1019 gests that intermittent drug-free intervals in the course of chronic neuroleptic treatment might increase the likelihood that any emergent dyskinesia would be irreversible. This is a very important issue in the practical management of chronic psychotic patients and until further definitive work is done it is, I feel, inappropriate to advocate such an untested treatment strategy. M.R.C. Neurochemical Pharmacology Unit, Department of Pharmacology, Medical School,
University of Cambridge, Cambridge CB2 2QD
ANGUS V. P. MACKAY
PSYCHOMETRIC TESTING AND ALCOHOL-INDUCED BRAIN DAMAGE
SIR,—The observations made by Dr Lee and her colleagues (Oct. 13, p. 759) on the early onset of alcohol-induced intellectual impairment in young alcoholics and the absence of correlation with liver damage or cerebral atrophy are important and
valuable.
Though computerised tomography (CT) of the brain will indicate organic disease which has resulted in structural changes it is unlikely to show the diffuse abnormalities associated with early alcoholic brain damage. At this stage psychometric testing is the most objective technique available for detecting intellectual deficiences. On standard intelligence scales there is a well described subtest profile associated with early alcoholic brain disease with particular impairment of visual/spatial and visual/ motor coordination, visual memory, abstract reasoning, and problem-solving.1-3 In contrast vocabulary is well preserved and correlates well with premorbid intelligence.4 Poor scores on object assembly with good scores on picture arrangement on the Wechsler Adult Intelligence Scale (WAIS) are strongly suggestive of alcohol-induced intellectual impairment.1,5 When the assessment is made on a single occasion, though the test profile may suggest evidence of organic impairment it cannot be evidence of deterioration without baseline levels. Dr Lee and her colleagues state that 22/37 of their patients "showed signs of intellectual deterioration". Without serial assessments such a conclusion cannot be drawn. The evidence of a particular test pattern of intellectual impairment, especially when associated with a decline in work history and a level of functioning below that expected from previous educational achievements, is suggestive of deterioration but not conclusive. It is interesting that only 13/18 patients with CT evidence of cortical atrophy had psychometric signs of intellectual impairment.
Of the 37 patients studied, 22 were described as showing of intellectual deterioration on psychometric tests, 11 of these to the extent of being "occupationally disabled". In contrast 17 patients were thought to be intellectually impaired on clinical grounds, though only 10 of these coincided with those
signs
showing impairment on psychometric testing. In other words, 7 clinically impaired patients had normal psychometric tests and 12 with psychometric evidence of intellectual impairment were judged normal clinically. In the results section, when clinical assessment of symptoms and signs of dementia were the criteria, only 7 patients were judged intellectually impaired (is this figure correct?) and there was no correlation between the symptomatic assessment and psychometric testing. These figures raise two important points. Firstly, are psychometric tests and clinical judgment assessing the same thing? Secondly, if they are, is one or other of them rather bad at it? 1. Wechsler D. The measurement and appraisal of adult intelligence, 4th ed. Baltimore: Williams and Wilkins, 1958. 2. Jones B, Parsons OA. Specific VS generalised deficits of abstractive ability in chronic alcoholics. Arch Gen Psychiat 1972; 26: 380-84. 3. Kleinknecht R, Goldstein S. Neuropsychological deficits associated with alcoholism. Quart J Studies Alcohol 1972; 33: 999-1019. 4. Rabin AI. Diagnostic use of intelligence tests. In: Wolman BB, ed. Handbook of clinical psychology. New York: McGraw-Hill, 1965. 5. Clarke J, Haughton H. A study of intellectual impairment and recovery rates in heavy drinkers in Ireland. Br J Psychiat 1975; 126: 178-84.
