Pain Processing Is Faster than Tactile Processing in the Human Brain

Abstract

Pain signals threat and drives the individual into a behavioral response that significantly depends on a short stimulus-response latency. Paradoxically, the peripheral and spinal conduction velocities of pain are much slower than of tactile information. However, cerebral processing times and reaction times of touch and pain have not yet been fully assessed. Here we show that reaction times to selective nociceptive cutaneous laser stimuli are substantially faster than expected from the peripheral conduction velocities. Furthermore, by using magnetoencephalography, we found that latencies between earliest stimulus-evoked cortical responses and reaction times are ϳ60 ms shorter for nociceptive than for tactile stimuli. These findings reveal that cerebral processing of pain is substantially faster than processing of tactile information and relatively compensates for the slow peripheral and spinal conduction velocities of pain. Our observation shows how the cerebral organization of pain processing enhances motor responses to potentially harmful stimuli and thereby subserves the particular behavioral demands of pain.

Gamma oscillations are involved in the sensorimotor transformation of pain

“…Our results would thus be compatible with the recent suggestion that the anterior midcingulate cortex integrates information about negative affect including pain to initiate adaptive motor responses (Shackman et al 2011). The direct thalamomotor route of nociceptive information could well reflect the particular biological relevance of complex but coordinated motor responses to pain and complements other evidence for a parallel organization of pain pathways in the human brain (Frot et al 2008;Ploner et al 2006bPloner et al , 1999.…”

Functional integration within the human pain system as revealed by Granger causality

“…The longer reaction times to painful than to tactile stimuli are due to the lower conduction velocity of nociceptive peripheral pathways (10-20 m/s) compared with tactile pathways [Vallbo et al, 1979;Meyer et al, 2006]. Pain-evoked S1 activations were located more medially and posteriorly than tactileevoked activations as shown in previous studies which directly compared locations of responses to painful and tactile stimuli [Kanda et al, 2000, Ploner et al 2000, 2006b]. …”

“…Thus, analysis was based on 10 subjects. Evoked responses to painful and non-painful stimuli have been reported in a previous analysis of the experimental data [Ploner et al, 2006b]. …”

“…Analysis of time courses was based on modalityspecific locations of tactile and pain-related responses as obtained from the spatiotemporal source model (see above). The usage of modality-specific locations of responses accounts for differences between locations of pain-evoked and tactileevoked responses [Kanda et al, 2000, Ploner et al 2000, 2006b into 1500 ms segments, running from 500 ms prior to the stimulus until 1000 ms after the stimulus. We applied a bandstopfilter (4 th -order Butterworth filter, stopband 33-36 Hz) to remove a well-known laboratory artifact.…”

“…The present study complements and extends these observations by showing directly the causal interactions, or better, the lack of causal interactions between these areas and thereby provides further confirmatory evidence for a parallel organization of S1 and S2 in human pain processing. Functionally, the parallel organization of pain may represent an evolutionary old, simple and robust substrate for fast and effective behavioral reactions to threatening and behaviorally relevant stimuli [Ploner et al, 2006b]. …”