We tried to establish possible correlations between clinical data and MRI in a group of patients with Wilson's disease. Eleven patients (6 male, 5 female), aged between 11 and 50 years old, with a duration of illness from 5 months to 32 years, were submitted to MRI on a 1.5 T System. Three patients were asymptomatic, two had mild neurological disturbances, two were moderately affected and the remaining four had a severe form of the disease. All were receiving D-penicillamine at the time of the study. In the most symptomatic patients there were abnormalities in five or more sites on MRI. The putamen was affected in all symptomatic patients, including five with dystonia. A striking feature was the peripheral location of high signal putaminal lesions on T2-weighted images. In five cases, lesions in the corpus striatum or substantia nigra explained the patient's Parkinsonian features. MRI is an efficient method for studying involvement of the central nervous system in Wilson's disease, and allows some interesting anatomoclinical correlations.

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We have recently shown ipsilateral dynamic deWcits in trajectory control are present in left hemisphere damaged (LHD) patients with paresis, as evidenced by impaired modulation of torque amplitude as response amplitude increases. The purpose of the current study is to determine if these ipsilateral deWcits are more common with contralateral hemiparesis and greater damage to the motor system, as evidenced by structural imaging. Three groups of right-handed subjects (healthy controls, LHD stroke patients with and without upper extremity paresis) performed single-joint elbow movements of varying amplitudes with their left arm in the left hemispace. Only the paretic group demonstrated dynamic deWcits characterized by decreased modulation of peak torque (reXected by peak acceleration changes) as response amplitude increased. These results could not be attributed to lesion volume or peak velocity as neither variable diVered across the groups. However, the paretic group had damage to a larger number of areas within the motor system than the non-paretic group suggesting that such damage increases the probability of ipsilesional deWcits in dynamic control for modulating torque amplitude after left hemisphere damage.

No abstract