Abstract

After incisional or alcoholic destruction of trigeminal posterior rootlets, constant dysesthesias of major degree referred to some part of the markedly denervated zone develop in 5 to 15% of the patients. The full severity may not appear for weeks or months. There is no allodynia or hyperpathia of the denervated zone. Bulbar trigeminal tractotomy with sparing of touch sensation produces severe dysesthesias in a tiny percentage of the patients, as does selective destruction of pain fibers by radiofrequency heating or glycerol. Spinal posterior rhizotomy elicits in less than 4% a lasting dysesthesia entirely different in temporal sequence, locus, and type of pain: (a) it tends to be maximal early after operation and to improve, (b) the spontaneous pain is accompanied by severe allodynia, and (c) the pain is usually referred beyond the margins of the insentient (rhizotomized) zone and may even be referred to the corresponding area on the opposite side. Sindou's "selective posterior rhizotomy," i.e., cutting of the small fiber lateral component of each rootlet as it enters the cord, has not given rise to dysesthesias. These do occur briefly in 50% of the cases following spinal ganglionectomy, the sensations being referred to the dermatomal segment of the ganglion in question. The secondary afferent neurons in the mesencephalic, principal, oral, and interpolar nuclei for the trigeminal posterior roots have no counterpart in the spinal cord for the spinal posterior roots. We suggest that the explanation for the fact that neither trigeminal neuralgia nor trigeminal anesthesia dolorosa have a spinal clinical counterpart is related to the as yet unexplained special functions of the elaborate trigeminal secondary afferent neuronal apparatus.(ABSTRACT TRUNCATED AT 250 WORDS)

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