Civil Case Example
Molly Johnson, Bradley Johnson, and Emily Johnson
v. Jefferson City Hotel
Business had been slow for a number of years at the Jefferson City Hotel. Hotel manager
Tom Lewis saw a national fraternity convention as a way out of this slump, with the
potential of more business in future years if the three-day meeting went well. An estimated
four thousand young men ranging in age from eighteen to twenty-two years old would
attend the convention, and 375 of them were registered guests of his hotel. By midnight of
the first day, it was apparent to hotel staff that alcohol was being freely consumed by the
young men: Chairs were knocked into the pool; objects were thrown from the upper floors
into the hotel atrium; the hallways were littered with broken glasses, beer bottles, and the
like; and housekeeping staff reported numerous rooms with vomit on the floors. Mr. Lewis
sent a note to staff on the second day to be patient—there was only one more day until the
unruly crowd left—and that he would approach the fraternity to pay for all damages to
the hotel. He did not attempt to deal directly with the disorderly conduct by adding additional
staff during the late shifts to prevent similar occurrences the next night.
The Jefferson City Hotel also rented rooms to parties who were not part of the convention
that weekend. One such party was Bradley, Emily, and Molly Johnson.
Around 2 a.m. on the last night of the convention, the Johnson family returned to the
hotel from a family celebration.Mr. Johnson was carrying two-year-old Molly, who was asleep.
As they walked through the atrium, several water balloons, beer cans, and glass bottles
rained down from the upper floors. As the Johnsons ran for cover, a broken vodka bottle
hit Mr. Johnson and Molly on their heads. As a result, a glass fragment lodged into Molly’s
eye. Molly permanently lost sight in her injured eye.
The Johnsons decided to sue the Jefferson Hotel. They argued that a hotel that brings
together a large number of people on its premises for financial gain has a responsibility for
using all reasonable care to protect others from injury from causes that can be reasonably
anticipated.
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CLASS ACTION
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Civil Case Example
Discussion Questions
1. What evidence is in this story that Mr. Lewis was negligent?Why should he have
anticipated that a hotel guest could be injured given what was happening at the
hotel?
2. What could Mr. Lewis have done to prevent the injury to Molly?
3. Was it reasonable for the Johnsons to think it was safe for them to walk through the
hotel lobby at 2 a.m.?
. . .
CLASS ACTION
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CLASS ACTION
© 2011 by Hazelden Foundation. All rights reserved. Duplicating this material for personal or group use is permissible.
Legal Vocabulary Puzzle
For each legal term shown, find the correct definition in the list below.
Write the number of the term next to the definition.
LEGAL TERMS
DEFINITIONS
_____ A written testimony of facts sworn under oath to be true
_____ A court case in which one party seeks compensation for damages caused by
another party’s negligence
_____ Legally responsible
_____ Evidence given by someone with a high degree of knowledge in a specific area
_____ A solemn promise to tell the truth
_____ A person who testifies about what he or she observed
_____ A public official authorized by the constitution to decide matters brought before
a court and preside over a trial
_____ The monetary compensation requested by a plaintiff
_____ Presenting the most convincing evidence in a trial
_____ Failure to provide reasonable care to prevent harm or injury
_____ The person accused of a crime (criminal) or being sued (civil)
_____ A person seeking compensation for damages in a civil court
_____ The attempt to contradict evidence given by the opposite side in a trial
1. Affidavit
2. Award
3. Breach of Duty
4. Civil Trial
5. Criminal Trial
6. Damages
7. Defendant
8. Deposition
9. Expert Testimony
10. Foreseeable Harm
11. Judge
12. Jury
13. Liable
14. Negligence
15. Oath
16. Party
17. Plaintiff
18. Preponderance
of Evidence
19. Prosecutor
20. Rebuttal
21. Sue
22. Witness
Legal Vocabulary Puzzle
CLASS ACTION
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_____ A person or persons on the same side of a legal case
_____ To file a lawsuit against a party, usually asking for money to compensate for
damages
_____ To give a judgment of money to a party to a lawsuit
_____ Failure to act in a reasonable way, either by doing something harmful or by not
preventing harm
_____ Recorded testimony sworn under oath to be true that can be used as evidence
_____ A court case in which an agent of the government seeks to prove that a person
is guilty beyond a reasonable doubt of breaking law(s) and should be punished
_____ The government’s representative presenting a case against the accused in a
criminal trial on behalf of the public good
_____ A group of peers who hear a court case and decide the outcome
_____ Ability of a responsible person to predict or anticipate harm that can occur as
a result of his or her actions
. . .
