Introduction

Schools are an efficient and convenient choice of setting for intervention programs targeting adolescents. Schools provide access to a large number of adolescents in a learning environment in which adolescents are more likely to be receptive toward instructions involved in an intervention. Moreover, monitoring the fidelity of program implementation and assessing program effectiveness in a school setting are relatively easy. In addition, the typical 4-year structure of school systems is conducive to tracking down students in order to obtain long-term follow-up data.

Prevention programming attempts to reach adolescents prior to the expected occurrence of certain problematic behavior such as drug abuse. The central focus of prevention is on the antecedents of problem behavior. Program participants are taught how to anticipate the impacts of these antecedents (e.g., such as desiring to feel good, cognitive exposure to drug-related cues, social influence, or cultural norms) and to counteract their potential impacts with instruction of protective cognitions, behaviors, or access to protective social units (e.g., drug-free communities). Among these strategies are selective or indicated approaches that attempt to prevent individuals who are either currently at-risk for drug use behavior, by virtue of their membership in certain segments of the population, or who are already demonstrating early signs of drug use behavior, from developing clinically diagnosed drug use disorders. Some researchers tend to refer to both indicated and selective programs as targeted programs.

Cessation (treatment) programs are designed to assist in stopping drug use, given that youth were either not exposed or did not respond to prevention efforts. Cessation programs provide participants with strategies to cope with psychological dependence (emotional reliance) on and physiological withdrawal from a drug (e.g., what types of withdrawal symptoms to expect, how long one will experience these symptoms, and how to cope with these symptoms without relapsing). Cessation programs focus on stopping a current behavior from continuing to arrest ongoing consequences and permit recovery of health. The goal may also involve teaching one how to live with permanent changes (e.g., drug-related injury).

In the school setting, prevention efforts are generally delivered school-wide (i.e., universal prevention), whereas cessation programs are usually delivered outside of the classroom (e.g., with student assistance programs, in clinics, or perhaps involving the school nurse, possibly involving self-help support groups, which meet during lunchtime or after school). Exposure to early prevention programming could provide proactive interference against later drug-facilitative–type information, resulting in protection against drug misuse. These prevention efforts may inhibit, delay, or halt addiction, which is what makes cessation so difficult. For older adolescents who are caught up in cycles of drug misuse or abuse, prevention programming could help minimize the time spent in a using cycle.

A recent focus of adolescent school-based drug abuse prevention and cessation programming involves applying models of neurobiology/neuropsychology as potential influences on program outcomes. This chapter provides a brief overview of the application of neuroscience to adolescent development, indicates current school-based prevention and cessation strategies that may impact neuroscience-relevant adolescent functioning, and suggests new directions for the development and implementation of drug use prevention and cessation programs.

Brief Overview: Neuroscience and Adolescents

Adolescent vulnerability to substance use has been associated with the protracted morphological development of the neural systems responsible for self-control and regulation, in conjunction with a heightened tendency to seek novel experiences (e.g., Steinberg and Chambers et al. ). The regions of the human brain linked to self-control and self-regulation are not fully developed until late adolescence. However, an increase in novelty-seeking behavior is evident when children transition into early adolescence. Thus increases in risk-taking and sensation-seeking tendencies among adolescents seem to precede the development of self-regulatory competencies.

Several animal as well as human studies suggest that novelty-seeking behavior increases rapidly during adolescence ; this has been attributed to the changes that occur in the pro-motivational dopamine systems during this stage of ontological development. The level of dopamine turnover among adolescents is likely to be higher than among children and adults. Dopamine in the ventral striatum, which includes the nucleus accumbens, is believed to modulate the conversion of thoughts and emotions into motivated actions. Dopamine release in the nucleus accumbens appears to filter and gate the motivational signals received from the cortical and limbic systems that are to be processed by the downstream motor systems.

