A simple electromagnetic mechanical stimulator for electrophysiological recording in man

In order to study peripheral nervous signals in response to a noxious or innocuous mechanical cutaneous stimulus we deviced an electromechanical stimulator of which stimulus duration, response frequency and delay are perfectly controlled. Using this device, stimulation of the finger has allowed us to record electrophysiological responses over the course of the median nerve.     

Tooth pulp-evoked jaw-opening reflex in the cat: evidence for central facilitation induced by noxious discharge in the intradental nerve fibers

The tooth pulp-evoked jaw-opening reflex was studied in the barbiturate-anesthetized cat. At liminal intensity of the stimulus, a stable short-latency response was obtained in the digastricus and in the tongue. At a higher stimulus intensity, there occasionally appeared to be a prolonged discharge of variable duration in the digastricus, and a second period of activity in the tongue after a silent period. The threshold intensity for these late discharges was supraliminal for the intradental A-fibers and subliminal for intradental C-fibers. Noxious conditioning stimulation of a tooth led to a temporary decrease of the threshold for the jaw-opening reflex elicited from a contralateral or adjacent tooth; only conditioning stimulation at an intensity producing a marked arousal reaction was effective in this respect. Infiltration of the tooth apex with epinephrine produced a local elevation of the threshold for the tooth pulp-evoked jaw-opening reflex. Distant noxious conditioning stimulation (tail pinch) did not influence the jaw-opening threshold. The results indicated that based on some central mechanisms, conditioning noxious stimulation of a tooth can produce a facilitation of the jaw-opening reflex.     

The effects of a distant noxious stimulation on A and C fibre-evoked flexion reflexes and neuronal activity in the dorsal horn of the rat

In the halothane-anaesthetized rat, the responses of 49 neurons in the lumbo-sacral cord and the reflex discharge in the common peroneal nerve following electrical stimulation of the sural nerve were recorded in order to study possible relations between neuronal events and reflex nerve discharges. A distant noxious stimulus (to activate Diffuse Noxious Inhibitory Controls (DNIC) of Le Bars et al.¹⁹) was used as a conditioning stimulus. Only the responses of neurons receiving an input from both A and C fibres were studied. The neurons were classified as class 1 (low threshold mechanoreceptive input only, n = 2), class 2 (nonnoxious and noxious inputs, n =34) or class 3 (responding to noxious stimuli only, n = 13). During conditioning stimulation the C fibre evoked discharge was inhibited in 32 out of 34 class 2 neurons. The A fibre-evoked discharge was simultaneously inhibited in 29 of these neurons. The main effect of the distant noxious stimulation on the C fibre evoked neuronal discharge was to decrease the discharge by a constant number of spikes, independent of the level of evoked activity. Only one class 3 neuron was inhibited during conditioning stimulation and none of the class 1 cells were influenced by DNIC. During conditioning stimulation the late and prolonged C fibre evoked reflex nerve discharge (latency 160–200 ms, duration up to several hundred ms) was strongly depressed. Concomitantly, a short-lasting reflex nerve discharge appeared over the interval 115–160 ms. This released reflex nerve discharge (RR) had a constant latency. There was no simultaneous change of the Aβ evoked reflex nerve discharge. After the end of the distant noxious stimulation the late C fibre evoked reflex nerve discharge (latency 160–200 ms) recovered. Concomitantly, the RR disappeared. The possibility that the class 2 neurons and the class 3 neurons are intercalated in different reflex pathways is discussed.     

Effects of a distant noxious stimulation on A and C fibre-evoked flexion reflexes and neuronal activity in the dorsal horn of the rat

