C H A P T E R

38
Human Neurophysiology: EEG and
Quantitative EEG in Addiction Research
Rebecca J. Houston*, Natalie A. Ceballos$
*
Research Institute on Addictions, University at Buffalo, The State University of New York, NY, USA
$
Texas State University, San Marcos, TX, USA

O U T L I N E

Electroencephalography 379 Opiates and ERPs 387

Hallucinogens 387
Quantitative Electroencephalography 380
3,4-Methylenedioxymethamphetamine
Event-Related Brain Potentials 380 and Quantitative EEG 387
3,4-Methylenedioxymethamphetamine and Event-
EEG and ERP Findings by Addictive Substance 382
Related Potentials 387
Nicotine 382
Marijuana and Quantitative EEG 388
Nicotine and qEEG 382
Marijuana and Event-Related Potentials 388
Nicotine and ERPs 382
Other Addictions and EEG/ERP 388
Alcohol 383
Disordered Eating 388
Alcohol and qEEG 383
Pathological Gambling 388
Alcohol and ERPs 384
Illicit Stimulants 385 Treatment Implications 389
Illicit Stimulants and qEEG 385
Summary 389
Illicit Stimulants and ERPs 386
Opiates 386
Opiates and qEEG 386

ELECTROENCEPHALOGRAPHY thought to represent summated postsynaptic potential

The first report on measurement of the human
brain’s electrical activity was published by Hans
Berger in 1929. Since then, electroencephalography
(EEG) methodology has evolved substantially. EEG
involves noninvasive measurement of neural activity
from scalp surface electrodes. This electrical signal
reflects the summation of synchronous activity of
a large group of neurons with similar spatial orienta-
tion. More specifically, these voltage fluctuations are
activity (changes in the membrane potential in relation
to neuronal firing). As a result, the EEG provides
a continuous time-sensitive index of neural activation.
Accordingly, a prime advantage of EEG as compared
to many other measures of functional brain activity
(i.e. functional magnetic resonance imaging (fMRI)
and positron emission tomography (PET)) is the high
temporal resolution. Changes in neural activity are
measured on the order of milliseconds as opposed to
minutes that are required for some functional brain

Biological Research on Addiction, Volume 2

http://dx.doi.org/10.1016/B978-0-12-398335-0.00038-8 379 Copyright Ó 2013 Elsevier Inc. All rights reserved.
380 38. HUMAN NEUROPHYSIOLOGY: EEG AND QUANTITATIVE EEG IN ADDICTION RESEARCH
measurement approaches. Thus, the EEG provides an
index of brain activity that is particularly sensitive for
reflecting moment-to-moment changes in neural acti-
vation (up to a thousand times faster), whereas other
methods may rely on slower processes such as cerebral
blood flow.
Although the EEG has high temporal resolution, the
spatial resolution (ability to detect the source of a given
EEG signal in the brain) can be quite low and the
signal from subcortical structures is diminished
considerably, if detectable at all. In an attempt to over-
come this shortcoming, specialized techniques have
been applied, some of which involve the combination
of EEG/ERP with structural (e.g. magnetic resonance
imaging (MRI)) information. For instance, source local-
ization involves the application of mathematical
parameters in an attempt to identify the location,
orientation, and strength of a given source of the elec-
trical information recorded at the scalp. These para-
metrics must be applied to human head models
which can vary from generic multilayer nested concen-
tric spheres to individualized computed tomography
(CT) or MRI scans. The combination of two methods
(i.e. EEG plus MRI) provides both the temporal resolu-
tion of the EEG and the superior spatial resolution of
the MRI.
Given the noninvasive and cost-effective nature of
EEG (it is fairly inexpensive compared to other
approaches), it has developed its own niche as a useful
tool for increasing our understanding of brain function
and dysfunction. Moreover, the use of EEG and its deriv-
atives has been particularly valuable for examining the
neurobiological precursors and consequences of
a number of addictive disorders.
Although more recent assessment methodologies
with high spatial resolution have decreased the clinical
use of the traditional EEG, quantitative EEG (qEEG)
remains a popular tool in research studies. qEEG
reflects ongoing functional brain activation during
a given time period or task. Differences in qEEG char-
acteristics such as frequency and amplitude have been
reliably associated with distinct behavioral and mental
states (e.g. relaxed wakefulness, changes in mental
activity/processing) and thus provide an excellent
basis for comparison when abnormal activity is sus-
pected. Event-related potentials (ERPs), a derivative of
the EEG signal, are used to assess sensory and cognitive
processing. Typically, the EEG signal is time-locked to
a discrete event (e.g. a stimulus or response) and aver-
aged over several trials to eliminate noise and identify
a specific pattern in the change in electrocortical
activity with regard to that event. A number of ERPs
have been identified and each represents a different
means for assessing various aspects of specific psycho-
logical processes.
II. NEUROSCIENCE
QUANTITATIVE
ELECTROENCEPHALOGRAPHY
qEEG measures consist of frequency analyses in
which the signal is deconstructed into its sub-band
frequencies or a power spectrum is obtained. Perhaps
the most commonly used spectral estimation method
is the fast Fourier transformation (FFT); this method
uses an algorithm to decompose the signal into compo-
nent frequencies so that changes or levels of different
frequencies can be observed. Power spectral analysis
focuses on the study of the EEG in several nonoverlap-
ping frequency bands, typically defined as delta waves
(1–4 Hz; deep sleep), theta waves (5–7 Hz; drowsiness),
alpha waves (8–13 Hz; relaxed wakefulness), and beta
waves (>13 Hz; alert wakefulness). Some researchers
have partitioned frequency bands further, for instance,
alpha 1 (8–10 Hz), alpha 2 (10–12 Hz), beta 1 (12.5–
16 Hz), beta 2 (16–20 Hz), and beta 3 (20.5–28 Hz) bands.
Power is typically expressed in either absolute or rela-
tive units. Relative power, a proportion of power in
the entire spectrum, minimizes the individual differ-
ences across subjects in absolute power magnitude and
may obscure group differences.
