The borderline diagnosis II: biology, genetics, and clinical course

Skodol, Andrew E.; Siever, Larry J.; Livesley, W. John; Gunderson, John G.; Pfohl, Bruce; Widiger, Thomas A.

doi:10.1016/s0006-3223(02)01325-2

Cited by 349 publications

(217 citation statements)

References 97 publications

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“…There is evidence that oligogenic, developmental, and environmental risk factors operate and interact to produce the full phenotypic expression of BPD (Silk, 2000;Skodol et al, 2002). Consequently, it would seem likely that disturbances at other chemical nodal points in the neural systems mediating the dimensions of BPD, such as the glutamate, GABA, and 5-HT signal transduction cascade pathways, may serve as additional risk factors for the disorder.…”

Section: Discussionmentioning

confidence: 99%

“…Impulsive aggression appears to be directly related to a deficiency in CNS 5-HT activity across a wide range of ages, psychiatric diagnoses, and normative personality types (Silk, 2000;Skodol et al, 2002). Recent evidence supporting the role of 5-HT dysfunction in impulsive aggression in BPD has been provided by neuroimaging studies (Soloff et al, 2000;Leyton et al, 2001).…”

Section: Pfcmentioning

confidence: 99%

“…There is strong evidence of 5-HT dysfunction in impulsive aggression across a broad population range including BPD (Silk, 2000;Skodol et al, 2002). Neuroimaging studies consistently demonstrate a decrease in 5-HT function in the medial PFC of subjects with BPD, which correlates with the degree of impulsive aggression (Soloff et al, 2000;Leyton et al, 2001).…”

Section: Da Effects On Impulsivity In Human and Animal Studiesmentioning

confidence: 99%

“…Research on the biological basis of BPD has focused primarily on the relationships between impulsive aggression and serotonin (5-HT) dysfunction (Silk, 2000;Skodol et al, 2002). To a lesser degree, emotional dysregulation has been correlated with imbalances in cholinergic, noradrenergic, and GABAminergic neurotransmission (Skodol et al, 2002;Gurvits et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Dopamine Dysfunction in Borderline Personality Disorder: A Hypothesis

Friedel

2004

Neuropsychopharmacol

121

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Research on the biological basis of borderline personality disorder (BPD) has focused primarily on the serotonin model of impulsive aggression. However, there is evidence that dopamine (DA) dysfunction may also be associated with BPD. Pertinent research and review articles, identified by Medline searches of relevant topics, books, references from bibliographies, and conference proceedings from 1975 to 2003, were reviewed. Evidence of DA dysfunction in BPD derives from the efficacy of traditional and atypical antipsychotic agents in BPD, and from provocative challenges with amphetamine and methylphenidate of subjects with the disorder. In addition, human and animal studies indicate that DA activity plays an important role in emotion information processing, impulse control, and cognition. The results of this review suggest that DA dysfunction is associated with three dimensions of BPD, that is, emotional dysregulation, impulsivity, and cognitive-perceptual impairment. The main limitation of this hypothesis is that the evidence reviewed is circumstantial. There is no study that directly demonstrates DA dysfunction in BPD. In addition, the therapeutic effects of antipsychotic agents observed in BPD may be mediated by non-DA mechanisms of action. If the stated hypothesis is correct, DA dysfunction in BPD may result from genetic, developmental, or environmental factors directly affecting specific DA pathways. Alternatively, DA dysfunction in BPD may be a compensatory response to alterations in the primary neural systems that control emotion, impulse control, and cognition, and that are mediated by the brain's main neurotransmitters, glutamate, and GABA, or in one or more other neuromodulatory pathways such as serotonin, acetylcholine, and norepinephrine.

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Section: Discussionmentioning

confidence: 99%

Section: Pfcmentioning

confidence: 99%

Section: Da Effects On Impulsivity In Human and Animal Studiesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Dopamine Dysfunction in Borderline Personality Disorder: A Hypothesis

Friedel

2004

Neuropsychopharmacol

121

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“…The past few years have seen a rapidly growing body of research in the field of neurobiological correlates of borderline personality disorder (BPD) (Lieb et al, 2004;Schmahl et al, 2002;Skodol et al, 2002). In addition to research on the genetic basis of the disorder (Jang et al, 1996;Torgersen et al, 2000), psychopharmacological treatment , and neuroendocrinology (Rinne et al, 2002), progress in neuroimaging has been fruitful in the elucidation of the underlying neurobiology of this severe and chronic disorder.…”

Section: Introductionmentioning

confidence: 99%

Neuroimaging in borderline personality disorder

Schmahl¹,

Bremner²

2006

Journal of Psychiatric Research

171

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Neuroimaging has become one of the most important methods in the investigation of the neurobiological underpinnings of borderline personality disorder. Structural and functional imaging studies have revealed dysfunction in different brain regions which seem to contribute to borderline symptomatology. This review presents relevant studies using different methodologies: volumetry of limbic and prefrontal regions, investigations of brain metabolism under resting conditions, studies of serotonergic neurotransmission, and challenge studies using emotional, stressful, and sensory stimuli. Dysfunction in a frontolimbic network is suggested to mediate much, if not all of the borderline symptomatology.

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