Schizophrenia Bulletin Advance Access originally published online on February 9, 2005
Schizophrenia Bulletin 2005 31(1):175-182; doi:10.1093/jschbul/sbi001
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Neurocognition, Symptomatology, and Functional Skills in Older Alcohol-Abusing Schizophrenia Patients
Instructor, Department of Psychiatry, Mount Sinai School of Medicine, New York, NY
Associate Professor, Department of Psychology, Hofstra University, Hempstead, NY; and Associate Professor, New York University School of Medicine, New York, NY
Associate Professor, Department of Psychiatry, Mount Sinai School of Medicine; and Director, Schizophrenia Treatment and Research Program, Mount Sinai School of Medicine/Bronx Veterans Affairs Medical Center
Professor and Chief of Psychology Services, Department of Psychiatry, Mount Sinai School of Medicine
Send reprint requests to Dr. C.R. Bowie, Mount Sinai School of Medicine, Department of Psychiatry, 1425 Madison Avenue, 4th Floor, New York, NY 10029; e-mail: christopher.bowie{at}mssm.edu.
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Deficits in neurocognitive functioning are common to both schizophrenia and alcoholism. Recent studies suggest that neurocognitive functioning is the most significant predictor of social-adaptive functioning in schizophrenia. Cognitive impairment induced by alcoholism may result in more impaired functional outcome for comorbid patients. Past research examining alcohol-abusing schizophrenia patients has not examined correlates with functional outcome and has generally been limited to relatively younger patients. This study examined neurocognitive functioning and its correlates in alcohol-abusing schizophrenia patients between the ages of 40 and 80. Outpatients with schizophrenia (SZ; n = 17) or both schizophrenia and alcohol abuse or dependence (SZ + ETOH; n = 18) were tested on a neurocognitive battery, rated for symptomatology, and assessed for functional abilities. The results suggest that alcohol abuse in schizophrenia is associated with more impaired functioning across many domains, including memory impairment, negative and general psychopathology symptoms, and adaptive functions. The only significant predictor of impaired functional status in the overall sample and the SZ + ETOH group was neurocognitive functioning.
Keywords: Schizophrenia / alcohol / cognition / adaptive functions
People with schizophrenia are at an increased risk for substance abuse, compared to the general population (Regier et al. 1990
). Alcohol is by far the most frequently abused substance in this population, with 33.7 percent meeting lifetime criteria for diagnosis (Regier et al. 1990). People with schizophrenia and concomitant alcohol abuse are at an increased risk for psychosocial problems that may interfere with their ability to function in many life domains. Past studies, for example, have found alcohol-abusing schizophrenia patients, compared to their nonabusing counterparts, to be more medication noncompliant and to have greater difficulty maintaining a healthy diet, managing their finances, and maintaining stable housing (Drake et al. 1989). In addition, alcoholic schizophrenia patients were more likely to have medical problems and more likely to return to a hospital for inpatient services than nonabusers (Drake et al. 1989). Alcohol-abusing schizophrenia patients, compared to their nonabusing counterparts, also have been found to show increased hostility, disorganization, incoherent speech, paranoia, depression, anxiety, and suicidal behavior (Drake et al. 1989; Nixon et al. 1996).
It is less clear, however, how alcohol affects schizophrenia patients' neurocognitive and functional skills. The few studies have found mixed results, with some studies finding no impairment associated with alcohol abuse (e.g., Nixon et al. 1996; Addington and Addington 1997) and others finding mild to moderate deficits associated with abuse (e.g., Richarme et al. 2000; Allen et al. 1999; Allen and Remy 2001). Methodological differences between studies may account for disparate findings, including the age range of subjects and length of abstinence before testing. The studies that found no group differences, for example, studied younger patients with limited cognitive assessment batteries. Furthermore, these studies either recruited patients who had been abstinent for a length of time sufficient for recovery from the acute neurotoxic effects of alcohol, or did not report length of abstinence.
Interestingly, neurocognitive deficits associated with alcohol abuse may be a function of patients' age. This is particularly relevant because cognitive impairments found in schizophrenia become more substantial in a subset of late-life patients (Harvey et al. 1999; Friedman et al. 2001). This impairment may not be limited exclusively to older, institutionalized patients, however, in that Allen et al. (1999) found a significant acceleration in global cognitive impairment for a dually diagnosed group between the fourth and fifth decade of life, compared to schizophrenia patients without alcohol abuse. This finding of cognitive impairment is consistent with recent neuroimaging studies of alcohol-abusing schizophrenia patients that show reductions in whole brain volume, particularly in prefrontal regions (Mathalon et al. 2003), the cerebellum (Sullivan et al. 2000), and the pons (Sullivan et al. 2003), relative to patients receiving a single diagnosis of alcohol dependence or schizophrenia alone.
