Dementia symptoms

Excess alcohol and long-term exposure to everyday organic solvents can express as symptoms of a
dementing illness. Both are difficult to characterize and diagnose. Both are capable of presenting in
the long-term care setting where the symptoms can be mis-diagnosed and the behaviours misinter-
preted. Acute use of alcohol impairs attention, memory, executive functions and visuo-spatial skills,
while chronic abuse causes neurocognitive deficits in memory, learning, visuospatial functions,
psychomotor speed processing, executive functions and decision-making, and may
lead to persistent amnesic disorder and alcoholic dementia.

Deliberate inhalation of solvents for recreational use is associated, in some users, with a
behavioural syndrome showing profound impairment in motor control and associated impairment
of some intellectual and memory capacity. Continuing use can result in physical impairment in
different organs, peripheral nerve damage, and neurobehaviourai effects.
By Shailesh Nadkarni and Luis Fornazzari

Neuro-pathological effects
of alcohol and solvents
Histories of alcohol or excessive exposure to solvents are capable of presenting
in the long-term care setting where the symptoms can he mis-diagnosed

T lhere are certain conditions and ill-
nesses that can express symptoms of
dementia. Alcoholism is responsible for
cognitive deficits of various severity, which
could be reversible, or not, with alcohol
abstinence, but can also contribute to the cog-
nitive impairment related to other patholo-
gies, such as Alzheimer's disease (Pierucci-
Lagha 2003).
Recently, two such medical conditions
were profiled and bring to the fore the
necessity of recognizing those conditions
or illnesses that have the ability to cause
memory deficits and cognitive impair-
ment - symptoms usually associated with
the more traditional neurological disor-
ders, such as Alzheimer's disease, frontal-
lobe dementia, dementia with Lewy bodies,
and vascular dementia, among others. The
first condition has been dubbed chronic
paint syndrome, and the second, alcohol-
related dementia.
Characterizing
alcoholic dementia
The diagnostic criteria for alcoholic
dementia are neither well defined nor
consistent (Saunders, et al., 1991; Lishman,
1990). The objective of a recently concluded
study was to describe the clinical profile of
alcoholic dementia, and involved a review
of clinical cases and a literature search.
The study sample consisted of patients
consecutively admitted to the Geriatric
Mental Health Program at the Centre for
Addiction and Mental Health (CAMH) in
Toronto, Ontario.
The records of eleven patients with a
diagnosis of alcoholic dementia that were
admitted to the inpatient program were re-
viewed. The diagnosis and type of demen-
tia were determined within two months of
admission by a behavioural neurologist
using patient interviews, chart reviews, and
information from structured interviews.
Results
The sample was 82% male, with an
average age of 67 years ranging from 62
to 75 years. The highest level of education
completed was grade seven. 9t% of the
patients were separated or divorced, and
all were previously employed as unskilled
labourers. 75% were smokers and 27%
had a history of substance abuse. 82%