In the halothane-anaesthetized rat, the responses of 49 neurons in the lumbo-sacral cord and the reflex discharge in the common peroneal nerve following electrical stimulation of the sural nerve were recorded in order to study possible relations between neuronal events and reflex nerve discharges. A distant noxious stimulus (to activate Diffuse Noxious Inhibitory Controls (DNIC) of Le Bars et al.) was used as a conditioning stimulus. Only the responses of neurons receiving an input from both A and C fibres were studied. The neurons were classified as class 1 (low threshold mechanoreceptive input only, n = 2), class 2 (nonnoxious and noxious inputs, n = 34) or class 3 (responding to noxious stimuli only, n = 13). During conditioning stimulation the C fibre evoked discharge was inhibited in 32 out of 34 class 2 neurons. The A fibre-evoked discharge was simultaneously inhibited in 29 of these neurons. The main effect of the distant noxious stimulation on the C fibre evoked neuronal discharge was to decrease the discharge by a constant number of spikes, independent of the level of evoked activity. Only one class 3 neuron was inhibited during conditioning stimulation and none of the class 1 cells were influenced by DNIC. During conditioning stimulation the late and prolonged C fibre evoked reflex nerve discharge (latency 160-200 ms, duration up to several hundred ms) was strongly depressed. Concomitantly, a short-lasting reflex nerve discharge appeared over the interval 115-160 ms. This released reflex nerve discharge (RR) had a constant latency. There was no simultaneous change of the A beta evoked reflex nerve discharge. After the end of the distant noxious stimulation the late C fibre evoked reflex nerve discharge (latency 160-200 ms) recovered. Concomitantly, the RR disappeared. The possibility that the class 2 neurons and the class 3 neurons are intercalated in different reflex pathways is discussed.     

Neural activity related to self- versus externally generated painful stimuli reveals distinct differences in the lateral pain system in a parametric fMRI study

Self-generated sensory stimulation can be distinguished from externally generated stimulation that is otherwise identical. To determine how the brain differentiates external from self-generated noxious stimulation and which structures of the lateral pain system use neural signals to predict the sensory consequences of self-generated painful stimulation, we used functional magnetic resonance imaging to examine healthy human subjects who received thermal-contact stimuli with noxious and non-noxious temperatures on the resting right hand in random order. These stimuli were internally (self-generated) or externally generated. Two additional conditions served as control conditions: to account for stimulus onset uncertainty, acoustic stimuli preceding the same thermal stimuli were used with variable or fixed delays but without any stimulus-eliciting movements. Whereas graded pain-related activity in the insula and secondary somatosensory cortex (SII) was independent of how the stimulus was generated, it was attenuated in the primary somatosensory cortex (SI) during self-generated stimulation. These data agree with recent concepts of the parallel processing of nociceptive signals to the primary and secondary somatosensory cortices. They also suggest that brain areas that encode pain intensity do not distinguish between internally or externally applied noxious stimuli, i.e., this adaptive biological mechanism prevents harm to the individual. The attenuated activation of SI during self-generated painful stimulation might be a result of the predictability of the sensory consequences of the pain-related action.     

Prefrontal influences upon the midbrain: A possible route for pain modulation

After implanting stimulating electrodes in the prefrontal cortex (PFC) of adult male rats, the response to PFC stimulation was studied in widely scattered neurons of the midbrain. Subsequent testing was performed to determine if the firing rates of PFC-responsive neurons could also be altered by either a noxious stimulus (foot pinch) or the microiontophoretic administration of various neurotransmitter substances (methionine-enkephalin, ME; norepinephrine, NE; acetylcholine, ACh). Numerous mesencephalic neurons were identified which altered their spontaneous firing rates in response to PFC stimulation. Following PFC stimulation, most (71%) neurons decreased their firing rates. It was also noted that most (78%) PFC-responsive neurons were also responsive to noxious stimulation. Of these neurons, 65% altered their firing rates in a similar manner in response to both PFC and noxious stimuli. The remainder of the neurons which altered their firing rates in response to both PFC and noxious stimulation responded to the two types of stimuli in opposite manners. Of this latter type, it was found that when PFC and noxious stimuli were administered concurrently, PFC stimulation abolished the response to the noxious stimulus. It was also observed that the microiontophoretic administration of either ME or NE frequently (100% and 52% respectively) mimicked the response to PFC stimulation, thereby suggesting that these neurotransmitters may be involved in mediating the PFC influence upon neurons in the midbrain.     

SI nociceptive neurons participate in the encoding process by which monkeys perceive the intensity of noxious thermal stimulation

The activity of primary somatosensory (SI) cortical nociceptive neurons was recorded while the monkeys performed a psychophysical task in which they detected small increases in skin temperature superimposed on noxious levels of thermal stimulation. The detection latency to these stimuli, expressed as detection speed, was used as a measure of the perceived intensity of sensation. Two-thirds of the neurons that responded to noxious thermal stimulation increased their discharge in response to graded increases in stimulus intensity. The remaining neurons responded to noxious thermal stimulation, but did not grade their response with the intensity of the stimulus. The response of SI nociceptive neurons that encode the intensity of noxious thermal stimulation was significantly correlated with the monkey's detection speed. We conclude that SI nociceptive neurons are involved in the encoding process by which monkeys perceive the intensity of noxious thermal stimulation.     

