral venous thrombosis by transcranial Doppler ultrasound.
upl KM. Monitoring of venous hemodynamics in patients with cerebral venous thrombosis by transcranial Doppler ultrasound.
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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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16. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 9, 2013, No. 2 , , ,

Internal Jugular Vein Thrombosis Due to Central Venous Catheter – Diagnosis and Clinical Significance.
Internal Jugular Vein Thrombosis Due to Central Venous Catheter – Diagnosis and Clinical Significance.
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In vitro evaluation of dual mode ultrasonic thrombolysis method for transcranial application with an occlusive thrombosis model.
Wang Z, Moehring MA, Voie AH, Furuhata H. In vitro evaluation of dual mode ultrasonic thrombolysis method for transcranial application with an occlusive thrombosis model.
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These initial studies have shown the potential of USPIO -enhanced MRI, 18F-FDG PET, IL2 scintigraphy, and low-density lipoprotein scintigraphy to identify inflammation, the potential of annexin A5 scintigraphy to identify cell death, and platelet scintigraphy to depict plaque thrombosis.
Currently, there are few in vivo human studies on functional imaging of carotid plaques. These initial studies have shown the potential of USPIO -enhanced MRI, 18F-FDG PET, IL2 scintigraphy, and low-density lipoprotein scintigraphy to identify inflammation, the potential of annexin A5 scintigraphy to identify cell death, and platelet scintigraphy to depict plaque thrombosis. Biomarkers have been shown to improve prediction independent of conventional risk factors. High sensitivity C-reactive protein (hs-CRP) and lipoprotein-phospholipase A2 (PLA2) are two such candidates
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sickle cell disease, stroke prevention, transcranial Doppler, thrombosis.
sickle cell disease, stroke prevention, transcranial Doppler, thrombosis.
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cerebral venous and sinus thrombosis.
The cerebral venous outflow has been neglected for many years in neurology. Considering Neurosonology a first interest started with primarily venous disorders, e.g. cerebral venous and sinus thrombosis. In the last few years venous ultrasound analysis was performed in a variety of other neurological disorders like dural fistulas, transient global amnesia and even in acute arterial stroke. In multiple sclerosis a chronic impaired cerebral venous outflow has claimed to be the starting point of a cascade leading to the disease. This concept has not been reproduced by groups with a longstanding experience in venous duplex sonography. However, the debates increased the scientific interest on the venous side of the cerebral circulation and its outflow.
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Asymptomatic thrombosis are 67 (87%), and symptomatic-10 (13 %), p
Arterial hypertension (AH) was the most common risk factor (RF) in 75% of all patients, dyslipidemia in 64% and diabetes mellitus in 28%. A symmetrical hypertrophy of the left ventricle and a decrease of its contractility was found as typical diastolic dysfunction. Mild ICA stenoses predominated in all groups while the moderate or severe carotid stenoses were relatively rare, especially with positive EST. ICA symptomatic thromboses were seen in 4,5% with positive EST. The IMT of the ICA correlated positively with the AH (r=+0.60,p0,05). Asymptomatic thrombosis are 67 (87%), and symptomatic-10 (13 %), p
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17. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 10, 2014, No. 1 , , ,

Development of malignant cerebral infarction in distal portion of the internal carotid artery or proximal middle cerebral artery thrombosis is a therapeutic challenge as the massive cerebral ischemia limits the effectiveness of medication therapy.
Development of malignant cerebral infarction in distal portion of the internal carotid artery or proximal middle cerebral artery thrombosis is a therapeutic challenge as the massive cerebral ischemia limits the effectiveness of medication therapy. ln cases of supratentorial infarctions resulting in death, the autopsy shows severe
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The microvascular changes are characterized by spasm, Raynaud's phenomenon, and thrombosis secondary to vibration exposure.
Microvascular damages and dysfunctions are some of the morphological and functional markers of hand-arm vibration syndrome (HAVS), a specific occupational disease caused by exposure to vibration at work, characterized by peripheral vascular, nervous and musculoskeletal abnormalities in the upper limbs. The microvascular changes are characterized by spasm, Raynaud's phenomenon, and thrombosis secondary to vibration exposure.
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18. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 10, 2014, No. 2 , , ,

Both AD and VaD changes are present in smaller vessels, where occlusion secondary to stenosis/thrombosis or spasm (which occurs as a reaction to an elevation in mean arterial pressure) results in elevated total peripheral resistance.
Both AD and VaD changes are present in smaller vessels, where occlusion secondary to stenosis/thrombosis or spasm (which occurs as a reaction to an elevation in mean arterial pressure) results in elevated total peripheral resistance. These dementias may thus represent end-organ failure secondary to the effects of vascular disease [25]. Several years ago a study by Rundek et al. described the changes of CVMR in patients with VaD, and to a lesser extent in those with AD [26]. A reduction in CVMR was associated with cognitive decline at 12 months follow-up, as reported by Silvestrini [16]. These results suggest that vascular factors are important in the pathogenesis of cognitive impairment in some patients with AD.
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In cases with cerebral infarctions ipsilateral to high-grade stenosis or thrombosis of the internal carotid
The impairment of the hemodynamic reserve capacity is frequently observed in patients with multiple asymptomatic subcortical infarctions, the results suggesting vasculopathy of the small vessels and hypoperfusion pathogenetic mechanism of their origin. When investigating patients with cerebral infarctions and symptomatic carotid stenoses Jolnic W. et al. [15] established that the TCD examined VMR has not identified the subgroup with high risk of stroke recurrence. Our studies with estimation of the VMR in the MCA in patients with unilateral cerebral infarctions showed its bilateral decrease [30]. In cases with cerebral infarctions ipsilateral to high-grade stenosis or thrombosis of the internal carotid
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19. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 11, 2015, No. 1 , , ,

The study was carried out in 28 clinically healthy subjects (15 men and 13 women in the age range from 22 to 79, mean age 51.3±20.5 years without a history of ophthalmic diseases and syndromes) and 20 patients (12 women and 8 men in the age range from 21 to 85 years, mean age 45±17 years) with ocular pathology: 10 of the patients were with papilledema caused by various pathological processes (bilateral papillitis or intracranial hypertension, brain tumors, arteriovenous malformation, dural transverse sinus venous thrombosis), 6 of the patients were with retinal detachment, 1 – with macular degeneration, 1 – with intraocular metastasis of the right eye, 1 – with amaurosis and visual hallucinations and 1 – with hemophthalmos.
The study was carried out in 28 clinically healthy subjects (15 men and 13 women in the age range from 22 to 79, mean age 51.3±20.5 years without a history of ophthalmic diseases and syndromes) and 20 patients (12 women and 8 men in the age range from 21 to 85 years, mean age 45±17 years) with ocular pathology: 10 of the patients were with papilledema caused by various pathological processes (bilateral papillitis or intracranial hypertension, brain tumors, arteriovenous malformation, dural transverse sinus venous thrombosis), 6 of the patients were with retinal detachment, 1 – with macular degeneration, 1 – with intraocular metastasis of the right eye, 1 – with amaurosis and visual hallucinations and 1 – with hemophthalmos.
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20. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 11, 2015, No. 2 , , ,

