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INTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, VOL.

13: 203212 (1998)

ALCOHOL RELATED DEMENTIA: PROPOSED CLINICAL CRITERIA


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DAVID OSLIN,1* ROLAND M. ATKINSON,2 DAVID M. SMITH3 AND HUGH HENDRIE4

University of Pennsylvania, Section of Geriatric Psychiatry, Philadelphia, USA; 2Oregon Health Sciences University, Oregon, USA; 3 Portland VAMC and Oregon Health Sciences University, USA; 4 Indiana, University, School of Medicine, USA

ABSTRACT
Current diagnostic criteria for Alcohol Related Dementia (ARD) are based almost exclusively on clinical judgment. Moreover, there are no guidelines available to assist the clinician or the researcher in distinguishing Alcohol Related Dementia from other causes of dementia such as Alzheimer's Disease (AD). However, this distinction may have implications for the prognosis and treatment of patients. In this article, provisional diagnostic criteria for establishing a diagnosis of Alcohol Related Dementia are proposed for further study. The criteria are based on the available literature on the relationship between alcohol consumption and dementia and were modeled after existing diagnostic criteria for AD and Vascular Dementia. Validity of these criteria for distinguishing AD from ARD will require further study. # 1998 John Wiley & Sons, Ltd.
Int. J. Geriat. Psychiatry, 13: 203212, 1998.
KEY WORDS alcoholism;

dementia; diagnosis

BACKGROUND Dementia is a leading cause of morbidity and mortality in late life and leads to tremendous caregiver burden. Furthermore, the economic and social costs of caring for patients with dementia are staggering. The need to better understand the risks of developing dementia and to develop eective treatments is clear. An area of continued controversy is the role of alcohol use as a causative factor for dementia (Alcohol Related Dementia, ARD) or as a risk factor for other types of dementia. The purpose of this article is to propose diagnostic criteria for the syndrome of ARD. The ultimate goal of developing improved classication criteria is to help clarify the relationship between alcohol use and dementia. The relationship between alcohol use and dementia is complex. Alcohol use may have direct neurotoxic eects leading to the characteristic dementia syndrome of Alcohol Related Dementia
* Correspondence to: David Oslin, University of Pennsylvania, Section of Geriatric Psychiatry, RalstonPenn Center, 3614 Chestnut Street, Philadelphia, PA 19104, USA. CCC 08856230/98/04020310$17.50 # 1998 John Wiley & Sons, Ltd.

(ARD), but this is not a universally accepted concept. Indeed, several authors have cast doubt on the existence of ARD as a neuropathologic disease and suggest that the majority of cases of ARD are in fact WernickeKorsako syndrome (Victor, 1993). We do not challenge the possible validity of this view; however, we wish to propose diagnostic criteria that rene the criteria for ARD proposed by DSM IV and focus more on ARD as a syndrome. Thus, the proposed criteria represent a dierence in perspective. WernickeKorsako syndrome is a specic neuropathological disease with a specic clinical presentation that in some cases is secondary to alcohol use. The broader diagnostic scheme we propose may include cases of Wernicke Korsako syndrome but also other cases of dementia that appear to be alcohol-related. Our purpose in taking this approach is twofold. First, based on epidemiologic data presented below, dementia associated with heavy alcohol use is more prevalent than WernickeKorsako syndrome, suggesting that either WernickeKorsako syndrome is under-diagnosed or that alcohol may contribute more broadly to dementia, perhaps through multiple mechanisms. Secondly, although
Received 5 May 1997 Accepted 22 October 1997

