In 13 patients with central (thalamic) pain after stroke, CT, MRI, PET scan and intraoperative thalamic microrecordings were performed. Electrophysiological studies showed that irregular burst discharges were often encountered in the posterolateral thalamus. The more often the irregular burst discharges were encountered, the greater the decrease of sensory response in the posterolateral thalamus. Metabolic studies showed that regional cerebral glucose metabolism decreased in both the posterolateral thalamus and in the cortical postcentral area on the lesioned side in all cases. In the thalamic lesion cases in which many irregular burst discharges were found in the posterolateral thalamus, regional cerebral glucose metabolism and the relative value of glucose to oxygen metabolism increased in the cortical precentral area on the lesioned side. It was suggested that decreased activity with abnormal burst discharge in the posterolateral (sensory) thalamus associated with changes in cortical activity adjacent to the central sulcus might be related to the genesis of central (thalamic) pain. It is emphasized that cortical activity decreased in the postcentral area, but often increased in the precentral area.