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Regional cerebral blood flow during alcoholic blackout
Psychiatry
49
Research. 21,49-54
Elsevier
Regional Cerebral Blood Flow During Alcoholic Mats Berglund,
lsak Prohovnik,
Blackout
and Jar1 Risberg
Received April 29, 1987; first revised version received version received August I, 1988; accepted November
September 7. 1988.
23. 1987; second revised
Abstract. Regional cerebral blood flow was measured during alcoholic blackout in a 61-year-old man with a blood-alcohol level of 0.389& The mean flow level was found to be elevated by about 30-60% compared to repeated studies during long-term abstinence. The regional pattern did not change greatly. Increases of mean regional cerebral blood flow have previously been reported during social drinking and in Wernicke-Korsakoff’s syndrome. A common disturbance of subcortical activation systems is hypothesized.
Key Words. Alcoholism,
blackout,
regional cerebral blood flow, xenon inhalation.
The alcoholic blackout is an important phenomenon both for the clinical evaluation of alcoholism and for the understanding of memory mechanisms. The phenomenon is characterized by amnesia which has a definite starting point and in which memory loss for significant events results in a sense of “lost time.” Memory loss is total and seemingly permanent (Goodwin et al., 1969a). The blackout has been experimentally related to a rapid rise in the blood-alcohol level (Goodwin et al., 19696; Ryback, 1970) but not to memory functioning in the sober state (Tarter and Schneider, 1976). Heber and Kryspin-Exner (1966) found no obvious differences in the electroencephalogram (EEG) during alcoholic intoxication between alcoholics with blackouts (n = 11) and those without (n = 22). This is a case report of regional cerebral blood flow in one alcoholic during a blackout state.
Methods Regional cerebral blood flow (rCBF) was measured by the ‘33Xe inhalation technique (Obrist et al., 1975; Risberg et al., 1975; Risberg, 1980). The patient inhaled 13’Xe mixed with air (3 mCi/l) for I min by means of a face mask and a rebreathing system. The I-min inhalation period was followed by IO min of normal air-breathing. The gamma radiation was recorded by 32 scintillation detectors (3/4” X 3/4” Nal [Tl] crystals; Novo Diagnostic Systems, Denmark) placed in parallel at right angles to both lateral surfaces of the head. The radiation from a continuous sample of the expired air was recorded by a separate detector for determination of
Mats Berglund, M.D., is in the Department of Alcohol Diseases, Malmii General Hospital, Malmo, Sweden. lsak Prohovnik, Ph.D., is in the Department of Biological Psychiatry, Columbia Presbyterian Medical Center, New York, NY, USA. Jarl Risberg, Ph.D., is in the Department of Psychiatry I., University Hospital, Lund, Sweden. (Reprint requests to Dr. M. Berglund, Department of Alcohol Diseases, Malmd General Hospital, S-214 01 Malmii, Sweden.) 01651781/89/$03.50
@ 1989 Elsevier Scientific
Publishers Ireland
Ltd.
50 end-tidal concentrations of r3’Xe (the “air curve”) used to correct the “head curves” for recirculation of the tracer. The results presented here are based on the initial slope index (ISI), a parameter dominated by gray matter blood flow. The arterial pC0, was estimated from recordings of end-tidal CO, concentrations (Beckman, LB2-analyzer). The subject was studied with closed eyes and was told not to fall asleep. Noise levels were kept to a minimum. Case Report. The patient was a 6l-year-old man who had abused alcohol for 25 years and was alcohol dependent according to DSM-III(American Psychiatric Association, 1980). He had never previously had alcohol withdrawal delirium or epileptic seizures during abstinence. He had had no severe physical complications from his abuse. The patient had been examined I year previously with rCBF measurements on four different occasions during a study of the first 7 weeks of the abstinence period (Berglund et al., 1987). Measurements were done after I, 3, 5, and 7 weeks of abstinence. During that time, the patient was not receiving psychopharmacological treatment. He had no obvious cerebral impairment and performed within the lower half of alcoholic subjects in the psychometric tests used (Trail A, Trail B., Digit Symbol). The investigator was the same at both examinations (M.B.). At the time of the current admission, the patient was clearly intoxicated, but his speech was coherent and he cooperated well during the rCBF measurement. His blood-alcohol level was 0.38% (breath analyzer). The patient received no psychopharmacological treatment before the rCBF measurement. Twelve hours after the examination, he had a total amnesia for the 2-3 hours around the time of the examination. His memory of the rCBF examination never returned. The next 2 days, the patient had rCBF examinations after medication with melperonhydrochloride (75 ml) and carbamazepine (600 mg). He left the ward 2 days later in good condition. He had mild withdrawal symptoms but no hallucinations, epileptic seizures, or clouding of the sensorium. A few months after the examination, he suffered a stroke resulting in continuing disability. It was therefore not meaningful to do any additional rCBF studies.
