It is no surprise when insurance companies find ways to restrict what they will cover as a service for their clients, whether flood insurance liability insurance, or any other branch of this financial industry.  This is especially true for medical insurance companies, which are always finding reasons to restrict payments.

This decision restricts the payment for a qEEG to be an extension of the analysis of an EEG analysis, which makes the qEEG a medical procedure requiring licensure adequate to provide credentials to do a medical EEG interpretation. If further restricts the payments to applications that match the American Academy of Neurology position paper, which approves the technique in vascular cases, encephalopathies such as dementia cases, or for epilepsy, as well as longer term EEG monitoring, where quantitative analysis allows the selection of segments for review visually, assisting the electroencephalographer in eliminating long time segments from detailed analysis.

Specifically restricted from payment are these applications:

• Alcoholism
• Asperger’s syndrome and other autism spectrum disorders
• Attention disorders
• Depression
• Drug abuse
• Fibromyalgia
• Hypoxic ischemic encephalopathy
• Insomnia
• Learning disability
• Mild or moderate head injury
• Panic disorder
• Post-concussion syndrome
• Predicting response to psychotropic medication
• Schizophrenia
• Tinnitus

The list above is not an appropriate reason to do an EEG medically… at least not on the surface. In many of these cases the clinical decision may include ruling our an encephalopathy, a a vascular or epileptic process. As an example of this, approximately 30% of those with autism have undiscovered epileptiform discharges in the EEG, and respond well to anticonvulsants. An EEG is the only way to rule out epilepsy in such a case, and this may be allowed under the coverage listed, if the testing is ordered appropriately and the chart supports the order for the testing.

This is generally the same for TBI, where a post-traumatic vascular issue or epileptiform response to the TBI may be suspected, such as with contusion or post traumatic edema/ischemia.
In atypical clinical presentation, an alcoholic can be evaluated for dementia (Korsakov’s syndrome), as well as epilepsy (PLEDS are a common withdrawal pattern in chronic alcoholics). The chart needs to support the evaluation diagnostically for ruling out any of these covered categories.

The report can comment on medication implications, even if the testing was not done for that purpose diagnostically.

Attentional and affective disorders will not be covered, but if the physician is trying to rule out epilepsy (absence can mimic ADD) or an encephalopathy or dementia as the etiology of the psychiatric changes, then the insurance may cover the EEG and subsequent qEEG examination.

The important thing is to have the documentation in the chart to support the diagnostic/treatment question being posed with the testing.

The fact that they cover any of the qEEG at all is only due to the AAN position paper’s support for these areas. As the neuroscience is done to support more applications, then the carriers will have to amend their coverage statements. It is up to us to do the hard work to open these other areas up to payment…. and to argue for some other licenses to be covered for payment.

HOUSTON – A Houston doctor is working on something that could help the many service members who return from the battle field suffering from post-traumatic-stress disorder.

By its own admission, The Veterans Administration has had little success treating people who are suffering from both traumatic brain injury and post traumatic stress disorder.

“They end up not having any cognitive strategies to manage the therapy, and they’ll either get out of therapy, or end their lives and that’s what’s happening,” said Dr. Ron Swatzyna, a psychotherapist, neuro-therapist, and biofeedback therapist for Houston’s Tarnow Center. “I’ve been working on this issue for about four years now.”

He said resetting the brain, lining it back up through stimulation, is the key.  And by mapping the brain, he believes he can tell when the patient is ready for therapy.

“Not at the beginning. If you push them too quick that’s a problem. If they are pushed into therapy too quick,” he said.

Swatzyna said the defense department and the VA both realize more research is needed, and if he can get funding, and cooperation from a group in the Texas Medical Center, he would like to open up a research center in Houston.

Vietnam veteran Billy Miller, who one of Swatzyna’s patients, is now helping him pull it off.

“Everyone I had been to before, all 25 doctors had never had military experience, they didn’t know what I was going through,” Miller said.