Several motivational stimuli have been associated with dopamine stimulation in the nucleus accumbens, including the drugs of misuse and agents of natural reward (e.g., food, sex). Furthermore, novel experiences tend to cause higher levels of dopamine stimulation compared with previously learned behaviors that have expected outcomes. Hence, the same mesolimbic dopamine systems appear to mediate both drug- and novelty-seeking behaviors. Conversely, concentrations of inhibitory motivation neurotransmitters such as serotonin appear to be lower in adolescent cerebrospinal fluid, which has been associated with higher impulsivity. A greater tendency to act along with decreased inhibitory tendencies for self-destructive action could contribute to drug use experimentation.

Adolescents’ vulnerability to drug use due to developmental changes in the dopaminergic system is further exacerbated by the relatively underdeveloped prefrontal cortex. Brain structure and function undergo significant changes throughout adolescence, notably in the forebrain regions, which comprise the prefrontal cortex. The prefrontal cortex is one of the last cortical structures to reach full ontogenetic development and may not achieve complete maturation until the third decade of a person’s life. This region of the brain is responsible for the spatiotemporal organization of goal-directed actions, which involve the carrying out of relevant actions in response to internal (e.g., memory) or external (e.g., environmental context) cues. In other words, the principal function of the prefrontal cortex is to perform executive function. Executive function represents a complex set of interrelated functions that make the temporal organization of goal-directed behavior, language, and reasoning possible. Methodologically, brain researchers find it difficult to separate the interrelated components of the executive system into discrete units (e.g., attention, working memory, decision-making) and localize them to specific areas of the prefrontal cortex. For example, the functional contribution of a specific prefrontal cortex area is difficult to measure after a discrete lesion, for such a lesion is likely to functionally affect the entire executive system. Nonetheless, researchers have linked deficiencies in executive function to abnormalities related to attention, working memory, long-term memory retrieval, planning, temporal integration of memory and goal, decision-making, monitoring, and inhibitory control.

Ability to exert sustained attention or manipulate the focus of one’s attention is necessary to formulate a goal-directed thought or bring an action to completion. In turn, one needs to control distracting or interfering urges, both internal (e.g., thoughts, memory, instinctual) and external (e.g., environmental), in order to maintain sustained attention. Working memory refers to the ability to retain information and utilize the information to execute a related action. Like most executive functions, working memory and sustained attention are interrelated and are essential for task perseverance. Furthermore, execution of actions involves foresight and planning. Planning represents the ability to utilize information obtained from selective retrieval of long-term memory, such as memory of past actions, for the anticipation of future events. Planning provides a conceptual scheme for the execution of a goal-directed behavior, and based on the anticipation of consequences, lays out the order of prospective actions. Individuals often have to choose among competing actions. The executive function of decision-making involves choosing an action after rationally evaluating the potential risks and rewards associated with its outcomes. Successful execution of goal-directed behaviors also depends largely on the ability to self-monitor. Monitoring enables one to assess the discrepancies between one’s actions and one’s goals, thus creating feedback which allows one to correct subsequent actions.

Inhibitory control involves controlling an impulse by inhibiting a response. According to Barkley, response inhibition involves three processes: (1) inhibition of the prepotent response (i.e., a response linked in associational memory to immediate reinforcement), (2) stopping of an ongoing response in order to delay the final decision to respond, and (3) protecting this decision-making time interval from being interfered with by other competing stimuli and responses (i.e., interference control). Primary response inhibition partially aids the functioning of working memory, regulation of motivation, verbal internalization, and behavioral analyses.

Hence executive functions make the self-regulation of thoughts, emotion, and behavior possible. Conversely, deficiencies in executive function may result in poor impulse control, poor judgment, and disinhibited behavior. Among adolescents, poor executive functioning has been consistently associated with higher rates of drug use (e.g., Grekin and Sher, Mezzich et al., Tarter et al., and Xiao et al. ). Furthermore, early adolescent deficiencies in executive function have been found to predict later drug use disorders. For example, Habeych et al. found that attenuated amplitude of the P300 wave, an indicator of executive cognitive function, in late childhood predicted substance use disorders in late adolescent males.

