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. 1994 Aug;93(4):265-75.
doi: 10.1016/0168-5597(94)90028-0.

Short-latency neck muscle responses to vertical body tilt in normal subjects and in patients with spasmodic torticollis

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Short-latency neck muscle responses to vertical body tilt in normal subjects and in patients with spasmodic torticollis

L Mazzini et al. Electroencephalogr Clin Neurophysiol. 1994 Aug.

Abstract

EMG responses in the sternocleidomastoid (SCM) and dorsal neck muscles (DNM) to vertical head acceleration were studied in normal subjects and in patients with spasmodic torticollis, standing on a platform that could be tilted upwards. The vertical body displacement and the induced changes in the head-neck angle (a flexion-extension sequence) were recorded. Excitatory responses, symmetrical on the two sides, were elicited in normal subjects in both muscle groups, at a latency of about 60 msec (DNM) and 90 msec (SCM). With the head initially extended, the latency of DNM response increased, leaving that of SCM unchanged. During an isometric rotatory effort, an early inhibitory period was recorded in the active muscles at a latency of about 40 msec. Downward tilt did not evoke the responses. The DNM excitatory responses appeared to be related to muscle stretch, while those in SCM, as well as the inhibitory responses in both muscles, were thought to originate in the vestibular receptors. During active head rotation the response increased in amplitude in the active SCM and decreased in the lengthened antagonist; decreased responses in the lengthened muscle persisted during passive head rotation. This was attributed to an influence from the tonic neck receptors. In the patients, SCM responses had normal latency, but were reduced in amplitude or absent in the dystonic muscle, in spite of tilt-induced head movements comparable to those recorded in normals. The diminution was even bigger if compared to normal subjects with the head actively rotated to a similar extent. It persisted when the head was returned to normal position by the "geste antagoniste." The inhibitory responses were unaffected in the active normal and dystonic muscles. The possible role of a deficit of the central vestibular connections in the decreased excitatory SCM response in dystonic patients is considered.

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