Results Results from the seven rCBF measurements are presented in Fig. I and compared to normative data from 33 healthy nonalcoholic males with a mean age of 59 years (Hagstadius and Risberg, in press). During the blackout state the average ISI was 53, > I SD above the mean of normal controls. This value was 32-61% higher than the other mean rCBF values recorded in the patients. The results during withdrawal and abstinence showed values around I SD below the normal mean. In the present study the rCBF values were not corrected to those of a standard pC02 of 40 mmHg. With The such a correction (Maximilian et al., 1980) the increase would be 25-46s. finding is thus not greatly changed by the pC0, correction. The regional CBF variations, expressed as yc of the hemispheric mean, are shown in Fig. 2. Fig. 3 shows the differences between the patient’s patterns and the pattern of the normal control group. Although the differences are not statistically significant, some interesting trends appear. The blackout state seems to be characterized by higher than normal distribution values in temporal and superior frontal regions, while lower values are seen in basal frontal and occipital areas. The patient’s pattern during non-blackout states is characterized by low frontal and high posterior values as compared to normal controls.
51
Fig. 1. Mean regional cerebral blood flow during the blackout state (filled circle) and during l-7 weeks of abstinence (open circles) B.K. d 61~
ISI 55
0
0
40-1st)
0
0
-________________________________~-------
xi-
0
0 0
0
3oL
01ays Pm2
34
31
32
0I
1* 38
1 31 1 51 * 33
32
71) weeks 33
The solid line indicates the mean of a normal reference group of similar age (Hagstadius and Risberg, 19137)and the interrupted lines f 1 SD. The flow values are not corrected for variations of pCOt. shown in the lower part of the figure.
Fig. 2. Regional cerebral blood flow during the blackout state and after 7 weeks of abstinence Blackout
-25%
BAL 38%
No Blackout
+25%
31
The clock symbols should be read as follows: 12 o’clock denotes mean hemispheric value as indicated in boxes. Black markings denote a regional value above the mean value and striped field denotes a value below the mean (9tY = 25%). The regional patterns were similar. The somewhat higher relative frontal flows during the blackout state are not significantly different from the other measurements. ISI = initial slope index. BAL = blood-alcohol level.
52
Fig. 3. Differences between the regional cerebral blood flow distributions of the patient and the normal reference group Blackout
No Blackout
Lt
Black indicates higher values for the patient and striped, lower. Note that 180% now denotes 25%. White or black line indicates 1 SD for regional group data in those regions with a deviation > 1 SD.
