Baldwin DS, Leonard BE (eds): Anxiety Disorders. Mod Trends Pharmacopsychiatry. Basel, Karger, 2013, vol 29, pp 98–110 (DOI: 10.1159/000351931)
The Early Phases of Anxiety Disorders: From Prevention to Treatment Javier Vázquez-Bourgon ⋅ Andres Herrán ⋅ José Luis Vázquez-Barquero Department of Psychiatry, Psychiatric Research Unit of Cantabria, University Hospital Marqués de Valdecilla, IFIMAV, CIBERSAM, Santander, Spain
Abstract The ‘early intervention’ model has been applied with good results to the care of a range of serious medical conditions. The key rationale for this model is to guarantee early identification and treatment for the illness, thus preventing its progression to a more advanced and severe stage. It would also provide a framework for optimal treatment according to the stage of the disorders. Although in the field of psychiatry this model has mainly been implemented in nonaffective psychosis, research evidence supports its application in other mental disorders. To promote this initiative, the chapter explores the available evidence demonstrating the feasibility of adopting the key elements of the model in the care of the whole spectrum of anxiety disorders. In addition, the chapter describes the different stages that are possible to identify in the process of developing an illness, and also the phase-specific interventions that could be applied. Finally, the service repercussions of implementing an early intervention model in anxiety disorders are discussed.
The advantages of prevention and the benefits of early diagnosis and treatment have been assumed for a long time as a major standard of medical practice. So much so that in modern health care systems this model has been successfully applied to malignant medical conditions. This has not been the case, however, in the area of mental health where psychiatric knowledge and practice have been derived from patients with wellestablished, often chronic, disorders. In these circumstances, the nature of the illness tends to be confounded with variables related to long-term treatment and clinical course. This has conditioned the understanding of key elements of mental disorders in general and particularly of the entire spectrum of anxiety disorders. Although the application of the early intervention model has proved to be useful in advanced medical care, it has only recently been extended to mental health, focusing mainly on psychosis [1]. As a result of this, there has been a significant emergence of early interven-
Downloaded by: Univ. of California San Diego 132.239.1.231 - 3/12/2017 9:40:09 PM
Copyright © 2013 S. Karger AG, Basel
tion services for psychosis worldwide. Despite this, there have been only limited initiatives to extend the clinical staging model to other mental disorders. In anxiety disorders, the onset of the illness is difficult to distinguish from transient and benign psychopathological changes. The situation is even more critical when we consider their differentiation from unspecific emotional dysfunctions and from normal anxiety states. This means that the application of an early intervention model to anxiety disorders is dependent both on the differentiation of the boundaries between normal and preclinical psychological experiences, and on a more precise characterization of the different stages of the illness process. The focus of this chapter is on describing the different stages that it is possible to identify in anxiety disorders, and reviewing their early clinical manifestations. In addition, the foundations of the application of the early intervention model to these disorders are discussed.
Application of the Early Intervention Model to Anxiety Disorders
The application of the early intervention model is based on the idea that the course of a disease is likely to progress from an ‘at-risk’ to a prodromal state and finally to a fully developed diagnostic entity. It also implies that the disease progresses through different stages that are characterized by phase-specific clinical manifestations and treatment susceptibility. From a clinical perspective, it also assumes that the earlier stages have better prognosis, require less intensive treatments, and tend to respond better to interventions. A series of concepts are incorporated into this model, the most relevant of which are reviewed in this chapter.
In modern health care, the focus of prevention has been extended to noninfectious and chronic diseases, including mental illness and emotional disturbances. For this, the traditional classification system for prevention, differentiating the three levels of primary, secondary and tertiary prevention has been regarded as unsatisfactory. In the early 1990s the Committee on Prevention of Mental Disorders of the Institute of Medicine (IOM) proposed a new model of preventive intervention describing the three levels of universal, selective and indicated prevention. At the universal level, prevention is focused on the general public or on a whole population group that has not been identified on the basis of individual risk. At the selective level, interventions are directed at asymptomatic populations, with a higher risk of a particular disorder. Finally, at the indicated level, preventive interventions are targeted at high-risk individuals who are identified as having minimal, but detectable, signs or symptoms foreshadowing a particular mental disorder, but who do not meet the diagnostic criteria for the disease. In these populations, defined for example by the occurrence of atten-
The Early Phases of Anxiety Disorders Baldwin DS, Leonard BE (eds): Anxiety Disorders. Mod Trends Pharmacopsychiatry. Basel, Karger, 2013, vol 29, pp 98–110 (DOI: 10.1159/000351931)
99
Downloaded by: Univ. of California San Diego 132.239.1.231 - 3/12/2017 9:40:09 PM
New Concepts for Health Prevention
uated and/or subthreshold ‘illness-specific’ clinical symptoms, or by the presence of a decline in functioning and a positive family history, phase-specific interventions could be implemented to prevent or postpone the onset of a ‘full-blown’ disorder. The relevance of this model of prevention is due to the fact that it allows the integration into a comprehensive construct of the clinical manifestations of different stages of a particular psychiatric condition, with interventions directed at promoting mental health and preventing the illness. As exemplified in its application to anxiety disorders by Lau and Rapee [2], the new concept of indicated prevention set the basis for implementing preventive strategies in the early phases of the disease.
