24
Child Clinical Neuropsychology
of Drug Abuse
ARTHUR MACNEILL HORTON, JR.
AND ARTHUR MACNEILL HORTON, III
Introduction
The use of substances to modify moods, behaviors
and perceptions, drug abuse has been a problem
since the beginning of recorded history. Human
beings for centuries have used alcohol and natural
substances such as peyote from the cactus and
leaves from the opium plant for their psychoactive
properties. After the industrial revolution, chemi-
cal technology has produced new psychoactive
substances with abuse potential such as heroin,
cocaine, LSD, PCP, designer drugs and Ecstasy.
Indeed, the likelihood is that new psychoactive
drugs will be developed in the future and they
will present additional potential for abuse.
Addiction to drugs of abuse is an important
issue for a number of reasons. One reason is that
prohibition of drugs of abuse has not been very
successful as a social policy. Tobacco use was
discouraged in England in the early 1600s but
smoking still increased and growing tobacco was
a major source of income for the British colonies
Sections of this chapter have been adapted and updated from,
‘‘Horton, A. M., Jr. (1996) Neuropsychology of drug abuse. In
R. J. Sbordone and C. J. Long (Eds.) Ecological validity of
neuropsychological testing (pp. 357–368) Delray Beach, Fla.:
GR Press/St. Lucie Press.’’
ARTHUR MACNEILL HORTON, JR.  Psych Associ-
ates, Towson, Maryland. ARTHUR MACNEILL
HORTON, III  Eastern Virginia Medical School,
Norfolk, VA.
C.R. Reynolds, E. Fletcher-Janzen (eds.), Handbook of Clinical Child Neuropsychology,
DOI 10.1007/978-0-387-78867-8_24, Ó Springer ScienceþBusiness Media, LLC 2009
in the Americas. England also made chocolate
illegal in the 1700s with little success. Later,
England, going the other way, in order to over-
come a balance of payments problem over tea
purchases with China fought two wars with
China in the 1700s and 1800s to be allowed to
export opium into China and gain control of the
island of Hong Kong as a site to store imported
opium. The United States prohibited alcohol use
in the 1920s but prohibition was a complete fail-
ure as a social policy and the sale of alcohol was
legalized by a constitutional amendment in 1933.
The United States has also prohibited drug use
of a number of substances but the effort has not
been a complete success and significant illegal
drug use has continued (SAMHSA, 2006).
Survey data indicate that in 2005 (the most
recent available findings) 19.7 million Americans
or 8.1% of the US population aged 12 or older
used illicit drugs during the month prior to the
survey interview (SAMHSA, 2006). Of illicit drug
users, marijuana is the most commonly used illicit
drug, with 14.6 past month users or 6.0% in 2005
(SAMHSA, 2006). For other commonly used illicit
drugs in 2005, 2.4 million persons (1.0%) were
current cocaine abusers, 1.1 million or 0.4% used
hallucinogens (including 502,000 or 0.2% users of
Ecstasy) (SAMHSA, 2006). For prescription psy-
chotherapeutic drugs non-medical use there were
6.4 million (2.6%) users aged 12 and older, of these
users 4.7 used pain relievers, 1.8 million used tran-
quilizers, 1.1 million used stimulants (including
512,00 using methamphetamine) and 272,000
599
600 CHAPTER 24
used sedatives (SAMHSA, 2006). For youths aged
12–17 in 2005, 9.9% were current illicit drug users
(SAMHSA, 2006). The rate of illicit drug use
among youths aged 12–17 in 2005 was similar to
the rate of illicit drug use in 2004 (10.6%) but
significantly lower than the rate of illicit drug use
in 2002 (11.2%) (SAMHSA, 2006).
Alcohol use was higher. In 2005, it was
estimated that 126 million Americans, aged 12
or older, were recent alcohol drinkers (51.8%) or
more than half of the US population in that age
range (SAMHSA, 2006). Of those current alco-
hol users age 12 or older, 55 million (22.7%)
were monthly binge drinkers and 16 million
(6.6%) were heavy drinkers (SAMHSA, 2006).
For youths aged 12–20, 10.8 million reported
monthly drinking (28.2%) in 2005 (SAMHSA,
2006). Generally speaking there were few
increases in illicit drug and alcohol use from
2004 to 2005 (SAMHSA, 2006).
Numbers, however, fail to capture the
damage to society caused by drugs of abuse.
Drug abuse has been estimated as costing the
United States more than 275 billion dollars a
year (Harwood et al., 1998). Drug abuse costs
are from multiple sources. Health costs increase
due to the pathological consequences of alcohol
and illicit drug use. In addition, there are costs
from the results of domestic violence, traffic
accidents and crime (Hubbard et al., 1989). In
addition, there are significant traumatic stress
effects on the spouses and children of drug
addicts and alcoholics that produce initial and
later delayed psychological damage.