Post-trial hormonal treatment effects: memory modulation or perceptual distortion?

An extensive literature has developed in recent years demonstrating that a variety of peripheral-acting hormonal and pharmacological treatments, administered in post-trial learning paradigms, can substantially influence memory. Careful analysis of the effects of such treatments in passive avoidance paradigms has provided evidence for an interaction between these treatments and the hormonal and physiological events triggered by the noxious stimulation used to induce passive avoidance behavior. The argument developed in this paper is that such post-trial manipulations distort the relationship between the intensity of the noxious stimulus and its physiological sequelae. Considered in this light, changes in passive avoidance behavior appear to represent perceptual distortions rather than memory effects, per se. That is, rather than interfering or enhancing memory processes, peripheral hormonal treatments may simply produce distortions in the perceived intensity of the noxious stimulus.     

Modeling pain circuits: how imaging may modify perception

Pain is the unpleasant sensory experience following tissue damage or the threat of damage. The activation of cortical regions during noxious stimulation is believed a result of the negative affect and sensations generated by the stimulus. How a noxious event is translated into pain experience remains uncertain, and pain that occurs in the absence of a noxious event remains mysterious. Acute pain and chronic pain depend on a categorization of feeling that occurs collectively rather than individually. Capturing that process inside a brain scan is problematic. Resolving this problem requires an approach to imaging that transgress the boundaries of physical and social concepts.     

Stimulation of the periaqueductal gray matter of the rat produces a preferential ipsilateral antinociception.

The few studies analyzing somatotopic organization of stimulation-produced antinociception (SPA) from the periaqueductal gray matter (PAG) have reported contradictory results. In the present study, the distribution of SPA on the hindquarters was assessed by measuring the threshold for inhibition of withdrawal reflexes to noxious heat applied to the hindpaws and tail in pentobarbital-anesthetized rats. Of the 3 body regions tested, the hindpaw contralateral to the stimulating electrode required the highest level of PAG stimulation to inhibit withdrawal. Reducing the intensity of the heat stimulus applied to the hindpaws caused a concomitant reduction in SPA threshold. As before, a higher stimulation current was needed to inhibit the withdrawal reflex in the contralateral than in the ipsilateral paw. These data indicate the antinociception from PAG stimulation is not equally distributed throughout the body, and that the intensity of the noxious stimulus influences the threshold for SPA.     

Long-lasting neuronal activity in rat dorsal horn evoked by impulses in cutaneous C fibres during noxious mechanical stimulation

The responses of 44 nociceptive neurones in the lumbar dorsal horn evoked by controlled mechanical stimulation of the skin, with or without conduction block in myelinated afferent fibres, were studied in the halothane-anaesthetized rat, in order to evaluate the effects of impulses in cutaneous nociceptive C fibres on dorsal horn neurones. Continuous non-noxious pinch of the skin evoked a short-latency discharge (mean latency 15 ms) in all the 13 class 2 neurones (i.e. neurones responding to both non-noxious and noxious stimulation of the skin) tested. The short-latency discharge was followed by weak prolonged activity in 6 neurones. Following noxious pinch of the skin a prominent late discharge (peak latency 150 ms-2 s) was evoked, which in all but two class 2 neurones outlasted the stimulation period (5-10 s). The discharge evoked by noxious pinch in class 3 neurones (i.e. neurones responding to noxious stimulation only) did not usually outlast the stimulation period. In all but two nociceptive neurones tested (n = 26) the late activity evoked by noxious pinch remained, albeit at a lower frequency in some neurones, during a conduction block in A fibres2,3. Hence this late discharge is probably mainly generated by impulses in nociceptive C fibers. It is concluded that nociceptive C fibres have an important role in sustaining long-lasting activation of class 2 neurones during noxious stimulation of the skin and that long-lasting discharges in these neurones indicates tissue damage to their receptive fields.     