The Following is an introduction into CLASS ACTION Curriculum. Please read.
Why is it important to teach students so early—even in
middle school—about alcohol prevention?
Underage drinking is a dangerous, persistent, widespread problem for America’s youth.
About 10.7 million persons aged twelve to twenty (28 percent of this age group) reported
drinking alcohol during the past month.1 Research shows that the risk for alcohol and
other drug use skyrockets when children enter the sixth grade, between the ages of twelve
and thirteen.2 By the end of sixth grade, 19 percent of our nation’s youth will have used
alcohol, and almost 6 percent will have been intoxicated at least once in their lives.3
In the 2007 Monitoring the Future (MTF) study conducted by the University of
Michigan, the percentage of students reporting ever using alcohol is 39 percent by the end
of eighth grade, and it climbs to 72 percent by the end of high school. Approximately 16
percent of eighth graders, 33 percent of tenth graders, and 44 percent of twelfth graders
admitted to drinking an alcoholic beverage thirty days prior to being surveyed.4
Underage drinkers consume about 10 percent of all alcohol purchased in the United
States, and, according to the U.S. Department of Justice, the “vast majority of this alcohol
is consumed in a risky fashion.” 5 Almost 18 percent of eighth graders and 55 percent
of twelfth graders report having been drunk.6 The more we can do to prevent underage
drinking, the better off our children will be in the future.
Why is underage alcohol use sometimes referredto as a “gateway to risk”?
Drinking alcohol during adolescence is dangerous. Car crashes are the leading cause of
death for teenagers, and nearly one-quarter of youth in fatal traffic crashes have been
drinking.7 Alcohol-related traffic crashes and risky driving behavior are serious consequences
of alcohol use by youth.8 Nearly one in three high school students nationwide has ridden
during the previous month in a car driven by someone who had been drinking, and 10
percent had driven a car after they had been drinking alcohol.9
Underage drinking is associated with many other social, emotional, behavioral, and
legal problems during adolescence, including alcohol abuse and dependence, violence and
injuries, truancy, risky sexual behavior, and other drug use throughout adolescence and
into adulthood.10
The earlier teens begin to drink alcohol, the more risky it is. Several studies have shown
that adolescents who initiate alcohol use early during adolescence are at increased risk for
subsequent abuse and dependence into adulthood.11 The risk associated with alcohol in
adulthood is substantial:
Introduction to Underage Alcohol Issues
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• Alcohol is the third leading actual cause of death in the United States.12
• Long-term heavy alcohol use increases the risk of
– several cancers13
– cardiovascular disease14
– stroke15
What does research on the adolescent brain contribute to thediscussion about underage drinking?
Not all that long ago, scientists believed the human brain was 90 to 95 percent formed
by the time a child entered kindergarten, around age six,16 and by the onset of puberty,
brain development was considered largely completed.17 We now know those ideas to be
false. Recent advances using brain imaging techniques called magnetic resonance imaging
(MRI), functional MRIs (fMRIs), and studies of event-related potentials (ERPs), combined
with animal models and research of teens’ performance on neuropsychological measures—
standardized tests of thinking and memory skills—are greatly advancing our knowledge
about the adolescent brain and the impact of alcohol on its development, including possible
long-term negative consequences that may extend into adulthood.18
When the thickening of the brain’s gray matter is finished at puberty (about eleven
years for girls and twelve years for boys), the brain starts a thinning process to eliminate
unused neural connections—a process that continues into early adulthood and results in
increased speed and better information processing.19 The “use it or lose it” principle is
involved in this synaptic pruning, and its result is believed to be related to a person’s ability
to sustain high-level cognitive control over behavior.20 Myelination (the insulation of established
neural connections that optimizes transfer of neural information across the central
nervous system) is another key feature of adolescent brain maturation,21 also thought to
be related to cognitive control of behavior.22
The maturation of the prefrontal cortex—the region of the brain associated with critical
thinking and decision making—is not completed until early adulthood.23 The subcortical gray
matter and the limbic system structures (which includes the hippocampus and amygdala)
increase in volume during adolescence.24 Figure 1 shows these and other important areas
What Is fMRI?Functional magnetic resonance imaging (fMRI) is a specialized type of neuroimaging
scan or MRI. Unlike the MRIs used by doctors as diagnostic tools, the fMRI is primarily
used in research studies to learn which regions of the brain are active during a specific
cognitive function by measuring the blood flow response to neural activity. Because it is
a noninvasive procedure, it can be used in studies of normal children and adolescents.
