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Symptoms of Posterior cerebral artery infarct

Origin of Posterior cerebral artery
  • The two PCAs are the terminal branches of the basilar artery in majority of people
  • In 20%—25% one of the posterior cerebral artery (PCAs) may originate from the internal carotid artery (ICA) via a posterior communicating artery
The clinical presentation of PCA territory infarction is determined by the  
  • Site of occlusion 
  • Availability of collaterals. 
1.Occlusion of the precommunal PI segment results in midbrain, thalamic, and hemispheric infarction.
2.Occlusion of the PCA in the proximal ambient segment before branching in the thalamogenictulate pedicle results in lateral thalamic and hemispheral symptoms 
3.Sometimes the occlusions may affect a single PCA branch, primarily the calcarine artery cause a large hemispheric infarction of the PCA territory.
Causes of PCA infarct
PCA infarct may be due to
  • Embolic
  • Thrombotic
  • Migrainous
  • Intrinsic atherosclerotic disease
  • PCA infarcts can also occur  due to compression of the artery against the tentorium during uncal herniation
Whether embolic, thrombotic, migrainous, or due to intrinsic atherosclerotic disease, partial syndromes of the PCA are the rule
1.Visualfield defect in PCA infarct
1.Infarction in the distribution of the hemispheric branches of the PCA may cause a contralateral homonymous hemianopia
This is due to infarction of
  • Striate cortex
  • Optic radiations
  • Lateral geniculate body
There is partial or complete macular sparing if the infarction does not reach the occipital pole.
2.The visualfield defect may be sometimes limited to a quadrantanopia. 
A superior quadrantanopia is due to infarction of the striate cortex inferior to the calcarine fissure or due to involvement of the inferior optic radiations present  in the temporo-occipital lobes.
An inferior quadrantanopia is the caused by an infarction of the striate cortex superior to the calcarine fissure or due to the superior optic radiations in the parietooccipital lobes
3.Complex visual changes observed in  PCA infarct are 
  • Formed or unformed visual hallucinations
  • visual and color agnosias 
  • Prosopagnosia.
Right hemispheric PCA infarctions may result in cause contralateral visual field neglect
2.Sensory findings in PCA infarct
Some alteration of sensation are also observed in PCA infarct
They  are paresthesiae, or altered position, pain, and temperature sensations
Sensors findings are due to thalamic ischemia  as a result of occlusion  of the precommunal or proximal postcommnual segments of the PCA
Thalamoparietal ischemia due to occlusion of the more distal PCA or its parieto-occipital branches
Brainstem ischemia is caused by vasoocclusive disease in the proximal vertebrobasilar arterial system
3.Alexia without agraphia (pure word blindness)
Infarction in the area of distribution of the callosal branches of the Posterior cerebral artery (PCA) tha affect  the left occipital region and the splenium of the corpus callosum results in alexia without agraphia (pure word blindness), occasionally this is associated with color anomia and object and photographic anomia .
In this syndrome, patients is able to write, speak, and spell normally but are they are unable to read words and sentences. The ability to name letters and numbers is intact, but there may be inability to name colors, objects, and photographs.
 .4.Behavioural disturbance in PCA infarct
Agitated delirium is seen with unilateral or bilateral penetrating mesiotemporal infarctions .
Large infarctions in the left posterior temporal artery territory may produce an anomic or transcortical sensory aphasia
Infarctions in the area of distribution of the penetrating branches of the PCA to the thalamus can result in aphasia
If the left pulvinar is involved, akinetic mutism, global amnesia, and the Dejerine-Roussy syndrome can be seen
5.Occlusion of calcarine artery
Occlusion of calcarine artery may be associated with pain in the ipsilateral eye .
Bilateral infarctions in the area of distribution of the PCA may result in bilateral homonymous hemianopia.
Anton’s syndrome
Bilateral occipital or occipitoparietal infarctions may cause  cortical blindness with preserved pupillary reflexes. Patients often deny or unaware of their blindness this is called as Anton’s syndrome.
Bilateral altitudinal visual held defects rarely result from bilateral occipital lobe infarcts
Infarction in the territory of the hemispheric branches of the PCA may also be accompanied by formed or unformed visual hallucinations called as release hallucinations ,
Visual and color agnosias
Prosopagnosia (agnosia for familiar faces). 
Apraxia of ocular movements is often present with bilateral lesions.
Balints syndrome
Some patients with bilateral occipital or parietooccipital infarctions present with  Balints syndrome.
Some patient with Proximal PCA occlusion may simulate MCA occlusion when it result in
  • Hemiparesis
  • Hemianopsia
  • Hemispatial neglect
  • Aphasia
  • Sensory  inattention .
Cortical signs are probably explained by thalamic involvement