Hippocampal dysfunction in Gulf War Syndrome. A proton MR spectroscopy study.

P Mohanakrishnan Menon, Henry A Nasrallah, Roy R Reeves, Jeffrey A Ali

Journal: Brain research 2004;1009(1-2):189-94

PMID: 15120596

Abstract

The pathogenesis of Gulf War Syndrome (GWS) is not clearly understood. Data exist to suggest that GWS may originate from a combination of chronic fatigue and sensitivity to the exposure of exogenous agents. Since the head region of hippocampus is highly vascularized and thus vulnerable to toxic substances in circulation, we postulated that hippocampal impairment occurs in GWS. To test this, single volume localized in vivo proton MR spectroscopy (MRS) studies of the left and right hippocampi of consenting Gulf War veterans (N=15; 10 with GWS, and 5 without GWS) and control Vietnam veterans (N=6) were conducted in accordance with approved human study protocols. The N-acetyl aspartate (NAA) to creatine and choline to creatine ratios were computed from the spectra. The NAA/creatine ratio of the GWS group (N=10) was found to be significantly lower than that of the entire control group (N=11) or the unaffected GW control group (N=5). No laterality differences were observed among any of the three groups. The choline/creatine ratio of the GWS group was not different from that for either control group. To check the existence of any relationship between age and the NAA/creatine ratios, the entire study population was grouped into those below or above the median age (44.3 years). It was found that the NAA/Cre ratio of the younger group (only Gulf War veterans) was significantly lower than that of the older group. The lower NAA/creatine ratio for the GWS group points to the existence of hippocampal dysfunction.

Address: Department of Psychiatry and Human Behavior, University of Mississippi Medical Center, Jackson 39216, USA. [email protected]

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