Alcohol and the brain

Current Opinion in Psychiatry

Volumn 10, Issue 3, 1997, Pages 205-210

  Chick, Jonathan ^a  

^a UNIVERSITY OF EDINBURGH   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

ALCOHOL; ENDORPHIN; NEUROTRANSMITTER; THIAMINE;

ALCOHOLISM; ANIMAL EXPERIMENT; BRAIN; CLINICAL ARTICLE; COGNITIVE DEFECT; CONTROLLED STUDY; DEMENTIA; HUMAN; KORSAKOFF PSYCHOSIS; NEUROPHARMACOLOGY; NONHUMAN; NORMAL HUMAN; RAT; SEROTONINERGIC SYSTEM; SHORT SURVEY; THIAMINE DEFICIENCY;

EID: 0030917286     PISSN: 09517367     EISSN: None     Source Type: Journal    
DOI: 10.1097/00001504-199705000-00005     Document Type: Short Survey

References (59)

1. O'Brien CP, McLellan AT: Myths about the treatment of addiction, Lancet 1996, 347:237-240.
2. Meyer RE: The disease called addiction: emerging evidence in a 2000-year debate, Lancet 1996, 347:162-166.
3. Joyce EM: Aetiology of alcoholic brain damage: alcohol neurotoxicity or thiamine malnutrition. Br Med Bull 1994,50:99-114.
4. Emsley R, Smith R, Roberts M, Kapnias S, Pieters H, Mantz S: Magnetic resonance imaging in alcoholic Korsakoffs syndrome: evidence for an association with alcoholic dementia. Alcohol Alcoholism 1996, 31:479-486.
5. Shear PK, Sullivan EV, Lane B, Pfefferbaum A: Mammillary body and cerebellar shrinkage in chronic alcoholics with and without amnesia. Alcohol Clin Exp Res 1996, 20:1489-1495. Chronic alcoholic patients showed mamillary body and cerebellar shrinkage on magnetic resonance imaging compared with control individuals but alcoholic patients with amnesia did not differ from those without.
6. Langlais PJ: Alcohol-related thiamine deficiency: impact on cognitive and memory functioning. Alcohol Health Res World 1995, 19:113-121. A very accessible review in a helpful monograph on cognition and alcohol.
7. Hommer D, Momenan R, Rawlings R, Ragan P, Williams W, Rio D. Eckhardt M: Decreased corpus callosum size among alcoholic women. Arch Neurol 1996, 53:359-363.
8. Pfefferbaum A, Lim KO, Desmond JE, Sullivan EV: Thinning of the corpus callosum in older alcoholic men: a magnetic resonance imaging study. Alcohol Clin Exp Res 1996, 20:752-757.
9. Pfefferbaum A, Sullivan EV, Mathalon DH, Shear PK, Rosenbloom MJ, Lim KO: Longitudinal changes in magnetic resonance imaging brain volumes in abstinent and relapsed alcoholics. Alcohol Clin Exp Res 1995. 19:1177-1191.
10. Rooprai HK, Pratt OE, Shaw GK, Thomson AD: Thiamine pyrophosphate effect and normalised transketolase activity ratio in Wernicke-Korsakoff patients and acute alcoholics undergoing detoxification. Alcohol Alcoholism 1996, 31:493-502.
11. Zimatkin SM, Simatkina TI: Thiamine deficiency as predisposition to, and consequence of, increased alcohol consumption. Alcohol Alcoholism 1996, 31:421-427.
12. Holzbach E: Thiamine absorption in alcoholic delirium patients. J Stud Alcohol 1996, 57:581-584.
13. Agabio R, Cortis F, Fadda GL, Gessa C, Lobina C, Reali R, Colombo G: Circadian drinking pattern of Sardinian alcohol-preferring rats. Alcohol Alcoholism 1996, 31:385-388.
14. Nutt D: Addiction: brain mechanisms and their treatment implications. Lancet 1996, 347:31-36. A very helpful summary for the nonspecialist seeking signposts in the neurotransmitter maze.
15. Lewis MJ: Alcohol reinforcement and neuropharmacological therapeutics. Alcohol Alcoholism 1996, 31 (suppl 1 ):17-26.
16. Hoffman PL, Tabakoff B: Alcohol dependence: a commentary on mechanism. Alcohol Alcoholism 1996, 31:333-340. The decreased mesolimbic dopaminergic function that occurs in alcohol withdrawal, may be involved in the initiation of further drinking and this increased dopaminergic function could be secondary to the alcohol-induced increase in N-methyl-D-aspartate receptor function.
17. Kalant H: Current state of knowledge about the mechanisms of alcohol tolerance. Addict Biol 1996, 1:133-141.