Variance in EEG pattern is heritable and typically
stable throughout the lifetime. Current models suggest
that genetic predisposition to alcohol dependence, in
particular, is linked to central nervous system (CNS)
homeostatic imbalance, which may be observed using
qEEG methods. In fact, the Collaborative Study on the
Genetics of Alcoholism (COGA) has identified a signifi-
cant linkage for beta EEG power and the gamma-amino-
butyric acid A (GABAA) receptor a2 subunit gene
(GABRA2). Subsequent work has shown that GABRA2
alleles affect subjective responses to alcohol and may
play a role in the risk of alcohol use disorders. Predis-
posed individuals tend to have higher than typical levels
of disinhibition or CNS hyperexcitability, for which
alcohol consumption may provide temporary normali-
zation. This initial state of hyperexcitability may facili-
tate the neuroadaptive changes associated with chronic
alcohol use, and may lead to a more rapid development
of physical dependence.
EVENT-RELATED BRAIN POTENTIALS
ERPs are derived from the ongoing EEG signal and
are time-locked to a specific event. For example, contin-
uous electrocortical activity is collected while individ-
uals are attending to and/or performing a given task.
The EEG is then epoched, which means that a window
of time is marked around each stimulus presentation.
The activity is then examined for a change in voltage
 EVENT-RELATED BRAIN POTENTIALS
in response to the stimulus in question (the “event” in
this example). The primary ERP characteristics that
are examined in response to specific “events” are ampli-
tude, the change in voltage, and latency, the point in
time where this change occurs. The topographic distri-
bution of a given ERP is another important character-
istic and thus careful attention to electrode locations is
required for proper interpretation. ERPs are frequently
labeled based on polarity, whether the change
in voltage is positive or negative in relation to a pre-
stimulus baseline, and latency (e.g. N100 reflects a nega-
tive change in polarity peaking approximately 100 ms
after stimulus onset). Other naming conventions may
incorporate topographical characteristics (e.g. frontal
P300) or functional interpretation (e.g. error-related
negativity (ERN)).
There is a distinction between those ERPs whose
characteristics depend largely on the physical features
of an external stimulus or event (exogenous) and those
whose characteristics are thought to be determined by
internal processes related to the event (endogenous).
Exogenous ERPs, such as the P100 or N100, are elicited
in response to the presentation of a stimulus and
changes in the physical features of this stimulus can
result in changes in the exogenous ERP. For example,
the presentation of an auditory tone will elicit the P100
and N100, but an increase in the loudness (i.e. intensity)
of the tone can result in changes in P100 and N100
amplitude. These ERPs are also termed evoked poten-
tials as they are elicited (or evoked) simply by the
presentation of a stimulus. Endogenous ERPs, on the
other hand, are linked to internal processes surrounding
a given event, such as decision making and error moni-
toring. Changes in endogenous ERP characteristics such
as amplitude or latency are dependent on these internal
mechanisms (e.g. the amount of time the individual
spends in evaluating a stimulus to meet task demands).
There are, however, some ERPs that may exhibit both
exogenous and endogenous properties. In addition,
some studies have suggested links between particular
ERP components and specific neurochemical processes,
such as neurotransmitter function. For instance, ampli-
tude increases in the mid-latency ERPs in response to
increases in auditory stimulus intensity have been
repeatedly linked to low serotonin function and favor-
able response to selective serontonin reuptake inhibitors
(SSRIs). Dopamine function has also been associated
with conflict processing (P300, ERN) and attention
(N100, mismatch negativity (MMN)). Given the complex
electrical and neurochemical processes involved in
neural communication, our extant understanding of
how these electrocortical measures are directly related
to neurochemical transmission remains an area of
debate. More is known about the anatomical basis for
specific ERPs, although this varies considerably by
II. NEUROSCIENCE
381
ERP, the modality and characteristics of the external
event (if applicable), and the elicitation method. Below
is a brief description of ERPs that have significantly
contributed to addiction research.
One of the movement-related potentials, the contin-
gent negative variation (CNV), is a slow negative wave
that occurs between a warning stimulus and target stim-
ulus that requires a rapid motor response. It consists of
two distinct components: an early negativity which
peaks about 1 s after the warning stimulus (the orienting
wave or O-wave) and a late negativity which increases
up to the point at which the imperative stimulus appears
(expectancy wave or E-wave). The late CNV is thought
to reflect both anticipation of the imperative stimulus
and movement preparation. Thus, the CNV has been
described as reflecting expectancy, attentional prepara-
tion, and motivation/intention to act.
The ERN occurs approximately 100 ms after an incor-
rect response, regardless of whether or not the partici-
pant is consciously aware of committing an error, and
is hypothesized to reflect error detection or conflict
monitoring processes. Often observed in conjunction
with the ERN are the error positivity (Pe), a positive
deflection occurring slightly later than the ERN after
an error and thought to reflect conscious processing of
an error, and the feedback negativity (sometimes called
the fERN), which is strongly associated with negative
feedback outcomes (particularly in reward contexts),
and typically occurs 250–300 ms after feedback
presentation.
The MMN is an auditory ERP that is elicited during
a passive attention task in which infrequent stimuli are
embedded within a sequence of frequent standard
stimuli while the individual’s attention is typically
engaged in another task (e.g. watching a silent video).
The MMN is thought to reflect involuntary attention to
the change in stimuli (i.e. deviance or “mismatch” detec-
tion) and/or may be a marker of early pre-attentive
sensory memory processes.
Mid-latency ERPs reflect the segue from exogenous to
endogenous ERPs depending on the stimuli and task
demands used to elicit these components. The visual
P100 occurs approximately 100 ms after stimulus onset
and is thought to represent sensitivity to an attended
stimulus. The N100 or N1 is hypothesized to indicate
the allocation and orienting of attention. The N200 or
N2 refers to a group of related components that occur
around 200 ms poststimulus, although the latency range
and topography can vary depending on task demands
and modality. Early work on the N2 hypothesized that
this component reflected the detection of deviant stimuli
or a mismatch between a stimulus and some previous
mentally stored expectation (the N2a is similar to the
MMN, but other N2 components differ from the MMN
in that the individual’s attention is consciously
382 38. HUMAN NEUROPHYSIOLOGY: EEG AND QUANTITATIVE EEG IN ADDICTION RESEARCH
engaged). Continued research on the N2 has indicated
the versatility of this component and the identification
of the N2b and N2c. The N2b is thought to be related
to cognitive control and response inhibition, and is the
most popular N2 component for the study of psycholog-
ical processes. The N2c is more common in visual
perception research and is related to visual attention
processes.
The P300 or P3 is probably the most frequently
studied ERP component in addiction research. The
“classic” P3 or P3b is elicited via an oddball paradigm
(e.g. presentation of stimuli requiring discrimination
between target and nontarget events) and is usually
maximal at posterior sites; its amplitude provides an
index of cognitive efficiency within the context of atten-
tion and memory updating whereas its latency reflects
stimulus evaluation time or task complexity. The P3a
(i.e. frontal P3 or novelty P3) is elicited in response to
infrequent and/or novel stimuli, has a more anterior
topographic distribution, and provides an index of
attention to novelty.
Other ERP components, such as the P50, N400, or
negative slow wave (NSW), have been explored in rela-
tion to addictive disorders. The findings related to these
components are relatively recent and/or less consistent,
but are also described where relevant.
EEG AND ERP FINDINGS BY
ADDICTIVE SUBSTANCE
Important issues for research on addictive substances
include the distinction between acute versus chronic
effects, the route of administration, and the differentia-
tion and/or control of facilitation/inhibition versus
withdrawal effects on cognition. Chronicity, extent of
dependence, and family history are also crucial factors.
The double-blind, placebo-controlled design presents
the “best practice” method of measuring the effects of
a drug; however, this technique has not consistently
been applied to studies assessing the effects of addictive
substances on EEG/ERPs. Lack of methodological conti-
nuity may be a contributing factor to inconsistent find-
ings in this field.
In terms of acute effects, the EEG/ERP findings asso-
ciated with a given class of addictive substances may be
predicted based on their CNS-activating or -inhibiting
effects. For instance, administration of a stimulant has
an excitatory effect on the CNS, resulting in an “alert”
EEG pattern (typically most evident frontally) and
increased amplitude with decreased latency of atten-
tion-related ERPs. Conversely, administration of a seda-
tive drug typically results in the opposite pattern of
findings. As noted above, it is important to acknowledge
II. NEUROSCIENCE
that a family history of addiction may influence acute
response to various substances.
Studies of the chronic effects of substances on EEG/
ERP indices also encounter a host of confounding
factors. For instance, certain EEG/ERP patterns may
serve as an endophenotype for risk of substance depen-
dence and may be associated with a family history of
alcohol/drug use or a predisposition for disinhibited
or externalizing behavior. Because few studies follow
participants from birth to their entry into substance
abuse treatment it is difficult to definitively determine
whether or not EEG/ERP deficits among substance-
dependent individuals reflect predisposing CNS factors
or merely the toxic effects of chronic substance use.
Nicotine
Nicotine and qEEG
Most studies of nicotine’s effects on qEEG have
focused on acute administration, which results in a stim-
ulant-like EEG profile, including reduction in ampli-
tude/power in slow wave delta and theta frequency
bands, and increases in amplitude/power in fast wave
alpha and beta frequency bands. When alpha is parti-
tioned into slow (alpha 1: 8–10 Hz) and fast (alpha 2:
10–12 Hz) varieties, acute nicotine results in decreases
in slow alpha and fast alpha amplitude/power. EEG
activation is widespread; however, low nicotine-yield
cigarettes tend to produce more localized posterior acti-
vation, which spreads to central and frontal regions with
increasing nicotine concentration. Administration
methods may also influence the EEG profile (e.g. ciga-
rette smoking is a more efficient activator of the EEG
versus nicotine nasal spray).
Chronic smoking increases the risk of attention and
working memory deficits; however, the literature is
contentious concerning the question of whether or not
chronic smoking results in cognitive deficits that may
be reflected via qEEG. This work is typically
confounded by lingering effects of overnight abstinence
from nicotine and/or acute abstinence occurring
throughout the testing session itself. As such, the acute
facilitative effects of nicotine may partially mask cogni-
tive deficits associated with long-term use, particularly
in the frontal brain regions. However, longitudinal
studies of EEG changes during smoking cessation have
revealed an overall slowing of the EEG, which persists
for up to a month following cessation.
Nicotine and ERPs
• CNV: CNV amplitude tends to increase in response to
higher doses of nicotine, suggesting an increased
orienting response reflected at frontal scalp electrodes
and readiness for movement reflected at central scalp
 EEG AND ERP FINDINGS BY ADDICTIVE SUBSTANCE
electrodes. Further, studies suggest that personality
traits may also influence smokers’ CNVs with an
increase in amplitude for extroverts and a decrease for
introverts. Overall, these findings tend to apply to the
global CNV waveform or to the E-wave component.
• MMN: Nicotine administration tends to be associated
with MMN amplitude increase and latency decrease,
reflecting an enhancement of deviance detection in
a string of otherwise common stimuli. Other work has
focused on patients treated or not treated with
acetylcholinesterase inhibitors; nicotine increased
MMN amplitude among untreated patients and
decreased latency among patients in both groups.
• Mid-latency ERPs: Acute improvements in task
performance are thought to be related to nicotine’s
facilitative effects on identification and encoding of
rare deviant stimuli at early sensory levels. Nicotine
enhances P100 and P200 amplitudes; however,
findings for the N100 waveform have been less
consistent.
Chronic smoking is thought to reduce amplitude and
increase latency of early ERP components. N100 find-
ings among smokers might reflect delayed information
processing and perhaps short-term memory distur-
bances, both related to prefrontal cognitive dysfunction.
However, it is possible that preexisting frontal dysfunc-
tion could have contributed to the initiation of partici-
pants’ tobacco use.
• P300: Acutely, nicotine/cigarette smoking shortens P3
latency and/or increases P3 amplitude, reflecting
enhanced efficiency of attentional allocation to target
stimuli. Evidence of a P3 endophenotype for tobacco
dependence has also been noted in studies of chronic
smokers, who exhibit lower P3 amplitude compared
to nonsmokers. Other research indicates diminished
P3 amplitudes in both current smokers and former
smokers, as compared to never smokers. Although
some researchers attribute these findings to
neurotoxicity, one could also argue that these data
reflect a trait or risk factor contributing to tobacco
dependence.
