THALAMUS AND NEUROGENIC PAIN - PHYSIOLOGICAL, ANATOMICAL AND CLINICAL-DATA

MICROELECTRODE recordings in the medial thalamus of 45 neurogenic pain patients undergoing medial thalamotomy revealed that most units (316/ 318) did not respond to somatosensory stimuli, and that half exhibited low-threshold calcium spike bursts. After medial thalamotomy, 67% of the patients reached a 50 to 100% pain relief, without somatosensory d eficits. Colocalization of bursting activities and of the most efficie nt therapeutic lesions in the central lateral nucleus suggests a key r ole of this structure in neurogenic pain. We propose that neurogenic p ain is due to an imbalance between central lateral and ventroposterior nuclei, resulting in an overinhibition of both by the thalamic reticu lar nucleus.