18. Chick J, Erickson CK, Amsterdam Consensus Conference Participants: Consensus conference on alcohol dependence and the role of pharmacotherapy in its treatment. Alcohol Clin Exp Res 1996, 20:391-402.
19. Erickson CK: Review of neurotransmitters and their role in alcoholism treatment. Alcohol Alcoholism 1996, 31(suppl 1):5-12.
20. Anton RF: Neurobehavioural basis for the pharmacotherapy of alcoholism: current and future directions. Alcohol Alcoholism 1996, 31 (suppl 1):43-54.
21. De Witte P: The role of neurotransmitters in alcohol dependence: animal research. Alcohol Alcoholism 1996, 31 (suppl 1):13-16.
22. Lancaster FE: Alcohol and the brain: what's NO got to do with it? Metab Brain Dis 1995, 10:125-133.
23. Rommelspacher H, Dufeu P, Schmidt LG: Harman and norharman in alcoholism: correlations with psychopathology and long-term changes. Alcohol Clin Exp Res 1996, 20:3-8. Levels of the beta-carboline compound, harman, were elevated in the plasma of alcoholic patients proportionate to positive family history and severity of alcoholism. The abnormality was present during intoxication and after 3 and 6 months of abstinence.
24. Ripley TL, Whittington MA, Butterworth AR, Little HJ: Ethanol withdrawal hyperexcitability in vivo and in isolated mouse hippocampal slices. Alcohol Alcoholism 1996, 31:347-358.
25. Randoll LA, Wilson WR, Weaver MS, Spuhler-Phillips K, Leslie SW: N-methyl-D-aspartate-stimulated increases in intracellular calcium exhibit brain regional differences in sensitivity to inhibition by ethanol. Alcohol Clin Exp Res 1996, 20:197-200.
26. Soyka M (Editor): Acamprosate in relapse prevention of alcoholism. Proceedings of the 1st Campral Symposium, ESBRA (Stuttgart, September, 1995). Berlin: Springer; 1996. A set of review papers on laboratory and clinical research with a drug shown in large randomized controlled studies to reduce relapse. Its action may be partly through correcting the effects of alcohol-induced up-regulation of N-methyl-D-aspartate receptors in the gamma aminobutync acid and glutamate system.
27. Sass H, Soyka M, Mann K, Ziegelgansberger W: Relapse prevention by acamprosate: results from a placebo controlled study on alcohol dependence. Arch Gen Psychiatry 1996, 53:670-672. In a 1-year study, 43% of patients taking acamprosate, compared with 21% taking placebo, maintained complete abstinence. The mean total number of abstinent days was 163 in placebo treatment and 224 with acamprosate.
28. Whitworth AB, Fischer F, Lesch OM, Nimmerrichter A, Oberauer H, Platz T, Potgieter A, Walter H, Fleischhacker WW: Comparison of acamprosate and placebo in long-term treatment of alcohol dependence. Lancet 1996, 347:1438-1442. Over a 1-year study (n=448) acamprosate was well tolerated and was associated with 40% more days of abstinence and slightly more than double the rate of complete abstinence. The advantage with acamprosate was maintained into the second year of the study after medication had ceased.
29. Sullivan EV, Marsh L, Mathalon DH, Lim KO, Pfefferbaum A: Relationship between alcohol withdrawal seizures and temporal lobe white matter volume deficits. Alcohol Clin Exp Res 1996, 20:348-354.
30. Worner TM: Relative kindling effect of readmission in alcoholics. Alcohol Alcoholism 1996, 31:375-380.
31. Schuckit M, Tipp JE, Reich T, Hesselbrock VM, Bucholz K: The histories of withdrawal convulsions and delirium tremens in 1648 alcohol dependent subjects. Alcohol Alcoholism 1995, 90:1335-1347.
32. Reid LD, Gardell LR, Chattopadhyay S, Hubbell CL: Periodic naltrexone and propensity to take alcoholic beverage. Alcohol Clin Exp Res 1996, 20:1329-1334. In laboratory rats, the inhibition of ethanol drinking because of naltrexone did not reduce when naltrexone was continued. There was no carry-over of its effect during repeated periods when it was replaced by placebo: drinking immediately resumed at the level of the control rats.
