Atherothrombotic occlusion of posterior cerebral artery

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Pathophysiology of atherothrombotic occlusion of posterior cerebral artery

Anatomically, 70% of both the posterior cerebral artery originated from the bifurcation at the top of the basilar artery. In 22 % of cases, one of the posterior cerebral artery runs from the ipsilateral internal carotid artery. In 8% of both the posterior cerebral artery originate from the same internal carotid. Atherosclerotic plaque, formed at the top of the basilar artery or prekommunalnom segment posterior cerebral artery, may block or narrow the lumen of one or more small branches penetrating the brain stem. These arterial branches supply blood to:

  • middle part of the cerebral peduncles
  • ipsilateral substantia nigra
  • red nucleus
  • nucleus of the oculomotor nerve
  • midbrain reticular formation
  • subtalamicheskie lyuisovy body
  • crossing the upper legs of the cerebellum
  • posterior longitudinal bundle
  • medial loop

Percheron artery, ie, the posterior thalamo-subtalamo-paramedian artery - is the only artery, branching off to the right or left of the median prekommunalnogo (mesencephalic) segment of the posterior cerebral artery. At the level of subtalamusa it dissolves and supplies blood to both sides of the lower middle and anterior thalamus and subthalamus.

The mechanism and consequences of blockage of the lumen of the coronary vessels and cerebral artery.

Thalamic branches, also originating from prekommunalnogo segment posterior cerebral artery that supply blood to the dorsal, dorsomedial, anterior and inferior parts of thalamus and medial geniculate body. These branches include the medial and lateral posterior choroidal artery.

The medial posterior choroid plexus artery supplies blood upper dorsal-medial and anterior part of dorsal thalamus and medial geniculate body, and the vascular basis of 3 ventricle.

Lateral posterior choroid plexus artery supplies blood choroid plexus of lateral ventricle. Both rear artery of the choroid plexus sends branches anastomosing with branches of the anterior artery of the same name. But other small branches of the pre communicating posterior cerebral artery segment ends without forming anastomoses.

Plaques formed in the posterior cerebral artery distal to (above) the merger with the posterior communicating artery may lead to clinically manifest occlusion of small branches of the envelope, going around the midbrain and the side legs of the envelopes of the brain, the medial loop of the midbrain tegmentum, corpus bigeminum top, side geniculate body, posterolateral nucleus of the thalamus, choroid plexus and hippocampus. In rare cases, a more distal location of plaque in the posterior cerebral artery occlusion can cause ischemia and infarction in nizhnesredinnoy part of the temporal lobe, and paragippokampovoy gippokampovoy convolutions of Mr. occipital lobe, including the calcarine sulcus along the cortex and associative visual fields 18 and 19.


Posterior cerebral artery syndrome:

Signs and symptoms
Structures involved
Peripheral territory
Homonymous hemianopia (often upper quadrantic) Calcarine cortex or optic radiation nearby
Bilateral homonymous hemianopia, cortical blindness, awareness or denial of blindness; tactile naming, achromatopia (color blindness), failure to see to-and-fro movements, inability to perceive objects not centrally located, apraxia of ocular movements, inability to count or enumerate objects, tendency to run into things that the patient sees and tries to avoid Bilateral occipital lobe with possibly the parietal lobe involved
Verbal dyslexia without agraphia, color anomia Dominant calcarine lesion and posterior part of corpus callosum
Memory defect Hippocampal lesion bilaterally or on the dominant side only
Topographic disorientation and prosopagnosia Usually with lesions of nondominant, calcarine, and lingual gyrus
Simultanagnosia, hemivisual neglect Dominant visual cortex, contralateral hemisphere
Unformed visual hallucinations, peduncular hallucinosis, metamorphopsia, teleopsia, illusory visual spread, palinopsia, distortion of outlines, central photophobia Calcarine cortex
Complex hallucinations Usually nondominant hemisphere

Central territory

Thalamic syndrome: sensory loss (all modalities), spontaneous pain and dysesthesias, choreoathetosis, intention tremor, spasms of hand, mild hemiparesis Posteroventral nucleus of thalamus; involvement of the adjacent subthalamus body or its afferent tracts
Thalamoperforate syndrome: crossed cerebellar ataxia with ipsilateral third nerve palsy (Claude’s syndrome) Dentatothalamic tract and issuing third nerve
Weber’s syndrome: Third nerve palsy and contralateral hemiplegia Third nerve and cerebral peduncle
Contralateral hemiplegia Cerebral peduncle
Paralysis or paresis of vertical eye movement, skew deviation, sluggish pupillary responses to light, slight miosis and ptosis (retraction nystagmus and “tucking” of the eyelids may be associated) Supranuclear fibers to third nerve, interstitial nucleus of Cajal, nucleus of Darkschewitsch, and posterior commissure
Contralateral rhythmic, ataxic action tremor; rhythmic postural or “holding” tremor (rubral tremor) Dentatothalamic tract

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.

MRI of the brain with intracerebral hemorrhage patients in the thalamus (indicated by arrows).

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).

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