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Intracranial atherosclerosis (ICAS) refers to a narrowing of an artery inside the brain that can lead to stroke.
Intracranial atherosclerosis is a major cause of stroke worldwide.
Mechanisms by which ICAS causes TIA or stroke, include acute occlusion or artery to artery embolization due to plaque rupture, branch atheromatous disease where the large artery plaque overgrows the ostium of a perforator artery, hypoperfusion of distal territory, due to low flow, or combination of these mechanisms.
Approximately 12% of White patients with a history of acute ischemic stroke or TIA have some form of intracranial atherosclerosis detected on routine screening in predominantly older adults, but accounts for an estimated up to 1/3 of ischemic strokes in Black, Asian, and Hispanic populations at comparatively young ages.
Caused by a buildup of plaque, atherosclerosis, inside the artery wall that reduces blood flow to the brain.
Intracranial arterial stenosis is difficult to distinguish from other causes a stroke or TIA such as, arterial dissection, intracranial vasculitis, moyamaoya disease, artery to artery embolism, in situ thrombotic occlusion of large vessels, local branch of occlusion of small perforated vessels, hemodynamic insufficiency: all of which influence prognosis and treatment.
Associated with a high risk for strokes and treatment aims to reduce the risk of stroke by controlling or removing plaque buildup and by preventing blood clots.
Blood is supplied to the brain by two paired arteries, the internal carotid arteries and the vertebral arteries.
The internal carotid arteries supply the front areas and the vertebral arteries supply the back areas of the brain.
Asymptomatic internal carotid artery stenosis develops and 7-9% of patients by 75 years.
1-2% age 65-84 will have sufficiently severe asymptomatic internal carotid artery stenosis to consider carotid artery revascularization.
The right and left vertebral arteries join together to form a single basilar artery.
The basilar artery and the internal carotid arteries join with each other in a ring at the base of the brain called the Circle of Willis.
Arteries most likely to be affected by stenosis are the internal carotid artery, the middle cerebral artery, the vertebral arteries, and the basilar artery.
Intracranial artery stenosis can result in a stroke: by severely narrowing the artery and reducing blood flow to the brain, causing blood clots to form and plaque can rupture and embolize downstream to lodge in a smaller artery and blocking blood flow to the brain.
The symptoms of intracranial artery stenosis are a transient ischemic attack (TIA) or stroke.
Atherosclerosis caused by high blood pressure, diabetes, smoking, and hyperlipidemia, obesity, heart disease, family history, and advanced age.
One of the most common causes of stroke worldwide, and is associated with a high risk of recurrence.
Patients with recent TIA or stroke and 70-99% stenosis of a major intracranial artery have a high risk of recurrent stroke in the territory of the stenotic artery of approximately 23% at one year, despite treatment with aspirin and standard management of vascular risk factors.
Therapeutic strategies for secondary stroke prevention in patients with ICAS include antithrombotic therapy, risk factor management, surgical and vascular procedures.
Risk management and dual antiplatelet therapy have resulted it in incremental improvements and lowering the risk of recurrent stroke.
Intracranial percutaneous transluminal angioplasty and stenting with self expanding Wingspanstent available for patients with 50-99% stenosis who have had a TIA or stroke while receiving anti-thrombotic therapy.
In a randomized study in patients with intracranial arterial stenosis, aggressive medical management with superior to percutaneous transluminal angioplasty and stenting: the rate of stroke or death was 14.7% in the stenting group and 5.8% in the medical management group (SAMMPRIS trial).
Among patients with TIA or ischemic stroke due to symptomatic severe intracranial atherosclerotic stenosis, the addition of percutaneous transluminal angioplasty and stenting to medical therapy, compared with medical therapy alone, resulted in no significant difference in the risk of stroke or death within 30 days of a stroke in the qualifying artery territory beyond 30 days through one year: these findings do not support the addition of percutaneous transluminal angioplasty and standing to medical therapy for the treatment of patients with symptomatic severe intracranial atherosclerotic stenosis (CASSISS Trial Investigators).
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