Neurological Development and Behavior in Adolescence
Until recently, the prevailing belief was that brain development ceased at around the time a child entered kindergarten (i.e., that the brain is 90-95% formed by age six). However, recent findings indicate that the maturation of the prefrontal cortex, the region of the brain involved in critical thinking and decision making, is not complete until early adulthood (e.g., Casey et al. 2000; Luna and Sweeney 2004; Thompson et al. 2000). The brain grows, as evidenced by the thickening of gray matter, until about puberty (approximately 11 for girls and approximately 12 for boys), at which point the brain begins a process of thinning where unused neural connections are eliminated (Giedd et al. 1999; Gogtay et al. 2004). The thinning process continues into early adulthood and results in increased speed and enhanced information processing (Giedd et al. 1999; Sowell et al. 1999). During the thinning process, synapses associated with redundant connections and skills that remain untapped begin to be pruned or discarded (i.e., the "use it or lose it" principle; Durston et al. 2001; Gogtay et al. 2004). More specifically, pruning of synapses results in an enhanced ability of distinct regions of the brain (those that have been extensively utilized) to sustain high-level cognitive control of behavior (Luna and Sweeney 2004).
In addition to the thinning process, adolescent brain maturation is also characterized by myelination, which is the insulation of established neural connections and serves to optimize transfer of neural information across the central nervous system (Geidd et al. 1999; Yakovlev and Lecours 1967). An increase in myelination allows for increased response speed and improved integration of neural circuitry necessary in modulation of behavior (Geidd et al. 1999; Yakovlev and Lecours 1967). Adolescent structural brain maturation has important implications for adolescent development because parallel improvements have been found in several cognitive processes, such as problem solving, reasoning, working memory, response inhibition, and attention allocation (Anderson et al. 2001; Diamond 1988; Fuster 1989). These processes are important in the development of higher order functions such as mood regulation, decision making, and impulse control (Gogtay et al. 2004). Adolescent brain maturation may therefore facilitate the acquisition of a more sophisticated cognitive and perceptual understanding of the adolescent's environment (Chambers et al. 2003).
Neurological development in adolescence, particularly executive cognitive functioning (ECF), influences adolescent risk taking behavior by creating an imbalance in the reward and harm avoidance systems. According to the triadic model of adolescent decision making, ECF serves as a regulatory system that balances anticipated rewards (reward/approach system) and avoidance of harmful outcomes (harm avoidance system; Ernst et al. 2006). A result of immature ECF in adolescence is an imbalance between the reward/approach system, involving the ventrial striatum, and the harm avoidance system, involving the amygdala. Evidence of this imbalance can be observed in adolescence as high sensitivity to rewards (Chambers et al. 2003), lower sensitivity to risk in goal-directed behavior (Steinberg 2004), higher susceptibility to and rates of substance use (Chambers et al. 2003; Johnston et al. 2006a), higher rates of substance use (Johnston et al. 2006a), and the overestimation of peer substance use and underestimation of consequences associated with substance use (Prinstein and Wang 2005).
Findings from recent studies support the link between an immature prefrontal cortex and difficulties in response inhibition, defined as the ability to select which ideas and stimuli to attend to in guiding behavior, as well as the ability to suppress responses toward competing ideas or behaviors that may lead to problematic outcomes (Bjorklund and Harnishfeger 1995; Fuster 1997; see Luna and Sweeney 2004, for a review). Researchers have found age-related increases in prefrontal functioning (e.g., Bunge et al. 2002; Rubia et al. 2000) and a rapid age-related decrease in the number of errors associated with poor response inhibition (e.g., Fisher et al. 1997; Klein and Foerster 2001; Luna et al. 2004) in studies examining response inhibition. These findings suggest that cognitive functions associated with response inhibition are not fully developed through most of adolescence and that youth do not develop the ability to inhibit responses in a consistent manner until late adolescence (e.g., Luna and Sweeney 2004).
As stated above, lack of response inhibition (Luna et al. 2004) and a general inclination toward greater risk taking (Ernst et al. 2006) (a) may compound the effects of incomplete neurological development on adolescents' decision making abilities and (b) may place adolescents at a disadvantage when faced with making decisions on whether to use substances. During the decision making process, the adolescent brain has to integrate and decide from among several internal states (e.g., hunger, sexual desire, pain) and environmental contexts (e.g., possibility or presence of danger; Bechara et al. 2001). When faced with each possible substance use situation, the adolescent also has to consider multiple goals (e.g., be part of the group, abide by family rules about substance use) and behaviors designed to meet each goal (e.g., agree to use substances, refuse substance use). It is likely that all of these factors may serve to compound the effects of incomplete neurological development on adolescent risk behavior.
