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Verbal Information Retention in Alcoholics
... These results confirm and extend those of previous studies demonstrating that alcohol dependence increases the risk of postoperative delirium and POCD in patients undergoing noncardiac surgery [18,19]. The neurocognitive tests in the current investigation were designed to measure performance in recent verbal and nonverbal memory and executive functions because previous studies suggested that cognitive impairments may develop in these domains after surgery [10,3233343536. The current investigation was specifically conducted in older patients (age ≥55 years) who are known to be at substantially greater risk for POCD [1,37383940. Advanced age is associated with reduced brain weight and volume, loss of cellular bodies and myelinated fibers in several brain regions (e.g., hippocampus), synaptic density, and DNA repair capability41424344. ...
... Advanced age is associated with reduced brain weight and volume, loss of cellular bodies and myelinated fibers in several brain regions (e.g., hippocampus), synaptic density, and DNA repair capability41424344. Patients with a history of alcohol dependence may also demonstrate preexisting cognitive impairment [10,32,33,36,39,4546474849505152. For example, impaired visuospatial recent memory and the ability to learn new verbal material were previously described in abstinent alcoholics [32,33,39]. ...
... Patients with a history of alcohol dependence may also demonstrate preexisting cognitive impairment [10,32,33,36,39,4546474849505152. For example, impaired visuospatial recent memory and the ability to learn new verbal material were previously described in abstinent alcoholics [32,33,39]. Similarly, executive dysfunction may be another characteristic sign of chronic alcohol dependence [10,36]. ...
Postoperative cognitive dysfunction (POCD) commonly occurs after cardiac surgery. We tested the hypothesis that a history of alcohol dependence is associated with an increased incidence and severity of POCD in male patients undergoing cardiac surgery using cardiopulmonary bypass. Recent verbal and nonverbal memory and executive functions were assessed before and one week after surgery in patients with or without a history of alcohol dependence. Cognitive function was significantly reduced after cardiac surgery in patients with versus without a history of alcohol dependence. The results suggest that a history of alcohol dependence increases the incidence and severity of POCD after cardiac surgery.
... Indeed, literature reports that not all AUD-related cognitive deficits are reversible following abstinence, and not all cognitive functions need the same amount of abstinence time to be recovered [50]. However, across all cognitive domains, impairment in AUD-associated memory processes may already partially recover with an intermediate abstinence period (between 2 weeks and 2 months [51][52][53]) and fully recover with a long-term abstinence (greater than 2 months [52,[54][55][56][57]), therefore having a good recovery potential. From the clinical practice perspective, if replicated, our findings would support the implementation of computerized cognitive rehabilitation programs aimed at targeting specifically memory recall deficits, instead of broader memory deficits, through heterogeneous stimuli (where AUD exhibit a specific pattern of impairments), rather than through both homogeneous and heterogeneous stimuli. ...
... Indeed, literature reports that not all AUD-related cognitive deficits are reversible following abstinence, and not all cognitive functions need the same amount of abstinence time to be recovered [50]. However, across all cognitive domains, impairment in AUD-associated memory processes may already partially recover with an intermediate abstinence period (between 2 weeks and 2 months [51][52][53]) and fully recover with a long-term abstinence (greater than 2 months [52,[54][55][56][57]), therefore having a good recovery potential. From the clinical practice perspective, if replicated, our findings would support the implementation of computerized cognitive rehabilitation programs aimed at targeting specifically memory recall deficits, instead of broader memory deficits, through heterogeneous stimuli (where AUD exhibit a specific pattern of impairments), rather than through both homogeneous and heterogeneous stimuli. ...
Aim: Alcohol use disorder (AUD) has been associated with recognition memory deficits. However, it remains unclear whether these deficits occur at the general recognition memory level or whether they selectively affect its subcomponents. Evidence suggests that recognition memory deficits may vary according to the heterogeneity of memory stimuli. Our aim was to investigate stimuli pair-dependent recognition memory deficits in AUD, using a
cued recall task including homogeneous and heterogeneous stimuli pairs.
Methods: Twenty-three patients with AUD (days since last alcohol consumption: 11.70 ± 10.20) and 23 healthy controls (HC) underwent a neuropsychological examination tapping attention, verbal fluency, logical, working and long-term memory, and a recognition and recall task involving both homogeneous (tool-tool) and heterogeneous (tool-scene, tool-animal) stimuli pairs. Group (AUD-HC) by condition (tool-tool, tool-scene, tool-animal) ANOVAs were performed on all neuropsychological indices.
