Behavioral Inhibition: Temperament or Prodrome?

Abstract

Individual differences in temperament emerge in the first months of life. Some infants display a heightened sensitivity to novelty and uncertainty in the world around them, leading a subset to fearfully withdraw from the social environment. Extreme forms of this temperament, Behavioral Inhibition (BI), are associated with increased risk for social anxiety disorder. Indeed, the link is so strong that some suggest that BI is not simply a risk factor for anxiety, but rather a milder form of the disorder. The current overview describes the literature linking BI and anxiety, highlighting the unique biobehavioral profiles evident in each construct. It then highlights specific evidence that may help distinguish the form and function of BI and anxiety. Finally, we briefly discuss unresolved issues that may help inform future work aimed at improving our understanding of individual development and shape therapeutic interventions directed at specific mechanisms of disorder.

Frontolimbic functioning during threat-related attention: Relations to early behavioral inhibition and anxiety in children

“…It is important to note that due to the cross-sectional design, we cannot infer the directionality of the effects or how these relations unfold over the course of development (Maxwell & Cole, 2007). By the same token, the finding cannot rule out the alternative causal relation, in which BI acts as a moderator, shaping the link between early neural risk-marker and later anxiety (Perez-Edgar & Guyer, 2014). Notwithstanding this limitation, our data extend longitudinal studies examining the relation between threat-related attention processes and internalizing problems in adolescents (Perez-Edgar et al, 2010a) and adults (Hardee et al, 2013) to childhood BI by indicating that the link between threat-attention neural patterns, BI levels, and anxiety are evident in childhood, preceding the emergence of socioemotional maladjustment and full-fledged anxiety disorders later in life (Beesdo et al, 2007).…”

“…BI-related neural perturbations parallel perturbations evident in clinically anxious individuals, and are apparent even in the absence of current psychopathology. These studies have important implications for translational research in suggesting that there may be enduring neural mechanisms that serve as the foundation for the link between early BI and subsequent anxiety (Perez-Edgar & Guyer, 2014; Pine & Fox, 2015). …”

“…These processes may influence each other through a feedback loop, contributing to the formation of a maladaptive response repertoire that perpetuates and strengthens anxious behaviors over time (Crick & Dodge, 1994). Indeed, longitudinal studies indicate that early BI predicted subsequent social withdrawal only in adolescents and children showing AB (Perez-Edgar et al, 2010a; 2011), underscoring that deeply-entrenched AB might bind at-risk children to a developmental trajectory marked by elevated anxiety symptoms (Perez-Edgar & Guyer, 2014; Perez-Edgar et al, 2014b). These data also support the presumption that BI may act as an endophenotypic marker of risk, aiding attempts to link variations in neural functioning with observed patterns of behavior (Perez-Edgar & Guyer, 2014).…”

Opportunities for Neurodevelopmental Plasticity From Infancy Through Early Adulthood

“…() examined whether shyness predicted change in resting state neural connectivity across three time points in middle childhood and early adolescence in 147 youth. Temperamental shyness is an early appearing individual trait that is relatively stable over time and, when coupled with specific additional risk factors, can lead to a marked increase in risk for anxiety (Pérez‐Edgar & Guyer, ). Over the course of development, changes in neural connectivity are thought to underlie more effective and efficient regulatory mechanisms, potentially blunting the risk for developing psychopathology.…”

Adolescent Social Phobia in Clinical Services

“…However, it is worth noting that the same study concluded that BI was best construed as a generalized risk factor for SAD, not an early precursor; in support of this contention, Clauss and Blackford ( 2012 ) cite that the majority of children with BI do not develop SAD, and children with BI do not automatically suffer from the same defi cits in emotional regulation and pervasive fear of negative evaluation seen in children with SAD. On the other hand, as noted by Perez-Edgar and Guyer ( 2014 ), the precise relationship between BI and SAD has not been defi nitively established by any direct research.…”