olivopontocerebellar atrophies/ataxia

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Olivopontocerebellar atrophy and Friedreich's ataxia: neuropsychological consequences of bilateral versus unilateral cerebellar lesions.

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This chapter deals with neuropsychological disturbances in patients with bilateral cerebellar damage (BCD), i.e., epileptic patients chronically receiving phenytoin, patients with olivopontocerebellar atrophy (OPCA), and Friedreich's ataxia (FA) versus those with unilateral cerebellar damage (UCD),

A case of spinocerebellar ataxia type 6 mimicking olivopontocerebellar atrophy.

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Spinocerebellar ataxia type 6 (SCA6) is an autosomal dominant, slowly progressive cerebellar ataxia without multisystem involvement. We report a 57-year-old woman with genetically confirmed SCA6 who showed clinical features of olivopontocerebellar atrophy. Conventional T2-weighted and FLAIR MRI

Early onset cerebellar ataxia with retained tendon reflexes (EOCA) and olivopontocerebellar atrophy (OPCA): a computed tomographic study.

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Computed tomographic (CT) studies in olivopontocerebellar atrophies (OPCA) and 'early onset cerebellar ataxia with retained tendon reflexes (EOCA)' are few and vary widely in methodology and criteria for cerebellar and brainstem atrophy. In this prospective study, CT scan observations on 26 patients

Early onset cerebellar ataxia with retained tendon reflexes comparison with Friedreich's ataxia and olivopontocerebellar atrophy : an evoked potential study.

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14 patients with the clinical diagnosis of early onset cerebellar ataxia with retained tendon reflexes (EOCA) were evaluated by multimodal evoked potential (EP) studies. The results were compared with observations made on 10 patients with Friedreich's ataxia (FA) and 16 patients with

[Familial olivo-ponto-cerebellar atrophy with myoclonus. Limits of cerebellar myoclonic dyssynergia (Ramsay-Hunt syndrome)].

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The case is described of a woman of 26 suffering (like her mother, a brother and a sister) from a progressively degenerating cerebellar syndrome, at first considered to be hereditary cerebellar ataxia, but which, after action myoclonus appeared, was diagnosed as dyssynergia cerebellaris myoclonica

Cerebellar ataxia, dementia, pyramidal signs, cortical cataract of the posterior pole and a raised IgG index in a patient with a sporadic form of olivopontocerebellar atrophy.

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Middle-aged patients who initially present with a progressive cerebellar ataxia, in the absence of a known familial pattern are often referred to under the descriptive diagnosis of 'idiopathic' late onset cerebellar ataxia. If these patients in time develop additional pyramidal or extrapyramidal

Structural and immunocytochemical features of olivopontocerebellar atrophy caused by the spinocerebellar ataxia type 1 (SCA-1) mutation define a unique phenotype.

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Neuropathological investigations performed on autopsied brain and spinal cords from 11 patients showed that spinocerebellar ataxia type 1 (SCA-1) can be distinguished from autosomal dominant spinocerebellar ataxia linked to SCA-2 and -3 loci on chromosomes 12 and 14, spinopontine, and the

Olivo-ponto-cerebellar atrophy (Marie's ataxia).

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Olivopontocerebellar atrophy (heredocerebellar ataxia of Marie) with encephalographic findings.

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Linkage study of dominantly inherited olivo-ponto-cerebellar atrophy (OPCA) and Holmes' ataxia.

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[An autopsy case of olivopontocerebellar atrophy clinically manifested by parkinsonism and not accompanied by marked cerebellar ataxia throughout the course (author's transl)].

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The cerebellar serotoninergic system and its possible involvement in cerebellar ataxia.

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A review concerning the characteristics of the cerebellar serotoninergic system is presented. In rat, cat and oppossum, the perikarya of origin are located in the brain stem raphe nuclei and in other brainstem structures. The projections to the cerebellar layers and deep nuclei include synaptic

Treatment of cerebellar ataxia with 5-HT1A agonist.

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Effective, pharmacologic approaches to the treatment of cerebellar ataxia are lacking or inadequate. We recently reported preliminary evidence that tandospirone citrate (tandospirone), a 5-HT1A agonist, improved cerebellar ataxia in patients with Machado-Joseph disease (MJD). In the course of that

Role of Corticotropin-Releasing Factor in Cerebellar Motor Control and Ataxia.

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Cerebellar ataxia, characterized by motor incoordination, postural instability, and gait abnormality [1-3], greatly affects daily activities and quality of life. Although accumulating genetic and non-genetic etiological factors have been revealed [4-7], effective therapies for cerebellar ataxia are

A family with hereditary ataxia: HLA typing.

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In a previously unreported family with olivopontocerebellar atrophy, the kindred contained over 600 individuals in five generations. Of 83 offsping of affected individuals who over over 38.8 years of age (the mean age of the onset of disease in this family), 47 had ataxia; there was autosomal

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