Discussion It was possible to make technically perfect measuremen:a during the blackout state. The main reason for this was that the patient had been examined previously. In most cases, it is probably not possible to examine alcoholics during blarkout with the rCBF technique, because the patient has to lie on his back without moving his head for I1 min. Our first main finding was that the patient had a large increase in mean rCBF during blackout compared with his own values during abstinence and also in comparison with normal values. The difference between blackout and non-blackout values (32-6 1%) is larger than the 5- 15% global increase commonly found in normal subjects during mental activation (Risberg, 1980). Investigators using the Kety-Schmidt-technique for measuring global CBF (Hine et al., 1952; Battey et al., 1953; Sutherland et al., 1960) have reported that CBF in some subjects increased while that in others decreased when they drank moderate amounts of alcohol. Battey et al. (1953) reported that low doses of alcohol given intravenously did not influence CBF or cerebral oxygen consumption. Larger doses of alcohol in alcoholics (blood-alcohol level = 0.3%) were, however, associated with a decrease of cerebral oxygen consumption and an increase of global CBF in line with our findings. Our results also corroborate the findings of Newlin et al. (1982) who studied rCBF with the l)“Xe inhalation technique in 10 social drinkers first in a sober condition and then after consumption of alcohol (0.75 g/kg), yielding a blood-alcohol level of 0.05%. They reported a 20% increase of cortical gray matter flow after drinking. The study by Battey et al. (1953) included seven patients who were examined in a
53
“stuporous state.” An average CBF increase of 42% was reported while the cerebral oxygen consumption (CMRO,) was normal. The blood-alcohol level was 0.32%. It is possible that these patients were studied during blackout states. The results are in agreement with ours. A phenomenological similarity between the alcoholic blackout state and the chronic state of Wernicke-Korsakoffs syndrome has been noted by Ryback (197 1). Both states are characterized by a severe deficit in short-term memory. Simard et al. (1971) described three cases of chronic states of Wernicke-Korsakoff’s syndrome who underwent rCBF examinations. One case had a mean rCBF increase of 25-65% and another had an increase of CMRO,? of 25%. Berglund and lngvar (1976) reported higher,mean rCBF values in seven cases of Wernicke-Korsakoff’s syndrome compared with alcoholics. Thus, there are rCBF similarities in blackout states and in chronic states of Wernicke-Korsakoffs syndrome. It is possible that the general activation system of the brain is disturbed in both states. In Wernicke-Korsakoffs syndrome, these disturbances are probably in the dorsal medial part of thalamus while the localization of disturbance during the blackout state is not known. A similar localization to that for Wernicke-Korsakoffs syndrome has been suggested (Ryback, 1971) with the disturbance possibly reflecting rapid changes of the blood-alcohol concentration level. The regional CBF findings were not statistically significant, but the trends noted (Figs. 2 and 3) still merit comment. The tendency for CBF in temporal areas to be more elevated during blackout is of interest in light of the well-known coupling between temporal
this area and memory functions. hyperfunction and dysfunction.
of abstinence
are less surprising;
has been reported
CBF in frontal et al., 1987).
decreased
earlier (Berglund
The blackout state might thus be linked to The low frontal values seen after 7 weeks
areas in chronic
alcoholics
Acknowledgments. The study was supported by the Swedish Medical Research Council (grants 4969 and 7099) and the Swedish Council for Planning and Coordination of Research.
References American Psychiatric Association. DSM-III: Diagnostic and Statistical Manual of Mental Disorders. 3rd ed. Washington, DC: APA, 1980. Battey, L.L.; Heyman, A.; and Patterson, J.L. Jr. Effects of ethyl alcohol on cerebral blood flow and metabolism. Journal of the American Medical Association, I52:6- IO, 1953. Berglund, M.; Hagstadius, S.; Risberg, J.; Johanson, M.; Bliding, A.; and Mubrin, Z. Normalization of regional cerebral blood flow in alcoholics during the first seven weeks of abstinence. Acta Psychiatrica Scandinavica, 75:202-208, 1987. Berglund, M., and Ingvar, D.H. Cerebral blood flow and its regional distribution in alcoholism and in Korsakoffs psychosis. Journal of Studies on Alcohol, 37586-597, 1976. Goodwin, D.W.; Crane, J.B.; and Guze, S.B. Phenomenological aspects of the alcoholic “blackout.” British Journal of Psychiatry, I 15: 1033-1038, 1969a. Goodwin, D.W.; Powell, B.; Bremer, D.; Hoine, H.; and Stern, J. Alcohol and recall: Statedependent effects in man. Science, 163: 1358-l 360, 19696). Hagstadius, S., and Risberg, J. Regional cerebral blood flow characteristics and variations with age in resting normal subjects. Brain and Cognition, in press. Heber, G., and Kryspin-Exner, K. Experimentelle Untersuchungen zur Frage der sogenannten Palimpseste bei Alkoholkranken. Wiener Zeitschrifi fir Nervenheilkunde. 24~2 19-226, 1966.
