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Neuropsychological function in patients with Gerstmann-Sträussler-Scheinker disease from the Indiana kindred (F198S).

Three patients with Gerstmann-Sträussler-Scheinker disease (GSS) caused by a serine-for-phenylalanine substitution at codon 198 of the prion protein gene (PRNP) were compared to 9 age- and education-matched non-mutation-carriers from the same large Indiana kindred (GSS-IK) on a comprehensive neuropsychological test battery. Clinically significant impairments in intelligence, secondary memory, attention and cognitive processing speed, executive ability, and manual motor skills were noted in 2 patients. The wide range and the severity of the cognitive deficits indicated generalized cerebral dysfunction consistent with global dementia. One patient, symptomatic for less than 1 year, had more selective deficits involving memory, motor skills, and verbal fluency, suggesting early subcortical involvement.[1]

References

  1. Neuropsychological function in patients with Gerstmann-Sträussler-Scheinker disease from the Indiana kindred (F198S). Unverzagt, F.W., Farlow, M.R., Norton, J., Dlouhy, S.R., Young, K., Ghetti, B. Journal of the International Neuropsychological Society : JINS. (1997) [Pubmed]
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