Encoding of nociceptive thermal stimuli by diffuse noxious inhibitory controls in humans. J Neurophysiol

Laboratoire de Neurophysiologie, Faculté de Médecine Pitié-Salpêtrière, Paris, France.
Journal of Neurophysiology (Impact Factor: 2.89). 12/1989; 62(5):1028-38.
Source: PubMed


1. It has previously been shown that, in normal humans, heterotopic painful thermal conditioning stimuli induce parallel increase in the thresholds of a spinal nociceptive flexion reflex (RIII reflex) and the concurrent sensation of pain elicited by electrical stimulation of the sural nerve. On the basis of analogous animal studies, we proposed that such phenomena could be related to diffuse noxious inhibitory controls (DNIC), which have been described in the rat. The present study, which was carried out on normal volunteer subjects, was particularly concerned with the extent and temporal characteristics of the depressive effects of DNIC triggered by painful thermal stimuli on RIII reflex activity. In addition, because it was possible that these depressive effects could have resulted from a direct postsynaptic inhibition of motoneurons, a second part of the study was aimed at determining whether or not the heterotopic noxious thermal stimuli also affected the excitability of alpha-motoneurons, as monitored by the monosynaptic Hoffmann reflex (H reflex) technique. 2. In the 11 subjects under study, application of moderate, nonnoxious temperatures (40-44 degree C) to the contralateral hand (via a thermoregulated and agitated waterbath) did not modify the RIII reflex nor the associated sensation of pain. By contrast noxious temperatures clearly depressed the RIII reflex and the concurrent sensation of pain, both during and after the conditioning procedure (CP), in a direct linear relationship to the temperature of the waterbath in the 45-47 degree C range; the maximal depressive effect was observed with the highest conditioning temperature. A significant relationship was also found between the extent of the RIII depression during the CP and that during a 10-min period of post-CP observation. 3. The depressive effects observed on both the RIII reflex and pain were not associated with clear change in autonomic functions. Respiration remained stable during the sessions, with no significant relationship between the temperatures of the waterbath and respiratory rate. Heart rate was slightly but significantly increased during the immersion of the hand in the 46 or 47 degree C waterbaths; this increase, however, ceased with the end of CP. 4. Application of thermal conditioning stimuli produced a slight but nonsignificant increase of the monosynaptic H reflex during the first minute of CP, no matter what was the temperature of the waterbath. However, there were no subsequent variations during the 6-min period of post-CP observation.(ABSTRACT TRUNCATED AT 400 WORDS)

