If the primary visual cortex in the occipital lobe is affected, the patient will present with contralateral homonymous hemianopia with macular sparing. This sparing is thanks to the collateral branches of the MCA that also irrigate the region of the macula.
When there is bilateral damage to the occipital cortex, the patient develops cortical blindness without awareness of their deficit and possible confabulation.
When the thalamus is affected, the patient develops contralateral hemibody pain, allodynia, and hyperalgesia, also known as thalamic pain syndrome.
Pinealomas are the most common cause of dorsal midbrain lesion, but they can also be caused by a PCA stroke. Vertical gaze palsy, nystagmus, the collier sign, and pseudo-Argyll Robertson pupils are among the symptoms.
Hemispheric damage in a PCA stroke can cause contralateral hemiparesis and hemisensory loss.
It is important to remember that the corpus callosum allows visual input to reach the parietal cortex language centers, integrating visual signals to produce language. When there is a PCA infarct in the left hemisphere (usually the dominant hemisphere), the patient will present with dyslexia.
Another possible manifestation of a PCA stroke in the left hemisphere, in the area of the splenium of the corpus callosum, is alexia without agraphia (the patient can write but not read).
When a large stroke occurs in the left hemisphere, which is usually the dominant hemisphere, in PCA territory, aphasia can happen.
When it comes to the hippocampus, a PCA stroke on one or both sides can cause memory loss and confusion.
When the corpus callosum in the right hemisphere (usually the non-dominant side) is affected by a PCA stroke, the patient will have prosopagnosia, which means they won't be able to recognize familiar faces.
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