EEG responses to tonic heat pain

Abstract

The aim of the present study was to characterize the EEG response pattern specific for tonic pain which is an experimental pain model resembling clinical pain more closely than phasic pain. Tonic experimental pain was produced by a series of heat pulses 1 degree C above pain threshold over 10 min. A series of heat pulses 0.3 degree C below pain threshold and a constant temperature of 37 degrees C served as non-painful heat control and as baseline condition, respectively. The level of attention was experimentally manipulated by instruction and by a distraction task. Twenty male, pain-free subjects had to rate the sensation intensity and sensation unpleasantness during thermal stimulation. Furthermore, a German version of the McGill Pain Questionnaire was to be filled out after tonic painful heat stimulation. The EEG was recorded via 10 leads according to 10/20 convention. Power density was calculated for the usual frequency bands. The ratings showed that tonic painful heat was experienced clearly distinct from tonic non-painful heat. An EEG response pattern emerged characterized by a rather generalized increased delta(2) activity, a left-biased fronto-temporally diminished theta activity, a fronto-temporal decrease in the alpha(1) activity and a left-sided temporal increase in the beta(1) activity. This observation agrees well with the findings of others. However, there was no evidence in our data that these EEG changes are specific to tonic heat pain as opposed to changes observed during tonic non-painful heat stimulation. Accordingly, the repeatedly reported EEG patterns are also likely to be produced by other forms of strong somatosensory stimuli and to be not specific for pain.

Linear and nonlinear analyses of EEG dynamics during non-painful somatosensory processing in chronic pain patients

“…In the present study, several aspects of the EEG pattern elicited by non-painful somatosensory stimulation in chronic pain patients also resemble those reductions in alpha over parietal brain regions observed in healthy controls during experimental acute pain (Chang et al, 2002b;Chang et al, 2002aChang et al, , 2003Chang et al, 2004). Although the significance of these changes in EEG elicited by tonic painful stimulation is still controversial (Apkarian et al, 2005;Stevens et al, 2000), it has been argued that reductions in alpha activity over posterior brain regions could be part of a general orienting and attentional response towards any kind of stimulation (Hubert et al, 2006), or reflect a central and specific processing of the attention system during sustained painful stimulation (Chang et al, 2002a). According with these interpretations, the observed pattern of reduced alpha in chronic pain might indicate that persistent pain, as it occurs in chronic pain sates, would lead to a sustained activation of an attentional pain system or increased alertness in posterior parietal brain regions even during the processing of non-painful body information.…”

Effects of Verum Acupuncture Compared to Placebo Acupuncture on Quantitative EEG and Heart Rate Variability in Healthy Volunteers

“…This is also supported by the correlation of pain with the different parameters of the ECG and EEG. The EEG changes that exclusively arise due to pain normally show a rather generalized pattern with predominance of the ␤ band, 28,29 which remained statistically unchanged in our study.…”

Effective electromagnetic noise cancellation with beamformers and synthetic gradiometry in shielded and partly shielded environments

“…Contrast these findings with evoked potentials generated by the CHEPS and other similar heat stimulators (600 ms stimulus duration) which are slower and longer in duration (500-1000 ms) (Le Pera et al, 2002). Consequently, the sensation may be more comparable to that experienced in tonic thermal pain, for which delayed increases in beta power have also been reported (Huber et al, 2006). Finally, there is some evidence to suggest that a power increase in the beta frequency bandwidth may be indicative of selective activation of the A-delta nociceptive fibres only (Raij et al, 2004).…”

“…Pre-and post-stimulus time windows of half a second, 1 and 2 s length were compared for the frequency bands of 13-20 and 20-30 Hz, corresponding to the beta rhythm exhibited by the sensorimotor cortices (Hari and Salmelin, 1997;Lounasmaa et al, 1996) and in which changes have been reported in response to pain (Chang et al, 2002;Huber et al, 2006;Lalo et al, 2007). For each of the eight participants, the SAM comparison showing activation within the primary somatosensory cortex was converted into MNI (Montreal Neurological Institute) space using a method of normalisation (Friston et al, 1994) to enable comparisons across participants and with previously reported source reconstructions following stimulation of the hand.…”