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 0.5-1.1 s 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 X 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 spontaneous muscle sympathetic activity was much lower in the patients; no evidence of arterial baroreflex modulation of muscle sympathetic activity was obtained in the patients; and 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.

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Discharge properties of afferent units from experimentally produced stump neuromata in the superficial peroneal nerve of the cat hind limb were investigated electrophysiologically. The superficial peroneal nerves were cut and ligated 6-245 days before the experiments. Myelinated and chiefly unmyelinated axons were analyzed. The following results were obtained: (1) 3.9 +/- 3% (mean +/- S.D.) of axons from early neuromata (days 6-27) and 13.4 +/- 10.7% of axons from old neuromata (more than 50 days after nerve severance) showed ongoing activity. The rate of ongoing activity was usually below 1 imp/sec (73%) and rarely above 4 imp/sec and its pattern, in most cases, was irregular. Some myelinated afferents had regular or irregular bursting patterns. (2) Mechanical stimulation of the neuroma excited 19.4 +/- 9.6% of the axons from young neuromata and 32.8 +/- 14.9% of the axons from old neuromata. Part of these mechanosensitive units exhibited pronounced after-discharges. Some 20% of the units which could be excited, probably ephaptically, by stimulation of other afferent fibers in the common peroneal nerve were excited by pressure applied to the neuroma. (3) About 20-40% of the units with ongoing activity (3-5% of all axons) responded weakly to intravenous injections of adrenaline and noradrenaline and to repetitive stimulation of the lumbar sympathetic trunk. (4) Recording from distally cut fiber bundles showed that part of the axons could be activated by electrical stimulation of the nerve distal to the recording site and by mechanical stimulation of the neuroma. Most of these axons were unmyelinated. This result indicates that afferent axons either branch or interact ephaptically a long distance proximal to the neuroma in the neuroma nerve. (5) The results are discussed with respect to similar results obtained on afferent fibers from experimentally produced neuromata of the sciatic nerve of mice and rats.

SUMMARY1. Intraneural stimulation (i.n.s.) was made in the superficial peroneal nerve at the ankle in seventeen healthy subjects. The effect on skin blood flow was monitored by laser-doppler flowmeters and photo-electrical pulse plethysmographs inside and outside the innervation zone of the stimulated nerve fascicle. I.n.s. was applied before and after proximal local anaesthesia of the stimulated nerve.2. Painful i.n.s. (stimulation strength 0-3-4 V) induced skin vasodilatation with the following characteristics: (a) it occurred on the dorsal side of both feet, (b) the blood flow increase on the opposite foot was blocked by local anaesthesia of the nerve supplying the skin area under study, (c) the blood flow increase on the stimulated foot was abolished by proximal local anaesthesia of the stimulated nerve. The findings show that the vasodilatation was due to activation of a reflex pathway.3. The reflex vasodilatation was bigger in the stimulated than in the opposite foot. At the same time there were signs of skin vasoconstriction in the fingers. The reflex vasodilatation in the foot was enhanced by body cooling. It was unaffected by atropine or propranolol.4. After local anaesthesia of the nerve proximal to the stimulation site, i.n.s. with 2-6 times increased stimulation strength produced skin vasodilatation restricted to the innervation zone of the stimulated nerve fascicle. This response had greater amplitude and longer duration than the reflex vasodilatation.5. Intravenously administered atropine and propranolol did not affect the local dilatation to i.n.s. but after chronic treatment of the skin with capsaicin (1 % in ethanol), i.n.s. after a proximal nerve block induced skin vasoconstriction. In five of seven experiments subcutaneous injection of terbutaline (0'25 mg) in the innervation zone abolished the local dilatation.6. It is suggested that (a) the reflex vasodilatation is of sympathetic nature and is induced by stimulation of thin (Ad?) afferent fibres, (b) the local vasodilatation is due to centrifugally conducted impulses in (afferent?) non-myelinated fibres.

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