eMedicine Specialties > Neurology > Neuro-vascular Diseases

Posterior Cerebral Artery Stroke

Author: Michael D Hill, MD, Medical Director, Stroke Unit, Assistant Professor of Neurology, Department of Clinical Neurosciences, Foothills Hospital, University of Calgary, Canada
Coauthor(s): Alastair M Buchan, MBBCh, FCCPC, Professor, Department of Clinical Neurosciences, Foothills Hospital, University of Calgary, Canada
Contributor Information and Disclosures

Updated: Feb 27, 2007

Introduction

Background

Posterior cerebral artery (PCA) stroke is less common than stroke involving the anterior circulation. An understanding of PCA stroke phenomenology and mechanisms requires knowledge of neurovascular anatomy and of the structure-function relationships of this region of the brain. This article provides an overview of PCA stroke and focuses exclusively on stroke of arterial origin involving the PCA territory.

Anatomy

The PCAs are paired, branching off the top of the basilar artery and curving posterosuperiorly around the midbrain. The PCA supplies parts of the midbrain, the subthalamic nucleus, the basal nucleus, the thalamus, the mesial inferior temporal lobe, and the occipital and occipitoparietal cortices. In addition, the PCAs, via the posterior communicating arteries, may become important sources of collateral circulation for the middle cerebral artery (MCA) territory.

The PCA is divided angiographically into P1 and P2 segments by the posterior communicating artery. Penetrating branches to the mesencephalon, subthalamic and basal structures, and thalamus arise primarily from the P1 segment and the posterior communicating artery. These penetrating arteries include the thalamogeniculate (which may arise independently or more commonly as a branch of the medial posterior choroidal artery), the splenial (posterior paricallosal artery), and the lateral and medial posterior choroidal arteries. The P2 segment bifurcates into the posterior temporal artery (anterior division) and the internal occipital artery (posterior division).

The posterior temporal artery further divides into anterior and posterior temporal branches supplying the inferomedial temporal lobe and the lingual and occipitotemporal gyri, respectively. The internal occipital artery supplies 3 end arteries: 1) the calcarine artery, which supplies the calcarine cortex on the medial surface of the occipital lobe; 2) the occipitotemporal artery, which supplies the orbital surface of the temporal and occipital lobes; and 3) the occipitoparietal artery, which supplies the precuneus and surrounding cortex.

Normal variants of neurovascular anatomy

In approximately 30% of people, one or both PCAs take origin from the internal carotid artery (ICA) directly or via the posterior communicating artery. Direct origin from the ICA is termed "fetal PCA" (when the ipsilateral P1 segment is congenitally absent). This may have important consequences, in that stroke in the PCA territory may be caused by occlusive disease of the anterior circulation.

The central artery of Percheron arises from one P1, then gives rise to bilateral medial thalamic perforators. Occlusion results in bilateral paramedian thalamic infarction. This is one of the few examples in which a cerebral vessel supplies structures on both sides of the midline.

Pathophysiology

Ischemic stroke occurs when local blood flow is suddenly limited by vessel occlusion. The rate of neuronal death varies with blood flow. If blood flow falls to less than 15 mL/100 g/min, energy failure and subsequent cell death occur within minutes. Even suboptimal flow for longer periods may cause the cells to die by an apoptotic mechanism over days to weeks. Rapid restoration of blood flow is essential to save brain tissue.

The mechanism of stroke involving the PCA territory is variable. It is commonly due to embolization from the heart, the aortic arch, the vertebral artery, or the basilar artery. Other mechanisms include intrinsic atherosclerotic disease and vasospasm. Migrainous strokes tend to involve PCAs preferentially. Less commonly, the anterior circulation is to blame (eg, internal carotid stenosis), when a fetal PCA is present. Rare causes of stroke may be considered when usual culprits such as coagulation abnormalities, vasculitis, sympathomimetic drugs, and metabolic disorders are not present.

Frequency

United States

Approximately 5% of ischemic strokes involve the PCA or its branches.

Mortality/Morbidity

• Death from PCA stroke is uncommon. Concomitant basilar occlusion and infarction of the brain stem may cause death.
• Rate of morbidity from PCA stroke is high. Recovery of visual field deficits is very limited. Patients may be unable to drive or read, resulting in major limitations in their quality of life, despite normal motor function.
• Other neuropsychological deficits may include prosopagnosia (inability to recognize faces), visual agnosia, amnesia, and alexia without agraphia. Rarely, PCA stroke results in infarction of the ipsilateral cerebral peduncle with resultant hemiplegia. Thalamic involvement can also produce contralateral sensory loss.

Sex

In recently published data from the Tufts New England Medical Center posterior circulation stroke registry, 58% of patients were male and 42% were female.

Age

In recently published data from the Tufts New England Medical Center posterior circulation stroke registry, the mean age of stroke was 61.5 years.

Clinical

History

The approach to stroke in the PCA territory is no different from stroke elsewhere in the brain. A simple 3-step algorithm can be applied as follows:

• First, confirm the diagnosis of stroke. If the patient is seen within the 3-hour time window, consider thrombolytic therapy (ie, intravenous tissue plasminogen activator [tPA]).
• Second, confirm the PCA stroke syndrome by localizing the lesion.
• Third, use the stroke syndrome as a guide and perform investigations to determine the stroke mechanism or cause.
• Based on these 3 steps, decide upon appropriate secondary preventive strategies. In practice, these 3 steps are done almost simultaneously.
• The phenomenology of PCA stroke is a function of the neuroanatomy and corresponding vascular supply, as described above.
• PCA syndromes can be divided roughly into those involving the midbrain, thalamus, occipital cortex, medial temporal lobe, occipitoparietal cortex, and combinations of these.
• Historical features are discussed in the Physical section.

