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QEEG-Guided Neurofeedback in the Treatment of Obsessive Compulsive Disorder

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Introduction. Blinded, placebo-controlled research (e.g., Sterman, 2000) has documented the ability of brainwave biofeedback to recondition brain wave patterns. Neurofeedback has been used successfully with uncontrolled epilepsy, ADD/ADHD, learning disabilities, anxiety, and head injuries. However, nothing has been published on the treatment of obsessive-compulsive disorder (OCD) with neurofeedback.Method. Quantitative EEGs were gathered on two consecutive OCD patients who sought treatment. This assessment guided protocol selection for subsequent neurofeedback training.Results. Scores on the Yale-Brown Obsessive-Compulsive Scale and the Padua Inventory normalized following treatment. An MMPI was administered pre-post to one patient, and she showed dramatic improvements not only in OCD symptoms, but also in depression, anxiety, somatic symptoms, and in becoming extroverted rather than introverted and withdrawn.Discussion. In follow-ups of the two cases at 15 and 13 months after completion of treatment, both patients were maintaining improvements in OCD symptoms as measured by the Padua Inventory and as externally validated through contacts with family members. Since research has found that pharmacologic treatment of OCD produces only very modest improvements and behavior therapy utilizing exposure with response prevention is experienced as quite unpleasant and results in treatment dropouts, neurofeedback appears to have potential as a new treatment modality.
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QEEG-Guided Neurofeedback
in the Treatment
of Obsessive Compulsive Disorder
D. Corydon Hammond, PhD
ABSTRACT. Introduction. Blinded, placebo-controlled research (e.g.,
Sterman, 2000) has documented the ability of brainwave biofeedback to
recondition brain wave patterns. Neurofeedback has been used success-
fully with uncontrolled epilepsy, ADD/ADHD, learning disabilities,
anxiety, and head injuries. However, nothing has been published on the
treatment of obsessive-compulsive disorder (OCD) with neurofeedback.
Method. Quantitative EEGs were gathered on two consecutive OCD
patients who sought treatment. This assessment guided protocol selec-
tion for subsequent neurofeedback training.
Results. Scores on the Yale-Brown Obsessive-Compulsive Scale and
the Padua Inventory normalized following treatment. An MMPI was ad-
ministered pre-post to one patient, and she showed dramatic improve-
ments not only in OCD symptoms, but also in depression, anxiety,
somatic symptoms, and in becoming extroverted rather than introverted
and withdrawn.
Discussion. In follow-ups of the two cases at 15 and 13 months after
completion of treatment, both patients were maintaining improvements
in OCD symptoms as measured by the Padua Inventory and as externally
validated through contacts with family members. Since research has
D. Corydon Hammond is Professor, Physical Medicine & Rehabilitation, Univer-
sity of Utah School of Medicine.
Address correspondence to: D. Corydon Hammond, PhD, Professor, Physical Med-
icine & Rehabilitation, University of Utah School of Medicine, 30 North 1900 East,
Salt Lake City, UT 84132-2119 (E-mail: D.C.Hammond@m.cc.utah.edu).
The author is appreciative of the generous assistance of Stephen Shepperd, PhD, in
administering the Yale Brown Obsessive Compulsive Scale to these patients’ post-
treatment.
Journal of Neurotherapy, Vol. 7(2) 2003
http://www.haworthpress.com/store/product.asp?sku=J184
2003 by The Haworth Press, Inc. All rights reserved.
10.1300/J184v07n02_03 25
found that pharmacologic treatment of OCD produces only very modest
improvements and behavior therapy utilizing exposure with response
prevention is experienced as quite unpleasant and results in treatment
dropouts, neurofeedback appears to have potential as a new treatment
modality. [Article copies available for a fee from The Haworth Document De-
livery Service: 1-800-HAWORTH. E-mail address: <docdelivery@haworthpress.
com> Website: <http://www.HaworthPress.com> 2003 by The Haworth
Press, Inc. All rights reserved.]
KEYWORDS. Neurofeedback, EEG, biofeedback, quantitative EEG,
OCD, obsessive-compulsive disorder
INTRODUCTION
Obsessive compulsive disorder (OCD) has a lifetime incidence in the
range of 1% to 3% (Karno, Golding, Sorenson, & Burnam, 1988; Jenike
& Brotman, 1984) and is widely regarded as having a strong biological
basis. In a qEEG study, Kuskowski et al. (1993) discovered lower abso-
lute power in delta, beta 1 and beta 2 bandwidths frontally and in the
right hemisphere in OCD patients. They further discovered increased
alpha relative power across temporo-parietal, central and occipital re-
gions, along with decreased relative power in beta bands in the left fron-
tal region. Their research additionally revealed severe right hemisphere
hypoactivity, particularly in beta relative power. This is an interesting
finding since treatment with clomipramine has been found to result in
increased right hemisphere activity (MacCrimmon & Arato, 1991),
which may help normalize the electroencephalogram (EEG) in OCD
patients with this pattern.
On the surface these findings seem somewhat at odds with most PET
and SPECT studies of OCD which have reported increased frontal
blood flow and metabolism in mediofrontal, anterior cingulate, right
frontal, and/or orbitofrontal areas (Baxter et al., 1987; Baxter, Phelps, &
Mazziotta, 1988; Benkelfat et al., 1990; Harris, Pearlson, & Hoehn-
Saric, 1993; Machlin, Harris, & Pearlson, 1991; Nordahl et al., 1989;
Perani et al., 1995; Piacentini & Bergman, 2000; Rauch, Whalen,
Dougherty, & Jenike, 1998; Rubin, Villaneuva-Meyer, & Anath, 1992;
Sawle, Hymas, & Lees, 1991; Saxena, Brody, Schwartz, & Baxter,
1998; Swedo, Schapiro, & Grady, 1989; Szeszko et al., 1999). The
neuroimaging findings converge in implicating a cortico-striato-thalamo-
26 JOURNAL OF NEUROTHERAPY
cortical network. Resting studies of OCD seem to indicate hyperactivity
in the orbitofrontal and anterior cingulate cortex and caudate nucleus,
with this being attenuated under conditions of symptom provocation,
and which attenuate following successful treatment (Rauch, 2000).
There are some evoked potential studies that are more congruent
with neuroimaging findings. The anterior cingulate cortex may be in-
volved with monitoring of behavior (Posner & Rothbart, 1998). An
event related potential called error-related negativity (ERN) is a wave
form that is associated with making mistakes or errors (Gehring, Coles,
Meyer, & Donchin, 1990). It reflects the activity of a general error-pro-
cessing system and one of the symptoms of OCD consists of excessive
checking, rumination, and doubt–which amount to excessive response
monitoring. The size of an ERN is sensitive to the size of an error. ERN
has been localized as being generated from a single source in the medial
frontal cortex (Dehaene, Posner, & Tucker, 1994; Gehring, Goss, Coles,
Meyer, & Donchin, 1993; Holroyd, Dien, & Coles, 1998; Luu, Collins, &
Tucker, 2000). Gehring, Himle, and Nisenson (2000) found that the
ERN was increased in OCD patients compared with matched controls,
and the magnitude of the ERN was related with symptom severity. An
fMRI study (Ursu et al., 2001) documented increased error-related ac-
tivity in the anterior cingulate cortex in OCD patients, and this degree of
activity was likewise correlated with severity of symptoms. Supporting
Gehring et al. (2000), Hajcak and Simons (2002) also found a signifi-
cantly larger Fz maximal negativity was associated with error responses
in college undergraduates with OCD characteristics compared with stu-
dents without such characteristics.
Some of the discrepancy between neuroimaging and qEEG studies
may also stem from a bias in neuroimaging studies (Rauch, 2000); they
often concentrate on only a limited number of brain areas, producing a
potential confirmatory bias. Simpson, Tenke, Towey, Liebowitz, and
Bruder (2000) conducted the first qEEG study under conditions of
symptom provocation. Importantly, they found that only live exposure
(and not imaginal exposure) to contaminants produced significant EEG
changes. This is of importance since some OCD neuroimaging studies
only used imaginal exposure. Simpson et al. (2000), using only vertex
electrode sites, found a significant shift in the anterior-to-posterior to-
pography of alpha power during live exposure compared with a control
condition. Live exposure was associated with an increase in OCD
symptoms and an increase in posterior relative to anterior alpha. No sig-
nificant shifts occurred in the theta or beta bands. The observed changes
were interpreted as reflecting a relative shift in brain activation from
Scientific Articles 27
posterior to anterior, which would be consistent with neuroimaging
studies finding enhanced frontal activation during symptom provoca-
tion in OCD.
Other qEEG research has identified two subtypes of OCD patients
(Mas, Prichep, John, & Levine, 1993; Perros, Young, Ritson, Price, &
Mann, 1992; Prichep, Mas, & John, 1989; Prichep et al., 1993; Silver-
man & Loychik, 1990). Prichep et al. (1993) found one subgroup with
excess alpha throughout most of the brain, but most excessive at T5, P3,
O1 (which would coincide with findings by Kuskowski et al., 1993),
and the frontal poles, along with a mild excess of beta in frontal, central
and mid-temporal areas. Their other subgroup had a theta excess, most
extreme throughout frontal areas and at posterior temporal electrodes.
Figure 1 displays these subgroups. Theta abnormalities have also been
reported by others (Insel, Donnelly, Lalakea, Alterman, & Murphy,
1983; Jenike & Brotman, 1984; Pacella, Polatin, & Nagler, 1944; Rock-
well & Simons, 1947).
28 JOURNAL OF NEUROTHERAPY
OCD
(n = 27)
Clus I
(n = 10)
Clus II
(n = 17)
Delta Theta Alpha Beta
z
1.2
0
1.2
FIGURE 1. Group Average Topographic Maps (nose up) for Z Relative Power
in the Delta, Theta, Alpha, and Beta Frequency Bands for the Two Neurometric
Clusters of Patients with Obsessive-Compulsive Disorders
Reprinted from Prichep, L. S., Mas, F., Hollander, E., Liebowitz, M., John, E. R., Almas, M., DeCaria, C. M., & Le-
vine, R. H. (1993). Quantitative electroencephalography (QEEG) subtyping of obsessive compulsive disorder.
Psy-
chiatry Research
,
50
(1), 25-32, with permission from Elsevier Science.
