Chronic Traumatic Encephalopathy(CTE) is associated with repeated head traumas — concussions or sub-concussive hits — that are not allowed to properly heal. It is a progressive degenerative disease found in individuals who have been subjected to multiple concussions and other forms of head injury. A variant of the condition, dementia pugilistica, is primarily associated with boxing. CTE has been most commonly found in professional athletes participating in gridiron football, ice hockey, professional wrestling and other contact sports, who have experienced head trauma, resulting in characteristic degeneration of brain tissue and the accumulation of tau protein. Individuals with Chronic Traumatic Encephalopathy may show symptoms of dementia such as memory loss, aggression, confusion and depression which may appear within months of the trauma or many decades later.

A number of athletes have been affected by the condition with serious consequences. Recently a former NFL lineman committed suicide after serious mental decline. His wife said it started with the nightmares and progressively got worse.

Bob Probert’s brain was examined after his early passing at the age and was found to have CTE (read more here).

A couple of years back with the Chris Benoit tragedy the issue of CTE and it’s effects were put on the map and other athletes began to take notice.

Other players are worried and should be about the possible effects of concussions not only during their playing career but also long after they have retired. CTE is a serious medical condition that should not be taken lightly. A brain injury that goes untreated can have serious long term consequences. We should applaud efforts by the NHL and the NFL to address vicious hits to the head but they need to go farther. Teams need to be proactive in helping to identify possible head injuries.

Often athletes and coaches will push to play even when there may be some lingering effects of a head injury. Athletes have long tried to play through injuries and in certain sports it is almost a crime to take yourself out of a game. Teams and / or the league need to mandate some sort of criteria for athletes they suspect may have head injuries. This can hopefully help prevent or lessen the possibility of CTE. While we may not be able to prevent CTE – following certain procedures (such as a qEEG and ERP) after an “event” may lessen the likelihood of CTE occurring in the first place.

The Pittsburgh Penguins forward Sidney Crosby recently has been out almost three months with post-concussion symptoms.  This is a great loss for hockey fans when you have one of the sports top performers not playing due to a head injury. A recent study shows that more players are losing playing time due to concussions (see the full story on ESPN.com) The NHL is finally addressing this issue. One big step is pulling players out of the game for at least 15 minutes for a concussion test. The new Concussion Removal Protocol is designed to keep players with head injuries out of the game.

It was great to hear that the Pittsburgh Penguins, as part of a new initiative, will offer free baseline concussion testing and educational programs to youth hockey players in the region. “Heads Up Pittsburgh” is a combination effort with the Pittsburgh Penguins Foundation and UPMC Sports Medicine, aimed at making more hockey families aware of concussions in the sport.  Hopefully more teams will follow suit.

more relevant links..

-NHL governors discuss player safety – PEBBLE BEACH, Calif. — NHL Commissioner Gary Bettman said Tuesday that there was not enough data yet to draw conclusions about the link between concussions and a degenerative brain ailment that has been found in four dead hockey players….(full story)

-CTE found in Lew Carpenter’s brain – (full story)

-Head injuries: A growing issue in hockey – ONALASKA, Wis. — Concussions have been a hot topic and a cause for concern in the sport of hockey recently. Head injuries have had serious effects on many NHL players including the face of the league, Sidney Crosby. (full story)

-Report: Derek Boogaard had CTE – NEW YORK — Rangers enforcer Derek Boogaard suffered from chronic traumatic encephalopathy, a degenerative brain ailment related to Alzheimer’s disease that is caused by repeated blows to the head, the New York Times reported…(full story)

- Concussions in Sports from ESPN

- A simple way to curb concussions from SI.com

- Former NFL players sue league over head injuries - Men accuse league of misleading them, failing to take action to reduce head injuries… (full story)

Concussion is a common consequence of trauma to the head in contact sports, estimated by the Centers for Disease Control and Prevention to occur three million times in the United States each year. Among people aged 15 to 24 years, sports are now second only to motor vehicle accidents as the leading cause of traumatic brain injury. While the majority of concussions are self-limited injuries, catastrophic results can occur and the long-term effects of multiple concussions are unknown.

Members of the AAN specialize in treating disorders of the brain and nervous system, and some members have particular interest and experience caring for athletes and are best qualified to develop and disseminate guidelines for managing athletes with sports-related concussion. Based on the clinical experience of these experts, the AAN supports the implementation of policy that supports the following recommendations:

Recommendations

1. Any athlete who is suspected to have suffered a concussion should be removed from participation until he or she is evaluated by a physician with training in the evaluation and management of sports concussions
2. No athlete should be allowed to participate in sports if he or she is still experiencing symptoms from a concussion.
3. Following a concussion, a neurologist or physician with proper training should be consulted prior to clearing the athlete for return to participation.
4. A certified athletic trainer should be present at all sporting events, including practices, where athletes are at risk for concussion.
5. Education efforts should be maximized to improve the understanding of concussion by all athletes, parents, and coaches.

Position Statement History
Approved by the AAN Sports Neurology Section, Practice Committee, and Board of Directors
October 2010 (AAN Policy 2010-36).

ISNR invites you to their 18th Annual Conference for Health Professionals, Education Professionals, Researchers & Students. This conference offers workshops by the leading clinicians and researchers in the field of neuroscience. There will be many workshops and keynote talks on clinical as well as theoretical applications in the neuroscience field.

