Publications

Concept, neuroanatomy and surgical techniques

Reactualization of the medial thalamotomy, performed since the fifties in cases of neurogenic pain, has been guided by the discovery of low threshold calcium spikebursts at frequencies in the delta–theta range in the posterior part of the central lateral (CL) nucleus. This thalamic rhythmicity is transmitted to the cortex through thalamocortical resonant properties, giving rise to the thalamocortical dysrhythmia, proposed to be the mechanism of neurogenic pain as well as other central nervoussystem (CNS) dysfunctions
Following earlier stereotactic experiences, we re-explored the possibilities of a therapeutic lesion of the pallidothalamic tract in the fields H1 and H2 of Forel in patients with parkinsonian signs. The physiopathological rationale of the pallidothalamic tractotomy (PTT) is based on the presence in the parkinsonian brain of a state of thalamic overinhibition due to an increased output of the internal pallidum.

EEG techniques

Epilepsy, Tinnitus and Neuropsychiatry

Essential Tremor

Neurogenic Pain

Chronic neurogenic pain remains today a significant problem, at the clinical as well as anatomo-physiological levels. It is caused by a lesion along somatosensory pathways, from nerve to cortex and is characterized by thermal (burning, cold), exteroceptive (electrical, tingling, pins and needles) and proprioceptive (crushing, tearing) dysesthesias.
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 deficits. Colocalization of bursting activities and of the most efficient therapeutic lesions in the central lateral nucleus suggests a key role of this structure in neurogenic pain. We propose that neurogenic pain is due to an imbalance between central lateral and ventroposterior nuclei resulting in an overinhibition of both by the thalamic reticular nucleus.

Parkinson