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White matter brain and trigeminal nerve abnormalities in temporomandibular disorder

Moayedi, Massieha,b; Weissman-Fogel, Iritb; Salomons, Tim Vaughnb; Crawley, Adrian Philipc,d; Goldberg, Michael Briane,f; Freeman, Bruce Victore,f; Tenenbaum, Howard Charlesa,e,f; Davis, Karen Deboraha,b,g,*

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doi: 10.1016/j.pain.2012.04.003
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Summary Temporomandibular disorder patients have white matter abnormalities along the trigeminal nerve and pain-related brain pathways, and abnormal connectivity of cognitive-affective brain regions.

ABSTRACT Temporomandibular disorder (TMD) is a prevalent chronic pain disorder that remains poorly understood. Recent imaging studies reported functional and gray matter abnormalities in brain areas implicated in sensorimotor, modulatory, and cognitive function in TMD, but it is not known whether there are white matter (WM) abnormalities along the trigeminal nerve (CNV) or in the brain. Here, we used diffusion tensor imaging, and found that, compared to healthy controls, TMD patients had 1) lower fractional anisotropy (FA) in both CNVs; 2) a negative correlation between FA of the right CNV and pain duration; and 3) diffuse abnormalities in the microstructure of WM tracts related to sensory, motor, cognitive, and pain functions, with a highly significant focal abnormality in the corpus callosum. Using probabilistic tractography, we found that the corpus callosum in patients had a higher connection probability to the frontal pole, and a lower connection probability to the dorsolateral prefrontal cortex, compared to controls. Finally, we found that 1) FA in tracts adjacent to the ventrolateral prefrontal cortex and tracts coursing through the thalamus negatively correlated with pain intensity; 2) FA in the internal capsule negatively correlated with pain intensity and unpleasantness; and 3) decreases in brain FA were associated with increases in mean diffusivity and radial diffusivity, markers of inflammation and oedema. These data provide novel evidence for CNV microstructural abnormalities that may be caused by increased nociceptive activity, accompanied by abnormalities along central WM pathways in TMD.

Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.

aInstitute of Medical Science, University of Toronto, Toronto, ON, Canada

bDivision of Brain, Imaging and Behaviour – Systems Neuroscience, Toronto Western Research Institute, Toronto, ON, Canada

cDepartment of Medical Imaging, University of Toronto, Toronto, ON, Canada

dDepartment of Medical Imaging, University Health Network, Toronto, ON, Canada

eFaculty of Dentistry, University of Toronto, Toronto, ON, Canada

fMount Sinai Hospital Dental Clinic, Toronto, ON, Canada

gDepartment of Surgery, University of Toronto, Toronto, ON, Canada

*Corresponding author. Address: Division of Brain, Imaging and Behaviour – Systems Neuroscience, Toronto Western Research Institute, Toronto Western Hospital, University Health Network, 399 Bathurst Street, Room MP14-306, Toronto, ON, Canada M5T 2S8. Tel.: +1 416 603 5662; fax: +1 416 603 5745.

E-mail address:kdavis@uhnres.utoronto.ca

Article history: Received 25 November 2011; Received in revised form 22 February 2012; Accepted 5 April 2012.

© 2012 Lippincott Williams & Wilkins, Inc.
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