RESEARCH
FACT
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of the brain. The development of the hippocampus during adolescence may be especially
significant given its association with learning and memory.25 Recent studies using fMRIs
suggest that it is both the maturation of these distinct areas of the brain and the brain’s
increased ability to work in an integrated manner, perhaps due to the processes of synaptic
pruning and myelination occurring during adolescence, that result in adult-level cognitive
control of behavior.26
These changes in the brain’s underlying structure and physiology are likely related to
observed changes in adolescents’ emotional and cognitive processes and behavior.27 During
adolescence, changes are observed in several cognitive processes (for example, problem solving,
reasoning, working memory, response inhibition, attention allocation), as well as other
higher-order functions including mood regulation, decision making, and impulse control.28
Developmental fMRI studies of response inhibition show that brain function changes with
age and improved behavioral performance.29 Response inhibition, in general terms, is the
ability to suppress competing responses or distractions. Response inhibition is present in
every voluntary action people perform, since choosing a response requires the rejection of
other possible responses. Its development begins in infancy with continued improvement
throughout childhood. However, until recently, studies stopped at late childhood, leaving a
gap in our knowledge about the development of this crucial ability during adolescence.30
Recent fMRI studies of adolescents indicate that while some teens, at times, can
demonstrate mature response inhibition, the integration of brain circuitry supporting such
cognitive control over behavior does not work at adult levels. Even younger children can
perform isolated response inhibition trials accurately, but it is during adolescence that the
ability to do so consistently and with greater efficiency appears to develop.31 This suggests
that the underlying brain mechanisms supporting response inhibition, perhaps because
they are not yet fully formed in adolescents,may be especially vulnerable under high-demand
FIGURE 1Brain Development
Prefrontal cortex
LIMBIC SYSTEM
m
Septal regionHippocampus
Amygdala
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CLASS ACTION
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Introduction to Underage Alcohol Issues
situations.32 So, for example, the belief of some that parents can teach appropriate drinking
skills to adolescents by providing alcohol in the “safe” home environment may not translate
to other high-demand environments like parties or unsupervised teen gatherings with
heightened levels of emotion, motivations to drink, and distracting stimuli and competing
tasks because the underlying system or brain circuitry for exerting cognitive control over
behavior is not yet sufficiently established.
As research accumulates on the changes occurring in the brain during adolescence,
concern is increasing about what the introduction of a potent neurotoxin like alcohol
might do to these crucial developmental and maturational processes during the second
decade of life.33 For those surprised to hear alcohol described as a neurotoxin, consider the
harm that can be done to a fetus with in utero exposure to alcohol. Such exposure can lead
to fetal alcohol syndrome (FAS), a birth defect characterized by central nervous system
damage, among other features, resulting from prenatal alcohol exposure.
Adolescents’ smaller body mass, their initial lack of tolerance to and experience with
alcohol, and a pattern of use favoring heavy and rapid drinking suggest young people
may suffer greater negative effects of alcohol use than adults.34 Adolescent alcohol abuse
is associated with damage to the brain and neurocognitive deficits that can have direct
implications for learning and other cognitive abilities that could continue into adulthood.35
However, further research is needed to determine which comes first, the brain and neurocognitive
deficits or the adolescent’s heavy alcohol use.36 It is also unclear at present which
neurocognitive deficits evident in adolescents with alcohol-use disorders are reversible after
long-term abstinence, because longitudinal studies have yet to be conducted.37 Additional
research is urgently needed to determine the nature, extent, and persistence of alcoholrelated
brain injury in adolescence, given its potential for far-reaching consequences.38
For multiple reasons, scientists have turned to animal research to address some of
the questions about the neurotoxic effects of alcohol on the developing adolescent brain.