The resurgent interest in neurocognitive functioning in schizophrenia is partly attributable to its association with functional impairments and outcome in schizophrenia (see Green et al. 2000 for review). Harvey et al. (1998) found cognitive functioning to be more strongly predictive of adaptive functioning than negative and positive symptoms, in both acutely ill and institutionalized older schizophrenia patients. However, functional skills have not been examined in alcohol-abusing schizophrenia patients. It would follow that these patients may be at elevated risk for functional impairment if their cognition is further compromised by alcohol abuse.
It has been demonstrated that alcohol abuse has detrimental effects on cognitive functioning in older schizophrenia patients, and it is fairly well established that neurocognitive functions are related to social and adaptive functioning skills in schizophrenia. For this study, an older sample of schizophrenia patients was recruited to extend the findings of the Allen et al. (1999) study to an older sample and expand the literature by examining adaptive functional skills and symptomatology, as well as examining the interrelationships between these variables.
It is hypothesized that (1) schizophrenia patients who abuse alcohol will have more impaired global neurocognitive functioning than those who do not abuse alcohol (secondary analyses were conducted to examine differences in specific neurocognitive functions); (2) neurocognitive dysfunction will be positively associated with impaired functional skills in both groups; and (3) increased amount of alcohol abuse will be positively related to impaired neurocognitive functioning and functional skills.
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Participants.
All participants were patients in psychiatric outpatient treatment programs affiliated with the Northport Veterans Affairs Medical Center or the Bronx Veterans Affairs Medical Center. One group of subjects received comorbid diagnoses of schizophrenia and alcohol abuse or dependence (SZ + ETOH), and the other group of patients received a diagnosis of schizophrenia (SZ) without any other DSM–IV Axis I psychiatric disorders (APA 1994). A diagnostic interview was completed with the Comprehensive Assessment of Symptoms and History (CASH; Andreasen et al. 1992). This instrument is designed for documenting the signs, symptoms, and history of participants evaluated in research studies of major psychotic and affective disorders based on structured interviews with the caretaker and patient and chart review. This instrument also includes criteria necessary to make diagnoses of alcohol or other substance abuse or dependence. All final research diagnoses were generated at a consensus meeting with a senior diagnostician.
Potential participants were excluded from this study if they were in active treatment for a seizure disorder, if they had experienced a cerebral vascular accident; if they had experienced a head trauma with loss of consciousness; or if they have a concurrent pervasive developmental disorder, mental retardation, or other neurological diseases or damage, including alcohol withdrawal seizures, as these may influence the results of the neurocognitive testing. Patients who used any illicit drugs or nonprescribed medication within the week prior to the evaluation and/or those with a DSM–IV diagnosis of substance abuse or dependence other than alcoholism were also excluded, as this may have compromised their cognitive functioning.
The patients with a history of alcohol abuse or dependence were abstinent for no longer than 3 weeks prior to the evaluation, as there is evidence that some cognitive functions are at least partially restored after this interval (Jenkins and Parsons 1979; Brandt et al. 1983).
Subjects were not compensated for their participation in this study. Institutional review board approval was obtained at both facilities and separate, but comparable, consents for both of the centers were used, in accordance with the format preferred by the respective institutional review boards. All participants provided written informed consent after the study procedure was explained to them.
Materials.
The 12-item Khavari Alcohol Test (Khavari and Farber 1978), which is a self-report assessment that estimates the number and volume of alcoholic drinks the patient consumed during the past month, was administered with the symptom interview. The Annual Absolute Alcohol Index (AAAI; Khavari and Farber 1978) was calculated based on the scores to provide a consumption variable. Despite the inherent limitations of self-report, schizophrenia patients have been shown to give self-report information on alcohol abuse with adequate reliability and validity (Toland and Moss 1989; Searles et al. 1990; Bryant et al. 1992).
