POSTERIOR CEREBRAL ARTERY
zkadhem - 05-09-09 13:36

The posterior cerebral artery (PCA) is one of a pair of blood vessels that supplies oxygenated blood to the posterior aspect of the brain (occipital lobe)

* Contralateral loss of pain and temperature sensations.
* Visual field defects (contralateral hemianopia with macular sparing).
* Prosopagnosia, which is a form of visual agnosia characterized by an inability to recognize faces, with bilateral obstruction of the lingual and fusiform gyri.
* Medial Midbrain Syndrome (Weber syndrome)
* Ipsilateral deficits of Cranial Nerves V, VIII, IX, X, & XI
* Horners Syndrome.

The above signs and symptoms occurance depend on what branch of the PCA was occluded.
The major PCA stroke syndromes are described here. Often, many of the features occur concomitantly.

* Paramedian thalamic infarction
o This syndrome, resulting from bilateral medial thalamic infarction, is part of the differential diagnosis of delirium and coma. Patients often are obtunded to comatose or agitated, and they may or may not have associated hemiplegia or hemisensory loss. Occasionally, the cranial nerve III nucleus is involved, with resultant ophthalmoplegia.
o Patients may take days to weeks to recover and seem to be in a sleeplike state. Although alertness generally returns, prognosis for good functional recovery is poor because of severe memory dysfunction.
o The syndrome may result from a "top of the basilar" artery embolus. The artery of Percheron, referred to earlier, may be involved. This has been referred to as a posterior variant of the syndrome of akinetic mutism.
* Pure hemisensory loss
o Infarction of the ventral posterolateral nucleus of the thalamus results in hemisensory loss. This is one of the well-described lacunar syndromes. Usually, the vessel involved is the thalamogeniculate branch.
o A related disorder is Dejerine-Roussy syndrome, in which quickly resolving hemiparesis and hemiataxia leave the patient with delayed, persistent, hemisensory disturbance with paroxysmal pain on the affected side.
* Visual field loss
o A general rule of visual field examination is that the further posterior the lesion, the more congruous is the visual field loss.
o Bilateral infarctions of the occipital lobes produce varying degrees of cortical blindness depending upon the extent of the lesion. Patients often exhibit Anton syndrome, a state in which they fervently believe they can see when they cannot. Patients may describe objects that they have not seen previously in exquisite detail, completely in error and oblivious to that error. Another intriguing phenomenon is blindsight—although cortically blind, patients can respond to movement or sudden lightening or darkening of environment.
o Unilateral infarction produces homonymous hemianopia. Sparing of the macula is encountered frequently in infarction of the occipital lobes due to PCA occlusion. Macular sparing probably is caused by collateral vascular supply to the occipital pole from posterior branches of the MCA and preservation of the optic radiations, though bilateral representation of macular vision also has been suspected.
o Infarction of the lateral geniculate nucleus may produce hemianopia, quadrantanopia, or sectoranopia. The vascular supply is dual; the anterior choroidal artery supplies the anterior hilum and anterolateral areas, and the posterior choroidal artery supplies the rest. Occlusion of the posterior choroidal artery may produce a distinct syndrome of hemianopia, hemidysesthesia, and memory disturbance due to infarction of the lateral geniculate, fornix, dorsomedial thalamic nucleus, and posterior pulvinar.
* Visual agnosia
o This refers to a lack of recognition or understanding of visual objects or constructs. It is a disorder of higher cortical function.
o The strict diagnosis of visual agnosia requires intact visual acuity and language function. Most patients have bilateral lesions, sparing the visual cortex but disrupting or disconnecting visual information from reaching parts of the visual association cortex for reference to visual memories. The patient with visual agnosia can recognize objects presented in another modality; for example, the patient can identify keys by palpating them or hearing them jingle, but not by seeing them.
o True visual agnosia has been divided into apperceptive and associative subtypes.
o In apperceptive visual agnosia, patients cannot name objects presented to them, draw objects from memory, or identify or match objects. Yet, they can see and avoid obstacles when ambulating and detect subtle changes in light intensity.