Data were collected on vascular risk factors (hypertension, diabetes, dyslipidemia, smoking), as well as on the possible association between right-to-left cardiac shunt with changes in the carotid arteries (carotid intima-media thickness (CIMT), the presence of carotid plaque) and the presence of deep venous thrombosis (DVT).
We conducted a retrospective review of de-identified reports from 58 patients with positive TCD that were subsequently subjected to c-TEE examination. Data were collected on vascular risk factors (hypertension, diabetes, dyslipidemia, smoking), as well as on the possible association between right-to-left cardiac shunt with changes in the carotid arteries (carotid intima-media thickness (CIMT), the presence of carotid plaque) and the presence of deep venous thrombosis (DVT).
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Possible presence of deep venous thrombosis (DVT) was also recorded by ultrasound examination.
– IMT and the presence of carotid plaques), ultrasound examination of the carotid blood vessels using the ultrasonic device Aloka Prosound Alpha 10 (Aloka, Japan) with a linear ultrasound probe 5–13 MHz. Possible presence of deep venous thrombosis (DVT) was also recorded by ultrasound examination.
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P4 Preoperative Assessment of Cerebral Autoregulation in Patients with Carotid Stenosis and Thrombosis.
P4 Preoperative Assessment of Cerebral Autoregulation in Patients with Carotid Stenosis and Thrombosis.
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P8 Cerebral Venous Thrombosis of Straight Sinus and Right Transverse Sinus: a Case Report.
P8 Cerebral Venous Thrombosis of Straight Sinus and Right Transverse Sinus: a Case Report.
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Long-term results of the ABSORB study showed that on the fifth year of follow-up of 30 patients with implanted Absorb BVS, no stent thrombosis, need for revascularization as a result of in-stent restenosis and death due to cardiovascular event were reported.
The bio-absorbable stents are considered the third revolution in stent technology (after the development of the first bare metal stents and the first drug eluting stents). Long-term results of the ABSORB study showed that on the fifth year of follow-up of 30 patients with implanted Absorb BVS, no stent thrombosis, need for revascularization as a result of in-stent restenosis and death due to cardiovascular event were reported. Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors are a new opportunity for better lipid control in patients intolerable to statins or with poor control with the maximum tolerated statin dose. The three major trials for evolucomab (PCSK9 inhibitor) show a mean of 57% lowering
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PREOPERATIVE ASSESSMENT OF CEREBRAL AUTOREGULATION IN PATIENTS WITH CAROTID STENOSIS AND THROMBOSIS
PREOPERATIVE ASSESSMENT OF CEREBRAL AUTOREGULATION IN PATIENTS WITH CAROTID STENOSIS AND THROMBOSIS
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To assess the dynamics of CA in patients with stenosis and thrombosis of the carotid arteries in perioperative period.
To assess the dynamics of CA in patients with stenosis and thrombosis of the carotid arteries in perioperative period.
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Thirty-nine patients (27 men and 12 women) with atherosclerotic stenosis or thrombosis of carotid arteries aged 48-78 years were studied.
Thirty-nine patients (27 men and 12 women) with atherosclerotic stenosis or thrombosis of carotid arteries aged 48-78 years were studied. Critical stenosis was revealed in 28 patients. Severe stenosis was found in 5 patients, thrombosis – in 6. Fourteen patients had a history of stroke, 25 were always asymptomatic. Stenting of the carotid artery was performed in 16 patients, carotid endartherectomy – in 17, upper cervical sympathectomy – in 4, extra-intracranial arterial bypass
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Severe stenosis was found in 5 patients, thrombosis – in 6.
Thirty-nine patients (27 men and 12 women) with atherosclerotic stenosis or thrombosis of carotid arteries aged 48-78 years were studied. Critical stenosis was revealed in 28 patients. Severe stenosis was found in 5 patients, thrombosis – in 6. Fourteen patients had a history of stroke, 25 were always asymptomatic. Stenting of the carotid artery was performed in 16 patients, carotid endartherectomy – in 17, upper cervical sympathectomy – in 4, extra-intracranial arterial bypass
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CEREBRAL VENOUS THROMBOSIS OF STRAIGHT AND RIGHT TRANSVERSE SINUSES: A CASE REPORT
CEREBRAL VENOUS THROMBOSIS OF STRAIGHT AND RIGHT TRANSVERSE SINUSES: A CASE REPORT
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On MRI multifocal subcortical hemorrhages by cerebral venous thrombosis of sinus sagittalis superior and the right sinus transversus were detected.
On MRI multifocal subcortical hemorrhages by cerebral venous thrombosis of sinus sagittalis superior and the right sinus transversus were detected.
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cerebral venous sinus thrombosis.
cerebral venous sinus thrombosis.
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orbital pseudotumor, thrombosis of the cavernous sinus, collagenosis, lymphoma, metastasis at al.).
Our study confirms that the diagnosis of Tolosa-Hunt syndrome is difficult and based on exclusion of other causes of painful ophthalmoplegia (e.g. orbital pseudotumor, thrombosis of the cavernous sinus, collagenosis, lymphoma, metastasis at al.). The complex use of clinical, laboratory and neuroimaging methods allowed prospective follow-up of the clinical evolution of the syndrome. The multimodal neurosonology has a limited diagnostic value for imaging the retrobulbar granulomatous inflammation but contributes for the noninvasive assessment of the optic disc and optic nerve changes, associated with the disease.
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21. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 12, 2016, No. 1 , , ,

It is shown that a lot of factors influence the stroke outcome – the process of recanalization, time to the beginning of the thrombectomy, presence of combined cerebrovascular pathology (thrombosis of MCA and ipsilateral occlusion of the BCA), patient's age and type of anesthesia during the intervention.
uence outcomes [4, 14]. It is shown that a lot of factors influence the stroke outcome – the process of recanalization, time to the beginning of the thrombectomy, presence of combined cerebrovascular pathology (thrombosis of MCA and ipsilateral occlusion of the BCA), patient's age and type of anesthesia during the intervention.
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thrombosis of the cavernous sinus, whose clinical presentation and course resembles TolosaHunt syndrome.
thrombosis of the cavernous sinus, whose clinical presentation and course resembles TolosaHunt syndrome. Cavernous sinus thrombosis may be septic or aseptic, which requires further study of a complete blood count (CBC) with differential count (CCA), ESR and C – reactive protein. Those studies help to distinguish from collagenosis. In light of other processes such as retrobulbar orbital pseudotumor, lymphoma, metastasis of unidentified carcinoma requires study of tumor markers (carcinoembryonic antigen and prostate specific antigen). To exclude endocrine ophthalmoplegia is necessary to test
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Cavernous sinus thrombosis may be septic or aseptic, which requires further study of a complete blood count (CBC) with differential count (CCA), ESR and C – reactive protein.
thrombosis of the cavernous sinus, whose clinical presentation and course resembles TolosaHunt syndrome. Cavernous sinus thrombosis may be septic or aseptic, which requires further study of a complete blood count (CBC) with differential count (CCA), ESR and C – reactive protein. Those studies help to distinguish from collagenosis. In light of other processes such as retrobulbar orbital pseudotumor, lymphoma, metastasis of unidentified carcinoma requires study of tumor markers (carcinoembryonic antigen and prostate specific antigen). To exclude endocrine ophthalmoplegia is necessary to test
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22. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 12, 2016, No. 2 , , ,

