| Research Abstract |
(1) In the central pain patients with definite thalamic damage (superficial pain dominant), electrophysiological study of the thalamus using the depth microrecording showed that spontaneous neural activity(SNA) was markedly decreased in and around VIM (ventralis intermedius) nucleus. SNA in intralaminar nuclei (CL=centralis lateralis) was, however, higher than in VIM, especially in its dorsal part. Often, irregular burst discharge was encountered around the VC (ventralis caudalis) nucleus, especially in the dorsal part of the intralaminar nuclei along trajectories toward CL. In these cases, the greater the severity of superficial pain, the higher was the relative value of regional cerebral glucose metabolism as compared to oxygen metabolism in the cerebral cortex around central sulcus(Cxc) on the lesioned side. Also, regional oxygen extraction ratio increased in this area. Therefore, in central(thalamic) pain patients, the irritable state of thalamic intralaminar nuclei and the abnormal (increased) neural activity developed in the Cxc might play important roles for the genesis of central pain, especially superficial pain.
(2) In rigid type Parkinson's disease(PD), the glucose metabolism was high in the lenticular nucleus but low in the Cxc. In contrast, chorea group showed low glucose metabolism in the lenticular nucleus but high in the motor and premotor cortex. The neural function of the basal ganglia and the cerebral cortex in rigid type PD are suggested to be totally different from that in hyperkinesia. In cases with hemitremor, the glucose metabolism was high in the Cxc as well as in the motor thalamus on the contralateral side. We postulated that those structures, as basal ganglia, thalamus and cerebral cortex, played important roles in maintaining and mediating abnormal involuntary movements.
(3) Measurement of neurotransmitter using microdialysis was performed in the basal ganglia and the thalamus of normal or experimental tremor monkey.
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