Posterior Cerebral Artery Stroke


Overview of PCA Stroke

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. Identifying mechanisms of stroke is essential so that appropriate preventive therapies may be instituted. This article provides an overview of PCA stroke and focuses exclusively on stroke of arterial origin involving the PCA territory.

Common neurovascular anatomy

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

Various nomenclature methodologies have been used to describe PCA vascular anatomy. The PCA is divided into P1 and P2 segments by the PCOM. Penetrating branches to the mesencephalon, subthalamic, basal structures, and thalamus arise primarily from the P1 segment and the PCOM. These penetrating arteries include the thalamogeniculate, splenial (posterior paricallosal artery), and lateral and medial posterior choroidal arteries.

The P2 segment bifurcates into the posterior temporal artery and the internal occipital artery. The posterior temporal artery further divides into anterior, middle, posterior, and hippocampal branches. The internal occipital artery divides into calcarine and occipitoparietal branches.

Normal variants of neurovascular anatomy

The fetal PCA variant is seen in up to 30% of people, with various incidences depending upon how the variant is defined, and occurs when the P1 segment is congenitally absent or markedly hypoplastic and the PCA arises directly from the ipsilateral internal carotid artery (ICA). This can have diagnostic importance in that PCA territory stroke may be caused by atheromatous disease of the anterior circulation (ie, ipsilateral carotid bulb atheroma).

The central artery of Percheron variant is uncommon and occurs when the bilateral medial thalamic/rostral midbrain perforators arise from a single trunk from one P1 segment. Occlusion may result in bilateral paramedian thalamic and rostral midbrain infarction. This is an example in which a single cerebral artery supplies bilateral structures.

Pathophysiology of PCA Stroke

Ischemic stroke occurs when a region of cerebral blood flow is suddenly limited. This may occur by vessel occlusion or by relatively low flow. The rate of neuronal death varies with blood flow, variability in individual anatomy and collateralization, and inherent cerebral capacities (ie, some cerebral regions are more resistant than others).

Cerebral blood flow (CBF) rates less than 20 mL/100 g/min may produce infarction depending upon these individual differences plus the duration of oligemia, with lower CBF rates (< 10 mL/100 g/min) requiring less time to produce irreversible injury. Rapid restoration of blood flow is the most effective means of preserving brain tissue.

The mechanism of stroke involving the PCA territory is variable. Common etiologic considerations for PCA stroke include cardiogenic embolization, atheromatous disease of proximal vessels resulting in occlusion and/or artery-to-artery embolization, dissection of proximal vessels resulting in occlusion and/or artery-to-artery embolization, or intrinsic PCA atheromatous disease.

Less common etiologies include migrainous cerebral infarction (which preferentially affects the PCA distribution), anterior circulation disease (when fetal PCA variant is present), hypercoagulable disorders, illicit substance use, vasculitides, and other rare stroke disorders discussed elsewhere.

Epidemiology of PCA Stroke

An estimated 5-10% of ischemic strokes in the United States involve the posterior cerebral artery (PCA) or its branches. While stroke is the third leading cause of death in the United States and the leading cause of adult disability, death from PCA stroke is uncommon and would more likely occur in the setting of concomitant brainstem infarction.

Rate of morbidity from PCA stroke is high. Recovery of visual field deficits may be 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 or chronic pain syndromes.

Published data from the Tufts New England Medical Center posterior circulation stroke registry document that 58% of patients are male and 42% are female, with the mean age of stroke being 61.5 years.[1]

Initial Assessment and Management

The approach to stroke in the posterior cerebral artery (PCA) territory is no different from that with stroke elsewhere in the brain. The immediate goals of assessment are to correctly identify stroke as a diagnostic possibility, appropriately localize the lesion, and determine the time of symptom onset. A high clinical suspicion of stroke can be supported when there is an acute onset of neurologic symptoms referable to a cerebral arterial distribution.

Time of symptom onset needs to be precisely determined, as this may determine eligibility for acute stroke therapies. Rigorous questioning of the patient, family, or witnesses is often needed to clarify symptom onset.

If the patient is seen within 6-8 hours of onset, consideration may be given to various acute stroke therapies including intravenous (IV) thrombolysis or intra-arterial (IA) thrombolysis. Mechanical endovascular therapies, which are increasingly used for various intracranial large vessel occlusions, have been described and may be considered but are infrequently used for PCA occlusion.