The relative contribution of genetic and environmental factors for the development of anxiety disorders has been extensively explored. In this respect, clinical genetic studies propose a genetic contribution to the pathogenesis of anxiety disorders with a heritability of about 20–50%, suggesting that a significant degree of variance is explained by environmental factors and gene-environment interactions [3]. These findings emphasize the important role that discrete environmental factors play in the liability for anxiety psychopathology, and the relevance of interactions of candidate genes and stressful life events. A key issue related to the inherited spectrum of factors is to determine how much personality traits and personality disorders, may contribute to the development of anxiety disorders. Bienvenue et al. [4] have shown that avoidant and dependent personality traits are predisposing factors, or at least markers of risk, for panic disorders and agoraphobia. Similarly, the presence of higher scores on neuroticism was, in combination with stressful life events, associated with an increased risk of developing a panic attack [5], an association which has been replicated in the Cantabria First Episode Study of Panic Disorders [6]. It is clear, therefore, that certain personality traits, in combination with specific environment factors, appear to contribute to the development of anxiety disorders. An additional predisposing factor for these disorders is the presence of prenatal exposure to biological and psychological maternal stress [7]. This raises the possibility that preventing or reducing the presence of maternal distress during the prenatal period may have long-term beneficial effects through diminishing the risk for developing anxiety problems in the next generation. In addition to genetic components, considerable attention has been given to the impact that adverse experiences in early life have on the development of anxiety disorders later in life, and on the way in which these factors interact with any genetic predisposition. Evidence mainly from preclinical studies suggests that stress early in life results in persistent central corticotropin-releasing factor hyperactivity and increased stress reactivity in adulthood [8]. Thus, genetic disposition combined with early stress in critical phases of development may result in a phenotype that is neurobiologically vulnerable to stress and consequently reduces the threshold for develop-
100
Vázquez-Bourgon · Herrán · Vázquez-Barquero Baldwin DS, Leonard BE (eds): Anxiety Disorders. Mod Trends Pharmacopsychiatry. Basel, Karger, 2013, vol 29, pp 98–110 (DOI: 10.1159/000351931)
Downloaded by: Univ. of California San Diego 132.239.1.231 - 3/12/2017 9:40:09 PM
Predictors of Anxiety Disorders
ing an anxiety disorder under the exposure during adulthood to stress. Given this, research findings have increasingly supported the notion that certain adverse life events may be more substantive to their etiological explanations. Among these events, physical/sexual abuse and loss/separation experiences during childhood have received much research attention: the presence of childhood physical and sexual abuse constitutes an important predisposing factor for the development of anxiety disorders [9], as does the presence of loss/separation experiences in childhood [10].