Clinical judgment of the symptoms and signs of intellectual impairment is extremely subjective and often unreliable. Psychometric testing uses standard criteria in a reproducible way to compare with well-documented profiles found in various forms of brain damage. There may still be room for improvement but this study suggests that clinical assessment alone may be of no value in identifying the high-risk patient without evidence of liver damage or cerebral atrophy early in his progress to irreversible5 brain damage. The use in the at-risk population of a small group of psychometric tests which are good discriminators of the early stages of impairment may help to prevent further brain damage and to enable these pateints to be weaned from alcohol before the onset of liver damage. Department of Gastroenterology, Central Middlesex Hospital, London NW10
RODNEY H. TAYLOR
SIR,—In their paper on alcoholic brain damage and liver damage (Oct. 13, p. 759) Dr Lee and colleagues imply that previous workers had overlooked the fact that brain damage is than cirrhosis. They also suggest that undue attention has been given to radiological measures of brain damage commoner
(pneumoencephalography, computerised tomographic scans) compared with psychological ones. Although they refer to a paper by me and Dr Lance Perrett,l their remarks indicate that they have not read it carefully. We did both pneumoencephalography and psychometric tests on 33 patients and found, as have several others before and since, that brain damage is the rule rather than the exception in alcoholism. At the time, I think that ours was the largest reported series in which both radiological and psychometric examination were used, and, while we felt that each method could provide useful information, we specifically stated that "The combination is superior to either method used
singly". In our series "only one patient... showed evidence of clinically significant liver damage, although many showed mild and usually transient abnormalities of liver function tests". Since our patients were older than Lee’s, the rarity of cirrhosis is even more significant. Perhaps Lee et al. should have provided more clinical and biochemical information: the practical importance and impact of cirrhosis among their patients is surely not restricted to histological changes. Lee et al. found no correlation between the degrees of cerebral atrophy and of psychometric impairment, and suggest that psychometry alone suffices. Other studies are less dogmatic. We found a significant correlation, especially with cortical atrophy, and S. Borg, at the symposium on Biochemical Aspects of Dependence and Brain Damage (Oxford, September, 1979) reported similar findings. W. A. Lishman found a poor correlation, which is further complicated by variations in the CT scan results depending on the length of the drying-out period. In the present state of knowledge-and with competent psychologists so scarce-I think it is wiser to retain both
methods.
Although brain damage can be, as Lee et al. say, a devastating complication, and may well carry an adverse prognosis, the long-term follow-up of my series suggests that it is not always disastrous (unpublished). Lee et al., our paper,’ and R. E. Tarter at the Oxford symposium provide evidence that the frontal cortex is especially prone to alcoholic atrophy, and that alcoholics may therefore give themselves a kind of "chemical leucotomy". Is it possible that some patients function better if they are relieved of certain inhibitions and anxieties which perhaps only those with intact frontal lobes can fully appreciate? 14A Abercorn Place, London NW8 1. Brewer C, Perrett L. Brain
COLIN BREWER
damage due to alcohol consumption: an encephalographic, psychometric and EEG study. Br J Addict 1971; 170-82.
air66:
University of Cambridge, Cambridge CB2 2QD
ANGUS V. P. MACKAY
PSYCHOMETRIC TESTING AND ALCOHOL-INDUCED BRAIN DAMAGE
SIR,—The observations made by Dr Lee and her colleagues (Oct. 13, p. 759) on the early onset of alcohol-induced intellectual impairment in young alcoholics and the absence of correlation with liver damage or cerebral atrophy are important and
valuable.
Though computerised tomography (CT) of the brain will indicate organic disease which has resulted in structural changes it is unlikely to show the diffuse abnormalities associated with early alcoholic brain damage. At this stage psychometric testing is the most objective technique available for detecting intellectual deficiences. On standard intelligence scales there is a well described subtest profile associated with early alcoholic brain disease with particular impairment of visual/spatial and visual/ motor coordination, visual memory, abstract reasoning, and problem-solving.1-3 In contrast vocabulary is well preserved and correlates well with premorbid intelligence.4 Poor scores on object assembly with good scores on picture arrangement on the Wechsler Adult Intelligence Scale (WAIS) are strongly suggestive of alcohol-induced intellectual impairment.1,5 When the assessment is made on a single occasion, though the test profile may suggest evidence of organic impairment it cannot be evidence of deterioration without baseline levels. Dr Lee and her colleagues state that 22/37 of their patients "showed signs of intellectual deterioration". Without serial assessments such a conclusion cannot be drawn. The evidence of a particular test pattern of intellectual impairment, especially when associated with a decline in work history and a level of functioning below that expected from previous educational achievements, is suggestive of deterioration but not conclusive. It is interesting that only 13/18 patients with CT evidence of cortical atrophy had psychometric signs of intellectual impairment.
