Talal M. Ghazal, M.D., M.S., Kimberly D. Moran, Kerry Walton, Ph.D., Rodolfo Llinas, M.D., Ph.D., and Michel Dubois, M.D. New York University, New York, NY, USA
Thalamocortical dysrhythmias (TCDs) have been described by Llinas et al. as a basic element of the pathophysiology for selected neurological and psychiatric disorders, including centrally-generated pain. Recent evidence has shown a direct relationship between abnormal thalamic rhythmicity and the occurrence of central pain. Magneto-encephalography (MEG) provides a noninvasive technology for recording the magnetic component of the spontaneous and evoked electrical activity of the brain. Spectral analysis of the averaged spontaneous MEG data has shown, in central pain states, the presence of thalamic related, abnormal increased activation of low frequency (theta) rhythmicity. Using an experimental protocol previously described and tested, we recorded spontaneous neuromagnetic activity using MEG in a group of patients with Chronic Regional Pain Syndrome type I (CRPS I). Those patients had, at the time of testing, clinical diagnostic criteria of CRPS I and were either not treated or had inefficient treatments. Results: Compared to controls, all patients showed an abnormal increase in low-frequency theta rhythmicity in conjunction with a decrease of power in the alpha or gamma frequency range. Magnetic source imaging (MSI) and independent component analysis identified independent sources in the theta frequency range that were localized to somatosensory cortex. These findings are similar to TCDs previously found in patients with centrally generated and deafferentation pain. This preliminary study in clinically diagnosed CRPS I patients brings an objective confirmation to the hypothesized “brain involvement” in the pathophysiology of this disease. It also offers not only a diagnostic tool for central pain states, but also a possible mechanism for CRPS—thalamocortical dysrhythmia. TCD has been shown to be present, both in animals and humans, in other central neuropathic states and may be responsible for a cascade of neurophysiological aberrations leading to persistent disease states.
References: Llinas RR, Ribary U, Jeanmonod D, et al. “Thalamocortical dysrhythmia: A neurological and neuropsychiatric syndrome characterized by magnetoencephalography”. Proc Natl Acad Sci USA 96:15222-15227, 1999 Schulman JJ, Ramirez RR, Zonenshayn M, Ribary U, Llinas RR. “Thalamocortical dysrhythmia syndrome: MEG imaging of neuropathic pain”. Thal Related Sys 3: 33-40, 2004. Llinas RR, Leznik E, Urbano FJ. “Temporal binding via cortical coincidence detection of specific and nonspecific thalamocortical inputs: a voltage-dependent dye imaging study in mouse brain slices”. Proc Natl Acad Sci USA 99: 449-454, 2002
Funding: NYUSOM GCRC (NCRR M01 RR00096)
Talal M. Ghazal, M.D., M.S.
Nothing to disclose.