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. 2025 Sep;32(9):e70363.
doi: 10.1111/ene.70363.

Relieving Chronic Neuropathic Pain With EEG-Neurofeedback

Affiliations

Relieving Chronic Neuropathic Pain With EEG-Neurofeedback

Thibaut Mussigmann et al. Eur J Neurol. 2025 Sep.

Abstract

Background: Electroencephalography (EEG)-guided neurofeedback (NFB) is a rarely evaluated neuromodulation technique for the treatment of chronic neuropathic pain.

Methods: The analgesic efficacy of EEG-NFB based on two different EEG targets was assessed in two groups of 16 patients with peripheral neuropathic pain. Twelve EEG-NFB sessions were performed over 4 weeks to improve the β1/β2 or α/θ ratio in the EEG signal of the central cortical region contralateral to the pain side. Before and 1 week after treatment, pain interference with daily life (primary endpoint), pain intensity, neuropathic symptom profile, pain catastrophizing, anxiety, depression, fatigue, and sleep quality were evaluated. In addition, EEG was recorded in the resting state before and after EEG-NFB sessions, as well as during the sessions.

Results: Significant analgesic effects were observed on the primary endpoint in both groups. However, β1/β2 training specifically reduced the intensity of ongoing and evoked pain, while anxiety and depression were reduced after α/θ training. Responders to β1/β2 training increased β1 activities or β1/β2 ratio in the resting state or during the EEG-NFB sessions, while an increase in the β1/β2 ratio was also observed during the sessions in responders to α/θ training. In 12 of the 15 responders, a transfer task was performed and showed partial maintenance of therapeutic benefit.

Conclusions: EEG-NFB can produce analgesia with different clinical and neurophysiological impacts according to various EEG targets. These results open perspectives for the use of EEG-NFB protocols in the treatment of chronic neuropathic pain, based on well-defined EEG targets.

Keywords: alpha; beta; chronic pain; theta; treatment.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

FIGURE 1
FIGURE 1
Study design. AD‐2‐Fr, AttrakDiff questionnaire (French version of the abridged form); BFI‐Fr, dimension scores of the Big Five Inventory (French version); BIS, Barratt Impulsiveness Scale (brief form); BPI, 7‐item interference score of the Brief Pain Inventory; CSI, Central Sensitization Inventory (short form); DN4, 4‐item Neuropathic Pain Questionnaire; EEG, electroencephalography; Exp‐LoC‐Q, expectancies and locus of control questionnaire; FMI‐Fr, sub‐scores of the Freiburg Mindfulness Inventory (French version of the short form); FSS, Fatigue Severity Scale; HAD, Hospital Anxiety and Depression questionnaire parts A and D; LSEQ, Leeds Sleep Evaluation Questionnaire; NExT‐Q, sub‐scores of the NExT questionnaire; NFB, neurofeedback; NPSI, Neuropathic Pain Symptom Inventory; NRS, numeric rating scale of pain intensity; PCS, Pain Catastrophising Scale; rsEEG, resting‐state electroencephalography; TMT, Trail Making Test parts A and B; VRS, verbal rating scale of pain intensity. Responders: patients with at least 30% improvement on BPI after intervention (T2 vs. T1).
FIGURE 2
FIGURE 2
Flowchart of the study. NFB, neurofeedback.
FIGURE 3
FIGURE 3
Evolution of pain interference in the responders who completed the transfer task. Upper row: Evolution of the Brief Pain Inventory interference (BPI) scores in each participant: changes are indicated with a solid line when the benefit obtained at T2 (1 week after the end of EEG‐neurofeedback training) compared to baseline (T1) was maintained at T3 (1 week after the end of the transfer task) or with a dotted line when the BPI score tended to return to baseline value at T3. Lower row: Mean values (±standard deviation) of BPI scores in the group of patients with significant decrease at T2 (**p < 0.01), which remained significant at T3 (*p < 0.05) compared to BPI scores at T1.

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