Biomedical subjects
Publications and source records attributed to R E Tarter.
Fifteen alcoholic inpatients who had had a liver biopsy for medical reasons were given a series of laboratory tests and a neuropsychological test battery. Results indicated significant correlations between the biochemical measures of hepatic dysfunction and different aspects of cognitive test performance.
In exploring potential alcoholism typologies, this chapter critically examines findings of adoption, high-risk, and familial alcoholism studies and studies of psychiatric syndromes in alcoholic individuals and their families. The adoption studies revealed that familial alcoholism and childhood conduct disorder and hyperactivity are associated with subsequent alcoholism. However, the relationship between childhood hyperactivity and alcoholism is probably coincidental to the conjoint presence of aggressive and antisocial behaviors in the same individuals. Psychiatric diagnosis and family psychiatric history studies suggest a synergistic relationship between alcoholism and sociopathy. Clinical studies of familial and antisocial alcoholism indicate that both are associated with early onset, more severe alcoholism, and poorer treatment outcome. Both meet clinical criteria for an alcoholism typology, although the evidence is more compelling for antisocial alcoholism. The findings of metabolic, electrophysiological, and neuropsychological differences between high- and low-risk subjects are of potential import, although their present significance is uncertain. Further clinical evaluation of antisocial and familial alcoholism and their relationship to each other is necessary. High risk and familial alcoholism findings may be confounded by the subjects's antisocial characteristics.
A study was conducted of the relationships between psychopathology and neuropsychological deficit in chronic alcoholic patients who had received the Minnesota Multiphasic Personality Inventory (MMPI), the Halstead-Reitan Neuropsychological Test Battery, and the Wechsler Adult Intelligence Scale (WAIS). Classification of the MMPIs by code type resulted in the formation of groups of 10 subjects with normal MMPIs, 19 subjects with MMPI profiles suggestive of depression, and 10 subjects with profiles suggestive of psychosis. Analysis of covariance was performed for various Halstead-Reitan scores; the only significant findings emerged for several of the verbal subtests of the WAIS. The group with psychotic MMPIs did substantially more poorly on these measures than the other groups. It was concluded that depressed alcoholics do not show greater neuropsychological deficit than do individuals with no significant psychopathology other than alcoholism. However, alcoholics with MMPI profiles that suggest psychosis differ from the other groups studied with regard to certain verbal abilities.
Fifty alcoholics who reported a greater number of childhood hyperactivity/minimum brain damage (MBD) symptoms (HA+ alcoholics) were compared to 49 alcoholics low in childhood hyperactivity/MBD (HA- alcoholics) with respect to patterns and severity of alcoholism, psychosocial functioning and physical status, personality and psychopathology, and familial alcoholism. HA+ alcoholics were found to report considerably more psychopathology on the MMPI and the Psychopathic State Inventory (PSI), findings which were suggestive of an underlying personality disorder. HA+ alcoholics were also found to differ significantly from the HA- alcoholics in several areas of psychosocial functioning and with respect to their pattern of alcoholism. That is, HA+ alcoholics had more interpersonal difficulties and had experienced more psychological/emotional problems; they were more likely to use alcohol to alter their moods and to use non-alcoholic illicit drugs; and they had less ability to internalize control of their impulses to consume alcohol. These findings, taken together, suggest that alcoholics reporting more symptoms of childhood hyperactivity/MBD may represent a subgroup within the larger alcoholic population. High and low hyperactivity alcoholics did not differ in severity of alcoholism or in alcohol-related physical effects or medical problems. Additionally, no evidence was obtained for a significant relationship between childhood hyperactivity and familial alcoholism.
Hemispheric laterality, measured by the Wechsler Verbal IQ-Performance IQ differential score, in a large group of delinquents (N = 101) was not associated with violent-nonviolent behavior. Delinquents were, however, likely to be relatively more impaired on verbal than on nonverbal intellectual capacities.
In 76 alcoholic men who were Veterans Administration inpatients, the presence of familial alcoholism was ascertained by means of an investigator-expanded version of the family history section of the Renard Diagnostic Interview. Subjects who had experienced 5 min of unconsciousness resulting from trauma, or at least two periods of unconsciousness or hospitalization as a result of injury were categorized as head injured. Of the familial alcoholics, 60.4% were found to be head injured, as contrasted with 34.8% of nonfamilial alcoholics, a statistically significant group difference. The possible etiological origins of this difference and its behavioral and treatment implications are discussed.
In a group of delinquent adolescent boys, the sons of alcoholic fathers (N = 16) did not differ from the sons of nonalcoholic fathers (N = 25) on either the number or pattern of features characterizing hyperactivity-minimal brain dysfunction. The findings suggest that childhood hyperactivity cis not a risk factor specific to alcoholism.
The psychological and biological characteristics associated with the vulnerability to alcoholism are reviewed. The predisposing features can be accounted for on the basis of deviations in empirically established temperament traits, thereby supporting the viability of a behavior-genetic perspective for elucidating the susceptibility to alcoholism. The temperament perspective also has heuristic value for improving our understanding of the neurobiological mechanisms that link the genetic predisposition to overt behavior. In addition, the temperament approach has ramifications for the prevention and treatment of alcoholism, as well as for clarifying the etiology and classification of certain other psychiatric disorders. The questions of what may be inherited in alcoholism and how this information can be usefully applied to enhance our knowledge of alcoholism etiology, prevention and clinical management are addressed.