Results: In the neuropsychological examination, AUD individuals showed deficits in delayed recall and faster reaction times compared with HC. The administration of the recognition and recall task revealed specific performance decreases in cued recall occurring in the whole sample (AUD + HC) for heterogeneous (tool-scene, tool-animal) pairs compared with homogeneous pairs. Within this pattern, AUD patients showed a lower cued recall rate than
HC only for tool-animal pairs.
Conclusions: Our results support the existence of specific recall/recollection deficits in AUD which occurred for heterogeneous, but not for homogeneous stimuli pairs. This finding calls for further neuroimaging investigations aimed at investigating the neurobiological substrate of (i) different recognition memory subcomponents, and (ii) the processing of stimuli with different degree or type of heterogeneity.
... This finding conflicts with many investigations which have specifically studied raemory functioning in abstinent alcoholics. While providing support for the presence of continuing figural memory deficits in older, longer-term abstinent alcoholics (e.g., Ellenberg et al., 1980;Goldman & Rosenbaum, 1977) , the results of this study failed to provide support for the frequent finding of coraplete recovery of verbal raemory, regardless of age and drinking history, within three to four weeks of abstinence (e.g., Ellenberg et al., 1980;Goldraan & Rosenbaura, 1977;Sharp et al., 1977;Weingartner et al., 1971) and, in fact, suggest that verbal memory (especially verbal short-term memory) is more impaired than figural. The discrepancies between the results of this study and those which have found recovery of verbal meraory raay be at least partially due to the nature of the tests used to assess verbal raeraory functioning. ...
... Learning, at least during the first four weeks of treatment, should be expected to be slow and repeated performance of learned behavior should be required (Weingartner et al. , 1971) . In addition to traditional interventions such as grouD and individual therapy, training in raemorization should be initiated, especially if future research shows continuing meraory deficits over a greater time span of abstinence than demonstrated in this study. ...
... Using verbal learning tasks to assess cognitive deficits, Allen, Faillace, and Reynolds (1971) and Weingartner, Faillace, and Markley (1971) found some recovery of short-term memory and new learning ability over a 3week period after detoxification. Intellectual test scores have also been reported to increase over a 1-week span (Burdick, Johnson, & Smith, 1970), a 6-week span (Smith & Layden, 1972), and a 1-year span (Long & McLachlin, 1974). ...
Assessed the recovery of alcoholics' ability to learn meaningful verbal items after the cessation of drinking via 3 spaced administrations of the Synonym Learning Test (SLT) during a 1-mo inpatient alcohol treatment program. The SLT procedure also assessed Ss' vocabulary level. Three matched groups of 11 male alcoholics (mean ages 41.55, 45.45, and 43.36 yrs) were tested. The study design separated practice effects from actual recovery via the administration of the 1st testing to each group at a different time delay after drinking ceased––5, 15, and 25 days, respectively. To ascertain baseline SLT performance, a control group of 11 nonalcoholic hospitalized patients (mean age 37.55 yrs) were tested once. Results show that vocabulary knowledge was unimpaired by chronic alcohol abuse, whereas the ability to learn new vocabulary words was impaired immediately after cessation of drinking but recovered to normal levels by 2 wks postdrinking. Length of drinking history did not influence either vocabulary knowledge or new vocabulary learning. The correlation between new vocabulary learning and initial vocabulary suggested that SLT scores must be adjusted for vocabulary in future clinical use of the procedure. Implications for alcohol treatment are discussed.
... In the present studies, L-DOPA had no effect on a typical measure of short-term memory, immediate recall on trial 1 of the 8-word serial learning task, nor did it affect trial 1 of the free recall task. Rather, it improved performance on the incremental accumulation of repeated information in the serial word hst test; it had a similar effect on the free recall task which consists of an information overload in which associational grouping is thought to be of particular importance in the ]earning process (Mandler, 1967;Atkinson et al., 1968;Deese, 1965;Weingartner et al., 1971). Thus, the results on both tests suggest that L-DOPA treatment affects the intermediate or longer-term memory component. ...
Verbal learning was measured during the administration of l-DOPA in large oral doses to depressed patients. Longer-term memory on two different tasks improved during treatment, while short-term memory (immediate recall) was unaffected. In contrast, the catecholamine synthesis inhibitor α-methyl-p-tyrosine did not alter either memory process.
The effects of l-DOPA on learning may be related to increased arousal produced by this drug.
... Using verbal learning tasks to assess cognitive deficits, Allen, Faillace, and Reynolds (1971) and Weingartner, Faillace, and Markley (1971) found some recovery of short-term memory and new learning ability over a 3week period after detoxification. Intellectual test scores have also been reported to increase over a 1-week span (Burdick, Johnson, & Smith, 1970), a 6-week span (Smith & Layden, 1972), and a 1-year span (Long & McLachlin, 1974). ...
