title: Changes in regional cerebral blood flow following antidepressant treatment in late-life depression.
abstract: OBJECTIVE
  Reversible/irreversible abnormalities of regional cerebral blood flow (rCBF) are seen in patients with depression. However, in late-life depression there is little evidence of a longitudinal change in rCBF through remission. We examined whether the decreased rCBF in individuals with late-life depression resolves following treatment.
  
  
  METHODS
  Twenty-five depressed patients older than 55 years completed the Hamilton Rating Scale for Depression and single photon emission computed tomography before and after a mean of 13.7 weeks of pharmacotherapy. Quantitative analyses were performed using the Statistical Parametric Mapping procedure.
  
  
  RESULTS
  Patients with depression demonstrated decreased rCBF in the anterior ventral and dorsal medial prefrontal cortex (PFC), including anterior cingulate cortices, bilateral ventrolateral PFC to temporal cortices, and bilateral medial to lateral parieto-occipital lobes relative to healthy controls. No particular areas showed increased rCBF. Following pharmacotherapy, rCBF significantly increased in the left dorsolateral PFC to precentral areas and the right parieto-occipital regions. However, decreased rCBF at baseline in the anterior ventral/dorsal medial PFC, bilateral ventrolateral PFC, bilateral temporal lobes, and bilateral parietal lobes did not show significant improvement after treatment.
  
  
  CONCLUSIONS
  Remarkable improvements in rCBF in the left dorsolateral PFC to precentral regions are consistent with the hypothesis that neuronetworks including the left frontal cortex may be functionally and reversibly involved in late-life unipolar major depression (state-dependent). In contrast, neural circuits including bilateral medial, dorsolateral, and parietal areas may reflect underlying and continuous pathognomonic brain dysfunction of depression (trait-dependent).
authors.affiliation: Department of Neuropsychiatry, Showa University School of Medicine, Tokyo, Japan.
authors.forename: Junko
authors.initials: J
authors.lastname: Ishizaki
authors.forename: Hideki
authors.initials: H
authors.lastname: Yamamoto
authors.forename: Taro
authors.initials: T
authors.lastname: Takahashi
authors.forename: Maki
authors.initials: M
authors.lastname: Takeda
authors.forename: Madoka
authors.initials: M
authors.lastname: Yano
authors.forename: Masaru
authors.initials: M
authors.lastname: Mimura
mesh_terms: D000368:Aged; D000928:Antidepressive Agents / Q000627:therapeutic use*; D001921:Brain / Q000098:blood supply; D016022:Case-Control Studies; D002540:Cerebral Cortex / Q000098:blood supply / Q000000981:diagnostic imaging / Q000503:physiopathology*; D002560:Cerebrovascular Circulation / Q000187:drug effects* / Q000502:physiology; D003866:Depressive Disorder / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000503:physiopathology*; D003865:Major Depressive Disorder / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D017397:Prefrontal Cortex / Q000098:blood supply / Q000000981:diagnostic imaging / Q000503:physiopathology*; D012039:Regional Blood Flow / Q000187:drug effects* / Q000502:physiology; D015899:Tomography, Emission-Computed, Single-Photon / Q000379:methods
chemical_list: D000928:Antidepressive Agents