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WernickeKorsako syndrome can be diagnosed with some degree of validity, heavy alcohol use is often overlooked as a risk factor for the development of dementia or as a source of excessive morbidity in patients already suering from dementia. To this end, it is hoped that providing a broader, clinically based diagnostic scheme will heighten clinicians' awareness of the contribution of alcohol to the dementias. Alcohol Related Dementia as dened in this paper is a syndrome likely representing several dierent etiologic mechanisms including direct neurotoxic eects of ethyl alcohol, metabolic dysfunction, immune related injury, trauma, vascular injury, and thiamine or other nutritional deciencies. In this context, WernickeKorsako syndrome is understood to be one specic disease manifesting as ARD. Although the pathophysiology of WernickeKorsako syndrome is understood, the diagnosis is often missed. The criteria proposed in this article might improve the sensitivity for detecting the presence of Wernicke Korsako syndrome and lead to better clinical management. This article will focus on the epidemiologic and neuropathologic evidence supporting the proposed clinical criteria of ARD, then outline these clinical criteria and propose directions for future research. CLINICAL AND POPULATION BASED STUDIES Epidemiological evidence for the existence of ARD is inconsistent. The prevalence rates of ARD in late life dier according to diagnostic criteria used and the nature of the population studied. Most authors make no attempt at diagnosing ARD; rather they report the prevalence of the comorbidity between alcohol use and dementia. Among community dwelling adults over 55 years old assessed in the Epidemiologic Catchment Area study, the prevalence of a lifetime history of alcohol abuse or dependence was 1.5 times greater among persons with mild to severe cognitive impairment than those with no cognitive impairment (George, 1991). Furthermore, the Liverpool Longitudinal Study of mental health in community dwelling elderly, found that dementia was 4.6 times more likely to occur in men aged 65 and older who had a lifetime history of heavy drinking (Saunders, 1991). Three recent clinical studies have examined the prevalence of heavy alcohol use among patients
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who present for evaluation of dementia. Rains and Ditzler studied 383 men and women, 9% of whom had a history of heavy alcohol use (Rains, 1993). More recently, studies by King and by Smith and Atkinson both found the prevalence of heavy alcohol use to be 22% in patients presenting to a dementia clinic (King, 1986; Smith, 1994a). In one of the few studies of alcohol use among demented long-term care residents, Carlen and colleagues determined that 29% of 130 residents with dementia met criteria for ARD (Carlen, 1994). Studies have also suggested high prevalence rates of dementia among patients presenting for treatment of alcohol use disorders. Finlayson and colleagues found 49 of 216 (23%) elderly alcoholics presenting for addiction treatment to have a comorbid dementia (Finlayson, 1988). Similarly, in a study of older alcoholic veterans presenting for mental health treatment, Blow and colleagues found 9% of the 60 to 69 year old age group (n 3986) and 18.4% of those over 70 (n 543) to have a comorbid dementia (Blow, 1992). In contrast to the higher rates of heavy alcohol use associated with dementia, the prevalence of Wernicke Korsako syndrome has been estimated to occur in only 0.4 to 2.8% of autopsies regardless of the clinical history (Harper, 1995). Community based prevalence rates of WernickeKorsako syndrome are dicult to ascertain, thus making the comparison between autopsy ndings and heavy alcohol use dicult to interpret. Although these epidemiologic studies do not specically conrm the existence of ARD, they do point to an association between alcohol use, especially heavy use or alcohol dependence, and the development of dementia. NEUROPSYCHOLOGY AND NEUROPATHOLOGY Another way of understanding the association between alcohol use and dementia is to explore the neuropsychological performance of adults with signicant alcohol use histories. The extent to which alcohol use interferes with performance on neuropsychological tests has been well reviewed by Victor and by Grant (Grant, 1987; Victor, 1993). Several studies have demonstrated acute eects of alcohol on abstraction and visuospatial problems but not on verbal skills. Less is known about the role of alcohol use in causing permanent cognitive changes. Grant and colleagues and Brandt and
