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Decreased N ‐acetyl‐aspartate levels in anterior cingulate and hippocampus in subjects with post‐traumatic stress disorder: a proton magnetic resonance spectroscopy study
Author(s) -
Ham ByungJoo,
Chey Jeanyung,
Yoon Sujung J.,
Sung Younghoon,
Jeong DoUn,
Ju Kim Seog,
Sim Minyoung E.,
Choi Namhee,
Choi IhnGeun,
Renshaw Perry F.,
Lyoo In Kyoon
Publication year - 2007
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2006.05253.x
Subject(s) - proton magnetic resonance , anterior cingulate cortex , psychology , hippocampus , traumatic stress , magnetic resonance imaging , posttraumatic stress , clinical psychology , functional magnetic resonance imaging , neuroscience , psychiatry , nuclear magnetic resonance , medicine , cognition , physics , radiology
The purpose of this study was to investigate the concentration of N ‐acetyl‐aspartate (NAA) in the brain and its relationship with clinical characteristics in patients with post‐traumatic stress disorder (PTSD). Proton magnetic resonance spectroscopy was performed in order to measure NAA concentrations in the anterior cingulate cortex (ACC) and bilateral hippocampus in 26 subjects with fire‐related PTSD, who were survivors of a subway fire in South Korea, and 25 age‐ and sex‐matched healthy comparison subjects. There were decreased NAA levels in the ACC ( t = −3.88, d.f. = 49, P < 0.001) and bilateral hippocampus (right, t = −3.88, d.f. = 49, P < 0.001; left, t = −3.62, d.f. = 49, P < 0.001) in the PTSD group relative to the healthy comparison group. Also, NAA levels of the ACC ( r = – 0.43, n = 26, P = 0.027) and bilateral hippocampus (right, r = – 0.48, n = 26, P = 0.013; left, r = −0.40, n = 26, P = 0.04) were negatively correlated with re‐experience symptom scores in subjects with PTSD. In conclusion, our findings suggest that subjects with PTSD had decreased neuronal viabilities in the ACC and bilateral hippocampus, and that these deficits may play an important role in the pathophysiology of PTSD, especially regarding the re‐experiencing of traumatic events.