Establishment of a central post-stroke pain model using global cerebral ischaemic mice.

OBJECTIVES

Stroke is the leading cause of disability in the world. Central post-stroke pain (CPSP), an intractable secondary disease, is a serious problem that occurs following cerebral stroke. However, the detailed mechanisms underlying CPSP and standard treatments for it are not well established. Therefore, we examined the nociceptive threshold and alterations in the current stimulus threshold of primary afferent neurons in bilateral carotid artery occlusion (BCAO) mice.

METHODS

Male ddY mice were subjected to 30 min of BCAO. The development of mechanical and thermal hyperalgesia and changes in current stimulus threshold in the hind paws were measured after BCAO using the von Frey test, plantar test and a Neurometer, respectively.

KEY FINDINGS

The threshold for mechanical and thermal hyperalgesia in both hind paws was significantly decreased on day 3 after BCAO as compared with pre-BCAO treatment. Furthermore, the sensitivity of C and Aβ fibres (at stimulation of 5 and 2000 Hz, respectively) was increased on day 3 after BCAO as compared with pre-BCAO treatment, while that of Aδ fibres was not altered.

CONCLUSIONS

Our data show the development of bilateral hyperalgesia in this model. Potentially, C and Aβ fibre-specific hypersensitization after stroke may have contributed to these symptoms.