ALCOHOL-RELATED BRAIN DAMAGE: AN OVERVIEW WITH SPECIAL REFERENCE TO THE AUSTRALIAN SITUATION

* J o h n P r i c e

This paper will examine those disorders which present psychiatrically. A good deal has been written on the neurology of alcohol-related brain disorders and a useful review available in a psychiatric text is that of Lishman ~ . Ron has provided substantial reviews of the common organic psychosyndromes of the alcoholic. 2,3

Cutting proposed the following categories of chronic organic mental disorders in alcoholics as representing a consensus deriving from both his own work and his review of the literature4:

1. Sub-clinical psychological deterioration: Careful psychological testing in the majority of alcoholics with a drinking history of more than 15 years will reveal deficits in at least one area of cognitive functioning.5.6 7.

2. Korsakoff's syndrome: Superimposed on this back- ground of mild cognitive dysfunction, there may appear an abrupt and clinically recognizable syndrome whose development owes much to thiamin deficiency. Its clinical picture, when an initial confusional state has subsided, is characterized by a fairly pure disorder of memory, without any major intellectual deficits except those common to all chronic alcoholics with a comparable drinking history.

3. 'Alcoholic dementia' or 'accelerated psychological deterioration': Some patients present a picture which resembles that of Korsakoff's syndrome in many respects and is frequently diagnosed as such. However, the gradual development, relative independence of nutrition- al factors, longer drinking history, greater age, higher proportion of females and, most of all, the intellectual decline which is evident, justify its status as separate from Korsakoff's syndrome. Some degree of recovery is the rule rather than the exception.

Although the condition may not be homogeneous, it is proposed that at least some members of the group show 'accelerated cognitive dysfunction', more severe in degree but not different in nature from that which develops in the majority of chronic alcoholics with a lengthy drinking history. In this sense, it is the clinical expression of the subclinical psychological deterioration of Category 1. The term 'accelerated psychological deterioration' is more cumbersome than 'alcoholic dementia', but may confer a better understanding of the problem.

4. Combined Korsakoff's syndrome and 'alcoholic dementia'.

5. 'Sub-acute confusional state': There may exist a group of cases for whom this label is appropriate. In proposing this, one would need to assume the action of some pathogenic factor, other than the high blood alcohol level over long periods, which is probably responsibile for 'accelerated psychological deterioration'.

The only two factors identified in this context are with- drawal or relative withdrawal, regarded by IsbeU et al as responsible for delirium tremen@, and thiamin de- ficiency, which results in Wernicke's encephalopathy. The former condition lasts only a few days in most instances and the latter is believed by Victor et al to have cleared or progressed Korsakoff's syndrom within two months. 9

* Dr. J. Price, Head of Department, Department of Psychiatry,

The only place for 'sub-acute confusional state' in this scheme is as a description of cases which resemble either condition, but in which resolution is delayed beyond the usual period.

Cutting concludes his delineation of the various categories he describes as follows: for any chronic alcoholic the chances of developing one of these five types of cognitive impairment is probably determined by a variety of factors; among these are the extent and pattern of drinking, nutritional deficiencies and periods of absolute or relative withdrawal from alcohol

It seems doubtful whether it is absolutely necessary for Korsakoff's syndrome to occur against a background of mild cognitive dysfunction, as proposed by Cutting 10 and Walsh. This is because the Wernicke-Korsakoff syndrome can develop after a few months of heavy drinking if accompanied by gross dietary neglect and resultant acute thiamin deficiency. In pathological terms, this may correspond to that 17% of the Wernicke post-mortem material described by Harper as 'acute', rather than 'acute on chronic' (17%) or 'chronic' (66%).

The report of Cala is largely concerned with the first and third categories of Cutting. as outlined above. The role, if any, of thiamin deficiency in these two categories is difficult, to assess. One problem that bedevils research in this area is that of cause and effect. Thus, if one turns to another contentious area, one can find plenty of evidence to associate depression and folic acid deficiency. The question arises whether folic acid defici- ency results from depression (consequent on failure to eat) or whether folic acid deficiency causes depression. Similarly, the psychosocial deterioration resulting from alcohol abuse could lead to dietary neglect and vitamin deficiency.

HOW GLOBAL AND HOW IRREVERSIBLE IS 'ALCOHOLIC DEMENTIA'?

These are issues addressed in part by Walsh and examined in some detail by Ronl 1.12 and Eckardt 13, among others. A very large number of studies over the years have addressed the cognitive defects of the alcoholic and the social drinker, which these reviews summarize. Ron concludes that there is neuro- pathological, neuroradiological and psychometric evidence of more frequent and more severe damage in the frontal lobes than elsewhere, although atrophy elsewhere does occur. The neuropathological and neuroradiological findings, reported elsewhere in this volume by Harper and Cala respectively, agree with Ron's conclusion. The findings of Cala indicate that the neuroradiological appearances in alcoholics improve after a period of abstinence; similarly, Ron 14 summarizes evidence indicating an improvement in the psychological test perfor- mance of alcoholics after a period off alcohol.

Although Cutting referred to the global nature of the deficit in alcoholics, one very commonly applied psychological test, the Wechsler Adult Intelligence Scale (WAIS), does not yield in alcoholics' results diagnostic of organic impairment. Results of the WAIS, when applied to alcoholics, have been very variable, but Kleinknecht and Goldstein15 have pointed out that the only sub-tests consistently reported as impaired have been Object Assembly and Digit Symbol. There are thus marked differ- ences in impairment between alcoholics and patients with the

Universily of Queensland, Royal Brisbane Hospital, Bn~bane, Qld 9029

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most common of all the dementias, Alzheimer's disease. The latter yields many more WAIS sub-test deficits than does chronic alcoholism.

IS THE TERM 'ALCOHOLIC DEMENTIA' APPROPRIATE?

The Diagnostic and Statistical Manual of Mental Disorders (DSM 111)16 stipulates that the essential feature of dementia is a loss of intellectual ability sufficiently severe to interfere with social or occupational functioning - - a multifaceted deficit state. In the alcoholic, memory, judgment, abstract thought and other fuctions are frequently impaired to the point where social and occupational functioning are grossly impaired. Hence, there would seem to be no objection to the use of the term 'dementia' in this context. Consistent with its definition of dementia, the DSM III includes the category of Alcoholic Dementia, defined as follows: 1. Dementia following prolonged heavy use of alcohol; 2. Dementia persisting at least three weeks after cessation of

alcohol ingestion; 3. Exclusion of all other causes of Dementia, other than pro-

longed heavy use of alcohol, by the history, physical examination and laboratory tests.

THE WERNICKE-KORSAKOFF 0N-K) SYNDROME It is generally accepted that Wernicke's encephalopathy is a

frequent antecedent of the Korsakoff syndrome. When Cutting refers in his Category 2 to "an abrupt and clinically recognis- able syndrome whose development owes much to thiamin deficiency ..." he is clearly referring to Wernicke's encephalo- pathy. However, as Harper (op. cit) points out, the fult-b40wn encephalopathy, with ataxia and ophthalmoplegia, is not always present and this can lead to diagnostic difficulty.

The relationship of Wernicke's encephalopathy to thiamin deficiency is explored by Wood et aL (op. cit. Table 5) and the association emerges clearly in their study. There are two comments one might make: first, that the precise role of Vitamin B12 deficiency in some cases of Wernicke's ence- phalopathy might merit further examination as suggested by Cole et a1.17; and second, that there may be (to judge from Blass and Gibson 18, and Leigh et a119) an abnormality in the enzyme transketolase in patients with the Wernicke-Korsakoff syndrome. If this is so, the significance of the 'TPP effect' (which can generally be accepted as a sensitive indicator of thiamin deficiency) may need re-evaluation in patients with abnormal transketolase. (If the addition of thiamin pyrophos- phate (TPP) to a red cell preparation enhances transketolase by more than 14%, then a TPP effect is said to be present.)

There must be very few psychiatrists in Australia who would doubt that the Wernicke-Korsakoff syndrome is a good deal more common here than elsewhere. Harper comes to this conclusion with respect to autopsy findings. Price and Theodoros 20 found a higher incidence of the Korsakoff syndrome in Queensland, and Wood and Breen21 indicate its higher incidence in Victoria and, to a lesser extent, in New Zealand, than is cited for the U.S. by Centrewall and Criqui22. European data are hard to get, perhaps because the Wernicke- Korsakoff syndrome is regarded there as a rarity (e.g. by Leigh et at23).

WHY IS THE W-K SYNDROME SO COMMON IN AUSTRALIA?

One possibility that needs to be considered is that the Wernicke-Korsakoff syndrome is more common in Australia than elsewhere because Australians drink more alcohol. Moser provides a tabulation showing that Australia is about half-way down a list of 25 countries in terms of alcohol con- sumption per member of the population over the age of 15

years. 24 Most European wine-drinking countries, such as France, Portugal, Spain and Italy, are higher than Australia on this list. Although data on the Wernicke-Korsakoff syndrome in these European countries is not available, Professor Griffith Edwards, in a personal communication to the author, has indicated his belief that the syndrome is a comparative rarity in these countries.

