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An exteroceptive reflex in the sternocleidomastoid muscle produced by electrical stimulation of the supraorbital nerve in normal subjects and patients with spasmodic torticollis

MRC Human Movement and Balance Unit and University Department of Clinical Neurology, Institute of Neurology, Queen Square, London, England.

We examined suppression of EMG activity in the contracting sternocleidomastoid muscles, produced by electrical stimulation of the supraorbital nerve in 10 normal subjects and 9 patients with spasmodic torticollis. This exteroceptive reflex in the sternocleidomastoid muscle consisted of 2 or 3 phases: (1) an early, small, and unstable phase of facilitation, followed by (2) a period of suppression beginning 35 msec after the stimulus, lasting for 35 msec with a reduction in EMG activity to approximately 40% of the prestimulus level, and (3) a further phase of facilitation at a latency of 70 msec, with duration 35 msec and an increase in EMG activity to approximately 35% above prestimulus levels. The latency and duration of the suppressive phase of this reflex were similar to the exteroceptive suppression of EMG activity in the masseter muscle after supraorbital nerve stimulation (masseter silent period). In patients with spasmodic torticollis, the depth of this exteroceptive suppression in the sternocleidomastoid muscles was less than that observed in an age-matched cohort of normal subjects, although the latency and duration were normal. In contrast, exteroceptive suppression in the masseter muscle was normal. These findings suggest abnormal function of inhibitory interneuronal networks between the 5th cranial nerve and the motor neurons of the spinal accessory and upper cervical nerves which mediate exteroceptive suppression in the sternocleidomastoid muscle in patients with spasmodic torticollis.

Address correspondence and reprint requests to Dr. Marsden, University Department of Clinical Neurology, The National Hospital for Nervous Diseases, Queen Square, London WC1N 3BG, UK.

Supported by the Medical Research Council. J.C.R. was a Royal Society University Research Fellow. R.S. was supported by the Dystonia Foundation.

Received February 14, 1989. Accepted for publication in final form April 14, 1989.

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