Publications by authors named "Paul H Soloff"

Background: Borderline personality disorder (BPD) is characterized by instability in affective regulation that can result in a loss of cognitive control. Triggers may be neuronal responses to emotionally valenced context and/or stimuli. 'Neuronal priming' indexes the familiarity of stimuli, and may capture the obligatory effects of affective valence on the brain's processing system, and how such valence mediates responses to the repeated presentation of stimuli.

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Background: Individuals diagnosed with borderline personality disorder (BPD) often describe their lives as stressful and unpredictable. However, it is unclear whether the adversity faced by those with BPD is a product of stress reactivity or stress generation. Here, we examined the dynamic, prospective associations between BPD and stressful life events over 3 years.

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The 10-year outcome for patients with borderline personality disorder (BPD) is diagnostic remission in 85% to 93%; however, less than half achieve good social and vocational functioning, and few attain full psychosocial recovery. To assess the gap between diagnostic remission and psychosocial recovery, quantitative measures of outcome were compared with narrative reports of psychosocial functioning in 150 BPD subjects followed prospectively from 2 to 31 years (mean 9.94 years).

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In longitudinal studies, BPD symptoms diminish over time, though psychosocial functioning lags far behind. The effects of time and advancing age on BPD are poorly understood. We sought prospective predictors of psychosocial outcome and recovery in 150 BPD subjects followed 2 to 31 years (mean 9.

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Fronto-limbic brain networks involved in regulation of impulsivity and aggression are abnormal in Borderline Personality Disorder (BPD). However, it is unclear whether, or to what extent, these personality traits actually modulate brain responses during cognitive processing. Using fMRI, we examined the effects of trait impulsivity, aggression, and depressed mood on regional brain responses in 31 female BPD and 25 control subjects during a Go No-Go task using Ekman faces as targets.

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Emotion dysregulation in borderline personality disorder (BPD) is associated with loss of cognitive control in the face of intense negative emotion. Negative emotional context may interfere with cognitive processing through the dysmodulation of brain regions involved in regulation of emotion, impulse control, executive function and memory. Structural and metabolic brain abnormalities have been reported in these regions in BPD.

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This pilot study examined the integrity of the corpus callosum in a sample of patients with borderline personality disorder (BPD), as abnormalities in inter-hemispheric communication could possibly be involved in illness pathophysiology. We utilized magnetic resonance imaging (MRI) signal intensity (SI) and morphometric measures. Ten BPD and 20 healthy control subjects were assessed for current and past Axis I and Axis II comorbidities and histories of childhood abuse.

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Neuroimaging studies of impulsive-aggressive subjects with borderline personality disorder (BPD) demonstrate hypometabolism in areas of prefrontal and frontal cortex, and a blunted cortical metabolic response to challenge with serotonergic agonists. Neuroendocrine responses to serotonergic challenge are known to vary greatly by gender, and may be related to sex differences in expression of impulsive aggression. We conducted single-blind, placebo-controlled fenfluramine-activated positron emission tomography (PET) studies in impulsive male and female subjects with BPD to look for gender differences in cortical response.

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Hippocampal volume reduction has been reported in patients with borderline personality disorder (BPD), and is hypothesized to be associated with traumatic childhood experiences. We extended this investigation to explore additional brain regions and other potential clinical correlates of structural brain changes in BPD. Ten unmedicated BPD subjects and 20 healthy controls were assessed for current and past Axis I and II comorbidities and histories of childhood abuse.

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