Of the 37 patients studied, 22 were described as showing of intellectual deterioration on psychometric tests, 11 of these to the extent of being "occupationally disabled". In contrast 17 patients were thought to be intellectually impaired on clinical grounds, though only 10 of these coincided with those
signs
showing impairment on psychometric testing. In other words, 7 clinically impaired patients had normal psychometric tests and 12 with psychometric evidence of intellectual impairment were judged normal clinically. In the results section, when clinical assessment of symptoms and signs of dementia were the criteria, only 7 patients were judged intellectually impaired (is this figure correct?) and there was no correlation between the symptomatic assessment and psychometric testing. These figures raise two important points. Firstly, are psychometric tests and clinical judgment assessing the same thing? Secondly, if they are, is one or other of them rather bad at it? 1. Wechsler D. The measurement and appraisal of adult intelligence, 4th ed. Baltimore: Williams and Wilkins, 1958. 2. Jones B, Parsons OA. Specific VS generalised deficits of abstractive ability in chronic alcoholics. Arch Gen Psychiat 1972; 26: 380-84. 3. Kleinknecht R, Goldstein S. Neuropsychological deficits associated with alcoholism. Quart J Studies Alcohol 1972; 33: 999-1019. 4. Rabin AI. Diagnostic use of intelligence tests. In: Wolman BB, ed. Handbook of clinical psychology. New York: McGraw-Hill, 1965. 5. Clarke J, Haughton H. A study of intellectual impairment and recovery rates in heavy drinkers in Ireland. Br J Psychiat 1975; 126: 178-84.
Clinical judgment of the symptoms and signs of intellectual impairment is extremely subjective and often unreliable. Psychometric testing uses standard criteria in a reproducible way to compare with well-documented profiles found in various forms of brain damage. There may still be room for improvement but this study suggests that clinical assessment alone may be of no value in identifying the high-risk patient without evidence of liver damage or cerebral atrophy early in his progress to irreversible5 brain damage. The use in the at-risk population of a small group of psychometric tests which are good discriminators of the early stages of impairment may help to prevent further brain damage and to enable these pateints to be weaned from alcohol before the onset of liver damage. Department of Gastroenterology, Central Middlesex Hospital, London NW10
RODNEY H. TAYLOR
SIR,—In their paper on alcoholic brain damage and liver damage (Oct. 13, p. 759) Dr Lee and colleagues imply that previous workers had overlooked the fact that brain damage is than cirrhosis. They also suggest that undue attention has been given to radiological measures of brain damage commoner
(pneumoencephalography, computerised tomographic scans) compared with psychological ones. Although they refer to a paper by me and Dr Lance Perrett,l their remarks indicate that they have not read it carefully. We did both pneumoencephalography and psychometric tests on 33 patients and found, as have several others before and since, that brain damage is the rule rather than the exception in alcoholism. At the time, I think that ours was the largest reported series in which both radiological and psychometric examination were used, and, while we felt that each method could provide useful information, we specifically stated that "The combination is superior to either method used
singly". In our series "only one patient... showed evidence of clinically significant liver damage, although many showed mild and usually transient abnormalities of liver function tests". Since our patients were older than Lee’s, the rarity of cirrhosis is even more significant. Perhaps Lee et al. should have provided more clinical and biochemical information: the practical importance and impact of cirrhosis among their patients is surely not restricted to histological changes. Lee et al. found no correlation between the degrees of cerebral atrophy and of psychometric impairment, and suggest that psychometry alone suffices. Other studies are less dogmatic. We found a significant correlation, especially with cortical atrophy, and S. Borg, at the symposium on Biochemical Aspects of Dependence and Brain Damage (Oxford, September, 1979) reported similar findings. W. A. Lishman found a poor correlation, which is further complicated by variations in the CT scan results depending on the length of the drying-out period. In the present state of knowledge-and with competent psychologists so scarce-I think it is wiser to retain both
methods.
Although brain damage can be, as Lee et al. say, a devastating complication, and may well carry an adverse prognosis, the long-term follow-up of my series suggests that it is not always disastrous (unpublished). Lee et al., our paper,’ and R. E. Tarter at the Oxford symposium provide evidence that the frontal cortex is especially prone to alcoholic atrophy, and that alcoholics may therefore give themselves a kind of "chemical leucotomy". Is it possible that some patients function better if they are relieved of certain inhibitions and anxieties which perhaps only those with intact frontal lobes can fully appreciate? 14A Abercorn Place, London NW8 1. Brewer C, Perrett L. Brain
COLIN BREWER
damage due to alcohol consumption: an encephalographic, psychometric and EEG study. Br J Addict 1971; 170-82.
air66:
