Somatosympathetic Vasoconstrictor Reflexes in Human Spinal Cord Injury: Responses to Innocuous and Noxious Sensory Stimulation below Lesion

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.

Development of a decerebrate model for investigating mechanisms mediating viscero-sympathetic reflexes in the spinalized rat

“…Visceral stimulation in decerebrate animals led to increases in RSNA and MAP, which were accompanied by decreases in HR. This pattern is similar to what is reported in human subjects (3,4,25,30). Reflex reactivity is attenuated by the administration of anesthesia and abolished by ganglionic blockade.…”

Viscerosympathetic reflexes in human spinal cord injury: relationships between detrusor pressure, blood pressure and skin blood flow during bladder distension

“…Our main findings were as follows: (i) in all 16 patients with spinal lesions above the level of sympathetic outflow to the hand, bladder filling induced signs of cutaneous vasoconstriction in the fingers; (ii) in 10 of those patients the blood pressure increased by 10 mmHg or more, and in nine of them there was a significant inverse relationship between finger pulse amplitudes and mean blood pressure; and (iii) there was no evidence of sweat release throughout the procedure in any patient, supporting our contention that sweat release is not a reliable marker of cutaneous sympathetic outflow below the lesion in human spinal cord injury (Brown et al 2007, 2009 a , b ; Macefield et al 2012).…”

“…In addition, a variety of stimuli applied below the lesion may lead to sudden increases of blood pressure (autonomic dysreflexia), sometimes to alarmingly high levels (Erickson, 1980; Teasell et al 2000). Most commonly the stimuli originate from the viscera, but non‐noxious sensory inputs from the body wall may occasionally evoke strong somatosympathetic reflexes below the lesion (Macefield et al 2012). Stimuli applied to the urinary bladder are especially effective at evoking marked increases in blood pressure, and several studies have reported a high incidence of autonomic dysreflexia during cystoscopy (Snow et al 1978) or cystometry (Guttman & Whitteridge, 1947; Krum et al 1992; Curt et al 1997; Giannantoni et al 1998; Lee et al 2003).…”

Spinal Reflex Control of Arterial Blood Pressure: The Role of TRP Channels and Their Endogenous Eicosanoid Modulators

“…If the spinal cord injury is located above the level of the cardiac sympathetic output (i.e., higher cervical injuries), the reflex-mediated bradycardia is absent and a tachycardiac response is observed (Eldahan and Rabchevsky, 2018). Similar cardiovascular responses can be produced by cutaneous stimulation below the level of the spinal cord injury through activation of a somato-sympathetic reflex (Brown et al, 2007(Brown et al, , 2009Macefield et al, 2012). In addition to cardiovascular responses, activation of viscero-sympathetic reflex can result in throbbing headache, nausea, irritability, and sometimes even convulsion, cerebral hemorrhage or death (Eldahan and Rabchevsky, 2018).…”