Psychiatric developments最新文献

The definitional criteria of the 3 systems (DSM-III, DIB and Kernberg) have been compared. While there is rather weak agreement between the criteria of DIB and those of DSM-III, there is no agreement at all between Kernberg's criteria and those of the other 2 systems. When the 3 systems are compared in terms of empirical diagnosis, the agreement between DSM-III and DIB is moderate and clearly stronger than that between Kernberg and either DSM-III or DIB. In terms of sensitivity, the Kernberg borderline comprises the DSM-III and DIB borderlines as subsets. The findings are consistent with the idea that Kernberg's borderline concept is an instance of a severity or maturity level construct, while DSM-III and DIB are characterological constructs, orthogonally related to the level construct.

This article focuses on the measurement of 'negative symptoms'. Standardized scales used to rate negative symptoms are reviewed and compared, as are the individual items which comprise them. The overlap of negative symptoms, akinesia, and depression is explored, and means are suggested to improve the precision of defining and measuring negative symptoms. Flat affect is the only item present in all negative symptom scales and may overlap with depression and akinesia. Inappropriate affect and attentional disturbance should not be considered negative symptoms. Poverty of speech and anhedonia lack unified definitions, and in some scales, they can also be confounded with depression and akinesia. The psychometric properties of most scales have not been sufficiently studied. The lack of long-term studies of stability of the supposedly enduring negative symptoms is especially worrisome. Carpenter's deficit syndrome consisting of non-secondary negative symptoms lasting more than one year is a promising new step to try and address some of these problems.

Sex differences in social play are quantitative and not qualitative, referring to frequency and not the form of the behaviors. Whereas increased perinatal exposure to exogenous testosterone masculinizes social play, experimental manipulations of androgen levels after this period (i.e. following critical periods for neuronal differentiation) apparently have no effect on the expression of social play. This effect appears to involve, at least in part, androgen receptor occupancy in the amygdala. In the rat, there is a prominent sex difference in nuclear-bound androgen receptors in the amygdala during the sensitive period for the masculinization of play-fighting. Moreover, testosterone implants directly into the amygdala during this period masculinize social play in females. Progesterone exposure reduces play-fighting in male rats, as does corticosterone. This latter effect may be mediated by corticosteroid receptors in the limibic brain. Perinatal androgen exposure may also be important in humans, since girls born with congenital adrenal hyperplasia diagnosed and treated at birth still show male-like patterns of play. Theories concerning the function of sex differences in social play emphasize either the social or motor learning functions. Juvenile male primate social rank correlates with number of peer social interactions, which predominantly take the form of play-fighting. Females on the other hand appear to spend less time play-fighting and spend more time waiting and competing for interactions with infants, i.e. play-mothering, whereby they acquire the motor skills necessary for handling infants. Such differences may reflect socio-biological and developmental cascades that are, in some way, initiated by perinatal hormonal events.

There are large sex differences in the incidence of many psychiatric diseases. The bases for these sex differences are probably complex and are likely to involve the interaction of both social and biological factors. Probable social factors include child rearing practices, personal expectations and lifestyles, and societal institutions. Biological factors would likely include genetic effects, hormonally mediated neurodevelopmental effects and hormonally mediated neuroregulatory effects. This paper focuses upon the developmental effects of gonadal hormones. The sex differences observed in the neuroanatomy and behavior of nonhuman mammals are reviewed. The instances in which developmental exposure to gonadal hormones has been demonstrated to be involved in establishing these sexual dichotomies are surveyed. The molecular mechanisms by which differences in prenatal and early postnatal levels of gonadal hormones may generate such sex differences are examined. Sex differences in human neuroanatomy and cognitive function are discussed. Finally, we speculate on ways in which similar hormonal mechanisms might act to influence psychiatric disorders.

This report reviews current data on the familial aggregation of Alzheimer's disease (AD). Single pedigree reports indicate that in few families AD is inherited as an autosomal dominant single gene disorder. Family studies show that first-degree relatives of AD patients have a higher lifetime incidence of AD than the general population or groups of nondemented subjects. Case-control studies indicate that the risk of developing AD is significantly higher for subjects with family members affected by dementia than for those without. The concordance rate in monozygotic twin pairs was found to be much lower than expected from an autosomal dominant disease. These data are inconclusive; however, they suggest that in future etiologic studies 3 types of AD should be considered separately: autosomal dominant, familial, and sporadic. Subclassification of AD by type of occurrence generates groups of patients which are probably more homogeneous regarding etiology.

