Central Pain in the Absence of Functional Sensory Thalamus

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Abstract
Since the pioneering publication by Dejerine and Roussy, the thalamus has been commonly implicated in the pathogenesis of central pain. It is well known that cerebral lesions that spare the thalamus aswell as both small and large ones within that structure produce similar pain syndromes, but could such pain develop if the thalamus were completely destroyed? CT scans of our patients suggested that it could. Moreover, exhaustive physiological explorations of the thalamus with macro- and microstim-ulation and microelectrode recordings in 2 more patients in whom CT scans suggested thalamic preservation despite massive suprathalamic infarcts, for the purpose of carry-ing out deep brain stimulation (DBS), revealed no evidence of ascending or descending diencephalic function. Their sensory examinations were similar to those of patients with congenital hemiatrophy who had undergone hemispherectomy. In 1 case, micro-stimulation of periaqueductal grey-periventricular grey (PAG-PVG) on the unaffected side of the brain induced the spectrum of responses correctly associated with these areas and during acute Stimulation nearly abolished the patient''s allodynia and hyper-pathia. These observations suggest that processes occurring at a subdiencephalic level (or possibly ipsilaterally) may be involved in the generation of pain.Stroke-induced central pain remains a therapeutic dilemma for the pain surgeon, and the mechanisms underlying this pain state remain a mystery. Since the early publication of Dejerine and Roussy, the thalamus has been thought to play an important role in the pathogenesis of central pain. In fact, in most cases of pain due to brain pa-thology, the term ''thalamic pain'' is loosely applied, even though the lesions may be lo-cated in the cortex, subcortical white matter or brainstem.

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