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.

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.

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 and each PCA is divided into four segments (P1-P4)
P1: extends from origin of the PCA to the posterior communicating artery (PCOM)
P2: includes from junction with PCOM to its major branch, the lateral posterior choroidal artery, which supplies the posterior thalamus
P3/P4: distal segments of the PCA whose branches circulate blood to cortical regions, most importantly the undersurface of the temporal lobe, the posterior 1/3 of the interhemispheric surface, occipital pole, visual cortex, and splenium of the corpus callosum.

Anatomic localization of the point of vascular occlusion in the PCA infarcts may be simplified into (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 strokes, involving only cortical structures (P3,P4 branch areas)

Patients with PCA infarcts present with symtptoms such as:
- acute vision loss
- confusion
- new onset posterior cranium headache
- paresthesias
- limb weakness
- dizziness
- nausea
- memory loss
- language dysfunction

The most common examination finding is a homonymous visual field cut, usually a complete hemianopia, caused by a lesion in the contralateral occipital lobe.

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. 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)

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

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