Volume 17, Number 3, October, 2006 19

had experienced seizures in the past, and
more than half had a history of head in-
jury. The most common co-morbid disor-
ders were personality disorders and psy-
chosis.
Average length of stay was a little over
four years, ranging from 29 days to over 12
years; average number of admissions was
three, ranging from one to nine per pa-
tient. The average score on the Mini
Mental State Examination was 15, with
scores ranging from 1 to 27.
A significant portion of the patients dis-
played poor insight and judgement, im-
paired memory (immediate and delayed),
poor visual-spatial construction, impaired
verbal reasoning, and poor impulse con-
trol, all of which were consistent with
studies (Parson and Leber, 1981; Eckardt and
Martin, 1986; Tabakoff and Petersen, 1988).
Deficits were evident for all patients
in tasks requiring cognitive flexibility.
Computer tomography scans revealed that
more than half the patients in the study
had diffused cerebral and atrophy.
Other findings included: frontal white
matter disease and temporal lobe encepha-
lomalacia, peri-ventricular ischemic
changes, enlargement of the ventricular
system and subarachnoid spaces, and per-
fusion to the temporo-parietal region (Ron,
1979; Wilkinson, 1987). Malnutrition was
common in the study patients. All had in-
takes below the recommended standards in
one or more micro- or macronutrients.
Recap
Studies have demonstrated that alcohol
subjects perform more poorly on cognitive
testing than non-alcoholic subjects. This
poor performance in cognition persists
even after prolonged periods of sobriety
(Bowden, 1990; Hendrie et ai., 1996).
A diagnosis of alcoholic dementia is
based on evidence of general decline in
cognitive functions, including, but not re-
stricted to, memory, following prolonged
heavy ingestion of alcohol and no other
identified cause for dementia (Carien et ai.,
1994; DSM-III-R, 1987).
Typical impairments seen in alcohol re-
lated dementia include deficits in ab-
20
stracting abilities and short-term memory
and disturbed verbal fluency. These cog-
nitive patterns are in contrast to those
seen in AD, where the memory impair-
ment is profound and involves both rec-
ognition and recall, and individuals fre-
quently present with word-finding defi-
cits (Oslin 2003).
Alcohol dementia continues to distin-
guish itself as one of the more difficult
types to characterize (Munro, 2001). Fur-
ther studies with larger sample sizes are
required to further validate the diagnos-
tic criteria of the elusive concept of al-
cohol-related dementia (Nadkarni 2004).
Chronic paint syndrome
A review of the literature has shown that
chronic paint syndrome has not been re-
ported in Canada, although cases with this
unique syndrome have been reported in the
U.S. and Nordic countries.
The following profile is a case of
chronic paint syndrome that was identified
in a Canadian citizen who lived and
worked in the U.S. for most of his work-
ing life.
Clinicians and physicians have to con-
sider chronic paint syndrome in differen-
tial diagnosis of patients who report a
history of working with paint and other
solvents and who show excess of specific
symptoms that could otherwise be as-
signed to mood and behaviour, along with
memory impairment.
Prompt recognition and treatment are
important for many painters and solvent
users who may be mistakenly regarded
and treated as neurotic or depressive.
Case report
A 55-year-old white, Canadian male, was
transferred from Florida in response to
closure of the mental health facility he
was residing at.
The client posture is normal, but he has
an unsteady gait. He is co-operative, calm,
and friendly, but did establish eye contact
well. He exhibits no psychomotor agita-
tion or retardation, nor gesturing or man-
neristic behaviours. His mood is euthymic.
Although readily engaging, he does not
initiate conversation.
Neurotoxicity
It is argued that long-term exposure to
turpentine substitutes and paints, often
through a period with acute intoxication
symptoms, gradually may lead to the dev-
elopment of a chronic brain syndrome,
called chronic paint syndrome (Ariien-
Soborg et ai., 1979).
Epidemiological studies and case reports
have indicated that professional painters
under long-term exposure to organic sol-
vents may develop a chronic organic
brain syndrome dominated by memory im-
pairment, fatigue, personality changes,
headache, and dizziness.
The major constituent of paints or thin-
ners is toluene, which is a neurotoxic sol-
vent derived from the hydrocarbons in coal
tar. Painters, such as the one profiled in
this report, in their daily work, use large
amounts of turpentine substitutes, with
its use rapidly increasing in recent years.
This is primarily due to increasing use of
oil-based paint and an application technique,
which enables the painter to cover larger
surfaces faster. Thus, evaporation is in-
creased, as well as absorption.
Magnetic imaging (MRI) of the brains
in those chronically misusing paint thin-
ner or toluene may show cerebral and
cerebellar atrophy, atrophy of the corpus
callosum, and loss of grey-white matter.
Other imaging techniques show scat-
tered lesions in the white matter and brain
stem due to demyelination or gliosis, and
low intensity lesions in the basal ganglia,
thalami, and sub-cortical white matter
(Komiyama, 1999).
Neuro-behaviour effects
The neuro-psychological symptoms are
associated with heavy exposure to work-
ing with paints, a phenomena that is
likely to be found worldwide wherever
there is such exposure to solvent-based
paints (Chen et al., 1999).
There also appears to be a dose-re-
sponse relationship of solvent mixtures to
Canadian Nursing Home
neuro-behavioural effects in painters and
