The Need for Individualization in Neurofeedback: Heterogeneity
in QEEG Patterns Associated with Diagnoses and Symptoms
D. Corydon Hammond
? Springer Science+Business Media, LLC 2009
lized by neurofeedback practitioners, many of which are
not based on careful examination of raw EEG data fol-
lowed by scientifically objective quantitative EEG (QEEG)
database comparisons. Research is reviewed demonstrating
the great heterogeneity in the EEG patterns associated with
various diagnoses and symptoms. The fact that most
patients qualify for dual diagnoses, with co-morbid psy-
chiatric and medical conditions present, complicates the
ability of clinicians to estimate what electrophysiological
patterns may be associated with symptoms. In such cases
treatment planning is characterized by a great deal of
guesswork and experimentation. Peer reviewed publica-
tions have documented that neurofeedback treatment can
sometimes be associated with both transient side effects as
well as more serious negative effects. It is believed that the
lack of comprehensive and objective assessment of brain
functioning may increase the risk of neurofeedback either
being ineffective or causing iatrogenic harm. QEEG pro-
vides reliable, non-invasive, objective, culture-free and
relatively low cost evaluation of brain functioning, per-
mitting individualization of treatment and added liability
Very diverse assessment procedures are uti-
Iatrogenic effects ? Negative effects
QEEG ? Neurofeedback ? EEG biofeedback ?
In the field of neurofeedback there are a variety of
approaches to assessment for treatment planning. One
approach gathers a symptom history and then basically
begins with standardized placements, seeking to tailor
reinforcement and inhibit frequency bands to the individ-
ual’s response, and later altering electrode placements
based on the symptoms that are present (e.g., Othmer
2005). Another approach gathers a symptom history and
then studies the raw EEG patterns and amplitudes at sev-
eral locations to arrive at treatment decisions (e.g., Ayers
1999). A different system (Lubar 1995; Monastra et al.
1999) for treating ADD/ADHD has involved gathering
EEG frequency data at locations along the midline, and
then examining theta/beta and alpha/beta ratios to deter-
mine frequencies to be inhibited and reinforced along the
midline (Monastra 2005). A still different methodology
obtains data in sequence (rather than simultaneously) at
various electrode sites and basically examines amplitudes,
variability and asymmetries. A system also exists where
data can be gathered in one or two electrode sites at a time
and compared to a normative database.
An increasing number of professionals conduct assess-
ment by obtaining quantitative EEG (QEEG) data at 19 or
more electrode sites simultaneously. The raw data are then
examined, artifacts carefully removed, and then extensive
statistical comparisons are made to normative databases to
obtain scientifically objective data on brain function. This
data may include such measures as magnitude, absolute
and relative power, power ratios, coherence, phase lag,
comodulation, and analysis with sophisticated discriminant
functions (e.g., to assist in diagnosis of head injury, ADD/
ADHD, dementia, major affective disorder, bipolar disor-
der). Specific standards have been established by an
D. C. Hammond (&)
University of Utah School of Medicine, PM&R, 30 No. 1900
East, Salt Lake City, UT 84132-2119, USA
Appl Psychophysiol Biofeedback
interdisciplinary panel for the use of QEEG in neurofeed-
back (Hammond et al. 2004).
This paper examines some of the advantages in utilizing
a more thorough, comprehensive, and scientifically objec-
tive QEEG evaluation of brain function prior to undertak-
ing neurofeedback treatment.
Reliability and Practicality of QEEG Assessment
of Brain function
Although neuroimaging modalities (e.g., PET, SPECT,
fMRI) are very popular in academic research circles, the
conclusion Hughes and John (1999) made a decade ago
still remains true—of all the brain assessment modalities
the greatest volume of replicated evidence for pathophys-
iological concomitants in psychiatry is provided by EEG
and QEEG studies. Compared with neuroimaging modali-
ties, QEEG is non-invasive, much less expensive for
patients as well as for professionals procuring equipment,
and it is much more readily available. With the increasing
cultural diversity of our society it is also valuable that
QEEG has proven to be free of cultural biases (Hughes and
John 1999), with replications having been performed in
several different countries and cultures.
