The branches of the posterior cerebral artery are divided into two sets, ganglionic and cortical:
Central branches
Also known as the perforating branches:
Thalamoperforating and thalamogeniculate or postero-medial ganglionic branches: a group of small arteries which arise at the commencement of the posterior cerebral artery: these, with similar branches from the posterior communicating, pierce the posterior perforated substance, and supply the medial surfaces of the thalami and the walls of the third ventricle.
Peduncular perforating or postero-lateral ganglionic branches: small arteries which arise from the posterior cerebral artery after it has turned around the cerebral peduncle; they supply a considerable portion of the thalamus.
(Posterior) choroidal branches
Not to be confused with the Anterior choroidal artery The posterior choroidal branches of the posterior cerebral artery are sometimes referred to as a single posterior choroidal artery.
Lateral posterior choroidal branches: small branches to the cerebral peduncle, fornix, thalamus, caudate nucleus, and choroid plexus of the lateral ventricle.
Cortical branches
The cortical branches are:
Anterior temporal, distributed to the uncus and the anterior part of the fusiform gyrus
The development of the PCA in fetal brain comes relatively late and arises from the fusion of several embryonic vessels near the caudal end of the PCommA supplying the mesencephalon and diencephalon of the fetus. The PCA begins as such, as a continuation of the PCommA in the fetus with only 10–30% of fetuses having a prominent basilar origin. The fetal carotid origin of the PCA usually regresses as the vertebral and basilar arteries develop with the PCommA reducing is size. In most adults, the PCA sources from the anterior portion of the basilar artery. Only about 19% of adults retain PCommA dominance of the PCA with 72% having dominant basilar origin, and the rest having either equal prominence between PCommA and basilar artery, or a single exclusive source.
Clinical significance
Stroke
Contralateral loss of pain and temperature sensations.
Visual field defects.
Prosopagnosia with bilateral obstruction of the lingual and fusiform gyri.
Bilateral homonymous hemianopia, cortical blindness, awareness or denial of blindness; tactile naming, achromatopia, failure to see to-and-fro movements, inability to perceive objects not centrally located, apraxia of ocular movements, inability to count or enumerate objects, tendency to run into things that the patient sees and tries to avoid: Bilateral occipital lobe with possibly the parietal lobe involved.
Verbal dyslexia without agraphia, color anomia: Dominant calcarine lesion and posterior part of corpus callosum.
Memory defect: Hippocampal lesion bilaterally or on the dominant side only.
Topographic disorientation and prosopagnosia: Usually with lesions of nondominant, calcarine, and lingual gyrus.
Unformed visual hallucinations, peduncular hallucinosis, metamorphopsia, teleopsia, illusory visual spread, palinopsia, distortion of outlines, central photophobia: Calcarine cortex.
Complex hallucinations: Usually nondominant hemisphere.
Central territory (Ganglionic branches)
Thalamic syndrome: sensory loss, spontaneous pain and dysesthesias, choreoathetosis, intention tremor, spasms of hand, mild hemiparesis, contralateral hemianaethesia: Posteroventral nucleus of thalamus; involvement of the adjacent subthalamus body or its afferent tracts.
Weber's syndrome: third nerve palsy and contralateral hemiplegia: Third nerve and cerebral peduncle.
Contralateral hemiplegia: Cerebral peduncle.
Paralysis or paresis of vertical eye movement, skew deviation, sluggish pupillary responses to light, slight miosis and ptosis : Supranuclear fibers to third nerve, interstitial nucleus of Cajal, nucleus of Darkschewitsch, and posterior commissure.