Patient history

Once the appropriate acute therapies (if any) are instituted, the history should be directed at cerebrovascular risk factors and contributing historical elements that may reveal the underlying etiology. History should include past diagnoses (eg, diabetes mellitus, atrial fibrillation, hypertension), family history, social history, recent trauma to the head or neck, and a thorough review of systems.

The phenomenology of PCA stroke is a function of the neuroanatomy and corresponding vascular supply; therefore, historical information may have a highly localizing value. PCA syndromes can be divided roughly into those involving the midbrain, thalamus, occipital cortex, medial temporal lobe, occipitoparietal cortex, and combinations of these.

Physical examination

A complete neurologic examination is essential in any patient presenting with acute neurologic symptoms and aids in confirming the diagnosis of stroke and localizing the disorder.

When patients present early and may be eligible for acute stroke therapies, a standardized and abridged examination is recommended. The NIH Stroke Scale is a validated assessment commonly used as a guide to patient selection for acute stroke therapies. The complete neurologic examination may follow the abridged examination when appropriate.

The physical examination should encompass a cardiologic and vascular examination, searching for arterial bruits, murmurs that suggest valvular heart disease, and signs of atrial fibrillation. Other physical stigmata, if seen, may demonstrate a propensity for atherosclerosis, including corneal arcus or tendinous xanthoma.

Major Posterior Cerebral Artery Stroke Syndromes

The major PCA stroke syndromes comprise the following:

Often, many of the features occur concomitantly.

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, referred to earlier, may be involved.

Visual field loss

Unilateral infarction produces homonymous 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, and, additionally, bilateral representation of macular vision has been suspected.

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 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 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.

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 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.


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 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 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.

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

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. 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.

Determining Etiology

After stroke has been correctly identified and localized, the next step is to determine the mechanism by which the stroke occurred, as this will guide long-term preventive strategies. In some cases, all diagnostic possibilities need to be considered and the workup is extensive.

In other cases, however, the mechanism may be promptly suggested by the history and a focused work-up will reveal an immediate cause. An example would be a young individual with neck trauma in which vascular imaging demonstrates a cervical artery dissection with thrombosis.


Cardioembolism is the most common cause of PCA stroke, and emboli may arise from a number of different mechanisms. The most common cause is atrial fibrillation, in which emboli form due to vascular stasis frequently within the atrial appendage. Atrial fibrillation often represents a high-risk etiology for recurrence, particularly if the patient has other identified risk factors, including congestive heart failure, hypertension, age older than 75 years, diabetes mellitus, and prior stroke or transient ischemic attack. These risk factors are the basis of the CHADS2 score, which estimates the risk of recurrent stroke and suggests the benefit of oral anticoagulation based upon score.[2]

Other cardiogenic embolus possibilities include a mural thrombus on a hypokinetic wall segment (eg, postmyocardial infarction, dilated cardiomyopathy, ventricular aneurysm), endocarditis (bacterial, marantic, Libman-Sacks), prosthetic heart valve thrombosis, rheumatic heart disease, and paradoxical embolism via a patent foramen ovale or atrial septal defect.

Embolism may arise from aortic arch atheroma. This entity has been more recently elucidated by transesophageal echocardiography, which is more effective than transthoracic echocardiography in examining the aortic arch. Thickness of plaque greater than 4 mm or presence of mobile thrombus are strongly associated with stroke.

Proximal vertebrobasilar artery disease

Atheromatous disease may be found within the vertebral artery in patients with posterior circulation ischemia and may result in stenosis or occlusion of that proximal vessel. This may result in hypoperfusion or artery-to-artery embolism involving the PCAs.

Dissection of the vertebral arteries may result from trauma or occur spontaneously and result in arterial embolization. The vertebral arteries are uniquely prone to dissection due to their intracanalicular course within the vertebral bodies. PCA stroke secondary to vertebral artery dissection may occur when thrombus forms at an intimal tear and embolizes distally or when the dissection results in vessel stenosis/occlusion with subsequent vascular stasis and embolism.

Intrinsic basilar atheromatous disease may result in misery perfusion or artery-to-artery embolization in the PCA distribution.

Intrinsic PCA stenosis from atherosclerosis is a less common, but recognized, cause of stroke.

Migrainous cerebral infarction

Migraine represents a particular challenge in stroke medicine. Migraine typically affects the posterior circulation and the mechanisms by which stroke occurs are not known, although numerous postulated mechanisms exist.

