Posterior Cerebral Artery Stroke Clinical Presentation

Updated: Jul 30, 2018
  • Author: Erek K Helseth, MD; Chief Editor: Helmi L Lutsep, MD  more...
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Presentation

History

Patients with posterior cerebral artery (PCA) infarcts present for neurologic evaluation with symptoms including the following:

  • Acute vision loss

  • Confusion [8]

  • New onset posterior cranium headache

  • Paresthesias

  • Limb weakness

  • Dizziness

  • Nausea

  • Memory loss

  • Language dysfunction [9]

The approach to stroke in the PCA territory is no different from the approach to 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.

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, or occipitoparietal cortex or combinations of these.

Time of onset

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) 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.

Risk factors

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.

Visual symptoms and headache

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 1 eye, attributable to a refractive error that is correctable with 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 of PCA stroke. A computed tomography (CT) scan easily can differentiate between both conditions. Additionally, a migraine is characterized by a moving, scintillating scotoma, not a fixed, bilateral, homonymous field cut.

The presence of homonymous hemianopia also helps in differentiating between a middle cerebral artery and PCA stroke, as profound hemiplegia or somatosensory loss may occur in both conditions.

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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 National Institutes of Health (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.

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 posterior cerebral artery (PCA) infarcts. [7, 10]

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.

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