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17 results of 3 texts with exact phrase : 'intracranial stenosis'.

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

Clinical and Vascular Follow-up of Symptomatic Intracranial Stenosis Stenting.
Clinical and Vascular Follow-up of Symptomatic Intracranial Stenosis Stenting.
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Data concerning the sensitivity and specificity of TCCS in intracranial stenosis remain limited.
Data concerning the sensitivity and specificity of TCCS in intracranial stenosis remain limited. Furthermore, limited criteria for the quantification of intracranial stenosis by TCCS are available. The classification is based on conventional TCD studies.
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Furthermore, limited criteria for the quantification of intracranial stenosis by TCCS are available.
Data concerning the sensitivity and specificity of TCCS in intracranial stenosis remain limited. Furthermore, limited criteria for the quantification of intracranial stenosis by TCCS are available. The classification is based on conventional TCD studies.
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occlusion, intracranial stenosis.
occlusion, intracranial stenosis.
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CLINICAL AND VASCULAR FOLLOW UP OF SYMPTOMATIC INTRACRANIAL STENOSIS STENTING
CLINICAL AND VASCULAR FOLLOW UP OF SYMPTOMATIC INTRACRANIAL STENOSIS STENTING
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2. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 10, 2014, No. 2 , , ,

looking at the vasomotor response to an increase in CO2 can be important for studying cerebrovascular reserve in patients with carotid or intracranial stenosis: it allows assessing the risk of ischemia and identifying a group with high risk of recurrent stroke.
looking at the vasomotor response to an increase in CO2 can be important for studying cerebrovascular reserve in patients with carotid or intracranial stenosis: it allows assessing the risk of ischemia and identifying a group with high risk of recurrent stroke. This can help to make decisions regarding revascularization, when there is already an exhaustion of vasodilatation in the arterial territory of the proximal stenosis [20].
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atherosclerosis, endovascular treatment, hemodynamic effects, intracranial stenosis, ultrasound
atherosclerosis, endovascular treatment, hemodynamic effects, intracranial stenosis, ultrasound
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A systematic assessment of intracranial vessels by ultrasound is useful in diagnosing stroke patients with intracranial stenosis, understanding the nature of the stenosis, identifying ICAS patients at a higher risk of stroke recurrence.
A systematic assessment of intracranial vessels by ultrasound is useful in diagnosing stroke patients with intracranial stenosis, understanding the nature of the stenosis, identifying ICAS patients at a higher risk of stroke recurrence. In fact ultrasound can provide real-time flow information (grade of stenosis, collaterals), study hemodynamic changes with time (regression/progression/stability of stenosis) or in response to various stimuli including breath-holding index to induce or augment a steal, and it can also detect transient emboli. All the information gathered by ultrasound has immediate therapeutic implications: anticoagulants for a partially recanalized embolus, calcium channel blockers for vasospasm, antiplatelet agents for dissection, immunosuppressants for vasculitis, intensive risk factor management and dual antiplatelet treatment for ICAS. In patients with recurrent symptoms despite best medical therapy, ultrasound can detect a progression of the stenosis, check for a possible increase of the embolic count downstream, assess intracranial arterial hemodynamics changes postoperatively (angioplasty alone or combined with new stents). In the latter cases, when verifying treatment efficacy, it is important to know the effects of a stent on cerebral blood flow in order to avoid misdiagnosis.
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Analogously to intracranial occlusion, intracranial stenosis criteria are direct and indirect.
2) and dampened flow signal (TIBI 3) are criteria for distal occlusion. Indirect criteria of intracranial arterial occlusion comprise high resistance in the feeding vessel or in the proximal segment of the occluded vessel, flow diversion and signs of collateralization. Analogously to intracranial occlusion, intracranial stenosis criteria are direct and indirect. Direct criteria include progressive focal increase of lood flow velocities in 2 50% stenosis or paradoxical velocity decrease with very severe stenosis, near-occlusion or diffuse intracranial disease. Indirect criteria, which are present only in very severe stenosis (>80%), are the same as for occlusion: high resistance in the feeding vessel or in the proximal segment of the stenotic vessel, flow diversion and signs of collateralization. While transcranial ultrasound has very high specificity, sensitivity and negative predictive value, it has only modest positive predictive value, thus requiring confirmation by other imaging modality such as CTA or conventional cerebral angiography.
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Once the anatomical diagnosis of an intracranial stenosis is made, it is crucial to understand the functional significance and the hemodynamic effects of the stenosis.
Once the anatomical diagnosis of an intracranial stenosis is made, it is crucial to understand the functional significance and the hemodynamic effects of the stenosis. Transcranial ultrasound can surely help by studying collaterals, testing for vasomotor reactivity and detecting emboli. In fact TCD/TCCS can provide real-time information on collateral flow and in case of vessel obstruction, activation of collateral pathways is very important for the clinical outcome of the patient. A complete circle of Willis and the possibility to activate primary collaterals (anterior communicating artery, posterior communicating artery) or secondary collaterals (ophthalmic artery, leptomeningeal arteries) reduces the risk of hemodynamic ischemic stroke. Sometimes we see a compensatory increase of blood flow velocity in the donor vessel due to recruitment of collaterals by vasodilation in tissues with compromised perfusion. This is called flow diversion and represents a natural steal by vessels distal to an arterial occlusion.
