olivopontocerebellar atrophies/dopaminas

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Preclinical impairment of the striatal dopamine transporter system in sporadic olivopontocerebellar atrophy: studied with [(123)I]beta-CIT and SPECT.

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We investigated whether the dopamine (DA) transporter system is impaired in sporadic olivopontocerebellar atrophy (sOPCA) patients without clinical parkinsonism using the DA transporter radiotracer [(123)I]beta-CIT [2beta-carboxymethoxy-3beta-(4-iodophenyl)tropane] and single-photon emission

3-Acetylpyridine-induced degeneration of the nigrostriatal dopamine system: an animal model of olivopontocerebellar atrophy-associated parkinsonism.

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The effects of 3-acetylpyridine (3-AP) administration to rats on the mesotelencephalic dopamine system were assessed. A single 3-AP injection resulted in biochemical and immunohistochemical evidence of degeneration of the nigrostriatal dopamine system. Six weeks after 3-AP treatment decreases in

Dopamine deficiency in the weaver mutant mouse: an animal model of olivopontocerebellar atrophy.

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The dopamine system in weaver mutant mice, a model of cerebellar atrophy, was studied. Dopamine levels of 6-week-old weaver mice were 37%, 44%, 34%, and 41% of levels in age-matched controls in the cerebral cortex, hippocampus, septal region and striatum, respectively. Noradrenaline levels did not

Striatal monoamine neurotransmitters and metabolites in dominantly inherited olivopontocerebellar atrophy.

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We measured the levels of the monoamine neurotransmitters and metabolites in striatum of 14 patients with end-stage dominantly inherited olivopontocerebellar atrophy (OPCA). On average, dopamine levels were reduced in putamen (-53%), caudate (-35%), and nucleus accumbens (-31%). However, individual

[Extrapyramidal manifestations in hereditary olivopontocerebellar atrophy--clinical study of 10 cases in three affected pedigrees].

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We studied 3 pedigrees affected with autosomal dominant olivopontocerebellar atrophy (OPCA), and clinical features of 10 patients were reported. Clinically, 6 cases were dominated with cerebellar ataxia, one with Parkinsonism, and three with choreiform movements. Furthermore, they were characterized

L-dopa in Parkinsonism associated with cerebellar dysfunction (probable olivopontocerebellar degeneration).

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Two patients with combined cerebellar and Parkinsonian features consistent with olivopontocerebellar degeneration were treated with long term oral l-dopa. Both patients showed improvement of the Parkinsonian symptoms but the cerebellar symptoms were unchanged. It is suggested that the Parkinsonian

Amantadine hydrochloride treatment in olivopontocerebellar atrophy: a long-term follow-up study.

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The efficacy of amantadine, a dopamine-releasing agent and antagonist of the N-methyl-D-aspartate glutamate receptor, was evaluated in patients with olivopontocerebellar atrophy. By contrast to an untreated control group whose terminal performance deteriorated on 8 of 8 measurements of reaction time

3-Acetylpyridine results in degeneration of the extrapyramidal and cerebellar motor systems: loss of the dorsolateral striatal dopamine innervation.

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3-Acetylpyridine (3-AP) administration to rats results in degeneration of the dopamine (DA) innervation of the striatum as well as degeneration of the olivocerebellar system. We now report that administration of this pyridine neurotoxin results in a decrease in striatal DA concentration which is

Dopamine agonists suppress visual-cortical reflex myoclonus.

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Two patients with a diagnosis of olivo-ponto-cerebellar atrophy developed cortical reflex myoclonus to visual (flash) and somaesthetic stimuli. Oral treatment with levodopacarbidopa (1000/100 mg) or subcutaneous administration of apomorphine (1 mg) abolished the visually-triggered myoclonus, without

Presynaptic parkinsonism in olivopontocerebellar atrophy: clinical, pathological, and neurochemical evidence.

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The substrate for olivopontocerebellar atrophy parkinsonism is obscure due to the lack of clinical and pathological reports and the absence of studies on dopamine receptors in this entity. We describe a patient with olivopontocerebellar atrophy whose clinical presentation was levodopa-responsive

3-Acetylpyridine neurotoxicity to the nigrostriatal dopamine system in mice.

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Employing tyrosine hydroxylase (TH) immunohistochemistry, the neurotoxic effects of 3-acetylpyridine (3-AP), a potent neurotoxin selective to olivocerebellar climbing fibers, on the mesencephalic dopamine systems were investigated in mice. Systemic injections of 3-AP resulted in a large loss of

Striatal dihydroxyphenylalanine decarboxylase and tyrosine hydroxylase protein in idiopathic Parkinson's disease and dominantly inherited olivopontocerebellar atrophy.

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We measured the levels of dopamine, tyrosine hydroxylase (TH) protein, and dihydroxyphenylalanine (DOPA) decarboxylase (DDC) protein in the striatum of 10 patients with idiopathic Parkinson's disease (PD) and 23 patients with dominantly inherited olivopontocerebellar atrophy (OPCA). The levels of

Dominantly inherited olivopontocerebellar atrophy from eastern Cuba. Clinical, neuropathological, and biochemical findings.

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A form of dominantly inherited olivopontocerebellar atrophy (OPCA) occurs commonly in persons of Spanish ancestry in northeastern Cuba. Its prevalence in the Province of Holguin is 41 per 100,000, a figure much higher than that found in western Cuba or in other parts of the world. The high

[A case report of Shy-Drager disease].

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Shy and Drager in 1960 first described a disease of adult onset characterized by the progressive development of autonomic deficits. The most frequent symptoms are related to orthostatic hypotension, impaired gastrointestinal motility, and urinary and sexual dysfunction. Recently the syndrome has

Biogenic amine metabolites and thiamine in cerebrospinal fluid in heredo-degenerative ataxias.

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BACKGROUND The aims of the present study were: i) to measure levels of the dopamine metabolite homovanillic acid (HVA), the serotonin metabolite 5-hydroxindoleacetic acid (5HIAA) and precursor tryptophan, as well as the noradrenaline metabolite 3-methoxy-4-hydroxyphenylethylene glycol (MHPG) and

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