Migraine alone commonly results in focal neurologic deficits, which may include visual loss, language disturbances, vertigo, nausea/vomiting, and other symptoms suggestive of posterior circulation disease (frequently known as complicated or basilar migraine). Furthermore, stroke in the posterior circulation distribution is more commonly associated with headache, occurring in approximately 30% of patients. Therefore, distinguishing between complicated migraine, migrainous cerebral infarction, and stroke with headache may be challenging.

Other stroke etiologic considerations

Other stroke etiologic considerations may include vasculitides, illicit substances, hypercoagulable disorders, metabolic disorders, and other infrequent stroke etiologies discussed elsewhere.

Diagnostic Considerations

The usual differential diagnosis includes other vascular diseases such as intracerebral hemorrhage, cerebral venous infarction, subarachnoid hemorrhage, and subdural hemorrhage. Rarely, space-occupying lesions (eg, glioma) present as sudden onset of deficit. Other disorders in the differential diagnosis include the following:

Demyelinating lesions (eg, multiple sclerosis) rarely present as hemianopia, but this does occur in a few patients. Posterior reversible encephalopathy syndrome may present with visual disturbances and imaging abnormalities within the occipital lobes.

Laboratory Studies for PCA Stroke

In the acute phase, routine blood tests should include a complete blood count, prothrombin time (PT)/activated partial thromboplastin time (aPTT)/international normalized ratio (INR), electrolytes, creatinine, and serum glucose. These tests are a part of the stroke mechanism work-up and are required to assess whether the patient is a candidate for acute stroke therapies.

When the mechanism of stroke is atherosclerotic disease, additional blood tests should be performed to assess atherosclerotic risk factors. Diabetes screening should be performed. A fasting serum cholesterol profile should be obtained.

If the stroke mechanism is not evident from the medical history and routine workup, then special hematologic and serologic examinations should be considered, particularly in young patients with cryptogenic stroke. A full hypercoagulable workup should include assays for arterial thrombophilia, including antiphospholipid antibodies and lupus anticoagulant.

Additional assays for venous thrombosis may be obtained in the appropriate clinical setting (ie, patent foramen ovale with paradoxical embolism) and include protein C, protein S, factor V Leiden/activated protein C resistance, antithrombin III, and prothrombin gene polymorphism. Some of these assays give abnormal results in the setting of acute stroke or anticoagulant medications and may need to be obtained on a delayed basis. The use and value of hypercoagulable disorder assessments remains a somewhat imprecise and controversial area of stroke neurology.

Neuroimaging for PCA Stroke

CT and MRI

All patients with suspected stroke should undergo emergent neuroimaging with CT or MRI. An unenhanced head CT is usually performed, as this test is widely available, can be rapidly obtained, and is sensitive in identifying intracranial hemorrhage. (See the images below.)

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Unenhanced head CT demonstrating a subacute L PCA infarct.

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Unenhanced head CT demonstrating hemorrhagic conversion of an ischemic stroke, approximately 72 hours after symptom onset.

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Brain MRI demonstrating acute stroke: diffusion restriction is seen on diffusion weighted imaging.

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MR angiogram demonstrating bilateral fetal PCA variants (black arrows) with the basilar artery terminating in bilateral superior cerebellar arteries (....

An emergent CT or MRI scan is required prior to considering acute stroke therapies, including thrombolysis. CT aids in identifying hemorrhage, identifying strokes that may be less acute than reported by patients (ie, the presence of hypodensity suggests a more subacute than hyperacute process), identifying hyperdense vessels, and excluding alternate diagnoses that may masquerade as stroke (ie, neoplasm or other masses). CT is less sensitive for lesions in the infratentorial region than the supratentorial region due to bony signal artifact and decreased tissue detail.

In the acute stroke setting, the use of CT angiography (CTA) has greatly expanded. CTA can identify both extracranial vascular disease (cervical atheromatous disease and dissection) and intracranial disease (intracranial stenosis or embolism). CTA results are frequently used to guide both acute and chronic therapies, including medical, surgical, and endovascular treatments.

MRI produces a much better examination of midbrain, subthalamic, and thalamic structures than CT. It also identifies acute stroke much earlier than CT by highly sensitive, diffusion-weighted imaging. MRI offers various modalities that can aid in determining the age of the stroke, identify multiple or small lesions that would be missed on CT, and identify at-risk or penumbral tissue by way of perfusion imaging.