Assessed the recovery of alcoholics' ability to learn meaningful verbal items after the cessation of drinking via 3 spaced administrations of the Synonym Learning Test (SLT) during a 1-mo inpatient alcohol treatment program. The SLT procedure also assessed Ss' vocabulary level. Three matched groups of 11 male alcoholics (mean ages 41.55, 45.45, and 43.36 yrs) were tested. The study design separated practice effects from actual recovery via the administration of the 1st testing to each group at a different time delay after drinking ceased--5, 15, and 25 days, respectively. To ascertain baseline SLT performance, a control group of 11 nonalcoholic hospitalized patients (mean age 37.55 yrs) were tested once. Results show that vocabulary knowledge was unimpaired by chronic alcohol abuse, whereas the ability to learn new vocabulary words was impaired immediately after cessation of drinking but recovered to normal levels by 2 wks postdrinking. Length of drinking history did not influence either vocabulary knowledge or new vocabulary learning. The correlation between new vocabulary learning and initial vocabulary suggested that SLT scores must be adjusted for vocabulary in future clinical use of the procedure. Implications for alcohol treatment are discussed. (PsycINFO Database Record (c) 2006 APA, all rights reserved).
To assess the relative recoverability in chronic alcoholics of abilities that typically reflect differential functioning of the cerebral hemispheres, 3 spaced administrations of verbal and visuospatial tasks used by R. Stark (see PA, Vol 36:4JG82S) were conducted during a 1-mo inpatient alcohol treatment program. The Stark tasks require new learning of verbal and visuospatial paired-associate items, which were equated for difficulty level and found to successfully discriminate unilateral cerebral damage. The study design separated practice effects from actual recovery via administration of the 1st testing to each of 3 groups of 16 alcoholics (matched for age, education, and drinking history) at 5, 15, and 25 days, respectively, after drinking ceased. Baseline Stark task performance was assessed in 16 nonalcoholic matched controls. Results show that both verbal and visuospatial learning were impaired immediately after drinking ceased but were recovered within 2 wks in most alcoholics. Continued visuospatial, but not verbal, impairment lasted through 25 days in older alcoholics with long drinking histories. Greater right hemisphere damage thus does not appear to occur in most alcoholics but may be implicated in older, long-term alcoholics. Mechanisms that presume diffuse bilateral atrophy in all alcoholics are proposed to explain the differential impairment of visuospatial functions in long-term alcoholics. (33 ref)
There has been a rapid expansion of behavioral research on alcohol and alcoholism within the past 10 years. The relics of a complex mythology have begun to yield to empirical observations, and a clearer impression of some behavioral effects of alcohol has begun to emerge. However, the transition from mythology to an accurate descriptive phenomenology is still incomplete, and the neural mechanisms underlying the effects of alcohol are unknown. We now recognize that alcohol can change human behavior in many subtle and elusive ways that are modulated by experience and expectancy as well as by the drug itself. The nature of the behavioral change is often unpredictable because of the many factors that interact to determine the effect of drinking.
Wer beruflich mit Alkoholabhängigen zu tun hat, kennt die hohen Rückfälligkeitsquoten dieser Suchtkranken nach zunächst erfolgreich erscheinenden therapeutischen Rehabilitationsversuchen. Die Rückfälligkeit behandelter Alkoholiker wird häufig ausschließlich, zumindest jedoch primär auf (psycho)soziale Faktoren zurückgeführt. In den Hintergrund tritt dabei die Frage, inwiefern der Alkoholrückfall durch Defizite an intellektuellen bzw. geistigen oder kognitiven Fähigkeiten und Fertigkeiten mitbedingt sein könnte.
The past 20 years and the last 10 in particular have witnessed an impressive increase in interest both in treating and understanding chronic alcoholism. The early part of this period saw the introduction of disulfiram and citrated calcium carbimide. A little later, tranquilizers and antidepressants came to the fore. At the same time there was a rapid increase in the vogue for group as opposed to individual psychotherapy. (The latter, along with Alcoholics Anonymous, had been an established therapeutic mainstay since the Second World War.)
Although heroin addiction is more dramatic and newsworthy because of its stronger association with crimes against property, it is generally agreed among professionals in the field of alcoholism and drug dependence that alcoholism is by far the more extensive public health problem of the two. Four major stumbling blocks have always faced those who try to treat alcoholics: (1) The vast majority of alcoholics remain undetected and undiagnosed and do not receive treatment for their alcoholism, if they ever get it, until their condition is far advanced. (2) Once referred for treatment, a high percentage of alcoholics fail to negotiate successfully the jump from referring source to treatment facility. (3) Once in treatment, the alcoholic patient is likely to quickly drop out of it. (4) Among the variety of treatment approaches available, it is by no means clear which is most appropriate for a given patient.
