Sympathetic Activity in Man After Spinal Cord Injury

Abstract

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.

Cutaneous vasoconstriction as a measure of incipient autonomic dysreflexia during penile vibratory stimulation in spinal cord injury

“…However, we do know from microneurographic studies that there is coactivation of cutaneous and muscle vasoconstrictor neurones following stimulation below lesion in subjects with SCI. 3 Although constriction of cutaneous (capacitance) vessels will result in the displacement of blood to active circulation, there is no doubt that the increase in BP is due to the activation of muscle vasoconstrictor neurones and, most likely, splanchnic vasoconstrictor neurones, through a spinal viscerosympathetic reflex. Indeed, the magnitude of the pressor response implies the constriction of many arterioles and, given that the splanchnic outflow originates below T6, it is highly likely that constriction within the splanchnic vascular bed contributes to the increase in BP.…”

“…However, as segmental circuitry is intact, visceral or somatic stimuli originating below the lesion can cause reflex activation of vasoconstrictor neurones and a consequent increase in BP. 2,3 This condition, known as autonomic dysreflexia, is considered a medical emergency, as arterial pressure can rise so suddenly and remain at dangerously elevated levels that lifethreatening complications can occur. 1,4 It is common for midthoracic lesions and above, 5 that is above the level of sympathetic outflow to the splanchnic circulation, where many vascular beds may have lost central control.…”

Assessing the capacity of the sympathetic nervous system to respond to a cardiovascular challenge in human spinal cord injury

“…The BP responses we found in the spinal-injured group are what we would expect to find after SCI, given that in complete and incomplete lesions the descending sympathetic drive to the muscle vascular beds have often been interrupted. 12 We know from microneurographic recordings in SCI that MSNA is absent at rest 13 and is not evoked during an inspiratory-capacity apnoea (Macefield et al, unpublished observations). Due to this lack of sympathetic controlFand the fact that the vagus nerve is still intactFthe only means available to counteract the fall in arterial pressure during the manoeuvre is to increase HR.…”

A systematic review of the evidence supporting a role for vasopressor support in acute SCI

“…This may last for several days to 6 weeks until segmental neuronal connections and reflex cycles gradually reappear distal to the level of injury, even without sympathetic discharge return. 25 At that time, reflex hyperactivity begins manifesting as muscle spasms and elevation of blood pressure. 14,26 Furthermore, Ko and coworkers 27,28 specified that the time of return of deep tendon reflexes after SCI is within the first couple of weeks after injury with the delayed plantar reflex being the first followed by the bulbocavernous and cremasteric reflex.…”