title: Neural dysfunction in postpartum depression: an fMRI pilot study.
abstract: BACKGROUND
  With approximately 4 million births each year in the United States, an estimated 760,000 women annually suffer from a clinically significant postpartum depressive illness. Yet even though the relationship between psychiatric disorders and the postpartum period has been documented since the time of Hippocrates, fewer than half of all these cases are recognized.
  
  
  OBJECTIVE
  Because postpartum depression (PPD), the most common complication of childbearing, remains poorly characterized, and its etiology remains unclear, we attempted to address a critical gap in the mechanistic understanding of PPD by probing its systems-level neuropathophysiology, in the context of a specific neurobiological model of fronto-limbic-striatal function.
  
  
  METHODS
  Using emotionally valenced word probes, with linguistic semantic specificity within an integrated functional magnetic resonance imaging (fMRI) protocol, we investigated emotional processing, behavioral regulation, and their interaction (functions of clinical relevance to PPD), in the context of fronto-limbic-striatal function.
  
  
  RESULTS
  We observed attenuated activity in posterior orbitofrontal cortex for negative versus neutral stimuli with greater PPD symptomatology, increased amygdala activity in response to negative words in those without PPD symptomotology, and attenuated striatum activation to positive word conditions with greater PPD symptomotology.
  
  
  CONCLUSIONS
  Identifying the functional neuroanatomical profile of brain systems involved in the regulation of emotion and behavior in the postpartum period will not only assist in determining whether the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition psychiatric diagnostic specifier of PPD has an associated, unique, functional neuroanatomical profile, but a neurobiological characterization in relation to asymptomatic (postpartum non-depressed) control subjects, will also increase our understanding of the affective disorder spectrum, shed additional light on the possible mechanism(s) responsible for PPD and provide a necessary foundation for the development of more targeted, biologically based diagnostic and therapeutic strategies for PPD.
authors.affiliation: Department of Psychiatry, The Mount Sinai School of Medicine, New York, NY 10029, USA. michael.silverman@mssm.edu
authors.forename: Michael E
authors.initials: ME
authors.lastname: Silverman
authors.forename: Holly
authors.initials: H
authors.lastname: Loudon
authors.forename: Michal
authors.initials: M
authors.lastname: Safier
authors.forename: Xenia
authors.initials: X
authors.lastname: Protopopescu
authors.forename: Gila
authors.initials: G
authors.lastname: Leiter
authors.forename: Xun
authors.initials: X
authors.lastname: Liu
authors.forename: Martin
authors.initials: M
authors.lastname: Goldstein
mesh_terms: D000328:Adult; D000679:Amygdala / Q000473:pathology*; D002540:Cerebral Cortex / Q000473:pathology*; D003342:Corpus Striatum / Q000473:pathology*; D019052:Depression, Postpartum / Q000503:physiopathology*; D005260:Female; D005625:Frontal Lobe / Q000473:pathology*; D006801:Humans; D008279:Magnetic Resonance Imaging; D010865:Pilot Projects; D011247:Pregnancy; D011930:Reaction Time