Severity of symptoms was assessed using the Positive and Negative Syndrome Scale (PANSS; Kay 1991). This is a 30-item scale with 7 items measuring positive symptoms, 7 items measuring negative symptoms, and 16 items measuring general aspects of psychopathology and is completed after a structured interview. In this study, the total scores on positive, negative, and general symptom subscales are dependent measures. The symptom interview and diagnostic interview were conducted on the same day as the neurocognitive testing and functional skills evaluation.
Cognitive domains most strongly associated with functional outcome in schizophrenia (Green 1996) were assessed. Verbal learning and memory was assessed with the Rey Auditory Verbal Learning Test (RAVLT; Schmidt 2001). For the present study, the dependent variables from the RAVLT are total number of items produced during trials one through five of list A, delayed recall, and recognition hits. Letter Number Sequencing and Digit Span, from the Wechsler Adult Intelligence Scale—3rd Edition (WAIS–III; Wechsler 1997), were used as measures of verbal working memory and attention. Additionally, participants were asked to name as many animals as they could in 1 minute to provide a measure of semantic fluency.
The Wide Range Achievement Test—3rd Edition (WRAT3; Wilkinson 1993) word recognition reading subtest was administered as an estimate of premorbid intellectual functioning. This test measures the ability to pronounce words, a skill found to be relatively preserved in schizophrenia (O'Carroll et al. 1992; Tracy et al. 1996; Harvey et al. 2000). The dependent measure is the standard score.
The UCSD Performance-Based Skills Assessment (UPSA; Patterson et al. 2001) is designed to directly assess functioning and degree of disability among the severely mentally ill. This test is designed for older outpatients and measures performance in a number of domains of everyday functioning through the use of props and standardized role-play situations. The Comprehension/Planning domain measures the patient's ability to comprehend written material that describe recreational outings and then name appropriate items necessary to bring to the outings. The Finance domain has two parts. The patient must first count out given amounts from real currency and make change. Then the patient must fill out a check to pay a utility bill. The Communication domain involves a series of role-play situations that require the patient to dial 911 in the case of an emergency, recall and dial a requested telephone number, and recall critical information for a followup medical appointment. The Household Management domain requires the patient to prepare a shopping list of missing pantry items needed to make a recipe. The primary outcome measure was a composite z score that was derived by averaging the four domains. Other dependent variables for the UPSA are z scores for the four different domains, which were calculated from the scores of the healthy control sample used to validate the measure (Patterson et al. 2001).
Procedure. Potential participants were asked by their case worker if they would participate in the study. After written informed consent was obtained, the tests were administered according to the instructions from respective manuals, in a fixed order. All evaluations were performed by the primary author (C.R.B.), who was trained by a senior psychologist (P.D.H.). The neurocognitive and functional skills assessments were conducted in one session. First, the RAVLT trials 1–5, list B, and immediate recall were administered, followed by the WAIS subtests and then the RAVLT delayed recall. The semantic fluency task was then administered. If administration of the WAIS subtests did not result in a 20-minute delay, mazes were given to the participant to fill the delay before the RAVLT delayed recall trial was administered. The semantic fluency and WRAT reading tests were given last to avoid introducing a confound to the RAVLT learning by presenting additional verbal material. The interview was completed after the neurocognitive testing to keep the experimenter blind to the symptoms and presence or absence of current alcohol use during administration of the cognitive tests. Medications and dosages the participant took for the 7 days prior to testing and the day of the testing were recorded. The PANSS ratings were based on a structured diagnostic interview and the CASH interview.
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Demographic Data.
Demographic data are presented in table 1. Seventeen participants in the SZ group and 18 participants in the SZ + ETOH group were enrolled and completed the evaluation. Sixteen (94%) of the participants in the SZ group and 17 (94%) of the participants in the SZ + ETOH group were male. The mean age was 54.9 (standard deviation [SD] = 10.66) for the SZ group and 52.1 (SD = 6.74) for the SZ + ETOH group. The mean level of education and estimated premorbid functioning, as measured by the WRAT–R reading recognition subtest (Wilkinson 1993), were not significantly different between the groups. The trend in the SZ group toward more years of education, t(33) = –1.85, p = 0.072, was in part accounted for by one participant in the SZ group who had graduate education. A similar proportion of patients in both groups were taking typical, atypical, or both types of antipsychotic medications, 
2(2) = 2.05, p > 0.05. A similar proportion of patients at both research sites were in each group, 2(1) = 2.3, p > 0.05.