There is increasing evidence indicating that, even in countries with sophisticated health care systems, when a person develops a particular mental disease there is usually a long period of time before it is correctly identified and receives appropriate treatment [11]. This was initially demonstrated in psychosis, where the duration of the untreated illness ranged from several weeks to many years [12]. It is now assumed that this long period of untreated illness also appears in other mental disorders, including anxiety disorders, in which although the onset of the illness usually occurs during the first three decades of life, effective treatment is typically not initiated until a number of years later [13, 14] (see chapter on Duration of Untreated Illness and Duration of Illness in Anxiety Disorders, pp. 111–118). In accordance with this, findings from research in anxiety and obsessive compulsive disorders demonstrate that the duration of untreated illness (DUI) extends for at least one year. The Cantabria First Episode of Panic Disorders Study demonstrated that for these disorders the DUI reached one year [15]. Similarly, others have demonstrated that the DUI for panic disorders reached nearly 45 months, the one for generalized anxiety disorders 87 months, and for obsessive compulsive disorders 90.6 months [16]. The relevance of this long period of untreated mental illness is based on its presumed association with a poorer outcome and treatment response, as demonstrated for psychosis and other major mental disorders [12, 17–19]. Similarly, research evidence is accumulating to support the idea that also in anxiety and obsessive compulsive disorders the presence of a long DUI is associated with a poorer outcome and reduced treatment response [15, 20, 21]. It has been postulated that in psychosis and other major mental disorders this association is due to a possible neuro-psycho-socio-toxic effect of untreated illness. Regarding anxiety disorders, despite this hypothesis being coherent with impressions derived from clinical practice, we still lack sufficient research evidence to believe unequivocally that the existence of a long delay in initiating appropriate treatment may promote the progression of an illness-related neuro-psycho-socio-toxic effect. A complementary explanation for the association between long DUI and poor outcome is derived from the ‘critical period hypothesis’. This was originally formulated for psychosis, and proposes that the early phase of the illness constitutes a ‘critical period’ during which symptomatic and psychosocial deterioration progresses rapidly [22]. It also contends
The Early Phases of Anxiety Disorders Baldwin DS, Leonard BE (eds): Anxiety Disorders. Mod Trends Pharmacopsychiatry. Basel, Karger, 2013, vol 29, pp 98–110 (DOI: 10.1159/000351931)
101
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Duration of Untreated Illness in Anxiety Disorders
that subsequent progression of morbidity slows or stops and the level of the recovery attained, by the end of the critical period, persists into the long-term. There is increasing evidence supporting the notion that existence of a similar critical period could be postulated in major mental disorders [17, 18]. The relevance of this concept relies on the fact that it provides evidence for postulating an optimal period for neuroprotective interventions, in either the prodromal phase or early stages of the illness. Thus, it appears that there are grounds for arguing that effective early intervention procedures should be applied during this stage of maximum susceptibility to the damaging effects of illness and the neuro-psycho-socio protective effects of interventions. Whether this postulation is applicable to anxiety disorders is a pressing issue for future studies.
The Early Stages of Anxiety Disorders
A key element of the early intervention model is the operationalization of the sequence of the prediagnostic and diagnostic stages of the illness (table 1). As the different anxiety disorders do not as yet have biological markers to define these different stages, the characterization should be mainly identified by symptoms and signs. The stages may in turn correlate with prognosis and treatment, and potentially with a specific pathophysiology from which can be derived reliable and phase-specific biological markers. To guide clinicians in identifying the stages at which an individual is at a particular time, different concepts have been proposed. Although originally developed for psychosis, in recent years they have been applied, with certain adaptations, to other mental disorders, including anxiety disorders.
The first stage in the model (stage 0) is defined as a ‘at risk asymptomatic’ where a range of risk factors may be operating in asymptomatic persons. In the case of psychosis, several risk factors have been identified. Such is the case of family history of mental illness, substance abuse and premorbid personality traits [17]. Similarly, in patients who develop anxiety and obsessive compulsive disorders long before the illness appears, it is possible to identify a series of predisposing conditions: among them being prenatal and environmental factors and factors related to personality traits. In addition, the presence in young children of ‘behavioral inhibition’ (a conduct characterized by reactions of withdrawal, shyness and avoidance in novel, unfamiliar situations) and the subsequent development of anxiety disorders is well established [23]. It has also been demonstrated that children who have anxious parents or overinvolved mothers tend to develop anxiety disorders later in life [24]. The relevance of this is the fact that it can be used to identify potential candidates for early prevention and for establishing appropriate intervention targets.
