Handbook Qeeg Chapter 10
Handbook Qeeg Chapter 10
Abstract
This chapter presents my clinical approach to neuropsychiatric patients including application of
QEEG/LORETA for the confirmation of diagnosis and use of LORETA Z-score neurofeedback
(NFB) in therapy. Introduction of QEEG/LORETA brain imaging has improved our diagnostic abil-
ity in neuropsychiatric practice by identification of dysregulated cortical areas implicated in patients’
symptoms. Additional use of LORETA Z-score NFB enables us to directly target these areas of
dysregulation in order to improve symptoms associated with them. Based on approximately 260
patients treated in our clinic with Z-score LORETA NFB and suffering from different neuropsy-
chiatric conditions, detailed analyses of representative cases are presented. Specific areas of cortical
dysregulation identified by QEEG/LORETA are described, and results of computerized cognitive
testing are presented. Follow-up findings of QEEG/LORETA electrical imaging after NFB and com-
puterized cognitive testing indicating NFB mediated cognitive enhancement will be shown. Several
major groups will be discussed including patients diagnosed with TBI, cerebrovascular disease (CVA),
chronic pain/headaches, seizures/epilepsy, a static (non-progressing) cognitive dysfunction, progress-
ing cognitive dysfunction including Alzheimer’s disease (AD), anxiety/depression, ADD/ADHD, as
well as autistic spectrum disorder (ASD).
Introduction
Since the introduction of QEEG analysis to the neurofeedback (NFB) community, QEEG-brain
mapping has become increasingly utilized for the confirmation of diagnosis and targeted neuro-
therapy. The initial phase of NFB therapy (which utilized one or two channel technology) relied
mostly upon on a symptoms approach with no definite guidance as to whether or not the assumed
treatment was accurate. It was not unusual to see patients who were subjected to more than 100
NFB sessions with only minor or modest improvement of their symptoms. Therefore, the intro-
duction of the QEEG was one of the most important milestones in NFB development. By per-
forming a periodic analysis of brain maps between the neurotherapy sessions, every therapist is able
to see if a desired progress in brain wave neuromodulation was achieved. Another game changer
was the subsequent introduction of LORETA imaging and LORETA mediated NFB. LORETA
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imaging has added value of three dimensional visualization of the brain’s electrical activity and
enables us to see electrical dysregulations in deeper structures of the brain, which are not visible
with two dimensional electrical imaging. Several important structures of the brain including the
insula, amygdala, hippocampus and cingulate gyrus are able to be visualized with this type of
electrical imaging. Many neuropsychiatric symptoms are associated with electrical dysregulation
in these structures, as has been shown in my prior papers (Koberda, Koberda, Bienkiewicz, Moses
& Koberda, 2013; Koberda et al., 2014). Therefore, our ability to self-regulate these electrically
dysregulated structures with LORETA NFB gave us an additional therapeutic tool in neurotherapy
armamentarium. An additional benefit of QEEG/LORETA electrical imaging is the low cost
associated with this technology. Many insurance companies reimburse approximately $300 for
this testing, which is just a fraction of the cost when compared to other types of functional brain
imaging (functional MRI, PET, SPECT). QEEG/LORETA is based on portable electronics and
computer software; it can be administered in any type of clinical outpatient setting. In this chapter,
I would like to share my approach to evaluating patients suffering from common neuropsychi-
atric disorders and present several cases as an illustration of this model. The majority of patients
referred to my clinic have already been subjected to conventional therapy with no major clinical
benefits. Some patients have seen multiple specialists, including pain management/psychiatrists,
and were subjected to brutal therapies such as electroconvulsive therapy (ECT) in order to improve
symptoms of depression. A selection of referred patients endured previously administered failed
surgeries.
Initial Evaluation
During the initial evaluation (which usually takes around 60 minutes in addition to general neuro-
psychiatric examination) an extensive history is taken from the patient and his/her family. In order
to deliver correct diagnosis and effective therapy, I have to be well familiarized with all my patients.