Delayed onset of mu event-related desynchronization with prepara-
tion for movement and less post-movement beta (20 Hz) synchroniza-
tion was reported by Leocani et al. (2001), a finding also found in
Parkinson’s disease (Pfurtscheller, Pichler-Zalaudek, Ortmayr, Kiez, &
Reisecker, 1998). Leocani et al. (2001) suggested that a lower level of
beta synchronization in OCD after a simple, self-paced movement
raises a question about whether this may reflect the inability of these pa-
tients to inhibit themselves from compulsive actions. In this regard,
lower P300 amplitudes in orbitofrontal areas in OCD patients (Malloy,
Rasmussen, Braden, & Haier, 1989) likewise suggest impaired inhibi-
tory mechanisms. Reduced motor cortical inhibition has also been found
in this population with transcrancial magnetic stimulation (Greenberg
et al., 2000). Perhaps related to these findings, Flor-Henry, Yeudall,
Koles, and Howarth (1979) noted reduced left temporal (T3) variability
in beta frequencies, but they did not examine frequencies lower than al-
pha.
Similar to Prichep, Mas, and John (1989), Prichep et al. (1993) and
Mas, Prichep, John, and Levine (1993), Perros, Young, Ritson, Price,
and Mann (1992) noted theta excess in 10 of 13 OCD patients in the
6.0-7.5 Hz range, predominantly in the left fronto-temporal area. They
pointed out that such activity is frequently attributed to disturbances in
deep midline structures (Gloor, 1976), which would be supported by
some of the neuroimaging studies cited earlier. We might speculate that
this theta subtype of OCD may be the group which has often produced
some of the neuroimaging findings noted above. Relevant to one of the
case reports which will be presented, another qEEG study has also
pointed to abnormalities in the left posterior temporal area. Silverman
and Loychik (1990) examined three siblings ranging from 23 to 29
years of age, all of whom had OCD. The left posterior temporal area
was identified as abnormal in all three, both on qEEG evaluation and on
auditory and visual evoked potentials, while the asymptomatic parents
were entirely normal on all measures.
Treatments for OCD
Behavior therapy commonly uses exposure and response prevention
techniques to treat OCD (Foa & Franklin, 2001), with claims that 76%
to 86% of patients who complete treatment make improvements. In an
earlier review by Foa, Steketee, and Ozarow (1985), they reported that
in over 200 patients, 51% reduced their symptoms at least 70%. In
Greist’s (1990) review, however, he notes what I have experienced in
Scientific Articles 29
years past using a behavior therapy approach with OCD patients, which
is that the greatest problem is that many patients dislike this treatment
and fully one-quarter decline treatment or sabotage it with overt or co-
vert avoidance. He also notes that behavior therapy has proven less suc-
cessful with pure obsessional disorder (without rituals) and estimates
the percent improvement in symptoms experienced following behavior
therapy as 50%. Nonetheless, this psychiatrist’s review estimates the de-
gree of symptomatic improvement with serotonin drugs as only being
30%. Goodman, McDougle, and Price (1992) similarly found that
symptom amelioration in OCD treatment with serotonin uptake inhibi-
tors is about 35% on average, and that 50% of patients experience only
partial symptomatic improvement.
The mean from four separate samples (Goodman, Price, Rasmussen,
Mazure, Fleischmann et al., 1989; Goodman, Price, Rasmussen, Mazure,
Delgado et al., 1989) of OCD patients on the Yale-Brown Obsessive-
Compulsive Scale (Y-BOCS; Goodman, Price, Rasmussen, Mazure,
Fleischmann et al., 1989) is 24.7 (standard deviation = 6). A very recent
(Ackerman & Greenland, 2002) meta-analysis of 25 drug studies found
that with the most effective pharmacologic treatment for OCD (clomi-
pramine) that the average drug treatment effect on the Y-BOCS was
10.64 (uncorrected for placebo effects), which is a 1.33 standard devia-
tion improvement. In fluvoxamine (Prozac) studies, the mean Y-BOCS
improvement was only 5.4 points. Interestingly, they discovered that
the longer the clomipramine drug trial went on, the less improvement
they found. Thus, 12-week trials had 5.78 less points of improvement
than 10-week trials. Older patients also had less improvement on
clomipramine. They found that the longer the pre-randomization period
(during which some placebo responders are often dropped from inclu-
sion in drug studies), the less improvement in drug response and in pla-
cebo response. The reviewers concluded that “the numerous side effects
of clomipramine may have contributed to its greater effect size in pla-
cebo comparisons” (p. 315). This same conclusion was reached previ-
ously by the same group (Ackerman et al., 1996), as well as by
Abramowitz’s (1997) review. This is particularly relevant because re-
cent reviews of antidepressant drugs studies (Antonuccio, Danton, DeNelsky,
Greenberg, & Gordon, 1999; Kirsch & Sapperstein, 1998; Moncrieff,
2001) have identified that these studies commonly use inactive place-
bos which have no side effects, resulting in many patients and raters
correctly discerning to which group they have been assigned, essen-
tially unblinding the study. However, one review (Thomson, 1982)
where an active placebo (e.g., atropine, which causes anticholinergic
30 JOURNAL OF NEUROTHERAPY
side effects) was used found that only one in seven studies identified the
antidepressant as superior to placebo. Another similar review (Moncrieff,
Wessely, & Hardy, 1998) discovered that in only two of nine studies
was antidepressant medication superior to an active placebo.
Despite the very modest effects of medication, there is evidence that
qEEG has potential to assist in predicting medication response in treat-
ing OCD (Prichep et al., 1993). Those patients with excess alpha rela-
tive power (with some frontal and central beta excess) were found to
respond positively 82% of the time to serotonin mediated antidepres-
sants, whereas, the second subtype with increased theta relative power
(with some alpha minima) failed to improve 80% of the time with
SSRIs. Nonetheless, it must be emphasized that medication treated pa-
tients remain dependent on the medication, and in one study (Pato,
Zohar-Kadouch, & Zohar, 1988), 89% of patients treated with clomi-
pramine (Anafranil) relapsed after discontinuation of medication. Natu-
rally, medications such as clomipramine also have numerous side
effects which must be tolerated such as dry mouth, blurred vision, con-
stipation, sweating, sedation, dizziness, and retarded ejaculation.
Psychiatry has also resorted to neurosurgical treatment for OCD, per-
forming cingulotomies in cases that have proven resistant to both medi-
cation and a trial of behavior therapy. However, using a somewhat
liberal criteria of having produced at least 35% improvement on the
Yale-Brown Obsessive Compulsive Scale, such psychosurgery has only
benefited from one-quarter to one-third of patients (Dougherty et al.,
2002; Jenike et al., 1991), even with the confound that most of the pa-
tients continued receiving pharmacotherapy following cingulotomy.
Rauch (2000) summarized, “For neurosurgical treatment of OCD, the
overall rate of efficacy is quite modest, the costs are high, and the risks
are considerable” (p. 169). It is thus apparent that current psychiatric
treatment of OCD has significant limitations.
There also exists interesting neuroimaging research on pre-treatment
brain characteristics that predict successful outcome. What is particu-
larly interesting about these studies is that they show biological brain
changes occurring following successful behavior therapy (exposure and
response prevention), with such changes not occurring in persons who
did not change in treatment or in normal controls. Schwartz, Stoessel,
Baxter, Martin, and Phelps (1996) and Baxter et al. (1992) found signif-
icant changes in glucose metabolism in the right caudate following suc-
cessful behavior therapy. They also found a significant correlation
between change in left orbital frontal cortex with change in Y-BOCS
scores, which has also been found by Swedo et al. (1992) in successful
Scientific Articles 31
medication treatment. Brody et al. (1998) reported normalization of left
orbitofrontal cortex metabolism predicted positive treatment response
to behavior therapy. They found that higher metabolism in the left
orbitofrontal cortex predicted greater improvement with behavior ther-
apy, but a worse outcome from fluoxetine treatment.
METHOD
This paper will report on the treatment of two cases of OCD with
neurofeedback. In both cases following the initial history taking, a
quantitative EEG (qEEG) was done to evaluate brain function. Vigi-
lance-controlled EEG was digitally recorded from the patients with
Lexicor NRS-24 equipment with recording electrodes placed according
to the 19 standard regions defined by the International 10/20 System of
electrode placement, referenced to linked ears. All electrode impedance
levels were below 3 Kohms, with no interelectrode differences of more
than 500 ohms and ear references which were perfectly balanced. The
vigilance level was controlled by noting signs of drowsiness appearing
in the EEG, and then pausing the recording and verbally interacting
with the patients, while they moved their arms and legs in the chair. A
bipolar recording channel was used to monitor eye movement artifact.
In each case, approximately 20 minutes of eyes-closed resting EEG
were recorded and edited to reduce artifact. The recordings were of
good quality. From the digitally stored EEG, 132 seconds and 120 sec-
onds of EEG in the two cases were subjected to quantitative spectral
analysis. In the first case, a second sample of 62 seconds was also gath-
ered for purposes of establishing test-retest reliability. The R squared
value for alpha was 96.5%. The R squared values for single hertz topog-
raphies may be seen in Figure 3. The results of spectral analysis from
1-32 Hz were displayed as computed color-graduated topographic maps
and compared via a Z-score transformation to age-regressed data bases
of normal subjects using the Nx Link database and the Thatcher Life-
span database with the NeuroRep Analysis and Report System, the lat-
ter of which was used to generate one hertz topographic maps. The
female patient’s eyes-closed EEG was also analyzed utilizing low reso-
lution electromagnetic tomography (LORETA) to provide an estima-
tion of the localization of underlying generators of the patient’s alpha
activity. Both patients engaged in an informed consent process and
signed informed consent forms. The patients were tested pre-treatment
and post-treatment with the Yale-Brown Obsessive Compulsive Scale
32 JOURNAL OF NEUROTHERAPY
(Goodman, Price, Rasmussen, Mazure, Fleischmann et al., 1989; Good-
man, Price, Rasmussen, Mazure, Delgado et al., 1989) and the Padua In-
ventory (Burns, Keortge, Formea, & Sternberger, 1996), both of which
demonstrate good reliability and validity. In the first case, the Minne-
sota Multiphasic Personality Inventory (MMPI) was also administered
pre- and post-treatment.
