Posterior Cerebral Artery Stroke 

  • Author: Christopher Luzzio, MD; Chief Editor: Denise I Campagnolo, MD, MS   more...
 
Updated: Jan 18, 2012
 

Background

This article focuses on the anatomy, symptoms, examination findings, etiologies, chronic disability issues, and neurorehabilitation associated with posterior cerebral artery (PCA) ischemic and hemorrhagic infarctions (see the image below). For extensive details concerning acute treatment and workup issues, the reader is referred to neurology articles on acute Anterior Circulation Stroke and Posterior Cerebral Artery Stroke [Neurology].

Computed tomography (CT) scan of the brain showingComputed tomography (CT) scan of the brain showing hypodense areas in the right occipital lobe consistent with a recent posterior cerebral artery ischemic infarct.

Patients who have sustained PCA strokes present with an interesting and diverse spectrum of neurologic symptoms. The most common long-term sequelae of PCA strokes are visual and sensory deficits. In general, patients with PCA distribution strokes exhibit less overall chronic disability than those with anterior cerebral, middle cerebral, or basilar artery infarctions.

Active neurorehabilitation of patients following cerebrovascular accident is essential because evidence suggests that prolonged neural plasticity follows stroke. Active intervention, especially by a team of rehabilitation specialists, is beneficial, increasing the probability of the patient's achieving maximal independence in activities of daily living (ADL). The role of the physiatric clinician on the neurorehabilitation team is to avert medical complications and facilitate integration of the various therapeutic services.

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Pathophysiology

Ischemic strokes occur when blood cannot flow to cerebral structures. Neuron metabolism tolerates a brief period of interrupted oxygen and glucose delivery. Cell death is imminent after approximately 6 minutes of halted blood circulation. Large cortical neurons are especially sensitive to ischemia. Infarcts include a central area, or umbra, of highly concentrated cell death, surrounded by a penumbra of tissue containing stunned cells that may recover, assuming circulation is reestablished or produced through nearby collaterals.

Understanding of posterior cerebral artery (PCA) stroke symptoms and physical examination findings requires familiarity with PCA anatomy. The right and left PCA vessels are formed from bifurcation of the basilar artery near the junction of the pons and midbrain over the ventral aspect of the brainstem. Each PCA is divided anatomically into 4 segments (P1-P4) as follows:

  • P1 extends from origin of the PCA to the posterior communicating artery, contributing to the circle of Willis.[1] Posterior thalamoperforating arteries branch off the P1 segment and supply blood to the midbrain and thalamus.
  • P2 includes the portion of the PCA that courses laterally around the midbrain from its junction with the posterior communicating artery to its major branch, the lateral posterior choroidal artery, which supplies the posterior thalamus and lateral ventricular choroid plexus. Other thalamogeniculate arteries branch from the P2 segment and serve the crus cerebri, pulvinar, medial geniculate body, brachium of the superior colliculus, and, variably, the lateral geniculate body.
  • The medial posterior choroidal artery can originate from P1 or P2. This artery supplies portions of the midbrain and posterior thalamus.
  • P3 and P4 are distal segments of the PCA, the branches of which circulate blood to cortical regions. The inferior temporal, parietooccipital, calcarine, and posterior pericallosal arteries supply the undersurface of the temporal lobe, the posterior one third of the interhemispheric surface, occipital pole, visual cortex, and splenium of the corpus callosum.
  • Anatomic localization of the point of vascular occlusion in PCA infarcts may be simplified into the following 2 categories: (1) deep or proximal PCA strokes, causing ischemia in the thalamus and/or midbrain (regions supplied by P1 and P2), as well as in the cortex (regions supplied by P3 and P4); and (2) superficial or distal PCA, involving only cortical structures (P3, P4 branch areas).[2, 3]
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Epidemiology

Frequency

International

Approximately 5-10% of cerebral infarcts occur in the posterior cerebral artery (PCA) territory.

Mortality/Morbidity

Overall, the risk of death in patients with posterior cerebral artery (PCA) strokes is approximately 5% in the acute hospital setting. Most deaths occur in patients with deep or proximal PCA infarctions, particularly those involving bilateral midbrain and thalamic structures. Otherwise, most PCA infarctions result in chronic visual deficits (84%), sensory abnormalities (17%), and motor weakness (6%), as documented in the Brandt et al series of 127 patients.[4]

Race

Stroke is more common in African Americans than in white or Hispanic populations in the United States.

Sex

Stroke occurs more frequently in men than women.

Age

Stroke incidence dramatically increases in the elderly population secondary to cardiovascular disease.

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Contributor Information and Disclosures
Author

Christopher Luzzio, MD  Clinical Assistant Professor, Department of Neurology, University of Wisconsin at Madison School of Medicine and Public Health

Christopher Luzzio, MD is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

Coauthor(s)

Consuelo T Lorenzo, MD  Physiatrist, Department of Physical Medicine and Rehabilitation, Alegent Health Immanuel Rehabilitation Center

Consuelo T Lorenzo, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Specialty Editor Board

Elizabeth A Moberg-Wolff, MD  Medical Director, Pediatric Rehabilitation Medicine Associates

Elizabeth A Moberg-Wolff, MD is a member of the following medical societies: American Academy for Cerebral Palsy and Developmental Medicine and American Academy of Physical Medicine and Rehabilitation

Disclosure: Medtronic Neurological None Speaking and teaching

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Richard Salcido, MD  Chairman, Erdman Professor of Rehabilitation, Department of Physical Medicine and Rehabilitation, University of Pennsylvania School of Medicine

Richard Salcido, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Physician Executives, American Medical Association, and American Paraplegia Society

Disclosure: Nothing to disclose.

Kelly L Allen, MD  Medical Director, Medevals

Disclosure: Nothing to disclose.

Chief Editor

Denise I Campagnolo, MD, MS  Director of Multiple Sclerosis Clinical Research and Staff Physiatrist, Barrow Neurology Clinics, St Joseph's Hospital and Medical Center; Investigator for Barrow Neurology Clinics; Director, NARCOMS Project for Consortium of MS Centers

Denise I Campagnolo, MD, MS is a member of the following medical societies: Alpha Omega Alpha, American Association of Neuromuscular and Electrodiagnostic Medicine, American Paraplegia Society, Association of Academic Physiatrists, and Consortium of Multiple Sclerosis Centers

Disclosure: Teva Neuroscience Honoraria Speaking and teaching; Serono-Pfizer Honoraria Speaking and teaching; Genzyme Corporation Grant/research funds investigator; Biogen Idec Grant/research funds investigator; Genentech, Inc Grant/research funds investigator; Eli Lilly & Company Grant/research funds investigator; Novartis investigator; MSDx LLC Grant/research funds investigator; BioMS Technology Corp Grant/research funds investigator; Avanir Pharmaceuticals Grant/research funds investigator

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Computed tomography (CT) scan of the brain showing hypodense areas in the right occipital lobe consistent with a recent posterior cerebral artery ischemic infarct.
 
 
 
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