This allows me to know my patient almost as well as I know my family members when they come
back for a follow-up visit. For that purpose I collect extensive family and social history, and document
as many details as possible, since they may have influence on the patient symptoms. Individuals who
complain of cognitive problems are usually scheduled for computerized cognitive testing (NeuroTrax,
Inc., Bellaire, TX). This testing takes approximately 60 minutes to complete, and evaluates seven
different cognitive domains including memory, information processing speed, attention, executive
function, motor function, verbal function and visual-spatial function. The individual is compared to
education and age-matched controls. Standard deviations (SD) are used to show whether the patient’s
cognition is close to the expected one. For those who elect to be subjected to NFB or other forms
of neuromodulation, cognitive testing may be repeated in order to see if any benefits of this therapy
was accomplished.
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another cognitive enhancement group from our practice (consisting mostly of ADD patients),
the TBI group resulted in even greater cognitive recovery. These results are very encouraging
and indicate the high potential of Z-score LORETA NFB in rehabilitation of patients suffering
from TBI. When programming NFB sessions, we have focused on a symptoms check list (SCL),
and selection was made based on up to five of the most severe problems identified by either the
patient or cognitive testing.
The following case illustrates my approach to a patient with mTBI with mild cognitive problems.
Case 1
A 17-year-old male with a history of two mild concussions (last one two years ago) and a possible
overlapping attention deficit disorder was seen for consultation. The patient came with his mom from
Atlanta for consideration of NFB due to poor high school performance and possible overlapping
depression and behavioral problems. His initial computerized cognitive testing (NeuroTrax) showed
lower than expected (expected score, 100) global cognitive score (GCS), 90.9 (Table 10.1) with low
memory score, 89.3, as well as executive function, 85.6. After initiation of Z-score LORETA NFB, a
subjective improvement of his cognition (feeling sharper) as well as mood improvement was noted.
After 10 sessions of NFB, marked improvement of cognitive score was recorded (GCS-101.5). An
additional 10 sessions (total of 20 sessions) of NFB increased his GCS to 108.8, which was almost
18 points higher than the initial one. The initial QEEG showed an elevated frontal and temporal theta
power, as well as frontal alpha and beta power (Figure 10.1). An increased frontal and temporal theta
power may be seen in patients with cognitive difficulties including ADD. Elevated frontal alpha is
frequently seen in individuals with depression. High frontal beta may be encountered in patients with
anxiety. Also, abnormalities in amplitude asymmetry, coherence and phase lag were noted. Additional
TBI discriminant analysis showed TBI probability index of 97.5% and TBI severity index of 5.23,
confirming evidence of prior concussions. LORETA imaging showed electrical dysregulation of the
anterior cingulate and right temporal region—including several Brodmann’s areas (BA): BA 20, 24
and 37 (Figures 10.2a and 10.2b).
In addition to cognitive and behavioral improvements, a correction of previously identified QEEG
abnormalities was achieved.
Table 10.1 A 17-year-old with prior concussions and ADD. NeuroTrax computerized cognitive testing was
completed before NFB initiation (first vertical column from left) and after completion of 10 and 20
NFB sessions (second and third column).
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Figure 10.1 A 17-year-old with prior concussions and overlapping ADD and behavioral problems—QEEG
showed elevated frontal and temporal theta and alpha power (in red), increased frontal beta power
and right temporal delta power. Green color shows absolute and relative power within one standard
deviation (SD), yellow color within two standard deviations and red color within three SD.
QEEG and LORETA Z-Score Neurofeedback
(a)
(b)
Figures 10.2a and 10.2b LORETA of 17-year-old male with prior concussions, and ADD-area of electrical dys-
regulation of the right temporal lobe is shown in red (a) and anterior cingulate in blue (b).
Cerebrovascular Disease
We have completed Z-score LORETA therapy with more than 260 patients with different neuro-
psychiatric conditions including five patients suffering from stroke. One of the patients who was
diagnosed with occipital cerebrovascular accident (CVA) and complained of visual problems due to
homonymous hemianopia completed only three NFB sessions and reported subjective improvement
of his vision. However, no follow-up visual fields study was completed. All patients suffering from
CVA, regardless of the origin (ischemic or hemorrhagic), were found to have an improved perfor-
mance after completion of NFB (Koberda & Stodolska-Koberda, 2014). In this chapter, I will present
one of our representative patients who completed Z-score LORETA NFB due to ischemic stroke.
