Approximately 60% to 90% of patients with borderline personality disorder (BPD) show nonsuicidal self-injurious behavior (NSSI) with cutting being the most frequently applied method. One of NSSI's functions is to reduce aversive tension. Previous studies have found a tension-reducing effect of painful tissue injury by an incision. It is still unclear whether this effect is based on the effect of tissue injury or the effect of pain experience, or both. The aim of this study was to determine whether tissue injury leads to a stronger stress reduction than a sole pain stimulus in patients with BPD. After stress induction, 57 BPD patients and 60 healthy controls (HCs) received either an incision or a non–tissue-injuring mechanical nociceptive stimulus (“blade”) typically perceived as painful or a non-nociceptive tactile sham stimulus (blunt end of scalpel). Participants were unaware of which procedure was applied. For stress assessment, subjective and objective parameters were measured. As immediate response to the stimulus application, we found greater stress reduction after both painful stimuli (incision and blade) in BPD patients but no difference in stress decrease between the tissue-injuring incision and the non–tissue-injuring pain stimulus (blade). Compared with HCs, incision and blade were followed by greater immediate decrease of arousal in BPD patients. Our findings confirm that among BPD patients, the nociceptive input leads to stress reduction. In contrast, the impact of tissue damage on stress reduction was relatively small. In addition, the results suggest that painful stimuli lead to a greater stress reduction in BPD patients compared with HCs.
The tension-relieving effects of nonsuicidal self-injurious behavior in borderline personality disorder patients resulted from nociceptive processes.
aDepartment of Psychosomatic Medicine and Psychotherapy, Central Institute of Mental Health, Mannheim, Germany
bDepartment of Neurology, Johann Wolfgang Goethe University, Frankfurt, Germany
cDepartment of Psychosocial Medicine, University of Heidelberg, Heidelberg, Germany
dDepartment of Neurophysiology, Centre of Biomedicine and Medical Technology Mannheim, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany
eDepartment of Psychiatry, Schulich School of Medicine and Dentistry, Western University, London, ON, Canada
Corresponding author. Address: Department of Neurophysiology, Centre of Biomedicine and Medical Technology Mannheim, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany. Tel.: +49-621-383-9934; fax: +49-621-383-9921. E-mail address: firstname.lastname@example.org (U. Baumgärtner).
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Received April 18, 2016
Received in revised form November 09, 2016
Accepted November 16, 2016