Currently, the use of diffusion/perfusion imaging studies to identify mismatch (suggesting the presence of at-risk brain tissue that is not yet infarcted) is actively being studied but is not the accepted standard of care. MR angiography (MRA) is frequently used to assess the extracranial and intracranial vasculature, but it is more prone to artifact and tends to overestimate the degree of hemodynamic compromise within vessels.


Other possible brain imaging procedures include single-photon emission computed tomography (SPECT) and positron emission tomography (PET). SPECT is a nuclear medicine study using radioisotopes of technetium. It provides an analysis of relative blood flow by region, usually in the resting state. It is rarely useful in the clinical setting of acute stroke and can be considered a research tool. PET can be used to analyze neurometabolism in vivo; it is at present a research tool.


Catheter cerebral angiography remains the criterion standard for evaluation of vascular anatomy. It is a more invasive method and does carry a small risk of procedure-related morbidity. Increasingly, noninvasive methods of viewing the arterial anatomy are used (CTA, MRA, TCD) each of which has its own benefits, technical challenges, and limitations. In many cases, these noninvasive methods are sufficient for diagnosis and management; however, when these produce unclear findings or more information is needed about the vascular anatomy, angiography is required. In addition, angiography is required as a precursor to endovascular treatments. (See the images below.)

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Digital subtraction angiogram demonstrating an acute L PCA occlusion (red arrow) following balloon-assisted coiling of a basilar tip aneurysm.

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Digital subtraction angiogram demonstrating revascularization of acute L PCA occlusion (red arrow) during a balloon-assisted basilar tip aneurysm, rev....


Transcranial Doppler ultrasonography (TCD) is not widely used in acute stroke; however, it may become useful as an adjunct in both diagnosis and acute treatment of stroke. TCD is dependent upon the skill and experience of the operator. In skilled hands, both the distal basilar and P1 and P2 segments can be assessed and may detect acute clot in the PCA.

Carotid duplex ultrasonography may be considered in PCA stroke when a fetal origin PCA is present. In this setting, carotid atheromatous disease would be symptomatic and patients may be considered for carotid endarterectomy or stenting for recurrent stroke prevention.


Transthoracic echocardiography (TTE) is used routinely to investigate possible cardiac sources of embolus. Transesophageal echocardiography (TEE) is a more sensitive test. It is more effective than TTE at identifying valvular lesions, aortic arch atheroma, and interatrial shunts. Patent foramen ovale (PFO) and any PFO-associated abnormal anatomy (such as atrial septal aneurysms) are more frequently detected by TEE.


All patients with stroke should have an immediate ECG. ECG may identify stroke mechanisms or stroke-associated conditions, such as myocardial infarction, conduction abnormalities, and atrial fibrillation.

Treatment of PCA Stroke

The treatment of stroke necessitates an understanding of the mechanism of stroke. The approach to stroke is defined by localization of the problem to determine the vascular territory involved and subsequently by using the history, stroke subtype, and investigational tools to define the stroke mechanism. The medical treatment of stroke can be divided into acute (within 3-4.5 hours of stroke onset), subacute, and chronic phases.

If possible, patients with acute stroke should be cared for in a stroke unit by staff familiar with stroke etiology, workup, treatment, and poststroke complications. Patients may require intensive care unit monitoring if they have a large-volume stroke, significant concomitant brainstem infarcts or tissue at-risk, or significant comorbid medical conditions (ie, myocardial infarction), or if they have received acute stroke therapies.

The management of acute stroke in general may be complicated and extensive. Various considerations need to be made regarding issues such as management of hypertension, hyperglycemia, cerebral edema with increased intracranial pressure, hemorrhagic transformation of cerebral infarction, infections, aspiration, deep venous thrombosis, myocardial infarction, and other stroke-associated conditions. Isolated PCA stroke may not have all the attendant complications as the associated disability or volume of infarction may be less than with other stroke syndromes (eg, MCA or BA stroke syndromes).

rtPA and TPA

The National Institutes of Neurological Diseases and Stroke (NINDS) trial of recombinant tissue-type plasminogen activator (rtPA) administered within 3 hours of stroke onset, demonstrated an increased likelihood of improved outcome and included all types of ischemic stroke.[3] However, recent studies have provided new data on rtPA treatment in the 3- to 4.5–hour window in carefully selected patients.[4, 5]

In May 2009, the American Heart Association/American Stroke Association (AHA/ASA) guidelines for the administration of rtPA following acute stroke were revised to expand the window of treatment from 3 to 4.5 hours to provide more patients with an opportunity to receive benefit from this effective therapy.[6] This has not yet been FDA approved.

