PURPOSE: Central poststroke pain (CPSP) is one of the most refractory neuropathic pains following stroke. Injury in the spinothalamic pathway appears crucial for the development of CPSP, but changes in activity in multiple brain regions may also be related. We investigated brain metabolic changes in patients with CPSP following thalamic intracerebral hemorrhage (ICH). METHODS: Forty-three patients with thalamic ICH were examined. Overall brain metabolism was measured with F-FDG PET. Images were analyzed with statistical parametric mapping (SPM12). Patients with CPSP (n = 20) were compared with patients without CPSP (n = 23). In addition, the association between regional brain metabolism and the severity of CPSP was investigated. RESULTS: In comparison to patients in the non-CPSP group, the CPSP group exhibited significant hypometabolism in the ipsilesional precentral, postcentral gyri, and the contralesional cuneus (Puncorrected < 0.001), whereas significant hypermetabolism was found in the medial dorsal nucleus of the contralesional thalamus (Puncorrected < 0.001). In addition, brain metabolism in the ipsilesional Crus I and Crus II of the cerebellum was positively correlated to pain intensity ratings (Puncorrected < 0.001). CONCLUSION: Our findings suggested that an altered state of resting brain metabolism in various brain regions related to sensory processing and cognitive functioning may be involved in the underlying mechanism of CPSP following thalamic ICH.
PURPOSE:Central poststroke pain (CPSP) is one of the most refractory neuropathic pains following stroke. Injury in the spinothalamic pathway appears crucial for the development of CPSP, but changes in activity in multiple brain regions may also be related. We investigated brain metabolic changes in patients with CPSP following thalamic intracerebral hemorrhage (ICH). METHODS: Forty-three patients with thalamic ICH were examined. Overall brain metabolism was measured with F-FDG PET. Images were analyzed with statistical parametric mapping (SPM12). Patients with CPSP (n = 20) were compared with patients without CPSP (n = 23). In addition, the association between regional brain metabolism and the severity of CPSP was investigated. RESULTS: In comparison to patients in the non-CPSP group, the CPSP group exhibited significant hypometabolism in the ipsilesional precentral, postcentral gyri, and the contralesional cuneus (Puncorrected < 0.001), whereas significant hypermetabolism was found in the medial dorsal nucleus of the contralesional thalamus (Puncorrected < 0.001). In addition, brain metabolism in the ipsilesional Crus I and Crus II of the cerebellum was positively correlated to pain intensity ratings (Puncorrected < 0.001). CONCLUSION: Our findings suggested that an altered state of resting brain metabolism in various brain regions related to sensory processing and cognitive functioning may be involved in the underlying mechanism of CPSP following thalamic ICH.