Laboratory animals allow for better experimental control of the amount and type of neurotoxins
to introduce to the brain than do observational studies of teens already identified
as having alcohol or other drug abuse problems. Researchers today are reluctant to use
adolescents in studies about the neurotoxic effects of alcohol on the developing brain because
of ethical and legal concerns about providing alcohol to underage research participants
given the known risks.39
Animal models of underage drinking suggest that adolescents may be more sensitive to
some effects of alcohol and less sensitive to others. Adolescent rats show more sensitivity
than adult rodents to alcohol’s social facilitation effects, which could encourage increased
intake of alcohol.40 Adolescent rats also show more sensitivity than do adult rats to the
effects of alcohol on memory and learning that are believed to result from alcohol’s action
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on the hippocampus.41 Chronic alcohol exposure consistently results in long-term cognitive
impairments, with adolescent rats especially sensitive to these consequences.42 The rat
equivalent to adolescent binge-drinking—chronic intermittent alcohol exposure—was associated
with damage to the frontal association cortex and other frontal regions in adolescent,
but not adult, rats.43 Binge-drinking, a pattern of typical adolescent use, increases future
susceptibility to the memory-impairing effects of alcohol in animal models.44
This parallels what we know from humans about the important changes in the hippocampus
and prefrontal cortex during adolescence, described above. In addition, a preliminary
study of humans that compared twelve adolescents with diagnosed alcohol dependence or
abuse with twenty-four comparison adolescents found a reduction in the size of the hippocampus
among those with alcohol disorders.45 Further research is needed to clarify if these
changes persist into adulthood and how they relate to brain functioning in humans.
There are effects of alcohol that adolescent rats appear to have less sensitivity to than
do adult rats, including alcohol-related motor impairment and alcohol-induced sedation.46
Unfortunately, these negative effects of alcohol intake can serve to moderate use because
difficulty walking and/or becoming sleepy can serve as cues to limit intake; furthermore,
these adolescent-related insensitivities to alcohol may be most pronounced during early
adolescence.47 A rare study in human children and adolescents ages eight to fifteen years
demonstrated similar insensitivity.48 Subjects in this study, eleven boys with a family history
of alcoholism and eleven age-matched controls, were given a mixture of 0.5 ml/kg of
pure ethanol with 12 ounces of Diet 7UP to drink within three minutes, resulting in blood
alcohol levels within the intoxicating range for adults.49 However, “little gross behavioral
change occurred in the children,” and none behaved grossly “intoxicated” compared to what
the researchers observed with their “adult practice subjects.” 50
This brief overview of the exciting new research on the adolescent brain development
and maturation can be used to inform decisions today about prevention strategies for adolescent
alcohol use.51 More answers are likely forthcoming as research techniques improve,
more data are collected, and theories are developed about the brain/behavior connections
and age-related changes. Current adolescent brain research supports prevention programs
that have clear no-use messages, given what is now known about the significant maturation
and development occurring in the brain during adolescence. Alcohol is a neurotoxin that
may interfere with these important processes.
THERE IS NO SAFE LEVEL OF ALCOHOL USE
FOR TEENS. ALL UNDERAGE DRINKING SHOULD BE
DISCOURAGED BY RESPONSIBLE ADULTS.
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Introduction to Underage Alcohol Issues
No information is available to recommend a “safe” level of alcohol intake for adolescents.
Furthermore, adolescents are cognitively immature in neurological processes related to
decision making.52 Public policies to discourage underage drinking, like the maintenance
and enforcement of the minimum drinking age, are essential given the neurocognitive
effects of alcohol on adolescents and college students.53 Given that most people are currently
unaware of the association of underage alcohol use with brain damage and neurocognitive
deficits, efforts are needed to better publicize this information so that policy makers,
physicians, educators, parents, and adolescents better appreciate the risk of underage
drinking.54 Comprehensive programs like Project Northland, which include interventions for
the individual to learn and rehearse behavioral skills, as well as programs for the family,
school, and community to provide environments conducive to no-use norms, best match
the immature neurological development of adolescence.55
. . .
Notes
1. Substance Abuse and Mental Health Services Administration, Office of Applied Studies, Results
from the 2007 National Survey on Drug Use and Health: National Findings, NSDUH Series H-34, DHHS
Publication No. SMA 08-4343 (Rockville, MD: 2008).
2. J. E. Donovan, S. L. Leech, R. A. Zucker, C. J. Loveland-Cherry, J. M. Jester, H. E. Fitzgerald,
L. I. Puttler, M. M.Wong, and W. S. Looman, “Really Underage Drinkers: Alcohol Use among Elementary
Students,” Alcoholism: Clinical and Experimental Research 28, no. 2 (2004): 341–49.
3. Donovan et al., “Really Underage Drinkers.”
4. L. D. Johnston, P. M. O’Malley, J. G. Bachman, and J. E. Schulenberg, “Overall, Illicit Drug Use by
American Teens Continues Gradual Decline in 2007” (Ann Arbor, MI: University of Michigan News Service,
2007). Online at http://www.monitoringthefuture.org.
