The posterior cerebral artery is subdivided into 4 segments:
P1: pre-communicating segment
Originated at the termination of the basilar artery
May give rise to the artery of Percheron if present
P2: post-communicating segment
From the PCOM around the midbrain
Terminates as it enters the quadrigeminal ganglion
Gives rise to the choroidal branches (medial and lateral posterior choroidal arteries)
P3: quadrigeminal segment
Courses posteromedially through the quadrigeminal cistern
Terminates as it enters the sulk of the occipital lobe
P4: cortical segment
Within the sulci of the occipital lobe
The branches of the posterior cerebral artery are divided into two sets, ganglionic and cortical.
Central branches
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The following are central branches of the PCA, also known as 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
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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.[1]
Cortical branches
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The cortical branches are:
Anterior temporal, distributed to the uncus and the anterior part of the fusiform gyrus
Splenial, or the posterior pericallosal branch, sometimes anastomoses with the anterior cerebral artery (ACA), and may not be present if the ACA wraps around the corpus callosum
Development
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The prenatal development of the posterior cerebral arteries in the fetus comes relatively late and arises from the fusion of several embryonic vessels near the caudal ends of the posterior communicating arteries supplying the mesencephalon and diencephalon.[2] 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.[3]
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.[3]
Clinical significance
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Stroke
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Contralateral loss of pain and temperature sensations.
Visual field defects (contralateral hemianopsia with macular sparing).[4]
Prosopagnosia with bilateral obstruction of the lingual and fusiform gyri.
Bilateral homonymous hemianopsia, cortical blindness, awareness or denial of blindness; tactile naming, achromatopia (color blindness), 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.[4]
Memory defect: Hippocampal lesion bilaterally or on the dominant side only.[4]
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.[4]
Complex hallucinations: Usually nondominant hemisphere.[4]
Central territory (ganglionic branches)
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Thalamic syndrome: sensory loss (all modalities), 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.
Thalamoperforate syndrome: crossed cerebellar ataxia with ipsilateral third nerve palsy (Claude's syndrome): Dentatothalamic tract and issuing third nerve.[7]
Weber's syndrome: third nerve palsy and contralateral hemiplegia: Third nerve and cerebral peduncle.[5]
Contralateral hemiplegia: Cerebral peduncle.
Paralysis or paresis of vertical eye movement, skew deviation, sluggish pupillary responses to light, slight miosis and ptosis (retraction nystagmus and "tucking" of the eyelids may be associated): Supranuclear fibers to third nerve, interstitial nucleus of Cajal, nucleus of Darkschewitsch, and posterior commissure.
Medial surface of cerebral hemisphere, showing areas supplied by cerebral arteries. Areas supplied by the posterior cerebral artery shown in yellow.
The arteries of the base of the brain. Posterior cerebral artery labeled near center. The temporal pole of the cerebrum and a portion of the cerebellar hemisphere have been removed on the right side. Inferior aspect (viewed from below).