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Excerpt
Based upon presentations by a cadre of leaders in the field of psychopathology, genetics, and other disciplines from the 1998 annual meeting of the American Psychopathological Association, whose theme was by the same name, this well-known author and Chief of the Child Psychology Branch of the NIMH has edited an ambitious and scholarly text examining early forms of adult psychopathology. Historically, there has been a philosophical and intellectual gap between surveyors of developmental and adult psychopathology, which has led to reductionistic views by some that childhood onset disorders are either "miniaturized" versions of their adult counterparts or that they are fundamentally different, if only by the symptoms they exhibit. This book makes a reasonable attempt to bridge this gap by carefully examining the commonalties and differences associated with childhood and adult onset psychopathology. The book is primarily presented from a genetic perspective, though there is an attempt to provide some information on environmental factors that contribute to psychopathology. The premise of the book is that age at onset is a salient factor, which has the potential for understanding adult forms of psychopathology, identification of physiologically different disorders, and may yield insights leading to mechanisms of treatment.
The book is divided into five sections: a) age at onset, mechanisms, and methods; b) neurodevelopment pathways to adult psychiatric disorders, triggers of disease onset; c) schizophrenia, specific disorders; d) depression and anxiety; and e) early prevention of adult psychiatric disorders. The book addresses most major forms of major psychopathology. Schizophrenia is the most heavily emphasized, though there are sections exploring bipolar disorder, depression, anxiety, obsessive-compulsive disorder, fragile-X syndrome, alcoholism, and antisocial personality disorder.
The first section examines genetic mechanisms and methods of assessing the impact of genetic contributions on psychopathology. Information is provided throughout the chapters on two strategies: genomic scans of pedigrees and trinucleotide repeats. Badner and her colleagues (chapter 1) make the observation that early-onset illness may represent "an extreme instance along an onset curve." Further, they argue that when early-onset illness is under genetic influence that one can expect to find independent familial aggregation of prepubertal-onset cases in siblings of patients, a point that is substantiated by their findings with a large bipolar pedigree. Childs (chapter 2) outlines a eloquent model of individuality that views age of onset as the product of genetic and experiential forces whose contributions change relative to the developmental state of the organism. This perspective has been described for some time by other authors as the epigenetic model of development. Cemen and Warren (chapter 3) describe trinucleotide expansion of the FMR1 gene that causes fragile-X syndrome. The chapter provides welcome information about the basic characteristics of fragile-X syndrome, historical genetic findings, and current genetic knowledge about the disorder. Compelling arguments are presented concerning two mechanisms of phenotypic expression, the permutation allele and the Sherman paradox (pp. 46-47). The Sherman paradox is of particular interest because it suggests that there is a relatively high frequency of nonpenetrant male carriers who have affected offspring.
The second section on neurodevelopmental pathways begins with a chapter by Tarrant and Jones on biological markers of schizophrenia. There is an elaborate dissertation of risk modifiers and risk indicators for the disorder, including dermatoglyphic patterns (dermal ridges on the palms and soles; pp. 82-86) and their sensitivity and specificity for the disorder. The authors conclude that abnormal nervous system development precedes schizophrenia but is not specific to the disorder, which limits its usefulness as a definitive marker.
