Neuro-Pathological Effects of Alcohol and Solvents

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Dementia symptomsExcess alcohol and long-term exposure to everyday organic solvents can express as symptoms of adem enting illness. Both are difficult to characterize and diagnose. Both are capable of presenting inthe long-term care setting w here 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 impairmentof 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 effectsof alcohol and solventsHistories of alcohol or excessive exposure to solvents are capable of presentingin the long-term care setting w here the symptoms can he m is-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 - symptom s usually associated withthe more traditional neurological disor-ders, such as Alzheimer's disease, frontal-lobe dementia, dementia with Lewy bo dies,and vascular dementia, among others. The

first condition has been dubbed chronicpaint syndrome, and the second, alcohol-related dementia.

Characterizingalcoholic dementiaThe diagnostic criteria for alcoholic

dementia are neither well defined norcons is tent (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 GeriatricMen tal Health Program at the Centre forAddiction and Mental Health (CAMH) in

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.

ResultsThe sample was 82% male, with an

average 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%


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had experienced seizures in the past, andmore than half had a history of head in-jury. The most common co-m orbid 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 judgeme nt, 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-lomalac ia , per i -ven t r i cu la r i s chemicchange s, enlargement of the ventricularsystem and subarachnoid spaces, and per-fusion to the temporo-parietal region (Ron,1979; Wilkinson, 1987). Malnutrition wascomm on in the study patients. All had in-takes below the recommended standards inone or more m icro- or macronutrients.

RecapStudies have demonstrated that alcohol

subjects 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 de mentia (Carien et ai.,1994; D SM-III-R, 1987).Typical impairments seen in alcohol re-

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 ch aracterize (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 syndromeA 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 theU.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 reportA 55-year-old white, Canadian male, was

transferred 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-

Although readily engaging, he does notinitiate conversation.

NeurotoxicityIt is argued that long-term exposure to

turpentine 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 m ajor 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 w ork, 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 effectsThe neuro-psychological sym ptoms are

associated with heavy exposure to work-ing with paints, a phenomena that islikely to be found worldw ide w hereverthere is such exposure to solvent-basedpaints (Chen et al., 1999).There also appears to be a dose-re-


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neuro-behavioural effects in painters andthose involved in paint manufacturing(Seeber, 1996; Triebig, 2000; Ruijten, 1994).

ConclusionThere is considerable evidence that

long-term excessive occupational expo-sure to mixed organic solvents can causea wide range of chronic central nervoussystem abno rma lities (Mikkeison 1988).

The more severe cases of encephalopa-thy associated with chronic exposure tosolvents are characterised by mild tomoderate 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 Arlien-Soborg, P., Bruhn, P., Gyldensted,C, Melgaard, B., Chronic painters syn-drome: chronic toxic encephalopathy inhouse painters, Acta Neurology Scandina-via; 60{3);p.\49-l56; 1979. Bowden, S.C., Separating cognitive im-pairment in neurologically asymptomaticalcoholism 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 maleand female painters; an epidemiologicalstudy in dockyard workers. OccupationalEnvironmental Medicine; 56(6); 1999. Cunha P., Novaes M., Neurocognitiveassessment in alcohol abuse and depend-ence: implications for treatment. Rev BrasPsiquiatr, 26 (Suppl. 1); S23-7; 2005. DSM -III-R: Diagnostic and StatisticalManual of Mental Disorders (3rd. Ed., re-vised); American Psychiatric Association,

Eckardt, M.J. and Martin, P.R., Clinicalassessment 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 andfunctional 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 Am ericans, Jour-na l of the American Geriatrics Society;44(10); p.l 158-65; 1996. Komiyama, M., Chronic misuse of paintthinners. Journal of Neurology, Neurosur-gery and Psychiatry; 67; p.267; 1999. Lishman, W., Alcohol and the brain, Brit-ish Journal of Psychiatry; 156; p.635; 1990. Mikkelson S., Jorgensen M., Browne E.,et al.. Com parison with the findings ofsimilar 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. Mu nro, C.A., Saxton, J. and Butters, M.A.,Alcohol dementia: cortical or subcorticaldementia? Archives of Clinical Neuropsy-chology; 16; p.523-533; 2001. Nadkarni, S., Eomazzari, L., Ibram, G.,Understanding the evasive clinical profileof alcoholic dementia, Neurobiology ofAging; 25(2); S96; 2004. Oslin, D.W., Cary, M.S., Alcohol-relateddementia: 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 dysfunctionand brain damage in alcoholics: casual,interactive or epiphenomenal? Alcoholism:Clinical and Experimental Research; 5;p.326-343; 1981. Ron, M.A., Organic psychosyndromesin chronic alcoholics, British Journal ofAd-diction;! A; p.^57,-35^; 1979. Piemcci-Lagha, A, Derouesne, C, Alco-holism andaging: Alcoholic dementia oralcoholic cognitive impairment, PsycholNeuropsychiatr Vieil.: 1(4); p.237-249;

D e c , 2003. Ruijten, M.W., et al., Neurobehaviouraieffects of long-term exposure to xylene andmixed organic solvents in shipyard spraypainters, Neurotoxicology; 15(3); p.613-620;Fall, 1994. Saunders, PA., Copeland, J.R., Dewey,M.E., Davidson, LA., McWil l i am, C ,Sharma, V. and Sullivan, C, Heavy drink-ing as a risk factor for depression and de-mentia in elderly men: findings from theLiverpool 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 andpainters. Food Chemical Toxicology; 34( 11 -12); p. 1113-20; 1996. Tabakoff, B. and Petersen, R.C., Braindamage and alcoholism. The Counselor;6(5); p.13-16; 1988. Triebig, G., et al., Neuropsych iatric symp-toms in active construction painters withchronic 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 tosolvents . Occupational EnvironmentalMedicine; 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 authorsShai lesh K. N a d k a rn i , M. B . B . S . ,

M.H.S.A., is Clinical Manager, MemoryClinic, Research and Affiliated Services,Geriatric Mental Health Program, Centrefor Addict ion and Mental Heal th(CAMH), Toronto.

Luis Fornazzari, M.D., E.R.C.P. (C).), isthe Clinical Director, Memory Clinic, Geri-atric Mental Health Program, CAMH , andDepartment of Psychiatry, Division ofNeurology, University ofToronto.


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Neuro-Pathological Effects of Alcohol and Solvents

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