Modulated expression of c-Fos in the spinal cord following noxious thermal stimulation of monoarthritic rats

Peripheral noxious stimulation evokes functional and biochemical changes in the spinal cord which results in central sensitization and hyperalgesia, but at the same time also induces the activation of inhibitory control systems. The purpose of the present study was to investigate whether the adaptive changes induced by ongoing peripheral inflammation influence the spinal cord expression of c-Fos (a commonly used marker of neuronal activity) following an additional acute noxious stimulus. Therefore, the spinal expression of c-Fos was immunohistochemically investigated following noxious thermal stimulation of a rat monoarthritic hindpaw at various time points (1, 4, 8, 21 days) after induction of monoarthritis. Compared to normal rats, c-Fos expression following ipsilateral noxious thermal stimulation of monoarthritic rats was strongly modified in the deep laminae of the dorsal horn depending on the time course of inflammation. At 1 day of monoarthritis, an enhanced ipsilateral expression (135% and 208% of normal rats in laminae III–VI and VII, respectively) and at 3 weeks a reduced expression (38% and 23% of normal rats in laminae III–VI and VII, respectively) was detected. The amount of c-Fos-positive neurons in the ipsilateral superficial laminae I and II was unchanged at all time points investigated. To assess excitability changes on the contralateral side at an early stage of inflammation, a group of monoarthritic rats received a contralateral noxious stimulus at day 1 of monoarthritis. This resulted in a potentiated expression of c-Fos ipsilateral to the acute noxious stimulus (i.e., contralateral to the monoarthritic hindpaw) restricted to lamina II (137% of normal rats) of the dorsal horn. The data showed that changes in c-Fos expression depended on the time point of noxious heat stimulation (NHS) of monoarthritic rats, and differed in the ipsi- and contralateral side of the spinal cord. In addition to a possible habituation of c-Fos expression, it may be speculated that the time course-dependent changes reflect laminae-specific modulations of excitatory and inhibitory mechanisms during monoarthritis. Further studies are necessary in order to provide more insights into the contribution of these mechanisms on noxious stimulus-evoked c-Fos expression. J. Neurosci. Res. 53:203–213, 1998. © 1998 Wiley-Liss, Inc.     

Apomorphine can increase cutaneous inhibition of motor activity in Parkinson's disease

We studied the effect of non-nociceptive ipsilateral digital stimulation on EMG recorded from a small hand muscle before and after the administration of subcutaneous apomorphine in 6 patients with Parkinson's disease. All were receiving the drug to control “on-off” fluctuations in motor performance. Averaged rectified EMG was recorded from tonically contracted abductor pollicis brevis (APB) following index finger stimulation using a brief stimulus train. In 5 patients motor evoked potentials (MEPs) were also recorded from APB during tonic contraction. A conditioning stimulus train was applied to the index finger at intervals between 15 and 65 msec prior to the transcranial magnetic stimulus. After apomorphine administration the patient group showed a significant increase in both EMG and MEP inhibition induced by digital stimulation. In patients with Parkinson's disease who have marked motor fluctuations, the inhibitory response of upper limb motor neurones to low level digital cutaneous stimulation can be altered by dopamine agonists.     

Reticular formation influence on neuronal transmission from perforant pathway through dentate gyrus

Electrical stimulation of the perforant pathway discharges granule cell synchronously, giving rise to a characteristic evoked potential in the granule cell layer termed here the evoked action potential or EAP. In freely moving rats, we applied 3 pulses of low intensity electrical stimulation to the medullary reticular formation prior to the application of the perforant path pulse. The effect of prior reticular formation stimulation was a marked augmentation of the normal EAP response to the perforant path stimulus. The augmentation was dependent on the behavioral state of the experimental animal (it occurred during slow-wave sleep but not during still, alert behavior) and was eliminated by anesthetic agents. The latency of EAP augmentation effect (minimum effective time interval between application of the reticular formation stimulus and the perforant path pulse) was 13--18 msec. In order to localize the sites in the medullary reticular formation from which EAP augmentation could be elicited, threshold currents for producing the effect were determined during dorso-ventral penetrations of a reticular formation stimulating electrode. EAP augmentation was elicited at low stimulus currents from a relatively broad region of the reticular formation. It was also noted that reticular formation stimulation which produced EAP augmentation always elicited one or more motor responses of the neck, back, face or vibrissae. Subsequent investigation of the pathways underlying these motor responses suggested that the effect of reticular formation stimulation on granule cell excitability was mediated by a polysynaptic pathway, the first segment of which was a projection to cells of nucleus gigantocellularis of the caudal medulla.     