Case 2
A 69-year-old male came for rehabilitation with LORETA Z-score NFB after suffering from CVA
(four months earlier). During CVA he complained of confusion with memory problems, left-sided
numbness associated with pain and visual and spatial problems. MRI of the brain showed evidence of
the right thalamic and temporal/hippocampal CVA and occlusion of occipital cerebral artery.
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QEEG showed increased right temporal delta and theta power (Figure 10.3). LORETA showed
several areas of electrical dysregulation including the right temporal lobe including BA-36 and the
cingulate gyrus BA-24 (Figures 10.4a and 10.4b).
Figure 10.3 A 69-year-old with prior CVA. QEEG showed increased right temporal delta and theta power (in
yellow).
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(a)
(b)
Figures 10.4a and 10.4b LORETA showed several areas of electrical dysregulation, including right temporal
lobe BA-36 and cingulate gyrus BA-24 (in red).
Table 10.2 Computerized cognitive testing (NeuroTrax) of a 69-year-old with prior CVA before and after
10 sessions of NFB.
Number of NFB Sessions 0 10
Global Cognitive Score 83.6 94.8
Memory 85 99.7
Executive Function 87.5 103.9
Attention 80.2 94.2
Information Processing Speed 74.4 84.3
Visual Spatial 85.8 99.3
Verbal Function 86.1 83.7
Motor Skills 86 98.4
Initial (before NFB) NeuroTrax showed low cognitive score GCS, 83.6, with a low memory score,
85.0, and information processing speed (IPS), 74.4. After four sessions of NFB, the patient reported
some improvement of his cognitive symptoms. After 10 NFB sessions, repeated cognitive testing
showed an improvement in cognitive functions (GCS-94.8) including memory-99.7, IPS-84.3, as
well as improvement in other cognitive domains. In addition, a correction of QEEG/LORETA
abnormalities was noted after NFB therapy completion.
Overall, this patient has been able to come back to his accounting duties and perform at his
pre-stroke baseline level.
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1. 35 F Improved − 2 5
2. 20 F Improved + 3 15
3. 53 F Improved − 6 7
4. 22 M Improved − 2 4
5. 58 F Improved + 5 21
6. 50 F Improved − 4 10
7. 20 F Improved + 3 8
8. 20 F Improved + 3 6
9. 44 F No Improvement − - 10
10. 24 F Improved + 3 26+
11. 52 F Improved + 3 10
12. 43 F Improved − 4 8
13. 23 F Improved + 2 11+
14. 38 F Improved + 5 14
15. 36 F TN Improved + 2 10
16. 31 M Improved + 2 10
17. 49 F Improved + 6 7
18. 27 F Improved + 3 3
19. 50 F Improved + 2 10
20. 57 F Improved + 4 26+
21. 38 F Improved + 4 10
22. 65 M Improved + 1 10
23. 51 M Improved + 4 15
Case 3
This is a 36-year-old female with an 18-month history of the right trigeminal neuralgia. The
patient had been taking pregabalin (Lyrica) 100 mg PO BID for neuralgic pain and duloxetine
(Cymbalta) for depression and pain. The patient reported that despite taking increasing doses of
Lyrica (she previously was on 50 mg BID), the pain was not improving and she gained a lot of
weight (her weight exceeding 300 lbs.). The patient was interested in trying an alternative modal-
ity of therapy, exhibiting interest with starting Z-score LORETA NFB. Her initial QEEG showed
elevation of fronto-temporal delta and theta power, as well as frontal beta power (Figure 10.5).
In addition, LORETA analysis showed an area of dysregulation in the left insular cortex (Fig-
ure 10.6). She reported marked pain improvement after the first session of NFB, and was able to
reduce the dose of Lyrica after the second session and then discontinue Lyrica completely after
the fourth session. The patient completed 10 sessions of NFB and has been in remission for over
an 8-month period. The QEEG, completed after total pain resolution, showed an improvement in
frontal delta, theta and beta power, as well as a resolution of insular cortex electrical dysregulation
(Figures 10.7 and 10.8).
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Figure 10.5 A 36-year-old female with trigeminal neuralgia. Pre-treatment QEEG showed marked frontal and
temporal increase in delta and theta power (in red) and frontal beta power (in yellow).