Vein Thrombosis: A Rare Entity
Vein Thrombosis: A Rare Entity
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In clinical experience diagnostic ultrasound methods are used (transcranial Doppler sonography, duplex scanning of basal cerebral arteries, etc.) for recanalization of cerebral arteries with severe thrombosis [11, 54] – a phenomenon confirmed both in vivo and in vitro in randomized and non-randomized clinical studies of ischemic brain stroke [45, 55].
. This term indicates the degradation of thrombotic masses by ultrasound waves with or without using thrombolytics. In clinical experience diagnostic ultrasound methods are used (transcranial Doppler sonography, duplex scanning of basal cerebral arteries, etc.) for recanalization of cerebral arteries with severe thrombosis [11, 54] – a phenomenon confirmed both in vivo and in vitro in randomized and non-randomized clinical studies of ischemic brain stroke [45, 55].
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Bilateral Superior Ophthalmic Vein Thrombosis: A Rare Entity
Bilateral Superior Ophthalmic Vein Thrombosis: A Rare Entity
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Bilateral Superior Ophthalmic Vein Thrombosis: А Rare Entity
Bilateral Superior Ophthalmic Vein Thrombosis: А Rare Entity
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sinus thrombosis, superior ophthalmic vein thrombosis
sinus thrombosis, superior ophthalmic vein thrombosis
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We present a patient with bilateral superior ophthalmic vein thrombosis diagnosed with orbital MR examination.
We present a patient with bilateral superior ophthalmic vein thrombosis diagnosed with orbital MR examination. The patient had bubbling right-facial-pain and visual deterioration. Orbital MRI revealed dilated superior ophthalmic veins with thrombosis bilaterally. Ten days after treatment initiation, the patient left the hospital; completely pain free, with normal visual acuity and full motility of ocular bulbs.
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Orbital MRI revealed dilated superior ophthalmic veins with thrombosis bilaterally.
We present a patient with bilateral superior ophthalmic vein thrombosis diagnosed with orbital MR examination. The patient had bubbling right-facial-pain and visual deterioration. Orbital MRI revealed dilated superior ophthalmic veins with thrombosis bilaterally. Ten days after treatment initiation, the patient left the hospital; completely pain free, with normal visual acuity and full motility of ocular bulbs.
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Superior ophthalmic vein thrombosis (SOVT) is an uncommon and very rare condition, occurring secondary to various etiologies.
Superior ophthalmic vein thrombosis (SOVT) is an uncommon and very rare condition, occurring secondary to various etiologies. Risk factors for SOVT can be local or systemic, usually including at least one factor from the Virchow's triad: hypercoagulability, hemodynamic changes, and endothelial injury/dysfunction [9]. It usually presents with globe dystopia, proptosis, periorbital edema, ophthalmoplegia, and occasionally diminished visual acuity. Most commonly SOVT is found in cases of orbital congestion such as orbital cellulitis, idiopathic orbital inflammation, thyroid-related orbitopathy, and
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described bilateral superior and inferior ophthalmic veins thrombosis secondary to ethmoidal rhinosinusitis [6].
vascular malformation [17]. lnfection of the orbit or paranasal sinuses, trauma, or malignant process can also cause SOVT [1]. lt can also occur as a complication of oral contraceptive therapy, or secondary to antiphospholipid syndrome [3, 8]. Bilateral SOVT is an extremely rare entity, and only individual cases are described in the literature. Ogul et al. described bilateral superior and inferior ophthalmic veins thrombosis secondary to ethmoidal rhinosinusitis [6]. Rohana et al. described bilateral SOVT secondary to nasal furun-
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We present a 75-year old female with bilateral superior ophthalmic veins (SOV) thrombosis diagnosed with orbital magnetic resonance imaging (MRl) examination.
We present a 75-year old female with bilateral superior ophthalmic veins (SOV) thrombosis diagnosed with orbital magnetic resonance imaging (MRl) examination.
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Bilateral Superior Ophthalmic Vein Thrombosis: A Rare Entity
Bilateral Superior Ophthalmic Vein Thrombosis: A Rare Entity
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Based on clinical examination and neuroradiological findings, the patient was diagnosed with bilateral superior orbital vein thrombosis.
Based on clinical examination and neuroradiological findings, the patient was diagnosed with bilateral superior orbital vein thrombosis. lmmediately, low molecular weight heparin (LMWH) was administered together with the appropriate antibiotics parenterally. We started with dual broad spectrum antibiotics (Metronidazole and Ceftazidime). LMWH was adjusted according to prothrombin time (РTT) values. One week later visual acuity was normal, with full motility of ocular bulbs and without eyelid edema. She only suffered of occasional headaches with the same characteristics as before.
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Control CTs of the brain and orbits were performed on the 6th day of treatment introduction, and demonstrated a considerable reduction of thrombosis on the left side, and almost normal finding on the right side (fig. 2).
We started with dual broad spectrum antibiotics (Metronidazole and Ceftazidime). LMWH was adjusted according to prothrombin time (РTT) values. One week later visual acuity was normal, with full motility of ocular bulbs and without eyelid edema. She only suffered of occasional headaches with the same characteristics as before. The values of C-reactive protein and D-dimer returned to the normal range. Control CTs of the brain and orbits were performed on the 6th day of treatment introduction, and demonstrated a considerable reduction of thrombosis on the left side, and almost normal finding on the right side (fig. 2). These findings were confirmed with ultrasound examination (US)
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CT of the brain and orbits showed considerable reduction of thrombosis on the left side, and almost normal finding on the right side.
CT of the brain and orbits showed considerable reduction of thrombosis on the left side, and almost normal finding on the right side.
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Superior ophthalmic vein thrombosis (SOVT) is an unusual entity, which can lead to devastating complications, thus bilateral SOVT can be considered as an extremely rare and dangerous condition [9].
Superior ophthalmic vein thrombosis (SOVT) is an unusual entity, which can lead to devastating complications, thus bilateral SOVT can be considered as an extremely rare and dangerous condition [9]. We present a case of bilateral SOVT diagnosed in time, so luckily, the patient was cured and left the hospital at her own request, completely symptom and complaints free.
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Bilateral Superior Ophthalmic Vein Thrombosis: A Rare Entity
Bilateral Superior Ophthalmic Vein Thrombosis: A Rare Entity
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On the other hand infections of dental origin and teeth extractions in the maxilla are well-known triggers for cavernous sinus thrombosis, sometimes with extension to superior ophthalmic veins.
С-reactive protein. On the other hand infections of dental origin and teeth extractions in the maxilla are well-known triggers for cavernous sinus thrombosis, sometimes with extension to superior ophthalmic veins. Since our patient had teeth extractions three days prior to SOVT symptoms onset, this probably was the triggering factor of bilateral SOVT. She had also plasma von Willebrand factor antigen (vWfAg) almost 4-fold above normal values. Plasma concentrations of vWfAg are significantly elevated in patients with acute infectious diseases [12]. This is another proof that the infection was a SOVT trigger in our patient.
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MRl is sensitive even in early stages of the disease, and is recommended when there is a suspicion of SOVT or cavernous sinus thrombosis.
