Spontaneous pain and painful overreaction to external stimuli resulting from lesion confined central nervous system (CNS) were named as thalamic syndrome. Thalamic lesion and decreased regional cortical perfusion thought to the pathogenesis of thalamic syndrome due to decreased function of thalamocortical tract. We performed $^{99m}Tc-HMPAO$ regional cerebral perfusion in 10 patients with clinical diagnosis of thalamic syndrome due to thalamic lesion or near the thalamic lesion at Yonsei University Hospital, from January 1989 to August 1991. In contrast to five patients with lesions near the thalamus who did not show secondarily decreased perfusion at cerebral cortex, four among the five patients with thalamic lesions revealed decreased cortical perfusion in the ipsilateral cerebral cortex on brain SPECT. These phenomena may suggest the loss of afferent activating stimuli from the thalamus led to decreased neuronal activity and the followitng hypoperfusion of cerebral cortex, and might be one of the indirect signs for suggesting presence of the thalamocortical tract. A causal relationship between cortical hypoperfusion and neuropsychological deficit is strongly suggested.