AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

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. 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.

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 physician on the neurorehabilitation team is to avert medical complications and facilitate integration of the various therapeutic services.

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 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. 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).

Frequency

International

Approximately 5-10% of cerebral infarcts occur in the PCA territory.

Mortality/Morbidity

Overall, patients with PCA strokes have an approximate 5% risk of death 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.

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.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

History

Patients with PCA infarcts present for neurologic evaluation with symptoms including the following:

• Acute vision loss
• Confusion
• New onset posterior cranium headache
• Paraesthesias
• Limb weakness
• Dizziness
• Nausea
• Memory loss
• Language dysfunction

Because many individuals identify stroke with motor weakness or language loss, they may delay seeking medical care after experiencing only vision change or headache, unaware that a stroke has occurred.

Patients may report bumping into objects, hitting obstacles on the roadside, or not seeing half the printed page when reading.

• Small homonymous visual-field cuts often are mistaken for a loss or change of vision from one eye attributable to a refractive error correctable with optical glasses.
• A person with a hemifield visual loss and headache also may be discharged from urgent care with a diagnosis of migraine headache rather than a PCA stroke. A CT scan easily can differentiate between the 2. Additionally, a migraine is characterized by a moving scintillating scotoma, not a fixed bilateral homonymous field cut.
• The presence of homonymous hemianopia also helps the physician differentiate between a middle cerebral artery and PCA stroke, as profound hemiplegia or somatosensory loss may occur in both conditions.

Physical

The most common examination finding is a homonymous visual-field cut, usually a complete hemianopia, caused by a lesion in the contralateral occipital lobe. Macular or central field sparing can occur if the occipital pole remains intact through blood supply from a branch of the middle cerebral artery. Cortical blindness results from bilateral PCA infarcts.

• Deep or proximal PCA infarcts involve portions of the thalamus and midbrain. Thalamic lesions result in contralateral face and limb sensory loss. The midbrain cerebral peduncle carries corticospinal tract fibers that decussate caudally in the brainstem. A peduncle lesion is associated with contralateral motor weakness. Motor symptoms also are induced by thalamic edema near the internal capsule or a focal lesion in this structure. The posterior aspect of the internal capsule, variably, receives some blood from branches off the proximal PCA.
• Large or bilateral PCA infarcts that involve thalamus, temporal, and/or parietal-occipital lobes often result in a spectrum of possible findings (neuropsychologic deterioration and memory, language, or visual-cognitive dysfunction). Prosopagnosia and visual agnosia are representative examples.

Causes

Major etiologies of PCA infarction include cardiac embolism, vertebrobasilar disease, and PCA atherothrombosis.

• Vertebrobasilar disease includes atherosclerosis, dissection, and aneurysm, all of which may cause artery-to-artery embolic events. Less frequent causes include paradoxical embolism, migraine, hypotension, hypercoagulable state, and fibromuscular dysplasia.

DIFFERENTIALS

Section 4 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Subdural hematoma
Brain metastases
Migraine
Trauma
Infection
Cardiac embolism
Brainstem infarction
Subarachnoid hemorrhage

WORKUP

Section 5 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• See also the following articles: Magnetic Resonance Imaging in Acute Stroke, Neuroprotective Agents in Stroke, and Stroke Team Creation and Management. Essential components of workup depend on the patient's age, stroke risk factors, and prior medical history.
• Studies used to evaluate the older patient (whose stroke is associated with cardiovascular disease) may include those that assess (1) severe anemia or volume depletion that can cause, worsen, or confound cerebral ischemia, (2) early infection as a result of aspiration, and (3) baseline coagulation status in case treatment involves heparin, warfarin, or thrombolysis. Appropriate tests include the following:
• • Complete blood cell count
  • Platelet count
  • Serum electrolytes
  • Blood urea nitrogen
  • Creatinine
  • Glucose
  • Prothrombin time
  • Activated partial thromboplastin time
  • International normalized ratio
  • Urinalysis

