Case Report
Eur Addict Res 2003;9:5152DOI: 10.1159/000067734
Alcohol Consumption inAlzheimers DiseaseA Case Report
Tomas Mller-Thomsen Christian Haasen
Department of Psychiatry, University Hospital Hamburg-Eppendorf,
Hamburg, Germany
Dr. Tomas Mller-ThomsenMemory Clinic, Department of Psychiatry,
University Hospital Hamburg-EppendorfMartinistrasse 52D20246
Hamburg (Germany)Tel. +49 40 42803 2228, Fax +49 40 42803 9779,
E-Mail [email protected]
ABCFax + 41 61 306 12 34E-Mail
[email protected]
2003 S. Karger AG, Basel10226877/03/00910051$19.50/0
Accessible online at:www.karger.com/ear
Key WordsAlzheimers disease W Late-onset alcohol consumption
AbstractAs late-onset alcohol consumption is rare, it often
indi-cates a different underlying disorder. We present a casewhere
late-onset alcohol drinking occurred during theonset of Alzheimers
disease.
Copyright 2003 S. Karger AG, Basel
Introduction
Alzheimers disease (AD) is characterised by a slowlyprogressing
process with a specific loss of neurones, for-mation of amyloid
plaques and neurofibrillary tangles.Before getting demented,
patients are affected by slightcognitive changes in a pre-clinical
phase of 58 years. Theawareness of this impairment might lead to
feelings ofhelp- or hopelessness. Depression is the best-known
andmost 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 acuteintoxication 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 drinkingfor
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 earlyphase of AD. Our case
report attempts to fill this gap.
Case Report
A 68-year-old retired bank attendant came to our memory
clinicaccompanied by his wife. He reported having problems with
hismemory and with performing his everyday activities. He could
notremember when these problems started. His wife had realised
thesechanges two years ago and had also observed a slow
progression. Hereported having consumed 23 bottles of wine daily
during the lastfew years, but he was presently abstinent. At this
point his wife con-tradicted him, saying that he would still be
drinking if she would notpay attention, and that he was still
drinking once or twice a week.
He was not able to give a precise personal history. His
wifereported that he retired at the age of 60 due to increasing
problems inhis job as a leading banker. After retirement they had a
satisfying lifewith many activities and journeys. Two years later
he began to isolatehimself more and more, and she noticed more and
more often a smellof alcohol. She pressured him to go for
treatment, which lead to threedetoxification treatments in six
years. No withdrawal symptomswere reported during these treatments.
He always began drinkingagain after some days. During the last
treatment, half a year ago,memory problems and orientation
difficulties were recognised forthe first time. Retrospectively,
she realised changes in her husbandscharacter 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
sincethe age of 15. The family history for dementia was
negative.
The mental status showed a withdrawn and slightly
depressedpatient, who nonetheless reacted adequately. Orientation
in time wasimprecise, 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 signof 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 possiblepoints. Verbal (Wordlist from
the Nrnberger Altersinventar) andnon-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) wasclearly 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 interestin 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 inhis everyday
activities, and symptoms have been presentfor more than six months.
Diagnosing the aetiology of thedementia is much more difficult: the
history of drinkingmight lead us to think about an alcohol-induced
amnestic
syndrome (Korsakoff). However, if this was the case, theloss of
memory would be more accented compared withthe cortical deficits.
In addition, speed of functioning isnot decreased, as it would be
in alcohol-induced disor-ders. Symptoms began slowly and then
worsened progres-sively, hence a vascular dementia seemed unlikely.
Thiswas confirmed by a CCT scan. As other causes could beexcluded,
the diagnosis of a probable AD was given. Overtime, 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 oftenindicates
other psychiatric problems. In this case, it wasprobably 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-onsetdrinking 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. Gerontology2000;46:219227.
2 Abraham HD, Fava M: Order of onset of sub-stance abuse and
depression in a sample ofdepressed outpatients. Compr
Psychiatry1999;40:4450.
3 Tyas SL, Koval JJ, Pederson LL: Does an inter-action between
smoking and drinking influencethe risk of Alzheimers disease?
Results fromthree Canadian data sets. Stat Med
2000;19:16851696.
4 Schutte KK, Brennan PL, Moos RH: Predict-ing the development
of late-life late-onsetdrinking problems: A 7-year prospective
study.Alcohol Clin Exp Res 1998;22:13491358.
