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UMD PSYC 434 - Defining the neurocircuitry of borderline personality disorder

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Defining the neurocircuitry of borderlinepersonality disorder: Functionalneuroimaging approachesGARY R. BRENDEL, EMILY STERN, and DAVID A. SILBERSWEIGWeill Medical College of Cornell UniversityAbstractFunctional neuroimaging recently has been used to localize brain dysfunction in borderline personality disorder~BPD!. Initial studies have examined baseline activity or emotional reactivity, and our group has investigated whatwe consider to be a crucial interaction between negative emotion and behavioral ~ dys!control. This research isbeginning to identify abnormal frontolimbic circuitry likely underlying core clinical features of this condition. Wereview the evidence for dysfunction in specific frontolimbic regions, leading to a mechanistic model of symptomformation in BPD. In addition, we offer an integration of these neuroimaging findings with developmentalperspectives on the emergence of borderline psychopathology, focusing on the ways in which early psychosocialexperience may interact with developing brain systems. We also consider possible mechanisms of psychotherapeuticchange at the neural systems level in BPD. Finally, we propose that future neuroimaging studies of BPD shouldintegrate multiple levels of observation ~structural, functional, neurochemical, genetic, and clinical! in amodel-driven fashion to further understand the dynamic relationship between biological and psychological factors inthe development and treatment of this difficult condition.Using a variety of imaging technologies andmethodologies, neuroimaging investigationsare shedding light on brain structure and func-tion in both normal and pathological statesincluding psychotic, mood, anxiety, and de-velopmental disorders ~Dougherty & Rauch,2001; Stern & Silbersweig, 2001!. These var-ied approaches include using structural neuro-imaging, positron emission tomography ~PET!,and functional magnetic resonance imaging~fMRI! in the setting of symptom provoca-tion studies, cognitive activation paradigms,and resting state studies. By defining the dys-functional neural circuitry in individuals withthese conditions, neuroimaging studies pro-vide the possibility of enhanced diagnosticspecificity, novel targets for therapeutic inter-ventions, and more reliable predictors of treat-ment response.Initially focused on the investigation ofAxis I disorders, psychiatric neuroimaging re-searchers are beginning to study the functionalneuroanatomy of Axis II disorders, includingborderline personality disorder ~BPD!. BPD isa complex psychiatric disorder characterizedby affect dysregulation and behavioral impul-sivity. Individuals with this condition experi-ence rapid alterations of mood and intenseemotional responses, as well as impulsive, po-tentially self-destructive behaviors ~substanceabuse, self-mutilations, suicidal behaviors, bingeeating, sexual promiscuity!. Focusing on thesedomains of emotion and behavior, neuroimag-ing studies have begun to elucidate the neuralcorrelates of this disorder.Functional neuroimaging studies using cog-nitive activation paradigms in which subjectsare presented with emotional stimuli have be-gun to examine neural dysfunctions associatedwith emotional reactivity in individuals withBPD.An f MRI study using negative versus neu-tral valenced images showed activations in bi-lateral amygdala, bilateral fusiform gyri, leftAddress correspondence and reprint requests to: Gary R.Brendel, 295 Central Park West, Suite 2, New York, NY10024; E-mail: [email protected] and Psychopathology 17 ~2005!, 1197–1206Copyright © 2005 Cambridge University PressPrinted in the United States of AmericaDOI: 10.10170S095457940505056X1197medial prefrontal ~Brodmann area @BA# 10!,and right ventrolateral prefrontal ~BA 47! cor-tices in BPD subjects compared with normalcontrols ~Herpertz et al., 2001!. In another fMRIstudy, investigators found greater activation inthe left amygdala in response to facial expres-sions of emotion ~happy, sad, fearful! in BPDpatients versus normal control subjects ~Done-gan et al., 2003!. A PET study by Schmahl, El-zinga, et al. ~2003!, in which subjects listenedto personalized scripts of abandonment expe-riences, found increased activity in bilateral dor-solateral prefrontal cortex ~DLPFC; BAs 8, 9,10! and decreased activity in right dorsal ante-rior cingulate ~BAs 24, 32!, left superior0middletemporal gyri, left fusiform gyrus ~BA 37!, leftvisual association cor tex ~BA 19!, and rightamygdala0hippocampus in BPD subjects com-pared with non-BPD subjects who had compa-rable sexual abuse histories. Although thedirection of change in neural activation be-tween BPD subjects and controls varies in thesestudies, probably related to the specific meth-odologies used, these results nonetheless sup-port the broad notion of dysfunction in limbicand prefrontal regions in this disorder. In ad-dition, frontolimbic ~amygdala0hippocampus,orbitofrontal cortex @OFC#!volume loss ~Ruschet al., 2003; Schmahl, Vermetten, Elzinga, &Bremner, 2003; Tebartz van Elst et al., 2003!provides further evidence of dysfunction in theseregions, and suggests an underlying neuropath-ological correlate in BPD in regions that can beassociated with the symptomatology of thisdisorder.@18F#Fluorodeoxyglucose PET ~FDG-PET!imaging studies of BPD subjects consistentlyhave demonstrated evidence of frontal dys-function, most prominent in the prefrontal cor-tical areas ~De la Fuente et al., 1997; Juenglinget al., 2003; Soloff, Meltzer, Greer, Constan-tine, & Kelly, 2000!. Metabolic challengeFDG-PET neuroimaging studies using fenflur-amine, a serotonergic agonist, have foundblunted neural responses in a variety of re-gions including medial, orbital, dorsolateral,and ventromedial prefrontal cortices, as wellas in anterior cingulate cortex in BPD sub-jects ~Siever et al., 1999; Soloff et al., 2000!.Overall, these studies suppor t the hypothesisthat diminished serotonergic function in PFC,a region with neurotransmitter and neuroana-tomical systems known to be involved in emo-tional regulation and inhibitory behavioralcontrol, may constitute a biologic diathesisfor disinhibition, impulsivity, and affect dys-regulation in individuals with BPD.Using PET with a-@11C#methyl-l-trypto-phan ~a-MTrp, an l -tryptophan analog ! to as-sess brain serotonin ~5-HT! synthesis capacity,Leyton et al. ~2001! found significantly lowera-MTrp trapping in male BPD subjects com-pared with healthy controls in bilateral medialfrontal cor tices extending into


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