Evidence-Based Reviews

Risk taking adolescents: When and how to intervene

Current Psychiatry. 2004 October;3(10):40-55

References

1. Chambers RA, Taylor JR, Potenza MN. Developmental neurocircuitry of motivation in adolescence: a critical period of addiction vulnerability. Am J Psychiatry 2003;160:1041-52.

2. Chambers RA, Potenza MN. Neurodevelopment, impulsivity, and adolescent gambling. J Gambl Stud 2003;19:53-84.

3. Turner C, McClure R. Age and gender differences in risk taking behavior as an explanation for high incidence of motor vehicle crashes as a driver in young males. Inj Control Saf Promot 2003;10:123-30.

4. Bachanas PJ, Morris MK, Lewis-Gess JK, et al. Psychological adjustment, substance use, HIV knowledge, and risky sexual behavior in at-risk minority females: developmental differences during adolescence. J Pediatr Psych 2002;27:373-84.

5. Goldstein RZ, Volkow ND. Drug addiction and its underlying neuro- biological basis: neuroimaging evidence for the involvement of the frontal cortex. Am J Psychiatry 2002;159:1642-52.

6. Spear LP. The adolescent brain and age-related behavioral manifestations. Neurosci Biobehav Rev 2000;24:417-63.

7. Clayton R. Transitions in drug use: risk and protective factors. In: Glantz M, Pickens R (eds). Vulnerability to drug abuse. Washington, DC: American Psychological Association, 1992;15-52.

8. Tamm L, Menon V, Reiss AL. Maturation of brain function associated with response inhibition. J Am Acad Child Adolesc Psychiatry 2002;41:1231-8.

9. Jonah BA. Sensation seeking and risky driving: a review and synthesis of the literature. Accid Anal Prev 1997;29:651-6.

10. Vitaro F, Arseneault L, Tremblay RE. Dispositional predictors of problem gambling in male adolescents. Am J Psychiatry 1997;154:1769-70.

11. Malow RM, Devieux JG, Jennings T, et al. Substance-abusing adolescents at varying levels of HIV risk: psychosocial characteristics, drug use, and sexual behavior. J Subst Abuse 2001;13:103-17.

12. Donovan JE, Jessor R, Costa FM. Syndrome of problem behavior in adolescence: a replication. J Consult Clin Psychol 1988;56:762-5.

13. Vitaro F, Brendgen M, Ladouceur R, Tremblay RE. Gambling, delinquency, and drug use during adolescence: mutual influences and common risk factors. J Gambl Stud 2001;17:171-90.

14. Shope JT, Bingham CR. Drinking-driving as a component of problem driving and problem behavior in young adults. J Stud Alcohol 2002;63(1):24-33.

15. Potenza MN. The neurobiology of pathological gambling. Semin Clin Neuropsychiatry 2001;6:217-26.

16. Petry NM. Substance abuse, pathological gambling, and impulsiveness. Drug Alcohol Depend 2001;63:29-38.

17. Bechara A. Neurobiology of decision-making: risk and reward. Semin Clin Neuropsychiatry 2001;6:205-16.

18. Zuckerman M. Sensation seeking: the balance between risk and reward. In: Lipsitt LP, Mitnick LL (eds). Self-regulatory behavior and risk taking. Norwood, NJ: Ablex Publishing; 1992;143-52.

19. Masterman DL, Cummings JL. Frontal-subcortical circuits: the anatomical basis of executive, social and motivational behaviors. J Psychopharmacol 1997;11:107-14.

20. Horn NR, Dolan M, Elliot R, et al. Response inhibition and impulsivity: an fMRI study. Neuropsychologia 2003;41:1959-66.

21. Fallgatter AJ, Herrmann MJ. Electrophysiological assessment of impulsive behavior in healthy subjects. Neuropsychologia 2001;39:328-33.

22. Booth JR, Burman DD, Meyer JR, et al. Neural development of selective attention and response inhibition. Neuroimage 2003;20:737-51.

23. O’Donnell P, Greene J, Pabello N, et al. Modulation of cell firing in the nucleus accumbens. Ann NY Acad Sci 1999;877:157-75.

24. Nordin C, Eklundh T. Altered CSF 5-HIAA disposition in pathologic male gamblers. CNS Spectrums 1999;4:25-33.

25. Leyton M, Okazawa H, Diksic M, et al. Brain regional alpha-[11C] methyl-L-tryptophan trapping in impulsive subjects with borderline personality disorder. Am J Psychiatry 2001;158:775-82.

26. Cherek DR, Lane SD, Pietras CJ, Steinberg JL. Effects of chronic paroxetine administration on measures of aggressive and impulsive responses of adult males with a history of conduct disorder. Psychopharmacology (Berl) 2002;159:266-74.

27. Geller DA, Biederman J, Stewart SE, et al. Which SSRI? A meta-analysis of pharmacotherapy trials in pediatric obsessive-compulsive disorder. Am J Psychiatry 2003;160:1919-28.

28. Hollander E, Allen A, Lopez RP, et al. A preliminary double-blind, placebo-controlled trial of divalproex sodium in borderline personality disorder. J Clin Psychiatry 2001;62(3):199-203.

