ABSTRACT
OBJECTIVES: Cerebral ischaemia is a leading cause of death and disability, including severe complications such as memory disturbance, palsy, and spasticity. Central post-stroke pain (CPSP) is a complication of cerebral ischaemia, and is characterized clinically by spontaneous pain and attacks of allodynia and dysaesthesia. However, the detailed mechanisms of CPSP are not well established. Herein, we have examined alterations of the current stimulus threshold of primary afferent neurons or the nociceptive threshold against mechanical stimuli in mice receiving left middle cerebral artery occlusion (MCAO). METHODS: Alterations of current stimulus threshold and the development of mechanical allodynia in hind paws were measured after MCAO using a Neurometer and the von Frey filament test, respectively. KEY FINDINGS: Development of cerebral infarction was clearly observed on day 1 and day 3 after MCAO. For the estimation of current stimulus threshold measured by the Neurometer, the sensitivity of Aδ and Aß fibres (at 2000 and 250 Hz stimulation, respectively) was significantly increased on day 3 after MCAO, while that of C fibres (at 5 Hz stimulation) was unaltered. In addition, the paw withdrawal threshold of the left hind paw as measured by the von Frey filament test was significantly decreased on day 1 and day 3 after MCAO when compared with day 0, while that in the right hind paw was not different. CONCLUSIONS: The data suggested the development of bilateral hyperaesthesia in this model. Further, mechanical allodynia developed in the ipsilateral side to the MCAO. Potentially, myelinated A fibre-specific hypersensitization after stroke may have contributed to these symptoms.