A series of neuropsychological tests known to be sensitive to the effects of chronic alcoholism was administered to 25 detoxified alcoholic patients with histories of mild head injury and 25 detoxified alcoholics matched for age, race, socioeconomic status, education and drinking history parameters, but without histories of head injury. None of the tests was performed at significantly different levels by the two groups. It was concluded that mild head injury did not compound the effects of chronic alcoholism among these patients, although it was noted that both groups demonstrated the anticipated impairments on the tests. It was also suggested that researchers need not exclude alcoholic subjects with mild head injury histories from studies involving the use of standard neuropsychological tests.
With the recent emphasis on clinical research there has developed a greater sophistication in identifying and uncovering possible confounding subject variables. The investigator searching for etiologies and underlying relationships is accordingly increasingly faced with the question of how to deal with, or control numerous subject variables which may covary with the condition or disorder under study. The present paper describes some of these variables and the problems their presence raises for the conduct of clinical research. Although most of the examples described such as childhood hyperactivity, head injury, psychopathology, and physical disorders of the subjects are specifically relevant to neuropsychological research in alcoholism, many of them should be pertinent also for related areas of inquiry. The difficulties and problems in controlling, ruling out and taking such variables into account, as well as guidelines and strategies for their treatment and management, are considered. The question of the generality of findings which arises when so many subject variables are controlled is discussed. It is concluded that we are just on the threshold of identifying and clarifying the behavioral effects of numerous subject variables, conditions and disorders. The implications of this situation for the validity of our current research findings are discussed.
Evidence accrued during the past two decades points to a genetic predisposition for alcoholism. The biological expression of the genetic vulnerability, however, is unknown. This discussion addresses the neurological manifestation of alcoholism vulnerability, including the biochemical, physiological and behavioral characteristics which appear to be associated with an increased risk for alcoholism.
A small group of children with various types of immunodeficiency disorders, examined on a battery of neuropsychological and intellectual tests, was found to be impaired on perceptual speed, visuospatial sequencing, and visual attention span capacities when compared to a control group of closest aged siblings and normal children matched for age, education, and IQ. The results suggest that cerebral dysfunction may be associated with immunodeficiency disorders in children, although these findings are tentative since other factors, such as the effects of chronic illness, could not be excluded in this small cohort of patients.
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The literature on the causes of neuropsychological deficits (NDs) in alcoholics is reviewed. It is asserted that NDs are caused not simply by the neurotoxicity of alcohol but by the interrelationships of various factors. NDs might thus reflect problems antecedent to or concomitant with alcoholism and not just the consequences of alcohol use. The family histories of alcoholics have shown that a differential susceptibility to NDs might have a genetic basis. NDs might also be due to the fetal alcohol syndrome. Children who eventually become alcoholics have been shown to be more impulsive and hyperactive than other children, factors related to NDs. There seem to be multiple pathways leading to NDs--two ND syndromes, an acceleration of the normal aging process and an amnesic syndrome, seem to be a consequence of alcoholism. Depression and sociopathy are independently related to both alcoholism and NDs, so causal attributions are difficult to determine. The contribution of head injury to NDs in alcoholics might also be important. NDs in alcoholics suffering from liver disease seem to be caused in part by the liver disease and not the alcoholism per se. Liver disease is also associated with nutritional deficiencies which, in turn, can produce certain NDs. Dysfunction in several neurological mechanisms has been shown to be related to alcohol consumption. However, neuronal metabolism, metabolizing enzymes, membrane permeability, neurotransmitters, endocrine function, cerebrovascular pathology and cerebrospinal pathology have not been found to be related to NDs. The effect of congeners has not been investigated.(ABSTRACT TRUNCATED AT 250 WORDS)
A theory of the origins and mechanisms of denial, which is frequently characteristic of alcoholics, is proposed on the basis of a biopsychological rather than a psychodynamic model of emotion. The biopsychological approach views denial as a consequence of a developmental defect in the apperception of interoceptive stimuli and in the appraisal of the significance of environmental events. Three hypotheses must be substantiated in order to support this theory: (1) alcoholics were physiologically unstable in arousal regulation; (2) alcoholics cannot cognitively discriminate interoceptive cues and physiological states; and (3) alcoholics cognitively underestimate emotion-laden events in their lives. Research which demonstrates the validity of these hypotheses is reviewed and implications for future research and treatment strategies are discussed.
Portal-systemic encephalopathy (PSE) is a common condition affecting individuals with chronic hepatic dysfunction. The clinical presentation of PSE often mimics a number of psychiatric disorders and, as discussed in the text, complicates the treatment of persons who suffer from both liver dysfunction and psychiatric illness. This review of the literature addresses the etiology, natural history and treatment of PSE. Special attention is devoted to clarifying the cognitive and affective manifestations of chronic low grade PSE.
A neuropsychiatric study of individuals who underwent successful liver transplantation an average of 3 years previously was conducted to assess quality of life in terms of cognitive capacity and psychiatric status, as well as social and behavioral functioning. Compared with a control group of patients with Crohn's disease, liver transplant patients did not differ on measures of intelligence, language, attention, concentration, spatial organization, memory, or learning. Performance on these diverse aspects of cognitive functioning was in the normal ranges for both groups when compared with normative or standardized test values. The control and liver transplant patients were not different from each other on measures of psychiatric status or social functioning; however, both groups exhibited some disruption of functioning in these two areas when contrasted with normative values. We conclude that relatively young individuals (mean age in this study, 27.8 years) do not exhibit debilitating long-term neuropsychiatric disability after liver transplantation, although some disturbance in social and psychiatric adjustment was observed.
A 37-year-old female with Capgras syndrome was assessed on psychometric and neuropsychological measures. Significant neuropsychological deficits suggesting a frontal-temporal cerebral dysfunction were observed. The results demonstrate that the Capgras delusion involves more than an inability to recognize faces, although this deficit is one manifestation of the disorder.