Atherothrombotic occlusion of posterior cerebral artery

Clinical symptoms of atherothrombotic occlusion of posterior cerebral artery

Localization of atheromatous lesions in the posterior cerebral artery or the beginning of one of its branches, as well as the degree of narrowing is usually defined beginning, severity and nature of the clinical syndrome. Significant but less important role played by other factors including collateral blood flow via the posterior communicating artery or branch cortical and blood viscosity. However, even in the presence of atherosclerotic plaque in the posterior cerebral artery mechanism responsible for the development of stroke, embolic occlusion is usually of the artery or its branches.

Changes in the posterior cerebral artery gives rise to syndromes, which are divided into two groups:

• Syndromes lesions of the midbrain, thalamus and subtalamusa associated with atherosclerotic narrowing of atherosclerotic or embolic occlusion of the proximal segment prekommunalnogo posterior cerebral artery or the beginning of her penetriruyushih branches
• Syndromes, cortical lesions caused by atherosclerotic narrowing, atherothrombotic or embolic occlusion postkommunalnogo segment posterior cerebral artery

 

Poximal pre-communicating syndromes (central area)

Trunk occlusion of posterior cerebral artery evolving infarction from one-or two-way involving the medial thalamus and subtalamusa, as well as the damage of the same name on the side of the brain stem and midbrain with corresponding clinical symptoms. Obviously, for non-operation state of the posterior communicating artery (for example, it atresia are also symptoms of peripheral areas postkommunalnym supplies the segment of the posterior cerebral artery). If there is no complete occlusion at the beginning of the posterior cerebral artery, hemiplegia in myocardial stem of the brain is rare. Syndromes partial proximal lesions can think of occlusion of the middle cerebral thalamo-perforated artery, but did not serve her confirmation.

Syndrome of the upper lesion characterized by the involvement of the red nucleus and / or Dent- ruber-thalamic tract, say a rough contralateral ataxia.

With involvement of the sub thalamic Lewis body may cause contralateral gemiballizma. Percheron artery occlusion causes paresis gaze upward and hypersomnia. Such a damage is often accompanied by abulia and a state of euphoria conducive to the emergence of abulia.
CT and MRI can detect bilateral lesions, resembling in its outline of a butterfly, and in subtalamuse srednenizhnih parts of the thalamus. Extensive foci of infarction in the midbrain and bilateral occlusion in subtalamuse trunk posterior cerebral artery usually develop secondary embolism. In such cases, there is a deep coma, bilateral pyramidal symptoms and "decerebrate rigidity". Atheromatous occlusion of penetrating branches of thalamic and thalamo- genikular groups in their initial parts leads to thalamic and thalamo- capsular lacunar syndromes.

The most famous of thalamic syndrome Dejerine - Roussy. Its main manifestations are contralateral loss as superficial (pain and temperature), so-called deep (tactile and proprioceptive) sensitivity gemitipu. Sometimes suffer only pain and temperature or vibration and the musculo-articular sensitivity. Most often impairments are defined in the face, arm, hand, torso, legs, feet n, at least - only one limb. Often there is giperpatiya, and after a few weeks or months in the affected areas may develop a painful burning pain. Patients describe it as a compressed, contracting, chilling, cutting. This pain is persistent, debilitating nature, poorly amenable to analgesics. Sometimes effective anticonvulsants.

When engaging in the lesion of the internal capsule posterior thigh revealed hemiparesis or hemiplegia in combination with impaired sensitivity gemitipu. Other related motor disorders are gemiballizm, choreoathetosis, intention tremor, discoordination and poznaya setting her hands and arms, especially when walking.

 

Post-communicating syndromes (peripheral or cortical area)

Infarctions in the thalamus pillows can occur when plugging back of the thalamo-thalamic genikulyatnoy penetrating branches postkommunalnogo of the posterior cerebral artery. By itself, occlusion of the peripheral posterior cerebral artery often leads to heart attacks cortical surface of the medial side of the temporal and occipital lobes. Common symptom is hemianopsia contralateral gomonimnaya. Beli associative visual fields remain intact and in the pathological process involves only the bark near the calcarine fissure, the patient feels a sudden vision defect. Sometimes it drops only the upper quadrant of the visual field. Central vision may remain intact if the blood supply to the occipital pole is supported by the top of the branches of the middle cerebral artery.