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Available from: Daniel Le Bars, Aug 17, 2014
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    • "Another limitation is the lack of pain inhibition during HNCS, although pain-related brain activity was decreased. In previous studies using similar methods, HNCS produced a robust decrease of pain perception in healthy volunteers (Willer et al., 1989; Piché et al., 2009, 2011; Bouhassira et al., 2013). However, the present experimental design was different in comparison to these studies, with a lower stimulation frequency (every 60 s vs every 6–12 s) and a longer HNCS duration (20 min vs 1–2 min). "
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    ABSTRACT: The aim of this study was to investigate the association between the magnitude of anti-nociceptive effects induced by heterotopic noxious counter-stimulation (HNCS) and the basal μ-opioid receptor availability in the amygdala. In 8 healthy volunteers (4 females and 4 males), transcutaneous electrical stimulation was applied to the right sural nerve to produce the nociceptive flexion reflex (RIII-reflex), moderate pain, and scalp somatosensory evoked potentials (SEP). Immersion of the left hand in cold water for 20 min was used as HNCS. In a separate session, basal μ-opioid receptor availability was measured using positron emission tomography with the radiotracer [11C]carfentanil. HNCS produced a reduction of the P260 amplitude (p < 0.05), a late component of SEP that reflects activity in the anterior cingulate cortex. This reduction was associated with higher basal μ-opioid receptor availability in the amygdala on the right (R2 = 0.55, p = 0.03) with a similar trend on the left (R2 = 0.24, p = 0.22). Besides, HNCS did not induce significant changes in pain and RIII-reflex amplitude (p > 0.05). These results suggest that activation of μ-opioid receptors in the amygdala may contribute to the anti-nociceptive effects of HNCS. The lack of RIII-reflex modulation further suggests that μ-opioid receptor activation in the amygdala contributes to decrease pain-related brain activity through a cerebral mechanism independent of descending modulation.
    Full-text · Article · Apr 2014 · Neuroscience Research
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    • "We are therefore confident that lack of power should not be confounding in the present 8 subjects study. RIII inhibition in response to a noxious stimulus depends on its intensity (Willer et al., 1989). We cannot rule out the hypothesis that our dyspnogenic stimulus was insufficiently intense, but our subjects reported very high ratings of breathing difficulty at the end of the 5th minute of the CO 2 -V T period. "
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    ABSTRACT: Dyspnoea has distinct sensory modalities, including air hunger and the sensation of excessive breathing "work/effort". Both have analgesic properties. In the case of work/effort, spinal mechanisms have been documented (inhibitory effect on the spinal nociceptive flexor reflex, RIII). This mechanism involves C-fibres. As C-fibres are unlikely to play a major role in air hunger, we hypothesised that inducing this type of dyspnoea would not result in RIII inhibition. Eight healthy volunteers were exposed to a hypercapnic hyperoxic gas mixture (5% CO2 and 95% O2) and asked to voluntarily fight the corresponding ventilatory reflex response by reducing tidal volume below its spontaneous level. Ventilatory variables and dyspnoea intensity (ordinal scale) were measured. Electromyography of the biceps femoris was used to record the amplitude of RIII in response to painful electrical sural nerve stimulation. Air hunger failed to inhibit the RIII reflex. We conclude that the mechanisms of air hunger induced analgesia do not include a spinal contribution and are therefore mostly central.
    Full-text · Article · Oct 2013 · Respiratory Physiology & Neurobiology
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    • "Counter-stimulation involves the application of 2 competing stimuli on different regions of the body. Stimuli can be nociceptive or non-nociceptive, but it has been demonstrated that only nociceptive counter-stimulation may produce inhibitory effects [23] [47]. In the anaesthetised rat, when 2 nociceptive stimuli are applied, the strongest stimulus decreases the activity of widedynamic-range (WDR) neurons induced by the competing stimulus , through descending pathways [23] [24]. "
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    ABSTRACT: Neuroimaging methods such as functional magnetic resonance imaging (fMRI) have been used extensively to investigate pain-related cerebral mechanisms. However, these methods rely on a tight coupling of neuronal activity to hemodynamic changes. Because pain may be associated with hemodynamic changes unrelated to local neuronal activity (e.g., increased mean arterial pressure (MAP)), it is essential to determine whether the neurovascular coupling is maintained during nociceptive processing. In this study, local field potentials (LFP) and cortical blood flow (CBF) changes evoked by electrical stimulation of the left hind paw were recorded concomitantly in the right primary somatosensory cortex (SI), in 15 rats. LFP, CBF and MAP changes were examined in response to stimulus intensities ranging between 3 to 30 mA. In addition, LFP, CBF and MAP changes evoked by a 10-mA stimulation were examined during immersion of the tail in non-nociceptive or nociceptive hot water (counter-stimulation). SI neurovascular coupling was altered for stimuli of nociceptive intensities (p<0.001). This alteration was intensity-dependent and was strongly associated with MAP changes (r=0.98, p<0.001). However, when the stimulus intensity was kept constant, SI neurovascular coupling was not significantly affected by nociceptive counter-stimulation (p=0.4), which similarly affected the amplitude of shock-evoked LFP and CBF changes. It remains to be determined whether such neurovascular uncoupling occurs in humans, and whether it also affects other regions usually activated by painful stimuli. These results should be taken into account for accurate interpretation of fMRI studies that involve nociceptive stimuli associated with MAP changes.
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