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Altered structure and function in the hippocampus and medial prefrontal cortex in patients with burning mouth syndrome

Khan, Shariq A.a; Keaser, Michael L.a; Meiller, Timothy F.b; Seminowicz, David A.a,*

doi: 10.1016/j.pain.2014.04.022
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Summary Patients with burning mouth syndrome had altered structure and function of the medial prefrontal cortex and hippocampus, which was partially explained by ongoing pain and depression scores.

ABSTRACT Burning mouth syndrome (BMS) is a debilitating, idiopathic chronic pain condition. For many BMS patients, burning oral pain begins in late morning and becomes more intense throughout the day, peaking by late afternoon or evening. We investigated brain gray matter volume (GMV) with voxel-based morphometry (VBM), white matter fractional anisotropy (FA) with diffusion tensor imaging (DTI), and functional connectivity in resting state functional MRI (rsfMRI) in a tightly screened, homogeneous sample of 9 female, postmenopausal/perimenopausal BMS patients and 9 matched healthy control subjects. Patients underwent 2 scanning sessions in the same day: in the morning, when ongoing pain/burning was low, and in the afternoon, when pain/burning was significantly higher. Patients had increased GMV and lower FA in the hippocampus (Hc), and decreased GMV in the medial prefrontal cortex (mPFC). rsfMRI revealed altered connectivity patterns in different states of pain/burning, with increased connectivity between mPFC (a node in the default mode network) and anterior cingulate cortex, occipital cortex, ventromedial PFC, and bilateral Hc/amygdala in the afternoon compared with the morning session. Furthermore, mPFC-Hc connectivity was higher in BMS patients than control subjects for the afternoon but not the morning session. mPFC-Hc connectivity was related to Beck depression inventory scores both between groups and between burning states within patients, suggesting that depression and anxiety partially explain pain-related brain dysfunction in BMS. Overall, we provide multiple lines of evidence supporting aberrant structure and function in the mPFC and Hc, and implicate a circuit involving the mPFC and Hc in regulating mood and depressive symptoms in BMS.

aDepartment of Neural and Pain Sciences, University of Maryland School of Dentistry, Baltimore, MD, USA

bDepartment of Oncology and Diagnostic Sciences, University of Maryland School of Dentistry, Baltimore, MD, USA

* Corresponding author. Address: Department of Neural and Pain Sciences, University of Maryland School of Dentistry, 650 West Baltimore Street, 8 South, Baltimore, MD 21201, USA. Tel.: +1 410 706 3476. Fax: +1 410 706 0865.

E-mail address:dseminowicz@umaryland.edu

Article history:

Received 22 December 2013

Received in revised form 4 March 2014

Accepted 15 April 2014

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

© 2014 International Association for the Study of Pain
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