• Kevin C Thorburn, John W Paylor, Christine A Webber, Ian R Winship, and Bradley J Kerr.
• aDepartment of Pharmacology, University of Alberta, Edmonton, AB, Canada bNeuroscience and Mental Health Institute, University of Alberta, Edmonton, AB, Canada cDivision of Anatomy, University of Alberta, Edmonton, AB, Canada dDepartment of Psychiatry, University of Alberta, Edmonton, AB, Canada eDepartment of Anesthesiology and Pain Medicine, University of Alberta, Edmonton, AB, Canada.
• Pain. 2016 Mar 1; 157 (3): 627-42.

AbstractTrigeminal neuropathic pain is a well-recognized complication of the demyelinating disease multiple sclerosis (MS). However, the mechanisms underlying MS-related trigeminal neuropathic pain are poorly understood. This can be attributed, at least in part, to the lack of an animal model that exhibits trigeminal pathology similar to that described in MS. Experimental autoimmune encephalomyelitis (EAE) is an animal model that is commonly used to study the pathophysiology of MS. We show here that mice with EAE exhibit increased sensitivity to air puffs applied to the whisker pad. The increased sensitivity to air puff stimulation is accompanied by T cell infiltration and glial activation at several points along the trigeminal primary afferent pathway. We also observe demyelination of the intra- and extra-pontine aspects of the trigeminal sensory root and the spinal trigeminal tract. This is the first study to show orofacial sensory disturbances and trigeminal demyelination in EAE. Collectively, our data suggest that EAE may be a useful model for understanding MS-related trigeminal neuropathic pain conditions such as trigeminal neuralgia.

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