Case 1
This patient was a single, 25 year-old woman who was employed as
an elementary school teacher. She had been diagnosed as having OCD
at age 17 by a psychiatrist, and her previous treatment had consisted of
pharmacologic therapy. Her medications had included Prozac, Klonepin,
Zoloft, Anafranil, Haldol, Amitriptaline, Effexor, Serzone, and Xanax.
None of the medications had been very effective. She was on .25 mg of
Klonepin per day at the time of the intake interview, but had been off all
medication for over two weeks prior to her qEEG. No other family
member had been formally diagnosed with OCD, but she indicated that
there were many individuals in her father’s family who exhibited
OCD-like behavior. The MMPI was administered because she also de-
scribed significant depression. It confirmed severe depression and anxi-
ety, very low ego-strength, introversion and being withdrawn, and
intense over-emotionality with an extreme, classic pattern for develop-
ing somatic complaints. She previously had two suicide attempts, both
at the age of 17. She also suffered with insomnia, requiring two hours to
fall asleep. She engaged in bruxism and experienced considerable
anxiety. She had been a straight A student in high school. She started
dating at age 16, but had not done much dating since going to college.
Two years previous to our intake interview she was so overwhelmed by
her OCD that she was asked to resign at the end of the year. The year
previous to seeing me she had not taught because she felt too incapaci-
tated by her OCD symptoms. These symptoms particularly focused on
contamination obsessions and washing compulsions, as well as obses-
sional rumination about harming herself. She also engaged in a lot of
mental counting and excessive blinking. She had currently been teach-
ing again for two months, but she was wondering if she would have to
resign before long because she was becoming so overwhelmed by the
OCD. Her qEEG results from the Nx Link and Lifespan databases may
be seen in Figures 2 and 3. In Figure 4 you can study her LORETA anal-
ysis using a Poisson Maximal Frequency Test for alpha frequency. It lo-
calized the left temporal alpha to the superior temporal gyrus in the
Scientific Articles 33
vicinity of Brodmann areas 22 and 42, as well as in the middle temporal
gyrus, Brodmann area 39, which is in the area of the angular gyrus.
Following informed consent, we decided that due to the severity of
her depression, our initial focus would be on reducing depression.
Therefore, we utilized my depression protocol (Hammond, 2001a).
This protocol was designed in response to the extensive qEEG and
neuroimaging literature (summarized in Davidson, 1998a, 1998b) doc-
umenting a robust biological marker for depression which consists of
greater left frontal alpha activity (inactivation) compared with right
frontal activity. This protocol is also responsive to parallel research
(Davidson, 1992; Heller, Etienne, & Miller, 1995; Heller, Nitschke,
Etienne, & Miller, 1997; Isotani et al., 2001; Pizzagalli et al., 2002) con-
firming that a frontal asymmetry with greater right frontal beta activa-
tion (e.g., Fp2, F4) is associated with anxiety, and with panic disorder
34 JOURNAL OF NEUROTHERAPY
Z-Values
3.0
0.0
3.0
Absolute Power:
Relative Power:
Power Asymmetry:
Coherence:
Delta
Delta
Delta
Delta
Theta
Theta
Theta
Theta
Alpha
Alpha
Alpha
Alpha
Beta
Beta
Beta
Beta
FIGURE 2. Case 1: Quantitative EEG Results from the Nx Link Database
(Wiedemann et al., 1999). A large proportion of depressed patients also
experience anxiety. These latter qEEG studies are also congruent with
PET and MRI studies (Abercrombie et al., 1996; Canli, Desmond,
Zhao, Glover, & Gabrieli, 1998; Chua, Krams, Toni, Passingham, &
Dolan, 1999; Dolan et al., 1996; Dolski et al., 1996; George et al., 1995;
Scientific Articles 35
1: Rsq = 99.4% 2: Rsq = 95.6% 3: Rsq = 97.2% 4: Rsq = 99.2% 5: Rsq = 82.1%
6: Rsq = 91.6% 7: Rsq = 98.9% 8: Rsq = 90.5% 9: Rsq = 95.3% 10: Rsq = 98.0%
11: Rsq = 95.4% 12: Rsq = 96.8% 13: Rsq = 95.3% 14: Rsq = 96.1% 15: Rsq = 96.7%
16: Rsq = 99.1% 17: Rsq = 97.1% 18: Rsq = 97.5% 19: Rsq = 81.9% 20: Rsq = 90.4%
21: Rsq = 98.7% 22: Rsq = 97.2% 23: Rsq = 94.5% 24: Rsq = 95.6% 25: Rsq = 91.5%
26: Rsq = 93.9% 27: Rsq = 88.0% 28: Rsq = 75.8% 29: Rsq = 88.9% 30: Rsq = 91.6%
SINGLE-BAND MAGNITUDE TOPOGRAPHIES
0.1 0.8 1.6
MICROVOLTS
FIGURE 3. Case 1: Single Hertz Magnitude Topographic Maps
Naveteur, Roy, Ovelac, & Steinling, 1992; Reivich, Alavi, & Gur,
1984; Stapleton et al., 1997; Stewart, Devous, Rush, Lane, & Bonte,
1988) and transcrancial Doppler ultrasound studies (Troisi et al., 1999)
of anxiety which find more right than left fronto-temporal activity, sug-
gesting that the frontal cortex is involved in regulating and restraining
subcortical limbic structures associated with affect. As a bridge facili-
tating understanding between neuroimaging and EEG research, a recent
neuroimaging study (Nakamura et al., 1999) demonstrated a positive
correlation between beta activity (13-30 Hz) and cerebral blood flow.
The patient’s treatment began with twenty-one sessions of neuro-
feedback using the Roshi system (Hammond, 2001a) with two referen-
tial training sites at Fp1 and F3. The Roshi uses photic stimulation,
wherein LED lights embedded in glasses vary in their pulsation, from
moment to moment, pulsing on the peak frequency within the frequency
36 JOURNAL OF NEUROTHERAPY
L
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(Y)
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(Y)
(Y)
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(Y)
(Y)
(Z = 41)
(Z = 6)
(Z = 29)
(Z = 64)
(Z = 34)
(Z = 1)
(Z = 36)
(Z = 71)
(Z = 27)
(Z = 8)
(Z = 43)
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(Z = 57)
LORETA-KEY
0.000 1.691 3.381 5.072 6.763
FIGURE 4. Case 1: LORETA Analysis for Alpha Frequency Band
band being reinforced. The Roshi also has very low feedback latency.
The 30 to 35 minute sessions at Fp1 and F3 used a program called Beta
Max for the first half of the session, which reinforced 15-18 Hz while si-
multaneously inhibiting theta and alpha frequency bands, and finished
the last half of the session with a program called SMR Max (inhibiting
theta and alpha, reinforcing 12-15 Hz). Because it was observed that her
dominant frequency not infrequently dropped into the delta range dur-
ing this training, in the last 12 of these sessions we spent the first 10
minutes strictly inhibiting delta (1-4 Hz), followed by the Beta Max
program and SMR Max program for 10 to 13 minutes each.
After two sessions of this training she reported feeling more energy
and alertness, and being more social, “which is abnormal for me.” She
indicated that her depression level (0-10) had dropped from a 9 or 10 to
a level 7. After 9 sessions the patient noted that her depression was “a
lot better,” her anxiety was less, and her sister had noted that her OCD
symptom of excessive blinking had decreased. After 11 sessions she re-
ported that a co-worker had also commented that she was blinking less
and seeming calmer. After twelve sessions she said she had been feeling
“pretty up, and I’ve been having more energy than normal and sleeping
better too. The anxiety is really controllable now.” After 13 sessions she
commented, “I actually haven’t felt this good in my life.”
Based on her qEEG, our training now shifted and we now began us-
ing Neuropathways EEG equipment. This is a unit that samples at
250,000 samples per second and digitally filters the EEG signal, with a
common mode rejection ratio >110 db wideband and >120 db at 60 Hz.
I switched to Neuropathways to focus primarily on inhibiting inappro-
priate activity. Two sessions were done inhibiting 19.5-25 Hz at Pz-Cz
with a sequential (bipolar) montage, while setting the threshold liber-
ally to only mildly reinforce 12-14 Hz. This was followed by another
session inhibiting 18-25 Hz and mildly reinforcing 12-15 Hz at Cz-Fz
for 20 minutes and then inhibiting 19-25 Hz at Cz-T3 for 15 minutes.
After these sessions she said she was mellower, able to concentrate eas-
ier, and “my mind didn’t go as fast.” We then did four sessions at
T3-Cz, inhibiting 19-25 Hz while mildly reinforcing 12-15 Hz. After
the first two of these four sessions she reported feeling less preoccupa-
tion with food contamination, that her OCD was improving, and she felt
minimal depression. Due to some difficulty sleeping, we then did one
Roshi session of SMR Max at C3 and C4. The goal of this session was to
have a calming effect and to also encourage beta spindles and enhanced
ability to fall asleep.
Scientific Articles 37
Next, we began focusing on the excess alpha activity in the left poste-
rior area. Comparing her qEEG relative power alpha (Figure 2) with the
alpha subtype from Prichep et al.’s (1993) research (see Figure 1), you
will note that they are almost identical. It was my hope, therefore, that
training at this site would begin to seriously impact her OCD symp-
toms. For the next eight consecutive sessions we inhibited 6.5-11 Hz
while mildly reinforcing 15-18 Hz at T5-P3 with a sequential montage,
using the Neuropathways unit. As hoped, with each session she re-
ported that her OCD symptoms and brooding seemed to be improving.
After seven sessions with this placement she estimated that her obses-
sions had improved by 75%. We then returned for two sessions to the
left frontal area (Fp1-F3), using the Roshi depression protocol to rein-
force changes in depression. A couple of days following these sessions,
I spoke with the father of the patient on the telephone. He told me that a
few days earlier his daughter had told him, “Dad, for the first time in my
life I feel normal.” Twelve more sessions focused on T5-P3, and in one
of those sessions the time was split between T5-P3 and T5-O1. Two fur-
ther sessions to reinforce changes in depression were also done at
Fp1-F3. During this time she was reporting no problems with either de-
pression or OCD symptoms.
After 50 sessions of neurofeedback, another MMPI was adminis-
tered. The striking changes in her two MMPIs may be seen in Figure 5.
