Atherothrombotic occlusion of internal carotid artery

Proximal internal carotid artery atherosclerosis

Atherosclerosis of the upper (proximal) of the internal carotid artery is usually most pronounced during the first 2 cm and located on the back. Atherosclerosis often extends downwards (in the distal segment) of the common carotid artery. Frequently (in 50-80 % of strokes) is atherosclerosis lesion has an effect the development of small strokes (microstroke) or transient ischemic attack (TIA) caused by criticaly reduced cerebral blood flow or embolism from the carotid artery in its intracerebral branches.

Clinical experience and data Autopsy studies suggest that stroke with lesions of the carotid artery usually caused by emboli, than lack of blood flow. Embolism of atherosclerotic plaque, located at the beginning of the internal carotid artery can cause transient ischemic attack (TIA), but if they are repeated, short-lived and stereotyped, the more likely they are the cause of disorders of hemodynamics.

 

Cerebral ischemia caused by a reduction in blood flow

Weak arterial blood flow can lead to stroke (infarction) of the brain or cause a transient ischemic attack (TIA) in the border zone or in areas adjacent blood supply. Development of stroke and microstroke (TIA) with a deficit of cerebral blood flow contribute to the two conditions:

1. Decrease in blood pressure below (distal to) stenosis in the carotid artery lesions with a decrease in the diameter of the lumen by more than 80 %, or equivalently that, at a value of the diameter of the lumen of the remaining less than 1,5-2 mm.
2. Deficiency of collateral blood flow to areas of ischemia.

Cerebral blood flow usually occurs when the circle of Willis of inferiority due to congenital atresia of primary (A1) anterior cerebral artery or the anterior or posterior communicating artery. Less commonly, damage to the brain develops during occlusion (occlusion), the opposite carotid or basilar artery, limiting blood flow into the arteries of the circle of Willis. Sometimes adequate blood supply is ensured through the orbital collaterals from the external carotid artery or superficial cortical collaterals at the boundary of the arterial pool. Blood supply is adequate and the area of ischemia is limited even with the existing inferiority circle of Willis. It is a variety of collateral blood supply is due to a variety of localization of lesions in stroke and transient ischemic attacks (TIA) in the carotid artery on the background of insufficient blood flow to the brain.

There are other explanations for the development of transient ischemic attack (TIA) with a decrease in cerebral blood flow. It is believed that marked narrowing (stenosis) at the bifurcation of the common carotid artery can lead to transient overlap (occlusion in the lumen of the vessel due to spasm. In rare cases, systemic factors circulatory disorders lead to a reduction of blood flow through the area of gross narrowing of the lumen of the vessel to the critical values. On the other hand, the regional blood circulation in the hemisphere of the brain may vary in relation to the maintenance of decreased blood flow in the carotid artery, and transient decompensation of this mechanism can induce transient ischemic attack (TIA). Other factors, including polycythemia vera, thrombocythemia, cardiac arrhythmias, sometimes causing repeated transient ischemic attack (TIA) in the presence of insufficient blood flow in the vessels of the brain and other internal organs.

 

Embolization of the carotid artery

At the origin of blood clots from a narrowed vessel stenosis or ulcerated area in the early atherosclerotic internal carotid artery (local or arterioarternal embolism) symptoms usually associated with blockage (occlusion), ophthalmic artery, middle cerebral artery trunk, one or more of its branches, and sometimes anterior cerebral artery or its branches. Sizes appropriate to the caliber of the vessel embolus, which is subject to occlusion.

Small blood clots clog the farthest (distal) branch of the middle cerebral artery or the ophthalmic artery, causing the patient's transient blindness in one eye or minor asymptomatic infarctions in areas adjacent blood supply to the arteries in the brain. Larger emboli consisting of platelet-fibrin clots may cover primary and secondary branches of the middle cerebral artery. In this neurological syndromes can be judged on involvement in the pathological process of various brain regions.

Some blood clots is so large that block the "trunk" of the middle cerebral artery in the bud, causing severe ischemia of the entire blood supply of the middle cerebral artery (deep white matter, lenticular nucleus, the surface of the cortex). Other blood clots are large enough to cover the trunk of the middle cerebral artery can cause a deep infarct (stroke) in the presence of sufficient collateral blood flow through the superficial cortical arteries.

Large blood clots, overlapping large vessel can be moved to dissolve and break down. If the splitting of blood clots occurs quickly, the neurological deficit in a patient may be transient or disappear completely.

In some patients with neurological symptoms, vascular lesion can be represented by a single plaque in the carotid bifurcation, but more often observed narrowing (stenosis) with a residual lumen diameter of blood vessel of less than 2 mm.