Research suggests that executive function develops in sophistication at the same rate as the structural maturation of the prefrontal cortex; and age-related social and cognitive maturation during adolescence may be attributed to the concomitant structural changes in the brain. For example, improvements in planning and decision-making have been linked with the structural developments in the dorsolateral and ventrolateral prefrontal cortex, respectively. Most notable developmental changes in the forebrain region have been observed as changes in gray and white matter volumes. Recent neuroimaging studies suggest that there is a continuous increase in the brain white matter volume during adolescence. For example, a significant growth is noticed in the posterior corpus callosum, the collection of over 200 million nerve fibers that allow communication between right and left hemispheres of the brain. In addition, the gray matter volume, which increases substantially during childhood, appears to decrease during adolescence in certain cortical structures (e.g., the prefrontal cortex ).

Reduction in cortical gray matter volume might occur due to increased intracortical myelination and/or due to synaptic pruning. Increased myelination of neurons results in a more efficient propagation of action potentials. Synaptic pruning involves selective removal of synapses that “do not efficiently transmit information pertaining to accumulating experience.” Synaptic pruning appears to serve a number of functions that facilitate cognitive development. For example, the process appears to stabilize the firing patterns of cortical neurons, which in turn is thought to enhance working memory performance. In general, both myelination and synaptic pruning are believed to enhance the efficiency of cortical information processing as well as the connectivity between cortical and subcortical regions.

Thus because adolescent prefrontal cortex is not yet fully developed, the associated executive functions are expected to be inadequately developed. As a result, adolescents tend to have lower regulatory competence, which makes them highly susceptible to drug use risk factors such as rash impulsiveness and poor decision-making. For example, adolescents tend to be poor judges of the harmful consequences of drug use, yield easily to peer pressure, and seek immediate gratification. Therefore it is not surprising that most adult drug users are likely to have initiated drug use in the period between early to mid-adolescence, before the brain regions associated with self-regulation are optimally developed.

In summary, evidence suggests that the developmental upsurge in novelty seeking coupled with suboptimal brain development makes adolescents vulnerable to drug use. Thus to some extent, adolescent experimentation with drugs appears to be a normative behavior. However, it should be noted that individual differences exist among adolescents with respect to both novelty seeking and executive functioning; some adolescents are always at a higher risk for developing substance use disorders than others.

Negative Consequences of Drug Use on Teen Cognitive Function

Early onset of drug use, escalation of use, and possible dependence might subject adolescents to the risks of developing mental health disorders and experiencing social, academic, and legal consequences. The developing adolescent brain appears to be highly vulnerable to the neurotoxic effects of drugs, including those of licit drugs such as tobacco and alcohol and the so-called soft drugs such as marijuana. Prolonged exposure to drugs during adolescence may result in neuropsychological deficiencies and structural brain damage, especially in areas associated with memory and executive function. Brown et al. have reported that compared with a matched group of healthy youth, alcohol-dependent young adolescents (in the third week of abstinence) were found to perform poorly on verbal and visuospatial tasks, suggesting that protracted exposure to alcohol might have enduring adverse effects on the brain’s functional ability involving memory and information processing. In fact, magnetic resonance imaging results indicate that youth with alcohol use disorders tend to show smaller hippocampal and white matter volumes and smaller prefrontal cortices. De Bellis et al. further found that the total hippocampal volume among adolescents with alcohol use disorder increased with the age at onset and decreased with the duration of disorder.

Although, taken together, the relatively limited extant neuroimaging studies fail to conclude whether chronic marijuana use is related to structural abnormalities in the brain (for review, see Quickfall and Crockford ), some of the findings (e.g., Wilson et al. ) suggest a relationship between age at first onset and decreased total brain volume. Furthermore, it appears that early marijuana use initiators (e.g., before the age of 17) tend to show significant later cognitive deficits (e.g., indicated by verbal IQ; visual scanning tasks) in comparison with nonusers and late-onset users ^{. ,} Nicotine-dependent adolescents have been suggested to perform normally on working memory tasks following nicotine intake but poorly during withdrawal. One neuroimaging study indicated that despite poor task performance, nicotine-dependent adolescents on withdrawal exhibited increased activities in the prefrontal cortex regions (e.g., dorsolateral prefrontal cortex) associated with working memory. Because an optimal level of dopamine action is essential for normal working memory functioning, the adverse effects of tobacco use cessation on working memory suggest that regular nicotine use causes abnormal adaptations of the dopaminergic circuitries. In fact, research on rodents has shown that the normal development of catecholaminergic systems during adolescence might be disrupted by protracted exposure to nicotine. These studies have linked adolescent nicotine exposure with hippocampal damage and impairments in the midbrain catecholaminergic systems that play important roles in mood regulation and addiction development.