33. 2Apostsynaptic to serotonergic neurons.
34. O'Malley SS, Croup RS, Wroblewski MS, Labnola DF, Volpicelli JR: Naltrexone in the treatment of alcohol dependence: a combined analysis of two trials. Psychiatr Ann 1995,25:681-688.
35. O'Malley SS, Jaffe AJ, Rode S, Rounsaville BJ: Experience of a 'slip' among alcoholics treated with naltrexone. Am J Psychiatry 1996,153: 281-283. Compared with individuals who received placebo, patients who received nattrexone reported lower levels of craving for alcohol and were more likely to give reasons for terminating drinking that were consistent with decreased incentive to drink.
36. O'Malley SS: Six month follow-up of naltrexone and psychotherapy for alcohol dependence. Arch Gen Psychiatry 1996,53:217-224. It is important that the benefits experienced by naltrexone-treated patients in this randomized controlled trial over 3 months did not immediately disappear on cessation of the drug and there was no discontinuation syndrome.
37. O'Brien CP, Volpicelli LA, Volpicelli JR: Naltrexone in the treatment of alcoholism: a clinical review. Alcohol 1996, 13:35-39. The authors review preclinical work and the already published randomized controlled studies showing the efficacy of naltrexone in relapse prevention. They emphasize the importance of continuing with psychosocial treatment. Further analysis showed that its effect was greatest in patients who had attended all 12 research visits in the 3-month study and was not statistically significant in patients who had been less compliant. (A check to see if the two treatment groups had remained matched on possible predictors of outcome after the stratification by compliance was carried out but not reported in this paper.)
38. Gianoulakis C, Krishnan B, Thavundayil J: Enhanced sensitivity to pituitary β-endorphin to ethanol in subjects at high risk of alcoholism. Arch Gen Psychiatry 1996, 53:250-257.
39. del Arbol JL, Aguirre JC, Raya J, Rico J, Ruiz-Requena MA, Miranda MT: Plasma concentration of β-endorphin, adrenocorticotrophic hormone, and cortisol in drinking and abstinent chronic alcoholics. Alcohol 1995, 12:525-529.
40. Aguirre JC, del Arbol JL, Rico J, Raya J, Miranda MT: Classification of alcoholics on the basis on plasma β-endorphin concentration. Alcohol 12:531-534. Normal plasma beta-endorphin concentration was correctly found to identify most nonalcoholic patients (93.5%) in a general population and the level was low in 73% of alcoholic patients in that sample.
41. Aguirre JC, del Arbol JL, Rico J, Raya J, Ruiz-Requena MS: Effect of acute alcohol intoxication on the opioid system in humans. Alcohol 1995, 12:559-562.
42. Le AD, Tomkins DM, Sellers EM: Use of serotonin (5-HT) and opiate-based drugs in the pharmacotherapy of alcohol dependence: an overview of the preclinical data. Alcohol Alcoholism 1996, 31(suppl 1):27-32.
43. Kranzler HR, Burleson JA, Korner R del Boca FK, Bohn MJ, Brown J, Liebowitz N: Placebo-controlled trial of fluoxetine as an adjunct to relapse prevention in alcoholics. Am J Psychiatry 1995, 152:391-439. Fluoxetine (up to 60 mg/day) had no effect on drinking but reduced Hamilton Depression Rating Scale scores more than placebo.
44. Lejoyeux M: Use of serotonin (5-hydroxytryptamine) reuptake inhibitors in the treatment of alcoholism. Alcohol Alcoholism 1996, 31 (suppl 1):69-76.
45. Tihonen J, Ryynänen O-P, Kauhanen J, Hakola HPA, Salaspuro M: Citalopram in the treatment of alcoholism: a double-blind placebo controlled study. Pharmacopsychiatry 1996, 29:27-29. A minimum abstinence of 1 week was instigated before starting the drug. Sixtyeight per cent of the sample were 'Type II alcoholic patients' but an unspecified number of patients who did not take at least 1 week of the drug were excluded from analysis (which theoretically may have reduced the matching of the two groups). Self-reported abstinence through 3 months was 10% of individuals who took placebo and 19% of individuals who took citalopram (insignificant). The relativereported improvement was 7% (placebo) and 26% (citalopram) (P=0.05).