The ability to gather, process, store, and respond intelligently to incoming information is obviously affected by alcohol ingestion. However, most investigators interested in this topic have, until recently, focused their attention almost exclusively on the relatively small number of detoxified alcoholics who developed the Wernicke-Korsakoff syndrome. The primary reason for this emphasis is that patients with this neuropsychiatric disorder manifest a set of circumscribed, clinically apparent cognitive impairments that can be dissected and delineated with a great degree of precision. Thus, it is now known that learning and memory skills are most affected, problem-solving and visuopercep-tual abilities are somewhat less disrupted, and intelligence—as assessed by standardized IQ tests—is essentially intact. Armed with the knowledge that chronic alcohol abuse can produce this distinctive pattern of impairment, clinicians active during the 1940s and early 1950s sought evidence of similar deficits in that much larger group of detoxified alcoholics who never show signs of Korsakoff’s syndrome or any other neuropsychiatric disorder. Administering their rather gross measures of cognitive competence to this group of neurologically intact alcoholics, they found few, if any, obvious cognitive deficits and concluded that beverage alcohol was a rather innocuous drug and that significant intellectual impairments would appear only if the heavy drinker were also malnourished.
A number of empirical and conceptual issues are addressed in an effort to explain the diversity of neuropsychological deficits demonstrated by chronic alcoholics. In addition to consumption characteristics and the neurotoxic effects of ethanol, evidence is marshalled to implicate nutritional deficiency, hepatic disease, congeners in the beverage, and cognitive regression as also being contributory to the manifest impairments. Moreover, predrinking disturbances are considered that may be responsible in part for the neuropsychological deficits observed in chronic alcoholics.
Our understanding of the neuropsychological concomitants of alcoholism can be increased by the adoption of a life-span approach to alcohol effects, localizing the system or region of maximal cerebral damage and relating these findings to treatment intervention. The extent to which adaptive capacity in alcoholics and social drinkers is predicted by neuropsychological test performance is of utmost importance, especially since nonalcoholic social drinkers also demonstrate a number of impairments.
Chronic alcohol abuse is known to lead to brain dysfunction (Begleiter and Platz, 1972; Rankin, 1975). In an effort to ascer tain some parallel between acute and chronic alcohol intake, the effect of single doses of alcohol on normal brain functioning is being studied. Extensive research has been conducted in order to investigate the effects of acute doses of alcohol on the normal human evoked potential. This has been examined with the auditory evoked response (AER) (Gross et al., 1966), the somatosensory evoked potential (SEP) (Lewis et al., 1970; Salamy and Williams, 1973; Porjesz and Begleiter, 1973), and the visual evoked potential (VEP) (Lewis et al., 1969, 1970; Porjesz and Begleiter, 1975; Rhodes et al., 1975), P3 amplitude (Roth et al., 1977), the contingent negative variation (CNV) (Kopell et al., 1972; Roth et al., 1977), and the amplitude-intensity gradient (Spilker and Callaway, 1969).
Critically reviews the literature on neurophysical and neuropsychological studies of brain functioning in alcoholics and examines findings concerning 3 hypotheses of brain damage in alcoholics: (a) diffuse or generalized brain damage, (b) damage that is lateralized to the right hemisphere, and (c) damage to the frontal-limbic-diencephalic system. While currently available evidence clearly demonstrates brain damage in alcoholics, it is not adequate unequivocally to support or refute any specific hypothesis of brain damage due to alcoholism. (84 ref) (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Chronic alcoholics exhibit impaired performance on a variety of psychological measures. While no generalized intellectual deterioration is evident, specific deficits on spatial, cognitive, learning, and motor tasks are observed. The manifest pattern of deficits is amenable to a neuropsychological interpretation, of which the presently most comprehensive hypothesis asserts that alcoholics suffer from a neurological disorder that is primarily localized to the anterior-basal region of the brain. © 1975 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted.
A battery of cognitive tests was administered to groups of younger (34–49) and older (50–59) alcoholics and nonalcoholic control subjects. Regardless of age, alcoholics were found to be impaired on essentially all measures of learning and memory. The relevance of these findings to the premature-aging hypothesis is discussed.
The relationship between aging and various drinking styles was examined. Four age groups (25–34, 35–44, 45–54, and 55–65 years) and four drinking styles (nondrinkers, social drinkers, alcoholics, and abstinent alcoholics) were compared. A battery of eight neuropsychological tests was administered to 322 men; 72 nondrinkers, 100 social drinkers, 58 abstinent alcoholics, and 92 alcoholics. Cognitive dysfunction related to aging was found to be a more significant factor than decline with alcohol use. Cognitive dysfunction associated with alcohol use was significant for three Wechsler Adult Intelligence Scale subtests; Vocabulary, Digit Symbol and Block Design. Alcohol-related differences in intellectual functioning tended to diminish with increasing subject age.
