Abstract
It is known that the sudden increases in blood pressure associated with autonomic dysreflexia in people with spinal cord injury (SCI) are due to a spinally mediated reflex activation of sympathetic vasoconstrictor neurons supplying skeletal muscle and the gut. Apart from visceral inputs, such as those originating from a distended bladder, there is a prevailing opinion that autonomic dysreflexia can be triggered by noxious stimulation below the lesion. However, do noxious inputs really cause an increase in blood pressure in SCI? Using microelectrodes inserted into a peripheral nerve to record sympathetic nerve activity we had previously shown that selective stimulation of small-diameter afferents in muscle or skin, induced by bolus injection of hypertonic saline into the tibialis anterior muscle or the overlying skin, evokes a sustained increase in muscle sympathetic nerve activity and blood pressure and a transient increase in skin sympathetic nerve activity and decrease in skin blood flow in able-bodied subjects. We postulated that these sympathetic responses would be exaggerated in SCI, with a purely noxious stimulus causing long-lasting increases in blood pressure and long-lasting decreases in skin blood flow. Surprisingly, though, we found that intramuscular or subcutaneous injection of hypertonic saline into the leg caused negligible changes in these parameters. Conversely, weak electrical stimulation over the abdominal wall, which in able-bodied subjects is not painful and activates large-diameter cutaneous afferents, caused a marked increase in blood pressure in SCI but not in able-bodied subjects. This suggests that it is activation of large-diameter somatic afferents, not small-diameter afferents, that triggers increases in sympathetic outflow in SCI. Whether the responses to activation of large-diameter afferents reflect plastic changes in the spinal cord in SCI is unknown.
Highlights
While spinal cord injury (SCI) can cause devastating changes in the somatic nervous system below the lesion – paralysis and loss of sensation – compared to our knowledge of the sensory and motor disturbances following a spinal injury relatively little is known about changes to the sympathetic nervous system (McLachlan and Brock, 2006)
Because segmental spinal circuitry is intact, sensory stimuli originating below the lesion can cause a spinally mediated reflex activation of sympathetic vasoconstrictor neurons and a consequent increase in blood pressure
SOMATOSYMPATHETIC REFLEXES TO NOXIOUS INPUTS IN HUMAN SPINAL CORD INJURY We recently showed that selective stimulation of muscle nociceptors, induced by bolus intramuscular injection of hypertonic saline into the leg of awake human subjects, caused a strong, dull ache that lasted ∼8 min and produced an increase in muscle sympathetic nerve activity (MSNA) and modest increase in blood pressure and heart rate; these followed the time course of the subjective report of pain (Burton et al, 2009a)
Summary
While spinal cord injury (SCI) can cause devastating changes in the somatic nervous system below the lesion – paralysis and loss of sensation – compared to our knowledge of the sensory and motor disturbances following a spinal injury relatively little is known about changes to the sympathetic nervous system (McLachlan and Brock, 2006). Given that the sympathetic supply to the viscera and blood vessels is derived from the thoracic and lumbar segments of the spinal cord, an injury to the cord can – depending on the level and extent of the lesion – result in partial or complete loss of descending control of sympathetic function below the lesion. With high thoracic or cervical lesions the loss of sympathetic vasoconstrictor drive to blood vessels in muscles and the gut results in a low resting blood pressure and orthostatic hypotension; control of skin blood flow, and sweat release, and thermoregulatory control, is compromised (Mathias and Frankel, 2002). Because segmental spinal circuitry is intact, sensory stimuli originating below the lesion can cause a spinally mediated reflex activation of sympathetic vasoconstrictor neurons and a consequent increase in blood pressure. The purpose of this review is to contextualize recent experimental evidence that addresses the dogma surrounding the types of somatic inputs involved in the generation of spinal somatosympathetic reflexes
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