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Background   Central post-stroke pain (CPSP) is a type of neuropathic pain caused by dysfunction in the spinothalamocortical pathway. However, no animal studies have examined comorbid anxiety and depression symptoms. Whether the typical pharmacological treatments for CPSP, which include antidepressants, selective serotonin reuptake inhibitors (SSRIs), and anticonvulsants, can treat comorbid anxiety and depression symptoms in addition to pain remains unclear? The present study ablated the ventrobasal complex of the thalamus (VBC) to cause various CPSP symptoms. The effects of the tricyclic antidepressants amitriptyline and imipramine, the SSRI fluoxetine, and the anticonvulsant carbamazepine on pain, anxiety, and depression were examined.Results   The results showed that VBC lesions induced sensitivity to thermal pain, measured using a hot water bath; mechanical pain, assessed by von Frey test; anxiety behavior, determined by the open-field test, elevated plus-maze test, and zero-maze test; and depression behavior, assessed by the forced swim test. No effect on motor activity in the open-field test was observed. Amitriptyline reduced thermal and mechanical pain sensitivity and anxiety but not depression. Imipramine suppressed thermal and mechanical pain sensitivity, anxiety, and depression. Fluoxetine blocked mechanical but not thermal pain sensitivity, anxiety, and depression. However, carbamazepine did not affect pain, anxiety, or depression.Conclusion   In summary, antidepressants and SSRIs but not anticonvulsants can effectively ameliorate pain and comorbid anxiety and depression in CPSP. The present findings, including discrepancies in the effects observed following treatment with anticonvulsants, antidepressants, and SSRIs in this CPSP animal model, can be applied in the clinical setting to guide the pharmacological treatment of CPSP symptoms.

molecular pain

Tricyclic antidepressants and selective serotonin reuptake inhibitors but not anticonvulsants ameliorate pain, anxiety, and depression symptoms in an animal model of central post-stroke pain