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colleagues have demonstrated that among nondemented alcoholics, abstinence leads to marked improvement in cognitive decits (Brandt, 1983; Grant, 1984). However, Brandt and colleagues did demonstrate that among patients with prolonged periods of abstinence there were long-term decits in the learning of novel associations (Brandt, 1983). It should be noted that most of these patients were moderate consumers of alcohol; and all were healthy with no history of dementia. These studies may have excluded individuals predisposed to developing cognitive changes associated with toxic eects of alcohol or individuals who may have not been exposed to sucient levels of alcohol to cause chronic cognitive losses. A more recent epidemiologic study by Hendrie and colleagues of older African-American men found that increasing alcohol consumption was associated with a worsening performance on dementia screening scales (Hendrie, 1996). Research ndings have also been inconsistent in demonstrating eects of light to moderate drinking upon cognitive functioning. However, recent studies have suggested that drinking in excess of 30 standard drinks per week is associated with poorer performance on neuropsychological testing (Christian, 1995; Parker, 1983; Waugh, 1989). These studies of light to moderate drinking again do not examine the relationship of alcohol use to the development of dementia per se and for the most part have been studies of healthy middle aged adults. Neuropathologic correlates of heavy alcohol use have been suggested by neuroimaging, EEG, and post-mortem pathology studies in cases that did not meet criteria for WernickeKorsako syndrome. In a review of ndings from studies using CT scanning, Ron found that cortical atrophy and third and lateral ventricular enlargement had been consistently demonstrated in alcoholics (Ron, 1983). MRI ndings by Pfeerbaum and colleagues and Hayakawa and colleagues have more recently conrmed the earlier CT ndings; however, most of the imaging procedures in these studies were performed in the immediate detoxication period and may reect short term changes unrelated to neuron loss or other permanent damage ndings (Hayakawa, 1992; Pfeerbaum, 1992). In fact, Shear and colleagues demonstrated in a small sample of abstinent alcoholics increases in white matter volume and reductions in cerebrospinal uid (Shear, 1994). A recent article by Pollock and colleagues, however, supports long
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term eects of alcohol on brain pathophysiology (Pollock, 1992). In this study, an EEG was performed in alcoholics after a minimum of 5 years abstinence and demonstrated regional increases in theta activity compared to controls. As with the long-term neuropsychological data, this nding may represent a predisposing trait rather than an eect of the alcohol use. ANIMAL AND POST-MORTEM STUDIES Studies in rats have shown that chronic alcohol consumption, even in the absence of malnutrition, leads to decreases in hippocampal pyramidal cells and dentate gyrus granule cells (Cadet-Leite, 1988; Walker, 1980). Moreover, many authors have described neuropathologic changes in alcoholics such as neuronal loss and neuroglial proliferation in the cerebral cortex, cerebellar degeneration, arteriosclerotic changes, and evidence of lipid emboli (Arango, 1994; Courville, 1966; Courville, 1954; Harper, 1990; Harper, 1985; Ibanez, 1995; Lynch, 1960; Mott, 1910; Ron, 1977). Unfortunately, many of these studies did not correlate neuropathologic changes with cognitive changes or alcohol consumption, thus limiting any interpretation regarding ARD. A limited number of studies have focused on alcoholics who have a comorbid dementia. Torvik and colleagues reported lesions in the mammillary bodies in alcohol abusing patients with dementia, leading them to postulate a link between WernickeKorsako syndrome and ARD (Torvik, 1982). Akai and Akai reported that post-mortem studies of the brains of 9 patients diagnosed with Alcohol Related Dementia also had signicantly greater loss of neurons in the nucleus basalis compared to 3 alcoholics without dementia (Akai, 1989). The lack of consistent neuropathologic ndings associated with alcohol use has led many authors to cast doubt on the clinical relevance of any direct neurotoxic eects of alcohol use. Authors such as Victor have cast doubt on the existence of ARD, suggesting instead that dementia in alcoholics is secondary to WernickeKorsako syndrome, malnutrition, vascular dementia, hepatic disease, or coincident Alzheimer's disease (Victor, 1989). This indeed may be true; however, current vague diagnostic criteria for ARD limit the ability to collect cases reliably, compare studies and denitively draw such conclusions. Moreover, many of the studies relating alcohol use to
