Brain Advance Access published online on September 23, 2005
Brain, doi:10.1093/brain/awh631
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Universitätsspital, Funktionelle Neurochirugie, CH-8091 Zürich, Switzerland; Center for Integrative Human Physiology, Universität Zürich, Switzerland
* To whom correspondence should be addressed. 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.
Received April 20, 2005
Revised July 14, 2005
Accepted August 12, 2005
Article
Increased EEG power and slowed dominant frequency in patients with neurogenic pain
2 Universitätsspital, Funktionelle Neurochirugie, CH-8091 Zürich, Switzerland
3 Biostatistik, Universität Zürich, Switzerland
Johannes Sarnthein, E-mail: johannes.sarnthein{at}usz.ch
Abstract 
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  R. J. Chapman, P. F. Cilia La Corte, A. U. R. Asghar, and A. E. King Network-based activity induced by 4-aminopyridine in rat dorsal horn in vitro is mediated by both chemical and electrical synapses J. Physiol., June 1, 2009; 587(11): 2499 - 2510. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A M Drewes, A L Krarup, S Detlefsen, M-L Malmstrom, G Dimcevski, and P Funch-Jensen Pain in chronic pancreatitis: the role of neuropathic pain mechanisms Gut, November 1, 2008; 57(11): 1616 - 1627. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Weisz, S. Muller, W. Schlee, K. Dohrmann, T. Hartmann, and T. Elbert The Neural Code of Auditory Phantom Perception J. Neurosci., February 7, 2007; 27(6): 1479 - 1484. [Abstract] [Full Text] [PDF]
|
|