Positron-Emission Tomography and Personality Disorders

Pf, Goyer; Pj, Andreason; We, Semple; Ah, Clayton; King, Abby C.; Ba, Compton-Toth; Sc, Schulz; Rm, Cohen

doi:10.1038/npp.1994.3

Cited by 232 publications

(112 citation statements)

References 18 publications

Supporting

Mentioning

105

Contrasting

Unclassified

Order By: Relevance

“…We did not find a difference in the orbitofrontal cortical area between depressed patients with BPD and MDD without BPD in contrast to findings from both lesion (Butter et al, 1970;Grafman et al, 1996;Heinrichs, 1989;Raleigh et al, 1979) and neuroimaging studies (De La Fuente et al, 1997;Goyer et al, 1994;New et al, 2002New et al, , 2004Siever et al, 1999) that suggest a role for the orbitofrontal cortex in impulsive aggression. Our sample of depressed women with BPD did not differ significantly in terms of clinical measures of aggression and impulsivity from the depressed women without BPD (see Table 1).…”

Section: Orbitofrontal Cortex In Mdd With Bpd Compared To Mddcontrasting

confidence: 99%

“…Functional neuroimaging studies of brain glucose metabolism in borderline and other aggressive and impulsive patients have also implicated the anterior cingulate area. In agreement with our findings, most studies of BPD found low relative glucose metabolism and regional cerebral blood flow (rCBF) in the anterior cingulate gyrus at rest (De La Fuente et al, 1997;Goyer et al, 1994). PET studies report that FEN responses are blunted in the orbitofrontal cortex and anterior cingulate gyrus (Siever et al, 1999) in impulsive aggressive subjects compared to healthy controls, as are m-CPP responses (New et al, 2002), although not all studies agree (Soloff et al, 2000).…”

Section: Anterior Cingulate In Mdd With Bpd Compared To Mddsupporting

confidence: 87%

“…Previous imaging studies have implicated frontal and temporal brain region's metabolic changes to violence (Goyer et al, 1994;Volkow and Tancredi, 1987). Raine et al (1997) reported reduced glucose metabolism in PFC and posterior parietal cortex of a severely violent and mostly male sample.…”

Section: Psychopathology In Bpdmentioning

confidence: 99%

See 2 more Smart Citations

Positron Emission Tomography of Regional Brain Metabolic Responses to a Serotonergic Challenge in Major Depressive Disorder with and without Borderline Personality Disorder

Oquendo

Krunic

Parsey

et al. 2005

Neuropsychopharmacol

View full text Add to dashboard Cite

Previous neuroimaging studies of major depression have not controlled for the presence of personality disorders characterized by impulsive aggressive behavior, such as borderline personality disorder (BPD). Using positron emission tomography (PET), we studied regional glucose uptake in response to fenfluramine (FEN) in depressed subjects with BPD (n ¼ 11) and depressed patients without Cluster B Axis II disorders (n ¼ 8). Subjects were scanned while medication-free after a single blind placebo administration and after FEN on a second day. Brain responses were measured by PET imaging of [ 18 F]fluorodeoxyglucose (FDG) and serial prolactin levels. Scans were compared at a voxel level using statistical parametric mapping. Correlations of changes in relative regional cerebral uptake (rCMRglu) with clinical measures were assessed. Depressed borderline patients had greater relative activity in parietotemporal cortical regions (BA 40, BA 22, and BA 42) before and after FEN activation compared to those without BPD. They also had less relative uptake in the anterior cingulate cortex (BA 32) at baseline compared to depressed patients without BPD and FEN abolished this difference. Impulsivity was positively correlated with rCMRglu in superior and middle frontal cortex (BA 6 and 44). Hostility was positively correlated with rCMRglu in temporal cortical regions (BA 21 and 22). In conclusions, borderline pathology in the context of a Major Depressive Disorder is associated with altered activity in parietotemporal and anterior cingulate cortical regions. Controlling for the presence of BPD in future imaging studies of mood disorders may elucidate similarities and differences in regional serotonergic function in these two often comorbid disorders.

show abstract

Section: Orbitofrontal Cortex In Mdd With Bpd Compared To Mddcontrasting

confidence: 99%

Section: Anterior Cingulate In Mdd With Bpd Compared To Mddsupporting

confidence: 87%

See 1 more Smart Citation

Positron Emission Tomography of Regional Brain Metabolic Responses to a Serotonergic Challenge in Major Depressive Disorder with and without Borderline Personality Disorder

Oquendo

Krunic

Parsey

et al. 2005

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…Neuroimaging studies in subjects with BPD indicate structural and functional changes in brain regions critical to cognitive activity, such as decreases in frontal lobe and hippocampal volumes (Driessen et al, 2000;Lyoo et al, 1998;Rusch et al, 2003), and changes in frontal lobe glucose metabolism (Goyer et al, 1994;De la Fuente et al, 1997;Juengling et al, 2003). Tebartz van Elst et al (2001) report a significant reduction of N-acetylaspartate concentration (a proposed measure of neuronal integrity) in the dorsolateral prefrontal cortex (DLPFC) measured by 1 H-MRS in patients with BPD compared to controls.…”

Section: Da Dysfunction and Impulsive Behaviors In Animalsmentioning

confidence: 99%

Dopamine Dysfunction in Borderline Personality Disorder: A Hypothesis

Friedel

2004

Neuropsychopharmacol

124

View full text Add to dashboard Cite

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.

show abstract

“…Positron emission tomography (PET) has revealed reduced prefrontal cortical activity in patients with bipolar depression (Baxter et al 1989), patients with personality disorders characterized by impulsive aggression (Goyer et al 1994), alcoholic criminal offenders with a history of impulsive aggression (Linnoila et al 1983), impulsive murderers (Raine et al 1994), and violent psychiatric inpatients (Volkow and Tancredi 1987). Fenfluramine administration increases cortical metabolism and/or blood flow in orbital frontal cortex in normal subjects (Kapur et al 1994;Mann et al 1996).…”

mentioning

confidence: 99%