54
Hine, B.C.; Schick, A.F.; Margolis, L.; Burbridge, N.; and Simon, A. Effects of alcohol in small doses and tetraethylthiuramdisulphide (Antabus) on the cerebral blood flow and cerebral metabolism. Journal of’ Pharmacology and Experimental Therapeutics, IO6:253-260,
1952. Maximilian, V.A.; Prohovnik, I.; and Risberg, J. Cerebral hemodynamic response to mental activation in normo- and hypercapnia. Stroke, I 1:342-347, 1980. Newlin, D.B.; Golden, C.J.; Quaife, M.; and Graber, B. Effects of alcohol ingestion on regional cerebral blood flow. International Journal oJ’ Neuroscience, 17: l45- 150, 1982. Obrist, W.D.; Thompson, H.K.; Wang, H.S.; and Wilkinson, W.E. Regional cerebral blood flow estimated by rr”Xe-inhalation. Stroke, 6:245-256, 1975. Risberg, J. Regional cerebral blood flow measurements by 133xenon inhalation: Methodology and applications in neuropsychology and psychiatry. Brain and Language.
9:9-34, 1980. Risberg, J.; Ali, Z.; Wilson, E.M.; Wills, E.L.; and Halsey, J.H. Regional cerebral blood flow by 133xenon inhalation: Preliminary evaluation of an initial slope index in patients with unstable flow compartments. Stroke, 6:142-148, 1975. Ryback, R.S. Alcohol amnesia: Observations in seven drinking inpatient alcoholics. Quarterly Journal oJ’Studies on Alcohol, 3 I :6 16-632, 1970. Ryback, R.S. The continuum and specificity of the effects of alcohol on memory. Quarterly Journal of Studies on Alcohol, 32:995-IO 16, I97 I. Simard, D.; Olesen, J.; Paulson, O.B.; Lassen, N.A.; and Skinhbj, E. Regional cerebral blood flow and its regulation in dementia. Brain. 94:273-288, I97 I. Sutherland, V.C.; Burbridge, T.N.; Adams, J.E.; and Simon, A. Cerebral metabolism in problem drinkers under the influence of alcohol and chlorpromazine hydrochloride. Journal of Applied Physiology, 15: I89- 196, 1960. Tarter, R.E., and Schneider, D.U. Blackouts: Relationship with memory capacity and alcoholism history. Archives of’ General Psychiatry, 33: I492- 1496, 1976.
49
Research. 21,49-54
Elsevier
Regional Cerebral Blood Flow During Alcoholic Mats Berglund,
lsak Prohovnik,
Blackout
and Jar1 Risberg
Received April 29, 1987; first revised version received version received August I, 1988; accepted November
September 7. 1988.
23. 1987; second revised
Abstract. Regional cerebral blood flow was measured during alcoholic blackout in a 61-year-old man with a blood-alcohol level of 0.389& The mean flow level was found to be elevated by about 30-60% compared to repeated studies during long-term abstinence. The regional pattern did not change greatly. Increases of mean regional cerebral blood flow have previously been reported during social drinking and in Wernicke-Korsakoff’s syndrome. A common disturbance of subcortical activation systems is hypothesized.
Key Words. Alcoholism,
blackout,
regional cerebral blood flow, xenon inhalation.
The alcoholic blackout is an important phenomenon both for the clinical evaluation of alcoholism and for the understanding of memory mechanisms. The phenomenon is characterized by amnesia which has a definite starting point and in which memory loss for significant events results in a sense of “lost time.” Memory loss is total and seemingly permanent (Goodwin et al., 1969a). The blackout has been experimentally related to a rapid rise in the blood-alcohol level (Goodwin et al., 19696; Ryback, 1970) but not to memory functioning in the sober state (Tarter and Schneider, 1976). Heber and Kryspin-Exner (1966) found no obvious differences in the electroencephalogram (EEG) during alcoholic intoxication between alcoholics with blackouts (n = 11) and those without (n = 22). This is a case report of regional cerebral blood flow in one alcoholic during a blackout state.
