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• W1971378633 abstract "Multiple sclerosis is a chronic inflammatory demyelinating disease, associated, in 50-80% of patients, with persistent pain. While the type of pain that affects these patients is being more documented, the mechanisms underlying this pathology are still poorly understood and animal models of such chronic pain associated with MS are required. The aim of our study was to characterize the sensory abnormalities and in particular the clinical signs linked to persistent pain in two models of Experimental Autoimmune Encephalomyelitis (EAE) in the rat. This behavioural characterization tested several sensory modalities such as mechanical and thermal (heat/cold) hyperalgesia or allodynia and explored some of these modalities on two different extremities: the hindpaws and the tail. Our study showed that while one of the model produced more robust motor impairment, animals of both models suffer from mechanical hyperalgesia and thermal allodynia to cold, both at the level of the tail and the hindpaws. While the time-course changes of some of these modalities are shifted in the time between the two models, they represent good models of the sensory abnormalities experienced by MS patients. The second part of our study aimed at characterizing from a pharmacological point of view the most robust model (EAE+Cyclosporine) and showed that Gabapentin, Duloxetine and Tramadol partially relieved some of the clinical signs. Our results suggest that the model EAE+Cyclosporine in the rat is a good model of chronic sensory abnormalities observed in MS patients both from a behavioural and pharmacological point of view." @default.
• W1971378633 created "2016-06-24" @default.
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• W1971378633 date "2011-03-01" @default.
• W1971378633 modified "2023-10-09" @default.
• W1971378633 title "Characterisation of sensory abnormalities observed in an animal model of multiple sclerosis: A behavioural and pharmacological study" @default.
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• W1971378633 doi "https://doi.org/10.1016/j.ejpain.2010.07.010" @default.
• W1971378633 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20829083" @default.
• W1971378633 hasPublicationYear "2011" @default.
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