Neurophysiological studies at the cellular level (microelectrode unit activity recordings and local field potentials) as well as electro- and magnetoencephalographic recordings provide converging evidence for a thalamocortical dysregulation at the source of chronic neurogenic pain of both peripheral and central origin. These indicate an increase of low frequency thalamocortical rhythmicity originating in disfacilitation of thalamic relay neurons, followed by cortical activation due to asymmetries of corticocortical inhibition. This process, called thalamocortical dysrhythmia, might become self-sustained and, thus, chronic due to recurrent thalamoreticulothalamic and corticoreticulothalamic feedback inhibition. Our surgical approach is centered on re-establishment of normal thalamocortical oscillatory activity using small, strategically placed medial thalamic and prethalamic lesions. These reduce the increased low frequency thalamocortical recurrent network activity via low frequency desamplification and thalamic disinhibition, providing long term therapeutic efficiency coupled with sparing of the specific thalamocortical loops.

This physiopathological framework should be helpful when considering differential mechanisms and treatment modalities for different types of chronic pain. It underscores the risks of any surgical procedure aiming at reducing further the activation of specific thalamic relay cells and, thus, increasing thalamic disfacilitation and dysrhythmic pain mechanisms. In addition, the normal low frequency generation by activation of the paralimbic and high order association networks provides, in the context of a well established thalamocorticothalamic divergent and, thus, interactive organization, a basis for understanding the relevance of the conceptual-affective internal environment in the maintenance and amplification of many chronic neurogenic pain situations.

We simultaneously recorded local field potentials (LFP) in the thalamus and EEG on the scalp of 17 patients suffering from neurogenic pain, epilepsy and movement disorders. The EEG of 11 patients displayed enhanced power in the theta frequency range (4–8 Hz). The thalamic LFP of 14 patients peaked in the theta range. The theta coherence between EEG and LFP was significant for 12 patients and reached strengths up to 70%. These findings suggest that enhanced theta rhythmicity occurs in tight functional thalamocortical loops and is a major element in all three diseases investigated.

To investigate second-order phase-coupling between LFP frequency components, we computed the bicoherence and averaged over the group of patients. We found peaks in the theta band and the beta band (14–30 Hz), indicating phase correlations of oscillatory events in these frequency ranges with their first harmonic. A further peak indicates that phase coupling occurred also between theta and beta frequencies. This indicates a strong functional interaction between the generators of these oscillations. We also computed the cross-correlation between LFP spectral power at different frequencies. Although this measure is independent of phase, we found good agreement with the bicoherence patterns, pointing again to strong interaction between theta and beta rhythmicity. The overproduction of theta rhythms, the thalamocortical coherence and the correlation of theta with beta rhythms are key elements for the understanding of thalamocortical dysrhythmia (TCD).