[Differences in ipsilateral afferent currents in rats with and without pain syndrome in trigeminal neuropathy].

Ipsilateral evoked potentials in the caudal trigeminal nucleus, ventrobasal thalamus, and cortex during electrical stimulation of the injured and opposite intact nerves were studied in rats with trigeminal neuropathy caused by partial compression of the infraorbital nerve. In spite of abnormally increased long latent evoked activity in the caudal nucleus ipsilaterally to compression, amplitude asymmetry of the ipsilateral thalamic and cortical evoked potentials in rats with pain syndrome was shown to be absent during nerve stimulation of the snout sides. In rats without pain-evoked potentials in the caudal nucleus during injured nerve stimulation had small differences as compared with the latter group. At that time, the increased magnitude of ipsilateral evoked potentials at uninjured nerve stimulation was recorded in all structures in rats without pain syndrome as compared with the pain syndrome group and sham-operated rats, and as compared with ipsilateral evoked potentials during injured nerve stimulation in rats without pain syndrome. The neuropathic pain syndrome is considered to result from the formation of the pathologic algic system with a generator of abnormality enhanced excitation which arises in the nonspecific nociceptive structures in response to specific structural injury. This alternative process is the compensative increase in the ipsilateral input of agents into the brain cortex from the intact nerve that prevents the development of its abnormal activities.