102
Vázquez-Bourgon · Herrán · Vázquez-Barquero Baldwin DS, Leonard BE (eds): Anxiety Disorders. Mod Trends Pharmacopsychiatry. Basel, Karger, 2013, vol 29, pp 98–110 (DOI: 10.1159/000351931)
Downloaded by: Univ. of California San Diego 132.239.1.231 - 3/12/2017 9:40:09 PM
The ‘at Risk Asymptomatic’
Table 1. Application of the early intervention model to anxiety disorders Stage Clinical definition
Target population
Potential interventions
0
Increased risk of disorder No symptoms currently
Young age first-degree Psychoeducation for young relatives of probands persons and family Promotion of health life styles Resilience training
1
Mild or nonspecific subthreshold symptoms of the disorder Could include the presence of ‘ultrahigh risk’ syndrome (moderate but subthreshold symptoms) Mild functional (psychosocial) change or decline Mild/moderate neurocognitive deficits (GAF
The Early Phases of Anxiety Disorders: From Prevention to Treatment Javier Vázquez-Bourgon ⋅ Andres Herrán ⋅ José Luis Vázquez-Barquero Department of Psychiatry, Psychiatric Research Unit of Cantabria, University Hospital Marqués de Valdecilla, IFIMAV, CIBERSAM, Santander, Spain
Abstract The ‘early intervention’ model has been applied with good results to the care of a range of serious medical conditions. The key rationale for this model is to guarantee early identification and treatment for the illness, thus preventing its progression to a more advanced and severe stage. It would also provide a framework for optimal treatment according to the stage of the disorders. Although in the field of psychiatry this model has mainly been implemented in nonaffective psychosis, research evidence supports its application in other mental disorders. To promote this initiative, the chapter explores the available evidence demonstrating the feasibility of adopting the key elements of the model in the care of the whole spectrum of anxiety disorders. In addition, the chapter describes the different stages that are possible to identify in the process of developing an illness, and also the phase-specific interventions that could be applied. Finally, the service repercussions of implementing an early intervention model in anxiety disorders are discussed.
The advantages of prevention and the benefits of early diagnosis and treatment have been assumed for a long time as a major standard of medical practice. So much so that in modern health care systems this model has been successfully applied to malignant medical conditions. This has not been the case, however, in the area of mental health where psychiatric knowledge and practice have been derived from patients with wellestablished, often chronic, disorders. In these circumstances, the nature of the illness tends to be confounded with variables related to long-term treatment and clinical course. This has conditioned the understanding of key elements of mental disorders in general and particularly of the entire spectrum of anxiety disorders. Although the application of the early intervention model has proved to be useful in advanced medical care, it has only recently been extended to mental health, focusing mainly on psychosis [1]. As a result of this, there has been a significant emergence of early interven-
Downloaded by: Univ. of California San Diego 132.239.1.231 - 3/12/2017 9:40:09 PM
Copyright © 2013 S. Karger AG, Basel
tion services for psychosis worldwide. Despite this, there have been only limited initiatives to extend the clinical staging model to other mental disorders. In anxiety disorders, the onset of the illness is difficult to distinguish from transient and benign psychopathological changes. The situation is even more critical when we consider their differentiation from unspecific emotional dysfunctions and from normal anxiety states. This means that the application of an early intervention model to anxiety disorders is dependent both on the differentiation of the boundaries between normal and preclinical psychological experiences, and on a more precise characterization of the different stages of the illness process. The focus of this chapter is on describing the different stages that it is possible to identify in anxiety disorders, and reviewing their early clinical manifestations. In addition, the foundations of the application of the early intervention model to these disorders are discussed.
Application of the Early Intervention Model to Anxiety Disorders
The application of the early intervention model is based on the idea that the course of a disease is likely to progress from an ‘at-risk’ to a prodromal state and finally to a fully developed diagnostic entity. It also implies that the disease progresses through different stages that are characterized by phase-specific clinical manifestations and treatment susceptibility. From a clinical perspective, it also assumes that the earlier stages have better prognosis, require less intensive treatments, and tend to respond better to interventions. A series of concepts are incorporated into this model, the most relevant of which are reviewed in this chapter.
In modern health care, the focus of prevention has been extended to noninfectious and chronic diseases, including mental illness and emotional disturbances. For this, the traditional classification system for prevention, differentiating the three levels of primary, secondary and tertiary prevention has been regarded as unsatisfactory. In the early 1990s the Committee on Prevention of Mental Disorders of the Institute of Medicine (IOM) proposed a new model of preventive intervention describing the three levels of universal, selective and indicated prevention. At the universal level, prevention is focused on the general public or on a whole population group that has not been identified on the basis of individual risk. At the selective level, interventions are directed at asymptomatic populations, with a higher risk of a particular disorder. Finally, at the indicated level, preventive interventions are targeted at high-risk individuals who are identified as having minimal, but detectable, signs or symptoms foreshadowing a particular mental disorder, but who do not meet the diagnostic criteria for the disease. In these populations, defined for example by the occurrence of atten-
The Early Phases of Anxiety Disorders Baldwin DS, Leonard BE (eds): Anxiety Disorders. Mod Trends Pharmacopsychiatry. Basel, Karger, 2013, vol 29, pp 98–110 (DOI: 10.1159/000351931)
99
Downloaded by: Univ. of California San Diego 132.239.1.231 - 3/12/2017 9:40:09 PM
New Concepts for Health Prevention
uated and/or subthreshold ‘illness-specific’ clinical symptoms, or by the presence of a decline in functioning and a positive family history, phase-specific interventions could be implemented to prevent or postpone the onset of a ‘full-blown’ disorder. The relevance of this model of prevention is due to the fact that it allows the integration into a comprehensive construct of the clinical manifestations of different stages of a particular psychiatric condition, with interventions directed at promoting mental health and preventing the illness. As exemplified in its application to anxiety disorders by Lau and Rapee [2], the new concept of indicated prevention set the basis for implementing preventive strategies in the early phases of the disease.