This paper reviews the neuropsychological literature on the effects of chronic alcohol abuse. Research reveals a relatively consistent pattern of intellectual and adaptive ability deficits associated with alcoholism. Alcoholics frequently show deficits in abstract thinking and problem solving involving integration of novel material, particularly of a visual-spatial nature; at the same time, their verbal skills and general psychometric intelligence often appear intact. This pattern of cognitive functioning is moderated to some degree by demographic, drinking-related, and cognitive style variables, and is closely associated with morphological and functional impairment of the brain. While a precise neurological mechanism for these effects has not been clearly established, several hypotheses have been advanced to account for the behavioral deficits evidenced by alcoholics. Based on a knowledge of the neuropsychological functioning of alcoholics, several treatment-related implications are discussed.
The literature published in 1971 and 1972 on alcoholics in the United States was reviewed for objective psychological test data or behavioral measurements. The review was organized to facilitate further research by assembling information according to problem area and by including tests employed, significant findings ( p = .05), critical comments, and inferences for therapy. An appendix of references from 1968–1970 employing objective psychological measurements is included and cross-indexed.
It is generally believed that many non-Korsakoff alcoholics have subtle defects in memory. To determine whether such defects vary as a function of length of abstinence (LOA), we performed extensive memory testing with: (1) recently detoxified (n = 31; LOA-29 days); (2) intermediate-term abstinent (n = 28; LOA = 1.9 years); (3) long-term abstinent (n = 32; LOA-7.0 years) alcoholics; and (4) nonalcoholic controls (n = 37). All subjects were matched on age and education. Alcoholics were matched on years of alcoholic drinking. Memory measures were divided into the following domains: verbal learning, verbal recall, visual learning, visual recall, and paired associate learning. A series of MANOVAs were conducted that revealed a significant relationship between visual learning and length of abstinence, and a significant interaction between age and length of abstinence on visual recall. Long-term abstinent subjects were not significantly different from controls on any test. We conclude that memory disturbance demonstrable among recently detoxified alcoholics in the early weeks of their abstinence is not evident in demographically matched long-term abstinent alcoholics with similar drinking histories.
This paper reviews the relationship between cognitive status and treatment outcome in chronic alcoholics, the natural history of recovery, and the role of cognitively oriented remediation programs in facilitating recovery. Seven studies of experience-dependent recovery are described in which behavioral improvement was noted. Various recommendations for treatment over the course of recovery are made, guided by anticipated changes in capacity to process complex information over time.
Impaired cognitive functioning in alcoholics is widespread during the first months of detoxification. Between half and two thirds of abstinent alcoholics exhibit cognitive impairments during this period, with residual deficits persisting for years after detoxification in some patients. The most severe deficits have been observed in visuospatial abilities, perceptual-motor integration, abstract reasoning, and new learning. The most significant predictors of cognitive dysfunction in persons recovering from alcoholism are the time elapsed since the last drink and the person's age. Surprisingly, the pattern and duration of a patient's alcohol abuse are relatively weak determinants of neuropsychological impairment during abstinence. Research investigating the hypothesis that cognitive impairments may be related to alcoholic persons resuming drinking has yielded mixed results, but a higher level of neuropsychological functioning is associated with increased rates of completing treatment programs and with greater success in the work environment after discharge from treatment. The possibility of cognitive limitations should be taken into account in planning treatment programs for alcoholism.
Event-related potentials and visuospatial learning performance were examined to understand the effects of chronic alcohol use on complex information processing. A total of 18 alcoholic male in-patients in an alcohol treatment program served as participants. Nine persons were seen at time of admission to the program while intoxicated (mean BAC = 18.0 mg/dl). The second group of nine persons was seen detoxified after 4 weeks in the treatment program. Learning consisted of a paired-associate paradigm requiring participants to learn the distinct spatial positions of six, randomly presented "nonsense" shapes. The visuospatial learning performance of the intoxicated alcoholics was superior to that of the detoxified alcoholics. Evaluation of event-related potentials during the visuospatial learning task indicated that while both groups displayed greater right hemisphere amplitudes of P3, P2, N1, and N2-P3 components, the amplitudes of the latter three components were significantly greater in the intoxicated alcoholics. The overall results suggest that compared to the intoxicated alcoholic, the detoxified alcoholic may suffer a disruption in attentional mechanisms related to visuospatial information processing, providing support for a theory that alcohol ingestion serves to balance information processing in the chronic alcoholic.
