White matter involvement in idiopathic Parkinson disease: a diffusion tensor imaging study.

BACKGROUND AND PURPOSE: Diffusion tensor imaging (DTI) offers a unique window on the connectivity changes, extending beyond the basal ganglia, which accompany the cognitive symptoms of Parkinson disease (PD). The primary purpose of this study was to assess the microstructural damage to cerebral white matter occurring in idiopathic PD. MATERIALS AND METHODS: Our sample included patients with PD without dementia (n = 10; Hoehn and Yahr stages I and II; Unified Parkinson Disease Rating Scale, 20.5 +/- 8.3; and Mini-Mental State Examination, 28.3 +/- 1.5) and age-matched healthy control subjects (n = 10). DTI was performed on a 1.5T scanner, and mean diffusivity (MD) and fractional anisotropy (FA) maps were obtained. Regions of interest (ROIs) were drawn on the major fiber bundles as well as on gray matter nuclei. RESULTS: In patients, the MD was increased at borderline significance in the substantia nigra but was unaltered in the thalamus, globus pallidus, putamen, and in the head of the caudate nucleus. The FA and MD were unaltered in the corticospinal tract in the midbrain and at the level of the internal capsule, and in the splenium of the corpus callosum. By contrast, the MD was increased and the FA was decreased in the genu of the corpus callosum and in the superior longitudinal fasciculus; in the cingulum, only the MD was altered. The observed changes were not significantly lateralized. CONCLUSIONS: Widespread microstructural damage to frontal and parietal white matter occurs already in the early stages of PD.

Researching a differential impairment of frontal functions and explicit memory in early Parkinson's disease.

An impairment at tasks sensitive to frontal lobe damage has been repeatedly reported in Parkinson's disease, but the exact nature of these deficits has not yet been clarified. Similarly, deficits of visuo-spatial functions have been frequently observed, but it is still debated whether verbal and visuo-spatial memory can be differentially affected. In this study we have compared the performance of 20 mild Parkinson's disease patients (I-II Hoehn and Yahr stage) and 18 matched normal controls, at tasks assessing frontal functions and explicit memory. We detected a selective deficit in set shifting and maintaining, without impairment in categorization and set formation. The lack of a selective increase in perseverative errors might indicate that perseverations either measure something different from set shifting or that they do not represent an index sensitive enough to set shifting impairment. Parkinson's disease patients were also significantly impaired at Raven's Progressive Matrices, a task assessing both frontal and visuo-spatial aspects. However, they did not show any differential impairment of visuo-spatial memory. Indeed, despite a trend of lower performance in visuo-spatial learning, memory performance of Parkinson's disease patients was significantly different from that of controls only at a free recall test which involved both verbal and visuo-spatial memory. We suggest the exploration of set shifting and maintaining to detect 'frontal' deficits in mild Parkinson's disease. We argue that Raven's Progressive Matrices is a valuable task for detecting subclinical cognitive deficits in Parkinson's disease, even if it does not show a specific profile of impairment in these patients. According to our results, a differential evaluation of verbal vs. visuo-spatial memory is not necessary in clinical practice, whilst free recall confirms its usefulness to detect subclinical impairments of memory functions.