Her depression normalized from a severe level and she became much
less withdrawn, going from being introverted to extroverted. These lat-
ter changes have been commonly observed by me in pre-post testing us-
ing my depression protocol. Increasing left frontal activation would be
anticipated to produce such changes, since the left frontal area is associ-
ated with not only happy emotions, but also with approach motivation
(Davidson, 1998a). Her extreme levels of both over-emotionality and
somatic symptoms decreased to within normal limits. Her anxiety and
OCD symptoms, as measured in scales A and 7, dramatically decreased
and her ego-strength and resilience increased. She was defensive in her
test taking set at both administrations of the MMPI. Nonetheless, in her
pre-treatment testing she still showed extreme levels of psychological
disturbance, and in her post-treatment testing her defensiveness was
only mildly greater.
At this same time the Padua Inventory was readministered, and I had
a colleague administer the Y-BOCS to alleviate contamination effects.
The last eight sessions of neurofeedback had placements at T5-Pz, in-
hibiting 4-8 Hz while mildly reinforcing 15-18 Hz. The first three of
these maintenance sessions were held at two- to three-week intervals.
38 JOURNAL OF NEUROTHERAPY
The final five sessions were spaced out over a five-month period for fol-
low-up reinforcement and to check for maintenance of changes. Seven
and a half months after termination of the five-month maintenance
phase of treatment (and 15 months after the main treatment phase), I
spoke with the patient and the Padua Inventory was readministered to
the patient. I had a telephone interview with her mother at about the
same time, obtaining external confirmation of the maintenance of
changes.
Table 1 shows the changes in this patient on the Y-BOCS and the
Padua Inventory from pre- to post-treatment and on follow-up. The
Y-BOCS is the most respected measure of OCD and generally patients
must score over 16 to be included in medication trials. The patient
scored 26 initially, slightly above the averaged mean for four samples of
OCD patients (Goodman, Price, Rasmussen, Mazure, Fleischmann et
Scientific Articles 39
120
115
110
105
100
95
90
85
80
75
70
65
60
55
50
45
40
35
30
25
20
0
1
1
2
2
3
3
4
4
5
5
6
6
7
7
8
8
9
9
0
0
Tor T c
Tor T c
?
?
L
L
F
F
K
K
Hs+5K
Hs+5K
D
D
Hy
Hy
Pd+4K
Pd+4K
Mt
Mt
Pa
Pa
Pt+1K
Pt+1K
Sc+1K
Sc+1K
Ma+2K
Ma+2K
Si
Si
A
A
R
R
Es
Es
MAC
MAC*
130
120
110
100
90
80
70
60
50
40
30
15
10
5
0
30
30
25
25
20
20
15
15
10
10
5
5
0
0
40
35
30
25
20
15
10
5
0
50
45
40
35
30
25
20
15
10
45
40
35
30
25
20
15
10
50
45
40
35
30
25
20
15
10
5
15
20
25
30
35
40
45
50
30
25
20
15
10
5
0
60
55
50
45
40
35
30
25
20
15
10
65
60
55
50
45
40
35
30
25
20
15
10
5
40
35
30
25
20
15
10
5
70
65
60
55
50
45
40
35
30
25
20
15
10
5
35
30
25
20
15
10
5
0
40
35
30
25
20
15
10
5
65
60
55
50
45
40
35
30
25
40
35
30
25
20
15
10
FEMALE
FIGURE 5. Case 1: Pre- and Post-Treatment MMPI
al., 1989; Goodman, Price, Rasmussen, Mazure, Delgado et al., 1989)
on the Y-BOCS total score. The Y-BOCS (Goodman, Price, Rasmussen,
Mazure, Fleischmann et al. 1989) mean for the Obsessions subscale is
10.7 and her pre-treatment score was 12.5. The Y-BOCS mean for the
compulsions subscale is 11.2, and she scored 13.5. An independent ex-
aminer interviewed her with the Y-BOCS after 50 neurofeedback ses-
sions. Instead of 26, she now scored 4–twice the average reduction in
score that is usually found in drug studies with the most effective phar-
macologic treatment (Ackerman & Greenland, 2002). This is a 3.67
standard deviation improvement, compared with the 1.33 standard de-
viation average improvement that results from the most effective phar-
macologic treatment. Her score was now 3 on the Obsessions subscale,
and 1 on the Compulsions subscale. The reliability on both administra-
tions was rated as excellent. The Y-BOCS was not administered in a
follow-up interview because the patient had moved away to another
geographic area. However, in addition to a telephone interview with the
patient and her mother, she did take the self-administered Padua Inven-
tory 15 months following the second (post-treatment) administration of
the YBOCS and the Padua Inventory.
On the Padua Inventory, her pre-treatment score of 72 significantly
exceeded the mean for an OCD population (54.93; SD = 16.72; Burns et
al., 1996), placing her one standard deviation above the mean for OCD
patients. After 50 neurofeedback sessions her total score was 8, and on
follow-up 15 months later, her score was 12. These improvements were
comparable to those seen on the Y-BOCS (see Table 1). The mean total
score on the Padua Inventory for a normal sample is 21.78 (SD = 16.33).
Thus, at the completion of 50 sessions she was almost one standard de-
40 JOURNAL OF NEUROTHERAPY
TABLE 1. Case 1: Pre-Post-Follow-Up OCD Outcome Measures
TEST Y-BOCS Padua Inventory
OCD MEAN & S.D. 24.7 (S.D. = 6) 54.93 (S.D. = 16.72)
PRE-TREATMENT SCORE 26 72
POST-TREATMENT 4 8
FOLLOW-UP SCORE 12
S.D.’S IMPROVED 3.7 3.8 & 3.6
PERCENT IMPROVED 84.6% 88.9% & 83.3%
viation below the mean for a normative sample. On subscale 1 (Obses-
sive Thoughts about Harm to Self or Others; OCD Mean = 10.0), her
pre-treatment score was 18, her post-treatment score was 4, and her fol-
low-up score was 3. On subscale 2 (Obsessive Impulses to Harm Self or
Others; OCD Mean = 6.0), her pre-treatment score was 6, her post-treat-
ment score was 0, and her score on follow-up was 1. On subscale 3
(Contamination Obsessions and Washing Compulsions; OCD Mean =
13.87), her pre-treatment score was 25, her post-treatment score was 3,
and her follow-up score was 2. On subscale 4 (Checking Compulsions;
OCD Mean = 19.87), her pre-treatment score was 15, her post-treatment
score was 1, and her score on follow-up was 4. Finally, on subscale 5
(Dressing/Grooming Compulsions; OCD Mean = 5.2), her pre-treat-
ment score was 8, her post-treatment score was 0, and her score on fol-
low-up was 2. Thus, in her 15 month follow-up she scored at or below
the mean for normal, non-OCD individuals on all Padua Inventory
subscales. This is even more significant because she was feeling under
extra stress, having just begun teaching after a summer vacation. She
was on no medication.
Case 2
The second case was a 25-year-old male who initially presented as
having problems with attention deficit disorder. He had been “on heavy
doses of Ritalin” for years. He indicated that when he began taking it, “it
changed everything” and he felt he could think and function normally.
“I looked forward to using Ritalin,” he said, but at the same time it made
him feel stigmatized. He had recently read about neurofeedback and
wanted to experiment with its potential. His history included a signifi-
cant previous problem with marijuana abuse and a problem with alco-
hol abuse. He said, “I can’t stay with anything for more than five
minutes. I want instant gratification.” He had also had “breakdowns” in
which he became depressed and would cry to his parents on the tele-
phone. He had previously been on Effexor and Paxil, but was not cur-
rently depressed and was only taking Ritalin. He met the diagnostic
criteria for ADD and ADHD. After an intake interview, we gathered
qEEG data after he had been off Ritalin for three days.
In giving him feedback on the analysis, I commented on the mild ex-
cess of beta over the general area of the anterior cingulate gyrus (see
Figure 6, electrode sites Fz and Cz), and inquired about OCD symptom-
atology. It quickly became apparent that he had many OCD symptoms
(e.g., obsessions with contamination and washing rituals, and checking
Scientific Articles 41
compulsions) and he admitted to feeling he “must be absolutely per-
fect,” whether it was in playing music or making hamburgers. There-
fore, I administered the Y-BOCS and gave him the Padua Inventory to
take home. His Y-BOCS score of 25 and Padua Inventory score of 62
confirmed the dual diagnosis of OCD.
Forty-four 30-minute long sessions were spent inhibiting 19-25 Hz
beta, while mildly reinforcing 12-15 Hz, typically for 15 to 20 minutes
at Fz-Cz (using a sequential montage with a Neuropathways neuro-
feedback unit), followed by 15 minutes with the same protocol at
Cz-C4. Interestingly, after two sessions he indicated: “A lot has changed.
For two days I have felt I was no longer a prisoner to any situation. I feel
turned-on, in a non-sexual way.” He further volunteered that he had
tended to compulsively masturbate and had also used masturbation as a
soporific. However, he had been feeling no compulsion to masturbate.
He also felt that he tracked words more smoothly on a page in reading.
42 JOURNAL OF NEUROTHERAPY
Z-Values
3.0
0.0
3.0
Absolute Power:
Relative Power:
Power Asymmetry:
Coherence:
Delta
Delta
Delta
Delta
Theta
Theta
Theta
Theta
Alpha
Alpha
Alpha
Alpha
Beta
Beta
Beta
Beta
FIGURE 6. Case 2: Quantitative EEG Results from the Nx Link Database
Since there had been only two sessions, this could be the result of posi-
tive expectancy, but on the other hand, medication responses had not
been overly positive with antidepressants. After four sessions he re-
ported sleeping much better. After six sessions, he indicated that two
friends, his father, and a sister had all spontaneously indicated that he
seemed calmer. He said, “There’s an absence of rudimentary fear and
paranoia.” After another session, he described himself as “mellow,” and
said, “It’s much easier for people to be around me. Women actually
want to get to know me!” After still another session, he indicated he was
“in a good mood all the time.” Following nine sessions he said that the
Ritalin he was taking had been feeling more and more potent, and,
therefore, he had been cutting it down and was now taking only between
one-quarter and one-eighth of the prescribed dose daily.
