The reliability of two prospective cortical biomarkers for pain: EEG peak alpha frequency and TMS corticomotor excitability

Chowdhury, Nahian S.; Skippen, Patrick; Si, Emily; Chiang, Alan; Millard, Samantha K; Furman, Andrew J.; Chen, Shuo; Schabrun, Siobhan M; Seminowicz, David A.

doi:10.1016/j.jneumeth.2022.109766

Cited by 24 publications

(32 citation statements)

References 75 publications

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“…For the first time, a cognitive-affective construct has been identified as a potential link connecting PAF to pain. In line with other studies of PAF, 2,18 this result was not dependent on a particular PAF calculation method, which helps to further establish the robustness of PAF as a metric and potential biomarker of pain.…”

supporting

confidence: 90%

Fear and pain slow the brain

Mazaheri,

Furman,

Seminowicz

2023

Pain

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N europhysiological signals detected noninvasively at the scalp using techniques such as EEG/MEG contain rhythms (oscillatory activity) occurring at distinct frequency bands. The predominant rhythm in healthy humans occurs between the bandwidth of 8 to 14 Hz and is commonly referred to as the alpha rhythm. The frequency within the alpha band where power is maximal is called the peak alpha frequency (PAF) or individual alpha frequency. Peak alpha frequency varies considerably between individuals, 9,14 and this variability is believed to play a role in the individual differences in perceptual ability and temporal binding of sensory information. 1,8,21,23 The relationship of PAF to both acute and chronic pain is an exciting area currently under investigation by multiple laboratories. Patients with chronic pain often exhibit changes in alpha rhythms, particularly slower PAF, when compared with control subjects, 26 and the degree of PAF slowing has been found to correlate with chronic pain duration. 3 One interpretation of this PAF slowing is that it reflects brain processes that actively maintain chronic pain, such as excess "inhibition or disfacilitation" brought about by ongoing pain. 16 An alternative interpretation is that slower PAF reflects processes related to higher pain sensitivity and an increased disposition to develop chronic pain that predate disease onset. This latter interpretation is supported by a series of studies of acute pain in healthy subjects, which found that an individual's PAF recorded during a pain-free rest period was negatively correlated with the intensity of a future pain event. [5][6][7] This work has undergone initial clinical validation: In a cohort of patients undergoing thoracotomy, PAF collected before surgery was able to predict the severity of postsurgery pain. 20 Thus, PAF has been suggested as a biomarker of pain sensitivity, which has been hypothesized to be a key factor in the transition from acute to chronic pain. 10 Precisely how PAF fits into the myriad of biological, social, and psychological factors involved in the transition from acute to chronic pain has remained unexplored. One of these factors is the fear of movement, which has been demonstrated to be a significant predictor of the transition from acute low back pain to chronic low back pain (CLBP). 19,25

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supporting

confidence: 90%

Fear and pain slow the brain

Mazaheri,

Furman,

Seminowicz

2023

Pain

Self Cite

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“…For example, recording resting state EEG with eyes closed emphasises the contribution of occipital alpha oscillations, as opposed to when eyes are open (Berger, 1929). In addition, the peak picking method of PAF estimation in the included studies is less reliable than the centre of gravity (CoG) method (Chowdhury et al, 2023) and also overlooks the possibility of multiple alpha peaks in an individual's frequency spectra (Chiang et al, 2011(Chiang et al, , 2008. This oversight disregards the potential for changes in PAF speed through relative increases in the power of faster alpha oscillations compared to slower alpha oscillations (Furman et al, 2021).…”

Section: Recommendations and Future Directionsmentioning

confidence: 99%

Can non-invasive brain stimulation modulate peak alpha frequency in the human brain? A systematic review and meta-analysis

