Neuropsychological abnormalities in first degree relatives of patients with familial Parkinson’s disease
- Kathy Dujardina,b,
- Alain Duhamelc,
- Estelle Becqueta,
- Christine Grunberga,
- Luc Defebvrea,
- Alain Desteea
- aCHRU de Lille, Clinique Neurologique, Neurologie A, Hôpital R. Salengro, 59037 Lille Cedex, France, bUniversité Charles de Gaulle, Lille3, UFR de Psychologie, BP 149, 59653 Villeneuve d’Ascq Cedex, France, cUniversité de Lille 2, Faculté de Médecine, CERIM, 59037 Lille Cedex, France
- Dr Kathy Dujardin, Clinique Neurologique, Neurologie A, CHRU de Lille, Hôpital Salengro, 59037 Lille Cedex, France. Telephone 0033 320 44 67 52; fax 0033 320 44 66 80; email: kdujardin{at}nordnet.fr
- Received 6 November 1998
- Revised 31 March 1999
- Accepted 7 April 1999
Abstract
OBJECTIVE To investigate the cognitive profile of first degree relatives of patients with familial Parkinson’s disease to determine whether these subjects presented signs of neuropsychological dysfunction compared with healthy controls. Results of recent genetic and neuroimaging studies suggest a genetic contribution to the aetiology of Parkinson’s disease and underline the interest in identifying preclinical signs of the disease.
METHODS A battery of tests evaluating executive function was administered to 41 first degree relatives of patients with well documented familial Parkinson’s disease and 39 healthy controls. A factorial discriminant analysis allowed isolation of a subgroup of 15 first degree relatives who could be considered as impaired compared with the healthy controls. Among these 15 “deviant” relatives, nine performed globally worse than the control subjects on all tasks. The six other subjects had mean or even high scores on all task variables, except on those highly correlated with the discriminant score of the factorial discriminant analysis.
RESULTS AND CONCLUSION Among the first degree relatives of patients with familial Parkinson’s disease, some manifested executive dysfunction comparable with that typically associated with the disease. Such impairment could represent a preclinical form of Parkinson’s disease.