The relative contribution of genetic and environmental factors for the development of anxiety disorders has been extensively explored. In this respect, clinical genetic studies propose a genetic contribution to the pathogenesis of anxiety disorders with a heritability of about 20–50%, suggesting that a significant degree of variance is explained by environmental factors and gene-environment interactions [3]. These findings emphasize the important role that discrete environmental factors play in the liability for anxiety psychopathology, and the relevance of interactions of candidate genes and stressful life events. A key issue related to the inherited spectrum of factors is to determine how much personality traits and personality disorders, may contribute to the development of anxiety disorders. Bienvenue et al. [4] have shown that avoidant and dependent personality traits are predisposing factors, or at least markers of risk, for panic disorders and agoraphobia. Similarly, the presence of higher scores on neuroticism was, in combination with stressful life events, associated with an increased risk of developing a panic attack [5], an association which has been replicated in the Cantabria First Episode Study of Panic Disorders [6]. It is clear, therefore, that certain personality traits, in combination with specific environment factors, appear to contribute to the development of anxiety disorders. An additional predisposing factor for these disorders is the presence of prenatal exposure to biological and psychological maternal stress [7]. This raises the possibility that preventing or reducing the presence of maternal distress during the prenatal period may have long-term beneficial effects through diminishing the risk for developing anxiety problems in the next generation. In addition to genetic components, considerable attention has been given to the impact that adverse experiences in early life have on the development of anxiety disorders later in life, and on the way in which these factors interact with any genetic predisposition. Evidence mainly from preclinical studies suggests that stress early in life results in persistent central corticotropin-releasing factor hyperactivity and increased stress reactivity in adulthood [8]. Thus, genetic disposition combined with early stress in critical phases of development may result in a phenotype that is neurobiologically vulnerable to stress and consequently reduces the threshold for develop-
100
Vázquez-Bourgon · Herrán · Vázquez-Barquero Baldwin DS, Leonard BE (eds): Anxiety Disorders. Mod Trends Pharmacopsychiatry. Basel, Karger, 2013, vol 29, pp 98–110 (DOI: 10.1159/000351931)
Downloaded by: Univ. of California San Diego 132.239.1.231 - 3/12/2017 9:40:09 PM
Predictors of Anxiety Disorders
ing an anxiety disorder under the exposure during adulthood to stress. Given this, research findings have increasingly supported the notion that certain adverse life events may be more substantive to their etiological explanations. Among these events, physical/sexual abuse and loss/separation experiences during childhood have received much research attention: the presence of childhood physical and sexual abuse constitutes an important predisposing factor for the development of anxiety disorders [9], as does the presence of loss/separation experiences in childhood [10].