If a clear time of onset can be established, stroke in the PCA territory may be treated with intravenous TPA. However, because isolated PCA territory symptoms may be subtle or underappreciated, patients may mistake the time of stroke onset. Patients who experience significant motor, sensory, or language symptoms (middle cerebral artery [MCA] or basilar artery [BA] syndromes) are more likely to present urgently and with more precise time of onset. Administration of TPA beyond the recommended time limits likely offers no benefit to patients and exposes them to increased risk of intracerebral hemorrhage.

Endovascular therapy

Angioplasty, stenting, mechanical embolectomy, and intra-arterial thrombolysis are enjoying ever-expanding application and use in acute stroke, although their roles continue to be defined. However, their application in the PCA distribution is uncommon compared with other vascular distributions (internal carotid artery, MCA, BA, vertebral artery). This is likely due to small vessel size of the PCAs, low NIHSS scores in which treatment benefit may be offset by procedural risk, delayed recognition of isolated PCA stroke syndromes, and other factors. Numerous mechanical embolectomy devices have been studied and few have allowed or incorporated isolated PCA stroke for inclusion.

Endovascular therapies are more likely to be used if there is significant vertebrobasilar disease as the cause of PCA stroke or if the patient fails to respond to medical management. When the internal carotid artery (ICA) is the source of stroke via a fetal variant PCA, surgical endarterectomy or endovascular stenting of the ICA may be appropriate.

More recently, treatments such as vertebral artery stenting have been used and may replace the medical-treatment-only approach to intrinsic vertebral artery disease; however, endovascular treatments tend to be reserved for medically refractory cases.

Surgical care

In unusual circumstances, vertebral artery bypass may be considered; however, this surgical procedure remains an unproven therapy. Extracranial (EC)-to-intracranial (IC) vertebral artery bypass may be undertaken by connection of the occipital artery to the vertebral, superior cerebellar, anterior ICA, or posterior ICA. The superficial temporal artery has also been used as a donor artery. Shunting to the PCA may be accomplished by using veins or synthetic grafts. In general, EC-to-IC circulation shunting has been relegated to use in extenuating circumstances since the publication of the negative EC-IC bypass trial.[7]

Outpatient care

Patients who had PCA stroke should be observed on an outpatient basis to ensure that cerebrovascular risk factors are treated chronically, that changes in medication management following stroke are well tolerated, and that chronic disability is appropriately addressed.

Attention to rehabilitation should begin early. Involvement of a speech language therapist may be required if alexia is present, with or without aphasia. The occupational therapist should be able to help with teaching patients to turn to look in the blank visual hemifield.

An issue that frequently arises with infarction of the visual cortex or its afferent fibers is competency to drive a vehicle. Patients with infarction in the territory of the left PCA may have preserved macular vision but severe restriction of peripheral vision, as well as an inability to read in any visual field. Patients with infarction in the territory of right PCA may have significant visual hemineglect.

Careful examination of the patient and knowledge of local laws governing the right to drive are a necessity. Patients often have to relinquish their driver’s license because of the visual field loss. This may result in considerable loss of independence and provoke anger and grief in the patient, for which counseling may be required.

Dietary restrictions

Acute stroke patients should undergo a bedside sips test to grossly assess for dysphagia (excepting those who have frank severe dysarthria/dysphagia or altered mental status).

A speech pathologist and dietitian may provide advice on diet both immediately and in the long term. Enteral nutrition may need to be provided by alternative means, such as a nasogastric device or a percutaneous enteric gastrostomy tube in patients who have severe dysphagia.

As mentioned previously, dysphagia is generally not an issue with PCA strokes unless there are concomitant brainstem infarcts. However, patients may not be able to see one side of the plate and may neglect some of their food; they need to have the plate turned and eventually be taught to turn their head to see the blind hemifield.

A heart-healthy diet is really an antiatherosclerosis diet and may be applicable depending on stroke mechanism and underlying risk factors. This prescription should be based on follow-up testing and investigation.

