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Neuro-Pathological Effects of Alcohol and Solvents

Neuro-Pathological Effects of Alcohol and Solvents

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Dementia symptoms
Excess alcohol and long-term exposure to everyday organic solvents can express as symptoms of adementing illness. Both are difficult to characterize and diagnose. Both are capable of presenting inthe 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 maylead to persistent amnesic disorder and alcoholic dementia.Deliberate inhalation of solvents for recreational use is associated, in some users, with abehavioural syndrome showing profound impairment in motor control and associated impairmentof some intellectual and memory capacity. Continuing use can result in physical impairment indifferent organs, peripheral nerve damage, and neurobehaviourai effects.
By Shailesh Nadkarni and Luis Fornazzari
Neuro-pathological effectsof alcohol and solvents
Histories of alcohol or excessive exposure to solvents are capable of presentingin the long-term care setting where the symptoms can he mis-diagnosed
T
lhere are certain conditions and ill-nesses that can express symptoms ofdementia. Alcoholism is responsible forcognitive deficits of various severity, whichcould be reversible, or not, with alcoholabstinence, 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 conditionswere profiled and bring to the fore thenecessity of recognizing those conditionsor illnesses that have the ability to causememory deficits and cognitive impair-ment - symptoms usually associated withthe more traditional neurological disor-ders, such as Alzheimer's disease, frontal-lobe dementia, dementia with Lewy bodies,and vascular dementia, among others. The
Volume 17, Number3,October, 2006
first condition has been dubbed chronicpaint syndrome, and the second, alcohol-related dementia.
Characterizingalcoholic dementia
The diagnostic criteria for alcoholicdementia are neither well defined nor
consistent
(Saunders, et al., 1991; Lishman,
1990).
The objective of
a
recently concludedstudy was to describe the clinical profile ofalcoholic dementia, and involved a reviewof clinical cases and a literature search.The study sample consisted of patientsconsecutively admitted to the GeriatricMental Health Program at the Centre forAddiction and Mental Health (CAMH) inToronto, Ontario.The records of eleven patients with adiagnosis of alcoholic dementia that wereadmitted to the inpatient program were re-viewed. The diagnosis and type of demen-tia were determined within two months ofadmission by a behavioural neurologistusing patient interviews, chart reviews, andinformation from structured interviews.
Results
The sample was 82% male, with anaverage age of 67 years ranging from 62to 75 years. The highest level of educationcompleted was grade seven. 9t% of thepatients were separated or divorced, andall were previously employed as unskilledlabourers. 75% were smokers and 27%had a history of substance abuse. 82%
19
 
had experienced seizures in the past, andmore 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 overfour years, ranging from 29 days to over 12years; average number of admissions wasthree, ranging from one to nine per pa-tient. The average score on the MiniMental State Examination was 15, withscores 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, impairedverbal reasoning, and poor impulse con-trol, all of which were consistent withstudies (Parson and Leber,
1981;
Eckardt andMartin,1986;Tabakoff and Petersen, 1988).Deficits were evident for all patientsin tasks requiring cognitive flexibility.Computer tomography scans revealed thatmore than half the patients in the studyhad diffused cerebral and atrophy.Other findings included: frontal whitematter disease and temporal lobe encepha-lomalacia, peri-ventricular ischemicchanges, enlargement of the ventricularsystem and subarachnoid spaces, and per-fusion to the temporo-parietal region (Ron,1979; Wilkinson, 1987). Malnutrition wascommon in the study patients. All had in-takes below the recommended standards inone or more micro- or macronutrients.
Recap
Studies have demonstrated that alcoholsubjects perform more poorly on cognitivetesting than non-alcoholic subjects. Thispoor performance in cognition persistseven after prolonged periods of sobriety(Bowden, 1990; Hendrie et
ai.,
1996).A diagnosis of alcoholic dementia isbased on evidence of general decline incognitive functions, including, but not re-stricted to, memory, following prolongedheavy ingestion of alcohol and no otheridentified 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 memoryand disturbed verbal fluency. These cog-nitive patterns are in contrast to thoseseen 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 difficulttypes to characterize (Munro, 2001). Fur-ther studies with larger sample sizes arerequired 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 thatchronic paint syndrome has not been re-ported in Canada, although cases with thisunique syndrome have been reported in the
U.S.
and Nordic countries.The following profile is a case ofchronic paint syndrome that was identifiedin a Canadian citizen who lived andworked 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 ahistory of working with paint and othersolvents and who show excess of specificsymptoms that could otherwise be as-signed to mood and behaviour, along withmemory impairment.Prompt recognition and treatment areimportant for many painters and solventusers who may be mistakenly regardedand treated as neurotic or depressive.
Case report
A
55-year-old white, Canadian male, wastransferred from Florida in response toclosure of the mental health facility hewas residing at.The client posture is normal, but he hasan unsteady gait. He is co-operative, calm,and friendly, but did establish eye contactwell. He exhibits no psychomotor agita-tion or retardation, nor gesturing or man-neristic behaviours. His mood is euthymic.Although readily engaging, he does notinitiate conversation.
Neurotoxicity
It is argued that long-term exposure toturpentine substitutes and paints, oftenthrough a period with acute intoxicationsymptoms, 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 reportshave indicated that professional paintersunder long-term exposure to organic sol-vents may develop a chronic organicbrain 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 coaltar. Painters, such as the one profiled inthis report, in their daily work, use largeamounts of turpentine substitutes, withits use rapidly increasing in recent years.This is primarily due to increasing use ofoil-based paint and an application technique,which enables the painter to cover largersurfaces faster. Thus, evaporation is in-creased, as well as absorption.Magnetic imaging (MRI) of the brainsin those chronically misusing paint thin-ner or toluene may show cerebral andcerebellar atrophy, atrophy of the corpuscallosum, and loss of grey-white matter.Other imaging techniques show scat-tered lesions in the white matter and brainstem due to demyelination or gliosis, andlow intensity lesions in the basal ganglia,thalami, and sub-cortical white matter(Komiyama, 1999).
Neuro-behaviour effects
The neuro-psychological symptoms areassociated with heavy exposure to work-ing with paints, a phenomena that islikely to be found worldwide whereverthere is such exposure to solvent-basedpaints (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 thatlong-term excessive occupational expo-sure
to
mixed organic solvents
can
causea wide range
of
chronic central nervoussystem 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
otherneurodegenerative diseases, such
as
Alzhe-imer's
or
Parkinson's disease,
by the
staticnature
of
cognitive impairment
and pos-
sible selective improvements
in
neuropsy-chological functioning
if
exposure
to sol-
vents
is
discontinued.
References
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B.,
Chronic painters
syn-
drome: chronic toxic encephalopathy
in
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• Bowden,
S.C.,
Separating cognitive
im-
pairment
in
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L.,
Ibram,
G.,
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Leber, W.R., The rela-tionship between cognitive dysfunctionand brain damage
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of
long-term exposure to xylene andmixed organic solvents
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PA.,
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J.R.,
Dewey,M.E., Davidson,
LA.,
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and
Sullivan,
C,
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as a
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for
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• Seeber,
A.,
Sietmann,
B. and
Zupanic,M.,
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search
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dose-response relation-ships
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neuro-behav-ioural effects
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and
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neuropsy-chological assessments of alcoholism. In:
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About the authors
Shailesh
K.
Nadkarni, M.B.B.S.,M.H.S.A.,
is
Clinical Manager, MemoryClinic, Research
and
Affiliated Services,Geriatric Mental Health Program, Centrefor 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.
21

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