Heritability of Childhood Anxiety

Anxiety disorders often begin in childhood and are associated with significant long-term morbidity (Bernstein et al., 1996). Recognizing and treating children with early signs of vulnerability to anxiety disorders are, therefore, important clinical goals.

Twin studies have established a genetic contribution to childhood anxiety symptoms and disorders. Family-association studies have found anxiety disorders to be elevated in children of parents with anxiety disorders and, conversely, in parents of children with anxiety disorders. Specific genes linked to certain neurotransmitters implicated in anxiety are now being studied in anxiety-disorder populations. Further studies have demonstrated temperamental risk factors for anxiety disorders (most notably, behavioral inhibition) using both family-association and prospective designs (Biederman et al., 1990; Kagan et al., 1989; Manassis et al., 1995). While each type of study has certain methodological constraints, and constitutional factors undoubtedly interact with environmental ones, this group of findings makes an impressive case for a hereditary component in anxiety disorders. However, exploring environmental contributions to anxiety (for example, family problems or stressful life events) and developmental or medical contributors (for example, learning disabilities or hyperthyroidism) is also essential.

Behavioral Inhibition

In treating anxious children, research findings regarding behavioral inhibition have been among the most helpful. Behavioral inhibition is an aspect of temperament, present in about 10% of toddlers, characterized by a child's tendency to restrict exploration and avoid novelty (Kagan et al., 1989). Prospective studies have shown an increased risk of multiple anxiety disorders in middle childhood for behaviorally inhibited children (Biederman et al., 1990) and a more specific risk of social phobia in adolescence (Schwartz et al., 1999). Although initially studied in toddlers, precursors and sequelae of inhibition have now been elucidated in longitudinal studies (Bernstein et al., 1996). The typical features of behavioral inhibition at various ages are shown in the Table, and their relevance to practice is described below.

Physiological studies of inhibited children have suggested that they experience chronically high levels of sympathetic nervous system arousal, and such arousal accounts for many of the manifestations of inhibition (e.g., reduced exploration to avoid overstimulation, decreased spontaneous speech due to vocal cord tension) (Kagan et al., 1989). Sensory sensitivities (e.g., sensitivity to certain noises or smells) are also common in behaviorally inhibited children, suggesting they may have a lower threshold for sympathetic arousal in response to certain external stimuli. Therapies that promote sensory integration have been used in some children with these specific sensitivities.

Relevance to Clinical Practice

Many inhibited children do not develop psychopathology, especially if they receive empathic encouragement to face new situations rather than avoiding them. Facing new situations is thought to result in gradual desensitization for the inhibited child, just as facing a feared stimulus does in the treatment of phobias. Parents who are securely attached to their children and are not unduly anxious themselves often help their inhibited children face novelty without seeking professional advice. Persistent behavioral inhibition is thought to occur when parents either fear that the child cannot manage exposure to new situations (resulting in overprotection) or dismiss the child's distress (contributing to the child's insecurity) (Arcus et al., 1992, as cited in Kagan et al., 1998). Helping such parents gradually and empathically expose their child to new situations can be a very therapeutic intervention.

In infancy, children who later become inhibited are often described as difficult. Unable to avoid novelty at this age, they respond with a high degree of crying and movement. Helping parents remain calm, soothe the infant and find ways to promote self-soothing are all therapeutic at this age.

By school age, children with persistent behavioral inhibition can begin to manifest anxiety disorders. The stress of school entry is a common trigger. Besides the anxiety disorders listed in DSM-IV, selective mutism (lack of speech in unfamiliar situations, most commonly school) can be problematic. Increasing evidence suggests that this is an anxiety-related condition and should not be seen as a willful refusal to speak (Dummit et al., 1997). For school-age anxieties, behavioral interventions that promote exploration and desensitization to phobias (often in combination with positive reinforcement systems) are cornerstones of treatment (Kendall et al., 1997). The child can also learn relaxation techniques and cognitive strategies for ameliorating anxiety. Medications, especially serotonin reuptake inhibitors, have been found effective in childhood anxiety disorders (Birmaher et al., 1998), although their use in the treatment of extremes of temperament remains controversial (Garland and Weiss, 1996).

The presence of behavioral inhibition is assessed by behavioral observations of the child and sometimes by parent report. By school age, however, child-report and teacher-report inventories can also contribute to the assessment. Two common standardized measures (Achenbach, 1991; March, 1998) are listed in the Table. Some children, however, do not freely acknowledge anxiety (Manassis et al., 1997), so parental reports of avoidant, inhibited behavior should be taken seriously.

With the onset of adolescence, children with persistent behavioral inhibition can experience more intense social phobia (Schwartz et al., 1999). Previously untreated anxieties of middle childhood may also become problematic as expectations of independent functioning increase at adolescence. For example, the inhibited child who has always feared speaking to peers on the telephone can avoid this situation by asking parents to help. At adolescence, this reliance on parents may no longer be considered socially acceptable.

The failure to treat earlier anxieties may also erode self-esteem. There is an increased incidence of depression in anxious children at adolescence, especially in those severely impaired by their anxieties. This has led some authors to suggest a progression to depression in more impaired children (Brady and Kendall, 1992). Preventing this outcome through early treatment of anxiety could thus ameliorate the long-term morbidity associated with comorbid anxiety and depression. Furthermore, there is an unfortunate association between alcohol abuse and social phobia in adolescence (Ginsburg et al., 1998; La Greca and Lopez, 1998). Such teens are thought to self-medicate their social anxiety, not having learned more adaptive coping strategies.

Specific Risk Factors

Anxiety disorders are increasingly thought to be polygenic, suggesting that additional constitutional risk factors exist besides behavioral inhibition. Numerous biochemical and neuroimaging studies are examining correlates of specific anxiety disorders (Pine and Grun, 1999). Few of these disorder-specific findings are yet being applied clinically; one exception is the Anxiety Sensitivity Index and the corresponding child instrument (Silverman et al., 1999). Anxiety sensitivity is a predisposition to react to autonomic arousal with anxiety and has been specifically linked to panic disorder. People with this sensitivity tend to attribute physical signs of arousal as representing a serious illness (e.g., palpitations signaling imminent cardiac arrest) rather than a more benign cause (palpitations due to consuming a strong cup of coffee). Questionnaire measures of this tendency can be helpful in assessing vulnerability to panic disorder and in beginning cognitive interventions for panic that focus on realistic reappraisal of physical sensations.

This brief review of heritable factors relevant to assessing and treating anxiety in children has focused on interventions that are informed by an appreciation of inhibited temperament and anxiety sensitivity. It is hoped that early amelioration of these risk factors will reduce the negative sequelae of untreated childhood anxiety disorders.

References:

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