With the involvement of the medial temporal lobe and hippocampus may appear sudden memory disorders, especially in the dominant hemisphere lesions, but these disorders tend to disappear because the memory functions are carried out with both hemispheres of the brain.

With the damage of the dominant hemisphere with the spread of a heart attack in the lateral direction in the deep white matter with involvement in the pathological process of the splenium may develop Alexia without agraphia. Can also be observed on the faces of psychic blindness, objects, mathematical symbols and colors, as well as anosmia with paraphasias (anomia), even in the absence of lesions of the corpus callosum.

Occlusion of the internal carotid artery stenosis or occlusion of a sharp posterior cerebral artery on the same side can reduce blood circulation in the area adjacent the rear and middle cerebral arteries. Often this leads to visual agnosia, visual neglect and failure to count objects in the opposite half of the visual field. Sometimes the posterior cerebral artery occlusion followed by pedicellate hallucinosis (visual hallucinations in the form of gorgeous scenes called objects), but the exact location of infarction in such cases is not entirely clear.

Bilateral infarcts in the pool of blood supply of the distal posterior cerebral artery leads to the development of cortical blindness. The patient often does not realize in view of existing disorders, and normal pupil reacts to light. Even when the visual defect is completely one-or two-sided, can be saved of small islands, while the patient is usually reported on the instability of view, the impression that the images of objects it manages to retain at the expense of keeping a vision of their individual parts. In rare instances only lost peripheral vision, and heart remains intact, while the patient reported the presence of the tube.

Optical ataxia (inability to control eye movements of the limbs), ocular ataxia (inability to translate look at a particular point of view), the inability to account objects shown in the picture, or drawing representation of the image in the picture, the inability to bypass along the way things are characteristic of bilateral lesions of the associative visual pathways. This combination of symptoms is known as Balint syndrome. Usually it is observed in bilateral infarctions, developing, is believed to be accompanied by decreasing blood flow in the basin of the distal posterior cerebral artery blood flow in the zone adjacent to the middle cerebral artery, which happens when the heart stops.

Finally, occlusion of the upper part of the basilar artery, caused, as a rule, embolism, can give a clinical picture that includes all or any of the symptoms of the central or peripheral area of blood supply. Pathognomonic for it are the sudden onset of symptoms and bilateral in nature.

 

Diagnosis and imaging studies of ischemic stroke in the posterior cerebral arteries basin

Infarct in the peripheral basin posterior cerebral artery can be easily diagnosed by magnetic resonance imaging (MRI) and computed tomography (CT). Meanwhile, CT data not reliable in myocardial blood flow in the central zone of the posterior cerebral artery, especially in developing occlusive lesions in the second penetrating branches of the posterior cerebral artery. By magnetic resonance imaging (MRI) can detect brain infarcts of the localization of a diameter greater than 0.5 cm.

Angiography remains the only way to convincingly demonstrate atherosclerotic changes or embolic lesion posterior cerebral artery. End of the varieties of modern spiral CT angiography with intravenous contrast reveals occlusive lesion of small penetrating branches of the posterior cerebral artery.

Thus diagnosis for ischemic stroke in the pool the posterior cerebral artery is mainly based on clinical findings, confirmed by magnetic resonance imaging (MRI ) and computed angiography (CT angiography) with intravenous contrast.

 

Treatment of ischemic stroke in the posterior cerebral arteries basin

Cerebral infarction in the pool the posterior cerebral artery are usually a secondary character and occur against a background of embolism from the lower segments of the vertebrobasilar system, or from the cavity of the heart. In order to prevent repeated embolism of the arterial lumen prescribe anticoagulants (heparin ). When atherosclerotic occlusion of the posterior cerebral artery of a specific treatment is needed. Symptoms of transient ischemic attacks of the brain in the pool the posterior cerebral artery may be due to atherothrombotic stenosis of the proximal (underlying) region or one of its penetrating branches (lacunar TIA).

During this atherosclerotic lesion posterior cerebral artery remains unspecified. Therefore, there is no clear comparative data on the effectiveness of anticoagulants and antiplatelet agents or appointment of a treatment compared with no such. In general, the most gentle way to treat ischemia or ischemic stroke in the pool the posterior cerebral artery is the appointment of antiplatelet agents (aspirin, trental).