While there are multiple negative effects of
illicit drug use and excessive alcohol use, the
social question is not as simple as to suggest
simple prohibition of any psychoactive substance
as a creditable social policy. It must be noted that
under some circumstances, the use of certain sub-
stances to modify moods and behaviors may be
regarded appropriate. Social norms may be seen
as strongly influencing decisions as to whether
the use of a psychoactive substance is pathologi-
cal. For example, the fact that chocolate was
made illegal in England for a period of time,
years ago, suggests that social factors rather
than non-social issues are involved. In the United
States the government allows Native Americans
tribes in the southwestern United States to use
peyote in religious rites. Also, many adults use
caffeine in the form of coffee, tea or cola drinks.
In addition, on a state-by-state basis, limited use
of marijuana for certain medical diseases are
allowed by state legal authorities for selected
individuals in the United States but on the federal
level any use of marijuana is discouraged. In the
State of Nevada, a measure to make the use of
marijuana legal and a state monopoly was nar-
rowly defeated in recent years after substantial
federal pressure was applied.
The above examples argue that it is impor-
tant to realize that society’s views regarding the
use of addictive substances are dependent on
social factors and may change over time. The
first use of many psychoactive substances
abused today, it should be noted, was for allevia-
tion of pain during surgery. The father of psy-
choanalysis, Sigmund Freud, for example,
advocated the use of cocaine as a pain medica-
tion. Freud changed his mind regarding the use
of cocaine after the addiction potential became
clear. Substances such as chocolate, tobacco and
alcohol that were earlier prohibited by society
are legal and accepted today. Alternately, many
substances that are illegal now were legal some
years ago. The problem of psychoactive drug
abuse is of great importance and all persons
need to understand the multiple aspect of this
important problem as society must make wise
decisions as to which psychoactive substances
should be prohibited. Perhaps the most impor-
tant scientific factor that should be considered is
the physical effects of psychoactive substance on
the human brain. Psychoactive substances by
definition are drugs that affect the human brain.
The possible negative effects of drugs of abuse
on the human brain should be considered in
making social decisions regarding prohibition
of psychoactive drugs. The effects on the
human brain are, of course, not the only factor
to consider in formulating America’s drug abuse
policy but it is an area regarding which clinical
child neuropsychologists have unique scientific
expertise that can be used to inform national and
state policy makers.
The use of psychoactive drugs that may be
abused by children is an issue of great important
concern. Because children are in a developmen-
tal period and their brains are still maturing the
effects of drugs of abuse may be more impairing
than when adults whose brains are mature abuse
similar drugs. Also, drug abuse by children of
school age may preclude education processes.
The use of drugs of abuse by school age children
may interfere with learning and memory
 CHILD CLINICAL NEUROPSYCHOLOGY OF DRUG ABUSE
processes that underlie their mental abilities to
profit from educational instruction. The aim of
this chapter is to review what is currently known
about psychoactive drugs of abuse, the negative
neuropsychological effects of exposure to psy-
choactive drugs and approaches to the neurop-
sychological assessment of children and youth
that have been exposed to drugs of abuse, with
special attention to the role of child clinical
neuropsychologists.
Overview
Research has documented that there are
neuropsychological effects from psychoactive
drugs of abuse (Horton, 1996). Because of the
extent of drug abuse, as earlier reported, there
are important implications for the assessment
and treatment of drug abusers (Spencer &
Boren, 1990). Tarter and Edwards (1987) were
among the first researchers to address the issue
of impaired functional adaptive capacity of indi-
viduals with substance abuse problems. Tarter
and Edwards (1987) averred that the use of neu-
ropsychological assessment to measure an indi-
vidual’s organic integrity would provide a basis
for estimating an individual’s potential for
recovery and future adaptive ability. For chil-
dren who are of school age, the degree and pat-
tern of neuropsychological impairment can
provide important information to guide educa-
tional instructional decisions.
Studies to assess the neuropsychological
treatment implications in populations of drug
abusers are few because agreement that there
are residual neuropsychological effects of
abused drugs in adults and children is a recent
advance (Spencer & Boren, 1990). It should be
noted that a distinction should be made between
residual and transient neuropsychological defi-
cits caused by psychoactive drugs of abuse
(Spencer & Boren, 1990). As is well known,
selected drug-related states such as intoxication
and withdrawal and delirium are considered to
be relatively transient. For example a person
could drink too much alcohol and for a time be
incapable of operating a motor vehicle for a
period of time but after some hours would regain
the ability to drive safely. While the effects on
learning and memory and executive functioning
from intoxication from alcohol are serious, it is
expected that with most individuals these effects
601
are state dependent rather than enduring after
withdrawal from alcohol and in some cases other
abused substance or substances. The residual
neuropsychological effects of psychoactive
drugs to be examined in this chapter would be
expected to be enduring organic syndromes of
greater time duration.
Regarding the other substance abuse syn-
dromes, other than alcohol, the major sub-
stance abuse syndromes associated with
organic deficits recognized by (APA, 2000)
include post-hallucinogen perception disorder,
PCP organic mental disorder not otherwise spe-
cified and amnesic disorder caused by sedative
hypnotic drugs.
Brain Structures and Processes Underlying
Addictive Behaviors
Because the brain is the organ which sub-
sumes human behavior, a basis understanding of
the brain structures and processes underlying
addictive behavior is essential to understand
substance use and abuse. The notion is that
understanding brain–behavior relationships
will aid in gaining insight into behavior that
often appears painful and chaotic. Addiction
processes based in the brain result from changes
to the reward pathway upon exposure to psy-
choactive drugs such as cocaine, heroin, and
marijuana, among others (Figure 1).