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cognitive or neuropathological changes present limited clinical correlation and often do not specically include patients with dementia. OBTAINING CLINICAL HISTORY Obtaining adequate clinical information regarding alcohol consumption is the rst step in determining the relationship of alcohol use to dementia. The clinical interview remains the best tool for obtaining this history, but collateral sources such as family, other relatives, friends, or medical records should be used routinely. Curtis and colleagues have shown that clinicians under-report alcohol use problems, especially among older adults (Curtis, 1989). Special skills in eliciting relevant information about quantity and frequency of alcohol use and symptoms of abuse or dependence in older adults are required. Typically, this information has to be gathered in a retrospective manner from the patient. The major drawback with retrospective analysis, of course, is that reliability and validity of any information gathered may be suspect. This is a particularly dicult problem among older patients who have lived longer and, as such, have more information to process. To compound the problem, patients presenting with cognitive decits are also unlikely to accurately recall alcohol consumption practices or alcohol related problems that have occurred in the past. Furthermore, denial is often a clinical problem associated with alcohol abuse and may also lead to underestimates of alcohol use. Family, friends and past medical records can be invaluable sources of information when evaluating patients with dementia. However, the use of family or friends as a resource to diagnose alcohol use disorders or to accurately recall a patient's drinking practices has received little attention with regard to validity. Hendrie and colleagues found relatively poor correlation between a cognitively impaired patient's report of alcohol consumption and the family's recollection of drinking practices (Hendrie, 1996). Despite these concerns, among older adults without cognitive impairment, several studies have demonstrated that alcohol use histories can be reliably obtained (Blow, 1993; Buchsbaum, 1992; Chaikelson, 1994; Joseph, 1995; Longnecker, 1992). Several standardized screening instruments such as the CAGE or the MAST-G have been found to be reliable and valid in identifying
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patients with alcohol use disorders both lifetime and current (Blow, 1993; Buchsbaum, 1992; Joseph, 1995). Standardized methods that obtain information regarding lifetime alcohol use and problems related to alcohol include quantity and frequency questionnaires and instruments such as the Semi Structured Assessment for the Genetics of Alcoholism (SSAGA) or the Drinking Problems Index (Bucholz, 1994; Finney, 1991). Quantity and frequency measures of alcohol consumption have been shown to be reliable and valid methods for determining alcohol use in the remote past. Among women with an average age of 54 interviewed 6 to 12 months apart, the correlation between the two interviews for lifetime average alcohol consumption was 0.87 (Longnecker, 1992). The Concordia Lifetime Drinking Questionnaire (CLDQ), a measure of lifetime quantity and frequency of alcohol use, was also found to be reliable (0.78) when administered to older men 33 months apart (Chaikelson, 1994). The instrument was validated against collateral sources of information with a correlation of 0.87 for current drinking and 0.72 for past drinking. The time-line follow-back method of Sobell and colleagues is also widely used and validated (Sobell, 1992). Given the questionable reliability of these instruments in cognitively impaired individuals, these and other instruments will need further specic study using caregivers as proxies for demented patients.