Methods Regional cerebral blood flow (rCBF) was measured by the ‘33Xe inhalation technique (Obrist et al., 1975; Risberg et al., 1975; Risberg, 1980). The patient inhaled 13’Xe mixed with air (3 mCi/l) for I min by means of a face mask and a rebreathing system. The I-min inhalation period was followed by IO min of normal air-breathing. The gamma radiation was recorded by 32 scintillation detectors (3/4” X 3/4” Nal [Tl] crystals; Novo Diagnostic Systems, Denmark) placed in parallel at right angles to both lateral surfaces of the head. The radiation from a continuous sample of the expired air was recorded by a separate detector for determination of
Mats Berglund, M.D., is in the Department of Alcohol Diseases, Malmii General Hospital, Malmo, Sweden. lsak Prohovnik, Ph.D., is in the Department of Biological Psychiatry, Columbia Presbyterian Medical Center, New York, NY, USA. Jarl Risberg, Ph.D., is in the Department of Psychiatry I., University Hospital, Lund, Sweden. (Reprint requests to Dr. M. Berglund, Department of Alcohol Diseases, Malmd General Hospital, S-214 01 Malmii, Sweden.) 01651781/89/$03.50
@ 1989 Elsevier Scientific
Publishers Ireland
Ltd.
50 end-tidal concentrations of r3’Xe (the “air curve”) used to correct the “head curves” for recirculation of the tracer. The results presented here are based on the initial slope index (ISI), a parameter dominated by gray matter blood flow. The arterial pC0, was estimated from recordings of end-tidal CO, concentrations (Beckman, LB2-analyzer). The subject was studied with closed eyes and was told not to fall asleep. Noise levels were kept to a minimum. Case Report. The patient was a 6l-year-old man who had abused alcohol for 25 years and was alcohol dependent according to DSM-III(American Psychiatric Association, 1980). He had never previously had alcohol withdrawal delirium or epileptic seizures during abstinence. He had had no severe physical complications from his abuse. The patient had been examined I year previously with rCBF measurements on four different occasions during a study of the first 7 weeks of the abstinence period (Berglund et al., 1987). Measurements were done after I, 3, 5, and 7 weeks of abstinence. During that time, the patient was not receiving psychopharmacological treatment. He had no obvious cerebral impairment and performed within the lower half of alcoholic subjects in the psychometric tests used (Trail A, Trail B., Digit Symbol). The investigator was the same at both examinations (M.B.). At the time of the current admission, the patient was clearly intoxicated, but his speech was coherent and he cooperated well during the rCBF measurement. His blood-alcohol level was 0.38% (breath analyzer). The patient received no psychopharmacological treatment before the rCBF measurement. Twelve hours after the examination, he had a total amnesia for the 2-3 hours around the time of the examination. His memory of the rCBF examination never returned. The next 2 days, the patient had rCBF examinations after medication with melperonhydrochloride (75 ml) and carbamazepine (600 mg). He left the ward 2 days later in good condition. He had mild withdrawal symptoms but no hallucinations, epileptic seizures, or clouding of the sensorium. A few months after the examination, he suffered a stroke resulting in continuing disability. It was therefore not meaningful to do any additional rCBF studies.
Results Results from the seven rCBF measurements are presented in Fig. I and compared to normative data from 33 healthy nonalcoholic males with a mean age of 59 years (Hagstadius and Risberg, in press). During the blackout state the average ISI was 53, > I SD above the mean of normal controls. This value was 32-61% higher than the other mean rCBF values recorded in the patients. The results during withdrawal and abstinence showed values around I SD below the normal mean. In the present study the rCBF values were not corrected to those of a standard pC02 of 40 mmHg. With The such a correction (Maximilian et al., 1980) the increase would be 25-46s. finding is thus not greatly changed by the pC0, correction. The regional CBF variations, expressed as yc of the hemispheric mean, are shown in Fig. 2. Fig. 3 shows the differences between the patient’s patterns and the pattern of the normal control group. Although the differences are not statistically significant, some interesting trends appear. The blackout state seems to be characterized by higher than normal distribution values in temporal and superior frontal regions, while lower values are seen in basal frontal and occipital areas. The patient’s pattern during non-blackout states is characterized by low frontal and high posterior values as compared to normal controls.
51
Fig. 1. Mean regional cerebral blood flow during the blackout state (filled circle) and during l-7 weeks of abstinence (open circles) B.K. d 61~
ISI 55
0
0
40-1st)
0
0
-________________________________~-------
xi-
0
0 0
0
3oL
01ays Pm2
34
31
32
0I
1* 38
1 31 1 51 * 33
32
71) weeks 33
The solid line indicates the mean of a normal reference group of similar age (Hagstadius and Risberg, 19137)and the interrupted lines f 1 SD. The flow values are not corrected for variations of pCOt. shown in the lower part of the figure.
