April 22, 2010
By Dr. Stephen Sideroff, PhD
Over the last two decades a new research and clinical approach--neurofeedback--has shown promise in the treatment of substance abuse. This article addresses how it works, what makes it so effective, why it is a potentially important tool in addiction, the neurophysiological issues it might address, the existing promising research and, most importantly, that neurofeedback can be a significant adjunct...
Editor's Note: This article is the first in a two-part series on
Neurofeedback in the Treatment of Substance Abuse. This article
presents evidence of the neurological basis, specifically EEG
dysfunction, underlying addiction that makes it such a complicated
condition to treat, and explains how neurofeedback addresses cognitive,
emotional and physical symptoms. The second part of this article will
include a discussion of the efficacy models of neurofeedback and a
review of the research applying neurofeedback to substance abuse
treatment, as well as address the possible mechanisms of its
effectiveness in addiction.
Over the last two decades a new research and clinical
approach--neurofeedback--has shown promise in the treatment of substance
abuse. This article addresses how it works, what makes it so effective,
why it is a potentially important tool in addiction, the
neurophysiological issues it might address, the existing promising
research and, most importantly, that neurofeedback can be a significant
adjunct to the therapeutic and counseling process with addicts.
category of disorders associated with substance abuse is the most
common psychiatric set of conditions affecting an estimated 22 million
people in this country (SAMHSA, 2004). Furthermore, the disorder is
accompanied by serious impairments of cognitive, emotional and
behavioral functioning. These conditions and symptoms so significantly
alter a person's brain and its functioning, that we often refer to the
drug as hijacking the brain, making it very difficult to think logically
and appropriately weigh the consequences of the drug related behavior.
Detoxified addicts have been shown to have significant
alterations in brain electroencephalographic (EEG) patterns and children
of addicts also exhibit EEG patterns that are significantly different
than normal (Sokhadze et al., 2008, for review). This indicates that,
not only are we dealing with the neurological consequences of
drug-related behavior, but there appears to be a genetic pattern as
well, that places certain people at greater risk for addictive
behaviors. The complexity of these factors makes the treatment of
addiction one of the most difficult areas of mental, emotional and
Multiple factors in
Treating addiction is compounded by the many
factors contributing to its onset and maintenance. Furthermore, the
addiction itself masks many other clinical conditions that become more
evident once the drug user becomes abstinent. In fact, it is frequently
other psychiatric problems that lead to drug abuse as the addict
attempts self-medication. It has also been shown that people with
cognitive disabilities are more vulnerable, and more likely to have a
substance abuse disorder (Moore, 1998). These impairments appear to
include attentional issues as well as the hypo-functioning of the
frontal cortex, sometimes referred to as the executive brain, where
decision making takes place (Fowler, et al., 2007).
As a result, we
are learning that no one approach has all the answers. Multiple
mechanisms require multiple considerations and approaches. In addition,
addicts are a diverse group, resulting in the need for many tools and
approaches. It appears that programs offering the most diversified array
of treatment modalities are the most effective (Vaccaro & Sideroff,
2008). That is also why, for example, most programs urge the inclusion
of a 12-step program for ongoing support.
But how do you
address the biological and genetic aspects while also addressing the
traumatic and emotional factors, the social cognitive and attentional
factors? How do you deal with the apparent "procedural memory" and
conditioned factors that cause an abstinent addict, on his or her way
home from work, to all of a sudden take an inappropriate turn and end up
at the drug dealer? Neurofeedback appears to be a tool, a training that
has the facility to address many of these factors associated with
History of promising treatments
the years, there have been a number of developments that have been
promising in the treatment of addiction. Each time a new approach is
identified, it is immediately seen as being the long sought after
"silver bullet" that will solve the addiction problem. This occurred
with the development of methadone, and later Levo-Alpha Acetyl Methadol
(LAAM). When I entered the field in 1976, as a post-doctoral fellow of
the National Institute of Drug Abuse, Naltrexone was gaining popularity.