CURRENT CLASSIFICATION SCHEME The most commonly used clinical denition of ARD is given in the Diagnostic and Statistical Manual Version IV (DSM IV) (Frances, 1994). This denition requires the presence of dementia that in the opinion of the clinician is intrinsically linked to the abuse of alcohol. The diagnostic criteria are vague and subjective. There have been no published validation or reliability reports using these criteria. Most reports of the relationship between alcohol use and cognitive impairment rely on `heavy alcohol use' or `problem alcohol use' as a measure of alcohol use. However, criteria for these terms are also not standardized and vary from study to study. We have proposed diagnostic criteria for the purposes of improving the validity and reliability of the diagnosis of ARD in order to reduce subjective interpretation and standardize alcohol consumption criteria. We hope that
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renement of ARD diagnostic criteria will promote better studies on the etiology of putative ARD cases and more careful consideration of alcohol as a risk factor in various dementias. We also hope that these criteria can provide a framework leading to more rational treatment options for individuals with alcohol use problems and/or dementia. PROPOSED CLASSIFICATION SCHEME A classication scheme based upon current research and clinical experience is outlined in Table 1. The criteria have been developed using the format adopted by the NINCDS/Alzheimer's Disease and Related Disorders Association criteria (NINCDS/ ADRDA) and the California Criteria for Ischemic Vascular Dementia (Chui, 1992; McKhann, 1984). The relationship between alcohol use and dementia is dened using four categories: Denite, Probable, Possible and Contributing. As with the California Criteria, a category of mixed dementia species cases that are thought to have multiple causes for the dementia. The essential element in using this classication scheme is the presence of dementia. Dementia is broadly dened as a deterioration in cognition from a previous level of functioning that interferes with usual daily activities. The cognitive deterioration must include decits in at least two areas of cognitive functioning. The cognitive and functional deterioration must not be due to a state of withdrawal or intoxication or any other state of delirium. These criteria are based on DSM IV and are consistent with NINCDS/ADRDA and the California Criteria (Chui, 1992; McKhann, 1984). The diagnosis of dementia is a clinical interpretation based on history from the patient and collateral informants, neuropsychological testing or other cognitive screening, and a thorough physical and mental examination including other appropriate diagnostic procedures as indicated by exam. Although the treatment of alcoholism rests on the clinical diagnosis of an alcohol use disorder, the criteria proposed for ARD rely on information regarding the quantity and frequency of alcohol use and the duration of use in relation to the onset of cognitive changes. The use of alcohol consumption as a marker for disease is based on a toxicological model (ie alcohol functioning as a toxic substance). The DSM IV denition of alcohol abuse and dependence are based on dysfunction in
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a number of areas of psychosocial functioning and not on consumption levels. It is plausible that the behaviors associated with alcohol dependence, such as poor nutrition or self neglect, places the patient at risk for developing dementia that is not directly related to the neurotoxic eects of alcohol. On the other hand, several studies have demonstrated that the presence of end organ damage such as liver disease is predicted by the quantity of alcohol consumption (Lelbach, 1974; Pequignot, 1974a; Pequignot, 1974b; Skog, 1982; Tuyns, 1983). Recall also that the population based studies in the U.S. and the U.K. showed that prior heavy consumption (not an alcohol use disorder) predicted current cognitive loss (George, 1991; Saunders, 1991). Moreover, abuse and dependence criteria do not necessarily correlate with the quantity and frequency of alcohol use, especially among older patients; and these criteria are not known to correlate with the presence of alcohol related end organ damage (Dawson, 1994; Grant, 1989). Because the use of total alcohol consumption as a diagnostic criterion for ARD is based on theoretical considerations (ie alcohol as a neurotoxin) rather than empirical studies, clinicians and researchers applying our proposed criteria are encouraged to collect information regarding abuse and dependence as well as total consumption. The amount of alcohol (greater than 35 standard drinks per week) chosen as a threshold for probable ARD is based on generally accepted criteria for `heavy drinking'. Although there have been no validation trials using dierent thresholds for quantity and frequency, the threshold proposed for these criteria is felt to represent a sucient toxic burden. A review of studies of the cognitive eects of light to moderate drinking suggest that there is little or no lasting cognitive eect from drinking fewer than 20 drinks per week and that greater than 30 drinks per week is required to demonstrate neuropsychological decits (Alterman, 1989; Arbuckly, 1994; Bates, 1990; Christian, 1995; Parker, 1983; Waugh, 1989). Hendrie and colleagues also demonstrated a dose response eect of alcohol consumption on cognitive decits (Hendrie, 1996). The use of a lower threshold for women is based on higher peak blood alcohol levels per gram of alcohol ingested in women compared to men (Frezza, 1990; Tupler, 1995). The period of 5 years that is suggested as a duration of signicant alcohol use is based on the ndings from the Liverpool Longitudinal Study that demonstrated a 5 year period of heavy