Reward pathways promote positive condi-
tioning whereby behaviors that precipitate the
experience of pleasure are increased. The brain
associates the behavior to the feeling of plea-
sure, and the behavior increases in frequency in
expectation of eliciting the same pleasurable
experience again. An exposition of neurophy-
siology, admittedly very brief and over simpli-
fied, is presented and is followed by examples of
drug– brain interaction to provide for a simplis-
tic understanding of the brain processes under-
lying abuse of psychoactive substances
(Figure 2).
The brain is composed of 100 billion cells,
known as neurons, and functions intracellular
communication. Messages among and between
cells are transmitted through chemical and elec-
trical means. The parts of a given individual
neuron allow classification relevant to the trans-
mission of information (Figure 3).
602 CHAPTER 24

FIGURE 1. The reward pathway consisting of three brain structures the VTA, nucleus accumbens and prefrontal cortex,
and the connections between the parts (http://www.nida.nih.gov/pubs/teaching/Teaching3.html).

FIGURE 2. Two neurons able to communicate. The arrows designate the route of transferred information
(http://www.nida.nih.gov/pubs/teaching/Teaching2.html).

Information from other neurons comes
through the dendrites and soma. Initiation of
chemical processes in the neuron are elicited in
response to inter-neuron transmissions. Each
neuron’s membrane controls the internal chemi-
cal environment of the cell. Cell membranes
maintain an electrical potential. The electrical
potential is the difference of electrical charge
between the inside of the neuron and the outside.
The difference results from concentrations of
positively and negatively charged ions on each
side of the cell membrane. Such differences seek
 CHILD CLINICAL NEUROPSYCHOLOGY OF DRUG ABUSE
FIGURE 3. An overview of a neuron with its major parts labeled (http://www.nida.nih.gov/pubs/teaching/Teaching2.html).
equilibrium (balance) where the concentrations
of ions and thus electrical charge do not differ.
Membranes preclude this tendency impeding the
flow of ions between the two areas. Ions are
allowed to pass through the membrane through
channels in the membrane specific for that ion
and/or charge. These channels may be activated
through a number of mechanisms.
At baseline a neuron is said to be at resting
potential prior to receiving signals from other neu-
rons. The dendrites and soma of cells contain
receptors which bind selectively with the chemical
signals sent between neurons (neurotransmitters).
Certain neurotransmitters cause bindings in the
electrical potential through the opening and clos-
ing of ion channels nearby. When bombarded with
signals from surrounding neurons that excite, an
action potential is produced. With an action
potential, an electrical current travels from the
dendrites and/or soma to the axon of the neuron
as ion channels sensitive to electrical charge are
opened. The cascading effect of ions flowing across
the plasma membrane pushes the local electrical
potential past its resting equilibrium. The current
generated moves to the end of the axon at the
terminal. Packages of stored neurotransmitters
cause the release of the contained neurotransmit-
ters into the external cellular.
The membrane at the terminal is known as
the presynaptic membrane which in combination
603
with the postsynaptic membrane of another neu-
ron forms the synapse. The area in between the
two neurons that the neurotransmitters travel is
known as the synaptic cleft. When the synaptic
cleft is crossed, the neurotransmitters attach to
receptors on the postsynaptic membrane. The
response of the neuron to the attachment of a
receptor will vary with the type of neurotrans-
mitter and the type of receptor. Ion channels will
allow for the entering or exit of ions. Neuro-
transmitters leave the receptor after attaching
and then are taken from the synaptic cleft by
uptake pumps on the terminal of the presynaptic
membrane. The process of inter-neuron commu-
nication is the method by which information
moves through the brain. Reward pathways
related to the development of addiction have
been associated with the neurotransmitter dopa-
mine, among other neurotransmitters, because
of its prevalence in the reward pathway. Also,
neuromodulators (endorphins) bind to both pre-
synaptic and postsynaptic receptors to modify
neuronal responses synaptic activity (Figure 4).
The human brain has multiple structural
subdivisions. The different brain structures sub-
sume specific neuropsychological functions and
interact with one another to yield more complex
and abstract behaviors. Examples of brain struc-
tures related to function are the hippocampus and
memory, parietal lobes and tactual perception,
604 CHAPTER 24
FIGURE 4. A synapse with the presynaptic neuron on the top releases a neurotransmitter and on the bottom the postsynaptic
neuron contains two types of receptors (http://www.nida.nih.gov/pubs/teaching/Teaching4.html).
temporal lobes and auditory perception, visual
cortex and sight and hypothalamus and homeos-
tasis. Routes of communication between struc-
tures rely on intra-neuronal interaction, and the
interconnections send and integrate information
between and among brain regions. A particular
example is the brain reward pathway which is
associated with the development of addictions.
The brain reward pathway progresses from the
ventral tegmental area (VTA) to the nucleus
accumbens to the prefrontal cortex. The brain
reward pathway is activated when positive rein-
forcement (a reward) occurs paired in time with a
certain behavior (www.nida.nih.gov/pubs/Teach
ing/). The behavior in close temporal sequence
becomes associated to the reward. Living organ
isms perform the behavior so long as a positive
reinforcer (reward) accompanies the behavior.