Alcohol
EEG/ERPs have long played an integral role in the
understanding of the vulnerability for and neurocogni-
tive consequences of addictive disorders. Published
studies date back to the 1940s indicating EEG abnormal-
ities as a result of both acute and chronic alcohol use.
When the study of evoked and ERPs increased in popu-
larity, research on how these neural mechanisms relate to
alcohol consumption also grew steadily. Important
issues are similar to some of those noted for nicotine
II. NEUROSCIENCE
383
research such as acute versus chronic effects, length
and severity of use/dependence, as well as effects of
abstinence/recovery. Research on the effects of alcohol,
particularly chronic effects, on neurophysiological
measures is often rife with confounds related to a history
of head injury, seizure disorder, antisocial behavior, and
family history of alcoholism. Early work may not have
accounted for many of these issues, assuming that defi-
cits were a consequence of the neurotoxic effects of
alcohol. Studies in recent years have tended to take
a more rigorous and balanced approach. It is also imper-
ative to note that the neurophysiology of alcoholism is
inextricably linked to one’s genetic propensity to develop
such disorders or behavior patterns. To date, hundreds of
studies have been conducted; below is a summary of the
most consistent and notable findings in humans.
Alcohol and qEEG
Studies of acute alcohol administration on qEEG
indices have demonstrated increases in slow alpha
activity at low doses, although these results are not
always consistent. Moderate doses of alcohol tend to
result in increased slow alpha, increased theta, and
decreased beta activity. Several studies of acute alcohol
effects on qEEG have been specifically conducted on
offspring of alcohol-dependent individuals (family
history positive or FHP) in an effort to explore whether
these offspring may possess an underlying neurological
vulnerability that may be revealed via alcohol exposure.
In general, FHP individuals do not exhibit any differ-
ences from those without such a history in terms of the
uptake and clearance of alcohol in the bloodstream.
However, qEEG studies have demonstrated greater
increases in slow alpha and beta activity as well as
greater decreases in fast alpha in response to alcohol
consumption in FHP males as compared to non-FHP
males. In addition, non-FHP individuals classified as
at least moderate drinkers also exhibit more beta power
than lighter drinkers after alcohol consumption. Finally,
studies of FHP individuals have also indicated that
a diminished alpha response to alcohol administration
in these individuals may be related to later development
of severe alcohol use problems.
Studies examining the chronic effects of alcohol
consumption on qEEG have largely focused on patient
populations. Studies of resting EEG studies have tradi-
tionally indicated increased levels of slow wave activity
(e.g. theta) in alcoholic individuals as compared to
nonalcoholic controls. This effect appears to be more
robust in men and independent of length of abstinence.
Elevated theta during a normal waking EEG is abnormal
and this type of finding is consistent with increased EEG
slow wave patterns reported in other psychiatric disor-
ders such as depression and psychotic disorders. In
addition to theta differences, a series of early studies
384 38. HUMAN NEUROPHYSIOLOGY: EEG AND QUANTITATIVE EEG IN ADDICTION RESEARCH
reported low alpha activity in alcoholics, but later work
has reported opposite or null effects. Another series of
studies has shown that men with a paternal history of
alcoholism (FHP) exhibit increased alpha power
compared to men without such a paternal history. Inter-
estingly, alcohol-dependent patients in recovery (as long
as 12 weeks abstinent) do not exhibit the same increases
in alpha activity in response to increases in photic stim-
ulation intensity as control individuals; this suggests
impaired sensory/attentional processing. Also related
to alpha activity is the notion that individuals who
exhibit low voltage alpha activity (LVA), an EEG pheno-
type, may be at higher risk for alcoholism. It has been
demonstrated that alcohol-dependent individuals are
three to four times more likely to exhibit LVA, and
LVA is related to low P3 amplitude, a “classic” character-
istic of alcohol-dependent individuals.
Increased beta power in alcohol-dependent individ-
uals has been consistently reported and there is evidence
of elevated beta in those with a family history of alco-
holism as well. Moreover, increased qEEG fast beta
activity has also been demonstrated as a valuable
predictor for relapse in alcohol-dependent (and other
substance-dependent) patients over and above a number
of other comorbid factors, such as severity of illness,
depression level, and childhood conduct problems.
This association appears stronger for men than women.
Related to these findings is research demonstrating that
the beta frequency band of the EEG is genetically linked
to a GABRA2 receptor gene, which has been associated
with alcohol dependence. The current hypothesis is
that variations in this gene can influence neural excit-
ability which can then implicate a predisposition to alco-
holism. These studies on beta power in alcoholic patients
and nonalcohol-dependent individuals with a family
history of alcoholism suggest that these effects are likely
related to a premorbid vulnerability for alcoholism as
opposed to the consequences of alcohol consumption.
Alcohol and ERPs
• CNV: The acute effects of alcohol administration on
the CNV include decreases in CNV amplitude, and
thus a dampening of preparatory processes under the
influence of alcohol. However, some studies report no
difference in CNV amplitudes or latencies between
abstinent alcohol-dependent patients and controls,
and others demonstrate reduced CNV amplitudes in
heavy and/or chronic drinkers compared to controls.
These disparate findings may be related to the
severity of alcohol consumption history as well as the
effects of abstinence. Studies reporting reduced CNV
amplitudes in drinkers interpret this as evidence of
deficient cognitive and motor preparation (i.e.
reduced CNV amplitudes), and hence impaired
II. NEUROSCIENCE
frontal lobe functioning, which is consistent with
findings from neuropsychological and structural
imaging studies (see Neuropsychological Precursors
and Consequences of Addiction, Addiction and the
Human Adolescent Brain, Alcohol Neuroimaging in
Humans).
• MMN: Decreases in MMN amplitude in response to
acute alcohol suggest that consumption can impair
auditory detection processes for unexpected events. A
visual analog of the MMN called the rareness-related
negativity (RRN) is also adversely affected by acute
alcohol. These findings speak to the extent that acute
alcohol can diminish attentional processes during
everyday activities such as driving. Studies of the
MMN in recently detoxified alcohol-dependent
patients report larger MMN amplitudes, suggestive of
greater attentional distraction and impaired
reorienting, although this effect has not always been
consistent. Further, the MMN appears to reduce with
increased abstinence, and alcoholics who have
maintained abstinence for a minimum of 6 months
exhibit no differences in MMN when compared to
nonalcoholic controls. Thus, the MMN seems to be
more sensitive to state factors, such as recent alcohol
use, and less determined by factors which may persist
throughout long-term recovery.
• Mid-latency ERPs: Consistent with acute alcohol
effects on the MMN, alcohol administration results in
smaller N1 amplitude and increased N2b latencies,
suggesting attentional impairment. Findings are
somewhat similar in terms of chronic alcohol
consumption with reduced visual N1 amplitude and
a phenomenon termed “auditory N1 amplitude
suppression” (reduced amplitude with repetitive
stimuli) being demonstrated in alcohol-dependent
patients compared to controls. There is also evidence
of amplitude decrements in P100, N170, and N200.
Studies published in 2012 on binge drinkers have
demonstrated increased P100 and N200 latency over
the course of 9 months compared to nonbinge
drinkers, supporting the idea that binge drinking may
be on a continuum with other alcohol use disorders,
and thus result in neurotoxic effects. Taken together,
studies of mid-latency ERPs indicate impaired
sensory and attentional processing which is also likely
to contribute to deficits in later stages of cognitive
processing.
• P300: Acutely, alcohol has been found to reduce both
P3a and P3b amplitudes, even at low doses.
Decrements in P3b amplitude and prolonged P3b
latency, in response to both visual and auditory
stimuli, have been repeatedly demonstrated in
alcohol-dependent patients as compared to controls
reflecting inefficient attention and/or cognitive
processing. This is consistent with findings in
 EEG AND ERP FINDINGS BY ADDICTIVE SUBSTANCE
individuals with other psychiatric disorders and
likely reflects generalized impairment of attentional
allocation, as opposed to deficits directly due to
alcohol. Interestingly, these findings appear to be
more robust for male as opposed to female alcoholics.
Studies of P3a have also demonstrated smaller P3a
amplitude in alcohol-dependent individuals as
compared to controls in both visual and auditory
modalities, although contradictory reports do exist. In
general, these findings of smaller P3b and P3a are
hypothesized to be due to reduced inhibition of the
CNS, and although the majority of studies have been
conducted in alcohol-dependent patients, research in
the past 20 years has also demonstrated similar
findings in heavy versus light social drinkers. In
addition, research with alcohol-dependent patients
has also demonstrated that P3 amplitude decrements
do not fully recover with prolonged abstinence.
A line of research initiated in the early 1980s also
demonstrated that nonalcohol-dependent offspring of
alcoholics also exhibit P3b amplitude decrements. This
work along with other research examining family
history of substance use disorders has lead to a growing
series of twin studies, suggesting that P3b amplitude to
visual stimuli may be an endophenotype or biomarker
for the development of externalizing behavior disorders
including substance use disorders. However, not all P3
studies examining family history have found consistent
effects; some have suggested that these effects may be
better accounted for by other common comorbid factors
such as conduct disorder/antisocial personality, and
other related features (i.e. impulsivity). Again, most of
these studies have been conducted with male partici-
pants, thus the picture for females is less clear.
An interesting development in recent years is the use
of EEG/ERP measures in studies of cue reactivity; the
P3 has played a significant role in this area. Research
has demonstrated enhanced P3 amplitudes to alcohol-
related stimuli in individuals with a history of alcohol
use disorders, indicating an attentional bias for
alcohol-related cues. Further, individuals low in
alcohol sensitivity, who report needing more alcohol
to experience subjective alcohol-related effects versus
those high in sensitivity, tend to exhibit larger P3
amplitudes to alcohol cues. This sensitivity effect may
be specific to alcohol cues versus other arousing cues.
The P3 has been used to explore alcohol expectancies
as well. In general, the higher the individual’s self-
reported positive/arousing expectancies, the larger
the P3 amplitude in response to negative alcohol expec-
tancy stimuli.
• ERN: Acutely, alcohol reduces ERN and Pe
amplitudes during a cognitive control task,
suggesting that alcohol may have an attenuating effect
385
on both unconscious and conscious error detection. In
terms of alcohol dependence, ERN amplitude
findings have been mixed, although it is suggested
that psychiatric comorbidity may be an important
factor (i.e. comorbid anxiety disorders are related to
larger ERN). In addition, the feedback negativity does
not appear to be affected in alcoholic participants, but
it is smaller in those participants with a greater family
density of alcohol problems, consistent with a genetic
vulnerability theory of addictions.
Illicit Stimulants
Studies of the acute effects of illegal stimulant admin-
istration typically have focused on participants who are
already dependent on these substances. Given the
similar dopaminergic mechanisms of cocaine, amphet-
amine, and methamphetamine, it is not surprising that
acute administration studies tend to report a similar
pattern of CNS activation. In addition, as for other
substances, study results may vary based on partici-
pants’ severity of dependence, length of chronicity,
time since last use of an illicit stimulant, and comorbid-
ity in terms of other addictions and psychiatric
conditions.
Illicit Stimulants and qEEG
Acutely, cocaine produces rapid increases in absolute
theta, alpha, and beta power over the prefrontal cortex,
persisting up to approximately 25 min, although level
of experience with cocaine may influence the extent of
drug action (e.g. tolerance or reverse tolerance effects).
In particular, cocaine-related increases in theta power
have been correlated with the subjectively positive
effects of cocaine. Overall, research suggests that the
prefrontal cortex is activated by both acute cocaine
administration and the pleasurable effects of cocaine
on the brain’s reward pathways (i.e. ventral
tegmental–nucleus accumbens–prefrontal cortex).
Chronic cocaine use tends to be associated with
decreased absolute and relative power in the delta
band and increased relative alpha power. Although
causation cannot be inferred from such studies, it is
interesting to note that these abnormalities may persist
even after 6 months of abstinence, suggesting a persis-
tent neurobiological alteration resulting from chronic
cocaine exposure. Of course, because pre-addiction
measures are not possible in quasi-experimental studies
of this nature, it is unknown whether or not these alter-
ations resulted from cocaine use or if preexisting qEEG
abnormalities might have predisposed these patients
to addiction.
