DOI: 10.1159/000067734 Alcohol Consumption in Alzheimers Disease A Case Report Tomas Mller-Thomsen Christian Haasen Department of Psychiatry, University Hospital Hamburg-Eppendorf, Hamburg, Germany Dr. Tomas Mller-Thomsen Memory Clinic, Department of Psychiatry, University Hospital Hamburg-Eppendorf Martinistrasse 52 D20246 Hamburg (Germany) Tel. +49 40 42803 2228, Fax +49 40 42803 9779, E-Mail muellert@uke.uni-hamburg.de ABC Fax +41 61 306 12 34 E-Mail karger@karger. ch www.karger.com 2003 S. Karger AG, Basel 10226877/03/00910051$19.50/0 Accessible online at: www.karger.com/ear Key Words Alzheimers disease W Late-onset alcohol consumption Abstract As late-onset alcohol consumption is rare, it often indi- cates a different underlying disorder. We present a case where late-onset alcohol drinking occurred during the onset of Alzheimers disease. Copyright 2003 S. Karger AG, Basel Introduction Alzheimers disease (AD) is characterised by a slowly progressing process with a specific loss of neurones, for- mation of amyloid plaques and neurofibrillary tangles. Before getting demented, patients are affected by slight cognitive changes in a pre-clinical phase of 58 years. The awareness of this impairment might lead to feelings of help- or hopelessness. Depression is the best-known and most common clinical symptom in the early phase of AD [1]. Depression, on the other hand, can lead to self-treat- ment with alcohol [2], but alcohol leads both by acute intoxication and chronic use to decreased cognitive abili- ty, which makes a differential diagnosis of AD difficult. In studies published until now, the probable risk of drinking for the development of AD is a cause of controversy [3]. Little attention has been given to the role of alcohol con- sumption as an unsuccessful coping strategy in the early phase of AD. Our case report attempts to fill this gap. Case Report A 68-year-old retired bank attendant came to our memory clinic accompanied by his wife. He reported having problems with his memory and with performing his everyday activities. He could not remember when these problems started. His wife had realised these changes two years ago and had also observed a slow progression. He reported having consumed 23 bottles of wine daily during the last few years, but he was presently abstinent. At this point his wife con- tradicted him, saying that he would still be drinking if she would not pay attention, and that he was still drinking once or twice a week. He was not able to give a precise personal history. His wife reported that he retired at the age of 60 due to increasing problems in his job as a leading banker. After retirement they had a satisfying life with many activities and journeys. Two years later he began to isolate himself more and more, and she noticed more and more often a smell of alcohol. She pressured him to go for treatment, which lead to three detoxification treatments in six years. No withdrawal symptoms were reported during these treatments. He always began drinking again after some days. During the last treatment, half a year ago, memory problems and orientation difficulties were recognised for the first time. Retrospectively, she realised changes in her husbands character during the previous two years. The medical history showed 52 Eur Addict Res 2003;9:5152 Mller-Thomsen/Haasen no disorders, apart from a daily consumption of 40 cigarettes since the age of 15. The family history for dementia was negative. The mental status showed a withdrawn and slightly depressed patient, who nonetheless reacted adequately. Orientation in time was imprecise, but in the other parameters he showed complete orienta- tion. He was able to answer some questions consistently and correct- ly, yet other questions were only answered vaguely. There was no sign of acute intoxication or psychotic symptoms. In order to get an orien- tation about his cognitive level of functioning, we performed a Mini- Mental-Status Examination in which he reached 24 of the 30 possible points. Verbal (Wordlist from the Nrnberger Altersinventar) and non-verbal (Rey-Osterrieth-figure) memory was strongly impaired, and he also had difficulties in constructive tasks. The overall cogni- tive speed of functioning (Trial-Making-Test A) was within the nor- mal range, but executive functioning (Trial-Making-Test B) was clearly below the age norm. Physical examination was without pathological findings, especial- ly no perception disorder. MCV was 100.8 fl (normal 8094) and -GT 29 U/l (normal !28). Other blood and CSF parameters, includ- ing B vitamins, CA marker and TSH were within the normal range. ECG, EEG, CCT and FPG-PET showed no pathological findings. We treated the patient with an acetylcholinesterase inhibitor. After 3 months his mental status improved, both objectively and sub- jectively. He was more active and open to contacts, regained interest in his activities, and was able to stop drinking. Besides a slight pro- gress in constructive difficulties, he remained stable in neuropsycho- logical tests over one year. Discussion The patient is suffering from a mild dementia accord- ing to DSM-IV-criteria: he has a memory loss and difficul- ties in executive and practical functions, he is impaired in his everyday activities, and symptoms have been present for more than six months. Diagnosing the aetiology of the dementia is much more difficult: the history of drinking might lead us to think about an alcohol-induced amnestic syndrome (Korsakoff). However, if this was the case, the loss of memory would be more accented compared with the cortical deficits. In addition, speed of functioning is not decreased, as it would be in alcohol-induced disor- ders. Symptoms began slowly and then worsened progres- sively, hence a vascular dementia seemed unlikely. This was confirmed by a CCT scan. As other causes could be excluded, the diagnosis of a probable AD was given. Over time, apraxia worsened even when memory deficits re- mained stable under treatment with an acetylcholine- esterase inhibitor. This confirmed the initial diagnosis. Late-onset alcohol consumption is rare [4] and often indicates other psychiatric problems. In this case, it was probably the start of cognitive deterioration and the dif- fuse realisation of this problem that led to excessive drink- ing and worsened the problem. In conclusion, late-onset drinking was a reaction to the awareness of cognitive dete- rioration in the beginning of AD. References 1 Jorm AF: Is depression a risk factor for demen- tia or cognitive decline? A review. Gerontology 2000;46:219227. 2 Abraham HD, Fava M: Order of onset of sub- stance abuse and depression in a sample of depressed outpatients. Compr Psychiatry 1999;40:4450. 3 Tyas SL, Koval JJ, Pederson LL: Does an inter- action between smoking and drinking influence the risk of Alzheimers disease? Results from three Canadian data sets. Stat Med 2000;19: 16851696. 4 Schutte KK, Brennan PL, Moos RH: Predict- ing the development of late-life late-onset drinking problems: A 7-year prospective study. Alcohol Clin Exp Res 1998;22:13491358. Copyright: S. Karger AG, Basel 2003. Reproduced with the permission of S. Karger AG, Basel. Further reproduction or distribution (electronic or otherwise) is prohibited without permission from the copyright holder.