Positive reinforcers may vary in reinforcement
potency depending on temporal factors. For exam
ple, if a person has not eaten for several hours then
a preferred food may be a positive reinforcer but
after a heavy meal more food may not be seen as a
positive reinforcer (reward), but after several
hours things would change. It is well established
from experimental results that stimulation of the
nucleus accumbens or VTA with cocaine activates
the brain reward pathway. Activation of the brain
reward pathway did not occur with cocaine
administered to other parts of the brain even if in
close proximity to parts of the brain reward
pathway.
Psychoactive substance can establish rela-
tionships between feelings of pleasure and drug-
taking behavior by activating the brain reward
pathway. This activation of the brain reward path-
way causes drug-taking behavior to be selected
over behaviors such as eating or hygiene or par-
enting. Changes in brain function that are good
examples of drug–brain interaction are cocaine,
heroin and marijuana. Other psychoactive drugs
affect the brain in similar ways to these three
examples. For example, the frequently abused
drug cocaine when smoked, snorted or injected
yields high concentrations in the VTA and nucleus
accumbens where dopamine is heavily used in
transmissions between neurons. The high concen-
tration of the abused drug cocaine in these areas
binds to dopamine’s uptake pump precluding it
from removing dopamine from the synapse.
Thereby increasing brain reward pathway stimu-
lation and causing feelings of pleasure (Figure 5).
Synaptic dopamine levels and dopamine
receptors activity both increase. Dopamine
receptors bind to a G-protein. The G-protein
with the inclusion of an enzyme forms a dopamine
receptor–G-protein/adenylate cyclase complex.
The enzyme is turned on and produces cAMP
 CHILD CLINICAL NEUROPSYCHOLOGY OF DRUG ABUSE 605

FIGURE 5. The normal effects of the neurotransmitter, dopamine bound to a dopamine receptor. Here, an enzyme
is activated to produce a certain molecular compound (http://www.nida.nih.gov/pubs/teaching/Teaching2.html).

FIGURE 6. Cocaine in the synapse blocks the uptake pump increasing dopamine activity (http://www.nida.nih.gov/pubs/
teaching/Teaching4.html).

(cyclic adenosine monophosphate) molecules
which control the neurons ability to generate
action potentials (Figure 6).
Cocaine increases the amount of cAMP in
the postsynaptic neuron with the net effects of
increased activation of the brain reward path-
way (Figure 7). Because of the temporal associa-
tion of cocaine use with increased activation of
the brain reward system, use of cocaine is asso-
ciated with feelings of pleasure. The activation of
606 CHAPTER 24
FIGURE 7. The effects of increased dopamine in the presence of cocaine. Contrast to Figure 5 to see difference in activity
and production of cAMP (http://www.nida.nih.gov/pubs/teaching/Teaching4.html).
the brain reward pathway is responsible for the
addictiveness of cocaine. At the same time, how-
ever, cocaine invades other brain areas. For
example, use of cocaine impairs the brain’s abil-
ity to utilize glucose (energy fuel of the brain) for
metabolic activity. Ineffective use of glucose can
cause impairment of brain functions not related
to the brain reward system.
Opiates and other psychoactive drugs can
activate cells in the VTA and nucleus accumbens
of the reward pathway and increase dopamine
release. The cellular mechanisms by which opiates
activate the brain reward system, however, differ
from those of cocaine. Opiates bind to opiate
receptors other than the presynaptic neuron or
the postsynaptic neuron. Opiates bind rather to
an additional neighboring neuron. Opiate bind-
ing to the neuron influences the neuron to send
signals to the dopamine terminals to increase the
amount of dopamine released. Higher levels of
synaptic dopamine released produces greater pro-
duction of cAMP in the postsynaptic neuron and
the brain reward pathway is activated. Again, the
association of the use of opiates and other psy-
choactive drugs with feelings of pleasure produces
addiction to the drug (Figures 8 and 9).
Marijuana, in terms of drug–reward path-
way interaction, requires additional explanation
relative to the well-explained cocaine and opiates
reward pathway systems. Marijuana is repre-
sented by its active ingredient cannabinoids or
THC (delta-9-tetrahydrocannabinol). It is estab-
lished that regions of the reward pathway such as
the VTA and nucleus accumbens contain high
concentrations of THC receptors. It is postulated
that THC activation of the reward system follows
a process similar to that of the opiate with a
neighboring neuron yielding more production of
cAMP in the postsynaptic neuron (Figure 10).
The human reward pathway is activated by
impulses sent from the nucleus accumbens to the
prefrontal cortex. While the short term or tran-
sitory effects of THC are well studied, the resi-
dual effect of marijuana use on the reward
pathway will require additional study. As with
other psychoactive drugs, THC can be found in
brain areas other than the brain reward system
pathway. For example, it has been established
that presence of THC in the hippocampus
reduces memory function, and in the cerebellum
the presence of THC can cause transient lack of
coordination and loss of balance.
 CHILD CLINICAL NEUROPSYCHOLOGY OF DRUG ABUSE 607

FIGURE 8. A side view of the brain showing where opiates are found and active in the brain (http://www.nida.nih.gov/pubs/
teaching/Teaching4.html).

