Key result
Craniofacially evoked conditioned pain modulation increases pressure pain thresholds versus control.
Why the study?
The effect of craniofacially evoked conditioned pain modulation on trigeminal somatosensory function using quantitative sensory testing was not systematically investigated in healthy humans.
Does craniofacially evoked conditioned pain modulation affect trigeminal somatosensory function in healthy humans?
Does craniofacially evoked conditioned pain modulation affect trigeminal somatosensory function in healthy humans?
p-value: p=<.001
When extensive quantitative sensory testing protocols are applied, pressure pain threshold may be the most sensitive measure to detect endogenous pain inhibitory mechanisms.
No immediate clinical implications for trigeminal testing; leaves open PPT sensitivity for detecting endogenous inhibition in healthy humans.
The aim of the study was to systematically investigate the effect of craniofacially evoked conditioned pain modulation on somatosensory function using a quantitative sensory testing (QST) protocol applied to the trigeminal area in healthy humans. Pressure pain evoked by a mechanical compressive device was applied as conditioning stimulus (CS) in the craniofacial region, with a pain intensity of 5 on a visual analogue scale (VAS: 0-10 cm) (painful session) or with VAS score of 0 (control session). A full QST battery of 13 parameters was performed as test stimuli on the dominant-side cheek. The individual QST data from 11 men and 12 women were transformed into z scores, and the QST data and z scores were tested using analyses of variance. Analyses of variance of pressure pain threshold (PPT) data (log-transformed values and z scores) indicated significant session (P ≤ .003) and time (P < .001) effects with a session-time interaction (P < .001), but no main effect of sex (P ≥ .053, effect size ≥ .166). The session-time interaction showed that the PPTs in the painful session were associated with significantly higher log-transformed PPT values and significantly lower z scores compared with the control session at the time point during CS (hypoalgesia) (P < .001). No other QST parameters were significantly modulated by the CS. Sex differences were not detected in this study; a larger sample size may be needed to further explore this possibility. However, the findings indicate that when extensive QST protocols are applied, PPT may be the most sensitive measure to detect endogenous pain inhibitory mechanisms.
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Oono et al. (2013) studied Healthy humans (n=23). Craniofacially evoked conditioned pain modulation vs. Control session (VAS 0) was evaluated on Pressure pain threshold (PPT) (p=<.001). Craniofacially evoked conditioned pain modulation significantly increased pressure pain thresholds (hypoalgesia) compared with a control session (P < .001).
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