In recent years there has been increasing interest in oscillatory neural activity in the CNS and in the role that such activity may have in motor control. It is thought that physiological tremor may be a manifestation in the periphery of such central oscillatory activity and that some pathological tremors are the result of derangement of these oscillators. This review re-evaluates both early and recent studies on physiological and pathological tremors and other peripheral oscillations in order to gain a new perspective on the nature and function of their central progenitors. This approach, namely using tremor as a 'window' into the function of central oscillations, is particularly suited to human investigations because of the obvious limitations of direct central recording. It is argued that physiological tremor is likely to be multifactorial in origin, with contributions not only from CNS 10-Hz range oscillatory activity, but also from motor unit firing properties, mechanical resonances and reflex loop resonances. Different origins are likely to dominate under different conditions. While some pathological tremors appear to arise as a distortion of central or peripheral components of physiological tremor, others arise de novo, such as the pathological oscillation of 3- to 6-Hz parkinsonian tremor. CNS oscillations outside the 10-Hz range are also found to modulate limb activity in normal individuals, and oscillatory activity exists in other motor systems such as eye movements. Finally, it is shown how studies of peripheral oscillations may help develop hypotheses on the role of CNS oscillations in motor control, including the proposed 'binding' function of synchronized oscillations and the possibility that motor signals could be coded by frequency of modulating oscillation as well as by synaptic connectivity.

The output from the central nervous system to muscles may be rhythmic in nature. Previous recordings investigating peripheral manifestations of such rhythmic activity are conflicting. This study attempts to resolve these conflicts by employing a novel arrangement to measure and correlate rhythms in tremor, electromyographic (EMG) activity and muscle vibration sounds during steady index finger abduction. An elastic attachment of the index finger to a strain gauge allowed a strong but relatively unfixed abducting contraction of the first dorsal interosseous (1DI). An accelerometer attached to the end of the finger recorded tremor, surface electrodes over 1DI recorded EMG signals and a heart-sounds monitor placed over 1DI recorded vibration. This arrangement enabled maintenance of a constant overall muscle contraction strength while still allowing measurement of the occurrence of tremulous movements of the finger. Ten normal subjects were studied with the index finger first extended at rest and then contracting 1DI to abduct the index finger against three different steady forces up to 50% of maximal voluntary contraction (MVC). Power spectral analysis of tremor, EMG activity and muscle vibration signals each revealed three frequency peaks occurring together at around 10 Hz, 20 Hz and 40 Hz. Coherence analysis showed that the same three peaks were present in the three signals. Phase analysis indicated a fixed time lag of tremor behind EMG of around 6.5 ms. This is compared with previous measurements of electromechanical delay. Other experiments indicated that the three peaks were of central nervous origin. Introducing mechanical perturbations or extra loading to the finger and making recordings under partial anaesthesia of the hand and forearm demonstrated preservation of all the peaks, suggesting that they did not originate from mechanical resonances or peripheral feedback loop resonances. It is concluded that, at least for a small hand muscle, there exist not one but a number of separate peak frequencies of oscillation during active contraction, and that these oscillations reflect synchronization of motor units at frequencies determined within the central nervous system. It is proposed that the multiple oscillations may be a means of frequency coding of motor commands.

Maximum elbow flexor and extensor muscle strength was measured in 9 patients with Parkinson's disease on and off antiparkinsonian medication. In addition, the rate of force generation, the rate of actively returning force to resting levels, and passive release of force "relaxation" were measured in submaximal contractions. The measures of strength and contraction time were correlated with changes in clinical status as measured by the Unified Parkinson's Disease Rating Scale. When patients were off medication, their reduction in strength was significantly greater in extension than flexion. The reduction in flexion strength did not reach statistical significance. The extensor weakness was primarily due to decreased tonic activation of the extensor muscles and not to muscle coactivation. Muscle relaxation time was much more prolonged than was force generation time or active force return time. The increase in relaxation time and the decrease in extensor strength both correlated with changes in clinical status. Finally, changes in extensor torque correlated with the time to actively return force, suggesting that reduced strength is related to a reduced ability to generate rapid contractions in some patients with Parkinson's disease. These results suggest that there is an asymmetric distribution of muscle weakness in Parkinson's disease and that selected measures of muscle strength and muscle relaxation correlate with changes in clinical status.

The differentiation of psychogenic from organic tremors, particularly those of a dystonic nature, can be difficult on clinical grounds. Entrainment of tremulous movements of different body parts into a single rhythm has been used clinically as a means of distinguishing these tremor forms, based on the inability of a patient with hysterical tremor to generate voluntary tapping oscillations independent of their ongoing tremor oscillation. The coherence entrainment test is a quantified electrophysiological entrainment test performed on accelerometer or surface EMG tremor signals. This test was carried out on 25 patients referred with suspected psychogenic tremor or dystonic tremor and on 10 normal subjects attempting to tap two independent voluntary oscillations. Using established and new clinical diagnostic criteria, patients were assigned the following final clinical diagnoses: 6 cases of clinically definite dystonic tremor, 5 cases of probable dystonic tremor, 2 cases of classic essential tremor, 5 cases of clinically definite psychogenic tremor, 3 cases of probable psychogenic tremor and 4 uncertain cases. On comparing these clinical diagnoses with those reached by a coherence entrainment test subsequently carried out on each patient, there was 100% concordance in both clinically definite and clinically probable patients. In uncertain cases, when later clinical information came to light, this also corroborated with the coherence entrainment diagnosis. No normal subjects were able to "mimic" organic tremor. The coherence entrainment test appears to be a sensitive and specific means of distinguishing psychogenic tremor from dystonic and other organic tremors.