title: The hippocampus in patients treated with electroconvulsive therapy: a proton magnetic resonance spectroscopic imaging study.
abstract: BACKGROUND
  We monitored the effect of electroconvulsive therapy (ECT) on the nuclear magnetic resonance-detectable metabolites N-acetylaspartate, creatine and phosphocreatine, and choline-containing compounds in the hippocampus by means of hydrogen 1 magnetic resonance spectroscopic imaging. We hypothesized that if ECT-induced memory deterioration was associated with neuronal loss in the hippocampus, the N-acetylaspartate signal would decrease after ECT and any increased membrane turnover would result in an increase in the signal from choline-containing compounds.
  
  
  METHODS
  Seventeen patients received complete courses of ECT, during which repeated proton magnetic resonance spectroscopic imaging studies of the hippocampal region were performed. Individual changes during the course of ECT were compared with values obtained in 24 healthy control subjects and 6 patients remitted from major depression without ECT.
  
  
  RESULTS
  No changes in the hippocampal N-acetylaspartate signals were detected after ECT. A significant mean increase of 16% of the signal from choline-containing compounds after 5 or more ECT treatments was observed. Despite the mostly unilateral ECT application (14 of 17 patients), the increase in the choline-containing compound signal was observed bilaterally. Lactate or elevated lipid signals were not detected. All patients showed clinical amelioration of depression after ECT.
  
  
  CONCLUSIONS
  Electroconvulsive therapy is not likely to induce hippocampal atrophy or cell death, which would be reflected by a decrease in the N-acetylaspartate signal. Compared with an age-matched control group, the choline-containing compounds signal in patients with a major depressive episode was significantly lower than normal, before ECT and normalized during ECT.
authors.affiliation: NMR Research in Psychiatry, Central Institute of Mental Health, Postfach 1221 20, D-68072 Mannheim, Germany.
authors.forename: G
authors.initials: G
authors.lastname: Ende
authors.forename: D F
authors.initials: DF
authors.lastname: Braus
authors.forename: S
authors.initials: S
authors.lastname: Walter
authors.forename: W
authors.initials: W
authors.lastname: Weber-Fahr
authors.forename: F A
authors.initials: FA
authors.lastname: Henn
mesh_terms: D000328:Adult; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000737:chemistry / Q000378:metabolism; D016923:Cell Death; D002794:Choline / Q000032:analysis / Q000378:metabolism; D003401:Creatine / Q000032:analysis / Q000378:metabolism; D004565:Electroconvulsive Therapy; D005260:Female; D006624:Hippocampus / Q000033:anatomy & histology* / Q000737:chemistry / Q000378:metabolism*; D006801:Humans; D009682:Magnetic Resonance Spectroscopy / Q000706:statistics & numerical data; D008297:Male; D008569:Memory Disorders / Q000175:diagnosis / Q000209:etiology / Q000378:metabolism; D008875:Middle Aged; D010713:Phosphatidylcholines / Q000032:analysis / Q000378:metabolism; D010725:Phosphocreatine / Q000032:analysis / Q000378:metabolism
chemical_list: D010713:Phosphatidylcholines; D010725:Phosphocreatine; D001224:Aspartic Acid; C000179:N-acetylaspartate; D003401:Creatine; D002794:Choline