Increased calcium-mediated cerebral processes after peripheral injury: possible role of the brain in complex regional pain syndrome.

BACKGROUND

Among various diseases that accompany pain, complex regional pain syndrome (CRPS) is one of the most frustrating for patients and physicians. Recently, many studies have shown functional and anatomical abnormalities in the brains of patients with CRPS. The calcium-related signaling pathway is important in various physiologic processes calmodulin (CaM) and calcium-calmodulin kinase 2 (CaMK2). To investigate the cerebral mechanism of CRPS, we measured changes in CaM and CaMK2 expression in the cerebrum in CRPS animal models.

METHODS

The chronic post-ischemia pain model was employed for CRPS model generation. After generation of the animal models, the animals were categorized into three groups based on changes in the withdrawal threshold for the affected limb: CRPS-positive (P), CRPS-negative (N), and control (C) groups. Western blot analysis was performed to measure CaM and CaMK2 expression in the rat cerebrum.

RESULTS

Animals with a decreased withdrawal threshold (group P) showed a significant increment in cerebral CaM and CaMK2 expression ( = 0.013 and = 0.021, respectively). However, groups N and C showed no difference in CaM and CaMK2 expression.

CONCLUSIONS

The calcium-mediated cerebral process occurs after peripheral injury in CRPS, and there can be a relationship between the cerebrum and the pathogenesis of CRPS.