huntington disease/crise épileptique

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Juvenile Huntington's disease presenting as difficult-to-treat seizure and the first episode of psychosis.

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OBJECTIVE The objective was to describe a case of juvenile Huntington's disease that first presented with seizures and psychosis. METHODS A male patient with no history of epilepsy and psychiatric disorder had his first seizure at the age of 20 years, which was followed by 3 years of psychotic

Psychogenic non-epileptic seizures in early Huntington's disease.

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Huntington's disease (HD) is a neurodegenerative condition characterised by motor dysfunction with involuntary movements and loss of voluntary control, cognitive deterioration and psychiatric problems. We report a 51-year-old man with early HD who experienced stereotyped episodes of repetitive,

R6/2 Huntington's disease mice develop early and progressive abnormal brain metabolism and seizures.

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A hallmark feature of Huntington's disease pathology is the atrophy of brain regions including, but not limited to, the striatum. Though MRI studies have identified structural CNS changes in several Huntington's disease (HD) mouse models, the functional consequences of HD pathology during the

Seizures in juvenile Huntington's disease: frequency and characterization in a multicenter cohort.

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Little is known about the epilepsy that often occurs in the juvenile form of Huntington's disease (HD), but is absent from the adult-onset form. The primary aim of this study was to characterize the seizures in juvenile HD (JHD) subjects with regard to frequency, semiology, defining EEG

Structured cueing on a semantic fluency task differentiates patients with temporal versus frontal lobe seizure onset.

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Patients with frontal lobe dysfunction (e.g., Huntington's disease) reportedly benefit more from cueing on measures of semantic fluency than do patients with damage to temporal lobe structures (e.g., Alzheimer's disease). This differential benefit from cueing suggests that different neurocognitive

Huntington disease in a 9-year-old boy: clinical course and neuropathologic examination.

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Huntington disease is a dominantly inherited, neurodegenerative disorder, usually with onset in the fourth to fifth decade of life but in a small proportion of patients before the age of 20 years. The early-onset form, juvenile Huntington disease, is clinically different from that of more common

From mild ataxia to huntington disease phenocopy: the multiple faces of spinocerebellar ataxia 17.

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Introduction. Spinocerebellar ataxia 17 (SCA 17) is a rare autosomal dominant cerebellar ataxia (ADCA) caused by a CAG/CAA expansion in the TBP gene, reported from a limited number of countries. It is a very heterogeneous ADCA characterized by ataxia, cognitive decline, psychiatric symptoms, and

Limbic neurogenesis/plasticity in the R6/2 mouse model of Huntington's disease.

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Huntington's disease is an inherited neurodegenerative condition characterized by movement disorders, and mood and cognitive disturbance. Mammalian neurogenesis persists into adulthood in the subventricular zone and dentate gyrus of the hippocampus. Neurogenesis is abnormal in the dentate gyrus in

Regional cerebral glucose metabolism differs in adult and rigid juvenile forms of Huntington disease.

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A 7-year-old girl with the juvenile form of Huntington disease is described. She had personality changes, speech and gait disturbances, diffuse rigidity, dementia, and a well-documented family history of Huntington disease. Electroencephalography revealed bilateral epileptic foci; however, she had

Mice transgenic for the human Huntington's disease mutation have reduced sensitivity to kainic acid toxicity.

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The mechanism underlying the pathology of Huntington's disease (HD) is unknown, although there is substantial evidence supporting a role for excitotoxicity. The discovery of abnormal aggregations of protein in the brains of patients with HD, as well as in the brains of transgenic mice modeling this

Huntington disease in children: genotype-phenotype correlation.

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Huntington disease is a neurodegenerative disorder of adulthood; however, a subset of early-onset patients exists, representing 1% of all HD patients. We reviewed a population of 155 HD-families to determine the frequency, molecular and clinical characteristics of children with an onset before the

[Huntington chorea in children].

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BACKGROUND The onset of Huntington's disease, a dominantly inherited degeneration of the basal ganglia, usually occurs in middle age; cases of childhood onset are rare. METHODS Case 1. A boy from a family including several cases of Huntington's disease gradually developed behavior disorders from the

Hospitalizations of Children with Huntington's Disease in the United States.

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UNASSIGNED Juvenile Huntington's disease (JHD) is a childhood-onset neurodegenerative disorder. Although it is caused by the same pathologic expansion of CGA repeats as adult-onset Huntington's disease, JHD has distinct clinical features. Most clinical research in HD focuses in the adult-onset

[Huntington chorea in childhood].

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By the case report of a 7 years old girl problems and difficulties in diagnosing early manifested Chorea Huntington are discussed. Dementia, rigor and akinesis are the presenting signs; choreatic movements are usually not present. Seizures occur frequently. Family history gives important

Anaesthesia and juvenile Huntington's disease.

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Juvenile Huntington's Disease (JHD) is an involuntary movement disorder that comprises both neurological and psychiatric symptoms. Whilst it has many similarities to Huntington's Disease, it is regarded as a separate clinical entity. The anaesthetic plan should be based on careful assessment of the

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