Patients with SOVT may complain of facial and orbital pain and swelling, double and decreasedblurred vision. Сlinical findings depend on the specific etiology and may include proptosis, chemosis, ophthalmoplegia, and ptosis. lf the optic nerve is affected by compression, clinical sigs of optic neuropathy may occur, such as reduced visual acuity, abnormal color vision, and relative afferent papillary defect [1, 2]. ln this case, the patient presented with clinical features consistent with an orbital process. Before additional diagnostics, we suspected Tolosa-Hunt syndrome, but after the MRl we diverted the examination to SOVT. MRl is sensitive even in early stages of the disease, and is recommended when there is a suspicion of SOVT or cavernous sinus thrombosis. MRl may demonstrate a dilated SOV, and extraocular muscle enlargement [2, 9]. ln our case, orbital MR examination was of crucial importance for the diagnosis. Some authors suggest Doppler imaging with ultrasound to confirm the lack of flow in the SOV [6]. We performed an US Doppler examination on the 6th day of treatment introduction which helped us in establishing the definitive diagnosis of SOVT and also monitoring the positive therapy effects. On the same day we performed a control СT of the brain and orbits which was in compliance with the US findings and the good early clinical outcome.
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On the other hand, if not treated, SOVT can progress to cavernous sinus thrombosis.
The appropriate management of SOVT depends on the etiology. 1n all cases empiric treatment with broad spectrum antibiotics is recommended, because infection is one of the most common causes of SOVT; later on antibiotics could be changed according to the antibiogram. Antibiotics should be given for 2 more weeks after clinical resolution, because pathogens can be located and sequestered within the thrombus [14]. Since in our case maxillary teeth extractions were the probable trigger factor for SOVT, we started treatment with dual broad spectrum antibiotics, which fortunately proved to be successful. The role of anticoagulants in SOVT cases is unclear. On the other hand, if not treated, SOVT can progress to cavernous sinus thrombosis. Although the use of anticoagulant therapy is controversial, many authors suggest dose-adjusted intravenous heparin applications if there are no contraindications, such as risk of intracranial or any other hemorrhage [15]. The EFNS guidelines for treatment of cerebral venous and sinus thrombosis in adults recommend body weightadjusted subcutaneous LMWH or dose-adjusted intravenous heparin use with an at least doubled activated partial thromboplastin time [4]. A metaanalysis comparing the efficacy of adjusted-dose unfractionated heparin and fixed-dose subcutaneous LMWH for extracerebral venous thromboembolism found superiority for LMWH and significantly less major bleeding complications [4, 16]. Guided by these recommendations we started the therapy with LMWH. Einhapul et al.
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The EFNS guidelines for treatment of cerebral venous and sinus thrombosis in adults recommend body weightadjusted subcutaneous LMWH or dose-adjusted intravenous heparin use with an at least doubled activated partial thromboplastin time [4].
Antibiotics should be given for 2 more weeks after clinical resolution, because pathogens can be located and sequestered within the thrombus [14]. Since in our case maxillary teeth extractions were the probable trigger factor for SOVT, we started treatment with dual broad spectrum antibiotics, which fortunately proved to be successful. The role of anticoagulants in SOVT cases is unclear. On the other hand, if not treated, SOVT can progress to cavernous sinus thrombosis. Although the use of anticoagulant therapy is controversial, many authors suggest dose-adjusted intravenous heparin applications if there are no contraindications, such as risk of intracranial or any other hemorrhage [15]. The EFNS guidelines for treatment of cerebral venous and sinus thrombosis in adults recommend body weightadjusted subcutaneous LMWH or dose-adjusted intravenous heparin use with an at least doubled activated partial thromboplastin time [4]. A metaanalysis comparing the efficacy of adjusted-dose unfractionated heparin and fixed-dose subcutaneous LMWH for extracerebral venous thromboembolism found superiority for LMWH and significantly less major bleeding complications [4, 16]. Guided by these recommendations we started the therapy with LMWH. Einhapul et al. suggest maintaining an elevated РTT in SOVT patients, but no more than
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Bilateral Superior Ophthalmic Vein Thrombosis: A Rare Entity
Bilateral Superior Ophthalmic Vein Thrombosis: A Rare Entity
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S. Superior ophthalmic vein thrombosis: complication of ethmoidalrhinosinusitis.
S. Superior ophthalmic vein thrombosis: complication of ethmoidalrhinosinusitis.
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K. Superior ophthalmic vein thrombosis developed after orbital cellulitis.
K. Superior ophthalmic vein thrombosis developed after orbital cellulitis.
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Superior ophthalmic vein thrombosis as an initial manifestation of antiphospholipid syndrome.
Dey M. Charles Bates A, McMillan P. Superior ophthalmic vein thrombosis as an initial manifestation of antiphospholipid syndrome.
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EFNS guideline on the treatment of cerebral venous and sinus thrombosis in adult patients.
upl K, Stam J, Bousser MG, De Bruijn SF, Ferro JM, Martinelli I, Masuhr F. European Federation of Neurological Societies. EFNS guideline on the treatment of cerebral venous and sinus thrombosis in adult patients.
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Heparin treatment in sinus venous thrombosis.
upl KM, Villringer A, Meister W, Mehraein S, Garner C, Pellkofer M,Haberl RL, Pfister HW, Schmiedek P. Heparin treatment in sinus venous thrombosis.
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Color Doppler imaging of superior ophthalmic vein thrombosis.
Flaharty PM, Phillips W, Sergott RC, Stefanyszyn M, Bosley T, Savino PJ. Color Doppler imaging of superior ophthalmic vein thrombosis.
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Unilateral superior ophthalmic vein thrombosis in a user of oral contraceptives.
Jaasis F, Habib ZA. Unilateral superior ophthalmic vein thrombosis in a user of oral contraceptives.
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Spontaneous superior ophthalmic vein thrombosis: a rare entity with potentially devastating consequences.
Lim LH, Scawn RL, Whipple KM, Oh SR, Lucarelli MJ, Korn BS, Kikkawa DO. Spontaneous superior ophthalmic vein thrombosis: a rare entity with potentially devastating consequences.
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Massive thrombosis of bilateral superior and inferior ophthalmic veins secondary to ethmoidal rhinosunisitis: imaging findings.
Ogul H, Gedikli Y, Karaca L, Okur A, Kantarci M. Massive thrombosis of bilateral superior and inferior ophthalmic veins secondary to ethmoidal rhinosunisitis: imaging findings.
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thrombosis due to severe superior ophthalmic vein enlargement in a patient with graves ophthalmopathy.
thrombosis due to severe superior ophthalmic vein enlargement in a patient with graves ophthalmopathy.
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Bilateral ophthalmic vein thrombosis secondary to nasal furunculosis.
Rohana AR, Rosli MK, Nik Rizal NY, Shatriah I, Wan Hazabbah WH. Bilateral ophthalmic vein thrombosis secondary to nasal furunculosis.
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Superior ophthalmic vein thrombosis in a patient with dacryocystitis-induced orbital cellulitis.
Schmitt NJ, Beatty RL, Kennerdell JS. Superior ophthalmic vein thrombosis in a patient with dacryocystitis-induced orbital cellulitis.
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Southwick FS, Richardson EP Jr, Swartz MN: Septic thrombosis of the dural venous sinuses.
Southwick FS, Richardson EP Jr, Swartz MN: Septic thrombosis of the dural venous sinuses.
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Superior and inferior ophthalmic veins thrombosis with cavernous sinus meningioma. Middle
Vyas S, Das PJ, Gupta SK, Kakkar N, Khandelwal N. Superior and inferior ophthalmic veins thrombosis with cavernous sinus meningioma. Middle
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Well defined risk factors for ICH are age, alcohol consumption, hypertension, cerebral amyloid angiopathy, anticoagulant therapy, hemorrhagic transformation of ischemic stroke, vascular abnormalities, venous thrombosis, vasculitis, coagulopathy, and neoplasia.
Nontraumatic intracerebral hemorrhage (ICH) leads to a high rate of morbidity and mortality and constitutes a major public health problem worldwide, accounting for 10%– 15% of all strokes each year. Well defined risk factors for ICH are age, alcohol consumption, hypertension, cerebral amyloid angiopathy, anticoagulant therapy, hemorrhagic transformation of ischemic stroke, vascular abnormalities, venous thrombosis, vasculitis, coagulopathy, and neoplasia. Although CT is the first-line diagnostic approach, MR imaging with gradient echo sequences can detect hyperacute ICH with equal sensitivity and overall accuracy. Furthermore, MR imaging is more accurate for the detection of micro-hemorrhages.
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23. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 13, 2017, No. 1 , , ,