Although EEG/ERP studies of chronic methamphet-
amine abusers have increased in recent years, the litera-
ture remains relatively sparse with regard to this issue.

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386 38. HUMAN NEUROPHYSIOLOGY: EEG AND QUANTITATIVE EEG IN ADDICTION RESEARCH
However, existing research suggests that increased theta
power may be associated with poorer performance on
working memory tests among recently abstinent meth-
amphetamine abusers. Overall, the neuroelectric profile
of recently abstinent methamphetamine-dependent
participants is consistent with generalized encephalop-
athy. The issue of persistent neurobiological alterations
among chronic abusers is particularly relevant to studies
of methamphetamine, which by nature of its enhanced
lipid solubility, might be expected to create lasting
neuronal changes.
Illicit Stimulants and ERPs
Currently, most of the work in this area appears to
have focused on cocaine use; however, studies of meth-
amphetamine’s effects are on the rise.
• N200: Decrements of frontal lobe (i.e. executive)
function are frequently noted among chronic cocaine
abusers. Electrophysiological correlates of these
deficits are often elicited using flanker tasks with Go/
NoGo features. Described in simple terms, these are
tasks in which one class of stimulus requires
a behavioral response, whereas another requires the
participant to refrain from responding. Such tasks
require a variety of executive functions, including
cortical inhibition, selection of appropriate responses
from among several competing ones, withholding
inappropriate responses, and the ability to detect error
and exercise corrective control. Within this context,
the N200 ERP is considered to reflect inhibitory
executive functions in Go/NoGo tasks and conflict
monitoring in tasks that elicit incompatible response
tendencies. Decreased N200 amplitude and delayed
latency are often noted among chronic cocaine
abusers and may reflect an inability to override
automatic addiction-related cognitions and behaviors.
• P300: Cocaine-dependent individuals often exhibit
decreased amplitude and delayed latency of the P3,
elicited by the classic oddball paradigm. Such
decrements are thought to reflect a generalized deficit
of attentional functions in chronic cocaine abusers.
Other studies have noted a negative correlation
between P3 amplitude and impulsivity, and this
finding appears to be independent of childhood
conduct disorder symptoms.
Similarly, methamphetamine-dependent individuals
also exhibit P3 decrements, which appear to be indepen-
dent of methamphetamine psychosis. These persistent
decrements support the notion of long-term neurophys-
iological alterations of the cortex in chronic metham-
phetamine abusers.
• Cue reactivity: Much of this work has revealed a late
positive potential (LPP) and early positive negativity
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(EPN) relevant to cue reactivity. Among individuals
with cocaine use disorders, LPP amplitude generally
appears to be enhanced following presentation of
cocaine-related versus neutral stimuli. Level of self-
reported cocaine craving has also been positively
associated with LPP amplitudes. However, these
effects may be modulated by recency of cocaine use.
A 2011 study reported that while early LPP (400–
1000 ms poststimulus) amplitude to cocaine pictures
was enhanced in both “abstinent” and “currently
using” participants versus controls, late LPP
amplitude (1000–2000 ms poststimulus) was
enhanced for abstinent participants but attenuated
among current users.
Opiates
The available research on human neurophysiology
associated with opiate-related drug disorders has
largely been conducted on heroin users, although recent
work has begun to expand beyond this type of sample.
A significant proportion of the patient samples in these
studies also tend to abuse other substances, particularly
alcohol, nicotine, cocaine, and prescription drugs. Thus,
separating the individual effects of opiate use is one of
the biggest challenges in this area. However, several
studies have demonstrated consistent results and have
focused, in particular, on the effects of withdrawal.
Opiates and qEEG
Few studies that have examined the acute effects of
opioids on qEEG have primarily used morphine-like
drugs and report increases in theta and delta power
and decreases in alpha and beta power in both opioid
users and surgical patients. Alpha slowing also appears
to be highly dependent on dosage. One placebo-
controlled study of self- versus passive-administration
of fentanyl, a synthetic mu-opioid agonist, in heroin-
dependent, methadone-maintained individuals, reported
increased delta power with fentanyl administration.
However, when fentanyl was self-administered, the
increase in delta was doubled, highlighting the reinforc-
ing nature of the drug.
Early qEEG studies of individuals with chronic opiate
use tend to report increased slow wave activity
compared to nondrug using controls, even after
extended periods of abstinence (up to 6 months in
many cases). Increased relative beta 2 power has been
demonstrated in abstinent heroin users, as well. Recent
work has utilized rigorous methodological approaches
to explore functional cortical connectivity in the alpha
and beta frequencies in relation to opiate withdrawal.
Functional connectivity refers to the temporal correla-
tion between spatially distanced events (e.g. separate
 EEG AND ERP FINDINGS BY ADDICTIVE SUBSTANCE
groups of neurons firing synchronously), and thus is
thought to reflect coordination of neuronal areas or
systems. The basic theory underlying this approach is
that chronic opiate use results in disrupted or rear-
ranged neuronal assemblies, which in turn, affects
neuronal communication (i.e. produces a different
pattern of neural synchrony between brain regions)
and subsequently disrupts neurocognitive processing
and behavior. Most of this work suggests that individ-
uals with a history of opiate use exhibit a different
pattern of functional connectivity that is directly related
to the severity of their withdrawal symptoms and that
this facilitates drug-seeking behavior and reduces the
efficiency of rehabilitation. In addition, individuals in
opiate withdrawal exhibit a slowing of the EEG which
can be restored via methadone treatment.
Opiates and ERPs
• MMN: In the only published study examining MMN
in abstinent opioid-dependent men and women, the
MMN latency to novel sounds was delayed
suggesting deficits in pre-attentive auditory
processing. The MMN is thought to be modulated by
changes in dopamine such as attenuated MMN
responses after acute administration of a dopamine D2
antagonist. Thus this finding in opioid-dependent
individuals is hypothesized to be related to the
important role of dopamine in neural mechanisms of
reward; additional study is needed to further identify
how the MMN is connected to dopamine function in
the context of attentional processing.