At this time we began occasionally spending the first half of the ses-
sion inhibiting 20-25 Hz beta at Cz-C4 or Fz-Cz, and then moving the
electrodes to F7 and F8 and inhibiting 7-11 Hz while mildly reinforcing
13-16 Hz. This was done to begin addressing his ADD problems fur-
ther, since F7 and F8 were both areas of alpha excess on his qEEG, as
may be seen in Figure 6. After twelve sessions he said that his visual
tracking of words felt “improved immensely.” He also indicated, “I
can’t even drink coffee anymore” because rather than helping his con-
centration as it did before, it caused him to feel over stimulated. After
another session he commented that his concentration was better when
he was reading, and he was having fewer intrusive thoughts. Following
his fifteenth session he reported being able to read for long periods of
time. He continued to steadily report feeling better. After 26 sessions he
indicated that his memory with reading was improved, he had less so-
cial anxiety, felt more energetic, and found he could do things musically
that he could not do before due to anxiety.
As treatment progressed, we also did some prefrontal training at Fp1
and Fp2, inhibiting 7-11 Hz and mildly reinforcing 12.5-15 Hz. The pa-
tient felt that this frontal training improved his concentration “a lot,”
helped him to feel more confident and less afraid socially, and he be-
lieved that it felt as if it also assisted with the OCD symptoms. By the
time we had reached 50 total sessions, he was feeling excellent. Women
he dated found him much more mature and easier to relate to, and his
family found him to be much easier to get along with. OCD symptoms
were minimal. After 56 thirty-minute sessions, 35 of which had focused
on inhibiting beta in the Fz-Cz-C4 area, an independent colleague re-
administered the Y-BOCS. His score had now dropped from 25 to 10–a
decrease of 2.5 standard deviations.
Scientific Articles 43
The patient was feeling a desire to enhance his academic abilities fur-
ther in anticipation of returning to college, and he had the financial
resources to do so. Therefore, we continued neurofeedback. At the con-
clusion of treatment (93 total sessions), he had gone through 44 sessions
inhibiting beta over the Fz-Cz-C4 area, 22 sessions inhibiting alpha and
reinforcing low beta frequencies at F7-F8, 21 sessions at Fp1-Fp2, three
and a half sessions inhibiting 2-9 Hz at O1-O2, and two and a half ses-
sions inhibiting alpha in the parietal area.
A summary of the pre-, post-, and follow-up testing on this case is
found in Table 2. At the end of treatment, after the 44 thirty-minute ses-
sions of inhibiting beta along the vertex (and 93 total sessions), the
Y-BOCS was again administered and his score had decreased further
from 10 to 7. This translates to an improvement of 3 standard deviations
in his Y-BOCS score from the beginning of treatment. His score on the
Padua Inventory at that time had dropped from 62 to 7, representing a
3.4 standard deviation improvement from his pre-treatment level. At
the conclusion of treatment, the patient moved out of state. However, 13
months later I was able to speak with his sister who had just returned
from an extended visit with him. She reported that he remained dramati-
cally changed from his pre-treatment adjustment. I also interviewed
him on the telephone and had him complete the Padua Inventory. He
had always had anxiety about flying, and since the September 11, 2001
terrorist attack in New York City, his fear had been exacerbated, but he
no longer experienced any OCD symptoms. He was not on any medica-
tion for OCD and was not taking Ritalin. Nonetheless, he said, “My
concentration is still a million times better.” The improvement in con-
centration and OCD had given him the confidence to return to college.
His 13-month follow-up score on the Padua Inventory was now 5, a 3.4
44 JOURNAL OF NEUROTHERAPY
TABLE 2. Case 2: Pre-Post-Follow-Up OCD Outcome Measures
TEST Y-BOCS Padua Inventory
OCD MEAN & S.D. 24.7 (S.D. = 6) 54.93 (S.D. = 16.72)
PRE-TREATMENT SCORE 25 62
POST-TREATMENT 7 7
FOLLOW-UP SCORE 5
S.D.’S IMPROVED 3.0 3.3 & 3.4
PERCENT IMPROVED 72% 88.7% & 92%
standard deviation improvement from his pre-treatment score. His
Padua Inventory subscale 1 (Obsessive Thoughts about Harm to Self or
Others; OCD Mean = 10.0) pre-treatment score was 15, his post-treatment
score was 2, and his follow-up score was 2. On subscale 2 (Obsessive
Impulses to Harm Self or Others; OCD Mean = 6.0), his pre-treatment
score was 2, his post-treatment score was 1, and his score on follow-up
was 0. On subscale 3 (Contamination Obsessions and Washing Com-
pulsions; OCD Mean = 13.87), his pre-treatment score was 20, his
post-treatment score was 2, and his follow-up score was 2. On subscale
4 (Checking Compulsions; OCD Mean = 19.87), his pre-treatment
score was 19, his post-treatment score was 2, and his score on follow-up
was 1. Finally, on subscale 5 (Dressing/Grooming Compulsions; OCD
Mean = 5.2), his pre-treatment score was 6, his post-treatment score
was 0, and his score on follow-up was 0. Thus, in his 13 month fol-
low-up he scored at or below the mean for normal, non-OCD individu-
als on all Padua Inventory subscales.
SUMMARY AND CONCLUSIONS
In research with uncontrolled epilepsy (summarized in Sterman,
2000, which has included placebo-controlled, blinded studies) neuro-
feedback has proven capable of reconditioning brain wave patterns.
Outcome research has also been done on neurofeedback with ADD/
ADHD, learning disabilities, depression, anxiety, brain injury, fibro-
myalgia, and posttraumatic stress disorder (Hammond, 2001b). This is
the first publication, however, on the treatment of obsessive-compul-
sive disorder with neurofeedback. Quantitative EEGs were gathered on
two consecutive OCD patients seeking treatment. This assessment then
guided individualized protocol selection for subsequent neurofeedback
training. The qEEG findings in the first case almost identically matched
the average profile of an alpha subtype of OCD, leading to treatment
focused in the left posterior area after we alleviated her depression. The
author had never heard of anyone using this neurofeedback protocol
and would not have considered using it without being guided by a qEEG
assessment. The patient’s more significant OCD symptoms primarily
changed following treatment focused in the left posterior area. Scores
on the Yale-Brown Obsessive-Compulsive Scale and the Padua Inven-
tory normalized following neurofeedback. An MMPI was administered
pre-post to the first patient, who showed dramatic improvements in not
only OCD symptoms, but also in depression, anxiety, somatic symp-
Scientific Articles 45
toms, and in becoming extroverted rather than introverted and with-
drawn. In follow-ups of the two cases at 15 and 13 months after
completion of treatment, both patients were maintaining improvements
in OCD symptoms as measured by the Padua Inventory and as exter-
nally validated through contacts with family members.
Since research has found that pharmacologic treatment of OCD pro-
duces only very modest improvements, and behavior therapy utilizing
exposure with response prevention is experienced as quite unpleasant
and results in treatment dropouts, neurofeedback appears to have poten-
tial as a new treatment modality for OCD. Further controlled research
should be pursued in this area.
REFERENCES
Abercrombie, H. C., Larson, C. L., Ward, R. T., Schaefer, S. M., Holden, J. E.,
Perlman, S. B., et al. (1996). Metabolic rate in the amygdala predicts negative affect
and depression severity in depressed patients: A FDG-PET study. Neuroimage,3
(2), S217.
Abramowitz, J. (1997). Effectiveness of psychological and pharmacological treat-
ments for obsessive-compulsive disorder: A quantitative review. Journal of Con-
sulting & Clinical Psychology,65, 44-52.
Ackerman, D. L., & Greenland, S. (2002). Multivariate meta-analysis of controlled
drug studies for obsessive-compulsive disorder. Journal of Clinical Psychopharm-
acology,22 (3), 309-317.
Ackerman, D. L., Greenland, S., Bystritsky, A., & Katz, R. J. (1996). Relationship be-
tween early side effects and therapeutic effects of clomipramine therapy in OCD.
Journal of Clinical Psychopharmacology,16, 324-328.
Antonuccio, D. O., Danton, W. G., DeNelsky, G. Y., Greenberg, R. P., & Gordon, J. S.
(1999). Raising questions about antidepressants. Psychotherapy & Psychosomatics,
68, 3-14.
Baxter, L. R., Schwartz, J. M., Mazziotta, J. C., Phelps, M. E., Pahl, J. J., Guze, B. H., et
al. (1988). Cerebral glucose metabolic rates in non-depressed patients with obses-
sive-compulsive disorder. American Journal of Psychiatry,145, 1560-1563.
Baxter, L., Phelps, M., Mazziotta, J., Guze, B. H., Schwartz, J. M., & Selin, C. (1987).
Local cerebral glucose metabolic rates in obsessive-compulsive disorder. Archives
of General Psychiatry,44, 211-218.
Baxter, L., Schwartz, J. M., Bergman, K. S., Szuba, M. P., Guze, B. H., Mazziotta, J.
C., et al. (1992). Caudate glucose metabolic rate changes with both drug and behav-
ior therapy for obsessive-compulsive disorder. Archives of General Psychiatry,49,
681-688.
Benkelfat, C., Phelps, M., Mazziotta, J., Guze, B. H., Schwartz, J. M., & Selin, R. M.
(1990). Local cerebral glucose metabolic rates in obsessive-compulsive disorder
patients treated with clomipramine. Archives of General Psychiatry,147, 846-848.
46 JOURNAL OF NEUROTHERAPY
Brody, A. L., Saxena, S., Schwartz, J. M., Stoessel, P. W., Maidment, K., Phelps, M.
E., et al. (1998). FDG-PET predictors of response to behavioral therapy and
pharmacotherapy in obsessive compulsive disorder. Psychiatry Research,84, 1-6.
Burns, G. L., Keortge, S., Formea, G., & Sternberger, L. (1996). Revision of the Padua
Inventory of obsessive-compulsive symptoms: Distinctions between worry, obses-
sions, and compulsions. Behaviour Research & Therapy,34, 163-173.
Canli, T., Desmond, J. E., Zhao, Z., Glover, G., & Gabrieli, J. D. (1998). Hemispheric
asymmetry for emotional stimuli detected with fMRI. Neuroreport,9, 3233-3239.
Chua, P., Krams, M., Toni, I., Passingham, R., & Dolan, R. (1999). A functional anat-
omy of anticipatory anxiety. Neuroimage,9, 563-571.
