Parkinson's disease rigidity: magnetic motor evoked potentials in a small hand muscle.
Cantello R,Gianelli M,Bettucci D,Civardi C,De Angelis M S,Mutani R
We studied the EMG potentials evoked in the bilateral first dorsal interosseus muscle by electromagnetic stimulation of the corticomotoneuronal descending system in 10 Parkinson's disease patients and in 10 age- and sex-matched normal controls. We selected patients who did not have tremor but had predominant rigidity with asymmetric body involvement. On the rigid side of the PD patients, the threshold to cortical stimulation was lower than on the contralateral side or than normal values. On average, patients had normal central conduction times, but their motor evoked potentials (MEPs) on the rigid side were larger than those of controls when the cortical stimulus was at rest or during slight tonic contraction of the target muscle. In the latter condition, a silent period shorter than that of controls followed MEPs, whereas the peripheral silent period following ulnar nerve stimulation at the wrist was prolonged. Alpha motor neuron excitability, tested by the F-wave method, was enhanced on the rigid side at rest. In rigidity, spinal motor nuclei may be more responsive than normal to descending inputs from motor cortex, or the entire corticomotoneuron system may prove hyperexcitable under given conditions.
Parkinson's disease rigidity: EMG in a small hand muscle at "rest".
Cantello R,Gianelli M,Civardi C,Mutani R
Electroencephalography and clinical neurophysiology
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."
Effects of dopamine on postural control in parkinsonian subjects: scaling, set, and tone.
Horak F B,Frank J,Nutt J
Journal of neurophysiology
1. This study investigates the effects of parkinsonism and of dopamine replacement therapy (levodopa) on scaling the magnitude of automatic postural responses based on sensory feedback and on predictive central set. Surface reactive torques and electromyographic (EMG) activity in response to backward surface translations were compared in patients with parkinsonism ON and OFF levodopa and in elderly control subjects. Correlations between the earliest postural responses [initial rate of change of torque and integrated EMG (IEMG)] and translation velocity provided a measure of postural magnitude scaling using somatosensory feedback. Correlations of responses with expected translation amplitude provided a measure of scaling dependent on predictive central set because the responses preceded amplitude completion. 2. Parkinsonian EMG responses in six leg and trunk muscles were not later than in elderly control subjects. In fact, quadriceps antagonist latencies were earlier than normal, resulting in coactivation at the knee not present in control subjects. EMG activation was fragmented, with short burst durations and high tonic levels that often returned to baseline with multiple bursts. In addition, parkinsonian responses showed smaller-than-normal agonist extensor bursts and larger-than-normal activation in tibialis and rectus femorus antagonist flexors. 3. Although parkinsonian subjects scaled postural responses to both displacement velocities and amplitudes, their torque response were smaller than those of elderly controls, especially in response to the largest displacement amplitudes. The gain (slope) of postural response magnitude scaling to displacement velocity was similar for parkinsonian and control subjects, although parkinsonian subjects had smaller torques. Parkinsonian subjects were also able to use prediction to scale responses to small expected displacement amplitudes, but many patients did not generate the larger plantarflexion torques required at larger displacement amplitudes. Reduced torque at large amplitudes was associated with less agonist gastrocnemius IEMG, increased tibialis antagonist burst responses, and increased tibialis tonic background activity. 4. Levodopa further reduced the already low magnitude of initial torque and IEMG responses to displacement velocities and amplitudes in parkinsonian patients. The ability to scale postural responses to velocity feedback was not affected by levodopa, but the ability to scale responses to large displacement amplitudes based on central set was worsened by levodopa. Levodopa also significantly reduced the tonic, background levels of EMG, particularly the distal gastrocnemius and tibialis activity. 5. High baseline muscle tone was apparent in parkinsonian subjects from their high background EMG activity in quiet stance, especially in tibialis and quadriceps, and the slow initial velocity of center of mass falling in response to displacements. By reducing tone, levodopa reduced passive stiffness to perturbations without increasing EMG burst magnitudes, resulting in less resistance to external displacements and thus faster center of body mass (COM) displacements. 6. The biggest postural deficit in parkinsonian subjects was not in response latency, pattern, or reactive or predictive scaling of response magnitude, but in quickly generating an adequate level of postural force. Dopamine improved tonic background postural tone but further weakened automatic postural responses to external displacements. Thus the basal ganglia may participate in postural control by regulating appropriate levels of background postural tone and by enabling adequate force generation for resisting external displacements.
Stimulus-sensitive myoclonus in akinetic-rigid syndromes.
Chen R,Ashby P,Lang A E
Brain : a journal of neurology
The cutaneous reflexes of upper limb muscles were studied in five patients with Parkinson's disease and 10 patients with stimulus-sensitive myoclonus associated with akinetic-rigid syndromes. The middle finger was stimulated with ring electrodes and rectified electromyographs were averaged from seven upper limb muscles and orbicularis oculi. Responses from subjects with Parkinson's disease without stimulus-sensitive myoclonus were similar to those of normal subjects. The responses from patients with stimulus-sensitive myoclonus associated with Parkinson's disease or multiple system atrophy had the normal pattern except that a long latency facilitation, which is present in normal subjects and known as E2, was greatly exaggerated. Patients with stimulus-sensitive myoclonus associated with cortical-basal ganglionic degeneration had a completely different pattern of responses. There was synchronous activation of all recorded upper limb muscles with latencies substantially shorter than those of the long latency facilitation (E2) in normal subjects. Cutaneous reflex testing may therefore be useful in the differentiation of akinetic-rigid syndromes.