Figure 10.6 A 36-year-old female with trigeminal neuralgia. Pre-treatment LORETA showing left insular
cortex electrical dysregulation (in red).
Figure 10.7 A 36-year-old female with trigeminal neuralgia. Post-NFB treatment QEEG showed partial cor-
rection of previously identified abnormalities.
Figure 10.8 A 36-year-old female with trigeminal neuralgia. Post-NFB treatment LORETA showed resolution
of previously identified insular electric dysregulation.
J. Lucas Koberda
Cognitive Dysfunction
We have conducted a larger case series report where 35 consecutive patients complaining of cognitive
dysfunction were subjected to LORETA Z-score NFB therapy (Koberda, Moses, Koberda & Winslow,
2014). Before NFB initiation, these patients were evaluated with computerized neurocognitive test-
ing in order to document and confirm any cognitive dysfunction reported in chief complaint. Many
patients underwent brain imaging and laboratory testing to rule out any treatable condition which
could have contributed to the patient’s symptoms. Electrical imaging with QEEG/LORETA local-
ization was also completed in order to visualize any area of cortical electrical dysregulation which
could have been potentially responsible for the patient’s symptoms (with specific Brodmann areas).
The NFB protocol was based either on the patient’s symptoms, the area of cortical dysregulation, or
both. After 10 sessions of surface/LORETA Z-score NFB, the computerized cognitive testing and
QEEG were repeated in order to see if any increase in cognitive score and/or reduction in QEEG
abnormalities were achieved. In addition, the patient’s subjective response was recorded as to whether
or not they felt that the therapy was beneficial. Twenty-five patients (71%) were identified as having
a significant objective improvement (on average 10 points) in cognitive testing. In addition, subjec-
tive cognitive improvement and an objective reduction of QEEG abnormalities with NFB were also
achieved in most of the patients. These results are very promising and indicate good effectiveness of
LORETA Z-score NFB in cognitive enhancement.
This clinical data illustrates high effectiveness of Z-score LORETA NFB therapy in complex neu-
ropsychiatric patients, where an improvement of depression/anxiety and other associated cognitive
domains can be achieved in most of the patients within just 10 treatment sessions. However, many
patients requested to continue NFB for a longer period of time in order to continue benefits of this
therapy. The following case will illustrate my approach to patients with static cognitive dysfunction.
Case 4
A 19-year-old male was brought for appointment by his adoptive parents indicating problems with
cognition, mostly executive function and information processing speed dysfunction. After complet-
ing a QEEG and before initiation of NFB, neurocognitive testing was completed in March 2013.
Results showed low cognitive score—Global Cognitive Score 80.2—with low executive function,
87.2, and a very low information processing speed of 52.1. His LORETA and QEEG showed evi-
dence of anterior cingulate electrical dysregulation and increased frontal delta power (Figures 10.9a
and 10.10). After the first 10 sessions of NFB, his executive function improved to 89.9, and with
Figure 10.9a A LORETA imaging of 19-year-old patient showing area of electrical dysregulation of anterior
cingulate (AC) region BA-32 (in red).
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Figure 10.9b Resolution of AC dysregulation after 20 sessions of NFB.
Figure 10.10a QEEG before NFB—noticeable area of frontal increase in delta power.
Figure 10.10 QEEG of 19-year-old with cognitive problems before initiation of NFB (a) and after a course of
NFB sessions (b).
Figure 10.10b QEEG after NFB—an improvement in previously overexpressed frontal delta power is recorded.
QEEG and LORETA Z-Score Neurofeedback
Figure 10.11 Executive testing (NeuroTrax) before NFB (March 2013) and after each round of 10 sessions of
NFB (in May 2013, October 2013 and January 2014)—gradual increase in executive function
was recorded.
each round of NFB, repeated cognitive testing was giving better results with executive function (sub-
sequently 92 and 97; see Figure 10.11). Also previously electrically dysregulated AC area and frontal
delta power overexpression became normalized (Figures 10.9b and 10.10b). In addition to QEEG and
cognitive testing, his parents noted a tremendous improvement in social and cognitive performance
at home and work.
