Introduction

Schizophrenia is the most serious of mental disorders, leading to significant, although not always persistent, impairments in functioning in approximately 1% of the population [1]. From an evolutionary perspective, schizophrenia has been conceptualized as either a disadvantageous by-product of human brain evolution or an evolutionarily advantageous outcome [2]. In terms of day-to-day living, untreated schizophrenia has a clear deleterious effect on functioning, with seemingly minimal social or occupational advantage. Despite significant impairment, particularly in moderate to severe cases, some people with schizophrenia find partners and have children, most likely prior to their first psychotic episode. The offspring of these individuals are at increased risk for developing psychiatric disorders, including schizophrenia, because of both genetic and environmental factors. These risks may be exacerbated by the greater likelihood that schizophrenic women will have children with men who are also suffering from a psychiatric disorder [3].

The diathesis-stress model proposed by Meehl in 1962 [4] has been widely accepted as the most comprehensive explanation for the development of psychosis. Data gathered over the past 100 plus years provide strong support for the notion that both genetic vulnerability and environmental stressors play a role in the development of schizophrenia spectrum disorders. These factors either enhance or compromise the development of personality in a complex, multi-directional fashion. The latter point is illustrated in the case of the Genain sisters, a group of

Early Detection and Management of Mental Disorders.

Edited by Mario Maj, Juan Jose? Lopez-Ibor, Norman Sartorius, Mitsumoto Sato and Ahmed Okasha. ©2005 John Wiley & Sons Ltd. ISBN 0-470-01083-5.

monozygotic quadruplets concordant for schizophrenia but discordant for the severity and onset of their illness [5]. Despite identical genetic load, a combination of environmental idiosyncrasies and differential treatment by their parents has apparently either enhanced or diminished the expression of their genetic vulnerability [6,7]. Similarly, their genetic endowment appears to have interacted with the environment to affect outcome. For example, two of the girls were considered more attractive and less frail than the others, and consequently were treated as healthier and more likely to succeed. The less attractive girls were seen as more inept, even ''retarded'', and were treated by their parents accordingly [8]. In reality, this pairing of the twins was probably unfounded, as one of the ''less attractive'' girls was actually more functional than her parents' treatment would suggest [8]. More in-depth data gathered from the Genain quadruplets will be discussed in a later part of this chapter, with the main point here being that genetic and environmental factors seem to have additive and reciprocal effects. This reality complicates efforts to identify and separate the effects of genetic and neurobehavioural disease markers.

Another challenge to researchers looking for disease predictors involves disentangling prodromal signs from premorbid indicators [9]. For example, social isolation in adolescence may be a prodromal sign of schizophrenia whereas this same variable may be viewed as a premorbid indicator if present in early childhood. Longitudinal studies have been particularly helpful in identifying predictors of illness, although categorizing these predictors as prodromes versus premorbid indicators is difficult. The strength of longitudinal studies is that they allow for a comprehensive assessment of high-risk children over the life course, prior to the emergence of full-blown psychosis. Converging evidence from these studies strongly suggests that neurodevelopmental processes are involved in the aetiology of schizophrenia; that is, antecedents of schizophrenia spectrum disorders are evident as early as infancy and continue to evolve over the course of childhood.

Although investigations indicate a link between genetic factors and subsequent development of psychosis, not all vulnerable persons go on to develop schizophrenia or spectrum disorders. Correctly predicting which high-risk individuals will actually go on to develop schizophrenia always involves a degree of error. Specificity is the probability of concluding that someone is affected by a disorder when he or she is truly not (false positive rate), while sensitivity refers to the probability of concluding that someone is affected with a disorder when he or she actually is (true positive rate). The sensitivity and specificity of particular indicators is an important aspect of discerning whether or not an indicator will be useful. Classifying someone as likely to develop schizophrenia when this is not the case could result in costly and perhaps damaging intervention efforts, because of labelling, stigmatizing, etc. Conversely, underestimating who is likely to develop the disorder would lead to a higher preponderance of individuals being deprived of needed early intervention. This chapter provides an overview of empirical research related to children who are at high risk for developing schizophrenia, those children who are the offspring of a schizophrenic parent (or parents). Consideration will be given to genetic factors thought to be important in the development of schizophrenia, identification of possible predictors and their relative usefulness, and intervention strategies that may be suitable for high-risk children.

BiPolar Explained

BiPolar Explained

Bipolar is a condition that wreaks havoc on those that it affects. If you suffer from Bipolar, chances are that your family suffers right with you. No matter if you are that family member trying to learn to cope or you are the person that has been diagnosed, there is hope out there.

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