Table 19.1.
Original reports of human in vivo 1H magnetic resonance spectroscopy in alcohol use disorder (up to February 2013)
| Authors, year of publication |
Study groups | Duration of abstinence |
Age (mean ± sd) |
Major findings (all findings statistically significant unless otherwise stated) |
|---|---|---|---|---|
| Fein et al., 1994 | 11 alcoholics, 9 controls | 3–24 months | 65 ± 9 | Greater frontal than parietal cortical NAA loss in alcoholics vs controls |
| Martin et al., 1995 | 10 alcoholics, 9 controls | 0–28 days | 44 ± 9 | Increase of Cho/NAA in cerebellar vermis with abstinence |
| Jagannathan et al., 1996 | 10 alcoholics, 27 controls | 1 month | 45 ± 4 | Low NAA/Cr and NAA/Cho in cerebellum, frontal lobe, and thalamus |
| Seitz et al., 1999 | 11 alcoholics, 12 controls | 4 days | 41 ± 11 | Low NAA/Cr at TE = 135 ms and low Cho/Cr at TE = 5 ms |
| Behar et al., 1999 | 5 alcoholics, 10 controls | 5 weeks | 35 ± 7 | Low GABA + homocarnosine in occipital lobe |
| Schweinsburg et al., 2000 | 9 alcoholics, 5 controls | 5 weeks (n = 4) and ≥ 1.5 years (n = 5) |
46 ± 7 | High mI in anterior cingulate cortex and thalamus at 5 weeks. NAA, Cho, and Cr not altered. mI normal at 6 years |
| Schweinsburg et al., 2001 | 37 alcoholics, 15 controls | 1 month | 39 ± 9 | Low NAA in frontal WM, high mI in WM |
| Bendszus et al., 2001 | 17 alcoholics, 12 controls | 2 days and 5 weeks | 40 ± 8 | Low NAA/Cr in cerebellum and frontal lobe, low Cho/Cr in cerebellum (days 3–6) and normalized values after 5 weeks |
| O’Neill et al., 2001 | 8 treatment-naïve heavy drinkers, 12 alcoholics |
2 years (alcoholics) | 43 ± 7 | NAA, Cr, and Cho throughout brain similar between groups |
| Parks et al., 2002 | 31 alcoholics, 12 controls | 4 days and 3 months | 41 ± 9 | Low cerebellar NAA and Cho. NAA increase over 3 months (n = 11) |
| Schweinsburg et al., 2003 | 25 alcoholics (11 F, 17 M),25 controls (12 F, 13 M) |
40 days (F), 26 days (M) |
43 ± 8 (F) 36 ± 6 (M) |
Low frontal white-matter NAA in female and male alcoholics. Low frontal gray-matter NAA only in female alcoholics |
| Meyerhoff et al., 2004 | 46 treatment-naïve heavy drinkers, 52 controls |
12 hours | 41 ± 9 | Low NAA in frontal WM of heavy drinkers vs controls (driven by those without a positive family history of alcoholism, associated with lower executive and working memory functions and lower frontal P3b amplitudes). High Cr, ml, and Cho in parietal GM (but not WM) of heavy drinkers vs controls |
| Durazzo et al., 2004 | 24 alcoholics, 26 controls | 1 week | 50 ± 6 | Low NAA and Cho in frontal lobe, low Cho in thalamus and parietal lobe. Low NAA throughout brain of smoking vs non-smoking alcoholics. Normal Cr and mI |
| Ende et al., 2005 | 33 alcoholics (12 female), 30 controls (10 female) |
3 weeks, 3 months and 6 months |
45 ± 9 | Low Cho in cerebellum and frontal lobe, trend to low NAA in frontal WM; Cho increases over 3 months (n = 14); no longitudinal NAA changes over 3 and 6 months (n = 11) |
| Ende et al., 2006 | 42 social drinkers | ~40 ± 10 | Greater alcohol consumption correlates with higher frontal Cho | |
| Mason et al., 2006 | 12 alcoholics, 8 controls | 1 week and 1 month | 39 ±8 | No GABA group differences in occipital gray matter at 1 week. Higher GABA in non-smoking vs smoking alcoholics. GABA decrease in non- smoking alcoholics over 1 month |
| Durazzo et al., 2006a | 25 alcoholics, 29 controls | 1 week and 4 weeks | 49 ± 7 | NAA and Cho increase in frontal and parietal lobes over 4 weeks. mI and Cr in frontal white matter increase over 4 weeks. Changes more pronounced in non-smoking alcoholics |
| Lee et al., 2007 | 13 alcoholics (smokers), 18 controls (non-smokers) |
16 days | 33 ± 3 | Low Cho and Cr, high Glu/Cr, normal NAA in the anterior cingulate cortex (high Glu/Cr due to low Cr?). High Glu measures correlate with better short-term memory and attention, but greater past alcohol consumption. No metabolic differences in insula |
| Bartsch et al., 2007 | 15 alcoholics, 10 controls | 5 days and 6 weeks | 44 ± 8 | Low frontomesial NAA and low cerebellar Cho. Both increase over 6–7 weeks |