Naltrexone is a long-acting opiate antagonist that blocks the effects
of opiates, such as morphine, heroin and codeine.
around this time that the importance of addiction-related stimuli was
becoming widely recognized (Wikler, 1984). In research examining the
conditioned aspects of addiction, it was found that stimuli associated
with the drug using behavior could serve as conditioned stimuli that
would trigger an unconditioned psychophysiological response that had
similarities to withdrawal and included anxiety, fear and physiological
arousal (e.g. Sideroff & Jarvik, 1980). This conditioned patterning
of response lead to the proposal that relapse liability might be
determined by exposing addicts to these conditioned stimuli and
monitoring their responses (Sideroff, 1980).
conditioning model, one potential mechanism of Naltrexone treatment
would be the behavioral extinction of some of the conditioned
associations of addiction. In other words, if the addict attempted to
get high while on Naltrexone, the lack of reinforcing effect might
lessen the conditioned effects of drug related stimuli. This, in turn,
might reduce readdiction liability. All that needed to happen was for
the addict to use, without experiencing any effect; a perfectly
reasonable theoretical assumption. So, not only was Naltrexone expected
to be successful in keeping addicts from using, but it also could
address conditioned aspects of addiction.
When I arrived at
UCLA and the Veterans Administration at Brentwood in 1976, I was
surprised to discover that the treatment program to which I had been
awarded a fellowship, was already eliminated--almost before it began.
With the help of the director of the methadone clinic, I started a new
experimental Naltrexone treatment program, drawing recruits from the
VA's methadone maintenance population.
Naltrexone did not meet its high expectations. While many methadone
patients expressed interest in using Naltrexone, the long process of
withdrawing from methadone--necessary in order to begin taking the opiate
antagonist--eliminated more than 80 percent of volunteers. Also, as we
enrolled volunteers, we found that 90 percent of the addicts who began
using Naltrexone never used opiates while on the antagonist; and the 10
percent who did use, only used once. It was as if the addict immediately
experienced this "no reward" condition and thus didn't bother to waste
his money. This, in itself, was an interesting finding, as it showed
this population to be able to demonstrate impulse control under certain
circumstances (Sideroff et al., 1978). As a result, we never had the
opportunity to test our theory of extinction.
The use of Naltrexone
for opiate addiction has subsequently been viewed as an unworkable
model. Yet, for the small fraction of individuals who were able to detox
and begin taking Naltrexone, it did change their lives.
the "Silver Bullet" has been thought of in terms of a drug; something
that could either eliminate craving or eliminate the high of the drug of
abuse. What have become most useful, have been drugs of substitution,
such as buprenorphine, (Johnson, et al., 2000), as we continue to search
for an effective treatment combination that includes psychotherapy.
The EEG is one objective representation of
how the brain is functioning. The EEG is recorded from scalp electrodes,
and is a representation of electrical activity produced by the
collective firing of populations of neurons in the brain, in the
vicinity of the electrode. Figure 1 presents a chart of brain wave
frequencies and the primary functions associated with their production.
It should be pointed out that this is a gross representation and that
more precise differences--beyong the scope of this article - can be found
when you look at specific single frequencies within each range. While
all frequencies and frequency ranges are important and necessary,
problems arise when there is too much or too little of a particular type
of brain wave; there is difficulty shifting in response to changing
needs; or the EEG is to reactive.
For example, in a healthy
functioning brain, if we look at the amount of theta being produced and
we compared it (using 4-8 Hz) with beta frequencies between 13 and 21 Hz
(cycles per second), there is approximately a 2 to 1 ratio. When we
assess the EEGs of people with Attention Deficit Disorder (ADD), we see
ratios that are 3 to 1 and much higher (Lubar, 2003).
higher ratios indicate that the brain is producing too much of the slow
waves relative to the beta waves, where the beta waves represent a more
focused and engaged brain. In other words, these brains are
under-activated. On the other hand, if we look at the EEG patterns of
people with anxiety, worry and tension, there is typically too much
activity occurring in the higher frequencies, usually between 24 and 35
Hz. The EEGs of people with substance abuse problems can show both of
It has been demonstrated that the EEGs of
addicts show specific abnormalities when compared to normative data.