QEEG has high sensitivity, specificity, and reliability
(Arruda et al. 1996; Burgess and Gruzelier 1993; Corsi-
Cabrera et al. 1997; Fein et al. 1984; Gasser et al. 1985;
Hamilton-Bruce et al. 1991; Harmony et al. 1993; John
et al. 1983; John et al. 1987; John et al. 1988; Kaye et al.
1981; Kondacs and Szabo 1999; Lund et al. 1995; McEvoy
et al. 2000; Pollock et al. 1991; Salinsky et al. 1991; Van
Dis et al. 1979) that has been found to be equal or superior
to routinely used clinical tests in medicine such as mam-
mograms, cervical screenings, blood tests, MRI, and CAT
scans (Swets 1988). The QEEG has also proven to be
sensitive to alterations in cerebral blood flow (Ahn et al.
1980; Jonkman et al. 1985; Van Huffelen et al. 1984;
Ritchlin et al. 1992), and thus has the potential to make
unique contributions in evaluating patients with ischemia
or risk for stroke.
Heterogeneity in EEG Patterns
It has been found that similar symptoms may stem from
widely divergent etiologies. For example, attentional and
memory problems may result from ADD that is genetically
based, may be associated with mild head injury or anoxia,
originate from anxiety or obsessive-compulsive processes
that impair intellectual efficiency and cause the patient to
be easily distracted, be associated with medication side
effects, stem from developmental or learning disabilities,
arise from manic distractibility, derive from attention being
diverted by hallucinatory psychotic processes, be traced
back to encephalopathies, undiagnosed epilepsy, or even
represent early stage dementia in adults. It is not at all
uncommon for experienced clinicians to see cases that have
been diagnosed as ADD, but where after gathering a
careful history it has seemed likely that the origin of the
attentional problem is associated with problems in child-
birth or from an earlier head injury.
The point the author wishes to make is that diagnostic
categories and individual symptoms are not always asso-
ciated with the same brainwave patterns. In both my clin-
ical experience and in published literature I have seen cases
of anxiety that were associated with generalized excess
beta, but also with a beta excess localized along the mid-
line, or throughout the parietal area, in the right parietal
area, or in the right frontotemporal area. There are also
cases of anxiety where there was not an excess of beta at
all, but rather where there was excess alpha frontally in the
cortical areas associated with emotional regulation. Many
clinicians have considered anxiety to be one of the less
complex symptoms or diagnoses that they treat and yet the
diversity of EEG patterns that can be associated with
anxiety implies that optimal treatment outcomes would
require treatment that is individualized to address the
unique EEG patterns of the patient.
It is vitally important for clinicians to recognize the
presence of this kind of heterogeneity in the electrophysi-
ological patterns associated with different symptom com-
plexes. Another example is that an excess of frontal theta is
not specific to ADD/ADHD. It may also be associated with
OCD or head injury. Chabot and Serfontein (1996) iden-
tified two subtypes of children with ADD/ADHD, one
showing a relative power theta excess and another dis-
playing an excess in relative power alpha. As further
research was published several studies have reliably iden-
tified an excess beta subtype of ADHD (Chabot et al. 1996;
Clarke et al. 1998, 2001a, b), probably constituting about
10–15% of the ADHD population. Chabot’s later research
(Chabot et al. 1999) documented that the children with the
3 different subtypes of ADD or ADHD (theta excess, alpha
excess, and beta excess) displayed very different responses
to treatment with stimulant medication expanding on ear-
lier findings by Suffin and Emory (1995) and Satterfield
and Cantwell (1974). Chabot et al. (1999) further docu-
mented that children with learning disabilities were even
more heterogenous in their brainwave patterns than were
children with ADD/ADHD.
Appl Psychophysiol Biofeedback
The Further Complication of Co-Morbidities
In addition to the fact that diagnostic criteria for conditions
such as ADD/ADHD are broad, it is well known that only
rarely are pure cases of a diagnosis found in which co-
morbidities are not present (Barkley 1998; Jensen et al.
