The posterior circulation supplies the brainstem, cerebellum, occipital lobes, and parts of the temporal lobes and thalami. Its two paired vertebral arteries fuse in the cranium to form the basilar artery, which gives off the major brainstem and cerebellar branches and terminates at the basilar tip by dividing into the two posterior cerebral arteries. Posterior circulation strokes are about 25% of all ischemic strokes but produce some of the most distinctive and clinically important syndromes — Wallenberg, top of the basilar, locked-in, PCA infarction with homonymous hemianopia. This page covers the vertebrobasilar system and the posterior cerebral artery.

The Vertebral Arteries

The vertebral arteries arise from the subclavian arteries, ascend through the transverse foramina of cervical vertebrae C6 through C1, loop around the atlas, and enter the cranium through the foramen magnum. Each is divided into four segments:

  • V1: from origin to C6 transverse foramen.
  • V2: within the transverse foramina C6-C1.
  • V3: looping around C1 and ascending toward foramen magnum.
  • V4: intracranial segment, ending where the vertebral arteries unite to form the basilar.

Vertebral artery dissection — especially after neck trauma (including chiropractic manipulation), hyperextension injuries, or apparently trivial events — is a common cause of stroke in young patients. Dissection most often involves V2 or V3 and presents with neck pain followed hours to days later by posterior circulation stroke (often Wallenberg syndrome).

Branches of the Vertebral Artery

  • Anterior spinal artery: small branches from both vertebrals unite to form the single midline anterior spinal artery, supplying the anterior two-thirds of the spinal cord.
  • Posterior spinal arteries: paired vessels from the vertebrals.
  • Posterior inferior cerebellar artery (PICA): the largest branch. Supplies the lateral medulla and the inferior surface of the cerebellum. PICA occlusion produces Wallenberg syndrome plus cerebellar features.
  • Paramedian and circumferential branches: to the medial and lateral medulla.

The Basilar Artery

Formed by the union of the two vertebral arteries at the pontomedullary junction. Runs along the ventral midline of the pons. Terminates at the basilar tip by dividing into the two posterior cerebral arteries (P1 segments). Major branches:

  • Anterior inferior cerebellar artery (AICA): from the proximal basilar. Supplies the lateral lower pons, middle cerebellar peduncle, anterior inferior cerebellum, and (via the internal auditory artery) the inner ear.
  • Pontine perforators: paramedian and circumferential branches to the pons.
  • Superior cerebellar artery (SCA): from the distal basilar, just below the bifurcation. Supplies the upper pons, lateral midbrain, and superior cerebellum.
  • Posterior cerebral arteries (PCA): terminal branches.

The Posterior Cerebral Artery (PCA)

The terminal branch of the basilar. Divided into:

  • P1 (precommunicating): from basilar tip to PComA. Gives off paramedian (thalamoperforating) arteries to the thalamus and midbrain.
  • P2 (ambient): wraps around the midbrain. Gives off thalamogeniculate arteries (to lateral thalamus) and posterior choroidal arteries.
  • P3 (quadrigeminal): in the quadrigeminal cistern.
  • P4 (calcarine and terminal): terminal cortical branches to occipital and posterior temporal cortex.

PCA Territory

  • Occipital lobe.
  • Posterior medial temporal lobe (including hippocampus).
  • Posterior corpus callosum (splenium).
  • Thalamus (via paramedian and thalamogeniculate branches).
  • Midbrain (via paramedian branches).
  • Pulvinar (via posterior choroidal branches).

Posterior Circulation Stroke Syndromes

Vertebral Artery Occlusion — Wallenberg Syndrome

The lateral medullary syndrome, from vertebral artery or PICA occlusion. Cardinal features: ipsilateral facial pain/temperature loss, contralateral body pain/temperature loss, ipsilateral Horner, ipsilateral cerebellar ataxia, vertigo, bulbar dysfunction (dysphagia, dysarthria, palatal weakness). Detailed in the medulla page.

Medial Medullary Syndrome

Anterior spinal or paramedian vertebral artery occlusion. Contralateral hemiparesis sparing the face, contralateral dorsal column sensory loss, ipsilateral tongue weakness.

AICA Syndrome

Lateral lower pons + middle cerebellar peduncle + inner ear. Ipsilateral facial weakness (CN VII), hearing loss (CN VIII), vertigo, ipsilateral facial sensory loss, ipsilateral cerebellar ataxia. Contralateral body pain/temperature loss.

SCA Syndrome

Upper lateral pons + lateral midbrain + superior cerebellum. Ipsilateral limb ataxia, ipsilateral Horner, contralateral spinothalamic loss. Large SCA infarcts can present with mass effect in the posterior fossa, requiring suboccipital decompression.

Basilar Artery Occlusion

One of the most devastating stroke syndromes. Multiple potential presentations:

  • Top of the basilar syndrome: occlusion of the distal basilar, producing bilateral PCA territory infarcts (cortical blindness, amnesia from bilateral hippocampal involvement) plus midbrain and thalamic features (altered consciousness, vertical gaze palsy, pupillary abnormalities).
  • Locked-in syndrome: bilateral ventral pontine infarction from mid-basilar occlusion. Awake patient, quadriplegia, anarthria, preserved vertical eye movements.
  • Pontine paramedian infarcts: smaller bilateral pontine lesions producing various brainstem syndromes.