• P300: Several studies have described P3 amplitude
decrements and prolonged P3 latency among opioid-
dependent individuals in withdrawal. Interestingly,
active heroin users tend to exhibit normalized P3
amplitude, thus emphasizing the severe impact of
opiate withdrawal on cognitive and attentional
processes. Another study demonstrated reduced
auditory P3 amplitude in heroin and/or cocaine
addicts, but those addicts with a history of
dysregulated aggression exhibited even smaller P3
amplitudes than those without. Studies of emotional
processing in abstinent heroin addicts report small P3
amplitudes in response to unpleasant and neutral
emotional stimuli, but not to pleasant stimuli
suggesting a bias toward positive emotional cues.
This is further supported by evidence of enhanced P3
amplitudes in response to opiate-related images as
compared to the P3 response to emotional and neutral
images in recently detoxified heroin addicts, some of
which were methadone maintained. A study in
opioid-dependent men and their full brothers found
that the opioid-dependent men performed worst on
a battery of neurocognitive measures compared to
their brothers and control men, and the brothers
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387
performed worse than controls. Although not
statistically significant, a similar pattern was
demonstrated for the auditory P3 in which the opioid-
dependent men exhibited the smallest P3 amplitude
and longest P3 latencies, and the brothers exhibited
smaller P3 amplitudes and longer latencies compared
to the controls. Taken together, these findings are
consistent with P3 findings with other substances,
particularly alcohol, indicating deficits in attentional
resource allocation in opioid-dependent individuals
(in withdrawal) as well as some attentional bias
toward rewarding cues. This work also supports the
aforementioned alcohol research on the P300 as
a potential endophenotype for substance use risk.
Hallucinogens
Neurophysiological correlates of hallucinogenic drugs
are not well studied, although a growing body of work
now exists primarily for two hallucinogenic substances:
3,4-methylenedioxymethamphetamine (MDMA or
ecstasy) and marijuana (MJ). An important consideration
for these studies is that ecstasy users, and often MJ users
as well, tend to be polydrug abusers, thus it is difficult to
completely isolate the effects of these specific drugs in
studies of chronic use.
3,4-Methylenedioxymethamphetamine
and Quantitative EEG
In healthy volunteers, acute MDMA administration
results in a decrease in slow and medium wave activity,
particularly decreased frontal delta, a global decrease in
theta activity, and decreased alpha activity in fronto-
parietal regions. Acute MDMA also results in increased
beta activity, most prominent in the orbitofrontal cortex
and anterior temporal lobes, which is hypothesized to
play an important role in the enhanced mood effects of
MDMA.
A study of resting EEG in recreational ecstasy users
revealed a positive correlation between chronic MDMA
use and both alpha and beta powers. A negative correla-
tion between MDMA use and delta power was also
demonstrated. MDMA use was also inversely correlated
with performance on a test of frontal lobe function. The
authors interpreted these results as evidence that
MDMA produces mild frontal lobe impairment related
to impulsivity; however, this study did not include
a nondrug using comparison group.
3,4-Methylenedioxymethamphetamine
and Event-Related Potentials
• Mid-latency ERPs: Auditory intensity dependence
paradigms examine mid-latency ERPs (P1, N1, and
P2) in response to increasing stimulus intensities,
388 38. HUMAN NEUROPHYSIOLOGY: EEG AND QUANTITATIVE EEG IN ADDICTION RESEARCH
which has been linked to serotonergic functioning. In
general, MDMA users exhibit greater intensity
dependence (i.e. increased N1–P2 amplitudes with
increasing stimulus intensity), which is indicative of
serotonergic dysfunction. These findings also appear
to be independent of MJ use and related to the level of
MDMA consumption. However, a longitudinal study
applied this paradigm to a small sample of polydrug
ecstasy users and reported no significant
neurophysiological changes between the two time
points (18 months apart).
• N200: Slower N200 latencies have been reported in
MDMA users compared to controls during a facial
emotion discrimination task. This has been
interpreted as evidence of a delayed attention deficit
as a result of MDMA use.
• P300: Studies of P3 in ecstasy users have yielded mixed
results with some studies reporting P3b findings
consistent with most substance use disorders, namely,
reduced P3b amplitude and longer P3b latency.
However, most of these studies included polydrug
ecstasy abusers and these effects do not appear to be
differentiated from those found in MJ users.
Marijuana and Quantitative EEG
Studies of acute MJ exposure report global decreases in
theta power and frontal beta power in conjunction with
lower accuracy and slowed reaction times on behavioral
tasks. MJ exposure has also been associated with “alpha
hyperfrontality” (increased power over the frontal
cortex) in daily MJ users. Given the controversy, both in
the research literature and societal perception regarding
neurotoxic effects of MJ, these findings do suggest that
MJ is associated with subtle, but adverse effects.
Marijuana and Event-Related Potentials
Acute MJ exposure results in reduced P3 amplitude
during working memory tasks as well as smaller ampli-
tudes for attentional components (e.g. N200). The N400
ERP (detection of novelty in language processing) is
also adversely affected. It is not clear, however, whether
these results are the direct result of MJ’s neurochemical
effects or are indirectly related to the reduced motiva-
tional capacity experienced during MJ intoxication. In
terms of chronic effects, Native Americans meeting
criteria for MJ dependence alone and those with MJ and
other drug dependence both exhibit prolonged P350
and P450 latencies in response to a facial discrimination
task as compared to nondrug users. These results support
the notion that MJ dependence is associated with delays
in processing and identifying emotional stimuli.
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Other Addictions and EEG/ERP
In addition to drugs, which may be thought to hijack
the brain’s natural reward processes, other substances
and activities may also appropriate these dopaminergic
pathways, leading to addictive preoccupations that
affect daily activities. Recent research has focused on
disordered eating, ranging from anorexia to binge eating
and obesity, as well as gambling behaviors.
