While the media focus was on "Medical Road Rage," another article in the June 2006 issue of the Archives of General Psychiatry was more interesting to The Neurocritic:
Schmahl C, Bohus M, Esposito F, Treede RD, Di Salle F, Greffrath W, Ludaescher P, Jochims A, Lieb K, Scheffler K, Hennig J, Seifritz E.Do borderline patients injure themselves to "feel" (or "feel more normal") OR to down-regulate the emotional components of pain? The results don't really answer this question or the question posed in my title, but the authors give 2 options:
Neural correlates of antinociception in borderline personality disorder.
Arch Gen Psychiatry. 2006 Jun;63(6):659-66.
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.
Limbic deactivation has been found to correlate with the degree of coping in aversive situations in general. . . . Thus, in view of these findings, self-inflicted pain may function to normalize neural activity in specific brain regions involved in emotional and cognitive processing. Alternatively, repeated self-injury could lead to an adaptation of pain thresholds and pain processing reflected in the current findings of elevated pain thresholds and disturbed prefrontal and limbic pain processing.
Now back to road rage (aka Intermittent Explosive Disorder). Dr. Emil Coccaro, that study's co-author and chair of Psychiatry at the University of Chicago, thinks all those angry drivers stuck in traffic should just take Prozac (not public transit).
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