By adversely affecting the normal development of the cortical and limbic brain structures associated with risk and reward calibration, decision-making, and inhibitory control, drug use not only exacerbates the loss-of-control due to incentive-sensitization but also undermines the cognitive ability to stop using drugs voluntarily. Evidence suggests that drug addiction might be related to impairments in ventromedial prefrontal and anterior cingulate cortices, brain regions associated with decision-making and inhibitory control. Furthermore, acute withdrawal of drug use seems to affect the anterior cingulate cortex, consequently weakening inhibitory control.

However, it should be noted that most of the research linking adolescent drug use, drug use withdrawal, and neuropsychological deficiencies has been cross-sectional, which makes any conclusion on their causal relationships open for debate. Nonetheless, it seems that deficient neuropsychological functioning and adolescent drug use share a reciprocal relationship. For example, neuropsychological deficiencies in preteen years tend to predict drug use disorders (e.g., Tarter et al. ), and, similarly, early drug use onset or abuse also seems to predict neuropsychological deficiencies. Such bidirectional relationships imply that adolescents with impaired neuropsychological functioning face the additional risk of drug use–mediated further neuropsychological deterioration.

Thus there appear to be at least three important reasons that prevention or treatment targeting adolescent drug misuse should address motivation, decision-making, and inhibitory control. First, adolescents normally tend to show suboptimal development of regulatory competence. Second, this regulatory competence is likely to be markedly lower among drug-misusing adolescents due to possible impairments in certain brain regions such as the prefrontal cortex, anterior cingulate cortex, and hippocampus. Poor regulatory competence may not only make it difficult for these high-risk adolescents to stop using drugs but may also cause them to relapse easily in case of temporary successful cessation. Third, adolescents at high risk for using drugs or developing drug use disorders are already likely to rank low on neurobehavioral inhibition, which might additionally indicate that their executive functions have trait-based deficiencies. Thus drug-abusing adolescents and adolescents at risk for developing drug dependence would benefit greatly from supplemental programming that promotes adaptive coping, impulse control, problem solving, and self-monitoring.

Brain Development and School-Based Drug Use Prevention and Treatment

It has become increasingly important for prevention researchers to take into account the findings made in neuroscience to guide their approach in designing drug use prevention programs for youth. In particular, researchers are interested in knowing whether developmental neurobiological and neurocognitive variables moderate and/or mediate prevention effects. Currently, the research attempting to answer these questions seems to be at a preliminary stage. For example, there is some evidence that adolescents’ neurocognitive skills moderate their response to preventive intervention materials. In a study dealing with social competency skills training, adolescents with poor executive cognitive abilities were less likely to respond positively to the prevention curriculum. Hence not all youth may be equally able to process prevention messages and instructions, and program materials may need to be individualized to address differential neurocognitive skills.

Alternatively, prevention or treatment programs may aim to enhance adolescent neurocognitive skills in order to counteract drug use behavior. Recent evidence suggests that practice in tasks requiring regulatory skills may enhance one’s executive functioning, and this alteration appears to correspond to practice-induced structural changes in the brain (e.g., Kabat-Zinn and Quickfall and Crockford ). Hence one might argue that repeated practice of skills and tasks demanding the use of executive functions (e.g., attention control, working memory) during childhood and adolescence, when cortical structures are likely to be most malleable, may assist the age-related development of executive functions, and in turn protect adolescents from engaging in risky behaviors.