A R Burton1, R Brown, V G Macefield. 1. Spinal Injuries Research Centre, Prince of Wales Medical Research Institute and University of New South Wales, Sydney, New South Wales, Australia. a.burton@powmri.edu.au
Abstract
STUDY DESIGN: Measurement of sympathetic effector organ responses to selective activation of muscle and skin nociceptors below lesion in spinal cord-injured (SCI) subjects. OBJECTIVES: To test whether selective noxious stimulation below lesion causes exaggerated sympathetic responses in human SCI. SETTING: Prince of Wales Medical Research Institute, Australia. METHODS: Twelve subjects (C5-T10, ASIA A-C), none of whom had sensation below the lesion, were included in the study. Selective stimulation of muscle or cutaneous nociceptors was produced by bolus injection of hypertonic (5%) saline into the tibialis anterior muscle or overlying skin and compared with non-noxious electrical stimulation of the abdominal wall. Cutaneous vasoconstrictor (photoelectric plethysmography) and sudomotor (skin conductance) responses, in addition to respiration, heart rate and continuous arterial pressure were monitored. RESULTS: Electrical stimulation of the abdominal wall caused a significant increase in arterial pressure (31.8+/-6.1%). Conversely, intramuscular or subcutaneous injection of hypertonic saline caused no significant changes in blood pressure (-3.0+/-2.4%; -1.4+/-3.4%) heart rate, skin blood flow or sweat release. CONCLUSIONS: While hypertonic saline injected into muscle or skin induces strong pain, cutaneous vasoconstriction and sweat release in able-bodied subjects, we saw no evidence of exaggerated sympathoexcitation when these same noxious stimuli were delivered below lesion in subjects with SCI. This suggests that certain types of somatic noxious input may not trigger autonomic dysreflexia, and questions the concept that any painful stimuli originating below lesion can reliably trigger dysreflexia.
STUDY DESIGN: Measurement of sympathetic effector organ responses to selective activation of muscle and skin nociceptors below lesion in spinal cord-injured (SCI) subjects. OBJECTIVES: To test whether selective noxious stimulation below lesion causes exaggerated sympathetic responses in human SCI. SETTING: Prince of Wales Medical Research Institute, Australia. METHODS: Twelve subjects (C5-T10, ASIA A-C), none of whom had sensation below the lesion, were included in the study. Selective stimulation of muscle or cutaneous nociceptors was produced by bolus injection of hypertonic (5%) saline into the tibialis anterior muscle or overlying skin and compared with non-noxious electrical stimulation of the abdominal wall. Cutaneous vasoconstrictor (photoelectric plethysmography) and sudomotor (skin conductance) responses, in addition to respiration, heart rate and continuous arterial pressure were monitored. RESULTS: Electrical stimulation of the abdominal wall caused a significant increase in arterial pressure (31.8+/-6.1%). Conversely, intramuscular or subcutaneous injection of hypertonicsaline caused no significant changes in blood pressure (-3.0+/-2.4%; -1.4+/-3.4%) heart rate, skin blood flow or sweat release. CONCLUSIONS: While hypertonicsaline injected into muscle or skin induces strong pain, cutaneous vasoconstriction and sweat release in able-bodied subjects, we saw no evidence of exaggerated sympathoexcitation when these same noxious stimuli were delivered below lesion in subjects with SCI. This suggests that certain types of somatic noxious input may not trigger autonomic dysreflexia, and questions the concept that any painful stimuli originating below lesion can reliably trigger dysreflexia.