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The posterior cerebral artery (PCA) is one of a pair of arteries that supply oxygenated blood to the occipital lobe, part of the back of the human brain. It begins near where the posterior communicating artery and the basilar artery join, and connects with the middle cerebral artery of the same side and internal carotid artery via the posterior communicating artery.

Posterior cerebral artery
Gray's Anatomy plate 517 brain.png
The outer surface of the human brain, with the area supplied by the posterior cerebral artery shown in yellow.
Circle of Willis en.svg
The arterial circle and arteries of the brain. The posterior cerebral arteries (bottom forks) arise from the basilar artery (center).
Details
Sourcebasilar artery (most common in adults)
Veincerebral veins
Suppliesoccipital lobe of cerebrum
Identifiers
Latinarteria cerebri posterior
Acronym(s)PCA
MeSHD020769
TAA12.2.07.082
FMA50583
Anatomical terminology

StructureEdit

The branches of the posterior cerebral artery are divided into two sets, ganglionic and cortical:

Central branchesEdit

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 cerebral artery

(Posterior) choroidal branchesEdit

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.

Cortical branchesEdit

The cortical branches are:

  • Anterior temporal, distributed to the uncus and the anterior part of the fusiform gyrus
  • Posterior temporal, to the fusiform and the inferior temporal gyri
  • Lateral occipital, which branches into the anterior, middle and posterior inferior temporal arteries
  • Medial occipital, which branches into the:
  • 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

DevelopmentEdit

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.[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 significanceEdit

StrokeEdit

Signs and symptoms:Structures involved

See: Posterior cerebral artery syndrome

Peripheral territory (Cortical branches)Edit

  • Homonymous hemianopia (often upper quadrantic): Calcarine cortex or optic radiation nearby.
  • Bilateral homonymous hemianopia, 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.
  • Memory defect: Hippocampal lesion bilaterally or on the dominant side only.
  • Topographic disorientation and prosopagnosia: Usually with lesions of nondominant, calcarine, and lingual gyrus.
  • Simultanagnosia, hemivisual neglect: Dominant visual cortex, contralateral hemisphere.
  • 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)Edit

  • 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.
  • 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 (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.
  • Contralateral rhythmic, ataxic action tremor; rhythmic postural or "holding" tremor (rubral tremor): Dentatothalamic tract.

See alsoEdit

Additional imagesEdit

 
Arteriogram of the arterial supply.

ReferencesEdit

  1. ^ Atlas of Human Anatomy, Frank Netter
  2. ^ Osborn, Anne G.; Jacobs, John M. (1999), Diagnostic Cerebral Angiography, Lippincott Williams & Wilkins, p. 153, ISBN 978-0-397-58404-8
  3. ^ a b Krayenbühl, Hugo; Yaşargil, Mahmut Gazi; Huber, Peter; Bosse, George (1982), Cerebral Angiography, Thieme, pp. 163–165, ISBN 978-0-86577-067-6

External linksEdit