There is increasing evidence indicating that, even in countries with sophisticated health care systems, when a person develops a particular mental disease there is usually a long period of time before it is correctly identified and receives appropriate treatment [11]. This was initially demonstrated in psychosis, where the duration of the untreated illness ranged from several weeks to many years [12]. It is now assumed that this long period of untreated illness also appears in other mental disorders, including anxiety disorders, in which although the onset of the illness usually occurs during the first three decades of life, effective treatment is typically not initiated until a number of years later [13, 14] (see chapter on Duration of Untreated Illness and Duration of Illness in Anxiety Disorders, pp. 111–118). In accordance with this, findings from research in anxiety and obsessive compulsive disorders demonstrate that the duration of untreated illness (DUI) extends for at least one year. The Cantabria First Episode of Panic Disorders Study demonstrated that for these disorders the DUI reached one year [15]. Similarly, others have demonstrated that the DUI for panic disorders reached nearly 45 months, the one for generalized anxiety disorders 87 months, and for obsessive compulsive disorders 90.6 months [16]. The relevance of this long period of untreated mental illness is based on its presumed association with a poorer outcome and treatment response, as demonstrated for psychosis and other major mental disorders [12, 17–19]. Similarly, research evidence is accumulating to support the idea that also in anxiety and obsessive compulsive disorders the presence of a long DUI is associated with a poorer outcome and reduced treatment response [15, 20, 21]. It has been postulated that in psychosis and other major mental disorders this association is due to a possible neuro-psycho-socio-toxic effect of untreated illness. Regarding anxiety disorders, despite this hypothesis being coherent with impressions derived from clinical practice, we still lack sufficient research evidence to believe unequivocally that the existence of a long delay in initiating appropriate treatment may promote the progression of an illness-related neuro-psycho-socio-toxic effect. A complementary explanation for the association between long DUI and poor outcome is derived from the ‘critical period hypothesis’. This was originally formulated for psychosis, and proposes that the early phase of the illness constitutes a ‘critical period’ during which symptomatic and psychosocial deterioration progresses rapidly [22]. It also contends
The Early Phases of Anxiety Disorders Baldwin DS, Leonard BE (eds): Anxiety Disorders. Mod Trends Pharmacopsychiatry. Basel, Karger, 2013, vol 29, pp 98–110 (DOI: 10.1159/000351931)
101
Downloaded by: Univ. of California San Diego 132.239.1.231 - 3/12/2017 9:40:09 PM
Duration of Untreated Illness in Anxiety Disorders
that subsequent progression of morbidity slows or stops and the level of the recovery attained, by the end of the critical period, persists into the long-term. There is increasing evidence supporting the notion that existence of a similar critical period could be postulated in major mental disorders [17, 18]. The relevance of this concept relies on the fact that it provides evidence for postulating an optimal period for neuroprotective interventions, in either the prodromal phase or early stages of the illness. Thus, it appears that there are grounds for arguing that effective early intervention procedures should be applied during this stage of maximum susceptibility to the damaging effects of illness and the neuro-psycho-socio protective effects of interventions. Whether this postulation is applicable to anxiety disorders is a pressing issue for future studies.
The Early Stages of Anxiety Disorders
A key element of the early intervention model is the operationalization of the sequence of the prediagnostic and diagnostic stages of the illness (table 1). As the different anxiety disorders do not as yet have biological markers to define these different stages, the characterization should be mainly identified by symptoms and signs. The stages may in turn correlate with prognosis and treatment, and potentially with a specific pathophysiology from which can be derived reliable and phase-specific biological markers. To guide clinicians in identifying the stages at which an individual is at a particular time, different concepts have been proposed. Although originally developed for psychosis, in recent years they have been applied, with certain adaptations, to other mental disorders, including anxiety disorders.
The first stage in the model (stage 0) is defined as a ‘at risk asymptomatic’ where a range of risk factors may be operating in asymptomatic persons. In the case of psychosis, several risk factors have been identified. Such is the case of family history of mental illness, substance abuse and premorbid personality traits [17]. Similarly, in patients who develop anxiety and obsessive compulsive disorders long before the illness appears, it is possible to identify a series of predisposing conditions: among them being prenatal and environmental factors and factors related to personality traits. In addition, the presence in young children of ‘behavioral inhibition’ (a conduct characterized by reactions of withdrawal, shyness and avoidance in novel, unfamiliar situations) and the subsequent development of anxiety disorders is well established [23]. It has also been demonstrated that children who have anxious parents or overinvolved mothers tend to develop anxiety disorders later in life [24]. The relevance of this is the fact that it can be used to identify potential candidates for early prevention and for establishing appropriate intervention targets.
102
Vázquez-Bourgon · Herrán · Vázquez-Barquero Baldwin DS, Leonard BE (eds): Anxiety Disorders. Mod Trends Pharmacopsychiatry. Basel, Karger, 2013, vol 29, pp 98–110 (DOI: 10.1159/000351931)
Downloaded by: Univ. of California San Diego 132.239.1.231 - 3/12/2017 9:40:09 PM
The ‘at Risk Asymptomatic’
Table 1. Application of the early intervention model to anxiety disorders Stage Clinical definition
Target population
Potential interventions
0
Increased risk of disorder No symptoms currently
Young age first-degree Psychoeducation for young relatives of probands persons and family Promotion of health life styles Resilience training
1
Mild or nonspecific subthreshold symptoms of the disorder Could include the presence of ‘ultrahigh risk’ syndrome (moderate but subthreshold symptoms) Mild functional (psychosocial) change or decline Mild/moderate neurocognitive deficits (GAF
