[Thalamic pain: critical study of 43 cases]

Apart from hyperpathia, which is an entity in itself, thalamic pain presents a clinical spectrum of variable quality and intensity that justifies the description of "thalamic pains". Their mechanisms can be related to two basic mechanisms. The first involves the dependence of the thalamus to the afferent spinothalamic system. A lesion of the lemniscal system resulting from lesions of the thalamic sensory nuclei--capable of provoking a syndrome of paresthesia-hyperpathia (P-HI)--provokes a loss of gate control normally ensured by this discriminatory system and thus releases the pathologic nociceptive reactivity. Some authors think that the thalamic lesion alters the activity of control of the VPL nucleus on the lumbosacral spinothalamic tract. This concept considers thalamic pain as identical with brain stem spinothalamic pain provoked by exclusion of the control system arising in the giant-cell reticular nucleus and projecting onto onto the posterior horns. However, most cases of thalamic pain appear to be dependent on another mechanism involving the thalamocortical loop. In this case the thalamic sensory nucleus lesion is involved insofar as it implicates the reciprocal thalamocortical connections and the reticular nucleus. Involvement of the Th-C-Th loop as the ultimate representative of the lemniscal gate control is supported by "pseudo-thalamic" pains related to cortico-subcortical lesions with abolished SEP. But the numerous cases of painful thalamic syndromes with lemniscal sparing and normal SEP lead to incriminate a lesion of a specific thalamocortical control system for pain.(ABSTRACT TRUNCATED AT 250 WORDS)