5. D. K. Eaton, L. Kann, S. Kinchen, S. Shanklin, J. Ross, J. Hawkins, W. A. Harris, R. Lowry,
T. McManus, D. Chyen, C. Lim, N. D. Brener, and H.Wechsler, “Youth Risk Behavior Surveillance United
States, 2007,” Morbidity and Mortality Weekly Report 57, no. 4 (2008): 1–131.
6. Johnston et al., “Overall, Illicit Drug Use.”
7. National Highway Traffic Safety Administration, “Fatality Analysis Reporting System Data Files
1976–2002” (Washington, DC: National Center for Statistics and Analysis, 2006).
8. National Highway Traffic Safety Administration, “Fatality Analysis”; J. S. Zakrajsek and J. T. Shope,
“Longitudinal Examination of Underage Drinking and Subsequent Drinking and Risky Driving,” Journal of
Safety Research 37, no. 5 (2006): 443–51.
9. National Center for Chronic Disease Prevention and Health Promotion, “YRBSS Youth Online:
Comprehensive Results,” http://www.cdc.gov/HealthyYouth/yrbs (retrieved September 12, 2008).
10. B. F. Grant and D. A. Dawson, “Age of Onset of Drug Use and Its Association with DSM-IV Drug
Abuse and Dependence: Results from the National Longitudinal Alcohol Epidemiologic Survey,” Journal of
Substance Abuse 10, no. 2 (1998): 163–73; B. F. Grant, F. S. Stinson, and T. Harford, “Age at Onset of Alcohol
Use and DSM-IV Alcohol Abuse and Dependence: A 12-year Follow-up,” Journal of Substance Abuse 13
(2001): 493–504; E. Gruber, R. J. DiClemente, M. Anderson, and M. Lodico, “Early Drinking Onset and Its
Association with Alcohol Use and Problem Behavior in Late Adolescence,” Preventive Medicine 25, no. 3
Introduction to Underage Alcohol IssuesCLASS ACTION
Originally published in Amazing Alternatives, ©1998, 2009 by Hazelden Foundation.
All rights reserved. Duplicating this material for personal or group use is permissible.
6 of 9
(1996): 293–300; R. Hingson, T. Heeren, S. Levenson, A. Jamanka, and R. Voas, “Age of Drinking Onset,
Driving After Drinking, and Involvement in Alcohol Related Motor-Vehicle Crashes,” Accident Analysis and
Prevention 34, no. 1 (2002): 85–92; R. Hingson, T. Heeren, R. Zakocs, M.Winter, and H.Wechsler, “Age
of First Intoxication, Heavy Drinking, Driving After Drinking and Risk of Unintentional Injury among
U.S. College Students,” Journal of Studies on Alcohol 64, no. 1 (2003): 23–31; R. Hingson, T. Heeren, and
R. Zakocs, “Age of Drinking Onset and Involvement in Physical Fights After Drinking,” Pediatrics 108, no.
4 (2001): 872–77; R. Hingson, T. Heeren, M. R.Winter, and H.Wechsler, “Early Age of First Drunkenness as
a Factor in College Students’ Unplanned and Unprotected Sex Attributable to Drinking,” Pediatrics 111, no. 1
(2003): 34–41; R.W. Hingson, T. Heeren, and M. R.Winter, “Age at Drinking Onset and Alcohol Dependence—
Age at Onset, Duration, and Severity,” Archives of Pediatrics & Adolescent Medicine 160, no. 7 (2006): 739–46.
11. J. D. Grant, J. F. Scherrer, M. T. Lynskey, M. J. Lyons, S. A. Eisen, M. T. Tsuang,W. R. True, and
K. K. Bucholz, “Adolescent Alcohol Use Is a Risk Factor for Adult Alcohol and Drug Dependence: Evidence
from a Twin Design,” Psychological Medicine 36, no. 1 (2006): 109–18; J. Guo, L. M. Collins, K. G. Hill,
and J. D. Hawkins, “Developmental Pathways to Alcohol Abuse and Dependence in Young Adulthood,”
Journal of Studies on Alcohol 61, no. 6 (2000): 799–808; J. D. Hawkins, R. F. Catalano, and J. Y. Miller,
“Risk and Protective Factors for Alcohol and Other Drug Problems in Adolescence and Early Adulthood—
Implications for Substance-Abuse Prevention,” Psychological Bulletin 112, no. 1 (1992): 64–105; Hingson
et al., “Age at Drinking Onset.”
