The normal carotid artery circulation (in the neck) is shown. The common carotid artery (CCA) divides into the external carotid artery (ECA) and the internal carotid artery (ICA). The arrows indicate the direction of flow in these vessels. The ECA has many branches which supply structures of the head and neck. The ICA has no branches in the neck, but proceeds directly through the base of the skull and towards the base of the brain. Its terminal (end) branches at the base of the brain comprise the "anterior circulation" of the circle of Willis ( take me to the Section on Brain Arteries now)

When fatty and inflammatory tissue builds up on the inside surface of an artery, it forms a plaque. Platelets, fibrin and other blood products can stick to this as part of a clot (thrombus). This leads to some degree of blockage of flow through the artery, which is known as carotid stenosis. The figure shows moderate blockage, i.e., moderate stenosis. Risk factors for plaque formation include smoking, poor diet (high cholesterol, obesity) and little exercise ("sedentary lifestyle"), hypertension, and in some instances a family history of early vascular disease. Mild to moderate carotid stenosis may or may not cause any symptoms. However, sometimes, as shown in this figure, a fragment of the plaque (embolus) can break off and "seed" the more distant circulation leading to a transient ischemic attack (TIA; see below), or a full (completed) stroke ( take me to the Brain Attack Section). Symptoms of a TIA or stroke include sudden problems with speech (dysarthria or aphasia), vision (amaurosis fugax), limb power, sensation, etc.

If the plaque build up involves blockage of 70% or more of the inner opening (luminal diameter) of the internal carotid artery (ICA), the stenosis is referred to as "high-grade" (there is "moderate" stenosis if the blockage is measured to be 40-69%). High grade stenosis may result in only a trickle of flow (or at least impaired flow) in the ICA more distant to the blockage. The brain may recognize this via stroke-like symptoms (vision loss, sensory and muscle function loss, speaking difficulty, etc.). On a cerebral angiogram or MR angiogram or CT angiogram, this trickle may appear as a "string sign" because it looks like a string of remaining flow. On a carotid ultrasound, the blockage can be measured and it may create a jet effect that results in an abnormally high flow velocity. Another way blockage can be detected is using oculoplethysmography (OPG), where eye pressures are recorded and found to be abnormal. Sometimes, blockage of the carotid artery is associated with abnormal retinal findings on an eye exam (e.g., embolus or venous occlusive disease).

The treatment considerations for carotid stenosis are complex and should be discussed in detail with your physicians. Treatment is carried out to prevent stroke, or if a limited stroke has occurred, to prevent further debilitating stroke. Medical treatment options include life-style (risk factor) modification (more exercise, better diet, quit smoking), anticholesterol or antilipid and anti-hypertension agents, and antiplatelet agents (medications which stop platelets sticking) such as acetyl salicylic acid (ASA, Aspirin), clopidogrel (Plavix) and ticlodipine (Ticlid) and their equivalents. The surgical treatment option is carotid endarterectomy, as illustrated. Here, a surgeon makes an incision in the neck, accesses the carotid arteries as shown, opens them and cleans out the plaque. The vessel is then sewn closed with or without a synthetic patch graft (e.g., one made of Goretex or an equivalent biocompatible fabric). In the illustration, a graft is shown. Surgery is usually highly effective (see below).

The risks of surgery usually include the risk of stroke and the risk of a heart attack around the time of the surgery (as most patients with carotid disease also have some degree of coronary artery disease, whether they know it or not). Risks of surgery also include a small risk of infection and neck blood clot, as well as injury to the nerves of speech, swallowing and tongue movement. Altogether, the risks of surgery are less than 5% for most patients. That is, there is a 95% plus chance of highly effective and safe surgery being carried out. The endovascular alternative to surgery is carotid stenting as shown. Here, a catheter is fed through the thigh (femoral) artery up into the neck and a stent is deployed to "jimmy" (wedge or compress) the plaque against the artery wall to create a bigger opening for blood to flow in the center of the diseased ICA. Although there is no surgery involved, and usually little risk of heart attack, some studies suggest that the risk of stroke from embolism during stenting is increased. The risk of significant complication with stenting is probably around 5%, but the chances of recurrent stenosis are higher with stenting.