Neurotic Depression was among the most commonly used psychiatric diagnoses until the introduction of DSM-III. Because of multiple criteria and meanings and the lack of diagnostic stability on follow-up, Neurotic Depression was not included as a category in DSM-III and will be omitted in ICD-10. This article reviews recent research on the validity of Neurotic Depression and its relationship to other types of depressive disorders. Empirical studies do not support the validity of this diagnosis. There is no unitary clinical description or phenomenological discrimination from other disorders, and limited supporting family study, laboratory investigation, or specific treatment response. Revised criteria for Neurotic Depression, derived from three recently conducted studies, need to be validated in prospective studies. Pending new research findings, the decision to omit Neurotic Depression from the classification of depressive disorders in DSM-III, DSM-III-R and in the draft of ICD-10 remains scientifically justified.

The concept of cycloid psychosis or cycloid psychotic disorder has been used in the European psychiatric literature for almost half a century. However, it has now for the first time been comprised into the 10th revision of the World Health Organization's International Classification of Diseases (ICD-10) that is currently in the phase of field trials. In this article evidence is presented that supports the independence of cycloid psychotic disorder from other major psychotic disorders. In particular, evidence is presented in favour of the clinical and predictive validity of the cycloid psychosis construct. Issues related to treatment are discussed and suggestions for future research are given.

This paper discusses various factors that must be considered in designing histological studies of schizophrenic brain. An examination of the literature prior to 1952 reveals that much of the controversy arising during the first half of this century can be understood within the context of methodological flaws that included the use of inappropriate controls, the lack of systematic diagnosis of schizophrenia, an absence of blind quantitation and finally, a failure to control for the effects of several potential confounding variables. In addition to these latter concerns, the design of post-mortem structural analyses of schizophrenic brain must also consider what brain areas are reasonable to examine, what morphometric parameters should be evaluated to test a hypothesis in question and whether any differences noted represent primary, secondary or perhaps even epiphenomenal changes in the brain. The life cycle of schizophrenic patients should be considered in these designs so that factors intrinsic to the disorder, such as a genetic trait marker or the effects of perinatal insult, can be distinguished from changes that may arise later, perhaps in relation to the acquisition of the defect state. The basic principles of neurobiology and clinical psychiatry should be applied in developing a design and in interpreting data that emerges. Taking all of these issues into account, complex strategies will be required in order to obtain reliable, valid and clinically relevant information that can contribute to our understanding of the pathophysiology of schizophrenia.

In this paper we propose that theories of early personality development be revised to consider knowledge of neurodevelopment. Research findings are reviewed that have established the presence of regressive changes in the normal development of the brain. These regressive changes, consisting of neuronal death and process and synapse elimination, are theoretically linked to three precursors of personality: sex differences, temperamental traits and perceptual-motor coordination. Evidence supporting these hypotheses is provided from studies examining how the effects of genetic, environmental, and experiential factors on brain development may determine the development of these personality features.

The major goal of psychobiological research is to understand the neural and genetic mechanisms involved in the pathogenesis of psychiatric disorders. In recent years, developmental, neurobiological and molecular biological approaches have been used to investigate substrates of behavior in animals. Examples of innate or instinctual behavior, such as cowering before predator images, aggressive or reproductive responses to abdominal coloration, have in common a determined time course following triggering by stimulus. These 'modal action patterns' may have analogies with more complex human behaviors which are highly stereotyped. Many apparently innate behavior patterns have an experiential component, for example, imprinting or song development in birds. Birds are sexually differentiated as regards telencephalic regions which determine song. The example of alterations in occular dominance columns in the occipital cortex following eyelid suture at a critical development period illustrates the sensitivity of 'hard wired' neuronal systems to experiential factors. There are also examples of genetic determinants of behavioral expression. In Drosophila, a mutant has been discovered which develops hyperactive movement in response to exposure to ether anesthesia. This abnormal behavior has been shown to be associated with abnormal potassium conductance associated with a specific channel. The molecular determinants of learning have been studied in the gill and syphon withdrawal reflex of Aplysa. Short-term learning is associated with a change in a specific kinase which influences a voltage gated potassium conductance, leading to prolonged depolarization, enhanced calcium influx, leading in turn to augmented neurotransmitter release. Longer term learning depends on expression of specific mRNAs, and inhibitors of protein synthesis, administered at critical periods, disrupt the development of long-term memory. The author discusses the viability of passing from examples such as these to an eventual understanding of psychiatric disorders.