Fig. 2. Regional cerebral blood flow during the blackout state and after 7 weeks of abstinence Blackout
-25%
BAL 38%
No Blackout
+25%
31
The clock symbols should be read as follows: 12 o’clock denotes mean hemispheric value as indicated in boxes. Black markings denote a regional value above the mean value and striped field denotes a value below the mean (9tY = 25%). The regional patterns were similar. The somewhat higher relative frontal flows during the blackout state are not significantly different from the other measurements. ISI = initial slope index. BAL = blood-alcohol level.
52
Fig. 3. Differences between the regional cerebral blood flow distributions of the patient and the normal reference group Blackout
No Blackout
Lt
Black indicates higher values for the patient and striped, lower. Note that 180% now denotes 25%. White or black line indicates 1 SD for regional group data in those regions with a deviation > 1 SD.
Discussion It was possible to make technically perfect measuremen:a during the blackout state. The main reason for this was that the patient had been examined previously. In most cases, it is probably not possible to examine alcoholics during blarkout with the rCBF technique, because the patient has to lie on his back without moving his head for I1 min. Our first main finding was that the patient had a large increase in mean rCBF during blackout compared with his own values during abstinence and also in comparison with normal values. The difference between blackout and non-blackout values (32-6 1%) is larger than the 5- 15% global increase commonly found in normal subjects during mental activation (Risberg, 1980). Investigators using the Kety-Schmidt-technique for measuring global CBF (Hine et al., 1952; Battey et al., 1953; Sutherland et al., 1960) have reported that CBF in some subjects increased while that in others decreased when they drank moderate amounts of alcohol. Battey et al. (1953) reported that low doses of alcohol given intravenously did not influence CBF or cerebral oxygen consumption. Larger doses of alcohol in alcoholics (blood-alcohol level = 0.3%) were, however, associated with a decrease of cerebral oxygen consumption and an increase of global CBF in line with our findings. Our results also corroborate the findings of Newlin et al. (1982) who studied rCBF with the l)“Xe inhalation technique in 10 social drinkers first in a sober condition and then after consumption of alcohol (0.75 g/kg), yielding a blood-alcohol level of 0.05%. They reported a 20% increase of cortical gray matter flow after drinking. The study by Battey et al. (1953) included seven patients who were examined in a
53
“stuporous state.” An average CBF increase of 42% was reported while the cerebral oxygen consumption (CMRO,) was normal. The blood-alcohol level was 0.32%. It is possible that these patients were studied during blackout states. The results are in agreement with ours. A phenomenological similarity between the alcoholic blackout state and the chronic state of Wernicke-Korsakoffs syndrome has been noted by Ryback (197 1). Both states are characterized by a severe deficit in short-term memory. Simard et al. (1971) described three cases of chronic states of Wernicke-Korsakoff’s syndrome who underwent rCBF examinations. One case had a mean rCBF increase of 25-65% and another had an increase of CMRO,? of 25%. Berglund and lngvar (1976) reported higher,mean rCBF values in seven cases of Wernicke-Korsakoff’s syndrome compared with alcoholics. Thus, there are rCBF similarities in blackout states and in chronic states of Wernicke-Korsakoffs syndrome. It is possible that the general activation system of the brain is disturbed in both states. In Wernicke-Korsakoffs syndrome, these disturbances are probably in the dorsal medial part of thalamus while the localization of disturbance during the blackout state is not known. A similar localization to that for Wernicke-Korsakoffs syndrome has been suggested (Ryback, 1971) with the disturbance possibly reflecting rapid changes of the blood-alcohol concentration level. The regional CBF findings were not statistically significant, but the trends noted (Figs. 2 and 3) still merit comment. The tendency for CBF in temporal areas to be more elevated during blackout is of interest in light of the well-known coupling between temporal
this area and memory functions. hyperfunction and dysfunction.
of abstinence
are less surprising;
has been reported
CBF in frontal et al., 1987).
decreased
earlier (Berglund
The blackout state might thus be linked to The low frontal values seen after 7 weeks
areas in chronic
alcoholics
Acknowledgments. The study was supported by the Swedish Medical Research Council (grants 4969 and 7099) and the Swedish Council for Planning and Coordination of Research.