Carotid plaque pathology: thrombosis, ulceration, and stroke pathogenesis.
Fisher M, Paganini-Hill A, Martin A. Carotid plaque pathology: thrombosis, ulceration, and stroke pathogenesis.
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24. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 13, 2017, No. 2 , , ,

Heparin is recommended for the treatment of acute ischemic stroke in cases with embolism originating in the heart with a high recurrence risk, in cerebral venous thrombosis, arterial dissection of major brain arteries.
Heparin is recommended for the treatment of acute ischemic stroke in cases with embolism originating in the heart with a high recurrence risk, in cerebral venous thrombosis, arterial dissection of major brain arteries.
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25. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 14, 2018, No. 1 , , ,

Deep vein thrombosis
Deep vein thrombosis
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Follow up doppler ultrasounds showed spontaneous partial thrombosis of the malformation.
We present a patient with a clinically silent arteriovenous fistula of arteria thyroidea ima, diagnosed with color doppler examination and confirmed by CT angiography. Fine needle cytopunction of thyroid gland using anatomic landmark tehnique was performed at the age of 12 to confirm the diagnosis of autoimmune disorder. Later ultrasound follow up revealed vascular lesion of the right thyroid lobe. We presumed an iatrogenic small artery lesion during fine needle aspiration cytology (FNAC). Proposed therapy included right thyroid lobectomy and radiological vascular intervention. Follow up doppler ultrasounds showed spontaneous partial thrombosis of the malformation.
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CDUS control in 6/2016 was performed much earlier than suggested, showing partial thrombosis of PSAN, but was unable to depict
Vascular surgeon excluded surgery as method of choice, suggesting only yearly CDUS controls. The patient was cardialy well compensated, with one episode of dyspnea, but excluding bronchoobstructive disease; and one case of dysphagia, neck pain and neck swelling. CDUS control in 6/2016 was performed much earlier than suggested, showing partial thrombosis of PSAN, but was unable to depict
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B-mode ultrasound of partial thrombosis of arteriovenous fistula with pseudoaneurysm;
B-mode ultrasound of partial thrombosis of arteriovenous fistula with pseudoaneurysm;
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Color-coded display of partial thrombosis arteriovenous fistula with PSAN;
Color-coded display of partial thrombosis arteriovenous fistula with PSAN;
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The last CDUS performed in our institution (Aviva Medical Center) showed minimal progression of AVF thrombosis, leaving only half of malformation patent, still unable to define the draining vein.
The last CDUS performed in our institution (Aviva Medical Center) showed minimal progression of AVF thrombosis, leaving only half of malformation patent, still unable to define the draining vein. Right thyroid lobe decreased in size, maybe due to the compressive factor of AVF and lobe atrophy included in autoimmune disorder (Fig. 2).
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No venous vascular structures were identified, probably due to venous thrombosis (Fig. 3).
The findings were confirmed on 3DMR angiography (MRA), with good correlations between the two modalities. No venous vascular structures were identified, probably due to venous thrombosis (Fig. 3). The patient has been asymptomatic in this period of follow-up.
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Axial image of MR angiography showing partial thrombosis of the AVF with PSAN
Axial image of MR angiography showing partial thrombosis of the AVF with PSAN
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Spontaneous thrombosis of iatrogenic femoral artery pseudoaneurysms: documentation with color Doppler and two-dimensional ultrasonography.
Johns JP, Pupa LE, Jr., Bailey SR. Spontaneous thrombosis of iatrogenic femoral artery pseudoaneurysms: documentation with color Doppler and two-dimensional ultrasonography.
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In the group of patients with carotid dissection, one patient received thrombolytic therapy; she ameliorated, but afterward worsened, and during rehabilitation got deep vein thrombosis and pulmonary embolism.
In the group of patients with carotid dissection, one patient received thrombolytic therapy; she ameliorated, but afterward worsened, and during rehabilitation got deep vein thrombosis and pulmonary embolism.
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26. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 14, 2018, No. 2 , , ,

