This may not surprise too many old-time NF practitioners, except that it is now being proven with well done studies in the traditional neuroscience literature!  Neurofeedback can induce changes in brain plasticity!

Jay

First Direct Evidence of Neuroplastic Changes Following Brainwave Training

ScienceDaily (Mar. 12, 2010) — Significant changes in brain plasticity have been observed following alpha brainwave training.

A pioneering collaboration between two laboratories from the University of London has provided the first evidence of neuroplastic changes occurring directly after natural brainwave training. Researchers from Goldsmiths and the Institute of Neurology have demonstrated that half an hour of voluntary control of brain rhythms is sufficient to induce a lasting shift in cortical excitability and intracortical function.

Remarkably, these after-effects are comparable in magnitude to those observed following interventions with artificial forms of brain stimulation involving magnetic or electrical pulses. The novel finding may have important implications for future non-pharmacological therapies of the brain and calls for a serious re-examination and stronger backing of research on neurofeedback, a technique which may be promising tool to modulate cerebral plasticity in a safe, painless, and natural way.

Continued at http://www.sciencedaily.com/releases/2010/03/100310114936.htm

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.

We are honored to welcome several high-profile speakers, including:

• Personalized Medicine in the Age of Technology - Vilayanur S. Ramachandran, MD, PhD; Director of the Center for Brain and Cognition and Professor with the Psychology Department and Neurosciences Program at the University of California, San Diego, and Adjunct Professor of Biology at the Salk Institute

• Regeneration and Stress at Work: Strategies for Improved Employee Health - Tores Theorell, MD, PhD; Professor Emeritus at the University of Stockholm, Sweden

• An Overview of Mind Body Healing - C. Norman Shealy, MD, PhD; founder of the American Holistic Medical Association, and past president of the International Society for the Study of Subtle Energies and Energy Medicine

• Neurotherapy in the Treatment of Traumatic Brain Injury: A Physiological Hypothesis – Paul Rapp, PhD; Professor in the Department of Military and Emergency Medicine at the Uniformed Services University of the Health Sciences

The group suggested that an assessment tool be used in wartime to determine if a soldier should return to duty. It also recommended improvements to traumatic brain injury research,  identified the barriers to treatment and strategized on the improvements for continuum of care and more resources for families of troops with TBI. The Congressional Briefing was highlighted on front page of MSNBC in an article titled  “Better Brain Trauma Testing Urged for Troops”.

]]> http://qeegsupport.com/congressional-briefing-on-tbi-for-wounded-soldiers/feed/ 0 http://qeegsupport.com/200/ http://qeegsupport.com/200/#comments Thu, 12 Mar 2009 15:54:46 +0000 Brian Milstead http://qeegsupport.com/?p=200 This letter has been sent to the American Psychological Association because they have for so long seemly ignored a growing number of psychologists who provide neurofeedback and QEEGs to people who have many disorders , often, disorders that were”incurable”.

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
133526162
NYState Lic 7301
Tel: 212 807 8690

The participants of the International Conference on Behavioral Health and Traumatic Brain Injury will be holding a Congressional Briefing hosted by:

Congressman Bill Pascrell and  Congressman Todd Platts

Co-Chairs, Congressional Brain Injury Task Force presenting recommendations to improve the care of our wounded warriors NOW!

In October of 2008, St Joseph’s Regional Medical Center hosted the International Conference on Behavioral Health and Traumatic Brain Injury. 100 doctors, researchers and scientists from around the globe discussed issues facing our wounded warriors, identified the barriers to treatment and strategized on the improvements for continuum of care. This briefing will present their reccomendations.

The meeting will be held @ the Capitol Visitors Center- Congressional Meeting Room South

RSVP – rsvp@susandavis.com

I put two and two together, and figured he had a big likelihood of a subdural hematoma putting pressure on his language and speech motor areas on the left frontal dorso-lateral area. Subdurals are common in elderly individuals who fall and hit their head, and need to be ruled out if there is a recurrent or persistent complaint following TBI. He complained of headaches which were unrelenting, but they had not scanned him even with his returns to their medical plan 2-3 times in the weeks following the fall.

