Parkinson's disease rigidity: EMG in a small hand muscle at 'rest'.

The presence of excessive EMG at 'rest' might be an important factor in the genesis of Parkinson's disease (PD) rigidity, and we studied it in the first dorsal interosseous muscle (FDI) of 8 idiopathic PD patients. We had 8 age- and sex-matched normal controls. In the PD group, the average area of the surface EMG at 'rest' correlated significantly with the clinical evaluation of rigidity and remained abnormally enhanced for 10-15 min after a command to 'relax.' Later, it tended to decline, but its entity was still much greater than in controls. The EMG 'at rest' consisted of unwilled motor unit (MU) firing. A larger MU number was recruited in patients than in controls at 'rest.' MU rate coding was similar in both groups. Eventually, patients could get periods of EMG silence which, however, were interrupted by short EMG bursts, even if there was no muscle stretch. These bursts were interpreted as residual fragments of the original excessive EMG at 'rest.' MUs first recruited during such bursts showed high, but not total, overlapping with those first recruited by a gentle voluntary contraction or by a weak transcranial magnetic stimulus to motor cortex. We conclude that EMG activity at 'rest' was made up of the discharge of low-threshold MUs, with a recruitment order similar to that resulting from descending cortico-spinal volleys. However, we cannot exclude other possible input sources to the alpha-motoneurones at 'rest.'