Accordingly, the prototype/willingness model (Gibbons et al. 2004; Ouellette et al. 1999) holds that adolescents do not intend to pursue health risks, but rather that they are open to such risky behavior when opportunities are presented. Hence, Gerrard et al. (2002) have found that adolescents who associate with substance using and risk taking peers are most likely to use substances, even if they acknowledge the risks and negative consequences of substance use. These authors also found that, as parent-adolescent communication about substances increased, the perceived potential negative consequences of substance use increased and reports of actual substance use decreased. Moreover, Gibbons et al. (2004) found that willingness to use substances was most strongly associated with substance use among adolescents residing in high-risk neighborhoods. Given these neurocognitive and social-ecological risks, it may not be reasonable to expect adolescents to make these decisions rationally. It may be necessary for protective social processes (e.g., parental monitoring; parent-adolescent communication) to help keep adolescents away of these situations as a way to prevent substance use.
An underdeveloped prefrontal cortex may also have implications for mood regulation in adolescence. Findings from MRI studies indicate that adolescents have greater difficulty than adults in interpreting emotional expressions despite comparable activation of the amygdala (Baird et al. 1999). The amygdala is associated with emotional control (e.g., impulsive "gut" reactions, fear, and anger; Baird et al. 1999; Monk et al. 2003; Thomas et al. 2001). It may be that the use of the amygdala in processing emotionally charged information, in the absence of a fully developed prefrontal cortex, is likely to produce uninhibited and impulsive responses lacking in reasoning. The findings reported by Baird et al. (1999) suggest that ability to regulate mood, particularly the ability to alleviate distress or to change negative mood states, may not be fully developed in adolescence (Campos et al. 2004). Mood dysregulation has been found to be an important risk factor for substance use disorders, as substances may be used as a way to alleviate negative affect brought about by stressful situations (e.g., Hussong and Chassin 1994). Substance use may help to regulate mood for some adolescents for whom mood regulation is particularly problematic. Put together, the picture that emerges is that the incompleteness of the developing adolescent brain may underlie common adolescent behaviors such as impulsive decisions, difficulty interpreting and handling emotionally charged situations, trouble regulating negative emotions, and failure to consider the long-term implications of one's present choices and behaviors. Findings from studies on adolescent brain maturation and cognitive development represent a first step in examining the link between neurological development and behavior, as well as attending to the higher-order processing power, capacity, and speed that is required to handle pressured and emotionally charged situations. Because of individual differences in cognitive, social, and emotional development, this stage may occur at different ages for individual youth. Accordingly, assessment of neurological development may be necessary for preventive interventions to identify which adolescents (e.g., immature versus mature cognitive development) would benefit from specific interventions (e.g., child-centered or decision making only versus family-based or combined family-based and child-centered or decision making).
Research has shown that biology (e.g., genetics) and context interact to influence both neurological development (e.g., decision making) and psychopathology (e.g., substance use) (O'Connor et al. 1998; Pike et al. 1996). Research suggests that context can influence neurological development in several ways. These include maternal substance use and exposure to stress during pregnancy, exposure to stress during childhood and adolescence, and others (see Fishbein 2000 for a review). Prenatal and postnatal exposure to alcohol and drugs and stressful contexts and events (e.g., traumatic events, parental divorce, parental psychopathology, neglect or abuse, parental death, poverty, and repeated out of home placements for children) may negatively influence neurological development, resulting in structural and functional changes in the brain (Cicchetti and Tucker 1994; Fishbein 2000; Girdler et al. 2003; Ito et al. 1998).
According to Sinha's (2001) stress vulnerability model, stressful events during childhood and adolescence increase risk for substance use by altering the cognitive, affective, and social processes involved in behavior. Moreover, because cognitive development continues into emerging adulthood, the disruptive effects of chronic stress on neurological development can be associated with long lasting impairments (Thadini 2002). Chronic exposure to stress has been found to be associated with neurological changes (e.g., low levels of cortisol and ACTH/corticotrophin; Heim et al. 2004; Huether 1998), which in turn has been found to be associated with decreased hippocampal volume and impaired memory and decision making (Carrion et al. 2001; Kitayama et al. 2006; Nelson and Carver 1998; Sapolsky 1996). More specifically, neurocognitive impairments associated with stress exposure impact the ability of adolescents to make and carry out prosocial decisions and behavior (e.g., decision to use alcohol and drugs) (Fishbein et al. 2006). Indeed, Fishbein et al. (2006) found that stress exposure was associated with poor decision making. In summary, decision making for adolescents who have been exposed to stress may be an even more difficult task, and these adolescents may be even less suited for child-centered interventions than are adolescents who have not experienced traumatic events.
J Prim Prev. 2008;29(1):5-35. © 2008 Springer
Springer Science Business Media
Cite this: Adolescent Neurological Development and its Implications for Adolescent Substance Use Prevention - Medscape - Jan 01, 2008.