2001). Thus it is not uncommon to find cases of ADD/
ADHD qualifying for additional diagnoses such as oppo-
sitional defiant disorder, depression, Tourette’s, and
obsessive-compulsive disorder. Similarly, in clinical prac-
tice we find that the majority of patients with a diagnosis of
depression will also have comorbid conditions present such
as anxiety, insomnia, obsessive-compulsive disorder,
alcoholism or drug abuse.
Co-morbidities bring additional EEG patterns into the
mix, adding complexity to the individual cases coming into
our offices. Medical co-morbidities may likewise be pres-
ent and impact electrophysiologic readings. For example,
viral infections can elevate theta activity (Westmorland
1993), and headaches and migraines have been found to
have several different EEG patterns (Hammond 2006).
Type I diabetic patients with a history or recurrent severe
hypoglycemia have been found to display a slowing of
EEG frequencies (Howorka et al. 2000).
Therefore, it should not be surprising that Donaldson
et al. (1998) and Mueller et al. (2001) found elevated
frontal theta activity in two fibromyalgia samples, but in a
later sample Donaldson and Donaldson (2006) did not find
the same pattern to be present. In their latest study fibro-
myalgia patients were discovered to have eyes open
excesses in beta and alpha frequency bands. The authors
suggested that their different findings may have been due to
the use of stricter sampling to obtain more pure fibromy-
algia patients through excluding patients with comorbid
It seems reasonable to assume that the more complex the
disorder (or the larger the number of diagnoses or symp-
toms that are present), the less likely we are to reliably
identify a unitary EEG pattern that is correlated with the
condition. Some evidence for this conclusion is found from
Boutros et al. (2003) who reviewed 22 articles in the
electrophysiology literature on borderline personality dis-
order (BPD). Although finding a high prevalence of EEG
abnormalities, few studies had control groups or adequately
controlled for comorbidities (e.g., depression, child abuse,
psychotic features). Thus while clinicians are likely to find
that borderline patients have abnormal QEEG’s and that
neurofeedback may hold potential as a treatment for them,
one cannot hope to reliably identify in the literature an
EEG pattern unique to BPD on which to base neurofeed-
back training. As we would expect, evidence has suggested
the likelihood that there are subtypes of BPD (Korzekwa
et al. 1993; Lahmeyer et al. 1989). Similarly, obsessive-
compulsive disorder has been identified in research as
having two major subtypes (Prichep et al. 1993) associated
with excess alpha and excess theta, and neurofeedback
clinicians generally believe that there is also a subtype
associated with excess beta.
Perhaps the most extreme example of a heterogenous
group of conditions connected with a diagnostic category is
schizophrenia and psychosis. There is great consensus from
extensive research that psychosis is associated with a high
incidence of QEEG abnormalities. There are a few broad
general findings that are commonly present in this popu-
lation. All psychotic subtypes have shown power asym-
metry in almost all frequency bands, with greater power in
the right hemisphere (especially frontally, suggesting a
general impoverishment in language) (John et al. 2007). In
general individuals with psychosis also display disturbed
coherence (but it can be either hypocoherence or hyper-
coherence), usually have power excesses in theta or low
alpha (with lower frequency being associated with more
severe symptoms), and show extreme deficits in high alpha.
However, despite some commonalities there is great
pathophysiological heterogeneity in these patients and five
different subtypes have been identified (John et al. 1994).
More recent research has replicated this finding with a
significantly expanded sample wherein six subtypes were
identified (John et al. 2007).
Neurofeedback appears to have potential in treating
people who are schizophrenic (Gruzelier 2000; Gruzelier
et al. 1999; Schneider et al. 1992) and this author has
obtained improvement in individual cases. However, with
not only psychosis but with all of the various psychiatric
disorders, it is believed that a unitary neurofeedback
treatment approach that does not build on a comprehensive
pre-treatment QEEG assessment will be more likely to
increase the risk of being either ineffective or in some cases
harmful. Individuals with different QEEG subtypes require
different interventions, whether the treatment is with neu-
rofeedback or with the individualized prescription of
medication based on distinctive QEEG profiles (Prichep
et al. 1993; Chabot et al. 1999; Hoffman 2006; Suffin and
Confounding Effects of Medications
In addition to the diversity in EEG patterns noted with
psychosis and many other psychiatric/psychological dis-
orders, there are also the confounding effects of pharma-
cologic agents that are being prescribed to many patients.