12. A. H. Mokdad, J. S. Marks, D. F. Stroup, and J. L. Gerberding, “Actual Causes of Death in the United
States, 2000,” Journal of the American Medical Association 291, no. 10 (2004): 1238–45.
13. V. Bagnardi, M. Biangiardo, C. La Vecchia, and G. Corrao, “Alcohol Consumption and the Risk of
Cancer: A Meta-analysis,” Alcohol Research and Health 25, no. 4 (1997): 263–70.
14. G. Corrao, V. Bagnardi, A. Zambon, and C. LaVecchia, “A Meta-analysis of Alcohol Consumption and
the Risk of 15 Diseases,” Preventive Medicine 38, no. 5 (2004): 613–19; G. Corrao, L. Rubbiati, V. Bagnardi,
A. Zambon, and K. Poikolainen, “Alcohol and Coronary Heart Disease: A Meta-analysis,” Addiction 95, no. 10
(2000): 1505–23; J. Rehm, G. Gmel, C. T. Sempos, and M. Trevisan, “Alcohol-related Morbidity and Mortality,”
Alcohol Research & Health 27, no. 1 (2003): 39–51.
15. Corrao et al., “A Meta-analysis of Alcohol Consumption”; K. Reynolds, L. B. Lewis, J. D. L. Nolen,
G. L. Kinney, B. Sathya, and J. He, “Alcohol Consumption and the Risk of Stroke: A Meta-analysis,” Journal
of the American Medical Association 289, no. 5 (2003): 579–88.
16. B. Lopez, S. J. Schwartz, G. Prado, A. E. Campo, and H. Pantin, “Adolescent Neurological
Development and Its Implications for Adolescent Substance Abuse Prevention,” Journal of Primary
Prevention 29 (2008): 5–35.
17. S. A. Brown, M. McGue, J. Maggs, J. Schulenberg, R. Hingson, S. Swartzwelder, C. Martin, T. Chung,
S. F. Tapert, K. Sher, K. C.Winters, C. Lowman, and S. Murphy, “A Developmental Perspective on Alcohol
and Youths 16 to 20 Years of Age,” Pediatrics 121, no. S4 (2008): 290–310.
18. S. E. Tapert, L. Caldwell, and C. Burke, “Alcohol and the Adolescent Brain: Human Studies,” Alcohol
Research & Health 28, no. 4 (2004/2005): 205–12.
19. Lopez et al., “Adolescent Neurological Development”; B. Luna and J. A. Sweeney, “The Emergence of
Collaborative Brain Function: fMRI Studies of the Development of Response Inhibition,” Annals of the New
York Academy of Sciences 1021 (June 2004): 296–309.
20. Ibid.
21. Brown et al., “Developmental Perspective on Alcohol and Youths”; Lopez et al., “Adolescent
Neurological Development”; D.W. Zeigler, C. C.Wang, R. A. Yoast, B. D. Dickinson, M. A. McCaffree,
C. B. Robinowitz, and M. L. Sterling, “The Neurocognitive Effects of Alcohol on Adolescents and College
Students,” Preventive Medicine 40 (2005): 23–32.
22. Luna and Sweeney, “Emergence of Collaborative Brain Function.”
23. S. Hiller-Sturmhöfel and H. S. Swartzwelder, “Alcohol’s Effects on the Adolescent Brain:What Can
Be Learned from Animal Models,” Alcohol Research & Health 28, no. 4 (2004/2005): 213–21; Lopez et al.,
CLASS ACTIONOriginally published in Amazing Alternatives, ©1998, 2009 by Hazelden Foundation. 7 of 9
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Introduction to Underage Alcohol Issues
“Adolescent Neurological Development”; Luna and Sweeney, “Emergence of Collaborative Brain Function”;
E. F.Wagner, “Developmentally Informed Research on the Effectiveness of Clinical Trials: A Primer for
Assessing How Developmental Issues May Influence Treatment Responses among Adolescents with Alcohol
Use Problems,” Pediatrics 121, no. S4 (2008): 337–47.