FIGURE 9. Areas where THC is found and active in the brain (http://www.nida.nih.gov/pubs/teaching/Teaching5.html).

Psychoactive Substance Abuse Research
Issues
In order to understand the residual effects
of different psychoactive substances of abuse
some discussion of possible residual effects of
drug using behaviors would be necessary. Fol-
lowing sections will present cursory reviews of
the neuropsychological test research data cur-
rently available regarding the residual effects of
various psychoactive abused substances. There
are, however, many very serious methodological
608 CHAPTER 24
FIGURE 10. High level of dopamine resulting from THC binding to its receptor on a neighboring neuron (http://www.nida.
nih.gov/pubs/teaching/Teaching5.html).
difficulties involved with measuring residual
drug abuse effects in human beings. Prior
reviews by Reed and Grant (1990) and Horton
(1996) addressed many of these issues. As is well
known, some neuropsychological tests are cor-
related with demographic variables such as age,
gender, ethnicity and education. The issue of
correcting for age, gender and education metho-
dological confounds is very complex. While age,
gender, ethnicity and education norms for a
number of neuropsychological tests have been
developed to address this problem area (Heaton,
Miller, Taylor, & Grant, 2004), there are multi-
ple methodological limitations to the new demo-
graphic norms and the problems of correcting
demographic variables that are too numerous to
be detailed (Fastenau & Adams, 1996; Fastenau,
1998; Horton, 1999, Reitan, 1967; Reitan &
Wolfson, 1995, 2005).
Also there is the vexing issue of use of multi-
ple substances of abuse. What substances drug
abusers have abused is difficult to control in
research investigations. Most drug abusers are
known as ‘‘garbage can’’ abusers. In brief, they
have used a wide variety of psychoactive sub-
stances with the most critical variable being
availability. Research studies characterize drug
abusers as having a preference for one substance,
but in reality, their daily consumption of addictive
substances is primarily a product of drug avail-
ability. In short, the psychoactive substance
available is abused. In estimating residual neu-
ropsychological effects of a particular drug of
abuse such as cocaine, heroin or marijuana it is
very difficult to disengage the effects of a single
drug if the research subjects have used all three
drugs in combination with alcohol.
Similarly determining the amount of drugs
taken by research subjects is very problematic.
Most frequently research studies ask patients
to estimate post hoc the amount or amounts of
a drug or drugs they had previously abused.
The research subjects’ self-report is solicited
days, weeks, months and years after the epi-
sode or episodes of substance abuse. Substance
abusing patients may be expected in some cases
to have impaired memory abilities. Also recall
of what drugs were abused can be confounded
with the type and pattern of learning and mem-
ory deficits.
The issue of assessing residual drugs effects
based on the mode of consumption is also pro-
blematic. Psychoactive drugs such as cocaine or
heroin may be ingested through a number of
modalities. For example, drugs can be taken
through needle injection, orally or through the
nose. Each method of consumption can produce
different effects with respect to the action of the
 CHILD CLINICAL NEUROPSYCHOLOGY OF DRUG ABUSE
drug and possibly any residual neuropsycholo-
gical impairment.
In addition, pre-existing and co-existing
medical risk factors can also cause residual neu-
ropsychological deficits that could be mistaken
for residual neuropsychological deficits due to
exposure to drugs of abuse. Tarter and Edwards
(1987) were among the first researchers to iden-
tify many of these factors. They noted that pre-
morbid and co-existing risk factors could also
influence a person’s reactions to various drugs.
For example, pre-existing factors such as learn-
ing disabilities and attention-deficit hyperactiv-
ity disorder could both present as residual
neuropsychological deficits and possibly interact
with similar conditions to produce greater levels
of neuropsychological impairment. With respect
to co-morbid conditions or factors, a variety of
serious psychiatric conditions could co-occur
with substance abuse and these mental disorders
are very difficult conditions to diagnose in an
addict population. Also, it has been averred
that poor nutrition (Tarter & Edwards, 1987)
can impair neurocognitive functioning. In addi-
tion, drugs of abuse can produce medical pro-
blems in various organ systems other than the
human brain and thus have secondary effects on
a person’s mental ability. Multiple psychologi-
cal, psychiatric, medical and nutritional factors
can produce residual neuropsychological effects
that would need to be distinguished from resi-
dual neuropsychological deficits of drugs of
abuse in human beings Benedict and Horton
(1992).
An additional research issue is that of the
criteria to accept that a neurotoxic substance
may cause residual neuropsychological deficits
in human beings. In many cases, researchers are
willing to conclude that a drug may cause residual
neuropsychological deficits simply based on a
level of performance model. That is to say that
for many researchers the sole criterion, for con-
cluding that a drug of abuse causes residual neu-
ropsychological deficits, is low scores on various
neuropsychological and intelligence tests
(Parson & Far, 1981). The problem with such a
conceptualization is that multiple factors may
cause low scores on neuropsychological and intel-
ligence tests. When multiple factors are involved
selecting a single factor as the only cause is very
poor logic. The particular problem with drug
abuse research is that because of the health pro-
blems associated with drugs of abuse it is not
609
possible to use true random research designs.
