Psychiatric developments最新文献

The hypothesis is advanced that certain psychoses in adults devolve from attention deficit disorder (ADD), which has a fundamental impact on cognitive and social development and thus affects personality structure and psychodynamics. This 'ADD psychosis' often masquerades as schizophrenia or an affective disorder and hence is frequently misdiagnosed, precluding appropriate clinical intervention. Based upon clinical evidence and empirical research involving phenomenological comparisons, premorbid history, high risk studies, neurodiagnostic evaluations, and pharmacotherapeutic response, it is suggested that ADD psychosis in adults be regarded as a separate diagnostic entity. Distinguishing symptomatology, anamnesis, family history, therapeutics, as well as prognosis, are discussed. The concept of attention deficit disorder (ADD), until recently referred to as minimal brain dysfunction (MBD), has been conceived as a childhood affliction with rather specific and circumscribed manifestations. The diverse features which embrace this syndrome, such as hyperactivity and dyslexia, were first identified and subsumed under the collective banner of MBD about 2 decades ago. The complex hypotheses concerning its possible etiology have been detailed elsewhere and need not be repeated here. Rutter, based on his extensive literature review and seminal studies, has come to regard MBD as a subclinical brain disorder developing from a genetically determined biochemical abnormality, which produces symptoms of hyperactivity, impulsivity, attention deficit, aggressivity, and conduct disturbance. Indeed, factor analytic studies reviewed by Rutter support the co-occurrence of these pathological features in children, yet the empirical evidence for a distinct syndrome and for a precise etiology has been admittedly weak, with some contending that MBD or ADD is simply a catch-all for disparate neurological symptoms of unknown and variable pathogenesis.

Thomas Kuhn's model of the structure of scientific procedure is outlined and applied to salient aspects of recent psychopharmacological research into the bioneural substrates of the affective disorders. It is argued that the amine hypotheses of these disorders are irrefutable in practice although not in principle and that their survival despite a lack of convincing supporting evidence and dis-proof of their initial premises suggests that they serve a paradigmatic function and that the core of this paradigm is psychological in nature rather than neurobiological. An attempt is made to show how an awareness of such functions may help explain otherwise puzzling features of the literature on the psychopharmacology of the affective disorders. Such an awareness may also help to indicate the steps necessary to replace the amine hypotheses or the likely future prospects for these hypotheses.

Massive changes in suicide rates over time have been recognized in the United States. An attempt has been made to describe these changes with age-period-cohort analyses. A variety of approaches has led us to conclude that suicide rates of non-white males, white and non-white females can be described adequately without a cohort effect. Recent suicide trends lead to the conclusion that a model based on a rising rate in more recently born white male cohorts coupled with an independent age effect could be rejected. If a cohort effect is postulated for more recent birth cohorts, it would require that the cohort suicide rate is decreasing with each successive birth cohort. Models based on high suicide rates in recent cohorts and additive age effects are probably misleading for future predictions. An association was noted between recent changes in the teenage and young adult suicide rates and rates of depression. Both may be the product of similar social influences.

The proposition that Borderline Personality Disorders (BPDs) are atypical forms of affective disorder is reviewed in the light of pharmacological, outcome and clinical studies. The case can be summarized briefly as follows: that the basic underlying cause of borderline symptomatology is an effective disorder; that mood disturbance, which is viewed as primarily biological, is more important than developmental experience and life events in maintaining borderline personality features; that therapies aimed at treating the mood disorder should therefore be expected to relieve the personality disorder. However, the pharmacological studies suggest that antidepressant medications have been largely ineffective in treating well defined BPD, except in the presence of coexisting depressive disorder. Indeed low dose antipsychotics have a demonstrated efficacy in the treatment of BPD, which does not strengthen the case for an affective etiology. Follow-up studies of BPDs suggest that dramatic characterological features seen at the time of index hospitalization tend to recede by the time patients are in their 30s, that major affective disorders fail to emerge over time, and that long-term marginal functioning derives from long-term maladaptive patterns across a variety of areas. Clinical studies suggest that 20-60 per cent of patients with BPD have a concomitant depressive disorder. Conversely the prevalence of personality disorders in depressions varies with depressive category, with considerably higher incidence of personality disturbance found in non-endogenous depression. The high rate of coexistence of these two disorders does not imply causality or primacy, in the sense that it is the affective disorder which brings out and causes the personality disorder. The review concludes that the assertion that BPD represents atypical affective disorder begs the possibility that it is precisely in having borderline features that they are atypical, and hence distinct.

A new multivariate analytical technique for the analysis of medical classification, Grade of Membership analysis, is utilized to examine somatization disorder in a community population. The authors examine whether somatic symptoms will cluster into a clinical syndrome resembling somatization disorder, as defined by the Diagnostic and Statistical Manual of Mental Disorders (DSM-III), if no prior assumptions are made about the inter-relationship of somatic symptoms or their clustering into clinical syndromes. Using respondents in the US National Institute of Mental Health Epidemiologic Catchment Area project of the Piedmont Region of North Carolina, Grade of Membership analysis was applied to all respondents reporting 3 or more somatic symptoms from the somatization disorder section of the Diagnostic Interview Schedule. Seven 'pure' types, roughly analogous to clusters in cluster analysis emerged from the analysis. One 'pure' type in the analysis is nearly identical to DSM-III somatization disorder and is associated with demographic characteristics found among patients with DSM-III somatization disorder. The results indicate that symptoms associated with somatization disorder cluster in a highly predictable fashion and represent a strong validation of the natural occurrence of an entity resembling somatization disorder.

Maternity Blues, although seldom a serious problem in clinical practice, is potentially important to research on affective disorders in general. Childbirth is a major life event known to be associated with large changes in maternal hormones. The determinants of the Blues may therefore be psychological and social, or biological, or both. This paper reviews the relevant literature. Reported associations between Maternity Blues and psychiatric disorder are examined. Possible psychological, social and biochemical determinants are reviewed, but no firm inferences on causation can yet be drawn. Conflicting results in the literature may have been due to variations in definition and measurement of the syndrome. The authors have recently used psychometric methods to develop a questionnaire for detecting and measuring Maternity Blues. By cluster analysis of responses to the questionnaire, a 'Primary Blues' cluster was defined, consisting of 7 items: tearful, tired, anxious, over-emotional, up and down in mood, low spirited, muddled in thinking. The item 'depression' appeared in another less frequent cluster.

Although DSM III has removed the category of neurosis, the implied fragmentation of the generic concept has been regretted by some investigators. Since its introduction in 1769, when the term was used to denote conditions which had a hysterical and hypochondriacal character, the technical use of the term has undergone revisions and reinterpretations which at one extreme have been embedded in psychoanalytic theory, and at the other have resulted in the replacement of the single concept by a proliferation of operationally defined syndromes. The present paper discusses some of the nosological problems implicit in recent trends. Whereas depression appears in 10 ICD9 categories does the psychiatric/neurotic dichotomy in relation to depression still have meaning in the absence of the generic term 'neurotic'? The hierarchical principle is widely accepted as a basis for classification, and yet the hierarchically minor syndromes may be a source of major distress. The paper reviews epidemiological studies of prognosis and follow-up of neuroses, and shows a significant excess of mortality, which is both behavioural and organic in origin. One important difficulty with the loss of the generic term is the potential loss of generic research where, for example, evaluation of treatment of panic disorder is considered distinct from other types of anxiety and phobia. The paper argues for the practical and theoretical benefits of retaining an umbrella term such as 'neuroses'.

This paper focuses on problems that can be encountered in conceptualizing, executing and writing up large-scale psychiatric epidemiological studies. It makes no attempt to cover fundamental issues of design and analysis, rather it centers on problems associated with projects of considerable size. In the conceptual area, it discusses the prerequisites to be considered before deciding to launch such a study. It notes the administrative and scientific uses of epidemiological studies and considers the strengths and weaknesses of large-scale studies to address those concerns. Issues in carrying out such studies are discussed including decisions about study design, sampling method and instrumentation. All are dependent on the central purpose of the study but trade-offs between feasibility and scientific rigor are always present. Data collection and analysis problems highlighted in large-scale studies are examined. They include the difficulty, in the former, of adequately motivating and supervising field personnel and, in the latter, of dealing with problems that accompany missing data and complicated sampling strategies. Potential problems in data access and use and writing up the results are seen as arising from the presence of a large investigative team with diverse interests. Lastly, the comparative worth of these studies is considered.