Davidson, R. J. (1992). Emotion and affective style: Hemispheric substrates. Psycho-
logical Science,3, 39-43.
Davidson, R. J. (1998a). Affective style and affective disorders: Perspectives from af-
fective neuroscience. Cognition & Emotion,12, 307-320.
Davidson, R. J. (1998b). Anterior electrophysiological asymmetries, emotion, and depres-
sion: Conceptual and methodological conundrums. Psychophysiology,35, 607-614.
Dehaene, S., Posner, M. I., & Tucker, D. M. (1994). Localization of a neural system for
error detection and compensation. Psychological Science,5, 303-305.
Dolan, R. J., Fletcher, P., Morris, J., Kapur, N., Deakin, J. F., & Frith, C. D. (1996).
Neural activation during covert processing of positive emotional facial expressions.
Neuroimage,4, 194-200.
Dolski, I. V., Malmstadt, J. R., Schaefer, S. M., Larson, C. L., Abercrombie, H. C.,
Ward, R. T., et al. (1996). EEG-defined left versus right frontally activated groups
differ in metabolic asymmetry in the amygdala. Psychophysiology,33, S35.
Dougherty, D. D., Baer, L., Cosgrove, G. R., Cassem, E. H., Price, B. H., Nierenberg,
A. A., et al. (2002). Prospective long-term follow-up of 44 patients who received
cingulotomy for treatment-refractory obsessive-compulsive disorder. American
Journal of Psychiatry,159 (2), 269-275.
Flor-Henry, P., Yeudall, L., Koles, Z., & Howarth, B. (1979). Neuropsychological and
power spectral EEG investigations of the obsessive-compulsive subjects. Biologi-
cal Psychiatry,14, 119-130.
Foa, E. B., Steketee, G. S., & Ozarow, B. J. (1985). Behavior therapy with obses-
sive-compulsives: From theory to treatment. In M. Mavissakalian, S. M. Turner, &
L. Michelson (Eds.), Obsessive-Compulsive Disorder: Psychological and pharma-
cological treatment (pp. 49-129). New York: Plenum Press.
Foa, E. B., & Franklin, M. E. (2001). Obsessive-compulsive disorder. In D. H. Barlow
(Ed.), Clinical handbook of psychological disorders (3rd ed., pp. 209-263). New
York: Guilford.
Gehring, W. J., Coles, M. G. H., Meyer, D. E., & Donchin, E. (1990). The error-related
negativity: An event-related brain potential accompanying errors. Psychophysi-
ology,27, S34.
Gehring, W. J., Goss, B., Coles, M. G. H., Meyer, D. E., & Donchin, E. (1993). A neu-
ral system for error detection and compensation. Psychological Science,4, 385-390.
Gehring, W. J., Himle, J., & Nisenson, L. G. (2000). Action-monitoring dysfunction in
obsessive-compulsive disorder. Psychological Science,11, 1-6.
Scientific Articles 47
George, M. S., Ketter, T. A., Parekh, P. I., Horwitz, B., Herscovitch, P., & Post, R. M.
(1995). Brain activity during transient sadness and happiness in healthy women.
American Journal of Psychiatry,152, 341-351.
Gloor, P. (1976). Generalized and widespread paroxysmal abnormalities. In A. Redmond
(Ed.), Handbook of Electroencephalography & Clinical Neurophysiology, Volume
132, Part B. Amsterdam: Elsevier.
Goodman, W. K., McDougle, C. J., & Price, L. H. (1992). Pharmacotherapy of obses-
sive compulsive disorder. Journal of Clinical Psychiatry,53(Suppl.), 29-37.
Goodman, W. K., Price, L. H., Rasmussen, S. A., Mazure, C., Delgado, P., Heninger,
G. R., et al. (1989). The Yale-Brown Obsessive Compulsive Scale. II. Validity. Ar-
chives of General Psychiatry,46, 1012-1016.
Goodman, W. K., Price, L. H., Rasmussen, S. A., Mazure, C., Fleischmann, R. L., Hill,
C. L., et al. (1989). The Yale-Brown Obsessive Compulsive Scale. I. Development,
use, and reliability. Archives of General Psychiatry,46, 1006-1011.
Greist, J. H. (1990). Treatment of obsessive compulsive disorder: Psychotherapies,
drugs, and other somatic treatment. Journal of Clinical Psychiatry,51 (8), 44-50.
Greenberg, B. D., Ziemann, U., Cora-Locatelli, G., Harmon, A., Murphy, D. L., Keel,
J. C., et al. (2000). Altered cortical excitability in obsessive-compulsive disorder.
Neurology,54, 142-147.
Hammond, D. C. (2001a). Neurofeedback treatment of depression with the Roshi.
Journal of Neurotherapy,4(2), 45-56.
Hammond, D. C. (2001b). Comprehensive neurofeedback bibliography. Journal of
Neurotherapy,5(1-2), 113-128.
Hajcak, G., & Simons, R. F. (2002). Error-related brain activity in obsessive-compul-
sive undergraduates. Psychiatry Research,110, 63-72.
Harris, G. J., Pearlson, G. D., & Hoehn-Saric, R. (1993). Single photon emission com-
puted tomography in obsessive-compulsive disorder. Archives of General Psychia-
try,50 (6), 498-501.
Heller, W., Etienne, M. A., & Miller, G. A. (1995). Patterns of perceptual asymmetry
in depression and anxiety: Implications for neuropsychological models of emotion
and psychopathology. Journal of Abnormal Psychology,104, 327-333.
Heller, W., Nitschke, J. B., Etienne, M. A., & Miller, G. A. (1997). Patterns of regional
brain activity differentiate types of anxiety. Journal of Abnormal Psychology,106
(3), 376-385.
Holroyd, C. B., Dien, J., & Coles, M. G. H. (1998). Error-related scalp potentials elic-
ited by hand and foot movements: Evidence for an output-independent error-pro-
cessing system in humans. Neuroscience Letters,242, 65-68.
Insel, T. R., Donnelly, E. R., Lalakea, M. L., Alterman, I. S., & Murphy, D. L. (1983).
Neurological and neuropsychological studies of patients with obsessive-compul-
sive disorder. Biological Psychiatry,18, 741-751.
Isotani, T., Tanaka, H., Lehmann, D., Pascual-Marqui, R. D., Kochi, K., Saito, N., et al.
(2001). Source localization of EEG activity during hypnotically induced anxiety
and relaxation. International Journal of Psychophysiology,41, 143-153.
Jenike, M. A., Baer, L., Ballantine, T., Martuza, R. L., Tynes, S., Giriunas, I., et al.
(1991). Cingulotomy for refractory obsessive-compulsive disorder: A long-term
follow-up of 33 patients. Archives of General Psychiatry,48, 548-555.
48 JOURNAL OF NEUROTHERAPY
Jenike, M. A., & Brotman, A. W. (1984). The EEG in obsessive-compulsive disorder.
Journal of Clinical Psychiatry,45, 122-124.
Karno, M., Golding, J. M., Sorenson, S. B., & Burnam, M. A. (1988). The epidemiol-
ogy of obsessive-compulsive disorder in five U.S. communities. Archives of Gen-
eral Psychiatry,45, 1094-1099.
Kirsch, I., & Sapperstein, G. (1998). Listening to Prozac, but hearing placebo? A
meta-analysis of antidepressant medication. Prevention & Treatment,1, 0002a. (A
peer-reviewed APA journal available at http://www.journals.apa.org/prevention/
volume1/pre0010002a.html)
Kuskowski, M., Malone, S., Kim, S., Dysken, M., Okaya, A., & Christensen, K.
(1993). Quantitative EEG in obsessive compulsive disorder. Biological Psychiatry,
33, 423-430.
Leocani, L., Locatelli, M., Bellodi, L., Fornara, C., Henin, M., Magnani, et al. (2001).
Abnormal pattern of cortical activation associated with voluntary movement in ob-
sessive-compulsive disorder: An EEG study. American Journal of Psychiatry,158
(1), 140-142.
Luu, P., Collins, P., & Tucker, D. M. (2000). Mood, personality, and self-monitoring:
Negative affect and emotionality in relation to frontal lobe mechanisms of error
monitoring. Journal of Experimental Psychology: General,129, 43-60.
Machlin, S. R., Harris, G. J., & Pearlson, G. D. (1991). Elevated medial-frontal cere-
bral blood flow in obsessive-compulsive patients: A SPECT study. American Jour-
nal of Psychiatry,148, 1240-1242.
MacCrimmon, D. J., & Arato, H. (1991). Interhemispheric serotonergic asymmetry re-
flected in topographic pharmaco-EEG. Psychiatry Research: Neuroimaging,40
(1), 91-93.
Malloy, P., Rasmussen, S., Braden, W., & Haier, R. J. (1989). Topographic evoked po-
tential mapping in obsessive-compulsive disorders: Evidence of frontal lobe dys-
function. Psychiatry Research,28(1), 63-71.
Mas, F., Prichep, L. S., John, E. R., & Levine, R. (1993). Neurometric Q-EEG sub-
typing of obsessive compulsive disorders. In K. Maurer (Ed.), Imagining of the
brain in psychiatry and related fields (pp. 277-280). Heidelberg, Berlin, Germany:
Springer-Verlag.
Moncrieff, J. (2001). Are antidepressants overrated? A review of methodological prob-
lems in antidepressant trials. Journal of Nervous & Mental Disease,189 (5),
288-295.
Moncrieff, J., Wessely, S., & Hardy, R. (1998). Meta-analysis of trials comparing anti-
depressants with active placebos. British Journal of Psychiatry,172, 227-231.
Nakamura, S., Sadato, N., Oohashi, T., Nishina, E., Fuwamoto, Y., & Yonekura, Y.
(1999). Analysis of music-brain interaction with simultaneous measurement of re-
gional cerebral blood flow and electroencephalogram beta rhythm in human sub-
jects. Neuroscience Letters,275 (3), 222-226.
Naveteur, J., Roy, J. C., Ovelac, E., & Steinling, M. (1992). Anxiety, emotion and cere-
bral blood flow. International Journal of Psychophysiology,13, 137-146.
Nordahl, T. E., Benkelfat, C., Semple, W. E., Gross, M., King, A. C., & Cohen, R. M.