Swatzyna was a captain in the Air Force, and now many believe he is the best in the country at understanding veterans.

Army soldier Joel Brasier, who suffers from TBI and PTSD, believes Swatzyna is on the right track and is hoping research will lead to better, faster treatment.

“It’s an ongoing process, but eventually they are going to make a breakthrough and get us the help we need,” Brasier said.

Full story from khou.com

How can we live a fuller and healthier lifestyle as we get older? Perhaps keeping our body and brain engaged can help. That seems to be the case in Japan where the number of centegenarians is greater than 20,000.

THE ART OF AGING:THE LIMITLESS POTENTIAL OF THE BRAIN introduces a number of these “super-seniors” who lead healthy lives at nearly 100-years-old and, through them,searches for the “keys” to living a healthy and vital life regardless of age.

Click here to view the embedded video.

These results are from 300 seconds of linked ear EEG data, note the dominant slower alpha peak frontally…. And the raw coherence values of that linked ear data. The raw EEG file sample is also included, so you can see the waveforms these values are being drawn from.

Linked Ears

Raw Coherence Values of Linked Ear Data

Raw EEG

The same exact 300 seconds of EEG data, reprocessed now with the weighted average montage.  Note the difference in spectra, and waveform!!!  The temporal slower alpha is now seen as the source of that slower alpha content.

The alpha hypercoherence in the EEG is easily seen in this data, but not in the linked ears.

This shows that you need to find the EEG montage that shows the actual EEG data for your case first, and THEN calculate coherence.

Weighted Average Spectra

Weighted Average Waveform

Weighted Average Raw

The images below show the Spectral plot, coherence plot and raw EEGs. Just like the other montages did. The Cz coherences are so inflated with field effects they are at 0.8 across the full spectrum at some sites, obviously artifactually high.

Spectral Plot

Coherence Plot

Raw EEG

I suggested at the time that all the emotion was merely an example of someone yelling “the sky is falling”, like Chicken Little. There was no real problem, just lots of crying out and hand wringing.

I requested in an open international forum for anyone to send me a sample of the problem, and none could be produced. I suspected there was no real problem, as the sample issue was concerning a 500 sample/second device having a time skew… though this was in comparison to a database collected on a 100 sample per second device, with the waveforms interpolated from these samples.

It was highly suspect from my technical perspective when this issue was raised, and it was even more suspect when nobody could produce actual data showing the coherence or phase issue.

Testing now has shown that the old style Mitsar, with the non-simultaneous sampling is identical in performance to the new style amplifier that has simultaneous sampling, and thus no skewing error is possible in the newest amp.  There is also an intermediate style amplifier tested, which is one of the smaller amps, but with a more current sampling design.

The data clearly show that there is no difference in coherence between these devices.

The Mitsar amplifier also has been tested with the new BranMaster  Discovery amplifier, and it also was shown to have indenticle coherence findings with the Mitsar amplifier.

Clearly there is no real issue.

Data rules…. the experimental details are below.

Jay

We performed the following experiment.

We took three different Mitsar amplifiers:

1. Mitsar-EEG-201 – old model of amplifiers with relatively large time shift between channels (1.75 ms maximum) 2. Mitsar-EEG-201M – new model of amplifiers with relatively small time shift between channels (470 microsecond maximum) 3. Mitsar-EEG-202 – 32-channels amplifiers with zero time shift between channels.

Than we take Electro-Cap and put it on the head of one subject. We used linked ears referent for EEG recording.

We sequentially connect Electro-Cap and referents to three different amplifiers and perform independent recording of EEG in eyes closed condition. The duration of recording was longer than 300 seconds.

When we reconnect Electro-Cap and referents from one amplifier to another we do not touch to electrodes on the head and ears.

The total time of out experiment was approximately 20 minutes. This means the functional state of subject remain relatively stable.

Than we remontage the EEG to average referent (very important for time  shift influence measurements), compute the coherence for all three EEG recordings using the same processing parameters and compare them. The duration of time interval for processing was the same for these EEG recording and was equal to 300 seconds.

