Cases reported "Athetosis"

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1/6. Possible mechanisms in infants for selective basal ganglia damage from asphyxia, kernicterus, or mitochondrial encephalopathies.

    magnetic resonance imaging and neuropathologic studies have demonstrated remarkably selective patterns of injury to subregions of the basal ganglia in children. Examples are kernicterus and certain mitochondrial encephalopathies, which cause selective injury to the globus pallidus, and near-total perinatal asphyxia, which causes lesions in the putamen and thalamus. To explain the differential vulnerability of nuclei within millimeters of each other, we hypothesize that their locations within the neurotransmitter-specific circuitry of the basal ganglia motor loop are important. In severe hypoxic-ischemic encephalopathy, excitatory glutamatergic pathways into the putamen and thalamus are overactive, but the globus pallidus might be protected because its activity is silenced by inhibitory neuronal activity. In contrast, the relatively high resting neuronal activity in the globus pallidus might make it more vulnerable to less intense, subacute oxidative stresses from mitochondrial toxins such as bilirubin or from genetic mitochondrial disorders. This hypothesis has implications for designing neuroprotective therapies and for treating associated chronic movement disorders.
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2/6. Hemidystonia and hemichoreoathetosis as an initial manifestation of moyamoya disease.

    OBJECTIVE: To describe hemidystonia and hemichoreoathetosis in an adult patient with moyamoya disease without a previous history of cerebrovascular accident. DESIGN: Case report. SETTING: Tertiary care center. PATIENT: A 22-year-old woman suddenly developed dystonic spasms in her left hand and left foot after a severe emotional stress. The dyskinesia gradually subsided over the next 4 months. Five months after the onset, she suddenly developed choreoathetoid movement in her right hand and right foot. MAIN OUTCOME AND RESULTS: The patient had both somatic and cortical sensory deficits in the right hand and right foot. magnetic resonance imaging of the brain showed an infarction at the right putamen and lesions involving the right frontal lobe and the left frontotemporoparietal lobe. Magnetic resonance cerebral angiography showed severe stenoses of both internal carotid arteries at the supraclinoid portion and numerous collateral vessels, compatible with moyamoya disease. Single photon emission tomography of the brain showed hypoperfused areas at the right frontal and left frontotemporoparietal lobes. The choreoathetosis of the right limbs improved markedly, along with improvement of sensory deficits. CONCLUSIONS: To our knowledge, this is the first report of an adult patient presenting with hemidystonia and hemichoreoathetosis as the initial manifestations of moyamoya disease. Arch Neurol. 2000;57:1510-1512
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3/6. Bielschowsky bodies (Lafora bodies of Bielschowsky type): report of a case associated with Rosenthal fibers in the brain stem.

    Bielschowsky bodies are an uncommon type of polyglucosan body. Similar to Lafora bodies, they are characteristically identified within neuronal perikarya and neurites. However, they lack the diffuse distribution of Lafora bodies, and instead are typically restricted to the external pallidum, often in association with status marmoratus or atrophy of the putamen. Fewer numbers of Bielschowsky bodies have also been identified in other areas such as the substantia nigra, putamen and inner globus pallidus. We report an additional case with Bielschowsky bodies in an 18-year old female with cerebral palsy. This case demonstrated multifocal Bielschowsky bodies and abundant Rosenthal fibers in the midbrain and pons. To our knowledge the association of Bielschowsky bodies with this peculiar distribution of Rosenthal fibers has not previously been reported.
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4/6. Delayed choreoathetosis following acute carbon monoxide poisoning.

    Ten days after accidental exposure to carbon monoxide, a 17-year-old youth developed transitory choreoathetosis of both arms, face, and neck, with moderate dysarthria. CT revealed symmetric bilateral infarction in the head of the caudate nucleus, the putamen, and the small parts of the anterolateral globus pallidus.
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5/6. Glutaric acidemia: a metabolic disorder causing progressive choreoathetosis.

    A boy with glutaric acidemia had psychomotor retardation first noted at age 6 months, recurrent metabolic acidosis, and a progressive quadriparesis with choreoathetosis. He died at age 3 1/2 years. Cultured skin fibroblasts lacked glutaryl-coa dehydrogenase activity. There was a biochemical, but not a clinical, response to dietary restriction of lysine and tryptophan. The caudate and putamen of the brain showed severe loss of nerve cells and fibers with proliferation of astrocytes, as well as markedly reduced gamma-aminobutyric acid and glutamate decarboxylase activity.
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6/6. Paroxysmal kinesigenic choreoathetosis associated with prenatal brain damage.

    We describe a 15 year old patient with paroxysmal kinesigenic choreoathetosis. Neurological examinations revealed a paresis of the right arm and hand that was similar to ulnar nerve palsy, a right homonymous hemianopsia and an ocular movement disturbance of smooth pursuit to left. Attacks of dystonic spasms began abruptly, usually following running, and lasted less than 5 min. magnetic resonance imaging displayed a linear area of increased signal in the T2-weighted images along the lateral margin to the left putamen, atrophies of the frontal and temporal opercula and a large porencephalic cyst in the left parieto-temporo-occipital region. A cerebral blood flow study with single photon emission computed tomography showed hypoperfusion of the lenticular nucleus and the regions corresponding to the atrophies and the porencephalic cyst. Electroencephalograms during the attacks could not demonstrate epileptic abnormality. Only the neuronal plasticity of an immature brain could explain the discrepancy between the observed huge lesions of the brain and the minor neurological symptoms present. Attacks of paroxysmal kinesigenic choreoathetosis might occur when the basal ganglia maturate to some extent, even if the lesions in the brain were caused before birth.
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