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Anatomically, each thalamus lies rostral to the brainstem, lateral to the third ventricle, and medial to the internal capsule. As most blood to the thalamus arrives from the tip of the basilar artery and the proximal portions of the posterior cerebral arteries (PCAs), thalamic lesions may be associated with simultaneous lesions in the midbrain or in the distal territory of the PCA. Microangiopathy is the cause of most lateral thalamic infarcts although embolic sources are occasionally found. Large thalamic hemorrhages involve more nuclei and tracts, with or without ventricular extension, resulting in overlapping clinical syndromes. Common features seen in patients with thalamic hemorrhages include rapid onset of symptoms, inconstant impairment of consciousness even in large size hematomas, and a relatively good prognosis as compared with that for hemorrhages in the pons and basal ganglia. Venous thrombosis of the deep cerebral venous system usually leads to bilateral thalamic edema.
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.
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