Although alcoholic Korsakoff's syndrome has traditionally been considered an acute disorder related to a nutritional deficiency, recent evidence demonstrating that ethanol may be neurotoxic has raised the possibility that the perceptual, problem-solving, and memory deficits associated with this chronic neurological disorder may develop slowly over decades of alcohol abuse. A review of the recent cognitive literature provides only limited support for this "continuity hypothesis." Long-term alcoholics, as with patients with alcoholic Korsakoff's syndrome, are impaired on numerous visuoconceptual and learning tasks, but there is little or no evidence that the information-processing deficits underlying the two patient groups' anterograde memory problems are similar. Furthermore, experimental and clinical studies of retrograde amnesia have noted only mild remote memory impairments in non-Korsakoff alcoholics as well as clear indications that alcoholic Korsakoff patients' severe loss or access to remote memories occurs acutely with the onset of Wernicke's encephalopathy. It is concluded that while the continuity hypothesis has heuristic value, there is still insufficient evidence to place the Korsakoff patient, the detoxified long-term alcoholic, and the heavy social drinker at different points on a single continuum of cognitive impairment.
Thirty-seven middle-aged alcoholics and 20 nonalcoholic controls equated for age and education were examined on measures of verbal, learning/memory, abstracting/problem-solving, and perceptual-motor abilities 7 weeks after beginning detoxification and 13 months later. At 7 weeks, the alcoholics were significantly different from the controls on the verbal, abstracting/problem-solving, and perceptual-motor clusters and tended to differ on the learning/memory tests. At 13 months, the same pattern of differences was found except the groups no longer differed on the verbal tests. Alcoholics who resumed drinking during the 13 months differed from the controls to a greater extent than did abstainers on both the initial and final testings. These results have implications for treatment programs and recidivism.
Evidence for impaired verbal learning/memory in alcoholics is inconsistent. In part, this may be due to variations in task parameters such as difficulty level. The latter was varied in a paired-associate paradigm with 60 chronic male alcoholics abstinent 1 month and 60 nonalcoholic matched controls. Each subject was presented four lists with seven pairs of stimulus-response combinations of word meaningfulness of high-high, low-high, high-low and low-low values. The more difficult lists resulted in greater errors for both groups, but the predicted relative impairment of alcoholics with more difficult material did not occur, nor did the groups' learning curves differ. Under our experimental conditions, rote associative learning either remains intact or recovers satisfactorily with 1 month of abstinence in alcoholics. The results emphasize the importance of methodological variables and suggest restrictions on current generalizations about cognitive impairment in alcoholics.
The learning and retention of verbal information was compared in two populations of patients, chronic alcoholics and hospitalized normal controls. The verbal learning procedures involved the multiple presentation of 20 word lists, drawn at random from the common words in the English language. Each of the Ss learned seven equivalent word lists presented in association with a variety of reinforcement conditions. Three conditions involved positive reinforcement, money, while three word lists were presented along with a negative reinforcer, shock to the top of the nondomi-nant hand. One condition, as a control, involved no reinforcement contingencies. In one of the three positive and negative reinforcement conditions, Ss could learn to anticipate reinforcing consequences. In another condition Ss were reinforced only after an initial presentation of the words but not at the time of recall. A third pair of reinforcement conditions involved either reward or punishment at the time of recall but not at the time of stimulus presentation. Alcoholic Ss, as well as normal controls, tended to select out in recall, words previously positively reinforced, or words, that if recalled would again be positively reinforced. The same recall paradigms presented in association with negative reinforcers produced very different effects in alcoholic and normal Ss. Whereas normal Ss tended to avoid negatively reinforced stimuli in recall, particularly under those conditions in which recall of previously negatively reinforced words would again lead to negative reinforcement, the alcoholic did not differentiate between negatively reinforced and neutral stimuli. Testing on a second recall trial, after a second stimulus presentation, also differentiated alcoholic Ss from normal controls. As in previous studies, alcoholic Ss were less able to retain newly acquired information. That is, they demonstrate recall deficits that are focal in shifting information from short to long term storage.
The consumption of alcohol by women in Sweden is strongly increasing, especially in younger individuals. Since the rediscovery of the teratological properties of alcohol most of the studies concerning foetal alcohol damage in man have covered female skid row alcoholics. This investigation describes the medical and social characteristics of a group of women (n = 92) receiving inpatient care for alcoholism compared with an age-matched control group, in relation to obstetrical history. The conditions in the control group were in accord with those of the general population. Social problems and degree of alcoholism were noticeably advanced among the probands. The proband women who gave birth after established regular alcohol consumption were younger, showed more psychiatric complications during the treatment period, had started drinking and developing signs of advanced alcoholism earlier in life compared with probands who gave birth before established regular alcohol consumption. They also exhibited more social disturbances. The social problems caused by the mothers' alcohol abuse are expected to aggravate the biological consequences to their children.