Death rates from cirrhosis of the liver are often quoted as giving some indication of the physical damage present in the community as a result of alcohol abuse. Cirrhosis death rates in the United States are nearly twice those in Australia, although, as has already been indicated, the Wernicke-Korsakoff syndrome is probably a good deal less common there. It must be admitted, however, that cirrhosis death rates are a very crude index of alcohol-related morbidity and appear to relate particularly to wine drinking. 25 Moreover, there is little hard data from many countries on the Wernicke-Korsakoff syndrome. Nevertheless, it seems very unlikely that the high incidence and prevalence of the Wemicke-Korsakoff syndrome in Australia simply reflects the high amount of alcohol consumed by Australians.

Table 1 gives some of the data we have assembled at Queensland's largest mental hospital, relating to marital status, gastrectomy and the Wernicke-Korsakoff syndrome (males only). 26 A special effort was made to collect Wernicke- Korsakoff patients with gastrectomy for this Table. Overall, approximately one-fifth of male W-K patients had undergone partial gastrectomy (not one-third, as Table 1 appears to indicate). There are two points worth noting in Table 1 : first, the excess of single men (except in those who have undergone gastrectomy) and, second, the excess of widowers.

Table 1: Marital status, gastrecotmy and the Wernicke- Korsakoff syndrome. 1

W-K, W-K, General no gastrectomy a gastrectomy population

Single 16 (40%) 2 (9%) 9.7%

Married/ Separated 12 (30%) 16 (73%) 84.8%

Widowers 12 (30%) 4 (18%) 5.5%

Totals 40 (100%) 22 (t00%) 254,738 (100%)

1. Male patients only, aged matched using 1976 Queens- land census data.

2. This column differs from each of the others at the 1% level of significance.

Our perusal of the records of Wernicke-Korsakoff patients indicates the frequent occurrence of three patterns, whose main characteristics are: 1. The patient with gastrectomy: The patient may have had

a gastrectomy in response to persistent ulcer symptoms, some of which may have been alcohol-induced. Such patients' demands for surgery may indicate their need for 'dramatic and strong solutions '27 to 'ulcer problems', and this attitude may determine subsequent abuse of alcohol to the point of brain damage. Some begin drinking and others increase drinking after gastrectomy. The families of these patients tend to be supportive and tolerant of the drinking. (These patients do not have a defect of thiamin absorption) .28

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2. The Iosec A variety of losses are included here (e.g. parent, spouse, job). A typic.at example, and the most frequent, is the widower: the wife of the social drinker dies. He responds by selling the family home and moving into a flat or unit. He increases his alcohol intake massively and develops a Wemicke-Korsakoff syndrome within two years of bereavement.

He does this at a time when he has excellent financial resources, so dietary neglect does not result simply from impoverishment due to excessive expenditure on alcohol. This type of patient seems particularly likely to enter a mental hospital, as the excess of widowers with the W-K syndrome was not found in W-K data obtained from general hospital admissions.

3. The single man: This man commences drinking often in adolescence and is a heavy social drinker in his early twenties. He is much more likely than not to be a beer drinker. At a time when other men are involved in courtship, marriage and raising a family, he has a social life which pivots around his drinking. At most of the places where he goes to enjoy the company of others, alcohol is available. There the Australian custom of 'shouting' frequently puts him under pressure to drink more than intended. 29 Females of marriageable age tend to avoid men who have a reputation for heavy drinking and the hotel then becomes fixed as the focal point of his social life.

Once there, he receives very little pressure to stop drinking. Other drinkers are tolerant and share his lack of concern about alcohol. Family pressure to stop drinking is ignored or may even increase his drinking. Employers are seldom concerned. If they are, as one alcoholic put it: "1 told him, 'You know what you can do with your job'." The death of parents and the unwillingness of remaining relatives to open their homes to an individual who is a heavy drinker, ultimately contributes to dietary neglect.

