Posterior inferior cerebellar artery

The posterior inferior cerebellar artery (PICA) is usually the largest branch of the vertebral artery (VA). It typically arises from the intracranial (V4) part of the VA, below the vertebrobasilar junction.

Course: Segments of the posterior inferior cerebellar artery

From its origin, PICA follows a tortuous course around the medulla and cerebellar tonsil. Its course is divided into five segments:

• Anterior medullary segment: extends from the origin of PICA to the most prominent part of the inferior olive.

• Lateral medullary segment: This segment passes across the lateral aspect of the medulla, extending from the level of the olive to the region of the CN IX, X and XI rootlets.

• Tonsillomedullary segment: begins as PICA passes posterior to the lower cranial nerve rootlets and then courses toward the cerebellar tonsil.

• Telovelotonsillar segment: ascends along the medial surface of the tonsil and courses through the fissures between the tonsil, vermis and cerebellar hemisphere.

• Cortical segment: begins as the posterior inferior cerebellar artery reaches the suboccipital surface of the cerebellum and consists of its terminal cortical branches.

Branches

Along its course, posterior inferior cerebellar artery gives rise to perforating, choroidal and cortical branches that supply the medulla, fourth ventricle and inferior cerebellum.

• The perforating branches supply the medulla, particularly contributing to the dorsolateral region of medulla.

• The choroidal branches supply the tela choroidea and choroid plexus of the fourth ventricle,

• The cerebellar cortical branches supply the cerebellar tonsils, inferior vermis and inferior aspects of the cerebellar hemispheres.

Clinical correlate: Lateral medullary (Wallenberg/PICA) syndrome

Because PICA contributes to the blood supply of the dorsolateral medulla, interruption of this circulation can produce a dorsolateral medullary infarction and lateral medullary syndrome, also known as Wallenberg syndrome or PICA syndrome.

The clinical features reflect the important nuclei and tracts packed within the lateral medulla:

• Crossed sensory loss: Damage to the spinal trigeminal nucleus and tract causes loss of pain and temperature sensation from the ipsilateral face, whereas damage to the spinothalamic tract causes loss of pain and temperature sensation from the contralateral trunk and limbs. This produces the characteristic crossed sensory pattern because the ascending spinothalamic fibres have already crossed within the spinal cord.

• Cranial nerve dysfunction: Involvement of the nucleus ambiguus and associated CN IX and X fibres may cause dysphagia, hoarseness/dysarthria and a reduced gag reflex on the side of the lesion.

• Cerebellar and vestibular signs: Damage to the inferior cerebellar peduncle, spinocerebellar fibres or cerebellar connections produces ipsilateral ataxia and incoordination, often with a tendency to fall toward the affected side. Involvement of the vestibular nuclei and vestibulocerebellar connections produces vertigo, nystagmus, nausea and vomiting.

• Autonomic dysfunction: Damage to the descending hypothalamospinal sympathetic fibres produces ipsilateral Horner syndrome, characterised by ptosis, miosis and decreased sweating (anhidrosis) on the affected side.

A useful distinguishing feature is that the corticospinal tract and hypoglossal nerve structures lie more medially and are usually spared in a classic lateral medullary lesion. Therefore, unlike medial medullary syndrome, prominent limb paralysis and ipsilateral tongue weakness or deviation are not typical features.