Disordered Eating
Individuals with eating disorders (e.g. anorexia and
bulimia) may exhibit facilitated processing of food-related
images versus standard emotional and neutral pictures, as
indexed by early posterior negativity (220–310 ms) in the
ERP. In contrast, controls may demonstrate facilitated
processing only for high-calorie food images. Further,
food availability manipulations may modulate ERPs
to food cues among restrained eaters. Similarities between
food cue reactivity among eating disordered individuals
and substance cue reactivity among addicted populations
highlight the common mechanisms for behaviors utilizing
the reward pathway (see Common Neural Mechanisms in
Obesity and Drug Addiction).
On the other side of the spectrum, women with binge
eating disorder appear to differ from overweight control
participants in terms of their long latency ERPs to
pictures of high- versus low-calorie foods. In this case,
high-calorie foods may have high motivation properties
and consume significant attentional resources. This
pattern is similar to what is seen in other addictions
where binging occurs.
To further substantiate the parallel between addiction
and preoccupation with food, one might predict that the
responses of obese or food-addicted individuals to food-
related stimuli would be similar to cue-related activation
within substance-dependent individuals. In fact,
research has demonstrated a P200 ERP bias to food-
related words among obese participants, suggesting
a heightened automaticity that may contribute to exces-
sive eating behaviors. However, it is important to
acknowledge that only a portion of those with obesity
show characteristics of addiction (see Common Neural
Mechanisms in Obesity and Drug Addiction).
Pathological Gambling
Much of the work on EEG/ERP correlates of gambling
behaviors has taken place at a more basic level, focusing
on neurophysiological indices of reward sensitivity
evoked by “gambling” tasks among controls. Although
it is believed that individuals who develop problematic
gambling behaviors may exhibit pathological levels of
reward sensitivity, little work has been done in terms of
EEG/ERPs among groups of pathological gamblers.
Existing data suggest that the feedback negativity ERP
 SUMMARY
appears to be sensitive to reward versus nonreward feed-
back and outcome expectation. Compared to low-risk
conditions, high-risk conditions evoke a more negative
ERP deflection in areas overlying frontocentral brain
regions. This is thought to occur because high-risk condi-
tions lead to higher conflict between participants’ moti-
vationally based tendencies and task instructions. From
a qEEG perspective, both theta and delta activities have
also been correlated to various aspects of the decision-
making process. Perhaps the most consistent finding is
a change in theta activity (e.g. greater increase in theta
power negative feedback/losses), occurring 150–350 ms
post-feedback, which appears to be related to the valence
(e.g. positive or negative psychological value) that the
participant assigns to his or her performance.
In an exception to the trend toward “basic”
approaches, ERPs have been compared in problem
gamblers and controls using a computerized Black Jack
game. Problem gamblers tend to perseverate in making
high-risk decisions, even though such decisions have
led to failures in the past (i.e. the “gambler’s fallacy”).
This pattern is not apparent among controls, who are
more likely to make conservative decisions and to learn
from their mistakes. When compared to controls,
problem gamblers show more frontocentrally distributed
reward-related positive amplitudes 270–320 ms after
presentation of the card which leads to a “bust” (e.g.
failure) or “no bust” result. The level of risk taking has
been positively correlated with amplitude differences
between task conditions (“bust” versus “no bust”).
Such findings suggest that high-risk-taking behavior in
problem gamblers is associated with an increased
reward-related neural response to infrequent successes.
TREATMENT IMPLICATIONS
Although EEG/ERPs have been applied to addic-
tion research primarily with regard to determining
neurophysiological effects of, or risk for, addictive
disorders, the past decade has produced research sug-
gesting that it may also prove useful in treatment
contexts. The use of brain wave biofeedback, a process
that allows an individual to learn how to change phys-
iological activity to improve health and/or perfor-
mance, has been examined in addictive disordered
samples. Although initial studies were mixed with
regard to success, biofeedback has received more
recent attention and systematic study with regard to
addictions. Essentially the EEG provides a measure
of ongoing electrocortical activity which the individual
uses as a guide for inducing physiological changes
such as a more relaxed state. These studies have
been applied to a wide range of addictions including
alcohol, cocaine, heroin, and MJ.
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389
As mentioned previously, EEG/ERP measures have
been increasingly used in studies of cue reactivity or atten-
tional bias. Substance-dependent individuals exhibit
enhancements of some ERPs, such as the LPP, elicited by
stimuli related to their drug of choice (versus neutral
images), and this enhancement is related to drug-taking
characteristics such as recency of use and level of craving
for the drug. Such responses closely parallel cue-reactivity
data obtained using other techniques, such as behavioral
and eye-tracking measures. Using behavioral techniques
(i.e. reaction time to visual probe tasks), researchers
have implemented attentional bias modification (ABM)
training among groups of substance-dependent partici-
pants with the goal of changing attentional biases and
influencing subjective craving and drug-seeking behav-
iors. Although this growing body of research suggests
that a single session is not sufficient to affect long-term
changes in behavior, ABM training does appear to be
a promising target for future research. Given the amena-
bility of EEG/ERPs to the study of cue reactivity/atten-
tional bias, it is possible that this methodology could
provide a more complete picture of the psychophysiolog-
ical correlates of successful ABM training.
SUMMARY
Taken together, the body of research on EEG/ERPs
and related techniques in addictions is vast, innovative,
informative, and shows no signs of stopping. Although
human neurophysiology may be considered one of the
older techniques in addictions research, it is clear that
recent advancements in methodology and theory will
pave the way for an even more comprehensive body of
research in this area. Neurophysiological measures
posses several advantages for assessing neural function
in terms of risk for and effects of addictive substances
and behaviors. These include technical features such as
high temporal resolution during assessment, but also
practical points such as the ability to identify subtle
changes or features that may not always manifest them-
selves behaviorally. The extant literature provides
evidence for possible neurotoxic effects of various
substance of abuse, opportunities for exploring new treat-
ment avenues, and potential tools to help identify those
most at risk. The future of human neurophysiology in
addictions lies in the combination of these measures
with other techniques and study disciplines, including
behavioral, neuroimaging, and genetic approaches.
SEE ALSO
Neuropsychological Precursors and Consequences of
Addiction, Common Neural Mechanisms in Obesity and
Drug Addiction, Addiction and the Human Adolescent
390 38. HUMAN NEUROPHYSIOLOGY: EEG AND QUANTITATIVE EEG IN ADDICTION RESEARCH

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