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 misinterpreted. 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


lhere are certain conditions and illnesses 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 cognitive impairment related to other pathologies, such as Alzheimer's disease (PierucciLagha 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 impairment - symptoms usually associated with the more traditional neurological disorders, such as Alzheimer's disease, frontallobe dementia, dementia with Lewy bodies, and vascular dementia, among others. The Volume 17, Number 3, October, 2006

first condition has been dubbed chronic paint syndrome, and the second, alcoholrelated dementia.

Characterizing alcoholic dementia
The diagnostic criteria for alcoholic dementia are neither well defined nor
consistent (Saunders, et al., 1991; Lishman,

The records of eleven patients with a diagnosis of alcoholic dementia that were admitted to the inpatient program were reviewed. The diagnosis and type of dementia were determined within two months of admission by a behavioural neurologist using patient interviews, chart reviews, and information from structured interviews.

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 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% 19

had experienced seizures in the past, and more than half had a history of head injury. The most common co-morbid disorders were personality disorders and psychosis. 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 patient. The average score on the Mini Mental State Examination was 15, with scores ranging from 1 to 27. A significant portion of the patients displayed poor insight and judgement, impaired memory (immediate and delayed), poor visual-spatial construction, impaired verbal reasoning, and poor impulse control, 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 encephalomalacia, peri-ventricular ischemic changes, enlargement of the ventricular system and subarachnoid spaces, and perfusion to the temporo-parietal region (Ron, 1979; Wilkinson, 1987). Malnutrition was common in the study patients. All had intakes below the recommended standards in one or more micro- or macronutrients.

stracting abilities and short-term memory and disturbed verbal fluency. These cognitive patterns are in contrast to those seen in AD, where the memory impairment is profound and involves both recognition and recall, and individuals frequently present with word-finding deficits (Oslin 2003). Alcohol dementia continues to distinguish itself as one of the more difficult types to characterize (Munro, 2001). Further studies with larger sample sizes are required to further validate the diagnostic criteria of the elusive concept of alcohol-related dementia (Nadkarni 2004).

Although readily engaging, he does not initiate conversation.

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 development of a chronic brain syndrome, called chronic paint syndrome (AriienSoborg et ai., 1979). Epidemiological studies and case reports have indicated that professional painters under long-term exposure to organic solvents may develop a chronic organic brain syndrome dominated by memory impairment, fatigue, personality changes, headache, and dizziness. The major constituent of paints or thinners is toluene, which is a neurotoxic solvent 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 increased, as well as absorption. Magnetic imaging (MRI) of the brains in those chronically misusing paint thinner or toluene may show cerebral and cerebellar atrophy, atrophy of the corpus callosum, and loss of grey-white matter. Other imaging techniques show scattered 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).

Chronic paint syndrome
A review of the literature has shown that chronic paint syndrome has not been reported 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 working life. Clinicians and physicians have to consider chronic paint syndrome in differential 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 assigned 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.

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 restricted 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 related dementia include deficits in ab-

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 agitation or retardation, nor gesturing or manneristic behaviours. His mood is euthymic.

Neuro-behaviour effects
The neuro-psychological symptoms are associated with heavy exposure to working 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-response 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).

• Eckardt, M.J. and Martin, P.R., Clinical assessment of cognition in alcoholism. Alcoholism: Clinical and Experimental Research; 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 between alcohol consumption, cognitive performance, and daily functioning in an urban sample of older black Americans, Journal of the American Geriatrics Society; 44(10); p.l 158-65; 1996. • Komiyama, M., Chronic misuse of paint thinners. Journal of Neurology, Neurosurgery and Psychiatry; 67; p.267; 1999. • Lishman, W., Alcohol and the brain, British Journal of Psychiatry; 156; p.635; 1990. • Mikkelson S., Jorgensen M., Browne E., et al.. Comparison with the findings of similar studies (ch. 9); cited in: Mixed solvent 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 Neuropsychology; 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 relationship 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 ofAddiction;! A; p.^57,-35^; 1979. • Piemcci-Lagha, A, Derouesne, C , Alcoholism and aging: Alcoholic dementia or alcoholic cognitive impairment, Psychol Neuropsychiatr Vieil.: 1(4); p.237-249;

There is considerable evidence that long-term excessive occupational exposure to mixed organic solvents can cause a wide range of chronic central nervous system abnormalities (Mikkeison 1988). The more severe cases of encephalopathy 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 Alzheimer's or Parkinson's disease, by the static nature of cognitive impairment and possible selective improvements in neuropsychological functioning if exposure to solvents is discontinued. •

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 drinking as a risk factor for depression and dementia in elderly men: findings from the Liverpool longitudinal study, British Journal of Psychiatry; 159;p.213-216; 1991. • Seeber, A., Sietmann, B. and Zupanic, M., In search of dose-response relationships of solvent mixtures to neuro-behavioural 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 symptoms in active construction painters with chronic solvent exposure, Neurotoxicology; 21(5); p.791-794; October, 2000. • William, D. E., et al., Neuropsychological function in retired workers with previous long-term occupational exposure to solvents. Occupational Environmental Medicine; 56; p.93-105; 1999. • Wilkinson, D., CT scan and neuropsychological assessments of alcoholism. In: O. Parsons, N. Butters, and P. Nathan (Ed.); Neuropsychology of Alcoholism: Implicatons for Diagnosis and Treatment: p.78; Guildford Press, New York, N.Y.; 1987.

• Arlien-Soborg, P., Bruhn, P., Gyldensted, C, Melgaard, B., Chronic painters syndrome: chronic toxic encephalopathy in house painters, Acta Neurology Scandinavia; 60{3);p.\49-l56; 1979. • Bowden, S.C., Separating cognitive impairment in neurologically asymptomatic alcoholism from Wemicke-Korsakoff Syndrome: is the neuropsychological distinction justified. Psychological Bulletin; 107; p.355-366; 1990. • Carlen, P., et al.. Alcohol-related dementia in the institutionalized elderly. Alcoholism: Clinical and Experimental Research; 18(6); p.1330-34; Nov./Dec, 1994. • Chen, R., Wei, L. and Seaton, A., Neuropsychological 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 dependence: implications for treatment. Rev Bras Psiquiatr, 26 (Suppl. 1); S23-7; 2005. • DSM-III-R: Diagnostic and Statistical Manual of Mental Disorders (3rd. Ed., revised); American Psychiatric Association, Washington, D.C.; t987. Volume 17, Number 3, October, 2006

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, Geriatric Mental Health Program, CAMH, and Department of Psychiatry, Division of Neurology, University of Toronto. 21

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