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Functional characterization of a mouse model for central post-stroke pain
Simon Gritsch1, Kiran Kumar Bali1, Rohini Kuner1
1Institute for Pharmacology, University of Heidelberg, Heidelberg, Germany.
Molecular Pain
|April 1, 2016
Summary
Central post-stroke pain involves hypersensitivity due to thalamic pathway dysfunction. Targeting thalamic activity, not peripheral nerves, may alleviate this chronic pain after stroke.
Area of Science:
- Neuroscience
- Pain Research
- Neurology
Background:
- Central post-stroke pain is a neuropathic syndrome following stroke, causing hypersensitivity and spontaneous pain.
- Dysfunction in central pain pathways is implicated, but mechanisms are unclear.
- A mouse model with thalamic lesions was created to study central post-stroke pain.
Purpose of the Study:
- To investigate the underlying pathophysiology of central post-stroke pain.
- To identify the specific mechanisms driving pain hypersensitivity after thalamic injury.
Main Methods:
- Created a mouse model with unilateral stereotactic lesions of the thalamic ventral posterolateral nucleus.
- Conducted behavioral analysis to assess sensory changes.
- Used pharmacological inhibition of spinal and peripheral pain pathways.
- Administered lidocaine microinjections into the thalamic lesion.
Main Results:
- The mouse model exhibited sensory changes comparable to human central post-stroke pain.
- Spinal and peripheral pain system inhibition did not affect hypersensitivity.
- Lidocaine injection into the thalamic lesion reversed hypersensitivity.
Conclusions:
- Evoked hypersensitivity in central post-stroke pain is linked to ongoing neuronal activity in the lateral thalamus.
- The thalamus plays a critical role in the maintenance of central post-stroke pain hypersensitivity.