We do not find any dramatic differences in coherence corresponding to different amplifiers. The small fluctuations can be explaned by amplifiers noise and non-stationarity of EEG.

Mitsar Calibration

The Mitsar system is calibrated at the manufacturer. There is no need to recalibrate the amplifier unless there is a serious problem from damage. The calibration button is so the user can run a test calibration signal to demonstrate that the channels are in fact correct and equal. If these were ever not correct (or equal) then the manufacturer would recalibrate the hardware device. It is blocked so that a user cannot accidentally mess the calibrations up. So in summary the calibration button in the software is pressed and then the button to observe EEG is pressed. Then the test calibration signal is generated and can be recorded. This is a good idea if the case is a medical or legal evaluation so that when the data is presented as evidence there is validation that a microvolt equals a microvolt.

In Part 2 you see how Noah parents learn there are alternatives to Ritalin and other drugs that may be given to their child. Learn about how Neurofeedback and EEG Brain Mapping may be able to help without the use of dangerous pharmaceutical drugs.

Dr. Linden is a Clinical Psychologist and Nationally Certified in Neurofeedback and Biofeedback. He is the director of The Attention Learning Center, which has offices located in San Juan Capistrano, Irvine and Carlsbad, California.

Dr. Linden is a regular contributor to the Journal of Neurotherapy and has been a speaker in many seminars and conferences related to ADD/ADHD and neurotherapy.

The thalamic involvement in the generation of the alpha rhythm is being under-valued when looking at the LORETA images of alpha current source generators. The alpha power may come from the sources that LORETA identifies, but the thalamus is intimately involved in alpha rhythm generation, and this is not part of the LORETA image of the sources.

The polarization within the thalamus sets the base frequency of the alpha, but the cortical rhythm requires a complex multi-layer feedback loop from the thalamus to the cortex, and back to the thalamus. Without the cortex, there is a total disruption of the normal spatio-temporal distribution of the alpha wave’s spike trains within the thalamus, and cortical damage often disturbs coherence due to this mechanism.

The thalamus distributes the alpha posteriorly via specific sensory relays, which have a simple return circuit. Like the white matter relay from the lateral geniculate of the thalamus to the occipital lobe’s primary visual areas, and directly back. This thalamo-cortical-thalamic loop is relatively faster than the loop seen frontally. The frontal return circuitry is not simple, but the descending routes are complex and somewhat circuitous, taking more time, and thus it is common for the frontal lobe’s alpha to be at the slower end of the individual’s alpha frequency range. The frontal lobe has a return path through the striatum.

The five divisions of the frontal-striatal pathways are the motor circuit, the oculomotor circuit (from the frontal eye fields), the dorsolateral prefrontal circuit (cortical gating), lateral orbito-frontal circuit (emotive), and the anterior cingulate circuit (emotional and cognitive flexibility). The striatal-thalamic pathways are divided into two descending pathways which both start from the cortex to the head of the caudate and then the putamen, and then this pathway divides between the globus pallidus and substantia nigra, and then these both go to the thalamus. The thalamo-cortical completion of the circuit projects to both the premotor and motor cortex directly.

Not all circuits are simple thalamus-to-cortex-to-thalamus “echoic” returns to the original source…

A cortico-thalamo-cortical projection system exists which originates from the primary visual cortex, relayed by the lateral posterior nucleus of the thalamus, projecting to the suprasylvian visual area (which is involved in highest levels of visual integration and comprehension). This finding suggests that the thalamus modulates transmission of cortical signals from one cortical area to another… the coherence or “connectivity” of the cortex is not cortical-cortical, but cortical-thalamo-cortical.

With maturation, the cortex provides a stimulatory effect on the alpha frequency, raising it to a slightly faster frequency tuning through feedback to the thalamus, but the basic frequencies of alpha are generated by the reticular nucleus of the thalamus providing acetylcholine to the thalamic nuclei, and by the underlying polarization within the thalamus, which is effected by the NE levels from the brainstem, and by fluctuating DC field strength levels in the brain. The other effects are the thalamo cortical transmission times, and an effect of the cortical-thalamic processing time for any given pathway…. Longer time needed for frontal than posterior circuits.