The nature of the memory and visuospatial defects associated with chronic alcoholism, and the recovery of these functions, were investigated in a large group of alcoholic men and well-matched nonalcoholic controls. Both young and old alcoholics displayed significant impairments on tasks requiring the learning of novel associations and the holding of information in memory over longer delay intervals. The recovery of cognitive skills was found to depend on the length of abstinence and the particular behavioral functions examined. Whereas psychomotor skills and short-term memory improved significantly with prolonged abstinence, long-term memory was impaired even after seven years of continuous sobriety. We propose that recovery of short-term memory reflects reestablishment of cortical functioning, while the persistent long-term memory defect indicates more permanent damage to diencephalic structures.
A representative sample of 1,367 employed men and women in Detroit responded to questions about their drinking practices and then completed a cognitive test which measures abstraction abilities. Abstraction, tested while respondents were sober, decreased significantly as reported quantity of alcohol usually consumed per drinking occasion increased. (Am J Public Health 1983; 73:521-526.)
A prospective study was designed to determine the neuropsychological consequences of continued alcohol consumption after treatment for alcoholism. Performance on 24 commonly used clinical neuropsychological tests was examined in 56 male alcoholics approximately 7 months after completion of an inpatient alcoholism treatment program. Abstainers (n = 17) performed better than those who resumed alcohol consumption. Although there was a significant decrease in alcohol consumption, posttreatment drinking behavior still predicted cognitive performance, with increased frequency and quantity per occasion having more deleterious consequences even at consumption levels that are deemed by some to be socially acceptable. It is concluded that alcohol consumption by former alcoholics might serve to maintain cognitive performance at reduced levels, and that this possibility should be considered in determining appropriate treatment goals for alcoholic patients.
A battery of challening tests was used to assess learning ability and short-term memory in groups of detoxified chronic alcoholics with and without complaints of memory impairment, alcoholic Korsakoff patients, and nonalcoholic controls. While alcoholics without memory complaints did not differ from controls on standardized clinical memory tests, their performance was significantly impaired on our more demanding experimental tests. In contrast, the performance of alcoholics reporting memory complaints was impaired, relative to the other alcoholics, on both clinical and experimental memory tests, overlapping that of the alcoholig Korsakoff patients. These results are consonant with Ryback's continuum-of-impairment hypothesis.
A battery of cognitive tests was administered to groups of younger (34--49) and older (50--59) alcoholics and nonalcoholic control subjects. Regardless of age, alcoholics were found to be impaired on essentially all measures of learning and memory. The relevance of these findings to the premature-aging hypothesis is discussed.
The relationship between vitamin levels, alcohol intake and cognitive status was examined in a group of 19 chronic alcoholics who had just begun to withdraw from alcohol. The results indicate that during this stage of detoxification levels of folic acid are the best predictors of cognitive performance. Alcohol intake, as measured by either total life consumption or years of alcohol abuse, was only weakly associated with neuropsychological tests scores. It is suggested that the cognitive recovery that occurs during the first weeks of abstinence may be related to nutritional variables, whereas the longer-lasting neuropsychological impairments of alcohol abusers may be related to the direct neurotoxic effects of alcohol.
The Standardized Version of Luria's Neuropsychological Technique was administered to separate groups of alcoholics 3 and 11 weeks abstinent from alcohol and to an equated control group. The alcoholics were impaired compared to controls on most of the battery scales; 3-week abstinent alcoholics performed poorer than 11-week abstinent alcoholics on most scales, however, only on the Rhythm scale was the difference significant. These results and other analyses suggest that chronic alcoholics suffer from a mild diffuse-generalized brain dysfunction which persists for up to at least 11 weeks of abstinence.
Numerous neuropsychological tests have been used to assess the effects of chronic alcohol use on the brain. Recently, the introduction of the Standardized Luria-Nebraska Neuropsychological Battery has presented a fresh way of evaluating disorders due to brain dysfunction. The present paper is an investigation of deficits in alcoholics on the Luria-Nebraska Neuropsychological Battery. It was found that alcoholics differed from age--and education--matched controls on six of the fourteen scales of the test: Visual, Receptive Language, Arithmetic, Memory, Intelligence, and the Pathognomonic scale. An investigation of the individual items which differentiated alcoholics and controls found evidence that the effects of alcoholism are primarily seen in the more complex association areas of the brain, consistent with the conclusions reached by Gudeman and his associates. The implication and limitations of the present results were also discussed.