atrial fibrillation, prosthetic heart valves, valvular thrombosis) [6, 4, 17, 12], patent foramen ovale (PFO) [32, 33], and during carotid surgery and endovascular procedures (i.e.
Transcranial Doppler (TCD) is a safe and sensitive technique for real-time detection of microembolic signals (MES) in the intracranial cerebral arteries. MES have been defined as short lasting (3 dB) transients within the Doppler frequency spectrum; they appear randomly during the cardiac cycle and produce a “whistle”, “chirp”, or “click” sound when passing through the sample volume; they have been proven to represent microemboli passing within cerebral arteries [24, 14, 7, 5, 22, 36]. Since its first application in the field of cerebrovascular diseases in the late 1990s, MES detection improved in several technical aspects, such as reliability of automated MES count and exclusion of artifacts during continuous TCD monitoring [3, 27, 1, 2, 18]. MES have been detected in a large number of clinical conditions, such as carotid artery stenosis (especially due to unstable plaques) [25, 21, 31, 20, 19, 38, 23, 29], aortic arch plaques [25, 6], cardiac sources of cerebral embolism (i.e. atrial fibrillation, prosthetic heart valves, valvular thrombosis) [6, 4, 17, 12], patent foramen ovale (PFO) [32, 33], and during carotid surgery and endovascular procedures (i.e. stent implantation) [16, 26, 35, 34]. In all these conditions, the presence of MES within the cerebral circulation has shown to indicate an increased risk of stroke in both asymptomatic and symptomatic patients [36, 15, 13]. In symptomatic cases, after an index stroke, MES detection identifies patients at higher risk for recurrent stroke. Most studies about MES detection concern patients with carotid artery stenosis, but some tried to detect MES in different stroke subtypes disclosing a higher MES number when the underlying mechanism was a cardiac embolism [17, 12]. There are few data about MES detection in patients with cryptogenic stroke, and about its relationship with the different stroke subtypes, especially with the recently proposed category of embolic stroke of undetermined source (ESUS) [10].
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Legend: OR, odds ratio; CI, confidence interval; DVT, deep vein thrombosis; PFO, patent foramen ovale; RLS, right-to-left shunt; ASA, Atrial Septal Aneurysm; ESUS, embolic stroke of undetermined source; *statistically significant; NS, not significant.
Legend: OR, odds ratio; CI, confidence interval; DVT, deep vein thrombosis; PFO, patent foramen ovale; RLS, right-to-left shunt; ASA, Atrial Septal Aneurysm; ESUS, embolic stroke of undetermined source; *statistically significant; NS, not significant.
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For children with sinovenous thrombosis or arterial stroke due to dissection or cardiac embolism guidelines recommend anticoagulant therapy with warfarin or low molecular weight heparin for 3-6 months.
applicable to pediatric stroke due to maturational differences in coagulation and vascular systems as well as different stroke mechanisms. Current guidelines agree on the treatment of children with sickle-cell disease and stroke – initial and maintenance transfusion therapy to reduce the proportion of sickle-cell haemoglobin to less than 30%. For children with sinovenous thrombosis or arterial stroke due to dissection or cardiac embolism guidelines recommend anticoagulant therapy with warfarin or low molecular weight heparin for 3-6 months. Children with ischemic stroke of other etiology are empirically treated with antithrombotics including antiplatelet and anticoagulant drugs. Of major concern is also the risk of recurrent stroke, which affects up to 25% of children.
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In acute central retinal artery thrombosis hyperechoic artifact in the optic nerve and increased venous blood flow was detected.
Normal optic disc resulted in a smooth and sharp contour without swelling. Papilledema was presented as a hyperechoic prominence into the vitreous. On its side the optic sheath diameter was increased in association with the degree of optic disc swelling. The retinal detachment was imaged as a hyperechoic undulating membrane, the neovascular macular degeneration – as a hyperechoic membrane behind the retina, and the intraocular metastasis – as irregular uni-focal formation into the vitreous. In acute central retinal artery thrombosis hyperechoic artifact in the optic nerve and increased venous blood flow was detected. Eye injury causes various changes in shape, size and density of the ocular
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Thrombosis – a Case Report.
Thrombosis – a Case Report.
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The Role of Color Duplex Ultrasonography in Subclavian Vein Thrombosis in Pacemaker
The Role of Color Duplex Ultrasonography in Subclavian Vein Thrombosis in Pacemaker
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The intraluminal carotid thrombosis (ICT) is an infrequent finding in cases of transient ischemic attack or ischemic stroke.
The intraluminal carotid thrombosis (ICT) is an infrequent finding in cases of transient ischemic attack or ischemic stroke. Optimal treatment for patients with symptomatic ICT remains poorly defined. Treatment options include anticoagulation/antiplatelet therapy and/or revascularization procedures.
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We present two cases of symptomatic occlusion/thrombosis of the right internal carotid artery (RICA) and the beneficial effect of antithrombotic treatment at the 1st month of follow-up.
We present two cases of symptomatic occlusion/thrombosis of the right internal carotid artery (RICA) and the beneficial effect of antithrombotic treatment at the 1st month of follow-up.
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As part of the diagnostic procedures a Doppler ultrasonography was performed, establishing significant stenosis/thrombosis of RICA.
Two 44and 57-year-old women with several transient ischemic attacks and ischemic stroke in the right middle cerebral artery territory are presented. As part of the diagnostic procedures a Doppler ultrasonography was performed, establishing significant stenosis/thrombosis of RICA. Additional imaging included CT and conventional carotidography. The two patients were discussed and put on conservative therapy. An antiplatelet therapy with Aspirin 300 mg/day and 20 mg/day of statin were initiated. At the end of the first month both patients improved their neurological deficit. Ultrasonography and carotidography showed complete recanalization of the carotid artery.
