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Effect of hypnotic pain modulation on brain activity in patients with temporomandibular disorder pain

Abrahamsen, Randia; Dietz, Martinb; Lodahl, Sanneb; Roepstorff, Andreasb; Zachariae, Robertc; Østergaard, Leifb; Svensson, Petera,b,d,*

doi: 10.1016/j.pain.2010.09.020
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Hypnosis modulates pain perception but the associated brain mechanisms in chronic pain conditions are poorly understood. Brain activity evoked by painful repetitive pin-prick stimulation of the left mental nerve region was investigated with use of fMRI in 19 patients with painful temporomandibular disorders (TMD) during hypnotic hypoalgesia and hyperalgesia and a control condition. Pain intensity and unpleasantness of the painful stimulation was scored on a 0–10 Numerical Rating Scale (NRS). NRS pain and unpleasantness scores during hypnotic hypoalgesia were significantly lower than in the control condition and significantly higher in the hypnotic hyperalgesia condition. In the control condition, painful stimulation caused significant activation of right posterior insula, primary somatosensory cortex (SI), BA21, and BA6, and left BA40 and BA4. Painful stimulation during hypnotic hyperalgesia was associated with increased activity in right posterior insula and BA6 and left BA40 whereas hypnotic hypoalgesia only was associated with activity in right posterior insula. Unexpectedly, direct contrasts between control and hypnotic hyperalgesia conditions revealed significant decreases in S1 during hyperalgesia. Direct contrasts between control and hypnotic hypoalgesia conditions demonstrated significant decreases in right posterior insula and BA21, as well as left BA40 during hypoalgesia. These findings are the first to describe hypnotic modulation of brain activity associated with nociceptive processing in chronic TMD pain patients and demonstrate that hypnotic hypoalgesia is associated with a pronounced suppression of cortical activity and a disconnection between patient-based scores and cortical activity in S1 during hypnotic hyperalgesia.

aDepartment of Clinical Oral Physiology, School of Dentistry, Aarhus University, Aarhus, Denmark

bCenter of Functionally Integrative Neuroscience, Aarhus University, Aarhus, Denmark

cPsychooncology Research Unit, Aarhus University Hospital, Aarhus, Denmark

dDepartment of Oral Maxillofacial Surgery, Aarhus University Hospital, Denmark

*Corresponding author at: Department of Clinical Oral Physiology, School of Dentistry, Aarhus University, Vennelyst Boulevard 9, DK-8000 Aarhus C, Denmark. Tel.: +45 89424191; fax: + 45 8619 5665.

E-mail address:psvensson@odont.au.dk

Submitted March 31, 2010; revised September 14, 2010; accepted September 15, 2010.

© 2010 Lippincott Williams & Wilkins, Inc.
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