o In associative agnosia, patients can draw objects to command and match them or point to them but cannot name them. They can see shapes and reproduce them in drawing, yet not recognize the identity of objects.
* Balint syndrome
o This typically occurs in degenerative diseases but also may occur with bilateral parieto-occipital infarction, most often in the watershed between the PCA and MCA territories. It is a triad of visual simultanagnosia, optic ataxia, and apraxia of gaze.
o Visual simultanagnosia implies an inability to examine a scene and integrate its parts into a cohesive interpretation. A patient can identify specific parts of a scene but cannot describe the entire picture.
o Optic ataxia implies a loss of hand-eye coordination such that reaching or performing a motor task under visual guidance is clumsy and uncoordinated.
o Finally, apraxia of gaze is a misnomer describing a supranuclear deficit in the ability to initiate a saccade on command.
* Disorders of face recognition
o Prosopagnosia refers to an inability to recognize faces. Typically, this deficit results from bilateral lesions of the lingual and fusiform gyri; however, cases of unilateral nondominant hemisphere lesions resulting in prosopagnosia have been reported.
o Usually, it does not occur in isolation and other object agnosias coexist. Autoprosopagnosia, or inability to recognize one's own face in a picture or mirror, may occur as a subset of this syndrome.
* Palinopsia, micropsia, and macropsia
o These are illusory phenomena that are of uncertain pathophysiology. They may represent seizure activity and traditionally are treated with anticonvulsants.
o Palinopsia describes the persistence of a visual image for several seconds to days in a partially blind hemifield.
o Micropsia and macropsia describe situations where objects appear smaller or larger than expected.
* Disorders of reading (alexia, dyslexia)
o Pure alexia may result from infarction of the dominant occipital cortex. Words are treated as if they were from a foreign language. Patients may retain the ability to formulate a word and its meaning if spelled out to them orally or if they trace the letters with their hand. Patients may then learn to read, albeit terribly slowly, in a letter-by-letter fashion, being unable to integrate multiple letter groups.
o Classic alexia without agraphia was described by Dejerine in the late 19th century. In his case study, he emphasized a left occipital cortex lesion and also infarction of the splenium of the corpus callosum, which disconnected fibers from the right occipital lobe from reaching the angular gyrus.
o Rarely, the dominant-hemisphere, posterior temporal lobe is supplied by PCA. Damage to this area results in a Wernicke-type aphasia with associated dyslexia and right hemianopia due to concomitant left occipital infarction.
* Disorders of color vision (achromatopsia, dyschromatopsia)
o Lesions of the lingual gyrus in the inferior occipital lobe may produce disorders of color perception. Testing with Ishihara plates reveals a deficit. Colors may be described as washed out or gray. This deficit usually occurs only in the contralateral visual field and is called "hemiachromatopsia."
o A related problem is color anomia, also called color agnosia, in which patients can perceive and match colors but cannot associate them with the proper color names. This deficit also has been explained by a disconnection model.
* Memory (amnesia)
o Infarction of the medial temporal lobe, fornices, or medial thalamic nuclei may result in permanent anterograde amnesia.
o Although traditionally bilateral infarction has been thought to be required for amnesia, memory functions may be lateralized such that infarction of left-sided structures may have a more lasting impact on verbal function.
o Older patients frequently have lasting short-term memory impairment from unilateral PCA territory infarction.
o Recent imaging in patients with transient global amnesia has demonstrated diffusion-weighted lesions in unilateral temporal lobes resulting in temporary amnesia.
* Motor dysfunction
o When the blood supply to the cerebral peduncles arises from perforators of P1 segment, infarction may occur, resulting in hemiplegia or hemiparesis.
o The clinical syndrome is no different from capsular infarction but often includes concomitant hemianopia because of occipital lobe involvement.
o The syndrome may mimic a large MCA infarction


[http://en.wikipedia.org/wiki/File:Gray517.png]