Mechanism and the treatment of central deafferentation pain

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Deafferentation of the sensory pathways within the peripheral and central nervous systems has been demonstrated to cause hyperactivity of neurons within the sensory pathways above the level of deafferentation. Such hyperactivity has been implicated in the mechanism of deafferentation pain observed clinically. In this studies ; 1) We recorded single neuron activities within the thalamic nucleus ventralis posterolateralis (VPL) after transection of the spinithalamic tract (STT) and within the sensory cortex after VPL lesions. Sensory cortex neurons became hyperactive after VPL lesions, and VPL neurous became hyperactive after STT transection through recruitment of NMDA recetors. The hyperactibities of VPL and sonsory cortex neurons were inhibited by the motor cortex stimulation. 2) After unilateral lesions restricted to the posterior ventrobasal region of the thalamus, CYO activity decreased rapidly in layr IV of the sensorimotor cortex at lesioned side. Segmentations normally seen in layr IV corresponding to barrels remained absent. While less marked decreases were also noted in other layrs, obvious recovery was subsequently obserbed. These changes in metabolic activity reflect the process of reorganization of neural circuits after tha lamocortical deafferentation from which thalamic pain is sometime produced. 3) In clinical studies, we concluded that pharmacoligical classification of deafferentation pain is useful for finding the deafferentation pain and for predicting the efficiency of chronic brain stimuration therapy, 4) Based on these results, We treated 12 cases of thalamic pain syndrome by chronic motor cortex stimulation employing epidural plate electrodes. Good pain control was obtained without any complication and side effects.