Cerebellar infarction and cerebellar hemorrhage

Sombat Muengtaweepongsa MD (Dr. Muengtaweepongsa of Thammasat University has no relevant financial relationships to disclose.)
Salvador Cruz-Flores MD (Dr. Cruz-Flores of the St. Louis University of Medicine and Director of the Souers Stroke Institute received fees from Eli Lilly for consulting and research grants from Coaxia, IMRx Therapeutics, Neurobiological Technologies Inc, and PhotoThera Inc as an investigator.)
Steven R Levine MD, editor. (Dr. Levine of the SUNY Health Science Center at Brooklyn has received honorariums from Genentech for service on a scientific advisory committee and a research grant from Genentech as a principal investigator.)
Originally released October 3, 2004; last updated December 17, 2009; expires December 17, 2012
Notice: This article has expired and is therefore not available for CME credit.

This article includes discussion of cerebellar infarction and cerebellar hemorrhage, cerebellar hematoma, and cerebellar stroke. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

Overview

Cerebellar infarct and hemorrhage account for about 2% of all strokes. Both conditions are critical neurologic disorders with potential catastrophic outcomes. They frequently present with headache, nausea and vomiting, dizziness, and a striking difficulty standing or walking. Their management often requires surgical intervention, and the prognosis is usually good when the intervention is performed before the patient becomes comatose. In this article, the authors discuss the clinical presentations associated with the different vascular territories within the cerebellum, the potential to confuse its presentation with peripheral causes of vertigo, and the usefulness of the head thrust test to differentiate between peripheral and central causes of dizziness.

Historical note and terminology

Infarction and hemorrhage are at different ends of the spectrum of vascular disease of the cerebellum; they share clinical features and some management strategies; therefore, they will be reviewed together. These 2 entities have much in common with stroke in other areas of the brain such as risk factors; however; they have distinctive clinical symptoms, signs, and prognosis. Furthermore, the acute treatment often involves a surgical intervention.

Gordon Holmes described the classical clinical signs of ataxia and atonia attributed to pure cerebellar lesions in patients with missile wounds occurring during World War I (Holmes 1917). Compared to those injuries, cerebellar strokes have a distinctive clinical picture due to the temporal profile of the disorder and the different vascular territories that can be affected. Early large case series of cerebellar hemorrhage showed that many patients died suddenly while many others had coma as their only sign. Few patients had dizziness, cranial nerve palsies, headache, contralateral hemiplegia, and conjugate eye deviation (Mitchell 1942). Other authors reported that many patients with cerebellar hemorrhage were comatose on presentation and less than half of those conscious had signs suggesting cerebellar dysfunction. Three clinical groups were recognized: those with sudden onset and rapid progression to coma; those with headache, vertigo, vomiting and ataxia; and those with gradual hydrocephalus (McKissock et al 1960).

Cerebellar infarcts were not diagnosed during life until neuroimaging became available and was sensitive enough to identify small lesions in the cerebellum. The early reported cases were patients with large infarctions and a fatal course secondary to edema, compression of the brainstem, and hydrocephalus whose typical clinical symptoms were headache, vertigo, vomiting, and gait ataxia followed by a delayed progression to coma and death (Menzies 1893; Fairburn 1956).

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