Incidence and type of psychiatric disturbance in dropouts from a state university.
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Biomedical subjects
Publications and source records attributed to R J Cadoret.
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This study used an adoption design to investigate the relationships among genetic background, environmental factors, and clinical outcome of attention deficit/hyperactivity, aggressivity, and adult antisocial personality (ASP) in a sample of 283 male adoptees. A biologic parent adjudged to be delinquent or to have an adult criminal conviction predicted increased attention deficit/hyperactivity in the adopted away sons, as well as increased adult ASP diagnosis. Aggressivity in the adoptee was predicted by attention deficit/hyperactivity, and aggressivity in turn predicted increased adult ASP. Environmental factors of socioeconomic status (SES), and psychiatric problems in adoptive family members correlated significantly with various clinical outcomes of aggressivity, attention deficit/hyperactivity, and ASP. The results suggest that attention deficit/hyperactivity should be considered a syndrome that has a variety of correlated behaviors, such as aggressivity, and that each of these correlated behaviors is influenced by different genetic and environmental factors and their interactions. Depending on the mix of factors, adult ASP can be one of the outcomes.
Clozapine has proven to be more effective than typical antipsychotics in treatment-refractory schizophrenic patients, and some evidence suggests that it may be particularly useful in treating the negative symptoms of schizophrenia. However, it is unclear whether this observation reflects improvement in "primary" or "secondary" negative symptoms. We hypothesized that a portion of clozapine's effect on negative symptoms would be related to an improvement in positive (psychotic and disorganization) symptoms, a decrease in extrapyramidal side effects (EPSE), and/or a decrease in depressive symptoms. The remainder of its effect would be related to a direct effect on the neural circuits or pathologic processes responsible for the negative symptoms. Twenty-nine treatment-refractory schizophrenics treated with clozapine for 6 weeks were studied. The core negative symptoms measured by the Scale for the Assessment of Negative Symptoms ([SANS] affective flattening, anhedonia/asociality, avolition/apathy, and alogia) all improved with clozapine treatment. Overall, there was a 31% improvement in negative symptoms, a 32% improvement in psychotic symptoms, and a 35% improvement in disorganization. The improvement in negative symptoms was correlated with improvement in disorganization, but not with improvement in psychotic symptoms, depression, or drug-induced EPSE. Although there was a correlation between improvement in negative symptoms and improvement in disorganization, there was a suggestion that the two are changing in parallel, but are independent of each other. It appears that at least a portion of clozapine's effect on core negative symptoms is mediated through a direct effect on the underlying pathophysiology of schizophrenia associated with negative symptoms.
The contributions of genetic and both positive and negative environmental factors were tested in the prediction of alcohol abuse/dependence among 300 adult adoptees. No direct effects for either genetic or environmental factors were significant in the prediction of adoptee alcohol abuse/dependence. However, among women, early-life family conflict and psychopathology in the adoptive family interacted with a biological background of alcoholism. Among women with at least one alcoholic biological parent, conflict or psychopathology in the adoptive family increased the probability of alcohol abuse and/or dependence. Among men, no significant interactions were found between a biological background of alcoholism and environmental variables. Results suggest a pattern of gene-environment interaction among women.
The time course of patient initiated visits, somatic, functional, and other medical complaints was studied in a group of 58 patients from a family practice who had been diagnosed and treated for anxiety. The findings were contrasted with two other groups of patients from the same practice: 101 depressives and 101 controls. Results indicate that the anxiety patients differed markedly from the depressives in having a very short-lived episode of anxiety or somatic complaints in contrast to depressives' much longer history of somatic and functional complaints which appeared to precede by months the diagnosis of depression. The findings suggest that the anxiety patients in this practice either had a qualitatively different condition from the depressives, or possibly suffered from a short-lived and unrecognized depression.
In a sample of 102 women who had been adopted at birth, drug abuse/dependency was found by log-linear analyses to have a major pathway of genetic etiology that started with a biologic parent with antisocial personality and led to an adoptee with conduct disorder and then through aggressivity to drug abuse/dependency, as well as from conduct disorder directly to drug abuse. This result was similar to findings from a male sample collected from the same agencies and at the same time, wherein antisocial biologic parents produced aggressive and conduct-disordered off-spring, who in turn became drug abusers/dependents as adults. Results are compatible with family studies demonstrating that female drug abusers stem from deviant families and themselves demonstrate socially deviant behavior early in life. The present study shows that one element of familial factors is genetic, and that, in addition, the family environment directly affects behavior (aggressivity) that leads to drug abuse/dependency.
DSM antisocial personality disorder (ASPD) requires a retrospective diagnosis of conduct disorder-historical behavior not present in everyone with adult ASPD criteria. Using adoption study data, we examined the impact of this requirement on biological and environmental risk associations. We also compared clinical correlates of adult antisocial behavior with and without prior conduct disorder. We defined three subgroups: DSM-III ASPD (n = 30), adult antisocials without conduct disorder (n = 25), and controls (n = 142). By design, the sample had a high incidence of biological parent ASPD, which was partially confounded with fetal alcohol exposure. We compared the associations of both of these putative risk factors with subgroup membership after controlling for gender and adverse adoptive environment. We also examined differences in two sociopathy scales and the incidence of co-occurring affective, alcohol, and other substance use disorders. Finally, we explored differences in individual antisocial symptoms. Having an antisocial biological parent was a specific risk factor for ASPD. In contrast, fetal alcohol exposure, male gender, and adverse environment were associated with the adult antisocial syndrome, regardless of conduct disorder history. The two antisocial groups were similar with respect to sociopathy scales, co-occurring diagnoses, and the incidence of most individual symptoms. However, several adult and conduct disorder symptoms had significant specific associations with biological or environmental background or their interaction. Phenotypic expression of the biological-possibly genetic-risk for ASPD appears to be manifest before adulthood. The influence of other risk factors may not depend on antecedent conduct disorder. Despite this, we could not detect clinically important differences between the two sociopathic groups. The conduct disorder requirement therefore may be more relevant to etiological than clinical understanding of adult antisocial behavior.
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