(1989). Cerebral glucose metabolic rates in obsessive-compulsive disorder. Neuro-
psychopharmacology,2, 23-28.
Scientific Articles 49
Pacella, B. L., Polatin, P., & Nagler, S. H. (1944). Clinical and EEG studies in obses-
sive-compulsive disorder. American Journal of Psychiatry,100, 830-838.
Pato, M., Zohar-Kadouch, R., & Zohar, J. (1988). Return of symptoms after discon-
tinuation of clomipramine in patients with obsessive compulsive disorder. Ameri-
can Journal of Psychiatry,145, 1521-1525.
Perani, D., Colombo, C., Bressi, S., Bonfanti, A., Grassi, F., Scarone, S., et al. (1995).
18F]FDG PET study in obsessive-compulsive disorder: A clinical/metabolic corre-
lation study after treatment. British Journal of Psychiatry,156, 244-250.
Perros, R., Young, E., Ritson, J., Price, G., & Mann, P. (1992). Power spectral EEG
analysis and EEG variability in obsessive-compulsive disorder. Brain Topography,
4(3), 187-192.
Pfurtscheller, G., Pichler-Zalaudek, K., Ortmayr, B., Kiez, J., & Reisecker, F. (1998).
Journal of Clinical Neurophysiology,15, 243-250.
Piacentini, J., & Bergman, R. L. (2000). Obsessive-compulsive disorder in children.
Psychiatric Clinics in North America,23 (3), 519-533.
Pizzagalli, D. A., Nitschke, J. B., Oakes, T. R., Hendrick, A. M., Horras, K. A., Larson,
C. L., et al. (2002). Brain electrical tomography in depression: The importance of
symptom severity, anxiety, and melancholic features. Biological Psychiatry,52,
73-85.
Posner, M. I., & Rothbart, M. K. (1998). Attention, self-regulation and consciousness.
Philosophical Transitions of the Royal Society of London Series B-Biological Sci-
ences,353, 1-13.
Prichep, L. S., Mas, F., & John, E. R. (1989). Neurometric subtyping of obsessive com-
pulsive disorders in psychiatry: A world perspective. Chapter in C. N. Stefanis, A.
D. Rabavilas, & C. R. Soldatos (Eds.), Proceedings of the VIII World Congress of
Psychiatry, Athens, October 12-19, 1989 (pp. 557-562). New York: Elsevier Sci-
ence.
Prichep, L. S., Mas, F., Hollander, E., Liebowitz, M., John, E. R., Alman, M., et al.
(1993). Quantitative electroencephalography (QEEG) subtyping of obsessive com-
pulsive disorder. Psychiatry Research,50 (1), 25-32.
Rauch, S. L. (2000). Neuroimaging research and the neurobiology of obsessive-com-
pulsive disorder: Where do we go from here? Biological Psychiatry,47, 168-170.
Rauch, S. L., Whalen, P. J., Dougherty, D., & Jenike, M. A. (1998). Neurobiologic
models of obsessive-compulsive disorder. In M. A. Jenike, L. Baer, & W. E.
Minichiello (Eds.), Obsessive-compulsive disorders: Practical management
(pp. 222-253). St. Louis: Mosby.
Reivich, M., Alavi, A., & Gur, R. C. (1984). Positron emission tomographic studies of
perceptual tasks. Annals of Neurology,15, (Suppl.), S61-S65.
Rockwell, F. V., & Simons, D. J. (1947). The electroencephalogram and personality
organization in the obsessive compulsive reactions. Archives of Neurology & Psy-
chiatry,57, 71-80.
Rubin, R. T., Villaneuva-Meyer, J., & Anath, J. (1992). Regional 133Xe cerebral blood
flow and cerebral 99m-HMPAO uptake in unmedicated obsessive-compulsive dis-
order patients and matched normal control subjects: Determination by high-resolu-
tion single-photon emission computed tomography. Archives of General Psychiatry,
49, 695-702.
50 JOURNAL OF NEUROTHERAPY
Sawle, G. V., Hymas, N. F., & Lees, A. J. (1991). Obsessive slowness: Functional
studies with positron emission tomography. Brain,114, 2191-2202.
Saxena, S., Brody, A. L., Schwartz, J. M., & Baxter, L. R. (1998). Neuroimaging and
frontal-subcortical circuitry in obsessive-compulsive disorder. British Journal of
Psychiatry (Supplement), 35, 26-38.
Schwartz, J. M., Stoessel, P. W., Baxter, L. R., Martin, K. M., & Phelps, M. E. (1996).
Systematic changes in cerebral glucose metabolic rate after successful behavior
modification treatment of obsessive-compulsive disorder. Archives of General Psy-
chiatry,53, 109-113.
Silverman, J. S., & Loychik, S. G. (1990). Brain-mapping abnormalities in a family
with three obsessive-compulsive children. Journal of Neuropsychiatry & Clinical
Neurosciences,2, 319-322.
Simpson, H. B., Tenke, C. E., Towey, J. B., Liebowitz, M. R., & Bruder, G. E. (2000).
Symptom provocation alters behavioral ratings and brain electrical activity in ob-
sessive-compulsive disorder: A preliminary study. Psychiatry Research,95(2),
149-155.
Stapleton, J. M., Morgan, M. J., Liu, X., Yung, B. C., Phillips, R. L., Wong, D. F., et al.
(1997). Cerebral glucose utilization is reduced in second test session. Journal of Ce-
rebral Blood Flow & Metabolism,17, 704-712.
Sterman, M. B. (2000). Basic concepts and clinical findings in the treatment of seizure
disorders with EEG operant conditioning. Clinical Electroencephalography,31
(1), 45-55.
Stewart, R. S., Devous, M. D., Rush, A. J., Lane, L., & Bonte, F. J. (1988). Cerebral
blood flow changes during sodium-lactate-induced panic attacks. American Jour-
nal of Psychiatry,145, 442-449.
Swedo, S. E., Pletrini, P., Leonard, H. L., Schapiro, M. G., Rettew, D. C., Goldberger,
E. L., et al. (1992). Cerebral glucose metabolism in childhood-onset obsessive-
compulsive disorder: Revisualization during pharmacology. Archives of General
Psychiatry,49, 690-694.
Swedo, S. E., Schapiro, M. G., & Grady, C. L. (1989). Cerebral glucose metabolism in
childhood onset obsessive-compulsive disorder. Archives of General Psychiatry,
46, 518-523.
Szeszko, P. R., Robinson, D., Alvir, J. M., Bilder, R. M., Lencz, T., Ashtari, M., et al.
(1999). Orbital frontal and amygdala volume reductions in obsessive-compulsive
disorder. Archives of General Psychiatry,56 (10), 913-919.
Thomson, R. (1982). Side effects and placebo amplification. British Journal of Psychi-
atry,140, 64-68.
Troisi, E., Silvestrini, M., Matteis, M., Monaldo, B. C., Vernieri, F., & Caltagirone, C.
(1999). Emotion-related cerebral asymmetry: Hemodynamics measured by func-
tional ultrasound. Journal of Neurology,246, 1172-1176.
Ursu, S., van Veen, V., Siegle, G., MacDonald, A., Stenger, A., & Carter, C. (2001,
March). Executive control and self-evaluation in obsessive-compulsive disorder:
An event-related fMRI study. Poster presented at the Cognitive Neuroscience Soci-
ety Meeting, New York, Cited in Hajcak & Simons, 2002.
Scientific Articles 51
Wiedemann, G., Pauli, P., Dengler, W., Lutzenberger, W., Birbaumer, N., & Buck-
kremer, G. (1999). Frontal brain asymmetry as a biological substrate of emotions in
patients with panic disorders. Archives of General Psychiatry,56, 78-84.
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... Previous research has examined the potential of neurofeedback as a treatment for OCD and related disorders, indicating it as a safe alternative with similar e cacy to behavioural and pharmaceutical interventions (Ferreira et al., 2019;Hammond, 2003;Zafarmand et al., 2022). As these studies outline, neurofeedback seems to facilitate a reduction in OCD symptomatology by modulating speci c brain wave frequencies which might be associated with rumination and cognitive avoidance as vital contributors to the disorder's persistence, explaining the improvement observed in the current study, which can be attributed to neurofeedback's effect enhancing self-regulation capacities, enabling patients to manage intrusive thoughts and maladaptive avoidance strategies better, associated with rumination and The ndings of this study can be translated into practical implications for mental health practitioners. ...
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Introduction: Obsessive-compulsive disorder (OCD) is a psychiatric condition characterised by persistent, intrusive thoughts and ritualistic behaviours. This study assesses the impact of qEEG-assisted neurofeedback on two critical components of OCD: rumination, a maladaptive focus on problem causes and consequences, and cognitive avoidance (CA), the tendency to evade distressing thoughts aiming to evaluate neurofeedback’s effectiveness in reducing rumination and CA severity in patients with OCD. Methods: This controlled prospective clinical trial with parallel design included patients diagnosed with OCD, with Yale-Brown Obsessive Compulsive Scale (YB-OCS) scores ≥ 16. Subjects were alternately assigned to either the neurofeedback or control groups maintaining a 1:1 ratio. The neurofeedback group underwent 25 sessions over six weeks, with outcomes measured through the Rumination Response Scale (RRS) and the Cognitive Avoidance Questionnaire (CAQ) pre- and post-intervention. Results: Of the initial cohort, 30 participants finished the study. Significant reductions in Rumination and CA were observed in the neurofeedback group with multivariate ANCOVA showing a significant impact on CAQ and RRS scores (Lambda Wilks p = 0.001) and univariate ANCOVA indicating marked decreases in CA (p = 0.001, Eta² = 0.687) and Rumination (p = 0.001, Eta Squared = 0.636) compared to controls. Discussion: The findings substantiate qEEG-assisted neurofeedback’s role in significantly reducing rumination and cognitive avoidance in OCD, indicating neurofeedback’s potential to modulate brain regions implicated in OCD pathology, such as orbitofrontal cortex and anterior cingulate, thus enhancing self-regulation and reducing symptoms. Limitations: Limitations include no long-term follow-up, reliance on self-report measures, a small, single-centred sample, and convenience sampling, all of which affect the generalizability of the results. INTRODUCTION
... According to the literature, the length of NFT sessions targeting the subjects' positive improvements in attention levels should be 30 min long divided into 2-10 sub-training sessions. 40 NFT sessions with three sessions per week subdivided into 10 tryouts of 3 min and 5 tryouts of 6 min [34] and 44 NFT training sessions subdivided into two 15 min sessions were used previously [35]. According to [36], a 20 to 30-minutes long NFT session can successfully induce a change in brain waves, but these changes will be temporary. ...