This clinical data illustrates high effectiveness of Z-score LORETA NFB therapy in complex neuropsy-
chiatric patients, where an improvement of depression/anxiety and other associated cognitive domains can
be achieved in most of the patients within just 10 treatment sessions. However, many patients requested to
continue NFB for a longer period of time in order to continue benefits of this therapy. Some patients were
also treated with additional NFB (5–10 sessions) in case of reoccurrence of symptoms.
Based on our encouraging data, I recommend implementation of QEEG/LORETA brain mapping
testing in all patients suffering from depression, anxiety and cognitive dysfunction.
Alzheimer Disease
It is important to note that NFB seems to not only be effective in patients with static (non-progres-
sive) cognitive dysfunction, but also with progressive neurodegenerative disorders like AD. We have
completed therapy of six AD patients so far.
The NFB protocol included surface and LORETA (NF1/NF2-Neuroguide, Inc.) feedback, in an
alternating protocol while focusing on a symptom check list including: attention deficits, concentra-
tion problems, executive function problems and short-term memory. NFB sessions were conducted
with a frequency of once, twice or three times per week, using auditory or auditory and visual
feedback combined. The most frequent finding on QEEG of AD patients was increase in slow fre-
quencies (mostly theta and delta) in frontal and temporal locations. LORETA frequently indicated
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electrical dysregulation in temporal areas. Out of six AD patients who completed at least 10 ses-
sions of Z-score LORETA NFB, four achieved cognitive enhancement on cognitive testing and one
achieved a cognitive stabilization. One AD who deteriorated despite NFB therapy was not fully
compliant with treatment (not able to come for NFB sessions at least weekly).
Unfortunately, after NFB discontinuation, these patients usually deteriorate quickly. It is recom-
mended to at least continue NFB therapy on a weekly basis. My recommendation is to have NFB
therapy five times a week in order to counteract progressive neuronal degeneration due to disease
progression. Larger studies with prolonged administration of NFB may be beneficial to determine
optimal timing and duration of NFB for this group of patients.
Case 5
My representative case of AD is a 64-year-old who recently retired (dentist) who started having
short-term memory problems approximately five years before seeing me for consultation. He was
started (by another neurologist) on medications for memory improvement—initially on Exelon
(Acetylcholine esterase inhibitor) and subsequently Namenda (NMDA receptor modulator) was
added. Unfortunately, Namenda was causing major side effects including constipation, requiring
frequent use of laxatives and enemas. MRI of the brain was reported as normal. Initial QEEG
revealed central increase of delta and beta power with coherence abnormalities (Figure 10.12);
LORETA detected several areas of electrical dysregulation including anterior cingulate (BA-24) and
precuneus (BA-7) and BA-6 (Figure 10.13). This patient QEEG did not show any major area of
frontal or temporal slowing, which is typical for individuals suffering from AD. My assumption is
that Exelon, which has a cholinergic action, most likely was responsible for QEEG findings of delta
and theta reduction. This effect of Exelon was previously reported in QEEG literature (Fogelson
et al., 2003; Gianotti et al., 2008). His initial NeuroTrax testing showed marked reduction of GCS-
78.1 (Table 10.4) and low memory score-44.6 (expected score 100). After completion of six NFB
sessions NeuroTrax testing was repeated and marked cognitive enhancement was recorded (Table
10.4) with increased GCS-86.4 and memory score-53.7 as well as other cognitive domains. Due to
chronic constipation caused by Namenda, this medication was gradually discontinued based on the
patient’s request. Repeated NeuroTrax testing showed further increase in GCS-90.3 despite recent
discontinuation of Namenda. In addition, his chronic constipation was resolved which contributed
to marked improvement of his quality of daily living and reduction of other medication usage (laxa-
tives). At the same time, a partial correction of previously identified QEEG/LORETA abnormalities
was found. This patient will continue to be monitored with periodic cognitive testing in order to
see whether LORETA Z-score NFB may be able to hold its cognitive benefits.
Table 10.4 A 64-year-old with AD. NeuroTrax testing before NFB initiation (left column), after 6 NFB sessions
(middle column) and after 12 NFB sessions (right column).
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Figure 10.12 A 64-year-old male with AD. Initial QEEG showed central increase of delta and beta power (in
yellow) as well as coherence abnormalities.