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Table 1. Classication of alcohol related dementia


Dementia Dementia is dened as a signicant deterioration of cognitive function sucient to interfere in social or occupational functioning. As dened by DSM IV this requires a deterioration in memory and at least one other area of intellectual functioning. Moreover, the cognitive changes are not attributable to the presence of delirium or substance induced intoxication or withdrawal. Denite Alcohol Related Dementia At the current time there are no acceptable criteria to denitively dene Alcohol Related Dementia. Probable Alcohol Related Dementia A. The criteria for the clinical diagnosis of Probable Alcohol Related Dementia include the following: 1. A clinical diagnosis of dementia at least 60 days after the last exposure to alcohol. 2. Signicant alcohol use as dened by a minimum average of 35 standard drinks per week for men (28 for women) for greater than a period of 5 years. The period of signicant alcohol use must occur within 3 years of the initial onset of Dementia. B. The diagnosis ofAlcohol Related Dementia is supported by the presence of any of the following: 1. Alcohol related hepatic, pancreatic, gastrointestinal, cardiovascular, or renal disease ie other end-organ damage. 2. Ataxia or peripheral sensory polyneuropathy (not attributable to other specic causes). 3. Beyond 60 days of abstinence, the cognitive impairment stabilizes or improves. 4. After 60 days of abstinence, any neuroimaging evidence of ventricular or sulcal dilatation improves. 5. Neuroimaging evidence of cerebellar atrophy, especially of the vermis. C. The following clinical features cast doubt on the diagnosis of Alcohol Related Dementia. 1. The presence of language impairment, especially dysnomia or anomia. 2. The presence of focal neurologic signs or symptoms (except ataxia or peripheral sensory polyneuropathy). 3. Neuroimaging evidence for cortical or subcortical infarction, subdural hematoma, or other focal brain pathology. 4. Elevated Hachinski Ischemia Scale score. D. Clinical features that are neither supportive nor cast doubt on the diagnosis of Alcohol Related Dementia included: 1. Neuroimaging evidence of cortical atrophy. 2. The presence of periventricular or deep white matter lesions on neuroimaging in the absence of focal infarct(s). 3. The presence of the Apolipoprotein e4 allele. The diagnosis of Possible Alcohol Related Dementia may be made when there is: 1. A clinical diagnosis of dementia at least 60 days after the last exposure to alcohol. 2. Either: Signicant alcohol use as dened by a minimum average of 35 standard drinks per week for men (28 for women) for 5 or more years. However, the period of signicant alcohol use occurred more than 3 years but less than 10 years prior to the initial onset of cognitive decits. or Possibly signicant alcohol use as dened by a minimum average of 21 standard drinks per week for men (14 for women) but no more than 34 drinks per week for men (27 for women) for 5 years. The period of signicant alcohol use must have occurred within 3 years of the onset of cognitive decits. Mixed Dementia A diagnosis of mixed dementia is reserved for clinical cases that appear to have more than one cause for dementia. The classication of probable or possible should continue to be used to convey the certainty of the diagnosis of ARD. The classication of mixed dementia should not be used to convey uncertainty of the diagnosis or to imply a dierential diagnosis. Alcohol as a Contributing Factor in the development or course of dementia. The designation of alcohol as a contributing factor is used for the situation in which alcohol is used, but not to the degree required or within the time required to meet the classication of probable or possible Alcohol Related Dementia. This designation should not preclude the use of Probable Vascular Dementia or Probable Dementia of the Alzheimer's type.

drinking increased the likelihood of men subsequently developing dementia (Saunders, 1991). No other studies have examined the duration of heavy drinking as a risk factor for developing dementia. In order to diagnose probable ARD, we
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have chosen to require that an interval of no more than 3 years have elapsed between the period of heavy drinking and the development of dementia. This requirement is meant to strengthen the causal relationship between alcohol use and dementia.