Rather, only quasi-experimental research designs
using non-equivalent control groups can be uti-
lized. Therefore, all drug abuse research with
human beings has limited control of potentially
confounding variables. The point for concluding
that a specific drug of abuse may cause residual
neuropsychological deficits is that low neuropsy-
chological and intelligence test scores may be due
to another factor other than exposure to a specific
drug. In neuropsychological testing, it is well
established that there are four methodological
methods of inference (Reitan & Wolfson, 1993),
such as level of performance, patterns of impair-
ment, specific deficits and left–right comparisons.
The usual criterion used to conclude there are
residual neuropsychological deficits following
exposure to drugs of abuse is level of performance
or, in other words, low scores on neuropsycholo-
gical and intelligence tests. A better model would
require that the other methodologies of inference
of neuropsychological testing (Horton & Wedding,
1984; Parson & Farr, 1981; Reitan & Wolfson,
1993) such as patterns of impairment, specific
deficits and left–right comparisons be satisfied
before it can be concluded that a specific drug of
abuse would cause residual neuropsychological
deficits.
Marijuana/Cannabis
Residual neuropsychological deficits in
marijuana abusers are subtle as initial research
studies (Mendelson & Mayer, 1972; Grant,
Rockford, Flemming, & Stunkard, 1973; Carlin
and Trupin, 1977) failed to find significant neu-
ropsychological deficits in marijuana users.
The initial studies contained few measures of
short-term memory functioning and that could
be the reason for the negative results. Later stu-
dies which included better measures of short-
term memory, however, suggested that memory
functions may be impaired after consistent
marijuana use (Page, Fletcher, & True, 1988;
Schwartz, Gruenewald, Klitzner, & Fedio,
1989). Additional research (Pope & Yurgelun-
Todd, 1996) suggested there were residual
neuropsychological effects on memory and
executive functioning at least for a period of
6 weeks. Bolla, Eldreth, Matochik and Cadet
(2005) noted short-term (25 days abstinence)
decision-making deficits and decreased
610 CHAPTER 24
activation in the left medial orbital frontal cortex
and increased activation in the cerebellum.
Grant, Gonzalez, Carey, Natarajan and
Wolfson (2003) conducted an excellent quantita-
tive synthesis of empirical research (meta-analysis)
pertaining to the residual neuropsychological
effects of cannabis in adult human subjects.
After screening 1,014 studies for methodological
flaws, they found 15 studies that were methodo-
logically adequate and which provided data on
704 cannabis users and 484 non-users. Grant et
al. (2003) calculated effects sizes for eight neu-
ropsychological ability domains (motor ability,
executive functioning, learning and memory,
etc.). Essentially an effects size is a statistical
method for comparing disparate research stu-
dies. In the simplest case the means of control
and experimental groups are compared for dif-
ferences using either the standard deviation of
the control group or a pooled standard deviation
composed of the standard deviations of both the
experimental and control groups. In brief, if the
experimental and control groups differ less than
a quarter standard deviation the effect is small,
half a standard deviation a moderate effect and a
strong effect for a full standard deviation differ-
ence. The Grant et al., (2003) research group
found small but significant effects sizes only for
learning and forgetting domains. Grant et al.
(2003) postulated that where cannabis com-
pounds are found to have therapeutic value, the
use of marijuana for therapeutic purposes might
have an acceptable margin of safety in medical
settings as the effects size of residual neuropsy-
chological deficits was small and limited to a
single neuropsychological domain.
The quantitative meta-analysis described
above was limited to adult human subjects
only. There is no comparable meta-analysis for
children unfortunately. It has been argued that
children and adolescents who are in the process
of development and undergoing neuropsycholo-
gical developmental changes, however, may be
more vulnerable than adults to the residual neu-
ropsychological deficits effects of cannabis. For
example, Fried and Smith (2001) have published
research that concluded that executive dysfunc-
tion was found in children of mothers who
abused small amounts of cannabis in a Canadian
sample. Similarly, Goldschmidt, Day and
Richardson (2000) published research that con-
cluded there were residual neuropsychological
deficits in a United States sample of children of
mothers who used cannabis.
Hallucinogens/LSD
Research studies of hallucinogens/LSD
have not identified marked residual neuropsy-
chological deficits. Early studies by McGlothlin,
Arnold and Freeman (1969) and Acord and
Baker (1973) presented initial research findings
that suggested possible visual abstraction and
concept formation deficits. These neuropsycho-
logical deficits were extremely mild and may
have been due to the pre-existing or co-morbid
risk factors identified by Tarter and Edwards
(1987). In the period of time since the early stu-
dies no further replications had been conducted.
Additional well-controlled research that con-
firmed earlier findings would be necessary before
reaching a conclusion regarding residual neu-
ropsychological deficits.