Article
Electroencephalography (EEG) based Neurofeedback training (NFT) is a non-invasive, brain-modulation technique that can improve the subject’s attention. In this research, the effectiveness of long-term NFT on the subject’s attention is explored. Real-time frontal lobe alpha band (8–13 Hz) power was used as feedback. The subjects were divided into the NFT group (n = 25) which received training and the control group (n = 25) which did not. All the subjects participated in the attention network task (ANT) at three stages i.e., before, mid, and at the end of NFT sessions. The EEG and behavioral data (Response time (RT) of the ANT task) were recorded for all subjects. The EEG data were pre-processed using a manual artifact removal procedure to avoid event-related information loss. Alpha band modulation can affect other bands such as theta (4–8 Hz) and beta (13–30 Hz) hence event-related functional connectivity (FC) and band power (BP) were analyzed in these bands as well. In event-related analysis, a significant increase (ANOVA & T-Test: P < 0.05) in theta and alpha power and FC within the NFT group was observed after NFT sessions whereas the changes observed within the control group were not significant. The RT of the subjects in the NFT group decreased. The increase in event-related power and connectivity within the theta and alpha band and the decrease in RT in the NFT group indicate the effectiveness of NFT sessions in the enhancement of attention.
... Simultaneous recording of EEG and fMRI provides complementary information and allows for a more comprehensive understanding and research in neurofeedback by exploring EEG and fMRI correlation (EEG-informed fMRI), fusion analysis, and validation of the effectiveness of the applied paradigm for a specific purpose (Ebrahimzadeh et al., 2019a(Ebrahimzadeh et al., ,b, 2021(Ebrahimzadeh et al., , 2022Mosayebi et al., 2022). EEG-based neurofeedback has applications in the treatment of attentiondeficit/hyperactivity disorder (ADHD) (Lubar et al., 1995;Zuberer et al., 2018), schizophrenia (Bolea, 2010), insomnia (Hammer et al., 2011), drug addiction (Lackner et al., 2016), autism (Coben et al., 2010), epilepsy (Saxby and Peniston, 1995;Walker and Kozlowski, 2005;Kaur and Singh, 2017;Linhartová et al., 2019), anxiety (Mennella et al., 2017), pain (Kubik andBiedroń, 2013, eating disorders (Bartholdy et al., 2013), Parkinson disease (Rossi-Izquierdo et al., 2013), obsessivecompulsive disorder (Hammond, 2003), post-traumatic stress disorder (PTSD) (Gapen et al., 2016) in addition to other psychological applications e.g., emotion regulation (Dennis and Solomon, 2010;Quaedflieg et al., 2015;Linhartová et al., 2019). ...
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Despite the existence of several emotion regulation studies using neurofeedback, interactions among a small number of regions were evaluated, and therefore, further investigation is needed to understand the interactions of the brain regions involved in emotion regulation. We implemented electroencephalography (EEG) neurofeedback with simultaneous functional magnetic resonance imaging (fMRI) using a modified happiness-inducing task through autobiographical memories to upregulate positive emotion. Then, an explorative analysis of whole brain regions was done to understand the effect of neurofeedback on brain activity and the interaction of whole brain regions involved in emotion regulation. The participants in the control and experimental groups were asked to do emotion regulation while viewing positive images of autobiographical memories and getting sham or real (based on alpha asymmetry) EEG neurofeedback, respectively. The proposed multimodal approach quantified the effects of EEG neurofeedback in changing EEG alpha power, fMRI blood oxygenation level-dependent (BOLD) activity of prefrontal, occipital, parietal, and limbic regions (up to 1.9% increase), and functional connectivity in/between prefrontal, parietal, limbic system, and insula in the experimental group. New connectivity links were identified by comparing the brain functional connectivity between experimental conditions (Upregulation and View blocks) and also by comparing the brain connectivity of the experimental and control groups. Psychometric assessments confirmed significant changes in positive and negative mood states in the experimental group by neurofeedback. Based on the exploratory analysis of activity and connectivity among all brain regions involved in emotion regions, we found significant BOLD and functional connectivity increases due to EEG neurofeedback in the experimental group, but no learning effect was observed in the control group. The results reveal several new connections among brain regions as a result of EEG neurofeedback which can be justified according to emotion regulation models and the role of those regions in emotion regulation and recalling positive autobiographical memories.
... Neurofeedback training has been proven beneficial and is an effective treatment modality for various psychological disorders (Demos, 2005) such as Schizophrenia (Pazooki, et al. 2019;Nan, et al. 2017;Jones, 2012), Depression (Dias &Deusen, 2011;Hammond, 2000;Baehr, Rosenfeld, &Baehr, 1997), Post-Traumatic Stress Disorder (PTSD) (Noohi, et al. 2017) and Obsessive Compulsive Disorder (OCD) (Wong, et al., 2015;Koprivova, et al. 2013;Hammond, 2003). ...
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ADHD is characterized by developmentally inappropriate levels of inattention, impulsiveness and hyperactivity. Neurofeedback, an evidence based non-invasive technique, has been proven beneficial and is an effective treatment modality to train the individual to modify their brainwave activity in order to decrease the symptoms of ADHD. This includes improving attention & mental functions, reducing impulsivity and hyperactive behaviors. It regulates the behavior of the individual by reducing the dependency on medications or any form of therapy and increase positive behavioral effects. The meta-analysis of fifteen studies depicts that theta and beta neurofeedback protocol and site of electrode placement (Cz) are most commonly used neurofeedback strategy in the treatment of ADHD. Neurofeedback training increases the power or rewards the sensorimotor rhythm (SMR) at 12-15 Hz training at Cz and inhibits beta activity (15–18 Hz) and theta activity (4-7 Hz) which has been reported to improve ADHD. Hence, it can be efficiently used with a medication regimen.
... Most of studies included purely for the systematic review provided a significant remission in OCD symptoms after NFB sessions (Barzegary et al., 2011;D. Hammond, 2004;Hammond, 2003). ‫ا‬ Considering the meta-analysis evidence, the overall results indicated quite promising of neurofeedback in treatment of patients with OCD.. Control group in trials showed (Kopřivová et al., 2013;Simon et al., 2013) the type of this group is not the same, leading to prevention of precise between-group analysis on the effect size (Begemann et al., 2016). ...
Article
Full-text available
To evaluate the evidences related to the effectiveness of neurofeedback treatment for people with OCD. A literature review and meta-analysis of current controlled trials for patients with OCD symptoms was conducted across different databases. So, the primary outcome measure was OCD symptoms in subjects based on DSM IV. Y-BOCS was considered as primary outcomes. Nine met inclusion criteria (including 1211 patients). Analysis showed there was an important benefit of neurofeedback treatment in comparison to other treatments (MD = -6.815; 95% CI = [-9.033, -4.598]; P < 0.001). The results provide preliminary evidence that NFB is efficacious method for OCD and suggest that more clinical trials are needed to compare common treatment such as medication, neurological, and behavioral interventions.
Article
Araştırmanın amacı, öfke problemi olan bir danışanın öfke ile baş etme becerilerini kazandırmada neurofeedback yöntemini etkililiği belirlemektedir. Olgu sunum yöntemiyle yapılan araştırmada öfke sorunu yaşayan 27 yaşındaki evli ve bir çocuk babası danışan, araştırmanın katılımcısıdır. Aynı zamanda danışan, psikiyatri kliniğinde herhangi bir tanıyla ilişkili olmamasına ilişkin, ruhsal gerginliğe bağlı olarak 2 yıldır tranko-buskas kullanmaktadır. Öfke problemi olan danışanın alpha, theta ve delta dalgalarındaki değişim oturum sürecinde izlenmiş ve bu beyin dalgalarına uygun protokolleri içeren dokuz neurofeedback oturumu düzenlenmiştir. Uygulama öncesinde danışandan alınan ölçümlerde, delta dalgası sonucunun 57.42, theta dalgası sonucunun 16.98 ve alpha dalgası sonucunun 7.25 olduğu görülmüştür. Ayrıca, izleme amacıyla danışanla beş oturumluk psikolojik danışma süreci yürütülmüştür. Neurofeedback uygulaması sonucunda danışanın normal sınırların dışında olan delta ve theta beyin dalgasında pozitif yönlü değişimlerin olduğu belirlenmiştir. Neurofeedback yöntemiyle yapılan dokuz uygulama sonucunda danışanın delta beyin dalgası sonucunun 28.81, theta dalgası sonucunun 13.03 düzeyine indiği ve alpha dalgası sonucunun ilk ölçüme yakın 7.18 düzeyinde sabit kaldığı belirlenmiştir. Araştırmanın bulguları ilgili alan yazındaki sonuçlar ve değerlendirmelerle tartışılmış olup, bu bağlamda araştırmacılara ve uygulamacılara önerilerde bulunulmuştur.
Chapter
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The chapter deals with the transdisciplinary linking of knowledge in multiprofessional teams of out-patience health care and joint interdisciplinary education, within which, in addition to medicine, it is recommended to incorporate knowledge from other related fields (biology, physics, mathematics, philosophy, psychology, pedagogy, etc.) in the interest of a complex multidimensional healthcare for the patient. The content of the international educational study program including the aforementioned elements of multiprofessional education is part of the article.
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Kapitola sa zaoberá transdisciplinárnym prepájaním poznatkov v multiprofesionálnych tímoch ambulantnej zdravotnej starostlivosti a spoločným interdisciplinárnym vzdelávaním, v rámci ktorého sa okrem medicíny odporúča potrebné inkorporovať aj poznatky z iných súvisiacich odborov (biológia, fyzika, matematika, filozofia, psychológia, pedagogika a podobne) v záujme komplexnej viacdimenzionálnej zdravotnej starostlivosti o pacienta. Súčasťou článku je aj náplň medzinárodného vzdelávacieho študijného programu zahŕňajúceho spomínané prvky multiprofesionálneho vzdelávania.
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