title: Hippocampal damage in the human brain after cardiac arrest.
abstract: OBJECTIVE
  Very few reports are available on changes in the human hippocampus after cardiac arrest. The objective of this study was to investigate if specific hippocampal volume losses can be demonstrated in the human brain following reperfusion after cardiac arrest.
  
  
  METHODS
  We assessed the volumes of the hippocampal formation (HF) and temporal lobe excluding HF (TL) as the contrast using magnetic resonance (MR)-imaging-based volumetry in 11 vegetative patients after cardiac arrest and in 22 healthy controls of similar age, sex and body size distribution. The measured volumes were normalized for differences in the head size among subjects by dividing by the total intracranial volume (TICV). The MR images of the 11 patients were obtained between days 8 and 21 after cardiac arrest.
  
  
  RESULTS
  The observed volumes of HFs and TLs of both patient and control groups were as follows: right HF volume (HFV): 2.67 +/- 0.19 (mean +/- SD, cm(3)) in patients versus 3.89 +/- 0.44 in controls; left HFV: 2.72 +/- 0.17 versus 3.74 +/- 0.35; right TL volume (TLV): 73.37 +/- 6.54 versus 80.08 +/- 7.62, and left TLV: 72. 45 +/- 6.77 versus 78.59 +/- 6.68. The normalized indices (HFV/TICV and TLV/TICV) were as follows: right HF: 0.0021 +/- 0.0002 (mean +/- SD) in patients versus 0.0031 +/- 0.0001 in controls, p < 0.0001, left HF: 0.0022 +/- 0.0002 versus 0.0030 +/- 0.0001, p < 0.0001, right TL: 0.058 +/- 0.002 versus 0.064 +/- 0.004, p = 0.0007, and left TL: 0.058 +/- 0.002 versus 0.062 +/- 0.004, p = 0.0014. The HFV-TLV ratios (HFV/TICV divided by TLV/TICV) of both groups were: right HFV-TLV ratio: 0.037 +/- 0.004 in patients versus 0.049 +/- 0. 004 in controls, p < 0.0001, left HFV-TLV ratio: 0.038 +/- 0.004 versus 0.048 +/- 0.004, p < 0.0001.
  
  
  CONCLUSIONS
  The patient group had HFs that were 26.8-30.6% smaller than those of the control group, but in the patient group, the TLs slightly decreased in size by only 7.8-8.2% of the volume of those in the control group within 21 days after cardiac arrest. The volume reductions in the bilateral HFs of patients after cardiac arrest were significantly larger than those in the bilateral TLs. We speculate that this specific rapid hippocampal shrinkage reflects its greater vulnerability to global brain ischemia.
authors.affiliation: Department of Emergency and Critical Care Medicine, Nara Medical University, Nara, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Fujioka
authors.forename: K
authors.initials: K
authors.lastname: Nishio
authors.forename: S
authors.initials: S
authors.lastname: Miyamoto
authors.forename: K I
authors.initials: KI
authors.lastname: Hiramatsu
authors.forename: T
authors.initials: T
authors.lastname: Sakaki
authors.forename: K
authors.initials: K
authors.lastname: Okuchi
authors.forename: T
authors.initials: T
authors.lastname: Taoka
authors.forename: S
authors.initials: S
authors.lastname: Fujioka
mesh_terms: D000368:Aged; D001284:Atrophy; D001921:Brain / Q000473:pathology; D005260:Female; D006323:Heart Arrest / Q000150:complications / Q000473:pathology*; D006624:Hippocampus / Q000473:pathology*; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D015425:Myocardial Reperfusion; D013702:Temporal Lobe / Q000473:pathology