Crudely stated: The frequencies of alpha are set in the thalamus, and the spatial and temporal distribution of alpha are controlled by the cortex, with rhythmic “initiation” (phase reset) done by the DC system’s “modulatory” influence on the AC rhythms of the EEG.

The thalamus can provide rhythms in the range from 3 to 16, with the common range of 8-12 representing an adult group’s “average”. Hyperpolarization of the thalamus slows the alpha, and hypopolarization speeds it up until it desynchronizes at about 16 Hz, and becomes a low voltage fast EEG.

The addition of some GABA (an inhibitory neurotransmitter) easily acquired with the addition of some alcohol will slow the alpha back into a rhythmic pattern. This basic mechanism is the reason alpha-theta training works so well on the low voltage fast EEGs seen so commonly in alcohol addiction.

LORETA may show a generator in the precuneus/cuneus area for the occipital alpha component, and the posterior cingulate for the parietal component (when alpha modulators are identified with ICA analysis and then source localized)… but these localizations miss the full beauty of the real mechanism’s complexity and especially the primary importance of the thalamus.

The thalamus gates our perceptions into “perceptual packets”, with the “thalamic gate” being open during the negative half-wave (up-side of the waveform), and less open during the positive half wave (the downward going half). Two stimuli presented within 75 to 100 milliseconds of each other will be “perceptually synchronized”, or though of as being instantaneously simultaneous.

The alpha frequency is the perceptual sampling rate… how many perceptual packets are evaluated per unit time, with a better semantic or declarative memory function seen with faster alpha frequencies. This is from the work on IAF (individual alpha frequency) from Professor Dr. Wolfgang Klimesch’s lab in Salzburg Austria, with significant contributions from Drs Michael Doppelmayr and Simon Hanselmayr.

The databases have difficulty characterizing alpha frequency tuning issues, with many identifying too much power at a slower frequency (like 7 Hz)… although the power values would be healthy and normal if alpha were only faster (like 9 Hz)… the databases seldom tell you it is merely 2 Hz slow. The normal alpha coherence values, if the alpha is slowed, are seen as hypercoherence, although they are perfectly normal for alpha. Databases that rely on predetermined band’s peak frequency may miss a shift if it exceeds their defined band, and this will miss the mean frequency if the peak is good but the band width has less faster content than slower content.

Faster alpha may cause similar issues (too much 12-15 Hz power or 12-15 Hz hypercoherence) when it is not “too much” of either that is really wrong, just alpha being too fast.

Thus when there are tuning issues, databases often have difficulty characterizing the core issue of tuning. When a tuning issue is noted, the coherence and power values may be “off” according to the database, when the real values are not really abnormal, just that they are too slow or too fast.

Theoretically, these issues may prove to be an area where Z-score training may have difficulty, flagging red herrings of power and coherence… though this is an empirical question that will be answered with time and experience

I’d like to just throw out there a few other findings that were discovered in a few exploratory investigations while working on some studies with our colleague Alicia Townsend, at the time at Univ. of North Texas. Lexicor funded these projects and now the arrangements are such that I can’t disclose more than was published in the abstracts from our talks at ISNR and AAPB.  I did at least want to point to these very preliminary findings because theoretically they are in concert with your explanations.

First, we explored 10 participants between the ages of 65 and 85 were recruited at the University of North Texas Health Science Center.  Each was diagnosed by the Alzheimer’s Disease Assessment Scale and a medical interview.  The aim of the study was to identify current source density markers in AD.  EEG recording of the eyes closed condition of an AD group was compared to an age-sex matched control group using within-subject multiple t-test procedures. sLORETA difference maps in nine frequency bands were investigated. Interestingly the results showed that there was a significant increase in current source density in the delta and theta bands in the Brodmann Area (BA) 39 of the right temporal lobe and BA 31, the cingulate gyrus respectively.  Additionally there were decreases in alpha in the BA 21 of the right temporal lobe and right inferior parietal lobule (Sherlin, Townsend & Hall, 2006).