Studies of detoxified alcoholics indicate an increase in absolute and
relative power in the higher beta range, along with a decrease in alpha
and delta/theta power (Saletu, et al., 2002). Low voltage fast
desynchronized patterns (high beta) may be interpreted as demonstrating a
hyper arousal of the central nervous system (Saletu-Z et al., 2004);
and Bauer, showed a worse prognosis for the patient group with a more
pronounced frontal hyper-arousal (Bauer, 2001).
The fact that these
EEG patterns as well as alcohol dependence itself are highly inheritable
further supports the biological nature of this disease (Gabrielli et
al., 1982; Schuckit & Smith, 1996; Van Beijsterveldt & Van Baal,
These specific abnormalities show both a worse
prognosis and a predisposition to development of alcoholism.
Individuals with a family history of alcoholism were found to have
reduced relative and absolute alpha power in occipital and frontal
regions and increased relative beta in both regions compared with those
with a negative family history of alcoholism. In another study, these
abnormalities also were associated with risk for alcoholism (Finn &
It is a common belief that at least part of
the cause of addiction is an attempt at feeling better--self-medicating.
When someone with reduced or an absence of synchronous alpha rhythm
takes a drink of alcohol, it results in the generation of an alpha
rhythm or what is referred to as alpha synchrony, which a normal
functioning brain has much greater capacity to produce (Pollock et al.,
1983). Thus, it appears that the alcohol is helping the addicted person
compensate for their brain's inability to produce an alpha rhythm which
is associated with a state of calmness. This mechanism helps to explain
the use of alcohol by this group of addicts.
research on abstinent heroin-dependent subjects, it is interesting to
note similar abnormalities of deficits in alpha frequencies, along with
excessive high beta EEG activity (Franken et al. 2004; Polunina &
Davydov, 2004). Although it appears that in some studies, these changes
found in early abstinence normalize after several months of abstinence
(Shufman et al., 1966; Polunina & Davydov, 2004). Cocaine-dependent
subjects may show similar increases in beta activity, but in addition
show increases in frontal alpha (Herning, et al., 1994). These changes,
specifically the elevation of fast beta activity, appear to be
correlated with relapse in cocaine abuse (Bauer, 2001). In contrast,
methamphetamine abusers have been shown to have significant increases
in delta and theta frequency bands (Newton et al, 2003).
are many questions that this research does not answer with regard to
the relationship between abnormal EEG patterns and addiction. For
example, it is not known if these dysfunctional elements are
coincidental or causal. In addition, these EEG patterns are found in
many mental disorders, some that are typically coincident with substance
abuse. These questions do not minimize the probable conclusions that
the EEG dysfunction creates specific vulnerabilities of these subjects.
For example, frontal alpha, which is also found with some types of ADD,
results in impairment of executive functions, such as decision making;
and excessive fast beta activity can result in excess emotional and
physical tension as well, as obsessive qualities.
substances of abuse have also been shown to correlate with abnormal EEG
patterns. For example, studies have demonstrated that subjects with a
chronic history of marijuana use demonstrate EEG patterns of frontal
elevations of alpha frequencies. (Struve, Manno, Kemp, Patrick, &
Manno 2003). This is referred to as "alpha hyper-frontality." Another
common feature of the EEG of chronic users is a reduction of alpha mean
frequency, which may indicate some deficits in intellectual functioning.
as a subset of biofeedback, monitors a subject's brain waves and feeds
back selective information about these brain waves, in order to gain
control over these patterns. Neurofeedback programs typically allow for
the setting of thresholds within specific frequency bands or ranges so
that when the EEG either rises above the threshold or drops below the
threshold, some form of signal or reinforcement is presented to the
subject. This feedback lets the brain know when it has been successful,
thus, in an operant conditioning model, encourages this rewarded brain
wave response. When the goal is to have the signal go above a threshold,
we refer to this as "up training" or rewarding. When the goal is to
reinforce signals that drop below a threshold, we refer to this as "down
training," or inhibiting this component of the EEG.