46. Janiri L, Gobbi G, Manelli P, Pozzi G, Serretti A, Tempesta E: Effects of fluoxetine at antidepressant doses on short-term outcome of detoxified alcoholics. Int Clin Psychopharmacol 1996, 11:109-117. Complete abstinence (self-reported) over 2 months was attained by 62% of patients taking fluoxetine (20 mg/day) and by 5% on patients taking placebo. Chlordiazepoxide up to 25 mg/day was allowed. One-fifth of the patients were depressed at intake according to the Hamilton Depression Rating Scale. (Blood test data were not reported.)
47. McGrath PJ, Nunes EV, Stewart JW, Goldman D, Agosti V, Ocepek-Welikson K, Quitkin FM: Imipramine treatment of alcoholics with primary depression: a placebo controlled clinical trial. Arch Gen Psychiatry 1996, 53:232-240.
48. Mason BJ, Kocsis JH, Ritvo EC, Cutler RB: A double-blind, placebo-controlled trial of desipramine for primary alcohol dependence stratified for the presence or absence of major depression. JAMA 1996, 275:761-767.
49. Powell BJ, Campbell JL, Landon JF, Liskow BI, Thomas HM, Nickel EJ, Dale TM, Penick EC, Samuelson SD, Lacoursiere RB: A double-blind placebo-controlled study of nortryptiline and bromocriptine in male alcoholics subtyped by comorbid psychiatric disorders. Alcohol Exp Clin Res 1995, 19:462-468.
50. Krystal JH, Webb E, Cooney NL, Kranzler H, Southwick SW, Heninger GR, Charney DS: Serotonergic and noradrenergic dysregulation in alcoholism: m-chlorophenylpiperazine and yohimbine effects in recently detoxified alcoholics and healthy comparison subjects. Am J Psychiafry 1996, 153:83-92.
51. Hedlund L, Wahlstrom G: Buspirone as an inhibitor of voluntary ethanol intake in male rats. Alcohol Alcoholism 1996, 31:148-156.
52. Malec E, Malec T, Gagné MA, Dongier M: Buspirone in the treatment of alcohol dependence: a placebo controlled trial. Alcohol Clin Exp Res 1996, 20:307-312.
53. Hore B: Substance misuse: biological factors. Curr Opin Psychiatry 1996, 9:212-216.
54. Typology: the classification of alcoholism. Alcohol Health Res World 1996, 20. Seven excellent review papers covering the historical background, measurement, validity and implications of various typologies of alcoholism
55. Hallman J, von Knorring L, Oreland L: Personality disorders according to DSM-III-R and thromobocytic monoamine oxidase activity in type 1 and type 2 alcoholics. J Stud Alcohol 1996, 57:151-161.
56. Fils-Aime M-L, Eckhardt MJ, George DT, Brown GL, Mefford I, Linnoila M: Early-onset alcoholics have lower cerebrospinal fluid S hydroxyindoleacetic acid levels than late-onset alcoholics. Arch Gen Psychiatry 1996, 53:211-216. One-hundred and thirty-one alcoholic patients abstinent for a minimum of 3 weeks received a low monoamine diet for at least 3 days before a lumbar puncture was performed. None fufilled criteria for antisocial personality. Individuals whose excessive consumption had commenced before the age of 25 years had a more severe course of alcoholism and a lower mean cerebrospinal fluid level of 5-hydroxyindoleacetic acid (as well as low cerebrospinal fluid levels of homovanillic acid and tryptophan concentrations).
57. Virkkunnen M, Goldman D, Nielsen DA, Linnoila M: Low brain serotonin turnover rate (low CSF 5-HIAA) and impulsive violence. J Psychiatr Neurosci 1995, 20:271-275.
58. Risinger FO, Bormann NM, Oakes: Reduced sensitivity to ethanol reward, but not ethanol aversion, in mice lacking 5-HT1B receptors. Alcohol Clin Exp Res 1996, 20:1401-1405.
59. 1B serotonin receptors. Nature Genet 1996, 14:98-101.