Carotid artery stenosis can predispose towards platelets sticking to the abnormal (plaque) segment, especially if it has an ulcerated (raw) region as shown in Fig. 3, above. This leads to formation of a local clot (thrombus) which can block off flow distant to the diseased segment. This is referred to a carotid occlusion, and is illustrated here. Carotid occlusion can also occur following carotid dissection (see below). It may not cause any symptoms (asymptomatic in about 25% of persons), or it may cause ministroke like events (TIA) or a completed stroke, symptoms of which are described above and elsewhere ( see Brain Attack Section). The risk factors and investigation and complications are as for carotid stenosis (see above). Treatment of carotid occlusion may include one of the following (discuss in detail with your physician): direct endovascular thrombolysis (clot-dissolving medicines through a catheter) with, e.g., tPA, or surgical revascularization via urgent carotid endarterectomy and thrombectomy, or EC-IC (brain) bypass. The option(s) used depend(s) on many factors.

Carotid dissection refers to a tear between the layers of the carotid artery wall. Risk factors: It can occur following direct mechanical injury (e.g., external trauma involving the neck, or during endovascular procedures where a catheter is navigated through the carotid artery); It can also occur during vigorous neck turning (inlcuding chiropractic manipulation) or physical straining, or even in prolonged bouts of coughing and crying; In previously diseased carotid arteries, the chance of a dissection is increased. It may present with sudden or gradually worsening headache especially on the side of the dissection, sudden or worsening neurological impairment (TIA or stroke-like symptoms as mentioned above), or pain in the neck over the dissected carotid artery (carotidynia), or Horner's syndrome. In this diagram, a dissection has occurred where a flap of the inner artery lining (known as the initima; see Brain Arteries Section) has been torn (dissected), and blood now runs under this flap, causing it to further elevate from the inner wall of the artery. This is a subintimal dissection. There may alternatively or in addition be "medial" or "subadvential" dissection (other layers torn).

The main complication of carotid dissection is stroke (from carotid occlusion; see above), as well as carotid pseudoaneurysm formation (see below). The investigation of a patient suspected of having a carotid dissection may include any of the following: CT or MR (MRI) head scan to rule out a stroke, and a CT angiogram or MR angiogram or catheter angiogram of the head and neck (extracranial and intracranial circulation) to look at the neck and brain circulation in detail. Most carotid dissections start a few centimeters distant to the origin of the ICA, and may extend to the skull base. There may be a tapering of the blood flow pattern in the vessel, and the carotid bulb region is frequently spared (not involved) in the dissection. If a patient presents with a carotid dissection, there is a 5-10% of having a dissection elsewhere in the carotid/cerebral circulation in the first year after diagnosis, and a 1%/yr subsequent risk of arterial dissection. Patients with fibromuscular dysplasia (FMD), Marfan syndrome, Takayasu's arteritis, Moya Moya, and polyarteritis nodosa (PAN) are at higher risk for dissections. In patients with significant persistent symptoms from carotid dissection, a brain bypass may need to be carried out ( take me to the Section on Brain Bypass now for images and details of this procedure).

The other feared complication of a carotid dissection is formation of a dissecting aneurysm. Here, the torn carotid wall leads to escape of blood through the inner wall and into a pocket under the outer wall and/or through it into surrounding tissue (the latter is referred to as a pseudoaneurysm because its wall is made up of surrounding nonvascular tissue). Aneurysm formation here is a surgical emergency, and its treatment involves (wherever possible) surgical reconstruction of the carotid artery, or sometimes even carotid artery ligation or endovascular occlusion, as part of carotid artery sacrifice. Carotid artter sacrifice may indeed need a brain bypass procedure to compensate. For many carotid dissections, dissecting aneurysm or pseudoneurysm formation does not occur. So, in patients presenting with "regular" carotid dissection, in general, if there is no intracranial or neck hemorrhage or related aneurysm, and no significant stroke, the treatment is anticoagulation (anti-blood clotting therapy) with intravenous heparin followed by oral Coumadin (warfarin), the duration varies per circumstance and followup. Surgical treatment is generally reserved for dissecting aneurysms and progressive stroke-like symptoms from the dissection.