Activity restrictions

Activity restriction varies depending on the patient's deficits, but the patient should be encouraged to remain mobile if possible. At discharge, activities may be limited by neurological deficits. The patient may be required to give up driving.


Stroke care is a multidisciplinary process. Participants may include a neurointensivist, neurointerventionalist, vascular surgeon, neurological surgeon, stroke nurse specialist, physical therapist, occupational therapist, speech therapist, physiatrist or rehabilitation neurologist, and a case manager or social worker.

Early attention to rehabilitation and eventual reintegration into the community speeds recovery and shortens the length of hospital stay.

Prevention of Recurrent Stroke

Treatments for recurrent stroke prevention should be instituted as soon as possible. The identified etiology of the stroke will determine what treatments are indicated (medical, surgical, endovascular) for preventing recurrent events.

Warfarin and antiplatelet therapies

Long-term anticoagulation with warfarin is indicated in several settings for prevention of recurrent strokes including atrial fibrillation, significant global or regional cardiac hypokinesis (ejection fraction < 30%), patent foramen ovale with documented hypercoagulable condition, and arterial hypercoagulable state. The risks of recurrent stroke have to be balanced with the risk of oral anticoagulation therapy. For patients in whom no cause can be found despite extensive work-up, antiplatelet therapies are generally recommended instead of anticoagulant therapies.

Antiplatelet therapies are often the mainstay for recurrent stroke prevention. In most cases, they can be instituted immediately, and evidence suggests that doing so decreases recurrent events both immediately and chronically. Aspirin, 325 mg qd, has been shown to reduce the rate of acute recurrence of stroke (ie, in the first 14 days after first stroke) when administered within 48 hours of the first stroke.

Ticlopidine, clopidogrel, and aspirin plus extended-release dipyridamole (Aggrenox) also prevent recurrent stroke, although ticlopidine is rarely used due to a higher risk of side effects. These agents produce platelet inhibition by a number of different mechanisms.


Anticoagulation is infrequently indicated in the acute phases of PCA stroke. While historically early anticoagulation (generally with heparin infusion) has been used in acute stroke, significant supporting data have been absent.

Early anticoagulation, particularly with heparin, has been studied in a number of diagnostic settings but has not demonstrably proven to be beneficial. Recent Cochrane reviews of studies totaling more than 20,000 patients have suggested that early anticoagulation does not produce a mortality or morbidity benefit.[8, 9] In specific cases (large vessel, high-grade stenosis), some benefit may have been seen; however, this was offset by increased hemorrhagic complications.

The rationale for the acute use of anticoagulant therapy lies in preventing acute recurrence of stroke; however, trials have shown that this risk of early recurrent stroke is low and that heparin does not provide any functional or survival advantage. This remains a controversial area, however, in which some stroke experts have strong opinions about acute anticoagulation.

In general, the stroke mechanism should be identified so that a better informed decision can be made before long-term anticoagulation is chosen. PCA strokes that arise from vertebral artery dissection are more frequently treated with anticoagulation, although again there is a paucity of data to support this use.

Early anticoagulation may be the most appropriate preventive strategy in specific circumstances that are considered high-risk, such as the presence of an intracardiac thrombus or a dissection with visualized large intraluminal thrombus. Strokes caused by atrial fibrillation do not require early anticoagulation with heparin. Studies have demonstrated that the risk of recurrent stroke within the first weeks is approximately 1%.[10] Early heparinization in this setting is associated with no clear stroke prevention benefit but is associated with increased hemorrhagic complications.

Heparin and low-molecular-weight heparin (LMWH) should be titrated individually based on aPTT. A heparin bolus is infrequently given due to concerns of hemorrhage. This approach may be justifiable given recent evidence that heparin does not provide an acute advantage in nonselective use in ischemic stroke.

The optimal dosing regimen for heparin in stroke has not been established. Fractionated heparins, or LMWH, have become available in the last few years and have revolutionized therapy of venous thrombosis and acute coronary syndromes. LMWH therapy in the acute setting should be cautiously considered because no antidote is available for quick reversal of anticoagulation in the event of intracerebral hemorrhage. In the subacute setting, LMWH may be used as a bridge to long-term anticoagulation with warfarin.

Other prophylactic measures

Although deep venous thrombosis (DVT) is unusual in patients with isolated PCA stroke, any patient who has diminished mobility from stroke (ie, concurrent brainstem stroke) or a comorbid condition should receive prophylactic therapy for DVT.