24. Zeigler et al., “Neurocognitive Effects of Alcohol.”
25. Tapert et al., “Alcohol and the Adolescent Brain.”
26. Luna and Sweeney, “Emergence of Collaborative Brain Function.”
27. Brown et al., “Developmental Perspective on Alcohol and Youths”; Lopez et al., “Adolescent
Neurological Development”; Luna and Sweeney, “Emergence of Collaborative Brain Function.”
28. Lopez et al., “Adolescent Neurological Development.”
29. Luna and Sweeney, “Emergence of Collaborative Brain Function.”
30. Ibid.
31. Ibid.
32. Ibid.
33. Brown et al., “Developmental Perspective on Alcohol and Youths”; Lopez et al., “Adolescent
Neurological Development”; C. O’Brien, “Brain Development as a Vulnerability Factor in the Etiology of
Substance Abuse and Addiction,” Adolescent Psychopathology and the Developing Brain: Integrating Brain
and Prevention Science, ed. D. Romer and E. F.Walker (New York: Oxford University Press, 2007), 388–98;
Tapert et al., “Alcohol and the Adolescent Brain”; Zeigler et al., “Neurocognitive Effects of Alcohol.”
34. Zeigler et al., “Neurocognitive Effects of Alcohol.”
35. Brown et al., “Developmental Perspective on Alcohol and Youths”; Lopez et al., “Adolescent
Neurological Development”; Hiller-Sturmhöfel and Swartzwelder, “Alcohol’s Effects on the Adolescent
Brain”;Wagner, “Developmentally Informed Research”; Zeigler et al., “Neurocognitive Effects of Alcohol.”
36.Wagner, “Developmentally Informed Research.”
37. O’Brien, “Brain Development as a Vulnerability Factor.”
38. Brown et al., “Developmental Perspective on Alcohol and Youths.”
39. Hiller-Sturmhöfel and Swartzwelder, “Alcohol’s Effects on the Adolescent Brain”; M. D.Wood and
K. J. Sher, “Risks of Alcohol Consumption in Laboratory Studies Involving Human Research Participants,”
Psychology of Addictive Behaviors 14, no. 4 (2000): 328–34.
40. O’Brien, “Brain Development as a Vulnerability Factor”; M.Windle, L. P. Spear, A. J. Fuligni,
A. Angold, J. D. Brown, D. Pine, G. T. Smith, J. Giedd, and R. E. Dahl, “Transitions into Underage and
Problem Drinking: Developmental Processes and Mechanisms between 10 and 15 Years of Age,” Pediatrics
121, no. S (2008): 273–89.
41. Brown et al., “Developmental Perspective on Alcohol and Youths”; Hiller-Sturmhöfel and
Swartzwelder, “Alcohol’s Effects on the Adolescent Brain”; O’Brien, “Brain Development as a Vulnerability
Factor.”
42. Brown et al., “Developmental Perspective on Alcohol and Youths.”
43. Ibid.
44. Zeigler et al., “Neurocognitive Effects of Alcohol.”
45. M. D. DeBellis, D. B. Clark, S. R. Beers, P. H. Soloff, A. M. Boring, J. Hall, A. Kersh, and
M. S. Keshavan, “Hippocampal Volume in Adolescent-Onset Alcohol Use Disorders,” American Journal
of Psychiatry 157, no. 5 (2000): 737–44.
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46. Brown et al., “Developmental Perspective on Alcohol and Youths”; Hiller-Sturmhöfel and
Swartzwelder, “Alcohol’s Effects on the Adolescent Brain”; O’Brien, “Brain Development as a Vulnerability
Factor.”
47.Windle et al., “Transitions into Underage and Problem Drinking.”
48. D. Behar, C. J. Berg, J. L. Rapoport, and W. Nelson, “Behavioral and Physiological Effects of Ethanol
in High-Risk and Control Children: A Pilot Study,” Alcoholism: Clinical and Experimental Research 7, no. 4
(1983): 404–10.
49. Ibid.
50. Ibid.
51. Lopez et al., “Adolescent Neurological Development”; Zeigler et al., “Neurocognitive Effects of
Alcohol.”
52. Lopez et al., “Adolescent Neurological Development.”
53. Zeigler et al., “Neurocognitive Effects of Alcohol.”
54. Ibid.
55. Lopez et al., “Adolescent Neurological Development”; Zeigler et al., “Neurocognitive Effects of
Alcohol.”
. . .
CLASS ACTIONOriginally published in Amazing Alternatives, ©1998, 2009 by Hazelden Foundation. 9 of 9
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Introduction to Underage Alcohol Issues
