Major PCA stroke syndromes
The major posterior cerebral artery (PCA) stroke syndromes (many of which occur concomitantly) include the following:
-
Paramedian thalamic infarction
-
Visual field loss
-
Visual agnosia
-
Balint syndrome
-
Prosopagnosia
-
Palinopsia, micropsia, and macropsia
-
Disorders of reading
-
Disorders of color vision
-
Memory impairment
-
Motor dysfunction
Paramedian thalamic infarction
This syndrome results from bilateral medial thalamic infarction. The presentation in these patients varies from lethargic to obtunded to comatose, but some patients may be agitated and may have associated hemiplegia or hemisensory loss. Occasionally, the cranial nerve III nucleus is involved, with resultant ophthalmoplegia.
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.
The syndrome may result from a “top of the basilar” artery embolus. The artery of Percheron may be involved.
Visual field loss
Unilateral infarction produces hom*onymous hemianopia. Sparing of the macula is encountered frequently in infarction of the occipital lobes due to PCA occlusion. Macular sparing may be caused by collateral vascular supply to the macular region or by the very large macular representation in the occipital cortex; additionally, bilateral representation of macular vision has been suspected.
Bilateral infarctions of the occipital lobes produce varying degrees of cortical blindness depending on 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 their environment.
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
This refers to a lack of recognition or understanding of visual objects or constructs. It is a disorder of higher cortical function.
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; this interferes with the information’s ability to reach parts of the visual association cortex, for reference to visual memories. The patient with visual agnosia can recognize objects presented to a nonvisual sensory system; for example, the patient can identify keys by palpating them or hearing them jingle.
True visual agnosia has been divided into apperceptive and associative subtypes. 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.
In associative agnosia, patients can draw objects to command and can match them or point to them, but they cannot name them. Patients can see shapes and reproduce them in drawings, yet they do not recognize the identity of objects.
Balint syndrome
This may occur with bilateral parieto-occipital infarction, most often in the watershed between the PCA and middle cerebral artery (MCA) territories. It is a triad of visual simultanagnosia, optic ataxia, and apraxia of gaze, which are characterized as follows:
-
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
-
Optic ataxia - Implies a loss of hand-eye coordination such that reaching or performing a motor task under visual guidance is clumsy and uncoordinated
-
Apraxia of gaze - A misnomer describing a supranuclear deficit in the ability to initiate a saccade on command
Prosopagnosia
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.
Palinopsia, micropsia, and macropsia
These are illusory phenomena that are of uncertain pathophysiology. Palinopsia describes the persistence of a visual image for several seconds to days in a partially blind hemifield. Micropsia and macropsia describe situations where objects appear smaller or larger than expected.
Disorders of reading
Pure alexia may result from infarction of the dominant occipital cortex. Words are treated as if they are 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.
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, preventing them from reaching the angular gyrus.
Rarely, the dominant-hemisphere posterior temporal lobe is supplied by the 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
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.
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.
Memory impairment
Infarction of the medial temporal lobe, fornices, or medial thalamic nuclei may result in permanent anterograde amnesia. 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.
Older patients frequently have lasting short-term memory impairment from unilateral PCA territory infarction. In addition, diffusion-weighted Imaging in patients with transient global amnesia has demonstrated lesions in unilateral temporal lobes resulting in temporary amnesia.
Motor dysfunction
When the blood supply to the cerebral peduncles arises from perforators of the P1 segment, infarction may occur, resulting in hemiplegia or hemiparesis. The clinical syndrome is no different from capsular infarction but often includes concomitant hemianopia because of occipital lobe involvement. The syndrome may mimic a large middle cerebral artery (MCA) infarction.
