Changes in the Brain Metabolism Associated with Central Post-Stroke Pain in Hemorrhagic Pontine Stroke: An 18F-FDG-PET Study of the Brain

Central post-stroke pain (CPSP) is an intractable neuropathic pain that can occur following central nervous system injuries. Spino-thalamo-cortical pathway damage contributes to CPSP development. However, brain regions involved in CPSP are unknown and previous studies were limited to supratentorial strokes with cortical lesion involvement. We analyzed the brain metabolism changes associated with CPSP following pontine hemorrhage. Thirty-two patients with isolated pontine hemorrhage were examined; 14 had CPSP, while 18 did not. Brain glucose metabolism was evaluated using F-18-fluorodeoxyglucose-positron emission tomography images. Additionally, regions revealing metabolic correlation with CPSP severity were analyzed. Patients with CPSP showed changes in the brain metabolism in the cerebral cortices and cerebellum. Compared with the control group, the CPSP group showed significant hypometabolism in the contralesional rostral anterior cingulum and ipsilesional primary motor cortex (P-uncorrected < 0.001). However, increased brain metabolism was observed in the ipsilesional cerebellum (VI) and contralesional cerebellum (lobule VIIB) (P-uncorrected < 0.001). Moreover, increased pain intensity correlated with decreased metabolism in the ipsilesional supplementary motor area and contralesional angular gyrus. This study emphasizes the role of the many different areas of the cortex that are involved in affective and cognitive processing in the development of CPSP.

Automated summary

This study analyzed the brain metabolism changes associated with central post-stroke pain (CPSP) following pontine hemorrhage. The findings revealed alterations in brain metabolism in the cerebral cortices and cerebellum of CPSP patients. Hypometabolism was observed in the contralesional rostral anterior cingulum and ipsilesional primary motor cortex, while increased metabolism was found in the ipsilesional cerebellum and contralesional cerebellum. Increased pain intensity correlated with decreased metabolism in the ipsilesional supplementary motor area and contralesional angular gyrus.