This was corroborative previous findings of increased delta and theta and decreased alpha from a single case study of AD I analyzed with Tom Budzynski  (Budzyski, Budzynski, & Sherlin, 2002).  Results varied from previous studies that showed diffuse differences although the temporal lobe slowing is replicated.  We recognized that the proximity of the significant locations to the precuneus and fusiform gyrus which are both important in facial recognition and processing social information.  The precuneus is also involved in episodic memory retrieval and imagery of motor functions. A correlation study found similar patterns with sLORETA.

I believe that future investigation for patterns in different types of dementia (vascular vs. alzheimer’s vs. frontal lobe vs. mild cognitive impairment) may increase our ability to differentially diagnose.

The second study we completed was to examine the relationship between memory loss and brain electrical activity that was not AD diagnosable. Eighty-four participants between the ages of 50 and 85 were recruited for the original study. Participants were administered the Alzheimer’s Disease Assessment Scale – Cognitive (ADAS-Cog), a QEEG, and a clinical interview. The cross spectra was averaged and LORETA correlation maps.  Correlations were computed for each individual’s ADAS-Cog score compared to each voxel (7×7x7 mm) of their baseline sLORETA.

What we found were significant positive correlations between ADAS-Cog scores and frontal and parietal delta activity, and theta activity in the precuneus. Significant negative correlations were found between ADAS-Cog scores and temporal alpha. This corroborated prior findings and further alluded that as our memory continues to become impaired we expect frontal and parietal delta as well as anterior midline theta to increase. And that alpha will decrease as impairment grows (Townsend, Sherlin & Hall, 2006). This is exactly as you reported as expectations in the EEG.

Budzinski, T., Budzinski, H., & Sherlin, L. (2002).  Short and Long Term effects of Audio Visual Stimulation (AVS) on an Alzheimer’s Patient as documented by Quantitative Electroencephalography (QEEG) and Low Resolution Electromagnetic brain Tomography (LORETA) [Abstract].  Journal of Neurotherapy. Vol 6:1.

Sherlin, L. ,Townsend, A., & Hall, J. (2006). LORETA Analysis of Alzheimer’s Disease. [Abstract].  Journal of Neurotherapy. Vol 9:4.

Townsend, A., Sherlin, L., & Hall, J.  (2006).  LORETA and QEEG Correlations with the Alzheimer’s Disease Assessment Scale. [Abstract].  Journal of Neurotherapy. Vol 9:4.

The Foundation gives an award to the author(s) of the publication which has
“contributed the most to furthering the field of neurofeedback” during the
past year. Past recipients have included Drs Rob Coben, John Gruzelier, as
well as Johan Levesque and Mario Beauregard.

This year the Foundation has chosen Professor Dr. Juri Kropotov as recipient
of this years award, based on his book and the body of work Juri has
contributed over the years.

This award selection was announced recently at the EEG Spectrum Clinical
Interchange Conference in Los Angeles.  The award includes a gorgeous plaque
as well as an honorarium.

We salute both the Foundation for helping promote the fiend of NF, as well
as all the award recipients for their publications and the substantial
contributions they all have given to our field.

Our organization needs to provide information regarding the types of training/treatment that has been proven  over and over to help clients that have severe impediments to their lives.  If you feel similarly and would like to either sign this letter or write your own, it may cause some movement in APA and the Monitor to recognize the services we provide.