Millard,

Speis,

Skippen

et al. 2023

Preprint

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Peak alpha frequency, the dominant oscillatory frequency within the alpha range (8–12 Hz), is associated with cognitive function and several neurological conditions, including chronic pain. Manipulating PAF could offer valuable insight into the relationship between PAF and various functions and conditions and provide new treatment avenues. This systematic review aimed to comprehensively synthesise effects of non-invasive brain stimulation (NIBS) on PAF speed. Relevant studies assessing PAF pre- and post-NIBS in healthy adults were identified through systematic searches of electronic databases (Embase, PubMed, PsychINFO, Scopus, The Cochrane Library) and trial registers. The Cochrane risk-of-bias tool was employed for assessing study quality. Quantitative analysis was conducted through pairwise meta-analysis when possible; otherwise, qualitative synthesis was performed. The review protocol was registered with PROSPERO (CRD42020190512) and the Open Science Framework (https://osf.io/2yaxz/). Eleven NIBS studies were included, all with a low risk-of-bias, comprising seven transcranial alternating current stimulation (tACS), three repetitive transcranial magnetic stimulation (rTMS), and one transcranial direct current stimulation (tDCS) study. Meta-analysis of active tACS conditions (eight conditions from five studies) revealed no significant effects on PAF (mean difference [MD] = -0.12, 95% CI = -0.32 to 0.08, p = 0.24). Qualitative synthesis provided no evidence that tDCS altered PAF and moderate evidence for transient increases in PAF with 10 Hz rTMS. There is limited evidence that NIBS can modulate PAF, and existing evidence does not demonstrate robust effects. Further studies employing standardised stimulation protocols are necessary to determine the potential of NIBS to modulate PAF.

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“…In some participants, background EMG activity was observed due to placement of the thermode close to the EMG electrodes, which can influence MEP amplitude (Ruddy et al, 2018). To account for this, MEP amplitude was calculated by subtracting the root mean square (RMS) of background EMG noise from the RMS of the MEP window using a fixed window between 55 and 5ms before the TMS pulse (Chowdhury et al, 2023;Schabrun et al, 2017;Tsao et al, 2011).…”

Section: Data Processingmentioning

confidence: 99%

Alterations in cortical excitability during pain: A combined TMS-EEG Study

Chowdhury

Chiang

Millard

et al. 2023

Preprint

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Transcranial magnetic stimulation (TMS) has been used to examine the inhibitory and facilitatory circuits during experimental pain and in chronic pain populations. However, current applications of TMS to pain have been restricted to measurements of motor evoked potentials (MEPs) from peripheral muscles. Here, TMS was combined with electroencephalography (EEG) to determine whether experimental pain could induce alterations in cortical inhibitory/facilitatory activity observed in TMS-evoked potentials (TEPs). In Experiment 1 (n = 29), multiple sustained thermal stimuli were administered over the forearm, with the first, second and third block of stimuli consisting of warm but non-painful (pre-pain block), painful heat (pain block) and warm but non-painful (post-pain block) temperatures respectively. During each stimulus, TMS pulses were delivered while EEG (64 channels) was simultaneously recorded. Verbal pain ratings were collected between TMS pulses. Relative to pre-pain warm stimuli, painful stimuli led to an increase in the amplitude of the frontocentral negative peak ~45ms post-TMS (N45), with a larger increase associated with higher pain ratings. Experiments 2 and 3 (n = 10 in each) showed that the increase in the N45 in response to pain was not due to changes in sensory potentials associated with TMS, or a result of stronger reafferent muscle feedback during pain. This is the first study to use combined TMS-EEG to examine alterations in cortical excitability in response to pain. These results suggest that the N45 TEP peak, which indexes GABAergic neurotransmission, is implicated in pain perception and is a potential marker of individual differences in pain sensitivity.

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The reliability of two prospective cortical biomarkers for pain: EEG peak alpha frequency and TMS corticomotor excitability

Cited by 24 publications

References 75 publications

Fear and pain slow the brain

Fear and pain slow the brain

Can non-invasive brain stimulation modulate peak alpha frequency in the human brain? A systematic review and meta-analysis

Alterations in cortical excitability during pain: A combined TMS-EEG Study

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