Physical

• In general, because of the diversity of PCA syndromes, a complete neurologic examination is necessary.
• When thrombolytic therapy is being considered, an abridged 5- to 10-minute examination focusing on the major areas of neurological dysfunction is appropriate, for example, level of consciousness, language, hemi-inattention, visual fields, eye movements, lower cranial nerves, crude motor function, sensory loss, and ataxia. The NIH Stroke Scale is recommended as a guide to patient selection for thrombolytic therapy.
• The physical examination also should encompass a cardiologic and atherosclerosis examination, searching for arterial bruits, murmurs that suggest valvular heart disease, signs of atrial fibrillation, and signs of hyperlipidemia (eg, corneal arcus, tendinous xanthomata).
• The major PCA stroke syndromes are described here. Often, many of the features occur concomitantly.
  • Paramedian thalamic infarction
    • 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.
    • 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, referred to earlier, may be involved. This has been referred to as a posterior variant of the syndrome of akinetic mutism.
  • Pure hemisensory loss
    • 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.
    • 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
    • A general rule of visual field examination is that the further posterior the lesion, the more congruous is the visual field loss.
    • 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.
    • 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.
    • 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 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.
    • 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 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
    • 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.
    • 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.
    • Finally, apraxia of gaze is a misnomer describing a supranuclear deficit in the ability to initiate a saccade on command.
  • Disorders of face recognition
    • 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.
    • 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
    • These are illusory phenomena that are of uncertain pathophysiology. They may represent seizure activity and traditionally are treated with anticonvulsants.
    • 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 (alexia, dyslexia)
    • 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.
    • Classic alexia without agraphia was described by Dejerine in the late 19^th 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.
    • 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)
    • 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. This deficit also has been explained by a disconnection model.
  • Memory (amnesia)
    • 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.
    • Recent imaging in patients with transient global amnesia has demonstrated diffusion-weighted lesions in unilateral temporal lobes resulting in temporary amnesia.
  • Motor dysfunction
    • When the blood supply to the cerebral peduncles arises from perforators of 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 MCA infarction.

Causes

After an assessment of PCA stroke syndrome, the next step is to determine the mechanism of stroke. One approach is to start with the heart and proceed rostrally.

• Cardioembolism
  • Cardioembolism is the most common cause of PCA stroke.
  • Emboli may form in the heart from multiple underlying diseases. The most common cause is atrial fibrillation. Stroke from atrial fibrillation is preventable with long-term anticoagulation.
  • Other possibilities include a mural thrombus on a hypokinetic segment (eg, post-myocardial infarction [MI], dilated cardiomyopathy, atrial septal aneurysm), bacterial endocarditis, Libman-Sachs endocarditis, prosthetic heart valves, paradoxical embolism via a patent foramen ovale, and atrial septal defect.
  • Mitral valve prolapse and mitral valve strands are probably only weak risk factors for stroke.
  • Embolism from aortic arch atheroma
    • With the advent of transesophageal echocardiography, examination and quantitation of atheromatous disease of the aortic arch has been possible.
    • Thickness of plaque greater than 4 mm and/or presence of mobile thrombus are highly predictive of stroke.
  • Proximal vertebral artery disease
    • Stenosis of a vertebral artery origin often is found in patients with posterior circulation ischemia.
    • Analogous to the narrowed ICA, stenosis may lead to artery-to-artery embolism.
  • Dissection
    • The vertebral arteries are uniquely prone to dissection in the distal or V3 segment as they pass over the arch of C1, pierce the dura, and enter the foramen magnum.
    • Dissection may be spontaneous or related to minor or major trauma.
    • The mechanisms of PCA stroke secondary to vertebral artery dissection are believed to be due to formation of embolism or thrombus around an intimal tear.
    • The usual treatment of stroke secondary to dissection is anticoagulation; however, no solid evidence exists to support this practice.
  • Vertebral atherosclerotic disease
    • Caplan studied 10 cases of stroke due to arterioembolism from atherosclerotic vertebral arteries.
    • Most commonly, the cerebellum was affected, but PCA territory infarction also was reported.
  • Basilar artery disease: Emboli traveling up the posterior circulation may arrest at the top of the basilar, producing ischemia of both PCA territories, the thalamus, and midbrain.
  • Posterior cerebral artery disease: Intrinsic PCA stenosis from atherosclerosis is quite rare. Nevertheless, it is a recognized cause of stroke.
  • Vasospasm and migraine
    • Migraine typically affects the posterior circulation.
    • The clinical manifestations of an aura such as scintillating scotomata may represent spreading depression of Leão across the occipital cortex.
    • Angiography of patients with migraine shows a beaded pattern of vasospasm.
    • Migrainous stroke is said to occur most commonly in the occipital lobes.
• Other diagnostic considerations
  • Diagnosis of stroke is usually not difficult. Suddenness of onset should alert the clinician to the vascular nature of the insult. The usual differential diagnosis includes other vascular diseases such as intracerebral hemorrhage, vascular malformations, venous infarction, subarachnoid hemorrhage, and subdural hemorrhage. Rarely, space-occupying lesions (eg, glioma) present with sudden onset of deficit. One to two percent of patients in the large British TIA trial were found to have neoplastic lesions.
  • Demyelinating lesions (eg, multiple sclerosis) rarely present with hemianopia, but this does occur in a few patients. Migraine is usually evident by the accompanying headache and nausea and may ultimately (but rarely) progress to infarction. Hypoglycemia should be ruled out with simple laboratory studies.

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