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The two cases emphasize a possible beneficial effect of the conservative antiplatelet treatment of the severe stenosis/thrombosis of the carotid artery.
The two cases emphasize a possible beneficial effect of the conservative antiplatelet treatment of the severe stenosis/thrombosis of the carotid artery.
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conservative treatment, thrombosis of internal carotid artery
conservative treatment, thrombosis of internal carotid artery
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FORAMEN OVALE IN PATIENT WITH MASSIVE PULMONARY EMBOLISM AND DEEP VEIN THROMBOSIS – A CASE REPORT
FORAMEN OVALE IN PATIENT WITH MASSIVE PULMONARY EMBOLISM AND DEEP VEIN THROMBOSIS – A CASE REPORT
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Compression ultrasound and color coded duplex ultrasound showed proximal lower limb deep vein thrombosis.
Echocardiography revealed severe RA dilation, interatrial septum was bulging towards left atrium (LA), there was a serpingous thrombus protruding from RA into LA via patent foramen ovale (PFO). CT pulmoangiography confirmed massive pulmonary embolism and the atrial thrombus. Compression ultrasound and color coded duplex ultrasound showed proximal lower limb deep vein thrombosis. Patient management was discussed by Heart Team and decision to proceed with atrial/pulmonary thrombectomy and PFO closure was made. Immediately post-op, there were pulmonary bleeding and right
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THE ROLE OF COLOR DUPLEX ULTRASONOGRAPHY IN SUBCLAVIAN VEIN THROMBOSIS IN PACEMAKER IMPLANTATION
THE ROLE OF COLOR DUPLEX ULTRASONOGRAPHY IN SUBCLAVIAN VEIN THROMBOSIS IN PACEMAKER IMPLANTATION
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Subclavian vein thrombosis in pacemaker implantation is a fairly rare complication that depends on individual patient anatomy, operating physician experience and the type of implanted device.
Subclavian vein thrombosis in pacemaker implantation is a fairly rare complication that depends on individual patient anatomy, operating physician experience and the type of implanted device. In most cases it is asymptomatic. Ultrasonography is a safe, fast and a very informative diagnostic method in determining venous thrombosis and is the preferred initial imaging modality in cases of suspected occlusive venous disease in patients who are to receive upgrade to their artificial pacemaker system.
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Ultrasonography is a safe, fast and a very informative diagnostic method in determining venous thrombosis and is the preferred initial imaging modality in cases of suspected occlusive venous disease in patients who are to receive upgrade to their artificial pacemaker system.
Subclavian vein thrombosis in pacemaker implantation is a fairly rare complication that depends on individual patient anatomy, operating physician experience and the type of implanted device. In most cases it is asymptomatic. Ultrasonography is a safe, fast and a very informative diagnostic method in determining venous thrombosis and is the preferred initial imaging modality in cases of suspected occlusive venous disease in patients who are to receive upgrade to their artificial pacemaker system.
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pacemaker, pacemaker upgrade, subclinical venous thrombosis
pacemaker, pacemaker upgrade, subclinical venous thrombosis
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with a subclavian venous thrombosis where the heart pacemaker (PM) electrode has already been implanted.
with a subclavian venous thrombosis where the heart pacemaker (PM) electrode has already been implanted.
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On CCDS, thrombosis of the right subclavian vein was observed with a normal left subclavian vein.
On CCDS, thrombosis of the right subclavian vein was observed with a normal left subclavian vein. During the ipsilateral upgrade procedure to CRT the venous occlusion was confirmed with a continuous right subclavian vein occlusion present. For the left ventricular electrode implantation an alternative venous access site through the left subclavian vein was used. The LV electrode was implanted in a lateral branch of the coronary venous system. The connector head of the LV electrode was placed in the initial (contralateral) side by tunneling over the sternum. A CRT device was implanted by using the RA and RV electrodes already in place.
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upgrade, Cardiac resynchronization therapy, subclinical venous thrombosis
upgrade, Cardiac resynchronization therapy, subclinical venous thrombosis
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The CCDS examination showed a thrombosis of left IJV – distal part and greatly slow venous flow in left subclavian vein (SV) to the extent of venous sludge, as well as a heterogenous formation above the collarbone.
The first patient is a 34-year-old man. He has a leading complaint of tingling and stabbing in the left upper limb and a slight swelling of the left side of the neck and the area of left collarbone (supraclavicular fossa). The CCDS examination showed a thrombosis of left IJV – distal part and greatly slow venous flow in left subclavian vein (SV) to the extent of venous sludge, as well as a heterogenous formation above the collarbone. The second patient is 35-year-old man. His complaints include nonspecific tension and burden in the head at leaning.The examination via CCDS show dilation of right IJV with a poorly influenced blood flow; slightly influenced by breathing delayed blood flow in right SV; retrograde
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These data indirectly refer to thrombosis or exter-
blood flow in left IJV and slow blood flow in left SV. These data indirectly refer to thrombosis or exter-
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Perren, Switzerland), diagnosis of retinal artery thrombosis (P.
Republic; A. Alexandrov, USA), ultrasound-guided application of botulinum toxin in cervical dystonia (U. Walter, Germany), and use of contrast agents in ultrasound diagnosis and evaluation (E. Vicenzini, Italy). Among the discussed topics were also: prognostic markers for risk assessment of brain aneurysm rupture (F. Perren, Switzerland), diagnosis of retinal artery thrombosis (P. Castro, Portugal) and diagnosis of peripheral nervous system diseases such as Charcot-Marie-Tooth (D. Coraci, Italy) and other polyneuropathies (A. Kerasnoudis, Greece).
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27. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 15, 2019, No. 1 , , ,

