Ischemic stroke is an abrupt onset neurologic deficit due to interruption of blood flow to a portion of the brain. Focal weakness, numbness, facial asymmetry, or speech difficulties are classic presentations. The major etiologies of ischemic stroke are cardioembolism, small vessel vasculopathy involving the penetrating arteries, and large vessel atherosclerosis due to plaque rupture involving the intracranial or extracranial cerebral arteries. Carotid artery disease accounts for between 10% and 20% of ischemic stroke.
The carotid arteries provide about 80% of the blood supply to the brain. The most common disease of the carotid artery is atherosclerosis occurring at the carotid artery bifurcation, typically involving the distal common carotid and the proximal internal carotid artery (ICA). Carotid artery diseases other than atherosclerosis are spontaneous dissection, fibromuscular dysplasia, primary tumors of the vascular structures and radiotherapy.
Atherosclerotic stenosis in carotid arteries is a slower process. Atherosclerosis develops over the course of 50 years, beginning in the early teenage years. The causes of this process appear to be lipid retention, oxidation, and modification, which provoke chronic inflammation at susceptible sites in the walls of all major conduit arteries. Lesions begin in the inner lining of the arteries-the intima-and they progressively affect the entire arterial wall, including the media and the adventitia. Initial fatty streaks evolve into fibrous plaques, some of which develop into forms that are vulnerable to rupture, causing thrombosis or stenosis. Significant stenosis before 40 years is rare.
Several risk factors may intensify or provoke atherosclerosis through their effects on low-density lipoprotein (LDL) particles and inflammation. These risk factors most frequently include hypertension, tobacco smoking, diabetes mellitus, obesity, and genetic predisposition.
Carotid artery diseases cause transient ischemic attacks (TIAs) or ischemic stroke. Transient monocular blindness also known as amaurosis fugax may be considered a brief monocular visual obscuration described by patients as a fog, blur, cloud, mist, and so forth. The symptoms reported for TIAs involving the carotid territory within the ipsilateral hemisphere generally match those found in stroke involving these territories, except for their briefer duration. The commonest symptoms are weakness or numbness of part or all of the side of the body contralateral to the affected hemisphere, with the presence or absence of a speech disturbance, depending on whether the dominant hemisphere is affected. An association with very severe internal carotid artery stenosis (>95%) or occlusion should lead to consideration of hemodynamic mechanisms. While symptoms precipitated by documented hypotension or precipitants likely to cause peripheral or core vasodilatation, e.g., orthostasis, a hot bath, or a large meal are likely to be hemodynamic in origin. One distinctive if uncommon form of hemodynamic hemisphere TIAs involves limb shaking.
Carotid arteries can be evaluated with Doppler ultrasound, CT or MR angiography. Ultrasonography of the carotid arteries is the modality of choice for triage, diagnosis, and monitoring of cases of atheromatous disease. This is an operator-dependent examination that requires a good understanding of Doppler physics and hemodynamic physiology. The extent, location, and characteristics of atherosclerotic plaque in the internal carotid artery can be documented with ultrasonography.
For patients with a TIA or non disabling ischemic stroke within the past 6 months and ipsilateral carotid stenosis >70% should be treated with carotid endarterectomy (CEA) or stenting. For those with moderate (50% to 69%) carotid stenosis, CEA is recommended depending on patient specific factors, such as age, sex, and comorbidities; and for those with a degree of stenosis of less than 50%, CEA and carotid artery stenting are not recommended. The optimal timing of carotid revascularization via CEA after a completed non disabling stroke has been defined to be within 2 weeks if no contraindications exist.