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We acknowledge that there is scant literature to support this notion or to suggest the appropriate length of such an interval. In fact, the thresholds for quantity, duration and temporal relationship of drinking to dementia onset are arbitrarily set in our proposal and will need further validation. Further diculties in understanding the role of alcohol use in the development of dementia occur when distinguishing the acute eects of alcohol intoxication or withdrawal from the more permanent eects implied by a diagnosis of dementia. There are clear associations between alcohol intoxication and withdrawal and cognitive impairment (Grant, 1987). However, this eect is certainly not reective of the presence of dementia or of the role of alcohol use in the development of dementia. The criteria for establishing a diagnosis of dementia preclude the use of transient changes in cognition which are solely due to the intoxicating eects of alcohol or to withdrawal eects. Therefore, cognitive impairment that is only present during periods of withdrawal or intoxication or other states of delirium, such as hepatic encephalopathy, would not meet criteria for dementia and, thus, is not ARD. Previous studies have also demonstrated that in non-demented patients who maintain abstinence, there is a persistent improvement in cognition for weeks to months, even years (Brandt, 1983). Likewise, improvement may also occur in ARD, and such reversibility of dementia is used as supportive evidence for the presence of ARD, as opposed to AD or Vascular dementia. In order to distinguish any noted improvement in dementia from improvement more appropriately attributable to early abstinence, the proposed criteria suggest that a minimum of 60 days of abstinence elapse before establishing the cognitive baseline for an individual. In other words, improvement in cognition noted during early abstinence should not be used as evidence for ARD. In addition to criteria for consumption and the presence of dementia, several clinical signs and symptoms are characterized as either supportive or not supportive in making a diagnosis of ARD. On the basis of studies by Smith and colleagues the presence of ataxia or peripheral sensory neuropathy supports the diagnosis of ARD (Smith, 1994b). Of course, other causes for these neurologic ndings must be ruled out. For example, vascular and drug eects on cerebellar function can cause ataxia; and disorders such as diabetes mellitus and multiple sclerosis can cause peripheral neuropathy. Furthermore, demonstration of
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cognitive stability or cognitive improvement, or improvement in previously demonstrated ventricular dilatation or sulcal widening in neuroimaging studies is supportive of a diagnosis of ARD. As the proposed mechanism of ARD is based on toxic damage, one may conclude that the presence of alcohol related damage to other organ systems such as hepatic, pancreatic, gastrointestinal, cardiovascular, or renal would add circumstantial evidence to support a diagnosis of Alcohol Related Dementia. However, the cognitive impairment should not be due to delirium associated with end organ damage such as hepatic encephalopathy. We also propose certain clinical signs and symptoms that do not support a diagnosis of ARD. These include: the presence of prominent language impairment (dysnomia or anomia), the presence of lateralizing neurologic signs consistent with cerebrovascular pathology, neuroimaging evidence for cortical or subcortical infarction, subdural hematoma, or other focal brain pathology, or elevated Hachinski Ischemia Scale score. In general, all of these signs and symptoms are suggestive of vascular disease and may warrant a diagnosis of probable or possible vascular dementia. Anomia was not associated with ARD in a study using similar criteria to the proposed criteria (Smith, 1994b). These ndings are not designed to be exclusionary, but, rather their presence tends to lower the diagnostic certainty of ARD. There are also several clinical signs and symptoms that we feel are not helpful in establishing a relationship between alcohol use and dementia. Although neuroimaging evidence of ventricular dilatation or sulcal widening is common in patients with heavy alcohol use, these signs are non-specic, ie they are also present in Alzheimer's disease as well as other types of dementia, and, therefore, not helpful in the diagnosis of ARD. The reversibility of these changes is felt to support the diagnosis of ARD. The presence of periventricular or deep white matter lesions on neuroimaging in the absence of focal infarct(s) is also felt to be nonspecic and therefore are not diagnostically useful. The presence of the Apolipoprotein e4 allele is felt to be not helpful, as there is little published data on the presence of Apo e4 among cognitively impaired individuals with a history of signicant alcohol use. As with previously proposed criteria for vascular dementia and Alzheimer's disease, these criteria use a classication of denite, probable, and possible to convey the degree of diagnostic certainty. An additional category of mixed dementia is reserved