The frequency of massive embolic strokes (cerebral infarction), exclusively on the background of developing ulceration lesion of the vascular layer atherosclerosis, remains unclear. Perhaps the frequency of embolic stroke is low, and such cases are observed only for large ulcers of the vascular layer (4 mm or more). The development of single stroke or transient ischemic attack (TIA) with long-term persistent symptoms in the absence of narrowing (stenosis) of the lumen of the carotid artery or minor of its intensity suggests that the source of the embolus is the heart. Atheromatous lesions localized in the beginning of the large branches of the aortic arch may also be the cause of embolism in the vessels of the brain and cause its transient ischemia or infarction, but the frequency of occurrence of this mechanism is also unknown.

Blockage (occlusion) of the internal carotid artery in its initial part may take place entirely without symptoms for a brain at an adequate level of collateral blood flow of arterial blood through the arteries of the circle of Willis. On the other hand, the lack of collateral circulation may develop a stroke or transient ischemic attack (TIA). In addition, a clot burden or thrombus can extend upward from the blockage of the lumen of the vessel through its siphon to the initial segments of the middle and anterior cerebral arteries, leading to a stroke. But more often than fresh thrombotic emboli detached from the material and get stuck in the lumen of the middle, anterior artery or one of their branches. According to some authors, emboli may originate from the underlying internal carotid artery stump and transported through the external carotid artery collaterals, reaching the division of intracranial internal carotid artery and its branches. But these emboli is probably quite rare.

The reason for the delayed stroke that develops in a few months after complete occlusion of the lumen (occlusion) carotid artery often remains unclear, and its frequency is unknown. According to one study, delayed stroke occurs in 5 % of cases a year. But in view of clinical experience, this figure seems too high. In most cases, embolic occlusion of the lumen at carotid artery occurred within the first year, although they can be seen in two years. Strokes of the brain, caused by insufficient blood supply, are developing at an earlier date, usually within the first few weeks after occlusion of the lumen (occlusion) carotid artery.

 

Intracranial (intracerebral) portion of the internal carotid artery

Carotid siphon exposed to atherosclerosis with thrombosis of less than the lower lying part of his internal carotid artery. Lesions in the carotid siphon can cause strokes and transient ischemic attack (TIA), pathophysiological and clinical manifestations which mirror those that are given above. Clinical history of the patient at narrowing the lumen (stenosis ) carotid siphon nonspecific. Please note that the narrowing of the lumen (stenosis) carotid siphon to asymptomatic until atheromatous process does not reduce the remaining gap in it up to 1.5 mm or less. Accurately diagnose the narrowing (stenosis) carotid siphon above the ophthalmic artery allows only angiography. Collateral blood flow through the arteries of the circle of Willis, of course, influence the pathogenesis of these lesions and the effectiveness of their medical or surgical treatment.

 

Atherosclerosis with thrombosis of the middle cerebral artery (MCA)

Atherosclerosis with thrombosis of the trunk of the middle cerebral artery may cause symptoms of cerebral ischemia in connection with narrowing of the lumen of the artery, and as a result of blockage of the initial segment of one or more arteries lenticular nucleus and the striatum that supply blood to the deep white matter and basal ganglia. Clinically manifest atherosclerotic plaque is often lower than the first division (bifurcation) of the middle cerebral artery. Since arteries of the circle of Willis is below the beginning of the middle cerebral artery, the collateral blood supply in the basin of the middle cerebral artery should be carried out through the small superficial cortical areas adjacent vessels and blood supply to the anastomosis of the anterior and posterior cerebral arteries.

Available data indicate that before the development of cerebral infarction (stroke), a narrowing of the lumen of the vessel is usually "warn" transient ischemic attack (TIA) in the basin of the middle cerebral artery. Their symptoms were similar to that for transient ischemic attacks (TIA) associated with the deterioration of blood flow due to stenosis of the internal carotid artery. In contrast to the internal carotid artery trunk of the middle cerebral artery and one or more of its main branches are usually subjected to occlusion of embolus (arterioarternal, from the heart or from an unknown source).

 

Atherosclerosis with thrombosis of the anterior cerebral artery (ACA)

Atherosclerotic deposits in the lower segment of the anterior cerebral artery rarely produce clinical symptoms of neurological deficit, as the blockage of the lumen (occlusion) is offset by collateral blood flow through the anterior communicating artery. The probability of transient ischemic attack (TIA) and stroke is increased if the way of collateral blood flow is characterized by a congenital imperforate (atresia) or the higher part of anterior cerebral artery has atherosclerotic changes.