I figured it would be impossible for him to tell the ER what he needed (as CT or MRI to look for the subdural), so I wrote him an e-mail summary of the findings and pertinent history for my mother to print out and take with them. I sent my elderly father and mother off to the ER, and my dad didn’t want to go because he figured he would miss football games. By Sunday noon, he was in the neurosurgeon’s hands, and they removed a LARGE subdural of 150 Ccs. He is now fine, with all his language skills returned. He even caught the late game on the tube.

After the surgical prep my mother called, and I was asked to “call the doctor”, and I rang in on the neurosurgeon’s headset when he had my dad’s head open. It was a pretty routine evacuation of a subdural, but they were very happy to be handed the case on a platter with the e-mail. He said he was surprised at the “diagnosis” done via telephone and gut instinct, but even more by the accuracy of the localization of the subdural to the left dorso-lateral frontal as well as left temporal areas. The subdural was very large, and encompassed the entire area described.

I’ve had enough drama for the holidays. You would think maybe he will stop bugging me to be a doctor now.

Damage is seldom restricted to merely being exclusively either white or gray matter, and mixed findings are seen commonly.  There are studies showing the correlation of quantitative EEG findings with quantitative MRI findings that are instructive in identifying the nature of the effect on the EEG of the different types of damage.

The EEG changes following brain injury are spectrally different between white and gray matter damage, which helps when evaluating the nature of the damage with the EEG.  The white matter is a high speed relay system that innervates the cortex, both with primary sensory input relayed from the thalamus, and with cortical-cortical input via various fasciculi.

When the cortex has decreased innervation, delta content emerges, according to the IFCN’s position paper on the basic mechanisms of cerebral rhythmic EEG**.  Thus, traumatic brain injury resulting in white matter damage is associated with slower spectral increases in the areas cortically where decreased innervation is present.  These slow spectral increases are seen primarily as delta, and may also be seen as a slower band including theta, especially with larger increases in the slow spectra.

White matter also carries signals across the cortex, and from the cortex through subcortical structures to other cortical locations, resulting in the neural network’s “connectivity”.    There has been a small case series showing that in some direct frontal injuries, there is a decrease in correlation from the left to the right frontal lobe, seen as decreased spectral correlation, also referred to as co-modulation (M.B. Sterman and D. Kaiser’s SKIL software).  This is identical to the changes seen with damage to the anterior portions of the corpus callosum following surgery.  This data was presented by Dr. Sterman, and published by the Journal of Neurotherapy as a technical paper describing their co-modulation metric.

Coherence changes may also be seen with head injury, with both hypercoherence and Hypocoherence reported, depending on the nature of the specific case’s damage.  Isolated areas may become hypercoherent due to the lack of input, though separated areas will be hypocoherent due to the damage to their connective network.

Damage may be seen in gray matter, which is highly “plastic”, unlike white matter, where damage persists.  The neural plasticity allows for regeneration of the cortical gray matter following injury, so the spectral changes associated with gray matter damage may change over time, from the more acute stages, through a transition phase into a static phase, which may allow for re-integration into functional relationships with neural network activity.

The immediate changes seen spectrally with gray matter injury is a decrease in the function of the thalmo-cortical neural network activity, seen spectrally as decreased alpha and beta, as well as decreased gamma in the affected gray matter.  These changes last for the period of the healing, commonly seen across a period from 6 months to a year.

As the gray matter heals, but is not integrated into the neural network function, the idling rhythm in alpha may return and even be seen as an excessive value in database comparisons, since the cortical area is not “working”.  The beta and gamma remain low during this phase, since they are not seen at normal levels in the idled cortical areas.  Beta is generated in local gray matter network activity, and gamma is seen in functionally bound and active networks only.

