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Brain Advance Access originally published online on September 23, 2005
Brain 2006 129(1):55-64; doi:10.1093/brain/awh631
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© The Author (2005). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Increased EEG power and slowed dominant frequency in patients with neurogenic pain

Johannes Sarnthein1,2, Jair Stern1, Christoph Aufenberg1, Valentin Rousson3 and Daniel Jeanmonod1,2

1 Universitätsspital, Funktionelle Neurochirugie, CH-8091 Zürich, 2 Center for Integrative Human Physiology and 3 Biostatistik, Universität Zürich, Switzerland

Correspondence to: Johannes Sarnthein, Funktionelle Neurochirurgie, Universitätsspital, CH-8091 Zürich, Switzerland E-mail: johannes.sarnthein{at}usz.ch

To study the mechanisms of chronic neurogenic pain, we compared the power spectra of the resting EEG of patients (n = 15, 38–75 years, median 64 years, 6 women) and healthy controls (n = 15, 41–71 years, median 60 years, 8 women). On an average, the patient group exhibited higher spectral power over the frequency range of 2–25 Hz, and the dominant peak was shifted towards lower frequencies. Maximal differences appeared in the 7–9 Hz band in all electrodes. Frontal electrodes contributed most to this difference in the 13–15 Hz band. Bicoherence analysis suggests an enhanced coupling between theta (4–9 Hz) and beta (12–25 Hz) frequencies in patients. The subgroup of six patients free from centrally acting medication showed higher spectral power in the 2–18 Hz frequency range. On an individual basis, the combination of peak height and peak frequency discriminated between patient and control groups: discriminant analysis classified 87% of all subjects correctly. After a therapeutic lesion in the thalamus (central lateral thalamotomy, CLT) we carried out follow-up for a subgroup of seven patients. Median pain relief was 70 and 95% after 3 and 12 months, respectively. The average EEG power of all seven patients gradually decreased in the theta band and approached normal values only after 12 months. The excess theta EEG power in patients and its decrease after thalamic surgery suggests that both EEG and neurogenic pain are determined by tightly coupled thalamocortical loops. The small therapeutic CLT lesion is thought to initiate a progressive normalization in the affected thalamocortical system, which is reflected in both decrease of EEG power and pain relief.

Key Words: neuropathic pain; central pain; thalamocortical system; thalamotomy; EEG oscillations

Abbreviations: CL = central lateral nucleus; CLT = central lateral thalamotomy; LTS = low-threshold calcium spike; MEG = magnetoencephalography; TCD = thalamocortical dysrhythmia

Received April 20, 2005. Revised July 14, 2005. Accepted August 12, 2005.


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