Imaging Studies

• CT scan of the brain is used to determine the presence of primary cerebral hemorrhage or ischemic infarction with hemorrhagic change.
• Abnormal neurovascular anatomy and associated pathology are determined through carotid Doppler studies and magnetic resonance imaging (MRI) or CT angiography (if MRA is contraindicated or not available).
• Frequently, PCA infarcts have a cardioembolic etiology. ECG identifies atrial fibrillation and/or myocardial infarction. Echocardiography helps determine the presence of nonembolized thrombi, valvular and myocardial disease, septal defects such as a patent foramen ovale, and altered ejection fraction. Transesophageal echocardiography is preferred when medically feasible and safe for the patient.

Other Tests

• Strokes occurring in persons younger than 50 years require investigation for etiologies such as cardiac defects (patent foramen ovale), thrombophilia or hypercoagulable state (protein S or C or antithrombin III deficiency, activated protein C resistance, G20210A prothrombin mutation), arterial dissection, connective-tissue autoimmune disorders (antiphospholipid syndrome), and malignancy.
• Identification of other stroke risk factors, including hypertension, diabetes, elevated cholesterol and lipid panels, and hyperhomocystinemia, is also useful.
• Some authorities have expressed concern that chiropractic manipulation of the neck may cause vertebral artery dissection.

Procedures

• Intravenous tissue plasminogen activator may be given to patients who present within 3 hours of developing a disabling ischemic stroke. Because of the increased risk for complicating intracerebral hemorrhage, there are rigid guidelines for administering tissue plasminogen activator.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Rehabilitation Program

Physical Therapy

A small percentage of patients with a PCA infarct suffer chronic motor deficits. Approximately 5% of patients who do may require transfer, gait, and stair training with an assistive device. Orthotic devices (eg, ankle-foot orthosis) also may be beneficial. Patients with PCA infarcts may demonstrate delayed postural reactions due to sensorimotor deficits. Programs designed to improve postural control and balance may be helpful. Home exercise programs and family/caregiver training are important to sustaining improvement after discharge from therapy.

Occupational Therapy

The occupational therapist helps the patient adapt to homonymous hemianopia and visual-spatial function abnormalities. The patient benefits from scanning into the field deficit. A small percentage of PCA stroke patients require therapy for motor deficits of the upper limb.

Speech Therapy

Speech therapy usually is not required; however, in infrequent cases where there is neuropsychologic deterioration or memory-language deficits, a speech therapist should be consulted. Although dysphagia typically is not associated with PCA infarcts, evaluation of swallowing may be useful in patients who may be at risk for aspiration.

Recreational Therapy

Recreational therapy helps patients with PCA stroke adapt to visual deficits and facilitates a healthy affect, as depression is a common occurrence in stroke patients.

Medical Issues/Complications

• Recurrent ischemic event
• Hemorrhage into infarcted brain tissue
• Stroke-associated epilepsy
• Anticoagulation-associated intracranial, gastrointestinal, or retroperitoneal hemorrhaging
• Urinary tract and pulmonary infections
• Skin breakdown
• Depression
• Chronic pain
• Dyskinesia and dystonia

Consultations

• Ophthalmologists accurately plot visual-field loss and can recommend corrective lenses and compensation techniques.
• Pain specialists treat rare intractable thalamic pain with many methods including anticonvulsants (carbamazepine [Tegretol], gabapentin [Neurontin]) and tricyclic medications (amitriptyline [Elavil]). Recently, topiramate (Topamax) has been found helpful in treating headache and painful dysesthesias.
• A psychiatrist may assist with treatment of mood disorders and psychotic symptoms.
• A neuropsychologist can help to assess and document cognitive function, which is especially important for persons returning to professional duties, considering living alone, or applying for disability.

