Introduction

Early recognition of ischemia in the posterior circulation is important in an era of new therapeutic approaches such as thrombolysis therapy. For a long time, study of the territory of cerebellar infarcts and their related stroke syndromes has been neglected because neuroimaging most often failed to show the infarct and because the sensitivity and specificity of clinical symptoms and signs in diagnosing cerebellar strokes were low. Large cerebellar strokes mimicking posterior fossa tumours have been only diagnosed at surgery by Fairburn and Oliver and Lindgren, then recognized as a clinical entity: the cardinal signs of vertigo, headache, vomiting and gait ataxia became better known to neurologists (Fairburn & Oliver, 1956; Lindgren, 1956; Fisher et al., 1965; Lerich et al., 1970). These reports also emphasized the possibility of pressure effects leading to brainstem compression, hydrocephalus, cardiorespiratory complications and death due to either hemorrhage or edematous infarction (Fisher et al., 1965; Lerich et al., 1970). Later, Duncan et al. reported patients with PICA territory infarcts with mostly vestibular signs (Duncan, et al., 1975), and Sypert and Alvord, in a necropsy study, examined the vascular mechanisms associated with edematous pure cerebellar infarcts sparing the brainstem found at autopsy (Sypert & Alvord, 1975). However, this pseudotumoural form is rare (less than 20% of cases) and, even with CT scan, smaller cerebellar strokes have not been diagnosed. This is in constrast to other posterior circulation strokes presenting with well-defined brainstem and occipital and temporal lobes stroke syndromes. Likewise, diagrams representing the territories of cerebral arteries in anterior and posterior circulation never showed territories of the cerebellum because they simply remained unknown.