those involved in paint manufacturing
(Seeber, 1996; Triebig, 2000; Ruijten, 1994).
Conclusion
There is considerable evidence that
long-term excessive occupational expo-
sure to mixed organic solvents can cause
a wide range of chronic central nervous
system abnormalities (Mikkeison 1988).
The more severe cases of encephalopa-
thy associated with chronic exposure to
solvents are characterised by mild to
moderate degrees of cognitive impairment,
and are distinguished from those of other
neurodegenerative diseases, such as Alzhe-
imer's or Parkinson's disease, by the static
nature of cognitive impairment and pos-
sible selective improvements in neuropsy-
chological functioning if exposure to sol-
vents is discontinued. • ish Journal of Psychiatry; 156; p.635; 1990.
References
• Arlien-Soborg, P., Bruhn, P., Gyldensted,
C, Melgaard, B., Chronic painters syn-
drome: chronic toxic encephalopathy in
house painters, Acta Neurology Scandina-
via; 60{3);p.\49-l56; 1979.
• Bowden, S.C., Separating cognitive im-
pairment in neurologically asymptomatic
alcoholism from Wemicke-Korsakoff Syn-
drome: is the neuropsychological distinc-
tion justified. Psychological Bulletin; 107;
p.355-366; 1990.
• Carlen, P., et al.. Alcohol-related demen-
tia in the institutionalized elderly. Alco-
holism: Clinical and Experimental Re-
search; 18(6); p.1330-34; Nov./Dec, 1994.
• Chen, R., Wei, L. and Seaton, A., Neu-
ropsychological symptoms in Chinese male
and female painters; an epidemiological
study in dockyard workers. Occupational
Environmental Medicine; 56(6); 1999.
• Cunha P., Novaes M., Neurocognitive
assessment in alcohol abuse and depend-
ence: implications for treatment. Rev Bras
Psiquiatr, 26 (Suppl. 1); S23-7; 2005.
• DSM-III-R: Diagnostic and Statistical
Manual of Mental Disorders (3rd. Ed., re-
vised); American Psychiatric Association,
Washington, D.C.; t987.
Volume 17, Number 3, October, 2006
• Eckardt, M.J. and Martin, P.R., Clinical
assessment of cognition in alcoholism.
Alcoholism: Clinical and Experimental Re-
search; 10(2); p. 123-127; Nov./Dec, 1986.
• Fornazzari L, Wilkinson D.A., Kapur,
B.M., Carlen P.L., Cerebellar, cortical and
functional impairment in toluene abusers.
Acta Neurol Scand; 67 p.319-329; 1983.
• Hendrie, H.C., Gao, S., Hall, K., Hui, S.L.
and Unverzagt, F.W., The relationship be-
tween alcohol consumption, cognitive per-
formance, and daily functioning in an ur-
ban sample of older black Americans, Jour-
nal of the American Geriatrics Society;
44(10); p.l 158-65; 1996.
• Komiyama, M., Chronic misuse of paint
thinners. Journal of Neurology, Neurosur-
gery and Psychiatry; 67; p.267; 1999.
• Lishman, W., Alcohol and the brain, Brit-
• Mikkelson S., Jorgensen M., Browne E.,
et al.. Comparison with the findings of
similar studies (ch. 9); cited in: Mixed sol-
vent exposure and organic brain damage;
a study of painters. Acta Neurol Scand; 118
(suppl 118);79-93; 1988.
• Munro, C.A., Saxton, J. and Butters, M.A.,
Alcohol dementia: cortical or subcortical
dementia? Archives of Clinical Neuropsy-
chology; 16; p.523-533; 2001.
• Nadkarni, S., Eomazzari, L., Ibram, G.,
Understanding the evasive clinical profile
of alcoholic dementia, Neurobiology of
Aging; 25(2); S96; 2004.
• Oslin, D.W., Cary, M.S., Alcohol-related
dementia: validation of diagnostic criteria,
American Journal of Geriatric Psychiatry;
11(4); P.441-447; July-August, 2003.
• Parsons, O.A. and Leber, W.R., The rela-
tionship between cognitive dysfunction
and brain damage in alcoholics: casual,
interactive or epiphenomenal? Alcoholism:
Clinical and Experimental Research; 5;
p.326-343; 1981.
• Ron, M.A., Organic psychosyndromes
in chronic alcoholics, British Journal ofAd-
diction;! A; p.^57,-35^; 1979.
• Piemcci-Lagha, A, Derouesne, C , Alco-
holism and aging: Alcoholic dementia or
alcoholic cognitive impairment, Psychol
Neuropsychiatr Vieil.: 1(4); p.237-249;
Dec, 2003.
• Ruijten, M.W., et al., Neurobehaviourai
effects of long-term exposure to xylene and
mixed organic solvents in shipyard spray
painters, Neurotoxicology; 15(3); p.613-620;
Fall, 1994.
• Saunders, PA., Copeland, J.R., Dewey,
M.E., Davidson, LA., McWilliam, C ,
Sharma, V. and Sullivan, C , Heavy drink-
ing as a risk factor for depression and de-
mentia in elderly men: findings from the
Liverpool longitudinal study, British Jour-
nal of Psychiatry; 159;p.213-216; 1991.
• Seeber, A., Sietmann, B. and Zupanic,
M., In search of dose-response relation-
ships of solvent mixtures to neuro-behav-
ioural effects in paint manufacturers and
painters. Food Chemical Toxicology; 34( 11 -
12); p. 1113-20; 1996.
• Tabakoff, B. and Petersen, R.C., Brain
damage and alcoholism. The Counselor;
6(5); p.13-16; 1988.
• Triebig, G., et al., Neuropsychiatric symp-
toms in active construction painters with
chronic solvent exposure, Neurotoxicology;
21(5); p.791-794; October, 2000.
• William, D. E., et al., Neuropsychologi-
cal function in retired workers with previ-
ous long-term occupational exposure to
solvents. Occupational Environmental
Medicine; 56; p.93-105; 1999.
• Wilkinson, D., CT scan and neuropsy-
chological assessments of alcoholism. In: O.
Parsons, N. Butters, and P. Nathan (Ed.);
Neuropsychology of Alcoholism: Imp-
licatons for Diagnosis and Treatment: p.78;
Guildford Press, New York, N.Y.; 1987.
About the authors
Shailesh K. Nadkarni, M.B.B.S.,
M.H.S.A., is Clinical Manager, Memory
Clinic, Research and Affiliated Services,
Geriatric Mental Health Program, Centre
for Addiction and Mental Health
(CAMH), Toronto.
Luis Fornazzari, M.D., E.R.C.P. (C).), is
the Clinical Director, Memory Clinic, Geri-
atric Mental Health Program, CAMH, and
Department of Psychiatry, Division of
Neurology, University of Toronto.
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