The term “orthostatic tremor” was introduced by Heilman in 1984 to describe “quivering” or tremor of the legs and trunk during quiet standing accompanied by unsteadiness that was relieved by walking or leaning on nearby objects.1 Subsequently, the tremor was characterised as a unique 16 Hz tremor predominantly affecting the legs and trunk.2 3 Tremor was visible only as a fine ripple because of the rapid frequency,2 3 and often obscured by voluntary manoeuvres to relieve the overwhelming sensation of unsteadiness, perhaps explaining the obscurity of the entity to that time. The rhythmic 16 Hz activity was best appreciated in EMG recordings and was maximal in muscles of the legs and trunk during quiet standing.2 3 In some patients, tremor was detected in the outstretched arms and, rarely, it was evident in cranial muscles.4 The designation “orthostatic” implied that the upright posture was in some way important in the generation of tremor. However, “orthostasis” alone is not sufficient or necessary for the appearance of the characteristic 16 Hz tremor. Tremor could be abolished by simply lifting the standing patient off the ground,1 and when walking, tremor disappeared from the non-weight bearing limb during the swing phase of the gait cycle.3 Tremor persisted in the weight bearing leg and in trunkal (paraspinal) muscles throughout the gait cycle, even though the symptoms of unsteadiness were alleviated by walking.3Standing on all fours also induced a 16 Hz tremor in proximal upper limb muscles.3 4 In this issue of theJournal (pp 284–8) Boroojerdiet al expand these findings by showing that isometric cocontraction of arm and leg muscles also induces 16Hz tremor in some patients with orthostatic tremor when supine or suspended upright. These authors suggest that muscle contraction seems to be the critical factor in generating the 16 Hz tremor, along the lines of an “action” tremor, and accordingly, the tremor may be considered “orthostasis independent”.

All evidence suggests that 16 Hz tremor is generated by a central oscillator,5 and this is further supported by the finding of Boroojerdi et al that peripheral loading does not alter the tremor frequency. It seems that muscle activation, whether postural or voluntary muscle contraction, leads to the appearance of tremor presumably by facilitating the background 16 Hz oscillatory activity. The mechanism of the sensation of unsteadiness and the relation of this symptom to the 16 Hz tremor remains unclear. Difficulties in attempting to reconcile the description of a clinical phenomenon with a physiological mechanism are a common problem. In the case of orthostatic tremor, the present designation reflects the symptoms well, although there remains much to understand about its mechanisms.