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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.They performed a control study of 93 neurologically healthy individuals at risk for Huntington disease.

The 61-year-old man was admitted with dysphagia and dysarthria, which had developed gradually over 2 years.

The patient had no psychologic signs, dementia, paresis, involuntary movements, ataxia, or sensory disturbance in the limbs.

(1988) found that life-table estimates of age of onset of motor symptoms have produced a median age 5 years older than the observed mean when correction for truncated intervals of observation (censoring) was made.

The bias of censoring refers to the variable intervals of observation and loss to observation at different ages.

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.

The age at onset was highly variable: some showed signs in the first decade and some not until over 60 years of age.

Shiwach and Norbury (1994) clashed with the conventional wisdom that psychiatric symptoms are a frequent presentation of Huntington disease before the development of neurologic symptoms.

A characteristic atrophy of the caudate nucleus is seen radiographically.

Typically, there is a prodromal phase of mild psychotic and behavioral symptoms which precedes frank chorea by up to 10 years.

He found the minimal lifetime prevalence of depression to be 39%.

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