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We enjoyed reading the paper by Dujardinet al 1 who investigated possible preclinical features of asymptomatic relatives in families with Parkinson's disease. A battery of neuropsychological tests disclosed impaired frontal executive function in 15 of 41 first degree relatives of patients with familial Parkinson's disease. Nine showed general frontal executive impairment. The other six only had lower scores in parts of motor dynamic sequences and word fluency. The authors concluded that this dysexecutive syndrome could be a premorbid expression of Parkinson's disease. It could represent an early nigrostriatal dysfunction in first degree relatives of probands with familial Parkinson's disease who may thus carry a higher genetic risk of developing the disease.
Dujardin et al describe modifications of the cognitive status which we reported in unaffected co-twins of patients with Parkinson's disease2 After this, 3 years ago our group published a similar study3 to the one by Dujardinet al. As they do not mention our findings, we briefly discuss our data in relation to their results. We compared 35 motor asymptomatic first degree relatives (mean age 52.6 (SD 10.6) years) of families with at least two members affected by Parkinson's disease to 29 relatives (mean age 52.1 (SD 4.1) years) of patients with sporadic Parkinson's disease and to 32 healthy controls (mean age 51.9 (SD 4.6) years). To account for a possible “low dopamine syndrome”, we studied memory, frontal lobe function, mood, personality traits, somatic complaints, and fine motor abilities. Tests used were the short form of the Wechsler adult intelligence scale, the auditory verbal learning test, the controlled oral word association test, the Wisconsin card sorting test (Nelson version), the paranoid depression scale, the revised version of the Freiburg personality inventory, a list of complaints, and a standardised finger tapping test. We found that first degree relatives of both patients with familial Parkinson's disease and those with sporadic Parkinson's disease differed significantly from controls in several tests. They had lower scores in total fluency and fewer categories in the Wisconsin card sorting test. Relatives of both patients with familial Parkinson's disease and with sporadic disease expressed more impulsiveness, more strain, and less extraversion on personality assessment. In addition, relatives of patients with familial Parkinson's disease had more errors than controls in the Wisconsin card sorting test. Relatives of patients with sporadic Parkinson's disease showed more depression, more somatic complaints, and inhibitedness than controls and also less extraversion, less emotionality, and a lower tapping rate of the right hand. Our results, both motor and non-motor, were comparable with those of patients with early stage Parkinson's disease and are in keeping with some of the findings of Dujardin et al.
On average, our proband sample was 14 years older than that of Dujardinet al, and by contrast with these authors, we included assessment of depression as a possible confounder of the neuropsychological test results. Depression may have a substantial impact on cognitive function,4 and a history of depression is thought to be a risk factor for developing Parkinson's disease.5 In our study, there were no correlations between cognitive impairment and depression. We therefore considered frontal lobe dysfunction and depression as independent signs of the “low dopamine syndrome” in our samples. Another important result of our investigation was that, apart from one personality trait (“aggressiveness”), we could not establish differences between relatives of patients with familial Parkinson's disease and those of patients with sporadic Parkinson's disease in any test item, nor were there item clusters in subsets of probands. Thus, according to our data, frontal lobe dysfunction and depression can be found to a variable degree in some relatives of patients with both the familial and the sporadic form of Parkinson's disease. It should be kept in mind that the finding of such neuropsychological abnormalities does not prove that their origin is genetic.
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