Kamiya, a researcher at the University of Chicago, was the first
researcher to discover that when a subject was informed that he was
producing alpha brain wave frequencies, he would then be able to learn
to detect, on his own, when he was in alpha (Kamiya, 1968). As a result
of this finding, he designed a study in which he similarly gave feedback
to the subjects as to their production of alpha, with the instruction
to produce alpha. He found that when given this feedback, subjects were
able to increase their production of synchronous alpha waves (Nowlis
& Kamiya, 1970). Interestingly, his success led to the popularity of
alpha training in mass culture, which coincided with its loss of
credibility in the academic community.
and its acceptance took on a new impetus when Sterman, working with
cats, was able to train these animals using a similar operant
conditioning model, to increase the amount of synchronous spindle
activity in the 14 Hz frequency range (Sterman, 2000). Since these
spindles occurred over the sensorimotor cortex, he labeled them
sensorimotor rhythm (SMR). These studies confirmed that the production
of these brain waves--associated with motoric stillness--resulted in
animals that were more resistant to the triggering of seizures. Sterman,
then adapted this EEG biofeedback procedure with epileptic patients and
demonstrated its effectiveness in reducing the frequency and intensity
When a subject produces SMR activity, he is
mentally alert with relaxed muscles (lower muscle tone). Lubar, working
in Sterman's laboratory, recognized the potential of this discovery, and
in a series of research studies, he and his colleagues were able to
train children with hyperactive disorder to increase their production of
SMR activity with feedback, resulting in reduced hyperactivity (Lubar,
The training procedures have evolved so that in
addition to reinforcing SMR frequencies, the training of ADD also
typically reinforces slightly higher frequencies of either 15 to 18, or
15 to 20 Hz activity, and at the same time, down trains the slower
(theta) frequencies. The protocols address the ratio between the slower
(theta) brain waves, with the faster brain waves, with a goal of
training greater activation of the brain, which translates into improved
attention. In one follow up study, Lubar and associates were able to
demonstrate that gains made in variables of attention were maintained in
subjects 10 years following training (Lubar, 1995; 2003).
the same time that neurofeedback was being used to address attentional
and cognitive deficits, primarily by training the activation of the
brain, it also was being used to help people relax and establish
autonomic and neuromuscular balance. With populations demonstrating
aspects of anxiety, obsessive compulsive disorder and tension, the
procedure has been to train increases in alpha frequencies (8-12 Hz) or a
combination of alpha and theta (Moore, 2000). In these cases, the
process is one of training a lowering of activation of the brain. A wide
range of neurofeedback protocols have now been applied to cognitive,
emotional and physical symptoms and conditions with a growing range of
positive results. A bibliography covering these studies is available
Acknowledgement: The author wishes to
express his appreciation to Eleanor Criswell, Jay Gunkelman, David
Kaiser and Hugh Baras for their helpful comments.
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reprinted with author permission from counselormagazine.com
Dr. Stephen Sideroff, PhD, is a licensed clinical psychologist, consultant and Assistant Professor in the Psychiatry Department at UCLA and one of the Clinical Directors at Moonview Sanctuary. Dr. Sideroff is an internationally recognized expert in behavioral medicine, biofeedback and peak performance, and wa the founder and former clinical director of Santa Monica Hospital’s Stress Strategies, which presented programs for individuals and corporations to better cope with stress.