Relationship between electromyographic activity and clinically assessed rigidity studied at the wrist joint in Parkinson's disease.

The electromyographic (EMG) patterns recorded from wrist muscles during manually applied, repetitive flexion and extension movements of the wrist joint, used for simultaneous clinical assessment of rigidity, were studied in patients with Parkinson's disease and healthy subjects. Recordings were made whilst patients/subjects attempted voluntarily to relax the muscle of the arm whose wrist joint was manipulated. Individual patients were investigated before and at varying times after their routine daily medication as their clinical rigidity underwent associated modulations. It was often possible to induce additional alterations in clinical rigidity by instructing patients to perform an activation or Jendrassik-like manoeuvre (clenching the contralateral fist). In rigid patients, the approximately sinusoidal wrist displacements (60 deg, 1-1.5 Hz) typically elicited pronounced, cyclic modulations of EMG activities in wrist flexors and extensors; increases in EMG activity were phase-locked to the respective periods of muscle stretch. Stretch-related EMG activity reduced or disappeared as rigidity was abolished by drug therapy. The EMG patterns of patients showing cogwheel rigidity featured discrete, phasic bursts superimposed upon more generalized stretch-related increases in activity. In healthy subjects, showing no clinical rigidity, the pronounced cyclic modulations of EMG activity characteristic of rigid patients were absent during similar manually applied wrist displacements. Quantitative EMG measurements for individual patients, made 'on' and 'off' medication and as their rigidity fluctuated, indicated that mild (grade 1) and moderate (grade 2) rigidity was consistently associated with increased stretch-related activity compared with non-rigid conditions. Pair-wise statistical analysis indicated such increases in EMG to be significant. Similarly, the ratios of EMG activities in the stretched versus released muscles were significantly greater for grades 1 and 2 rigidity than in the absence of rigidity. Overall, the present findings support the view that enhancement of stretch reflex activity has a major role in the genesis of parkinsonian rigidity.