Saadé N E, Shbeir S A, Atweh S F, Jabbur S J
Department of Physiology, Faculty of Medicine, American University of Beirut, Lebanon.
Physiol Behav. 1996 Aug;60(2):559-66. doi: 10.1016/s0031-9384(96)80032-1.
Peripheral nerve lesions have been reported to produce deafferentation pain and persistent changes at various levels of the central nervous system. Using autotomy in rats following leg denervation, as a model for deafferentation pain, we studied the effect of various cerebral lesions on this abnormal behavior. Under deep anesthesia, rats were subjected either to massive hemidecortication or to subtotal hemispherectomy (involving parts of basal ganglia and limbic areas), which was followed 1 week later by a denervation of the ipsilateral or contralateral leg. Hemidecortication significantly delayed autotomy from 7.8 +/- 2.8 to 25.6 +/- 2.1 days without reducing its incidence, whereas hemispherectomy abolished the incidence of autotomy in the contralaterally denervated leg and delayed its onset from 7.8 +/- 2.8 to 34 +/- 6.1 days and decreased its incidence (from 100% to 60%) in the ipsilaterally denervated leg. Chemical lesions of the neostriatum produced similar effects on autotomy to those produced by hemispherectomy. Hemispherectomized and striatum-lesioned rats that failed to elicit autotomy in the contralaterally denervated leg were subjected after 7 weeks to denervation of the ipsilateral leg. Sixty to seventy percent of these rats showed autotomy and in half of them the attack was directed simultaneously to both legs. These results suggest an involvement of the cerebral cortex and a stronger contribution of subcortical structures (like striatum and limbic system) in the processing of nociceptive information.