There is clear evidence in the literature for permanent cerebral impairment due to prolonged alcohol abuse. Observation also suggests that there is a component of this cerebral impairment that is found immediately subsequent to heavy drinking and that is reversible. This study examined the time-course of recovery from this temporary impairment and delineated more specifically the neuropsychological functions that participate in the recovery. Four groups (N = 87) of hospitalized male alcoholics were tested after 6, 15, 21, and 110 days of abstinence using the Raven Progressive Matrices, the Trail-Making Test, the Memory for Designs, and the following subscales of the WAIS: Arithmetic, Digit Span, Block Design, Similarities, and Digit Symbol. The results indicated that significant improvement occurred during the third week of abstinence (between 15 and 21 days) on the Digit Span, Block Design, Similarities, Memory for Designs, Raven, and Trail-Making tests, but not on the Arithmetic and Digit Symbol tests. These results suggest that treatment programs that use a preliminary "drying-out" period should consider lengthening this period to 3 weeks to insure that patients are maximally responsive to psychotherapy.
The past twenty years have seen extensive study of cognitive deficits in a relatively rare species of alcoholic — the alcoholic with Korsakoff’s syndrome (e.g., Talland, 1965; Butters & Cermak, 1974, 1976). Much of this research has focused on the Korsakoff patients’ severe anterograde amnesia. Clinically, such individuals have difficulty retaining new information for more than a few minutes, and perform poorly on a wide variety of formal verbal learning and short-term memory tasks (e.g., Cermak, Butters, & Goodglass, 1971; Cermak & Butters, 1973). Recent studies have attributed these deficits to an alteration in the types of remembering strategies used by such patients. Compared to neurologically intact control subjects, Korsakoff patients are less likely to spontaneously rehearse verbal information (Cermak, Naus, & Reale, 1976), and are more likely to encode the phonemic, rather than the semantic, features of the to-be-remembered material (Cermak, Butters, & Gerrein, 1973). This more primitive processing is thought to produce relatively fragile memory traces (Craik, 1973; Cermak, 1977). Perhaps as a result of this defective encoding, Korsakoff patients also display a remarkable sensitivity to the effects of proactive interference (Cermak & Butters, 1972).
Postoperative cognitive dysfunction (POCD) affects a significant number of patients and may have serious consequences for quality of life. Although POCD is most frequent after cardiac surgery, the prevalence of POCD after noncardiac surgery in older patients is also significant. The risk factors for POCD after noncardiac surgery include advanced age and preexisting cognitive impairment. Self-reported alcohol abuse is a risk factor for postoperative delirium, but its significance for long-term POCD has not been investigated. The goal of this study was to determine whether neurocognitive function is impaired after noncardiac surgery during general anesthesia in older patients with a history of alcohol abuse.
Subjects aged 55 yr and older with self-reported alcohol abuse (n = 28) and age-, sex-, education-matched nonalcoholic controls (n = 28) were tested using a neurocognitive battery before and 2 weeks after elective surgery (n = 28) or a corresponding time interval without surgery (n = 28). Verbal memory, visuospatial memory, and executive functions were assessed. A neurologic examination was performed to exclude subjects with potential cerebrovascular damage.
Significant three-way interactions (analysis of variance) for Visual Immediate Recall, Visual Delayed Recall, Semantic Fluency, Phonemic Fluency, and the Color-Word Stroop Test implied that cognitive performance in the alcoholic group decreased after surgery more than it did in the other three groups.
The results suggest that a history of alcohol abuse in older patients presents a risk for postoperative cognitive impairment in the domains of visuospatial abilities and executive functions that may have important implications for quality of life and health risks.
Either diabetes or alcohol abuse can impair cognitive function, especially at older ages. Whether a history of alcohol abuse increases the risk for cognitive impairment in diabetic patients has not been examined. Cognitive function of type 2 diabetic subjects with a history of alcohol abuse was expected to be more impaired than that of subjects with either diabetes or alcohol abuse alone. Men, 55 years of age, were categorized as 15 alcoholic-diabetic; 15 alcoholic-nondiabetic; 15 nonalcoholic-diabetic; 15 nonalcoholic-nondiabetic, and matched on age, sex, and education. Participants' verbal memory, visuospatial memory, and executive functions were assessed using a neurocognitive test battery. Significant interactions of diabetes and alcoholism for Visual Delayed Recall, Story Immediate Recall, and Story Delayed Recall implied that diabetes and alcohol abuse enhanced each other's effect in lowering cognitive test scores. Alcohol abuse history in older diabetic subjects presents an increased risk for cognitive impairment.
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