Once the neural network of the local gray matter is re-integrated into the functional processing, the alpha will then be reduced, and the faster activity seen associated with local function will also be seen as returning to more normal levels.  This may not happen spontaneously, and may require specific interventions, such as neurofeedback, physical therapy, and/or various cognitive-behavioral interventions.

The work of Dr. Kirtley Thornton showed that the gamma and beta remain low, even when the alpha return has occurred.  These faster patterns returned following successful clinical therapy to re-integrate the neural tissue into the functional neural network of the cortical gray matter and white matter.

Some software provides multivariate discriminant analysis, differentiating normal controls from mild traumatic brain injured clients.  These were collected retrospectively, with clients in a specific state of the dynamically changing gray matter’s plasticity, within a 9 month range in one product that is commercially available.  Their prospective use clinically, like all other classification systems, provide false positive and false negative results (type 1 and type 2 errors).

When used indiscriminately, discriminants provide a significant “red herring” problem clinically.  They are not appropriately used as a screening test for individuals, but rather they are only appropriate when used to answer a specific clinical question: “Has my client who has had an actual head injury actually suffered a brain injury?”

I personally do not find them useful clinically, since they do not provide a full evaluation of a client’s brain’s specific injury, and have an unacceptable false negative rate in know head injured clients.  The dismissal of clinically significant findings by the relatively blind use of a head trauma discriminant would tell 20%-30% of those who have had a real brain injury that they are “normal”.  This is not acceptable in the real world when a better clinical judgment would be provided by a careful analysis of the EEG and qEEG by experts in this specific application area.  We have also found a 50% false positive rate when applied to a general clinical population (though this is not the intended use of the discriminant).

The neurological professional groups are divided on the use of traumatic brain injury discriminant classification, with the American Academy of Neurology (AAN) refusing to accept discriminant use clinically, but the 1994 position paper of AMEEGA, published in EEG and Clinical Neurophysiology, provides for the clinical acceptability of the technique in the hands of experts.  ECNS (EEG and Clinical Neuroscience Society)  has reiterated the AMEEGA position paper, and the AAN position paper has had specific responses to it from those who use discriminants.

I find the detailed evaluation of the client’s EEG and qEEG, and an understanding of the dynamics of the brain’s response to trauma, provide a superior working understanding of the client’s specific injury.  This is far superior compared with a simplistic sorting into classifications of “normal” or “TBI” by software that admittedly misses 20% of the actual cases of brain injury and 50% of other clinical cases would be classified positive for brain injury in the absence of any history of head injury in an open clinical series.

Therapeutic intervention is not specified by TBI discriminants, nor is it reasonably possible to customize a therapeutic approach using discriminants due to their sensitivity to artifact.  By contrast, the EEG and qEEG data can be used for both understanding the brain injury, as well as to help the clinician customize a therapeutic approach to the specific neural network areas injured traumatically.

**   M. Steriade, P. Gloor, R.R. Llinas, F.H. Lopes da Silva, and M.M. Mesulam (1990)
Report of IFCN Committee on Basic Mechanisms:  Basic mechanisms of Cerebral Rhythmic Activities,
Electroencephalography and Clinical Neurophysiology; 1990, 76: 481-508

References:

Nuwer, M, et al, Routine and Quantitative EEG in Mild Traumatic Brain Injury; Clinical Neurophysiology, 116 (2005) 2001-2025

Thatcher, R.W., Camacho, M,, Salazar, A, Linden, C., Biver, C. and Clarke, L.: Quantitative MRI of Gray-White Matter Distribution in Traumatic Brain Injury. Journal of Neurotrauma, Volume 14, No. 1, 1-14, 1997

Thatcher, R.W., Moore, N, John, E.R., et al.: QEEG and Traumatic Brain Injury: Rebuttal of the American Academy of Neurology 1997. A Report by the EEG and Clinical Neuroscience Society, Clinical Electroencephalography, 30(3): 94-98, 1999