The dosage of conventional antipsychotic medications was converted to a chlorpromazine-equivalent dosage to examine differences in doses of antipsychotic medications between groups. With mean chlorpromazine-equivalent dosages of 257.77 (SD = 182.89) in the SZ group and 343.61 (SD = 200.18) in the SZ + ETOH group, the two groups were not significantly different, t(14) = 0.856, p = 0.406. Significantly more patients in the SZ + ETOH group than in the SZ group were taking anticholinergic medication, 2(1) = 11.84, p < 0.01. See table 2 for a breakdown of medication status by group.
All patients met criteria for either schizophrenia or schizoaffective disorder but not other DSM–IV Axis I disorders, other than alcohol abuse or dependence in the comorbid group. The two groups were not significantly different on schizophrenia subtype, 2(3) = 2.43, p > 0.05.
In the SZ + ETOH, group 12 (66%) participants met DSM–IV (APA 1994) criteria for alcohol abuse and 6 (33%) met criteria for alcohol dependence. Participants in this group had been abstinent for a mean of 8.56 days before the assessment (SD = 6.43, range = 1–20) and consumed a mean of 545 units of alcohol per year (SD = 464.45, range = 129–2,214).
Neurocognitive Data.
Raw scores on the neurocognitive tests were transformed to z scores (mean = 0, SD = 1) based on normative data for the RAVLT measures (Schmidt 1996), the WAIS subtests (Wechsler 1997), and the semantic fluency test (Spreen and Strauss 1998). Averaging the z scores of six neurocognitive measures generated the neurocognitive composite score, which was examined in a one-way analysis of covariance, with anticholinergic dosage and years of education as covariates. The SZ + ETOH group was significantly more impaired on the neurocognitive composite score. Followup multivariate analysis of covariance (MANCOVA) tests were conducted to examine group differences on the individual neurocognitive tests. The overall MANCOVA was significant, F(6,26) = 2.58, p < 0.05. See table 3 and figure 1 for a summary of neurocognitive data.
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A 2 x 2 repeated measures analysis of variance, with group as the between-subjects factor and RAVLT Trials 1 and 5 as the within-subjects factors, was conducted to examine group differences in the extent of learning over the five trials of the RAVLT list A. There was a significant main effect for learning trial, F(1, 33) = 77.81, p < 0.001, which indicates that both groups learned words over the trials. The main effect for group was also significant, F(1, 33) = 9.01, p < 0.01, which indicates that the SZ + ETOH group produced fewer words than the SZ group at both learning trials. The learning by group interaction approached, but did not reach significance, F(1, 33) = 2.98, p = 0.09, which indicates that the two groups did not significantly differ in their ability to learn words over the trials.
A 2 x 2 repeated measures analysis of variance, with group as the between-subjects factor and RAVLT Trial 5 and RAVLT delayed recall as the within-subjects factors, was conducted to examine the group differences in delayed verbal recall as a function of learning capacity. The number of words recalled during the delayed recall trial, relative to the number of words produced at trial 5, which is the last learning trial, provides a measure of "retention" of verbal material. The main effect for retention was significant, F(1, 33) = 75.44, p < 0.001, indicating that both groups recalled fewer words after the delay than they learned during the last learning trial. The main effect for group was also significant, F(1, 33) = 7.97, p < 0.01, indicating that the SZ + ETOH group was able to recall fewer words during the trials than the SZ group. However, the group by retention interaction was not significant, F(1, 33) = 0.003, p = 0.96, which indicates that both groups retained a similar proportion of words, relative to their learning performance.
Symptom Data. A multivariate analysis of variance (MANOVA) was conducted to examine group differences in symptomatology. The overall MANOVA was significant, F(1, 33) = 8.8, p = 0.006. The SZ + ETOH group had significantly more severe symptoms than the SZ group for negative symptoms and general psychopathology, but not positive symptoms. See table 3 for a summary of symptom data.
Functional Skills Data.
A MANOVA was conducted to examine group differences in functional skills. The raw scores were converted to z scores based on normative data (Patterson et al. 2001). A one-way analysis of variance of global functional skills as measured by the composite score revealed more impairment in the comorbid group. Followup MANOVA tests were conducted to examine group differences in the specific functional skills. The overall MANOVA was significant, F(1, 33) = 20.45, p < 0.001. See table 3 for a summary of the individual domains.