Merlyn Hurd PhD;BCIAC/EEG Fellow
Editor of NeuroConnections the ISNR/AAPB Neurofeedback division

Letter to APA regarding qEEG – March 09 2009

James H Bray PhD, President APA
Rhea K. Farberman, Executive Editor Monitor on Psychology
750 First Street, N.E.
Washington, DC 20002-4242

Dear Drs. Bray and Farberman,

Imagine the excitement of seeing “Brain Imaging” on the front of the Monitor for the March 2009 edition.  Finally, the APA is writing about QEEGs (quantitative electroencephalograms) and the types of work that is being done by thousands of psychologists in the neurofeedback world.

No, the first article is “A pacemaker for your brain?” which reviews the effect of deep brain stimulation (DBS) for the treatment of depression.  The second article “From the Research Lab” informed us about implanting electrodes on the surface of the brain to pinpoint where to surgically remove parts of the brain to correct the disorder from which the client was suffering.  The instrument discussed is fMRI. Perhaps I have not been keeping up with the areas of scope of practice for psychologists but this falls under medical procedures and few psychologists can afford an fMRI machine in their private office.  Yes, many psychologists work with fMRI’s in hospital settings, still it is a small number compared to the number of psychologists/neurofeedback therapists in the United States.

It is time the APA and the Monitor recognize the value of the thousands of psychologists around the world and approximately 3000 in the USA who use non invasive imaging techniques and treatments/training to reduce/eliminate epilepsy, traumatic brain injury; depression; ADHD;  and a host of other disorders.  As you probably know, early on, neurofeedback was, studied and researched in psychology laboratories,and is based on the principles of operant conditioning, which is a major area of development and focus for psychologists (beginning with its founder, psychologist B.F. Skinner) Some of the most seminal research in brain imaging and neurofeedback was and is conducted by psychologists ( for example Barry Sterman, Ph.D whose research led to the validity of neurofeedback, Joel Lubar, Ph.D. and Robert Thatcher, Ph.D.)Also early studies by Steven S. Fox, Ph.D. ( Univ. of Iowa, dept of psychology) with his 1967-1971 EEG/EP operant conditioning studies in cats and humans as well as Peter Rosenfeld, Ph.D. and Alan Rudell, Ph.D. who also published rigorous scientific studies on EEG/EP biofeedback in the late 1960s and early 1970s need to be recognized.

Do not be persuaded by the American Neurolog ical Academy’s viewpoint that QEEGs are not valid.  Recently, in a court case in NY State the QEEG was admitted as meeting Daubert criteria. This is one of many in the United States courts that have admitted QEEG’S as part of the defense.   It submitted thousands of studies using QEEG to verify its validity. The criterion used to locate the studies were computerized analysis of QEEG results. Also do not be persuaded that the Neurofeedback training is not valid, especially, when hundreds of studies have shown excellent outcomes.  These studies have been published in numerous journals.

Furthermore, Carl U. Weitman, Phd., F. BCIA-EEG chaired a liaison task force from 1995-97 between APA and AAPB that resulted in the APA practice directorate and APA council recognizing neurofeedback and QEEG as proficiencies within the scope of psychology; applied psychophysiology and biofeedback.  Among the results, state boards aligned their views with those of the practice directorate. In the interim, the practice code  90876 came to be “Psychophysiological Psychotherapy.
Perhaps you could see to having an edition that looks at Brain Imaging that employs the techniques that psychologists use and the training that they employ guided by those images and interpretations which are against normative databases.

Please log on to isnr. org; aapb.org; skiltopo.com and appliedneuroscience.com to review the studies, member’s lists and activities of these professional organizations.

Thank you for your kind attention to this letter.

Sincerely,

Merlyn Hurd PhD; BCIAC/EEG Fellow
Editor of NeuroConnections.. ISNR/AAPB Neurofeedback division Newsletter
Gerald Gluck Ph.D     Marvin H. Berman Ph.D.       Laurence R. Lewis Ph.D.
Alfred Collins Ph.D.  BCIA-EEG     Anne Ward Steven Ph.D.    David Cantor Ph.D.

Merlyn Hurd PhD; BCIAC/EEG Fellow
88 University Place, 8th Floor
New York, New York 10003
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Tel: 212 807 8690