OBJECTIVE: This study was designed to investigate the mechanism of the primary afferent input to spread of contralateral hyperalgesia in the persistent muscle pain model in the rat. METHOD: Muscle pain was induced by twice repeated intramuscular injections of pH 6.0 buffered saline into the unilateral gastrocnemius muscle of the rats. Change of mechanical withdrawal threshold to von-Frey filament was measured after ipsilateral laser irradiation, anesthetic blockade with lidocaine and dorsal rhizotomy (L2~L6) to reduce primary afferent input from the tissue injury. RESULTS: Bilateral persistent mechanical hyperalgesia in the hind paw was evoked after second injection. Ipsilateral laser irradiation, lidocaine injection and dorsal rhizotomy had no effect on the contralateral spread of mechanical hyperalgesia. CONCLUSION: These results suggest that contralateral hyperalgesia was produced by, but didn't need to be maintained by inputs from an injury. Therefore, central nervous systems are responsible for the contralateral spread of hyperalgesia.