Brain, Vol. 109, No. 4, 695-715, 1986
© 1986 Guarantors of Brain
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SYMPATHETIC ACTIVITY IN MAN AFTER SPINAL CORD INJURY
OUTFLOW TO MUSCLE BELOW THE LESION
Departments of Rehabilitation Medicine and Clinical Neurophysiology, Uppsala University Uppsala, Sweden 1Department of Neurology, University of Freiburg Hansastrasse 9, D-7800 Freiburg, FRG 2Department of Clinical Neurophysiology, Sahlgrenska Hospital S-413 45 Gothenburg, Sweden
Correspondence to:
Correspondence to. Dr Leif Stjernberg, Department of Rehabilitation Medicine, Akademiska Sjukhuset, S-751 85 Uppsala, Sweden.
SUMMARY
Microelectrode recordings were made in peroneal muscle nerve fascicles in 9 patients with traumatic spinal cord lesions at the C5 to T8 level. In 4 patients the lesion was incomplete with some sensibility but no voluntary motor function below the level of the lesion. All patients had increased tendon jerks. EMG was recorded in 5 patients and showed signs of some peripheral denervation. Simultaneous recordings from nerves to skin and to muscle were made in 2 patients and control recordings were made in 19 normal subjects In the patients, spontaneous neural activity was sparse but after a latency of 0.5–1 Is strong mechanical and electrical stimuli applied to the skin below the level of the lesion, stimulation of the urinary bladder and deep breaths induced bursts of efferent impulses with a conduction velocity of 0.65 m.s-1. The discharges were often followed by cutaneous vasoconstriction and/or reduction of skin resistance. It is concluded that the neural bursts contained sympathetic impulses of spinal origin.
The main differences between patients and normal subjects were (1) spontaneous muscle sympathetic activity was much lower in the patients; (2) no evidence of arterial baroreflex modulation of muscle sympathetic activity was obtained in the patients; and (3) in the patients a given stimulus induced sympathetic reflex discharges which occurred synchronously in muscle and skin nerve branches. Increases of intravesical pressure induced only weak increases of muscle sympathetic activity in the patients but nevertheless marked hypertensive reactions occurred. It is suggested that the excitability of decentralized spinal sympathetic neurons to muscles is usually decreased and that mechanisms other than exaggerated sympathetic outflow must be important for evoking episodes of high blood pressure in patients with spinal cord injuries.
Received May 9, 1985. Revised October 14, 1985. Accepted November 29, 1985.
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