Price and Theodoros provide evidence that in the period just prior to the onset of Wernicke's encephaiopathy, beer was part, or all, of what was consumed in the way of alcoholic beverages by over half of those for whom this information was available. 3o Although Australia does not rank all that high in total per capita alcohol consumption, it does rank very high when it comes to beer drinking. For example, in 1972, the consumption of beer per head of the adult Australian population is given by Moser 31 as 228 litres, the highest figure of 15 countries included in her tabulation. Australia is regularly one of the top four countries in the world for beer drinking and was outranked in 1977 only by West Germany.32

Beer is, of course, a gaseous and relatively dilute alcoholic beverage. The beer drinker often reports that the large volume necessary to produce a pleasurable degree of intoxication during a bender induces a sense of gastric fullness which diminishes appetite. Food is avoided because previous experi- ence has ted him to conclude that if he eats, he will need more beer than he can consume without abdominal discomfort to maintain himself in a pleasurable state of intoxication. Further- more, beer drinkers often report that if they drink more than about 6 pints of beer, they lose all interest in eating.

FUTURE DEVELOPMENTS IN AUSTRALIA

It is difficult to predict whether or not there will be a downturn in the incidence of alcohol-related brain damage. The situation is subject to a very large number of pressures. The following are worth mention: the impact, if any, of increased public awareness of the problem; the impact, if any, of specific pre- ventive measures that may be introduced (for an example, see Price, elsewhere in this volume); an increased awareness by politicians, employers and insurers of the nature and sub-

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stantial extent of the problem and their response to this aware- ness; changes in drinking practices relating to economic conditions, and pressures from a variety of specially interested groups, including advertisers and the alcohol industry; and even the 'evolution of the ideal male Australian' to which Sargent33 refers.

One must beware of over-reliance on hospital statistics for assessing trends. The present policy of caring for those with alcohol-related brain damage increasingly within the com- munity may lead to an 'improvement' in hospital admission rates which merely reflects the unavailability of hospital beds for such individuals.

ACKNOWLEDGMENT

The author is grateful to Dr R.A. Kerr for his constructive criticism of this paper and for assistance with Table 1.

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9. Victor, M., Adams, R.D. & Collins, G.H., (1971), The Wernicke-Korsakoff syndrome, Contemporary Neurology Senes, Blackwell, Oxford.

10. Cutting, J. (1978), ibid. 11. Ron, M.A., (197-/), ibid. 12. .. (1979), ibid. 13. Eckardt, M.J., Parker, E.S., Noble, E.P., Feldman, D.J., &

Gottschalk, L.A. (1978), Biol. PsychiaL, 13: 551-565, 'Relationship between neuropsychological performance and alcohol consumption in alcoholics'.

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Stud. Alcohol, 33: 999-1019, 'Neuropsychological deficits associated with alcoholism'.

16. DSM III, (1980), Diagnostic and Statistical manual of mental disorders (3rd edition), American Psychiatric Association, Washington.

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18. Blass, J.P., & Gibson, G.E., (1977), New Eng/. J. Med., 297: 1367-1370. 'Abnormality of a thiamine-requiring enzyme in patients with Wemicke-Korsakoff syndrome'.

19. Leigh, D., McBumey, A., & Mcllwain, H. (1981a), Brit. J. Psychiat. 139: 156-159, 'Wemicke-Korsekoff syndrome in monozygotic twins: a biochemical peculiarity'.

20. Price, J. & Theodoros, M.T., (1979), Aust. N.Z.J. PsychiaL, 13: 315-320. 'The supplementation of alcoholic beverages with thiamine - - a necessary pre- ventive measure in Queensland'.

21. Wood, B.&Breen, K.J.,(1980),Med.J.Aust.,1:461-464 'Clinical thiamine deficiency in Australia: the size of the problem and approaches to prevention'.

22. Centrewail, B.S. & Criqui, MH. (1978), New Eng/. J. Med., 299: 285-289, 'Prevention of the Wemicke- Korsakoff syndrome'.

23. Leigh, D., McBurney, A., & Mcllwain, H. (1981b), Brit. J. Psychiat., 139: 153-156, 'Erythrocyte transketolase activity in the Wemicke-Korsakoff syndrome'.

24. Moser, J. (1974), Problems and programs related to alcohol and drug dependence, W.H.O., Geneva.

25. Whitlock, F.A., (1974), Quart. J. Stud. A/c., 35: 586--605, 'Liver cirrhosis, alcoholism and alcohol consumDtion'.

2 6 . P r ice , J. - - unpublished material 27. Viskum, K., (1975), Acta Psychiat, Scan., 51: 182-200.

'Mind and ulcer'. 28. Price, J. - - in preparation. 29. Sargent, M., (1979), Drinking and alcoholism in

Australia, Longman Cheshire, Melbourne. 30. Price, J. & Theodoros, M.T. (1979), ibid. 31. Moser, J. (1974),ibid. 32. British Brewers' Society, (1979) Auckland Star, 25th

January. 33. Sargant, M. (1979), ibid.

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