Dissociation between persistent central retinal artery thrombosis and clinical improvement of vision as an expression of functional brain reorganization is registered.
for early and fast diagnosis of CRAO and its follow-up in the presence of carotid pathology. Dissociation between persistent central retinal artery thrombosis and clinical improvement of vision as an expression of functional brain reorganization is registered.
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Embologenic central retinal artery thrombosis (CRAO) is an urgent condition resulting in ischemic stroke of the eye, clinically manifested by acute unilateral, non-painful loss of vision [13, 19].
Embologenic central retinal artery thrombosis (CRAO) is an urgent condition resulting in ischemic stroke of the eye, clinically manifested by acute unilateral, non-painful loss of vision [13, 19]. It was first described by von Graefe in 1859 in a patient with multiple systemic endocarditis embolisms [7, 20]. According to the literature, CRAO has a frequency of 1/100,000 population [19], with a prevalence of 1.67/100,000 in men [10], more commonly associated with high-grade ipsilateral stenosis of the internal carotid artery [3, 11].
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ciliaris posterior brevis is detected, affecting the cases with central retinal artery (CRA) thrombosis.
ciliares are divided into aa. ciliares posteriores longi and aa. ciliares posteriores breves [2]. In part of the population a. cilioretinalis, branch of a. ciliaris posterior brevis is detected, affecting the cases with central retinal artery (CRA) thrombosis. In literature a. cilioretinalis is seen in 25–30% (Beatty
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was hospitalized by emergency and consulted with an ophthalmologist who established thrombosis of the left central retinal artery.
was hospitalized by emergency and consulted with an ophthalmologist who established thrombosis of the left central retinal artery. The patient was followed up by parallel clinical, paraclinical and ophthalmologic examinations.
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Left CRAO thrombosis –
Left CRAO thrombosis –
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Degenerative changes in the vitreous body of the right ocular bulb, a typical CRA thrombosis image [6]: a small round hyperechoic artefact within the left optic nerve 14 mm behind the optical disc (Fig.
The Doppler ophthalmic test was positive on left (a sign of collateral blood flow through the left external carotid artery). Degenerative changes in the vitreous body of the right ocular bulb, a typical CRA thrombosis image [6]: a small round hyperechoic artefact within the left optic nerve 14 mm behind the optical disc (Fig. 4 D), increased vascular resistance in the left ophthalmic artery and increased venous flow in the CRA territory were seen.
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Central retinal artery thrombosis is apolyethiological disease.
Central retinal artery thrombosis is apolyethiological disease. The pathogenesis of CRA thrombosis is associated with atherosclerosis, emboli from various sources (platelet aggregates, cholesterol, fat, air embolism), vasculitis, vasospasm or hypotension. It has been shown that over 75% of patients have generalized atherosclerosis combined with arterial hypertension and diabetes mellitus [4], with risk factors similar to those in cerebrovascular disease.
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The pathogenesis of CRA thrombosis is associated with atherosclerosis, emboli from various sources (platelet aggregates, cholesterol, fat, air embolism), vasculitis, vasospasm or hypotension.
Central retinal artery thrombosis is apolyethiological disease. The pathogenesis of CRA thrombosis is associated with atherosclerosis, emboli from various sources (platelet aggregates, cholesterol, fat, air embolism), vasculitis, vasospasm or hypotension. It has been shown that over 75% of patients have generalized atherosclerosis combined with arterial hypertension and diabetes mellitus [4], with risk factors similar to those in cerebrovascular disease.
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Principles of Treatment of CRA Thrombosis according to S.
Principles of Treatment of CRA Thrombosis according to S. Cugati et al., 2013 [5].
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Most commonly CRA thrombosis occurs in case of ipsilateral ICA stenosis, orbital trauma, coagulopathy (especially sickle-cell anemia), vasculopathy (systemic lupus erythematosus, temporal arteritis, etc.), migraine, oral contraceptive use, cardiovascular diseases (especially valve disorders, myxoma), carotid angiography and endarterectomy [11].
Most commonly CRA thrombosis occurs in case of ipsilateral ICA stenosis, orbital trauma, coagulopathy (especially sickle-cell anemia), vasculopathy (systemic lupus erythematosus, temporal arteritis, etc.), migraine, oral contraceptive use, cardiovascular diseases (especially valve disorders, myxoma), carotid angiography and endarterectomy [11].
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Treatment of CRA thrombosis is aimed at early reperfusion and prevention of ocular complications.
Treatment of CRA thrombosis is aimed at early reperfusion and prevention of ocular complications. Although there is no unified international therapeutic algorithm of behavior, two basic approaches are applied – non-invasive and invasive (Table 1) [5, 19].
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Late effects occur in 18% of patients with acute thrombosis: neovascularization of the optic papilla (usually between weeks 2 and 16 after the symptoms
The invasive treatment method includes procedures aim the recanalization of the internal carotid artery (carotid endarterectomy, endovascular stenting and/or mechanical thrombectomy) [12, 15] and the ophthalmic artery through selective intra-arterial thrombolysis. In treatment with intra-arterial thrombolysis there is a 60-70% visual acuity improvement [19]. In some cases the use of anterior chamber paracentesis followed by aspiration of a small amount of fluid is recommended. Nd YAG laser (Neodymium: yttrium-aluminum-garnet laser) embolectomy and pars plana vitrectomy are not routinely used because of the high risk for vitreous hemorrhage. Late effects occur in 18% of patients with acute thrombosis: neovascularization of the optic papilla (usually between weeks 2 and 16 after the symptoms
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In conclusion, the study confirms that multimodal ultrasound imaging is a non-invasive screening method for early and rapid diagnosis of CRA thrombosis and follow-up of its evolution.
In conclusion, the study confirms that multimodal ultrasound imaging is a non-invasive screening method for early and rapid diagnosis of CRA thrombosis and follow-up of its evolution. There is a slight dissociation between the retinal artery occlusion and the clinical improvement of vision, which supports the theory of functional reorganization of vision in conditions of chronic ischemic damage to the retina [14].
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. The intravascular analysis shows thickening of the wall of the aortic arch and the walls of the common carotid arteries with peripheral thrombosis in the aneurysms and a stenotic proximal segment of the right internal carotid artery
. The intravascular analysis shows thickening of the wall of the aortic arch and the walls of the common carotid arteries with peripheral thrombosis in the aneurysms and a stenotic proximal segment of the right internal carotid artery
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The dimensions and extent of the thrombosis of carotid aneurysms are identical to those depicted by the CTA (Fig. 3).
of inflammation) (Fig. 2). Identical changes in the vascular wall were also found along the course of the thoracic and suprarenal abdominal aorta. The thoracic aorta is dilated to a varying degree along its entire course with a maximal dilatation in the thoraco-abdominal segment (Fig. 3). The dimensions and extent of the thrombosis of carotid aneurysms are identical to those depicted by the CTA (Fig. 3). On the dynamic contrast-enhanced MR angiography an asynchronous, delayed at the left, filling of the carotid arteries is observed (Fig. 4). The findings correspond to panvasculitis with involvement of the aorta, including the aortic arc and its branches and formation of aneurysms and segmental stenoses, probably
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After a three-month treatment (immunosuppressive therapy and corticosteroids) and normalization of immunological markers, a follow-up CTA shows a complete thrombosis of the aneurysm of the left common carotid artery and a collateral filling of the internal carotid artery at the left via the ipsilateral external carotid artery.
The patient is referred to Rheumatology Clinic for therapy, where immunological tests confirm Takayasu decease. After a three-month treatment (immunosuppressive therapy and corticosteroids) and normalization of immunological markers, a follow-up CTA shows a complete thrombosis of the aneurysm of the left common carotid artery and a collateral filling of the internal carotid artery at the left via the ipsilateral external carotid artery. The internal carotid artery on the left is poorly filled along its entire length up to the circle of Willis (Fig. 5). At the right no differences with the previous imaging results are seen.
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images show a complete thrombosis of the aneurysm of the common carotid artery at the left up to the level of bifurcation.
images show a complete thrombosis of the aneurysm of the common carotid artery at the left up to the level of bifurcation. The level of thrombosis is demonstrated of multiplanar reconstruction
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The level of thrombosis is demonstrated of multiplanar reconstruction
images show a complete thrombosis of the aneurysm of the common carotid artery at the left up to the level of bifurcation. The level of thrombosis is demonstrated of multiplanar reconstruction
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Our case demonstrates the whole spectrum of changes in Takayasu disease: intimal edema, inflammation, hemorrhages and fibrosis in the media and adventitia, and wall thrombosis in the lumen of the aneurysms.
Depending on the techniques used, the sensitivity, specificity and accuracy of the method ranges from 91%, 81% and 86% respectively in the non-contrast angiography and up to 100% for contrast-enhanced angiography. The assessment accuracy of the grade of stenotic lesions reaches 98% when the latter technique is used. The application of contrast allows seeing enhancement in the vascular wall, which is a sign of active inflammation [1]. Highresolution morphological images give information about the thickness of the vascular wall and the type of changes: edema, hemorrhages, thrombi, and calcifications. The individual layers of the wall are clearly distinguishable; it is also possible to localize the different types of changes. Our case demonstrates the whole spectrum of changes in Takayasu disease: intimal edema, inflammation, hemorrhages and fibrosis in the media and adventitia, and wall thrombosis in the lumen of the aneurysms. MRT provides coverage of a larger volume within one examination without ionizing
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Keywords related to: 'thrombosis'

● cerebral venous sinus thrombosis

● thrombosis of internal carotid artery

● subclinical venous thrombosis

● sinus thrombosis

● superior ophthalmic vein thrombosis

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