Other Treatment

Many experimental treatment modalities such as cognitive retraining, neuropharmacologic therapy (amphetamines), robot-assisted physical and occupational therapy, and virtual environments are reported to aid stroke recovery, but further evidence is needed to confirm their benefit.

MEDICATION

Section 7 of 11  

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• References

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Several new oral anticoagulant medications, including ximelagatran, are in the final stages of clinical trials for use in the prophylaxis of ischemic thromboembolic stroke. Once approved for use, the potential of such drugs in the arena of stroke treatment is significant.

Drug Category: Hematological agents

Patients entering the rehabilitation phase of their hospital course may be prescribed warfarin, clopidogrel, or aspirin. The selection of these agents is dependent on the etiology of the PCA stroke, associated complications, comorbidities, and prior medical history. These medications are used to prevent further cerebral vascular ischemic events.

FOLLOW-UP

Section 8 of 11  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Further Inpatient Care

• Patients with acute PCA infarcts generally are hospitalized, unless, due to late diagnosis, they can be seen safely on an outpatient basis. Aggressive rehabilitation begins once the patient is medically stable. Goals include maintaining range of motion, promoting active movement of the hemiplegic side if applicable, improving the patient's functional mobility and self-care capabilities, and monitoring medical conditions affecting recovery and prevention of further disability,

Further Outpatient Care

• Depending on the degree of motor loss, available insurance coverage and variables such as social situation, the patient may qualify for continued outpatient or home therapy.
• The patient with PCA stroke may want to drive or participate in activities dangerous to a person with homonymous hemianopsia vision loss. Some recovery of vision may occur. Repeated visual-field testing is required, as well as further assessment by occupational therapists and physicians.

In/Out Patient Meds

• Discharge medications may include specific agents for stroke prevention (eg, aspirin, clopidogrel, warfarin) that usually are recommended by the neurologist prior to transfer to a neurorehabilitation setting. Cholesterol-lowering drugs, antihypertensive therapies, muscle relaxants, and substances for treating rare thalamic pain or chronic headaches or depression may be prescribed.

Complications

• Complications that may occur in the patient with PCA stroke are described in other sections. See Medical Issues/Complications and Medical/Legal Pitfalls.

Prognosis

• On average, patients with PCA stroke sustain minimal or no chronic motor disability. These patients are usually able to adapt to their visual deficit so that many ADL tasks are manageable.
• Of young stroke victims, 30-70% return to work, with the higher fraction being men and those educated beyond high school.

Patient Education

• The patient must learn conscious scanning into the visual-field deficit. The hemiparetic patient who has sustained PCA stroke must learn transfer techniques, walking with mechanical assistance (if feasible), and modified ADL (eg, dressing, bathing, cooking). Some patients require a significant amount of assistance. The patient's caregiver should meet with therapists to learn how best to help the patient at home without causing personal or other injury.
• For excellent patient education resources, visit eMedicine's Stroke Center. Also, see eMedicine's patient education article Stroke.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Medical/Legal Pitfalls

• A number of medical issues must not be neglected, either in the acute setting or in the neurorehabilitation phase of their hospitalization.
• • Reviewing documentation and performing baseline neurologic examinations help the clinician recognize an evolving or recurring stroke, which is treatable, from a completed infarction.
  • Initial evaluation of stroke symptoms must include a CT scan of the head to rule out primary intracranial hemorrhage and to assess for hemorrhagic change within ischemic tissue.
  • An ECG assesses for concurrent myocardial infarction.
  • Evaluate patient's swallow function so that diet can be modified appropriately and aspiration pneumonia avoided.
  • Bedridden patients, especially those with flaccid limbs, are prone to deep venous thrombosis and subsequent pulmonary embolism. Prophylaxis to prevent deep venous thrombosis includes early mobilization, subcutaneous heparin, pneumatic pressure, and elastic stockings.
  • Decubitus ulcers develop rapidly in immobilized patients. Wet bedclothes facilitate skin breakdown. Attentive nursing care is essential.
  • Weakened patients may fall and suffer traumatic head injury or fractured hips. Close monitoring of patients with cognitive impairment and training of family is important.
  • Painful contractures develop rapidly in weakened limbs and may impede recovery. Early and frequent performance of range of motion can help prevent this problem.
• Patients with PCA stroke experience a dramatic alteration of visual function, requiring modification of ADL. Homonymous field loss makes these patients prone to burns, motor vehicle accidents, mechanical injury from falls, or walking into objects. Explain these risks clearly to the patient and his/her family. Do not allow driving until follow-up evaluations of visual-field loss have been completed and occupational therapists and physicians have tested patient for visual function.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  Posterior cerebral artery stroke. CT scan of the brain showing hypodense areas in the right occipital lobe consistent with a recent posterior cerebral artery ischemic infarct.
	View Full Size Image
Media type:  CT

