R. Cantello et al., PARKINSONS-DISEASE RIGIDITY - EMG IN A SMALL HAND MUSCLE AT REST, ELECTROMYOGRAPHY AND MOTOR CONTROL-ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY, 97(5), 1995, pp. 215-222
The presence of excessive EMG at ''rest'' might be an important factor
in the genesis of Parkinson's disease (PD) rigidity, and we studied i
t in the first dorsal interosseous muscle (FDI) of 8 idiopathic PD pat
ients. We had 8 age- and sex-matched normal controls. In the PD group,
the average area of the surface EMG at ''rest'' correlated significan
tly with the clinical evaluation of rigidity and remained abnormally e
nhanced for 10-15 min after a command to ''relax.'' Later, it tended t
o decline, but its entity was still much greater than in controls. The
EMG ''at rest'' consisted of unwilled motor unit (MU) firing. A large
r MU number was recruited in patients than in controls at ''rest.'' MU
rate coding was similar in both groups. Eventually, patients could ge
t periods of EMG silence which, however, were interrupted by short EMG
bursts, even if there was no muscle stretch. These bursts were interp
reted as residual fragments of the original excessive EMG at ''rest.''
MUs first recruited during such bursts showed high, but not total, ov
erlapping with those first recruited by a gentle voluntary contraction
or by a weak transcranial magnetic stimulus to motor cortex. We concl
ude 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 p
ossible input sources to the cy-motoneurones at ''rest.''