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 thalamo-cortical 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.
Thalamus & Related Systems, 2005, 3(1), 63–70