Developmental Risk Factors
Behavioural inhibition, an aspect of temperament characterized by a tendency to restrict exploration and avoid novelty, has been previously identified as a risk factor for multiple anxiety disorders in middle childhood. Because of its link to multiple anxiety disorders, however, it was thought to be a nonspecific risk factor for anxiety. Recent investigations have therefore attempted to identify risk factors (either biological or environmental) that are specific to particular disorders.
One approach has been to test anxious children for risk factors specific to particular anxiety disorders in adults. As in adults with panic disorder, changes in respiration with carbon dioxide exposure were found to be greater for anxious children (all types) than for nonanxious control children. Test-related hyperventilation in subjects with high test anxiety has also been confirmed in children. Motor soft signs, known to be elevated in agoraphobic adults, have been found to be increased in children of agoraphobic parents, compared with age- and sex-matched control subjects. By contrast, anxious children did not show the blunted growth hormone responses to clonidine found in many anxious adults. It is unclear whether this finding reflects a true discontinuity between child and adult disorders or a neurophysiological adaptation to anxiety that is not yet present in anxious children.
Anxiety sensitivity has been linked specifically to panic disorder in adults. Children and adolescents with panic disorder reported greater levels of anxiety sensitivity than did youngsters with nonpanic anxiety disorders matched for sex. Self-reported anxiety sensitivity was also correlated with depression in children and adolescents referred for anxiety, even when controlling for other aspects of anxiety.
Anxious adults have been found to selectively attend to and selectively remember threatening stimuli. Several investigators have sought similar cognitive biases in anxious children. To date, they have demonstrated threat-related biases in attention, memory functioning, dichotic listening, and interpretation of ambiguous stimuli in children with anxiety disorders or high trait anxiety. Exposure to threatening stimuli has also been found to interfere in the performance of other cognitive tasks.
Interestingly, many of the tasks used also test implicit aspects of cognition. In other words, children are not consciously choosing to attend to or remember threatening stimuli. Their biases appear to be due to subtle aspects of information processing. Informing parents of the limited control their children have over these biases can be clinically useful. This information often alleviates parental frustration with a child who appears to dwell on the most upsetting aspects of events despite repeated reassurance. Reduced parental frustration in turn alleviates some of the child's anxiety.
Genetic studies offer a second promising approach to understanding the development of anxiety disorders in children. Previous studies of twins and families have found a definite familial contribution to childhood anxiety disorders. Recent family studies have found anxiety disorders to be elevated in children of parents with anxiety disorders or mixed anxiety--depression, with social phobia, and with agora-phobia. Conversely, parents of school-refusing children had elevated rates of anxiety and depressive disorders. Many specific genetic loci are now being researched. The dopamine transporter gene (DAT1), genes involved in corticotropin release, and the serotonin transporter gene (HTT) have all been linked to internalizing disorders in children, but their specific contributions to the pathophysiology of childhood anxiety remain to be elucidated. Previous twin studies have established a genetic contribution to childhood anxiety symptoms and to anxiety disorders as a group, and the degree of genetic versus environmental contribution to specific anxiety disorders is now being studied. In a recent twin study, Topolski and others found that shared environmental effects played a moderate role in SAD but were not significant contributors in overanxious disorder, where genetic influences predominated.
Besides behavioural inhibition, additional aspects of temperament have been found to increase the risk of childhood anxiety disorders. High levels of emotionality predicted case status among siblings (where one sibling had an anxiety disorder), and obsessive difficult temperament (best described as pervasive rigidity or an extreme lack of adaptability) has also been found to be increased in anxious children. Inhibition itself may be a more specific risk factor than was previously believed. Two recent studies, one retrospective study and one prospective study using Kagan's cohort have now linked behavioural inhibition to social anxiety in adolescence, but not to other anxiety disorders.
Environmental studies of risk factors for the early development of anxiety disorders have focused largely on aspects of the parent--child relationship. Parental modeling, for example, has been cited as a possible reason for the association between parent and child anxiety. Onset of anxiety disorders in adolescents has been associated with high family conflict.
Many authors have reported an association between parental rejection and control (tendency to restrict a child's autonomy) and childhood anxiety. Unfortunately, most of their work is based on self-reports from anxious individuals concerning their experiences with parents, raising the possibility of bias due to cognitive distortions associated with anxiety. Caster and others, for example, found that socially anxious adolescents perceived their parents as being more socially conscious and less socially active than nonanxious adolescents did, but there were no differences in parental self-perceptions in these areas. One group in Australia has addressed this difficulty by observing families of anxious children engaging in problem-solving discussions. Children's anxious expectations and avoidant coping responses following such discussions were associated with specific parental behaviours during the discussion that subtly fostered such responses.
Kagan's group has associated maternal criticism with child behavioural inhibition, but only in mothers suffering from anxiety disorders, suggesting that nature and nurture may interact in producing inhibition. Interactive effects are also suggested by Kortlander and others, who found that mothers' expectations for their anxious children's coping reflected the actual lower coping ability of the children. Poorer child coping was associated with protective maternal responses, a possible maintaining factor for anxious behaviours.
Finally, the role of attachment as a predictor of anxiety disorders has been confirmed by an impressive longitudinal study by Warren and others. These investigators assessed psychopathology in 172 adolescents (mean age 17.5 years) who had previously been examined--shortly after birth using a screen for parental psychepathology and several temperament measures and at age 12 months using the Strange Situation Procedure for attachment. One subtype of attachment, termed "anxious/resistant," predicted adolescent anxiety disorders consistently, even after accounting for maternal anxiety and temperament. Some adolescents with other attachment histories also developed anxiety disorders but at significantly lower rates.
A remaining challenge is to integrate developmental and cognitive studies with the affective neuroscience pioneered in adults to develop a more comprehensive understanding of various subgroups of childhood anxiety disorder and their developmental trajectories. For example, early childhood risk factors such as behavioural inhibition and attachment status may increase a child's vulnerability to anxiety disorders, but the specific disorder may also relate to neurophysiological characteristics (for example, heightened sensitivity to carbon dioxide in panic disorder) that have only been examined in adults to date. Attempts at theoretical integration are now being proposed.
Clinically, it is often useful to inform families that, at least in part, their child's condition is constitutional. This information tends to relieve parental fears about having caused the child's anxiety and helps the clinician emphasize coping rather than cure as a treatment goal. Families are less likely to become discouraged with treatment if they recognize that their child, though likely to continue to be somewhat more anxious than the average, can learn to cope, to the point where anxiety does not interfere significantly in daily activities.
- Manassis, K. (2000). Childhood Anxiety Disorders: Lessons from the Literature. The Canadian Journal of Psychiatry,45(8), 724-730. doi:10.1177/070674370004500805
The box directly below contains references for the above article.
Anxiety Disorders of Childhood and Adolescence
- Rhoads, J. C., & Donnelly, C. L. (n.d.). Anxiety Disorders of Childhood and Adolescence. Retrieved November, 2018, from http://ppn.mh.ohio.gov/Portals/0/pdf/Anxiety Protocol.pdf
Reflection Exercise #2
The preceding section contained information
about childhood anxiety disorders. Write
three case study examples regarding how you might use the content of this section
in your practice.
Online Continuing Education QUESTION
16 What have studies of families found concerning familial contribution to childhood anxiety disorders? Record the letter of the correct answer
the CE Test.