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Cerebellar outflow lesions: a comparison of movement deficits resulting from lesions at the levels of the cerebellum and thalamus.

Previous work has shown that lesions in the lateral cerebellum involving the dentate nucleus impair both reaching and pinching movements in humans and monkeys. This study addressed the question of whether disruption of the cerebellar-thalamo-cortical pathway at the level of the thalamus would produce behavioral deficits similar to those seen after dentate damage. We compared the performance of both reaching and pinching movements in patients with lateral cerebellar lesions and in patients with discrete lesions of the ventrolateral thalamus. The patients with thalamic lesions had minimal or no sensory loss and no corticospinal signs, suggesting that the abnormal movements were due to disruption of the cerebellar projection to the thalamus. We found that lesions of the ventrolateral thalamus resulted in impaired pinching movements, but remarkably normal reaching movements with the exception of a slight tremor. This is in contrast to the profound pinching and reaching impairments of patients with lateral cerebellar lesions involving the dentate nucleus. Implications about the functional organization of cerebellar output are discussed.

Adult↗

Clinical observations in the acute phase of cerebellar hemorrhage and infarction.

Three cases of cerebellar hemorrhage and 5 of cerebellar infarction, diagnosed by brain CT, were examined from the early phase of the onset. All of our cases were mild to moderate in severity and were cured satisfactorily within 3 to 8 weeks of medical treatment. Dizziness and nausea were the commonest symptoms and cerebellar and other CNS signs could be detected only for a short period in some of the cases. Although neuro-otological examinations, especially gaze nystagmus, eye tracking and positional nystagmus tests, were useful for diagnosing the central vestibular lesion, no definite indication could be drawn in order to differentiate between cerebellar hemorrhage and infarction. Therefore, it is considered difficult in such mild cerebellar strokes to establish correct diagnosis by physical examinations alone. It was concluded that if central vestibular disorder is suspected, prompt brain CT examination is necessary in order to diagnose mild cases of cerebellar vascular diseases.

Cerebellar Diseases↗

Immunological characterization of a neuronal antibody (anti-Tr) associated with paraneoplastic cerebellar degeneration and Hodgkin's disease.

We studied an autoantibody (called anti-Tr), found in the serum and CSF of five patients with paraneoplastic cerebellar degeneration (PCD) and Hodgkin's disease (HD). Anti-Tr antibodies labelled the cytoplasm of Purkinje cells of human and rat cerebellum. The molecular layer of rat cerebellum showed a characteristic dotted pattern suggestive of immunoreactivity of dendritic spines of Purkinje cells. Patients with cerebellar disorders without HD (159) or HD without PCD (30) did not harbor anti-Tr antibodies. Immunoblots of human Purkinje cells or rat and mouse cerebellum were negative. Anti-Tr antibodies, as defined in this study, appear specific for HD-associated PCD. The immunohistochemical pattern described in the rat cerebellum coupled with the absence of reactivity in the immunoblot may be used to identify anti-Tr antibodies.

Adolescent↗