Effective treatment of hypertension has been proven to reduce the risk of recurrent stroke.

Elevated cholesterol is a potential risk factor for stroke; sustained reduction in cholesterol levels may reduce the chances of stroke. Numerous studies have demonstrated a modest stroke risk-reduction benefit in patients with coronary heart disease; however, the results of the SPARCL study (Stroke Prevention by Aggressive Reduction in Cholesterol levels) suggest that patients without CHD also have a lower incidence of stroke on statin therapy.[11]

Numerous statins (eg, lovastatin, simvastatin, pravastatin, atorvastatin) are available. All inhibit enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme in anabolism of cholesterol. These drugs are effective in reducing levels of low-density lipoprotein (LDL) cholesterol but have less effect on high-density lipoprotein (HDL) and triglycerides. They may have other pleiotropic effects in stroke prevention such as plaque stabilization, reduction of free radical formation, and anti-inflammatory, immunomodulatory, and antiplatelet effects. Additionally, prestroke use of statins may be associated with smaller infarct or better outcomes. Large vessel atherosclerosis may undergo regression in patients treated with statin therapy.

Emphasis should always be placed on smoking cessation, moderation of alcohol use, and discontinuation of illicit substance use.


Mortality associated with isolated posterior cerebral artery (PCA) stroke is low; therefore, prognosis is generally good. Visual field deficits improve to varying degrees; however, they may be permanent and associated with morbidity. Some neuropsychological deficits may improve with time but are also associated with morbidity.

Patient Education

At discharge, all patients who have had a stroke should be counseled about the symptoms and signs of acute stroke. They should know that the major symptoms of stroke include the following:

Since a delay in receiving emergency care is the major reason why patients cannot be treated with thrombolytic therapy, patients and their caregivers must be taught what to do if a stroke occurs. Patients should be instructed to call an ambulance (ie, call 911) if they or their friends/relatives suffer from any of these symptoms.

For patient education information, see the Stroke Center, Cholesterol Center, and Statins Center, as well as Stroke, High Cholesterol, Cholesterol FAQs, and Atorvastatin (Lipitor).


Erek K Helseth, MD, Fellow, Vascular and Interventional Neurology, Oregon Health and Science University

Disclosure: Nothing to disclose.

Specialty Editors

Thomas A Kent, MD, Professor and Director of Stroke Research and Education, Department of Neurology, Baylor College of Medicine; Chief of Neurology, Michael E DeBakey Veterans Affairs Medical Center

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Howard S Kirshner, MD, Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center

Disclosure: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD, Professor, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, Oregon Stroke Center

Disclosure: Co-Axia Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Concentric Medical Consulting fee Review panel membership

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors Michael D Hill, MD, and Alastair M Buchan, DSc, MB, BCh, to the development and writing of the source article.


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Unenhanced head CT demonstrating a subacute L PCA infarct.

Unenhanced head CT demonstrating hemorrhagic conversion of an ischemic stroke, approximately 72 hours after symptom onset.

Brain MRI demonstrating acute stroke: diffusion restriction is seen on diffusion weighted imaging.

MR angiogram demonstrating bilateral fetal PCA variants (black arrows) with the basilar artery terminating in bilateral superior cerebellar arteries (blue arrows).

Digital subtraction angiogram demonstrating an acute L PCA occlusion (red arrow) following balloon-assisted coiling of a basilar tip aneurysm.

Digital subtraction angiogram demonstrating revascularization of acute L PCA occlusion (red arrow) during a balloon-assisted basilar tip aneurysm, revascularization with use of balloon angioplasty.

Unenhanced head CT demonstrating a subacute L PCA infarct.

Unenhanced head CT demonstrating hemorrhagic conversion of an ischemic stroke, approximately 72 hours after symptom onset.

Brain MRI demonstrating acute stroke: diffusion restriction is seen on diffusion weighted imaging.

MR angiogram demonstrating bilateral fetal PCA variants (black arrows) with the basilar artery terminating in bilateral superior cerebellar arteries (blue arrows).

Digital subtraction angiogram demonstrating an acute L PCA occlusion (red arrow) following balloon-assisted coiling of a basilar tip aneurysm.

Digital subtraction angiogram demonstrating revascularization of acute L PCA occlusion (red arrow) during a balloon-assisted basilar tip aneurysm, revascularization with use of balloon angioplasty.