A double blind evaluation of cognitive decline in a Norwegian cohort of asymptomatic carriers of Huntington's disease

Previous studies investigating subclinical signs of cognitive decline in presymptomatic carriers of Huntington's disease (HD) have shown conflicting results. The current study examines cognition in 105 at-risk individuals, using a broad neuropsychological test battery and adopting strict inclus...

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Bibliographic Details
Published in:Journal of clinical and experimental neuropsychology 2010-07, Vol.32 (6), p.590-598
Main Authors: van Walsem, Marleen R., Sundet, Kjetil, Retterstøl, Lars, Sundseth, Øyvind
Format: Article
Language:English
Subjects:
Adult
Adult and adolescent clinical studies
Analysis of Variance
Asymptomatic
Biological and medical sciences
Cognition
Cognition Disorders - diagnosis
Cognition Disorders - etiology
Cognition Disorders - genetics
Cohort Studies
Cytosine-adenine-guanine
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Double-Blind Method
Female
Humans
Huntington Disease - complications
Huntington Disease - genetics
Huntington's disease
Male
Medical sciences
Middle Aged
Nervous system (semeiology, syndromes)
Nervous system as a whole
Neurology
Neuropsychological Tests
Norway - epidemiology
Organic mental disorders. Neuropsychology
Proximity to disease onset
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Retrospective Studies
Trinucleotide Repeats - genetics
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Summary:Previous studies investigating subclinical signs of cognitive decline in presymptomatic carriers of Huntington's disease (HD) have shown conflicting results. The current study examines cognition in 105 at-risk individuals, using a broad neuropsychological test battery and adopting strict inclusion criteria for attaining a homogeneous sample. Results obtained by analyses of variance and effect size calculations indicate no clinical evidence of significant cognitive decline in asymptomatic HD carriers very far from onset of illness compared to noncarriers. Closeness to disease onset amongst gene carriers influenced cognition negatively whereas cytosine-adenine-guanine (CAG) repeat size did not. The findings call for longitudinal follow-up studies using a combination of clinical instruments and experimental paradigms to pinpoint when subtle cognitive deficits occur and within which of the cognitive domains.
ISSN:1380-3395
1744-411X
DOI:10.1080/13803390903337878