INFLUENCE OF DOPAMINERGIC MEDICATION ON AUTOMATIC POSTURAL RESPONSES AND BALANCE IMPAIRMENT IN PARKINSONS-DISEASE

It is still unclear why balance impairment in Parkinson's disease (PD) often responds insufficiently to dopaminergic medication. We have stu died this issue in 23 patients with idiopathic PD and 24 healthy contr ols. Our specific purposes were (a) to investigate the contribution of abnormal automatic postural responses to balance impairment in PD and (b) to assess the influence of dopaminergic medication on abnormal au tomatic postural responses and balance impairment. Standing subjects r eceived 4 degrees ''toe-up'' rotational perturbations of a supporting forceplate. We bilaterally recorded posturally destabilizing medium la tency (ML) responses from the stretched gastrocnemius muscles and func tionally corrective long latency (LL) responses from the shortened tib ialis anterior (TA) muscles. We also assessed changes in the center of foot pressure (CFP) and the center of gravity (COG). All patients wer e tested in the ''off'' and ''on'' phases, All controls were tested an d retested after 1 h. During the off phase, we found enlarged ML ampli tudes and diminished LL amplitudes in patients, together with a marked ly increased posterior displacement of the COG. The abnormal ML and LL responses were partially responsible for the increased body sway in p atients because the initial forward (destabilizing) displacement of th e CFP was increased, while the subsequent backward displacement of the CFP (a measure of the corrective braking action of LL responses) was delayed. Abnormal late automatic possibly more voluntary postural corr ections also contributed substantially to the increased body sway. Dur ing the on phase, ML amplitudes were reduced in patients but remained increased compared with controls. LL amplitudes no longer differed bet ween both groups due to a modest, possibly dopamine-related increase i n patients and a simultaneous decrease in controls. The abnormal CFP d isplacement was only partially improved by dopaminergic medication. Th e later postural corrections were not improved at all. Consequently, t he increased posterior COG displacement was not ameliorated during the on phase. We conclude that (a) a combination of abnormal automatic an d perhaps more voluntary postural corrections contributes to increased body sway in PD and (b) dopaminergic medication fails to improve bala nce impairment in PD because early automatic postural responses are on ly partially corrected, while later occurring postural corrections are not improved at all. These electrophysiological results support clini cal observations and suggest that nondopaminergic lesions play a signi ficant role in the pathophysiology of postural abnormalities in PD.