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Once the anatomical and functional diagnosis of an intracranial stenosis is made, it is crucial to understand the nature of the stenotic lesion.
Once the anatomical and functional diagnosis of an intracranial stenosis is made, it is crucial to understand the nature of the stenotic lesion. The differential diagnosis includes atherosclerotic disease, a partially recanalized embolus/thrombus, arterial dissection, vasculitis, vasospasm. Intracranial stenosis can be a dynamic process and serial examinations by TCD/TCCS can help understanding its nature; in fact cerebral artery stenoses may undergo progression (usually a plaque), regression (embolus, dissection, vasospasm, vasculitis), or remain stable during follow-up.
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Intracranial stenosis can be a dynamic process and serial examinations by TCD/TCCS can help understanding its nature; in fact cerebral artery stenoses may undergo progression (usually a plaque), regression (embolus, dissection, vasospasm, vasculitis), or remain stable during follow-up.
Once the anatomical and functional diagnosis of an intracranial stenosis is made, it is crucial to understand the nature of the stenotic lesion. The differential diagnosis includes atherosclerotic disease, a partially recanalized embolus/thrombus, arterial dissection, vasculitis, vasospasm. Intracranial stenosis can be a dynamic process and serial examinations by TCD/TCCS can help understanding its nature; in fact cerebral artery stenoses may undergo progression (usually a plaque), regression (embolus, dissection, vasospasm, vasculitis), or remain stable during follow-up.
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Another limit is that ultrasound detection of hemodynamically relevant intracranial stenosis limits the search to the advanced stages of the disease.
Intracranial artery stenosis is assumed to represent atherosclerotic plaque when no other obvious disorder, like vasculitis or dissection, is found on diagnostic work-up. However, we know relatively little about the composition of these cerebral artery stenoses apparent on noninvasive and invasive imaging studies. Another limit is that ultrasound detection of hemodynamically relevant intracranial stenosis limits the search to the advanced stages of the disease. In fact, intracranial stenosis represents only the most advanced stage of intracranial atherosclerosis, because the vessel maintains the same lumen diameter up to 40-50% stenosis due to the remodeling of the arterial wall according to Glagov regardless of the progressing atherosclerotic process. When this compensatory mechanism fails, a vessel stenosis develops.
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In fact, intracranial stenosis represents only the most advanced stage of intracranial atherosclerosis, because the vessel maintains the same lumen diameter up to 40-50% stenosis due to the remodeling of the arterial wall according to Glagov regardless of the progressing atherosclerotic process.
Intracranial artery stenosis is assumed to represent atherosclerotic plaque when no other obvious disorder, like vasculitis or dissection, is found on diagnostic work-up. However, we know relatively little about the composition of these cerebral artery stenoses apparent on noninvasive and invasive imaging studies. Another limit is that ultrasound detection of hemodynamically relevant intracranial stenosis limits the search to the advanced stages of the disease. In fact, intracranial stenosis represents only the most advanced stage of intracranial atherosclerosis, because the vessel maintains the same lumen diameter up to 40-50% stenosis due to the remodeling of the arterial wall according to Glagov regardless of the progressing atherosclerotic process. When this compensatory mechanism fails, a vessel stenosis develops.
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All the information obtained on the nature of the intracranial stenosis will have immediate therapeutic implications: anticoagulants for a partially recanalized embolus of cardiac origin, cal-
All the information obtained on the nature of the intracranial stenosis will have immediate therapeutic implications: anticoagulants for a partially recanalized embolus of cardiac origin, cal-
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3. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 12, 2016, No. 2 , , ,

Pathologic findings of the VA that can be detected by EDS include caliber variations and hypoplasia, course anomalies and cervical compression, proximal and distal occlusion, proximal stenosis with and without cervical compensation, V4 segment intracranial stenosis, dissection, and subclavian steal [12].
Pathologic findings of the VA that can be detected by EDS include caliber variations and hypoplasia, course anomalies and cervical compression, proximal and distal occlusion, proximal stenosis with and without cervical compensation, V4 segment intracranial stenosis, dissection, and subclavian steal [12]. The most frequent locations of VA atherosclerotic damage are the sites of vessel bifurcation, namely at the V0/V1 origin and in distal V4 tracts,
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Carotid stenosis and intracranial stenosis are associated with recurrent stroke and that is why adding vascular imaging techniques to stroke risk evaluation provides better predictive accuracy.
Carotid stenosis and intracranial stenosis are associated with recurrent stroke and that is why adding vascular imaging techniques to stroke risk evaluation provides better predictive accuracy.
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