Basilar occlusion has poor prognosis without intervention; mechanical thrombectomy can be life-saving in selected patients.

PCA Territory Infarction

The classical PCA stroke produces contralateral homonymous hemianopia, often with macular sparing. Other features depending on extent:

  • Alexia without agraphia: dominant PCA stroke involving left occipital cortex plus splenium of corpus callosum.
  • Prosopagnosia, color anomia: bilateral fusiform involvement (rare from PCA alone).
  • Anton syndrome: bilateral PCA territory involvement with cortical blindness and denial.
  • Memory deficits: bilateral hippocampal involvement.
  • Balint syndrome: bilateral parieto-occipital damage producing simultanagnosia, optic ataxia, ocular apraxia.

Thalamic Stroke Syndromes

From paramedian, thalamogeniculate, polar (tuberothalamic), or posterior choroidal artery occlusion. Each has a distinct picture:

  • Polar/anterior thalamic: amnesia, apathy, executive dysfunction.
  • Paramedian thalamic: altered consciousness, vertical gaze palsy. Bilateral paramedian = artery of Percheron.
  • Thalamogeniculate (VPL/VPM): contralateral hemisensory loss; thalamic pain syndrome (Dejerine-Roussy) weeks later.
  • Posterior choroidal: visual field defects, sometimes wedge-shaped sectoranopia from LGN infarction.

Vertebrobasilar Insufficiency

Transient ischemia in the vertebrobasilar territory produces episodes of vertigo, diplopia, dysarthria, ataxia, hemianopia, or other posterior circulation features. Causes include atherosclerotic vertebrobasilar disease, subclavian steal (reversal of vertebral flow in the setting of subclavian stenosis when the arm is exercised), and embolic disease.

The Posterior Circulation in Aneurysmal Disease

Aneurysms in the posterior circulation are less common than anterior but include:

  • Basilar tip aneurysm: a major site, producing SAH that often presents with altered consciousness.
  • PICA-vertebral junction aneurysm: another important site.
  • Dolichoectasia: tortuous dilation of vertebrobasilar arteries, sometimes producing brainstem compression or recurrent strokes.

🔍 Did You Know?

The top of the basilar syndrome, first described by Caplan in 1980, is one of the most dramatic and underrecognized stroke syndromes. Occlusion of the distal basilar artery — most often from cardiac embolus — produces simultaneous infarction in multiple territories: bilateral PCA (cortical blindness, hippocampal amnesia), midbrain (vertical gaze palsy, pupillary abnormalities, altered consciousness), and thalamus (more altered consciousness, possible hemiparesis from internal capsule). The patient is often profoundly altered with prominent visual and oculomotor abnormalities and minimal motor weakness — easily mistaken for metabolic encephalopathy. Recognition matters enormously because mechanical thrombectomy can be effective even relatively late in the time course of basilar occlusion compared with anterior circulation strokes.

Pitfalls and Pearls

  • Vertebral artery dissection should be considered in any young patient with posterior circulation stroke, especially with neck pain or recent trauma.
  • Wallenberg syndrome is one of the most pathognomonic stroke patterns: ipsilateral face/Horner/ataxia/bulbar + contralateral body sensory loss, no hemiparesis.
  • Top of the basilar syndrome presents with altered consciousness, vertical gaze palsy, and bilateral visual symptoms — often mistaken for metabolic cause.
  • Locked-in syndrome from basilar occlusion: patient is awake but only vertical eye movements work. Always check for command-following blinks.
  • PCA infarction classically produces homonymous hemianopia with macular sparing.
  • Alexia without agraphia is left PCA stroke (occipital + splenium).
  • Bilateral paramedian thalamic infarction (artery of Percheron) presents with coma and vertical gaze palsy.
  • AICA infarction produces ipsilateral hearing loss (the artery supplies the inner ear).
  • Mechanical thrombectomy for basilar occlusion has a longer effective time window than anterior circulation thrombectomy.
  • Cerebellar stroke can produce mass effect, brainstem compression, and obstructive hydrocephalus. Surveillance and decompression considerations are critical.

References

  1. Caplan LR. Caplan’s Stroke: A Clinical Approach. 5th ed. Cambridge University Press; 2016.
  2. Caplan LR. “Top of the basilar” syndrome. Neurology. 1980;30(1):72-79.
  3. Mattle HP, Arnold M, Lindsberg PJ, Schonewille WJ, Schroth G. Basilar artery occlusion. Lancet Neurol. 2011;10(11):1002-1014.
  4. Searls DE, Pazdera L, Korbel E, Vysata O, Caplan LR. Symptoms and signs of posterior circulation ischemia. Arch Neurol. 2012;69(3):346-351.
  5. Brazis PW, Masdeu JC, Biller J. Localization in Clinical Neurology. 7th ed. Wolters Kluwer; 2017.