title: Baseline cerebral hypermetabolism associated with carbamazepine response, and hypometabolism with nimodipine response in mood disorders.
abstract: BACKGROUND
  Positron emission tomography (PET) studies have reported baseline (medication free) differences between mood disorder patients and healthy control subjects, but relatively little is known about relationships between baseline PET scans and treatment responses. Carbamazepine (CBZ) and to a more limited extent nimodipine (NIMO) seem useful in mood disorders. We explored whether baseline regional cerebral glucose metabolism (rCMRglu) could discriminate CBZ and NIMO responders from nonresponders and healthy control subjects.
  
  
  METHODS
  In refractory mood disorder patients, we examined relationships between responses to these drugs, assessed by Clinical Global Impression-Improvement scores, and baseline rCMRglu, determined with fluorine-18 deoxy-glucose and PET.
  
  
  RESULTS
  CBZ responders had baseline left insular hyper-metabolism compared to healthy control subjects and nonresponders, whereas nonresponders had widespread (including left insular) hypometabolism. Degree of CBZ response correlated with baseline paralimbic (including insula) and prefrontal hypermetabolism. In responders but not nonresponders, CBZ decreased widespread metabolism, with the degree of decrease in left insula correlating with response. In contrast, NIMO responders but not nonresponders had baseline widespread (including left insular) hypometabolism. Left prefrontal and left insular baseline hypometabolism, but not metabolic changes with treatment correlated with degree of NIMO response.
  
  
  CONCLUSIONS
  These data suggest that baseline anterior paralimbic and prefrontal hypermetabolism may be associated with CBZ response, and hypometabolism with NIMO response. Based on these preliminary data, further exploration of relationships between baseline PET scans and treatment responses is indicated.
authors.affiliation: Stanford University School of Medicine, California, USA.
authors.forename: T A
authors.initials: TA
authors.lastname: Ketter
authors.forename: T A
authors.initials: TA
authors.lastname: Kimbrell
authors.forename: M S
authors.initials: MS
authors.lastname: George
authors.forename: M W
authors.initials: MW
authors.lastname: Willis
authors.forename: B E
authors.initials: BE
authors.lastname: Benson
authors.forename: A
authors.initials: A
authors.lastname: Danielson
authors.forename: M A
authors.initials: MA
authors.lastname: Frye
authors.forename: P
authors.initials: P
authors.lastname: Herscovitch
authors.forename: R M
authors.initials: RM
authors.lastname: Post
mesh_terms: D000328:Adult; D018692:Antimanic Agents / Q000494:pharmacology*; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D002220:Carbamazepine / Q000494:pharmacology*; D002540:Cerebral Cortex / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000378:metabolism*; D003865:Major Depressive Disorder / Q000188:drug therapy* / Q000378:metabolism*; D005260:Female; D006801:Humans; D008297:Male; D009553:Nimodipine / Q000494:pharmacology*; D012016:Reference Values; D014055:Tomography, Emission-Computed
chemical_list: D018692:Antimanic Agents; D002121:Calcium Channel Blockers; D002220:Carbamazepine; D009553:Nimodipine