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for cases that appear to have more than one etiologic factor. This would allow, for example, the simultaneous diagnosis of ARD and vascular dementia in a patient who meets criteria for ARD and subsequently suers a cerebrovascular accident and develops worsening of the dementia. Finally, a category of alcohol use as a contributing factor is proposed for use in patients with dementia from a cause other than ARD who have signicant histories of alcohol use. This classication is meant to stimulate interest in alcohol use as a risk factor for other types of dementia or as a factor that modies the presentation or course of dementia. Alcohol use that continues despite the presence of dementia is also likely to contribute to excessive but possibly reversible impairment. If critics like Victor are correct, and ARD does not exist as a denable entity, the classication of alcohol use as a contributing factor in the development of various dementias may prove to be the most valid association. In using the classication of alcohol use as a contributing factor it is important to be descriptive about the alcohol use adding comments regarding alcohol abuse and dependence as well as consumption and the temporal relationship of these symptoms to the occurrence of dementia. DISCUSSION Alcohol use is a major public health concern among all age groups including the elderly. As reviewed by Liberto and colleagues, `heavy' drinking, dened as a minimum of 12 to 21 drinks per week, is present in 3% to 9% of the older population (Liberto, 1992). The consequences of abusive alcohol consumption are devastating and can eect every organ system. As lifespan lengthens and the proportion of older adults grows, there will be an increasing need for knowledge about the problems associated with continued use of alcohol and the sequelae of past alcohol use. In this article we have outlined a set of tentative diagnostic criteria for establishing the role of alcohol use in the development of dementia. The need for such criteria has been underscored by the inconsistencies in diagnostic criteria in previous studies of ARD. Moreover, the estimated prevalence of ARD in recent studies, especially in men, highlights ARD as a signicant clinical problem. The purposes of developing these criteria are to: 1) standardize and objectify diagnostic criteria for
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alcohol related cognitive impairment, 2) provide a clinical framework for validating the existence of, and understanding the pathophysiologic mechanisms of ARD, 3) increase awareness among clinicians of the long-lasting eects of alcohol on cognition, and 4) guide the develop of treatment options for alcohol and non-alcohol related cognitive impairment. The validity of the proposed criteria will only be established through further research. A possible criticism of this eort to propose criteria for ARD is that the elaboration of more detailed criteria may falsely tend to validate a disease that may not exist. These criteria may also be criticized as being in conict with or overlapping the clinical criteria for such disorders as WernickeKorsako syndrome. In our opinion, the criteria for ARD proposed in this paper do not represent the establishment of a new disorder, only the renement of diagnostic criteria for an entity presumed to exist according to mainstream psychiatric thought as reected in DSM IV. By establishing these criteria we intend to help answer questions about the existence of ARD and the relationship of ARD to Wernicke Korsako syndrome. The potential diculty in using these criteria lies in the ability to gather accurate and detailed clinical information regarding alcohol use. The authors are aware of the daunting nature of this task in many busy clinical settings, but suggest that through careful interviewing and the use of clinical records and family interviews, a history can be obtained that will provide the necessary basis for a clinical diagnosis. Although the proposed diagnostic scheme requires specic quantity, duration, and temporal information about alcohol use and the development of dementia, these thresholds are meant as guiding principles rather than absolutes. In conclusion, ARD remains a controversial syndrome that is not well understood in terms of its epidemiology or pathophysiology. The authors' intent in proposing these criteria is to provide a common language for clinicians and researchers in exploring the role of alcohol use in the development of severe and persistent cognitive impairment.

REFERENCES
Akai, J. and Akai, K. (1989) Neuropathological study of the nucleus basalis of meynert in alcoholic dementia. Arukoru kenkyuto Yakubutsu Ison 24, 8088.
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