Key result
Mental arithmetic (high arousal) abolished the systolic inhibition of nociceptive responding that was observed at 300 ms after the R-wave during rest.
Why the study?
Does physiological arousal (mental arithmetic) moderate systolic inhibition of the nociceptive flexion reflex in adults?
Does physiological arousal (mental arithmetic) moderate systolic inhibition of the nociceptive flexion reflex in adults?
Physiological arousal attenuates the systolic inhibition of nociceptive responding, likely due to baroreflex attenuation.
Answers are grounded in this paper and cite their sources.
Arousal state merits consideration in baroreflex-nociception studies; leaves open clinical translation to pain processing.
Inhibition of the nociceptive flexion reflex during systole could be due to activation of the arterial baroreceptors. Physiological arousal, characterized by raised blood pressure, increases afferent activity from the arterial baroreceptors but attenuates the baroreflex. This study examined the effects of arousal on systolic inhibition of the nociceptive flexion reflex in 38 adults. The threshold current to elicit the reflex in the leg was determined, and participants were stimulated at threshold intensity for 12 trials in two conditions: rest (low arousal) and mental arithmetic (high arousal). In each trial, stimulation was delivered 0 ms, 300 ms, or 600 ms after the R-wave of the electrocardiogram. Nociceptive responding was inhibited for stimulation at 300 ms after the R-wave during rest but not mental arithmetic. This moderation of systolic inhibition of nociception could be due to attenuation of the baroreflex with increased arousal.
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McIntyre et al. (2006) studied this question. Mental arithmetic (high arousal) vs. Rest (low arousal) was evaluated on Nociceptive responding (flexion reflex) at 0, 300, or 600 ms after the R-wave. Mental arithmetic (high arousal) abolished the systolic inhibition of nociceptive responding that was observed at 300 ms after the R-wave during rest.
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