Consumption Data. Pearson correlations were computed to examine the association of quantity of alcohol use (AAAI) with neurocognitive, symptom, and functional variables. Higher levels of consumption were significantly associated with greater levels of general psychopathology, r = 0.47, p < 0.05 and more impaired household management skills, r = –0.41, p < 0.05. There was a trend for significant correlations between higher consumption and higher levels of positive symptomatology, more impaired recognition, working memory, and lower neurocognitive composite score. See table 4 for correlations between alcohol consumption and neurocognitive, functional, and symptom variables.
Prediction of Functional Skills. Linear regression analyses were conducted to find predictors of functional skills. The neurocognitive composite score, negative symptom total, age, and education were examined as predictor variables for the functional skills global score for the entire sample and for both groups. Simultaneous regressions were first conducted to determine whether the variables predicted functional skills. If simultaneous regression yielded significant results, the variables were reexamined in a forward-entry stepwise regression analysis to determine which variables accounted for a significant proportion of the variance.
Simultaneous regression for the entire sample was significant, F(5, 29) = 5.71, p < 0.01, R2 = 0.47. Forward-entry stepwise regression analysis revealed that only the neurocognitive composite score entered the equation at a statistically significant level, F(1, 33) = 24.96, p < 0.001, R2 = 0.43. Simultaneous regression for the SZ group was not significant, F(5, 11) = 0.92, p = 0.51, R2 = 0.29. Simultaneous regression of the SZ + ETOH group was significant, F(5, 12) = 5.53, p < 0.01, R2 = 0.70. Forward-entry stepwise regression analysis revealed that only the neurocognitive composite score entered the equation at a statistically significant level, F(1, 16) = 29.51, p < 0.001, R2 = 0.65.
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Discussion |
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The purpose of the present study was to examine neurocognitive functioning, symptoms, functional skills, and the interrelationships between these variables in older schizophrenia outpatients who abuse alcohol. Comparisons were made between active alcohol-abusing schizophrenia patients and those without a history of alcohol abuse. The results support the hypothesis that the schizophrenia patients with alcohol misuse have more impaired neurocognitive functioning than schizophrenia patients without alcohol abuse or dependence. Impairments were most apparent in verbal learning and memory.
A detailed analysis of the verbal learning and memory test revealed interesting patterns. Specifically, the comorbid group did not differ from the schizophrenia group on the ability to benefit from learning over repeated trials and were not significantly worse in the proportion of words retained after a delay. Thus, alcohol-abusing schizophrenia patients may have a specific impairment in learning capacity (i.e., the number of words) rather than in learning over trials or retention, as compared to their nonabusing counterparts. The working memory and verbal learning and memory impairments in the comorbid group of the present study complement findings of a recent imaging study that detected volume deficits in prefrontal and anterior superior temporal regions (Mathalon et al. 2003). Learning and memory impairment may also be associated with cerebellar dysfunction, which has previously been reported in alcohol-abusing schizophrenia patients (Sullivan et al. 2000; Deshmukh et al. 2002). The recent discovery that alcohol abuse may have effects on the pons in schizophrenia patients abusing alcohol, but not those without substance abuse (Sullivan et al. 2003), suggests that alcohol abuse may have additive effects on the brain of schizophrenia patients.
The alcohol-abusing group demonstrated poorer functional skills than schizophrenia patients without alcohol abuse. Neurocognition was the strongest predictor of functional skills in alcohol-abusing schizophrenia patients. The small sample size and relatively intact neurocognitive skills in the nonabusing group may have precluded prediction of functional skills for this group.
Quantity of alcohol use (i.e., consumption) was associated with impaired neurocognitive functioning at a level that approached statistical significance. Previous research has found quantity of use to be associated with impairments in cognitive functioning in nonpsychotic populations (DeFranco et al. 1985; Pishkin et al. 1985; Page and Cleveland 1987). Interestingly, consumption was associated with higher levels of general psychopathology, which was also significantly more severe in the SZ + ETOH group than the SZ group. This scale measures, among other variables, mood disturbance (e.g., anxiety, depression, guilt, somatic concern). Previous work has demonstrated an association between alcoholism and mood disturbance in schizophrenia patients (Drake et al. 1989; Nixon et al. 1996).
There are limitations that reduce the generalizability of our findings. The cross-sectional design of this study limits the interpretation of our findings because group differences may have been present at baseline and not a result of chronic alcohol consumption. However, in support of our results, no group differences were found in patients' demographic background (e.g., years of schooling, age at first hospitalization) and estimated premorbid intellectual ability.