29. Swann AC. Treatment of aggression in patients with bipolar disorder. J Clin Psychiatry 1999;60(suppl 15):25-8.

30. Hollander E, Dolgoff-Kaspar R, Cartwright C, et al. An open trial of divalproex sodium in autism spectrum disorders. J Clin Psychiatry 2001;62:530-4.

Problem behavior syndrome. High impulsivity is predictive of problem gambling, drug use, and risky driving and sexual practices later in life.^1,2,9-11 Adolescents with what some authors describe as a “problem behavior syndrome” engage in behaviors—such as substance use, risky sexual behavior,¹² gambling,¹³ and reckless driving¹⁴—that share a common trend toward impulsivity.

Impaired data processing. Decision making has been proposed as a three-part cognitive process:

accumulating sensory input
processing this input and formulating a behavioral response appropriate to the situation
planning and implementing the resultant motor output.²

Impulsivity is believed to result from impaired ability of the brain to process accumulated information or to formulate a response to it—or both. Impulsive individuals thus experience impaired data processing, in which they:

misjudge the likely risk of a given action or overestimate their ability to accomplish a task
show impaired response inhibition and thus find it difficult to resist an impulse to participate in a given activity.

Sensation seeking. Adolescents who exhibit risk-taking behavior may wish to experience the thrill of the behavior (sensation or novelty seeking). Alcoholic or drug-dependent individuals and those who engage in pathologic gambling or take chances while driving also demonstrate significantly impaired decision making.^15-17 Adolescents who engage in these and other problem behaviors have similarly scored high on sensation-seeking scales.^10,18

DECISION-MAKING BIOLOGY

At least four neural circuits process decisions, weighing the risks and benefits of a given situation and formulating a response. These circuits are:

prefrontal cortices, including orbitofrontal, dorsolateral, and ventromedial
ventral striatum, including the nucleus accumbens
thalamus
monoaminergic brainstem nuclei (ventral tegmental area [VTA] and raphe nuclei).¹⁹

Functional imaging studies—including MRI and PET, EEG, and electrophysiology—have confirmed that these four brain regions are integral to response inhibition and show abnormal activity in impulsive individuals.^20,21 Indeed, prefrontal cortex damage has been extensively documented to cause marked impulsivity, poor decision making, and an increased propensity for substance abuse and dependency.¹

Functional imaging studies also have shown that adolescents appear to use these neural regions inefficiently during decision making. Extensive areas of the involved brain regions are activated in individuals ages 8 to 20, whereas only focal activation occurs in adults.²²

Box 2

How dopamine and serotonin affect impulsive behavior

Dopamine. The nuclear accumbens (NA) plays an important role in processing afferent excitatory glutamatergic projections and then instigating the given response.²³ Dopamine is released in the NA in response to a long list of stimuli, including:

exposure to substances
natural rewards such as food or sex
stimulating situations, such as playing video games, gambling, or thrill seeking.²

Novel experiences and rewards that are delivered erratically cause an elevated dopamine release in the NA. This may explain, in part, the excitement one gains from activities with unpredictable outcomes, such as gambling, bungee jumping, parachuting, white-water rafting, or taking risks while driving.

As rewarding stimuli are re-experienced, dopamine response accelerates in magnitude, and the reward becomes progressively stronger as the experience is repeated. This repeated dopamine release in the NA changes the cellular proteins involved in signaling pathways thought to be associated with the transition from impulsive to compulsive behavior.² Therefore, addiction may be caused by neurocircuitry changes induced by repeated dopamine release. Similarly, persons who engage in impulsive behavior may have hypersensitive dopamine-related reward circuitry, which may, in part, explain their predisposition to addictive behavior.

Serotonin. Serotonergic projections originate mainly in the midbrain’s raphe nuclei and are transmitted to the ventral tegmental area, NA, prefrontal cortex, amygdala, and hippocampus.¹ Abnormal serotonin levels have been implicated in impaired impulse control² and decreased CNS serotonin in impulsive behavior.²⁴

Functional brain imaging studies have shown reduced serotonin neurotransmission in highly impulsive individuals, compared with normal controls.²⁵ Administering serotonergic agents seems to markedly decrease impulsive behavior.²⁶

Activity within this network is modulated by excitatory glutamatergic transmission and inhibitory GABAergic transmission within the cortices and by dopaminergic and serotonergic transmission within the VTA and raphe nuclei, respectively.^2,20 Although all of these neurotransmitters have been implicated in impulsivity, dopamine and serotonin have been studied most extensively (box 2).^1,2,23-26

CASE CONTINUED: PSYCHIATRIC WORKUP

Josh clearly is engaged in worrisome behavior with potential long-term consequences. To evaluate him for underlying psychopathology, the psychiatrist used a structured psychiatric exam, Minnesota Multi-phasic Personality Inventory (MMPI), and SNAP-IV Rating Scale for ADHD (see Related resources). Josh endorsed some depressive symptoms—which were also evident on the MMPI—but did not meet DSM-IVTR criteria for major depressive disorder. Neither were his symptoms diagnostic for any other Axis I or Axis II disorder.

Given the risk of harm and likelihood of worsening behavior over time, the psychiatrist schedules Josh for weekly psychotherapy and possible medication.