In: Encyclopedic Reference of Pain, eds. R.F. Schmidt and W.D. Willis, 2006.
Neurophysiological studies at the cellular level (single unit activity and local field potentials or LFPs) as well as electroencephalographic (EEG) and magnetoencephalographic (MEG) recordings provide converging evidence for a thalamocortical dysregulation at the origin of chronic neurogenic pain of both peripheral and central origin. These data suggest an increase of low frequency thalamocortical rhythmicity originating in disfacilitation of thalamic relay neurons, followed by cortical activation due to asymmetries of corticocortical inhibition. The process, called thalamocortical dysrhythmia (TCD), may become self-sustained and thus chronic, due to recurrent thalamoreticulothalamic and corticoreticulothalamic feedback inhibition.