Chapter 4 - Central Pain: A Thalamic Deafferentation Generating Thalamocortical Dysrhythmia

Abstract

The mechanism responsible for the generation of central (or phantom) pain, as opposed to that resulting from the activation of nociceptive input, has been a perplexing medical puzzle. The possibility that such pain is ultimately a disconnection neurological syndrome will be the topic of this short essay. Abnormal recurrent thalamocortical resonance of intrinsic origin will be proposed as a plausible underlying mechanism in central pain generation. Electrophysiological studies in rodents and in humans reveal the presence of continuous, low frequency (theta/delta) thalamocortical loop recurrent oscillations that are most probably related to sensory deafferentation. For example, magnetoencephalographic (MEG) studies in humans with central pain show that low frequency activity is localized to the somatosensory cortical representation of the pain location, and to the fronto-mesial cortex. Animal studies demonstrate that low frequency oscillations originating in thalamus support an associated “edge effect” at beta or gamma band frequency at the level of the cortex. Co-localization of low and high frequency activity has also been observed in MEG studies. It is concluded that such thalamo-cortical activation at the somatosensory level provides subjective localization while the thalamic fronto-mesial loop is responsible for the emotional pain sensation.