Figure 10.13 A 64-year-old with AD. LORETA detected several areas of electrical dysregulation (in red)
including anterior cingulate and other BA (not shown).
J. Lucas Koberda
Figure 10.14 Summary of frequently identified QEEG/LORETA abnormalities in patients suffering from
depression and anxiety.
Figure 10.15 Orbitofrontal electrical (area in red) dysregulation (BA-11) seen in one of the patients with
depression and anxiety.
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Detailed analysis of our patients diagnosed with depression and/or anxiety showed that out of 31
included in the study, 24 (77%) were found to have both subjective and objective (improvement of
QEEG abnormalities) improvement of the symptoms within 10 sessions of LORETA Z-score NFB.
I would like to present one of our patients who successfully completed Z-score LORETA NFB with
marked improvement in both depression and cognitive function. Cognitive function, which is often
impaired in patients with depression, usually improves after NFB therapy.
Case 6
A 58-year-old university professor was seen in my office due to major depression associated with
anxiety and memory problems. She noticed problems with teaching due to possible cognitive dys-
function. Figure 10.16 shows her LORETA imaging before NFB, which identified several areas of
electrical dysregulation, including the cingulate cortex and left temporal region.
The computerized cognitive testing completed before NFB identified deficiency of memory and
executive function. Blood work was negative for B12 deficiency.
After 10 sessions of NFB, major improvement in memory (from 42.8 to 107.1) was recorded on
neurocognitive NeuroTrax testing (Table 10.5). In addition, marked improvement in the patient’s
mood and anxiety was reported. Post-NFB LORETA imaging confirmed an improvement in
electrical dysregulation of previously identified regions (picture not shown). Patient also reported
better performance in her academic settings.
Figure 10.16 A 58-year-old female: LORETA imaging before NFB shows two areas of electrical dysregulation,
(in red) including the cingulate cortex and left temporal region.
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Table 10.5 A 58-year-old female cognitive testing results before (left column) and after (right column) 10 sessions
of NFB. Expected score is 100 with 1 standard deviation = 15.
Global CS: 86.7 112.1
Memory: 42.8 107.1
Executive Function: 81.7 122.9
Attention: 110.5 108.6
Info Processing Speed: 96.2 108.6
Visual Spatial: 93.8 113.6
Verbal Function: 93.6 110.0
Motor Skills: 88.6 114.1
Table 10.6 ASD patients’ demographics and other clinical information. M-male, F-female.
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Case 7
This is a 12-year-old autistic boy whose family was interested in trying NFB as therapeutic modality. He
had practically no speech output except occasional single words, was restless and fidgety. MRI of the brain
was normal. His NeuroTrax cognitive testing was grossly abnormal with low memory score of 25.7 and
attention score of 39.7. QEEG showed marked increase of central and temporal beta power (Figure 10.17)
and LORETA demonstrated anterior cingulate (BA-24) electrical dysregulation (Figure 10.18).
Figure 10.17 This is a 12-year-old boy with ASD. Pre-NFB QEEG shows increased central and temporal beta
power (in red).
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Figure 10.18 Pre-NFB LORETA showed area (in blue) of anterior cingulate electrical dysregulation in theta
frequency.
This patient completed only five NFB sessions (due to insurance termination) after which his
family noticed some improvement in his behavior, mostly noticing him being less restless. In addition,
after five NFB sessions, reduction of excessive beta activity on QEEG was noted.
Case 8
This is a 15-year-old boy with history of Asperger Syndrome (AS) associated with ADHD and
behavioral problems including anger control. His cognitive profile showed Global Cognitive Score
(GCS) of 90.5 with weakness in memory (87.8) and verbal function (68.7). LORETA demonstrated
(Figure 10.19) area of electrical dysregulation in the right frontal lobe Brodmann area 9 (BA-9),
Figure 10.19 A 15-year-old male with AS/ADHD. LORETA showed electrical dysregulation of BA-9 (in red)
in delta frequency.
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which has a role in memory and other cognitive functions. QEEG showed mild increase in frontal
beta and delta power. Patient completed 10 NFB sessions; however, no follow-up cognitive testing
was accomplished due to insurance termination. Overall, his family and the patient noticed some
subjective improvement in his cognition. QEEG recorded after NFB also showed some improvement
of previously identified abnormalities.