Medications further complicate neurofeedback treatment
because they often modify the EEG in unspecified ways,
especially with the complex cocktails of different drugs
that are sometimes prescribed. However, even though the
Appl Psychophysiol Biofeedback
effects of some medications and drug interactions remain
unknown, a QEEG evaluation provides an objective base-
line of brain function at the current time, on the
Risks of Negative Effects and Liability Protection
Obviously there can be a great deal of guesswork involved
when a neurofeedback practitioner seeks to predict how a
person’s brain is functioning based merely on the patient
having a certain symptom or diagnosis. Clinicians need to
consider this—if you were faced with a malpractice law-
suit, how would a jury regard you when they were told that
you placed electrodes on someone’s head and then modi-
fied the way their brain was functioning based not on sci-
entifically objective information, but simply on your
guestimate about what was going on? Changing someone’s
brain function would be considered by most people to be a
fairly serious matter, and not something to be taken lightly
based on rough estimates. Similarly, making decisions
about changing brain function based on broad generaliza-
tions from published QEEG literature (which, as has been
shown, displays considerable diversity), rather than an
individualized, scientifically acceptable assessment, would
seem difficult to defend.
Lack of individualization of treatment has been found to
be an important element in causing iatrogenic effects in
both individual psychotherapy (Bergin and Lambert 1978)
and group therapy (Yalom and Lieberman 1971), and
almost without doubt in medicine as well. It seems logical
that this would likewise apply to neurofeedback treatment.
This is a serious ethical concern because we know that
inappropriate neurofeedback training can cause side effects
and in some cases iatrogenic harm.
Research and clinical papers (Chartier 2001; Hammond
and Kirk 2008; Lubar et al. 1981; Lubar and Shouse 1976,
1977) attest to this fact and have noted negative effects
from neurofeedback that have included seizures, manic
behavior, anger and irritability, increases in depression,
anxiety and agitation, fatigue, sleep disturbance, emotional
lability, OCD symptoms, tics, enuresis, somatic symptoms
(e.g., headaches, nausea, twitches), decline in cognitive
functioning, temporary disorientation or dissociation, and
enuresis and incontinence. If a patient were alleging harm
done, would the assessment on which you based your
treatment decisions and your record keeping withhold
Illustrating these points further, it can be noted that
although alcoholics and children of alcoholics have gen-
erally been found to have an excess of beta activity and a
deficit in alpha and theta activity (e.g., John et al. 1988),
another subtype representing 24% of alcoholics has been
identified that has a more classic ADD/ADHD pattern of
excess slow activity. Therefore, routinely utilizing a
‘‘standard protocol’’ of alpha/theta training with alcoholics,
rather than performing individualized assessment, would
seem to pose a one in four risk of exacerbating symptoms,
such as increasing impulsiveness and cognitive ineffi-
ciency, problems with emotional regulation and behavioral
self-control, and perhaps even risking seizure activity from
reinforcing slow activity that was already excessive. These
are matters to be taken seriously.
Summary and Conclusions
Assessment procedures utilized by neurofeedback practi-
tioners are very diverse and many of them are not based on
careful examination of raw EEG data followed by scien-
tifically objective database comparisons. QEEG provides
reliable, non-invasive, scientifically objective, culture-free
and relatively low cost evaluation of brain function.
Research has clearly shown that there is considerable het-
erogeneity in the EEG patterns that are associated with
diagnostic categories and symptoms, and even more so due
to the common presence of psychiatric and medical co-
morbidities. Papers have additionally documented that
neurofeedback treatment can be associated with both
transient side effects and more serious negative effects. It is
believed that a lack of objective and comprehensive
assessment of brain functioning, followed by individuali-
zation of neurofeedback treatment, may increase the risk of
treatment either being ineffective or of causing iatrogenic
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