References American Psychiatric Association. DSM-III: Diagnostic and Statistical Manual of Mental Disorders. 3rd ed. Washington, DC: APA, 1980. Battey, L.L.; Heyman, A.; and Patterson, J.L. Jr. Effects of ethyl alcohol on cerebral blood flow and metabolism. Journal of the American Medical Association, I52:6- IO, 1953. Berglund, M.; Hagstadius, S.; Risberg, J.; Johanson, M.; Bliding, A.; and Mubrin, Z. Normalization of regional cerebral blood flow in alcoholics during the first seven weeks of abstinence. Acta Psychiatrica Scandinavica, 75:202-208, 1987. Berglund, M., and Ingvar, D.H. Cerebral blood flow and its regional distribution in alcoholism and in Korsakoffs psychosis. Journal of Studies on Alcohol, 37586-597, 1976. Goodwin, D.W.; Crane, J.B.; and Guze, S.B. Phenomenological aspects of the alcoholic “blackout.” British Journal of Psychiatry, I 15: 1033-1038, 1969a. Goodwin, D.W.; Powell, B.; Bremer, D.; Hoine, H.; and Stern, J. Alcohol and recall: Statedependent effects in man. Science, 163: 1358-l 360, 19696). Hagstadius, S., and Risberg, J. Regional cerebral blood flow characteristics and variations with age in resting normal subjects. Brain and Cognition, in press. Heber, G., and Kryspin-Exner, K. Experimentelle Untersuchungen zur Frage der sogenannten Palimpseste bei Alkoholkranken. Wiener Zeitschrifi fir Nervenheilkunde. 24~2 19-226, 1966.
54
Hine, B.C.; Schick, A.F.; Margolis, L.; Burbridge, N.; and Simon, A. Effects of alcohol in small doses and tetraethylthiuramdisulphide (Antabus) on the cerebral blood flow and cerebral metabolism. Journal of’ Pharmacology and Experimental Therapeutics, IO6:253-260,
1952. Maximilian, V.A.; Prohovnik, I.; and Risberg, J. Cerebral hemodynamic response to mental activation in normo- and hypercapnia. Stroke, I 1:342-347, 1980. Newlin, D.B.; Golden, C.J.; Quaife, M.; and Graber, B. Effects of alcohol ingestion on regional cerebral blood flow. International Journal oJ’ Neuroscience, 17: l45- 150, 1982. Obrist, W.D.; Thompson, H.K.; Wang, H.S.; and Wilkinson, W.E. Regional cerebral blood flow estimated by rr”Xe-inhalation. Stroke, 6:245-256, 1975. Risberg, J. Regional cerebral blood flow measurements by 133xenon inhalation: Methodology and applications in neuropsychology and psychiatry. Brain and Language.
9:9-34, 1980. Risberg, J.; Ali, Z.; Wilson, E.M.; Wills, E.L.; and Halsey, J.H. Regional cerebral blood flow by 133xenon inhalation: Preliminary evaluation of an initial slope index in patients with unstable flow compartments. Stroke, 6:142-148, 1975. Ryback, R.S. Alcohol amnesia: Observations in seven drinking inpatient alcoholics. Quarterly Journal oJ’Studies on Alcohol, 3 I :6 16-632, 1970. Ryback, R.S. The continuum and specificity of the effects of alcohol on memory. Quarterly Journal of Studies on Alcohol, 32:995-IO 16, I97 I. Simard, D.; Olesen, J.; Paulson, O.B.; Lassen, N.A.; and Skinhbj, E. Regional cerebral blood flow and its regulation in dementia. Brain. 94:273-288, I97 I. Sutherland, V.C.; Burbridge, T.N.; Adams, J.E.; and Simon, A. Cerebral metabolism in problem drinkers under the influence of alcohol and chlorpromazine hydrochloride. Journal of Applied Physiology, 15: I89- 196, 1960. Tarter, R.E., and Schneider, D.U. Blackouts: Relationship with memory capacity and alcoholism history. Archives of’ General Psychiatry, 33: I492- 1496, 1976.