The study's relatively small sample size did not interfere with our ability to find a number of important differences between the groups, including overall differences in cognitive functioning and functional skills measures. Lack of power associated with this small sample size, however, does require that interpretations regarding the specificity of group differences remain tentative.
Participants were treatment-seeking outpatients. It is possible that this recruitment method may have excluded patients with more severe alcohol abuse. Alcohol abuse can lead to treatment noncompliance and symptom exacerbation (Drake et al. 1989). These occurrences would seemingly make more severe abusers less likely to attend programs and thus unavailable for recruitment into research studies. The fact that significantly more participants in the comorbid group were taking anticholinergic medication at the time of testing could confound interpretation of group differences, particularly on neurocognitive functions, which may be sensitive to anticholinergic effects (Strauss et al. 1990); the fact that groups differences remained significant after controlling for anticholinergic dosage allays this concern somewhat. While group differences in anticholinergic usage may be attributable to the slightly (although not significantly) higher percentage of participants in the comorbid group taking conventional antipsychotic medications, it is possible that alcohol abuse produces or exaggerates the extrapyramidal symptoms that are targeted by the anticholinergic medications. Alcohol-abusing schizophrenia patients are known to have a greater risk for tardive dyskinesia (Dixon et al. 1992), so it is plausible that other movement disorders are also associated with alcohol abuse in schizophrenia. This is an important question to be addressed in future research.
Longitudinal designs that examine the effects of alcohol abuse on schizophrenia patients' symptoms, neurocognition, and functional outcome are needed. Future studies may also examine recovery of neurocognitive functions in alcohol-abusing schizophrenia patients. The fact that cognitive functions are somewhat restored after abstinence from alcohol provides an opportunity for future research to study the direction of causality. If cognitive functions in alcohol-abusing schizophrenia patients improve after abstinence to levels consistent with those by schizophrenia patients not abusing alcohol, this would provide strong evidence that alcohol use compounds underlying neurocognitive deficits that are pathognomonic to schizophrenia.
Because polysubstance abuse is common in schizophrenia, it would be interesting to examine the combined effects of alcohol and cocaine on neurocognition and functional skills. The pattern of learning and memory deficits in the alcohol-abusing schizophrenia patients in the present study appears very similar to that found in samples of cocaine-dependent schizophrenia patients (Serper et al. 2000a, 2000b).
In treatment, schizophrenia patients are often faced with challenges to learn skills for coping with symptoms, generalize these skills to a variety of settings, and then evaluate complex information and act accordingly in the environment. Understandably, this is a challenge for people who have impaired attention, learning, memory, and mental flexibility. Alcohol abuse appears to further impair these neurocognitive functions. Treatment programs may prove ineffective if they rely on storage of large amounts of verbal information or mental flexibility. Yet in substance abuse treatment, patients are quickly faced with complex and abstract concepts (e.g., denial, powerlessness) and are expected to generalize skills to a number of environments. Accordingly, treatment strategies that consider the concomitant neurocognitive impairments of alcohol abuse have been proposed, such as delaying and slowly pacing aspects of treatment that rely on memory and abstract thinking and continually monitoring the patients' ability to benefit from treatment techniques (McCrady and Smith 1986). Given the demonstrated ability of alcohol-abusing schizophrenia patients to learn at a rate consistent with nonabusing patients, albeit at a lower capacity, they may still benefit from psychotherapy and rehabilitative techniques. However, it will be essential for clinicians to consider the amount of information to be learned and assist patients in retaining and generalizing skills.
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This article is based on a doctoral dissertation submitted by Christopher R. Bowie to the psychology department at Hofstra University. Support for this research was provided by the Mount Sinai Silvio Conte Neuroscience Center (National Institute of Mental Health [NIHM] Grant MH 36692, Kenneth L. Davis, Principal Investigator [PI], NIMH Grant MH63116, Philip D. Harvey, PI, and the Veterans Affairs, Veterans Integrated Service Network 3, Mental Illness Research and Education and Clinical Centers [VA VISN 3 MIRECC]), as well as a Graduate Student Grant from the American Psychological Society awarded to Christopher R. Bowie. The authors thank Asrat Tesfa, Ph.D., Rosemary Carlsson, Ph.D., the S.T.A.R. team at the Bronx VA Medical Center, and the Comprehensive Day Treatment Center at the Northport VA Medical Center for assistance in recruitment; and Thomas Patterson, Ph.D., for making available the UPSA.
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