Ecstasy
The drug ‘‘Ecstasy’’ (3, 4-methylenedioxy-
methamphetamine or ‘‘MDMA’’) has been con-
sidered a stimulant but it also has hallucinogenic
properties which have been more recently appre-
ciated. Ecstasy is different from other hallucino-
gens and research studies have demonstrated that
Ecstasy can impair memory in abstinent users
(Bolla, McCann, & Ricaurte, 1998; Zakzanis &
Young, 2001). More recent research has demon-
strated learning and memory deficits can persist
up to a year post-abstain (Parrott, 2001; Rene-
man, Booj, Majoie, van den Brink, & den Hee-
ten, 2001). In addition, use of Ecstasy was
associated with task-switching and the degree
of neuropsychological deficit was related to the
extent of drug usage (Dafters, 2006).
Opiates
Research studies on opiates and residual
neuropsychological deficits are contradictory.
An early study with heroin users in a Veterans
Administration Medical Center by Fields and
Fullerton (1975) found no evidence for residual
neuropsychological deficits. Rounsaville,
Novelly, Kleber, and Jones (1982) at Yale
 CHILD CLINICAL NEUROPSYCHOLOGY OF DRUG ABUSE
University published research that suggested
heroin addicts who also were polydrug users
had neuropsychological deficits and addicts
with the most impairment had childhood his-
tories of hyperactivity and a poorer academic
record. The next year, however, the same
research group (Rounsaville, Jones, Novelly,
and Kleber, 1982) who earlier found neuropsy-
chological impairment conducted a follow-up
study (using the same heroin addict subjects as
in 1981 study) also found their heroin addict
users performed better than demographically
similar controls on neuropsychological tests.
One possibility is the first study failed to ade-
quately control for demographic and premorbid
factors. Another possibility could be that heroin
addicts, like professional boxers, are a physiolo-
gically superior group and even with a degree of
neuropsychological impairment they are more
able than normal individuals. There has been
little subsequent research on residual neuropsy-
chological impairment in heroin addicts.
Sedatives
In an early study, Judd and Grant (1975)
reported residual neuropsychological deficits
among sedative abusers but their patients had
also been abusers of stimulants, alcohol and opi-
ates. Bergman, Borg, and Holm (1980) found
residual neuropsychological deficits in subjects
that were treated only for illicit sedative abuse
and better controlled for polydrug abuse. Allen
and Landis (1998) note the fact that elderly indi-
viduals are at greater risk for adverse reactions
such as confusion and delirium and neuropsy-
chological impairment. The evidence for organic
deficits is so well accepted that (APA, 2000)
contains a category for sedative–hypnotic,
amnestic impairment.
Phencyclidine (PCP)
PCP or ‘‘angel dust’’ has been reported to
provoke violent uncontrollable psychotic out-
bursts in the absence of an external threat.
Research studies have not found strong evidence
for residual neuropsychological deficits in PCP
users. In one of the few studies on PCP, Carlin,
Grant, Adams, and Reed (1979) found very
subtle evidence for neuropsychological deficits
611
and the study used a small sample size and has
not been replicated. Indeed, a PCP organic men-
tal disorder category that existed in DSM–III-R
was dropped from (APA, 2000). Few conclu-
sions can be confidently drawn regarding the
potential effects of PCP use on neuropsycholo-
gical functioning.
Cocaine
In an early study, O’Malley and Gawin
(1990) found a mild degree of neuropsychologi-
cal impairment in chronic cocaine users but the
level of deficits found was mild. More recent
studies (Bolla, Funderberk, & Cadet, 2000;
Simon et al., 2002; Strickland et al., 1993; Van
Gorp et al., 1999) clearly document residual
neuropsychological deficits with respect to
cocaine abusers. Jovanovski, Erb, and Zakzanis
(2005) note that neuropsychological abilities
with respect to attention, executive functioning,
working memory and declarative memory were
the most frequently observed pattern of residual
neuropsychological deficits.
There have also been neuroimaging find-
ings that support the notion of residual neuro-
psychological deficits. For example, Strickland
et al. (1993) correlated the results of neuropsy-
chological with single photon emission com-
puterized tomography (SPECT) findings. In
addition, Volkow et al. (1992) found decreased
blood flow in the frontal lobes of cocaine users.
Neurocognitive deficits in cocaine users were
suggested to be due to strokes and seizures
(Volkow, Mullani, Gould, Adler, & Krajewski,
1988).
Stimulants
Animal research has suggested the possibi-
lity of residual neuropsychological deficits in
humans due to stimulants but prior studies failed
to demonstrate deficits (Reed & Grant, 1990).
Recent human studies (Kalechstein, Newton, &
Green, 2003; Nordahl, Salo, & Leamon, 2003)
have indicated neuropsychological deficits in
attention executive functions and memory are
related to methamphetamine use. Verbal mem-
ory impairment in methamphetamine addicts
has been noted to be due to poor verbal encoding
and retrieval strategies (Woods et al. (2005).
612 CHAPTER 24
In addition, Thompson et al. (2004) found struc-
tural abnormalities in the brains of human sub-
jects who have used methamphetamine.
Inhalants/Solvents
There is strong evidence for residual neu-
ropsychological deficits after exposure to inha-
lants/solvents. One of the first studies was a case
report by Bigler (1979) which found a general-
ized pattern of neuropsychological deficits.
A subsequent study by Korman, Matthews and
Lovett (1981) found clear neuropsychological
impairment by inhalant abusers. Korman et al.
