PATHOPHYSIOLOGY OF THALAMIC PAIN

Abstract

A. Regional cerebral metabolism in patients with thalamic painPET studies were performed in 11 cases of thalamic pain after CVD (cerebrovascular disease) to elucidate its metabolic features in the brain. They consisted of either a C15O2-15O2 continuous inhalation study to measure regional cerebral oxygen consumption (rCMRO2), regional cerebral blood flow (rCBF) and regional oxygen extraction fraction (rOEF), or an 18F-fluoro-2-deoxy-D-glucose (18FDG) study to measure regional cerebral glucose utilization (CMRGL) Subjects (patients and controls) in the gas (C15O2-15O2) study were divided into 4 different groups : a thalamic lesion group with pain (P-Th group) (4 cases), a putaminal lesion group with pain (P-Put group) (6 cases), a thalamic lesion group without pain (NP-Th group) (2 cases) and a normal control group (N group) (3 cases). An FDG study was performed in 4 cases : 3 cases of thalamic pain and 1 normal control. Gas study was additionally performed in pain cases.In the P-Th group, rCMRO2 was relatively well maintained in most brain structures except lesioned sensory-thalamus. In the cerebral cortex around the central sulcus, the rCMRO2 level was almost normal. Furthermore, rOEF and the relative value of CMRGL, compared with rCMRO2, also increased in these structures. In the P-Put and NP-Th group, however, rCMRO2 decreased in all brain structures, as did rCBF, rOEF and CMRGL, and in the P-Put group, the oxygen-glucose molar utilization ratio (OGMUR) was within the normal limit. Therefore, CBF and oxygen metabolism in the thalamus on the CVD lesion side decreased in all cases with thalamic pain. In the P-Th group, it was suggested that the function of the nonspecific activating afferences, including the thalamic intralaminar nuclei, was maintained, and abnormal (excess) neural activity had occurred in the cerebral cortex around the central sulcus.B. Pathophysiology of thalamic painCT study in cases with thalamic pain showed that the damage to the ventral postero-lateral part of the thalamus was an important factor in the development of spontaneous pain. In the pain group the size of lesions was apparently smaller than that of other sensory disturbance groups in the chronic stage. Furthermore, thalamic electrophysiological study showed that the character of thalamic pain, both deep and superficial, was associated with that of local pathophysiology in the thalamic sensory nucleus. In the non-thalamic lesion group, we could recognize more deep than superficial pain, and BNA (background neural activity) was relatively well preserved in the ventral thalamus. It was also suggested that functional change or reorganization in the thalamic sensory nucleus occurred in this group. In the thalamic lesion group, superficial pain was predominant, and BNA decreased markedly in the ventral thalamus, particularly in the VC nucleus. Cerebral metabolic study in this group indicated that rCMRO2 was relatively well maintained in the cerebral cortex around the central sulcus, and rOEF and the relative value of CMRGL, compared with rCIVIRO2, also increased. These findings suggest that the function of the nonspecific activating afferences, including thalamic intralaminar nuclei, was maintained, and abnormal (excess) neural activity had occurred in the cerebral cortex around the central sulcus (senrori-motor cortex).These studies lead us to postulate that thalamic pain may be ascribed to both dysfunction of the thalamic relay nucleus and sensory cortex.