Repetitive noxious neonatal stimuli increases dentate gyrus cell proliferation and hippocampal brain‐derived neurotrophic factor levels

Neonatal noxious stimulation has been proposed to model pain triggered by diagnostic/therapeutic invasive procedures in premature infants. Previous studies have shown that hippocampal neurogenesis rate and the behavioral repertoire of adult rats may be altered by neonatal noxious stimuli. The purpose of this study was to evaluate whether noxious stimulation during neonatal period alters the nociceptive response and dentate gyrus neurogenesis when compared to rats subjected to a single noxious stimulus in late infancy. Plasma corticosterone and hippocampal brain‐derived neurotrophic factor (BDNF) levels were measured. Neurogenesis in the dentate gyrus was evaluated in adolescent rats (postnatal day 40; P40) exposed twice to intra‐plantar injections of Complete Freund's adjuvant (CFA) on P1 and P21 (group P1P21) or P8 and P21 (P8P21) or exposed once on P21 (pubertal). On P21, one subset of animals received 5‐bromo‐2′‐deoxyuridine (BrdU) and was euthanized on P40 for identification of proliferating cells in the dentate gyrus. Another subset was sampled for thermal response or plasma corticosterone measurement and hippocampal BDNF levels. Proliferative cell rate in dentate gyrus was the highest in all re‐exposed groups (P < 0.001), except for P8 females (P8P21F), revealing also a sex difference, where P8P21 males showed higher rate than females (P < 0.001). Stimulated groups took longer than CTL animals to lick the paws (P < 0.001), regardless of the age when the noxious stimulus was applied. Re‐exposed groups had lower corticosterone plasma level (P1P21 M and F, P8P21M) than controls. On the contrary, hippocampal BDNF was increased in males from both re‐exposed groups. These results show that infant noxious stimulation in neonatally previously stimulated rats is related to high proliferation in the DG and this association seems to be modified by the animal's sex. The new generated dentate granule cells in the hippocampus may have a role in the long‐term behavioral responses to neonatal nociceptive stimulation. Noxious stimulation in the neonatal period results in sex‐dependent neurogenic response. © 2013 Wiley Periodicals, Inc.     

Effects of serotonin and morphine on spontaneous and evoked firing of nociceptive neurons in the trigeminal spinal nucleus of rats

Spontaneously firing neurons that were responsive to noxious face pinch or noxious heat were studied in the trigeminal spinal nucleus of the rat brain. These eurons responded with either an increase or decrease in firing rate. In these neurons serotonin (5-hydroxytryptamine; 5-HT) apparently acts through two mechanisms to attenuate the response to a noxious stimulus. One mechanism is mimicked by morphine; these two drugs block the response to the noxious stimuli without having a consistent effect on spontaneous firing. The effects of the two drugs were somewhat selective depending on the noxious stimulus used and the effect of the noxious stimulus; morphine and 5-HT were more effective in blocking the increase in firing rate evoked by the face pinch but 5-HT and morphine were more effective in blocking the decrease in firing rate evoked by the noxious heat stimulus. Interestingly, the direction of the response to a particular noxious stimulus frequently predicted whether or not both morphine and 5-HT would act on the same or different neurons. A second mechanism by which 5-HT, but not morphine, acted was to change the spontaneous firing in a direction opposite that evoked by the noxious stimulus. This type of effect apparently modulated the response to a noxious stimulus by changing the spontaneous firing rate such that a noxious stimulus had to be more intense before it could significantly alter the neuronal firing in the opposite direction. Morphine occasionally produced a change in firing pattern in neurons; this effect remains to be documented more extensively.     

Carpal tunnel syndrome : Which finger should be tested? An analysis of sensory conduction in digital branches of the median nerve

Each digital branch of the median nerve was stimulated in turn in 34 women (55 hands) with carpal tunnel syndrome (CTS). The amplitude and conduction velocity of the sensory nerve action potential (SNAP) recorded at the wrist, and the threshold for patient perception of the electrical stimulus on the median innervated sides of each digit, were compared with the corresponding values in a group of asymptomatic, age-matched women. Sensory conduction velocity or SNAP amplitude were abnormal in more than 80% of all digital nerves studied apart from those in the index finger. Stimulation of digital nerves in the index finger proved the least sensitive means of detecting the electrophysiological abnormality. We conclude that selective digital nerve stimulation is a sensitive technique in the diagnosis of CTS. If ring electrodes are preferred, our results suggest that the middle rather than the index finger should be used.     

