Failure of frontolimbic inhibitory function in the context of negative emotion in borderline personality disorder.

OBJECTIVE: The authors sought to test the hypothesis that in patients with borderline personality disorder, the ventromedial prefrontal cortex and associated regions would not be activated during a task requiring motor inhibition in the setting of negative emotion. Such a finding would provide a plausible neural basis for the difficulty borderline patients have in modulating their behavior during negative emotional states and a potential marker for treatment interventions. METHOD: A specifically designed functional magnetic resonance imaging (fMRI) activation probe was used, with statistical parametric mapping analyses, to test hypotheses concerning decreased prefrontal inhibitory function in the context of negative emotion in patients with borderline personality disorder (N=16) and healthy comparison subjects (N=14). 3-T fMRI scanning was used to study brain activity while participants performed an emotional linguistic go/no-go task. RESULTS: Analyses confirmed that under conditions associated with the interaction of behavioral inhibition and negative emotion, borderline patients showed relatively decreased ventromedial prefrontal activity (including medial orbitofrontal and subgenual anterior cingulate) compared with healthy subjects. In borderline patients, under conditions of behavioral inhibition in the context of negative emotion, decreasing ventromedial prefrontal and increasing extended amygdalar-ventral striatal activity correlated highly with measures of decreased constraint and increased negative emotion, respectively. CONCLUSIONS: These findings suggest specific frontolimbic neural substrates associated with core clinical features of emotional and behavioral dyscontrol in borderline personality disorder.

Somatosensory processing and borderline personality disorder: pain perception and a signal detection analysis of proprioception and exteroceptive sensitivity.

Approximately two thirds of those with borderline personality disorder (BPD) who self-injure report diminished sensitivity to pain during acts of self-harm. Research on pain perception suggests that abnormalities of the motivational-affective domain likely contribute to the commonly reported hypo-analgesia evidenced in BPD. It is not that BPD individuals cannot detect or feel painful stimuli, rather their response to it seems to reflect differences in tolerance and willingness to report a stimulus as painful. Although specific processes involved with pain insensitivity have been debated in literature, the likelihood of generalized dysfunction in the somatosensory systems in BPD has not been considered. Prior BPD research has focused only on the pain submodality of somatosensation. This study assessed pain perception (nociception), basic touch (exteroception), and body sense (proprioception) somatosensory submodalities, in an effort to determine if generalized somatosensory deficits are present in BPD. Subjects diagnosed with DSM-IV BPD (n = 27) were compared with individuals who had a history of major depressive disorder with no current psychopathology (n = 20), and normal controls (n = 44), all drawn from a community setting. Individuals with BPD evidenced higher pain endurance and tolerance, but did not demonstrate generalized somatosensory deficits, as evidenced by appropriate functioning on tasks of exteroceptive and proprioceptive sensitivity. Findings are consistent with (but do not prove) a specific dysfunction in the pain-specific mechanism of sensitivity and perception in BPD, perhaps one that does not disturb the other somatosensory modalities. These data help to provide a firmer empirical basis for pain insensitivity as an endophenotype for BPD.

Somatosensory processing and borderline personality disorder features: a signal detection analysis of proprioception and exteroceptive sensitivity.

Pain perception in borderline personality disorder (BPD) may reflect abnormalities of the sensory-discriminative and/or motivational-affective domains in those patients. Although pain insensitivity has received considerable specific discussion, the likelihood of a generalized dysfunction in the somatosensory systems in BPD has not been explored. Prior BPD research has focused only on the pain submodality of somatosensation. This study assessed other prominent and basic touch and body sense somatosensory submodalities, exteroception and proprioception, respectively. Exteroception and proprioception were measured with two-point discrimination and weight discrimination tasks, respectively. A group of subjects with BPD features (n = 32) was compared with a control group (n = 29), both drawn from a nonclinical population, across objective laboratory measures of somatosensation. Results indicated that individuals with BPD features do not demonstrate generalized somatosensory deficits. Lack of group differences in these two somatosensation submodalities (particularly the exteroceptive sensitivity submodality) is consistent with (but does not prove) a dysfunction in the pain-specific mechanism of sensitivity and perception in BPD, perhaps one that does not disturb the other somatosensory modalities.

Diurnal cortisol amplitude and fronto-limbic activity in response to stressful stimuli.

The development and exacerbation of many psychiatric and neurologic conditions are associated with dysregulation of the hypothalamic pituitary adrenal (HPA) axis as measured by aberrant levels of cortisol secretion. Here we report on the relationship between the amplitude of diurnal cortisol secretion, measured across 3 typical days in 18 healthy individuals, and blood oxygen level dependant (BOLD) response in limbic fear/stress circuits, elicited by in-scanner presentation of emotionally negative stimuli, specifically, images of the World Trade Center (WTC) attack. Results indicate that subjects who secrete a greater amplitude of cortisol diurnally demonstrate less brain activation in limbic regions, including the amygdala and hippocampus/parahippocampus, and hypothalamus during exposure to traumatic WTC-related images. Such initial findings can begin to link our understanding, in humans, of the relationship between the diurnal amplitude of a hormone integral to the stress response, and those neuroanatomical regions that are implicated as both modulating and being modulated by that response.