Table 10.7 Summary of patients suffering from seizures and subjected to NFB therapy.
Case 9
An 18-year-old female high school senior whose seizures started at age 11, sometimes proceeded by
eye blinking episodes. Her current medications included Keppra XR 1500 mg daily and Lamictal
150 mg daily. Prior MRI of the brain was reported to be normal. EEG showed multiple sharps
in several locations including P3, P4, T5, T6, O1, O2. Cognitive testing showed low information
processing speed and memory (Figure 10.20). Despite extensive neurological evaluations at UCLA
and multiple medications, no seizure reduction was observed. Her mother even reported an increase
in seizure numbers with use of anti-epileptic mediations. Dr. Barry Sterman was also consulted,
and sensory-motor rhythm (SMR) NFB was initiated with some seizure reduction noted. However,
despite 90–100 sessions of NFB completion, seizures were still occurring, but with lower frequency.
This patient came to my office for one week of intensive therapy with Z-score LORETA NFB (twice
a day). LORETA imaging showed multiple areas of cortical electrical dysregulations (see Figure 10.21
below). After completion of eight NFB sessions, a long period of remission was achieved (approx-
imately four months seizure free). Further NFB therapy was continued at another location but
with much lower frequency. Since the initiation of Z-score LORETA NFB therapy (approximately
14 months) only three seizures were noted. In addition, marked improvement of cognitive status was
found with resultant admission to college and very good grades during the freshmen year (mostly
As—on the dean’s list).
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Figure 10.20 Illustrates lower than expected cognitive score, especially memory and attention, as well as infor-
mation processing speed (too low to be scored).
Figure 10.21 An 18-year-old female with medication resistant epilepsy. LORETA showed several areas of elec-
trical dysregulation including left temporal region (in red).
QEEG and LORETA Z-Score Neurofeedback
Conclusion
As we can see from the reviewed cases, Z-score LORETA NFB has proven to be a very effective
therapeutic modality in many neuropsychiatric disorders. Some cases, such as the one pertaining
to intractable epilepsy, were left with practically no medical options except possible neurosurgical
interventions. Many progressive neurodegenerative disorders have no effective medical alternatives
to slow the progression of AD. Assuming that NFB may have some neuroplastic properties (Ghaziri
et al., 2013), we can hope that this treatment modality may slow relatively rapid cognitive decline of
neurodegenerative disorders. Longer studies with five-year follow-ups will be needed to see if NFB
is able to hold cognitive benefits in those AD patients (and for how long).
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11
CONCUSSIONOLOGY
Sport Concussion Management
Harry Kerasidis
Abstract
There is a growing awareness of the repercussions of a concussion and, increasingly, clinicians are
called on to treat post-concussion syndromes. This review covers the elemental basics of concus-
sions in terms that will not only inform clinicians but patients themselves. Standard neurological
concussion treatment is described. Advanced treatment techniques of neurofeedback and neuro-
modulation are presented. Case studies illustrate treatment protocols using QEEG-driven selection
of targets for training.
The brain is beautiful, the new frontier of science. However, the brain is also vulnerable. Its fragile, gel-
like consistency floats unattached inside the skull. When force is applied, as it does many times in sports
collisions, military injuries, work accidents and motor vehicle accidents, the brain sloshes from side to
side, end to end, almost like scrambling the yolk of an egg as it floats inside, without breaking its shell.
The consequences from concussions and undiagnosed brain injuries can be seen immediately or
take several hours or even days for symptoms to materialize. However, their effects can be life altering.
It is a mystery that medical science is unraveling.
For example, the Wall Street Journal reported on the front page in 2008 that undiagnosed brain
injuries are a major cause of:
• Homelessness
• Psychiatric illness
• Depression and anxiety
• Alcoholism and drug abuse
• Suicide
• Learning problems
To understand concussions and mild traumatic brain injury, first we need a better understanding of
the brain itself. It is a wonderfully complex organ, and “command central,” literally responsible for
regulating or executing every move we make, every word we say, every emotion we feel and every
thought we think.
Brain health is so critical to proper life functioning that maybe protective helmets should include
a label: “WARNING: Contents Are Fragile.”
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