The effect of morphine on responses of nucleus ventroposterolateralis neurons to colorectal distension in the rat

In 71 halothane-anesthetized rats, we characterized the responses of single neurons in the nucleus ventroposterolateralis (VPL) of the thalamus to a noxious visceral stimulus (colorectal balloon distension; CRD) and studied the effects of intravenous morphine on these responses using standard extracellular microelectrode recording techniques. One hundred nine neurons were isolated on the basis of spontaneous activity. Sixty-four (59%) responded to CRD, of which 52 (81 %) had excitatory and 12 (19%) had inhibitory responses. Neurons showed graded responses to graded CRD pressures (20-100 mmHg), with maximum excitation or inhibition occurring at 80 mmHg. Responses to noxious (pinch, heat) and innocuous (brush, tap) cutaneous stimuli were studied in 95 of the VPL neurons isolated. Eighty-three of these neurons (48 CRD responsive and 35 CRD nonresponsive) (87%) had cutaneous receptive fields, of which 96% were small and contralateral and 4% were large and contralateral or bilateral. Ninety-four percent of these neurons responded to both noxious and innocuous cutaneous stimulation, and 6% responded to only noxious stimulation. No neurons responded solely to innocuous stimulation. Cumulative doses of morphine (0.125, 0.25, 0.5, 1, and 2 mg/kg, i.v) produced statistically significant dose-dependent attenuation of neuronal responses to CRD. Naloxone (0.4 mg/ kg, i.v.) reversed the effects of morphine. Morphine and naloxone had no significant effects on spontaneous activity. These data support the involvement of VPL neurons in visceral nociception and are consistent with a role of VPL in sensory-discriminative aspects of nociception.     

Relationship between event-related beta synchronization and afferent inputs: analysis of finger movement and peripheral nerve stimulations.

OBJECTIVE: We compared beta synchronization associated with voluntary finger movement with beta synchronization produced by sensory stimulation, in order to better understand the relationship between event-related beta synchronization (ERS) and the different afferent inputs. METHODS: Twenty-four subjects performed an index finger extension. They also received three types of electrical stimulation (cutaneous stimulation of the index finger, single and repetitive stimulation of the median nerve). An EEG was recorded using 38 scalp electrodes. Beta ERS was analyzed with respect to movement offset and the stimulus (or the last stimulus in the series, for repetitive stimulation). RESULTS: Median nerve stimulation and finger extension induced more intense beta ERS than cutaneous stimulation. The magnitude of beta ERS induced by movement or by single median nerve stimulation were not different but post movement beta synchronization duration was longer than beta ERS induced by single median nerve stimulation and cutaneous stimulation. CONCLUSIONS: This study demonstrates that beta ERS depends on the type and quantity of the afferent input. SIGNIFICANCE: This work reinforces the hypothesis of a relationship between beta ERS and processing of afferent inputs.     

Magnetoencephalographic study of event‐related fields and cortical oscillatory changes during cutaneous warmth processing

Thermoreception is an important cutaneous sense, which plays a role in the maintenance of our body temperature and in the detection of potential noxious heat stimulation. In this study, we investigated event‐related fields (ERFs) and neural oscillatory activities, which were modulated by warmth stimulation. We developed a warmth stimulator that could elicit a warmth sensation, without pain or tactile sensation, by using a deep‐penetrating 980‐nm diode laser. The index finger of each participant (n = 24) was irradiated with the laser warmth stimulus, and the cortical responses were measured using magnetoencephalography (MEG). The ERFs and oscillatory responses had late latencies (～1.3 s and 1.0–1.5 s for ERFs and oscillatory responses, respectively), which could be explained by a slow conduction velocity of warmth‐specific C‐fibers. Cortical sources of warmth‐related ERFs were seen in the bilateral primary and secondary somatosensory cortices (SI and SII), posterior part of the anterior cingulate cortex (pACC), ipsilateral primary motor, and premotor cortex. Thus, we suggested that SI, SII, and pACC play a role in processing the warmth sensation. Time–frequency analysis demonstrated the suppression of the alpha (8–13 Hz) and beta (18–23 Hz) band power in the bilateral sensorimotor cortex. We proposed that the suppressions in alpha and beta band power are involved in the automatic response to the input of warmth stimulation and sensorimotor interactions. The delta band power (1–4 Hz) increased in the frontal, temporal, and cingulate cortices. The power changes in delta band might be related with the attentional processes during the warmth stimulation.