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13809126]" pmid="13809126"Reed and Neel (1959) found only 8 in which both parents of a single patient with Huntington chorea were 60 years of age or older and normal.The clinical features developed progressively with severe increase in choreic movements and dementia.Preclinical HD individuals had substantial morphologic differences throughout the cerebrum compared to controls.The volume of cerebral cortex was significantly increased in preclinical HD, whereas basal ganglion and cerebral white matter volumes were substantially decreased.Although decreased volumes of the striatum and cerebral white matter could represent early degenerative changes, the finding of an enlarged cortex suggested that developmental pathology occurs in HD. (2007) compared psychiatric manifestations among 29 HD mutation carriers with no clinical symptoms, 20 HD mutation carriers with mild motor symptoms, 34 manifesting HD patients, and 171 nonmutation controls.The mild motor symptoms group and the manifesting HD group showed significantly higher scores for obsessive-compulsive behavior, interpersonal sensitivity, anxiety, paranoia, and psychoticism compared to the nonmutation control group.
1985) contrasted HD in 2 very large Maryland pedigrees: an African American family residing in a bayshore tobacco farming community and a white Lutheran family living in a farming community in the western Maryland foothills and descended from an immigrant from Germany.
However, the whole group of heterozygous and homozygous normal at-risk individuals showed a significantly greater number of psychiatric episodes than did their 43 spouses, suggesting stress from the uncertainty associated with belonging to a family segregating this disorder. (1995) performed extensive neuropsychologic evaluations on 8 genotype-positive individuals comparing them to 8 genotype-negative individuals from families with Huntington disease.
They found no significant differences between these 2 groups, casting further doubt on earlier reports that suggested cognitive impairments are premonitory signs of the classical neurologic syndrome of Huntington disease. (1995) performed a double-blind study on 33 persons at risk for HD who had applied for genetic testing.
Significantly inferior cognitive functioning was disclosed in gene carriers by a battery of neuropsychologic tests covering attentional, visuospatial, learning, memory, and planning functions.
Primarily, attentional, learning, and planning functions were affected. (1995) performed a prospective analysis of neuropsychologic performance and CT scans of 60 individuals with Huntington disease.