Cerebellar infarcts, review

based on Amarenco,The Spectrum of cerebellar infarctions. Neurology 91:41:973-979. Review.

The PICA, which comes from the termination of the VA, has a medial branch that supplies the lateral medulla, and a lateral branch that almost never does.

The AICA, which emanates from the caudal third of the BA, supplies the lateral pons, including the nuclei of V, VII, and VIII (both cochlear and vestibular),the root of the VII and VIII nn, and the spinothalamic tract. The AICA can encompass the PICA territory when the latter is hypoplastic.

The SCA arises from the rostral BA, near the ostia of the PCA and thalamoperforating arteries. It supplies the rostral cerebellum vermis and dentate nucleus. The lateral tegmentum in pons is gotten affecting the superior cerebellar peduncle, the st tract, the lateral lemniscus, corticotegmental tract, decending sympathetics and the root of IV nerve.

Clinically Amarenco "concurs with Heros" that a patient able to walk normally is unlikely to have a substantial cerebellar infarct. In addition to the symptoms in other post, including dysarthria, lateropulsion, vertigo, nausea, vomiting, posterior headache, nystagmus and dysmetria, coma is common, as are signs of brainstem or PCA involvement.

AICA infarcts (figure 3, C through F; table). Considered uncommon, AICA infarcts are certainly underestimated. They involve the lateral portion of the pons, the middle cerebellar peduncle, the flocculus, and the anterior caudal part of the Cerebellum. The main clinical manifestation is a crossed syndrome, often misdiagnosed as lateral medullary infarction (Wallenberg’s
syndrome) because of dysmetria, vestibular signs, Homer’s syndrome, facial sensory impairment, contralateral pain and temperature sensory loss in the limbs, and sometimes dysphagia. Other signs, unusual in Wallenberg’s syndrome, are severe facial palsy, deafness
with or without tinnitus, lateral gaze palsy, and multimodal sensory impairment over the face. There may be an isolated vestibular manifestation, as recently shown in a case of probable occlusion of an accessory supplementary AICA.


PICA infarcts are as frequent as SCA infarcts . If restricted to the PICA territory, they are often small in size and benign. In a clinical series, only one-fourth of 36 patients had signs of brainstem compression (all of these had full PICA territory infarct), one-fifth had
obstructive hydrocephalus, and one-ninth died from cerebellar swelling.In this series, PICA infarcts presented mainly with vertigo, headache, gait ataxia, Wallenberg’s
syndrome or appendicular ataxia, and horizontal nystagmus. Infarcts of the medial branch
may be clinically silent or present with three mainpatterns: (1) isolated vertigo often misdiagnosed as labyrinthitis with ipsilateral axial lateropulsion of trunk and gaze,SOa nd dysmetria or
un~teadiness(h~e~n ce, cerebellar signs can be minimal,
and MRI may be required for diagnosis); (3) Wallenberg’s
syndrome when the medulla is also involved.
3*32.61C.6l2in ical manifestations of infarcts of the
lateral branch of the PICA are unknown since reported
cases have been chance autopsy findings with no available
clinical information