In: Textbook of Stereotactic and Functional Neurosurgery. Lozano A., Gildenberg P. (eds.).
Springer-Verlag: Berlin, Chapter 123, pp. 2081-2096, 2009.
Read a part of this chapter on Google Books
Introduction
Head and Holmes postulated in 1911 the existence of an ‘‘essential medial thalamic centre,’’localized medial to a pain-generating lesion in the thalamic ventroposterior (VP) nucleus, and responsible for the pathogenesis of central pain [1]. This centre was thought to be exposed
to a decreased inhibitory influence from thalamo-cortico-thalamic loops. A generation of abnormal impulses in VP and their amplification in a reverberating circuit between lateral and medial thalamic nuclei were also proposed in the seventies by Sano [2]. Furthermore, the medial
thalamus has been known for years to be an amplifier/synchronizer for low electroencephalographic (EEG) frequencies [3]. From the beginning of stereotaxy in the fifties and in contrast to all other lesional surgeries, medial thalamotomies against neuropathic (synonym:
neurogenic) pain were recognized as procedures with low complication rates and absence of risk for the development of iatrogenic pain manifestations. They were shown to bring pain relief to all body localizations, and that without producing somatosensory deficits. Although
cases with total and stable pain relief were published, recurrence of the original pain, partial or complete, was frequent [2,4–10]. These observations were commonly reported, but many studies were relatively small and included inhomogeneous pain patient populations. These data provided us with the necessary basis and incentive to pursue the medial thalamic path, with the goal to re-actualize this promising therapeutic option on the basis of newly developed anatomical, physiological and technical tools. Other reports of our experience in this field have been published elsewhere [11–16].