Cerebral Metabolites on the Descending Limb of Acute Alcohol: A Preliminary 1H MRS Study

Abstract

Choline-containing compounds (Cho) and the summed peak of glutamate and glutamine (Glx) increased in the thalamus on the descending limb of alcohol, relative to baseline. Findings suggest neuroinflammatory and/or compensatory mechanisms in effect during the process of alcohol clearance.

Proton Magnetic Resonance Spectroscopy in Post-Traumatic Stress Disorder—Updated Systematic Review and Meta-Analysis

“…For example, shared metabolic effects have been reported between PTSD and anxiety, 101 or abnormalities reported in PTSD groups with comorbid depressive symptoms, 51 the latter of which has a documented association with PTSD. 50 Changes in brain morphology 52 , 55 and neurometabolite concentrations have also been found with both acute 102 and chronic 103 alcohol use, as in tobacco or nicotine use, 104 also possibly confounding putative findings attributed to PTSD status. As such, parsing the specific effects of PTSD on metabolite concentrations apart from those associated with comorbid conditions remains a significant challenge.…”

Meta-analysis and Open-source Database for In Vivo Brain Magnetic Resonance Spectroscopy in Health and Disease

“…These age ranges allowed for the greatest number of studies to be included in each of the categories while leaving a gap (e.g., 46-49 years of age) to set groups apart. There were 8 [141–147], 19 [148,149,158–166,150–157], 199 [23,67,174,264–273,175,274–283,176,284–293,177,294–303,178,304–313,179,314–323,180,324–333,181,334–343,182,344–353,183,354–359,165,184–193,167,194–203,168,204–213,169,214–223,170,224–233,171,234–243,172,244–253,173,254–263], and 45 [183,205,360–369,207,370–379,234,380–389,251,279,294,343,346,349] studies within the four age categories (early life, adolescent, young adult, aged), respectively. To determine the concentration ranges, values were separated by metabolite and units (i.u./mM and 1/tCr) reported.…”

“…Studies that investigated clinical groups and included a healthy control group were included in the clinical population analysis. There were 180 publications [141,142,157,305,306,308,310–312,317,321,322,328,160,329–333,335,337,339–341,161,342,345,350–354,359–361,162,362,364,365,368–374,163,377,378,380–387,165,388–397,166,398–407,167,408–414,169,171,143,174,175,178,179,181,183–185,187,188,144,190,192,193,195–201,145,203,204,207–211,213–215,146,217,219,220,223,227,229–231,233,235,150,237,238,240,243,247,249,250,253,254,256,151,…”

Imaging neuroinflammation in individuals with substance use disorders

“…Another study in which alcohol was infused intravenously to a target breath alcohol concentration of 60 mg/dL showed a similar reduction in Cho in the occipital cortex within an hour of administration but, in contrast to the previous study, found a trend for increasing mI as well as a decrease in NAA ( 45 ). Measurement of brain metabolites in the descending limb of the blood alcohol curve, approximately 4–5 hours following alcohol administration, demonstrated significant elevation in Cho/Cre and glutathione/Cre (GSH/Cre) in the thalamus but no effects on mI/Cre or NAA/Cre ( 46 ). The inconsistent findings of these studies raises questions about the temporal (i.e., ascending vs. descending limb) and regional (i.e., differing brain regions) effects of alcohol on brain metabolites.…”