title: The relationship between the acute cerebral metabolic response to citalopram and chronic citalopram treatment outcome.
abstract: OBJECTIVE
  Given the challenges in the clinical management of geriatric depression, research over the past decade has focused on developing early neurobiological markers of antidepressant treatment response. This study tested the hypothesis that lower baseline glucose metabolism and greater acute cerebral metabolic responses to a single, intravenous (IV) dose of the selective serotonin reuptake inhibitor (SSRI) citalopram would be associated with greater improvement of depressive symptoms after 12 weeks of citalopram treatment in geriatric depression.
  
  
  METHODS
  sixteen geriatric depressed patients underwent two scans to measure cerebral glucose metabolism after administration of either a saline placebo or citalopram infusion (40 mg, IV). Then, the patients were treated with the oral citalopram medication for 12 weeks.
  
  
  RESULTS
  greater improvement of depressive symptoms was associated with lower baseline metabolism in anterior cingulate, superior, middle, and inferior frontal gyri (bilaterally), inferior parietal lobule (bilaterally), precuneus (right), insula (left), parahippocampal gyrus (right), caudate (bilaterally), and putamen (left) regions. Greater improvement of depressive symptoms was associated with greater reductions in metabolism after acute citalopram administration in similar brain regions, including additional posterior cortical regions.
  
  
  CONCLUSIONS
  lower baseline cerebral metabolism and greater decreases with acute citalopram administration are associated with better antidepressant response to chronic citalopram treatment. These data are consistent with previous studies of total sleep deprivation and suggest that dynamic, early adaptive changes or normalization of cerebral metabolism may represent early neurobiological markers of chronic SSRI treatment response in geriatric depression.
authors.affiliation: Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA. gsmith95@jhmi.edu
authors.forename: Gwenn S
authors.initials: GS
authors.lastname: Smith
authors.forename: Clifford I
authors.initials: CI
authors.lastname: Workman
authors.forename: Elisse
authors.initials: E
authors.lastname: Kramer
authors.forename: Carol R
authors.initials: CR
authors.lastname: Hermann
authors.forename: Rachel
authors.initials: R
authors.lastname: Ginsberg
authors.forename: Yilong
authors.initials: Y
authors.lastname: Ma
authors.forename: Vijay
authors.initials: V
authors.lastname: Dhawan
authors.forename: Thomas
authors.initials: T
authors.lastname: Chaly
authors.forename: David
authors.initials: D
authors.lastname: Eidelberg
mesh_terms: D000284:Administration, Oral; D000368:Aged; D001921:Brain / Q000000981:diagnostic imaging / Q000187:drug effects / Q000378:metabolism*; D015283:Citalopram / Q000008:administration & dosage / Q000493:pharmacokinetics / Q000627:therapeutic use*; D003863:Depression / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000378:metabolism*; D005260:Female; D019788:Fluorodeoxyglucose F18; D005947:Glucose / Q000378:metabolism; D006801:Humans; D007262:Infusions, Intravenous; D008297:Male; D049268:Positron-Emission Tomography / Q000379:methods; D016896:Treatment Outcome
chemical_list: D015283:Citalopram; D019788:Fluorodeoxyglucose F18; D005947:Glucose