(1981) found that inhalant abusers were signifi-
cantly more impaired than other drug abusers
with clear neuropsychological effects found on
both global measures (such as intelligence and
achievement measures) and more specific tests
(such as perception of speech sound, sensory
perception and set shifting ability). The nature
of the neuropsychological deficits found by
Korman et al. (1981) suggested that inhalant
abuse produces neuropsychological deficits that
are severe and widespread. Similarly, Tsushina
and Towne (1977) found glue sniffers were neu-
ropsychologically impaired. Moreover, Berry,
Heaton, and Kirley (1977) found a group of
chronic inhalant abusers impaired on
neuropsychological tests. Exposure to organic sol-
vents has also been shown to cause long-term
neuropsychological impairment on measures of
speed of processing, memory and verbal fluency
(Wood and Liossi (2005). Another study (Rosen-
berg, Grigsby, Dreisbach, Busenbark, & Grigsby,
2002) found that solvent abusers performed worse
than other drug abusers on neuropsychological
tests of working memory and executive cognitive
functions. Interestingly, Rosenberg et al., 2002)
also found a dose– response relationship between
solvent abuse and MRI findings. Consistent and
strong research findings make it possible to con-
clude that inhalants/solvents cause residual neu-
ropsychological impairment.
Polydrug Abuse
Polydrug abusers are more the norm than
an exception in drug abuse research. An early
national study by Grant, Mohns, Miller, and
Reitan (1976) demonstrated neuropsychological
impairment in 50% of a sample of polydrug
users. In addition, Judd and Grant (1975) pro-
vided evidence for impairment of neuropsycho-
logical functioning. There is concern, however,
that polydrug users who demonstrate neuropsy-
chological deficits suffer from possible con-
founds with respect to risk factors that are
medical and psychiatric in nature. Some of the
poly drug users studied also abused alcohol and
the effects seen are more due to alcohol con-
sumption than specific drug effects but others
have suggested greater impairment when cocaine
and alcohol are combined (Bolla et al., 2000).
Additional research is needed to address this
issue.
Summary
As noted by Spencer and Boren (1990) there
are residual neuropsychological deficits from
repeated drug abuse. Nonetheless, the magni-
tude of effects is subtle. Future research should
investigate subcortical effects of the action of
drug abuse on the brain rather than use instru-
ments that were developed to focus on cortical
functioning. As the most common pattern of
deficits found are on measures of attention,
memory and executive functioning, very subtle
assessments of memory, attention and executive
functioning are needed.
In terms of general conclusions regarding
residual neuropsychological deficits, it is clear
that
1) These neuropsychological deficits are
very subtle.
2) They do not impair gross language,
motor functioning or sensory– perceptual
functioning.
3) They involve higher levels neurocognitive
abilities such as attention, short-term
memory and executive functions such as
visual abstract problem solving and com-
plex concept formation.
It may very well be that some drug abusers
can perform relatively well at low level positions
or relatively non-demanding social situations,
yet they will show pronounced problems with
mentally demanding employment tasks or in
complex social situations.
This chapter has briefly discussed brain
structures and processes underlying addictive
 CHILD CLINICAL NEUROPSYCHOLOGY OF DRUG ABUSE
behaviors. Difficulties involved in assessing the
residual neuropsychological effects of various
psycho–active substances have been alluded to
and a very selective review of neuropsychologi-
cal test results with drug addicts has been pre-
sented. The current research with respect to the
neuropsychological effects of abused drugs is
composed of a small number of flawed studies
so there is ample room for additional research.
A crucial research issue is that of the criteria
to accept that exposure to a drug may cause
residual neuropsychological deficits in human
beings. In the past, researchers were willing to
conclude that a drug may cause residual neurop-
sychological deficits simply based on a level of
performance model. Many researchers would
accept that a drug of abuse causes residual neu-
ropsychological deficits if there are low scores on
various neuropsychological and intelligence
tests. The conceptualization is flawed because
multiple factors may cause low scores on neuro-
psychological and intelligence tests. When multi-
ple factors are involved selecting a single factor
as the only cause is very poor logic. The major
problem with drug abuse research with human
beings is that because of the health problems
associated with drugs of abuse it is not possible
to use true random research designs. Rather,
only quasi-experimental research designs using
non-equivalent control groups can be utilized.
Therefore, all drug abuse research with human
beings has limited control of potentially con-
founding variables. The point for concluding
that a specific drug of abuse may cause residual
neuropsychological deficits is that low neurop-
sychological and intelligence test scores may be
due to another factor that exposure to a specific
drug. In neuropsychological testing, it is well
established that there are four methodological
methods of inference (Reitan & Wolfson, 1993),
such as level of performance, patterns of impair-
ment, specific deficits and left–right compari-
sons. The usual criterion used to conclude there
are residual neuropsychological deficits follow-
ing exposure to drugs of abuse is level of perfor-
mance or, in other words, low scores on
neuropsychological and intelligence tests. A bet-
ter model would require that the other meth-
odologies of inference of neuropsychological
testing (Reitan & Wolfson, 1993) such as pat-
terns of impairment, specific deficits and left–-
right comparisons be satisfied before it can be
613
concluded that a specific drug of abuse would
cause residual neuropsychological deficits.
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