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

• Adams DS. Stroke rehabilitation: indications, outcomes, recent developments. J La State Med Soc. Nov 1996;148(11):498-502. [Medline].
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• Brandt T, Steinke W, Thie A. Posterior cerebral artery territory infarcts: clinical features, infarct topography, causes and outcome (1). The authors dedicate this paper to Michael S Pessin, MD, who died before publication. Multicenter results and a review of the literature. In: Cerebrovasc Dis. May-Jun 2000;10(3):170-82. [Medline].
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• Georgiadis AL, Yamamoto Y, Kwan ES. Anatomy of sensory findings in patients with posterior cerebral artery territory infarction. Arch Neurol. Jul 1999;56(7):835-8. [Medline].
• Ghika J, Bogousslavsky J, Henderson J. The "jerky dystonic unsteady hand": a delayed motor syndrome in posterior thalamic infarctions. J Neurol. Aug 1994;241(9):537-42. [Medline].
• Gustafsson D, Elg M. The pharmacodynamics and pharmacokinetics of the oral direct thrombin inhibitor ximelagatran and its active metabolite melagatran: a mini-review. Thromb Res. Jul 15 2003;109 Suppl 1:S9-15. [Medline].
• Hanlon RE, Dobkin BH, Hadler B. Neurorehabilitation following right thalamic infarct: effects of cognitive retraining on functional performance. J Clin Exp Neuropsychol. Jul 1992;14(4):433-47. [Medline].
• Hassid EI. Neuropharmacological therapy and motor recovery after stroke. Mil Med. May 1995;160(5):223-6.
• Hasso AN, Stringer WA, Brown KD. Cerebral ischemia and infarction. Neuroimaging Clin N Am. Nov 1994;4(4):733-52. [Medline].
• Rose FD, Brooks BM, Attree EA. A preliminary investigation into the use of virtual environments in memory retraining after vascular brain injury: indications for future strategy?. Disabil Rehabil. Dec 1999;21(12):548-54. [Medline].
• Steinke W, Mangold J, Schwartz A. Mechanisms of infarction in the superficial posterior cerebral artery territory. J Neurol. Sep 1997;244(9):571-8. [Medline].
• Traversa R, Cicinelli P, Bassi A. Mapping of motor cortical reorganization after stroke. A brain stimulation study with focal magnetic pulses. Stroke. Jan 1997;28(1):110-7. [Medline].
• Volpe BT, Krebs HI, Hogan N. Robot training enhanced motor outcome in patients with stroke maintained over 3 years. Neurology. Nov 10 1999;53(8):1874-6. [Medline].
• Yamamoto Y, Georgiadis AL, Chang HM. Posterior cerebral artery territory infarcts in the New England Medical Center Posterior Circulation Registry. Arch Neurol. Jul 1999;56(7):824-32. [Medline].
• Zweifler RM. Management of acute stroke. South Med J. Apr 2003;96(4):380-5. [Medline].

Article Last Updated: Jan 24, 2007