| Durazzo et al., 2008 | 70 alcoholics | 1 month | 51 ± 9 | Low -3NAAintemporal gray matter and frontal white matter and low Cho in frontal gray matter predict relapse within 6–12 months of treatment |
| Gazdzinski et al., 2008a | 35 alcoholics, 32 heavy drinkers |
1 week (alcoholics) | 44 ± 8 | Low NAA, Cho, and mI throughout the brain of treatment-seeking alcoholics vs non-treated heavy drinkers |
| Gazdzinski et al., 2008b | 24 alcoholics, 14 controls | 1 week and 4 weeks | 49 ± 9 | Low NAA and Choin medial temporal lobe. NAA and Cho increase in non- smoking alcoholics over 4 weeks |
| Wang et al., 2009 | 48 alcoholics (26 smoking, 22 non-smoking), 26 controls |
1 month | 49 ± 8 | Only in smoking alcoholics, NAA lower in frontal WM region of low fractional anisotropy (FA) than in controls. No NAA differences in frontal WM with normal FA |
| Durazzo et al., 2010b | 51 alcoholics 26 controls | 1 week | 48 ± 9 | Low NAA and Cr in brain reward system of those who relapse within 6–12 months of treatment vs abstainers and controls |
| Gazdzinski et al., 2010 | 54 alcoholics | Approx. 1 month | 50 ± 8 | Higher BMI associated with lower NAA, Cho, Cr, and m-Ino in frontal lobe, subcortical nuclei, and vermis. Increased alcohol intake related to elevated m-Ino in multiple brain regions and to smaller volumes of frontal and temporal GM |
| Umhau et al., 2010 | 33 alcoholics (15 acamprosate, 18 placebo) |
Days 4 and 25 of study medication |
33 ± 1 | Longitudinal decrease of Glu/Cr in anterior cingulate cortex of those treated with acamprosate. No significant change in any metabolite concentrations in those treated with placebo. |
| Modi et al., 2011 | 9 alcoholics, 13 controls | 1 week | 44 ± 7 | High Cho/Cr in occipital lobe (high Cho? low Cr?) |
| Yeo et al., 2011 | 146 treatment-naïve heavy drinkers |
≤3 weeks | 32 ± 9 | A specific type of genetic mutation (copy number variation) correlated with NAA, Glx, and Cr in anterior cingulate cortex |
| Thoma et al., 2011 | 7 treatment-naïve heavy drinkers, 6 alcoholics, 17 controls |
>1 year (alcoholics) | 34 ± 7 | Significant substance use and psychiatric comorbidity. In anterior cingulate cortex low Glu and high Gln in both drinking groups. Related to drinking severity. No differences between drinking groups |
| Durazzo et al., 2013 | 76 alcoholics (43 smoking, 33 non-smoking), 42 controls (non- smoking) |
1 week | 51 ± 9 (alcoholics), 45 ± 9 (controls) |
Lower NAA in smoking vs non-smoking alcoholics and controls in the DLPFC, insula, superior corona radiata, and the total brain reward system. Differences between alcoholic groups not mediated by alcohol consumption, hypertension, psychiatric comorbidities |
| Abé et al., 2013 | 40 alcoholics, 28 polysubstance users, 16 controls |
1 month | 49 ± 9 | No significant metabolic differences between abstinent alcoholics and controls. In the DLPFC of alcohol-dependent polysubstance users, significantly lower concentrations of NAA, Cho, and mI than both alcoholics and controls. Cr was significantly lower in polysubstance users compared to alcoholics |
| Hermann et al., 2012 | 47 alcoholics, 57 controls | 1 day and 14 days | 46 ± 1 | High Glu at 1 day in prefrontal cortex of alcoholics vs controls. Normal Glu at 14 days. Confirmed in parallel rat studies |
| Mon et al., 2012 | 44 alcoholics, 16 controls | 9 days and 5 weeks | 51 ± 9 | Low NAA, Cho, Cr, and Glu in anterior cingulate cortex at 1 week recover to normal levels at 5 weeks. GABA and mI normal at both times. No abnormalities or changes in DLPFC and POC. Higher cortical mI at 1 week correlates with worse cognition and greater alcohol consumption |
| Xia et al., 2012 | 49 treatment-naïve heavy drinkers, 45 controls (all non-smoking) |
0 | 46 ±6 | Low NAA/Cr in prefrontal GM and WM and worse executive function. NAA levels and executive skills influenced by different SNPs of the metabotropic glutamate receptor 3 (GMR3) gene. Some of these genotypic differences also found in controls |
NAA, N-acetylaspartate; Cho, choline-containing metabolites; Cr, creatine; TE, echo time; GABA, γ-aminobutyric acid; mI, WM, white matter; BMI, body mass index; m-Ino, myo-inositol; GM, gray matter; Glx, glutamate; Gln, glutamine; DLPFC, dorsolateral prefrontal cortex; POC, parieto-occipital cortex; SNP, single nucleotide polymorphism.