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Journal Article

Neural Correlates of Antinociception in Borderline Personality Disorder

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons84187

Bohus M, Esposito F, Treede R-D, di Salle F, Greffrath W, Ludaescher P, Jochims A, Lieb K, Scheffler,  K
Department High-Field Magnetic Resonance, Max Planck Institute for Biological Cybernetics, Max Planck Society;

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Citation

Schmahl, C., Bohus M, Esposito F, Treede R-D, di Salle F, Greffrath W, Ludaescher P, Jochims A, Lieb K, Scheffler, K., Hennig, J., & Seifritz, E. (2006). Neural Correlates of Antinociception in Borderline Personality Disorder. Archives of General Psychiatry, 63(6), 659-666. doi:10.1001/archpsyc.63.6.659.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0013-D127-A
Abstract
Context A characteristic feature of borderline personality disorder (BPD) is self-injurious behavior in conjunction with stress-induced reduction of pain perception. Reduced pain sensitivity has been experimentally confirmed in patients with BPD, but the neural correlates of antinociceptive mechanisms in BPD are unknown. We predicted that heat stimuli in patients with BPD would activate brain areas concerned with cognitive and emotional evaluation of pain. Objective To assess the psychophysical properties and neural correlates of altered pain processing in patients with BPD. Design Case-control study. Setting A university hospital. Participants Twelve women with BPD and self-injurious behavior and 12 age-matched control subjects. Interventions Psychophysical assessment and blood oxygen level–dependent functional magnetic resonance imaging during heat stimulation with fixed-temperature heat stimuli and individual-temperature stimuli adjusted for equal subjective pain in all the participants. Main Outcome Measure Blood oxygen level–dependent functional magnetic resonance imaging signal changes during heat pain stimulation. Results Patients with BPD had higher pain thresholds and smaller overall volumes of activity than controls in response to identical heat stimuli. When the stimulus temperature was individually adjusted for equal subjective pain level, overall volumes of activity were similar, although regional patterns differed significantly. Patient response was greater in the dorsolateral prefrontal cortex and smaller in the posterior parietal cortex. Pain also produced neural deactivation in the perigenual anterior cingulate gyrus and the amygdala in patients with BPD. Conclusion The interaction between increased pain-induced response in the dorsolateral prefrontal cortex and deactivation in the anterior cingulate and the amygdala is associated with an antinociceptive mechanism in patients with BPD.