Letter from the Conference Chair:

It is with great pleasure that I welcome you to an ISNR conference for the third year as the conference chair. For this 18th Annual International Conference of the International Society for Neurofeedback and Research I am delighted to host you in Denver, Colorado, one of the few cities in history that was not built on a road, railroad, lake, navigable river or body of water when it was founded. It just happened to be where the first few flakes of gold were found in 1858. ISNR, like Denver, has grown from golden ideas and holds a bright and rich future.  With this spirit I invite you to join in a collective reflection on what our field has accomplished during these past 18 years, and on the scholarly challenges before us.

In addition to the parallel oral presentations, panel sessions, and workshops, here are a few highlights of the plenary sessions:

• Keynote Speaker- Norman Doidge, MD, NY Times best-selling author, will present “The Brain That Changes Itself: The Neuroplasticity Revolution and Film Clips of People Undergoing Plastic Change”
• Keynote Speaker- Alvaro Pascual-Leone, MD, PhD- “Multimodal Brain Imaging: Combining Brain Stimulation and Functional Neuroimaging to Understand A Changing Brain”
• Keynote Speaker- Jonathan Marks, MA, BCL- “Beyond Neurotherapy: The Ethics of National Security Neuroscience”

Invited Speakers:

• Dirk DeRidder, MD, PhD – “Alcohol Addiction: A Clinical Pathophysiological Approach”
• Matthew Nock, PhD – “Single-Case Experimental Design: A Valuable Method for Evaluating Neurofeedback in Clinical Practice”
• Hartmut Heinrich, PhD – “Theta / Beta and SCP Training in Children with Attention-Deficit/Hyperactivity Disorder: Behavioral and Neurophysiological Results from a Randomized Controlled Trial”
• Michael Schmidt, PhD – “Nutrient Modifiers of Neuroplasticity and Performance and the Exploration of Novel QEEG Assessment Metrics”
• Donald Cooper, PhD – “Single Cell Memory: How individual Neurons Route and Store Temporary Information to Maintain Attention”
• Paul Rapp, PhD – “Could Neurofeedback Reconstruct Synchronous Networks Lost Following Traumatic Brain Injury?”
• Jason Soss, MD- ” Neural Network Mapping”

As in our previous conferences, you can expect the opportunities to network with a diversity of colleagues from a variety of institutions. On Wednesday, there will the ISNR golf tournament with a portion of the proceeds going to the INSR Research Foundation. The tournament and Wednesday pre-conference workshops will be followed by an evening reception and our now traditional special panel Neurofeedback: The Past, Present and Future from the “Pioneering Women’s Perspective” featuring Genie Bodenhamer-Davis, PhD, Judith Lubar, MSW, and Lynda Thompson, PhD.

On Thursday evening, there will be a reception during the poster presentations and a first time evening plenary session. Our conference wouldn’t be complete without a Saturday evening presentation of honors, dinner and entertainment this year by Swing Essence, where attendees will enjoy conversation and dining with live jazz that you would expect in the finest clubs, featuring a jazz-inspired rhythm section, and accomplished instrumentalists.

During the past few years, the ISNR conference has achieved steady growth as evident from the support received from professionals, academia and industry. I would like to express sincere thanks to all the presenters and the members of the conference committee that has made this event a success. Also I would like to thank Deymed Diagnostic (Platinum), BrainMaster (Gold) and Nova Tech EEG, Thought Technology and Stens Corporation (Silver) for their sponsorship of the conference. Because of all of your efforts, the conference program is very rich with exciting papers and events.

Finally, I hope that you will find the presentations and discussions to be a valuable resource in your professional, research, and educational activities whether you are a student, academic, researcher, or a practicing professional. I encourage you to take part in this international conference, and I very much look forward to welcoming you personally to Denver in September!

Leslie Sherlin, PhD
2010 Conference Chair

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.

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.

Whenever a client presents with the question of dementia, all other forms of
dementia need to be ruled out before you are left with the diagnosis of AD.
There are many EEG signatures of various forms of dementia, all of which are
helpful in evaluating a client’s presentation of dementia.

Done by experts in EEG in dementia, the EEG and qEEG may be of substantial
additive value in the differential diagnosis puzzle that all cases of
dementia represent clinically.

One EEG pattern seen in dementia is the presence of periodic triphasic
slowing in the EEG, which is actually diagnostic of subacute sclerosing
panencephalitis (SSPE). SSPE is a “spongiform encephalopathy” where the
brain becomes like “Swiss cheese”, with holes scattered throughout. This
periodic triphasic finding is differentiated from MULTIFOCAL triphasics
which are diagnostic of Crutzfeld-Jacob Syndrome (CJD), which in lay terms
is a form of mad cow disease in humans.

Other helpful EEG signatures include PAFA (periodic anterior fast activity)
which is seen in many with Pick’s disease (a fronto-temporal dementia),
FIRDA (frontal intermittent rhythmic delta activity) or in children OIRDA
(an occipital variant), and also diffuse slowing patterns are all reported
in those with hypoxic/anoxic encephalopathies… as well as the rather
differentiation of multi-infarct dementia (MID) versus AD, where the
difference is seen in coherence, which in AD is seen as anterior posterior
hypocoherence, and from MID, which is seen as fronto-temporal hypocoherence.

This doesn’t speak to more common dementias where non-specific slowing is
seen, like Korsakov’s Syndrome, and Binswanger’s Disease, and some
interesting ones that have more specific EEG signatures, like atypical
frontal and/or temporal Status Epilepticus, which in EEG terms may be seen
as PLEDS (periodic lateralized epileptiform discharges) which is also common
in chronic alcohol related presentation of an “acute dementia”.

The progressive slowing of the alpha peak and increased slower content may
be seen in normo-tensive hydrocephalus, which is a reversible dementia.
This is reversed with the simple surgical placement of a V-P shunt
(ventricular-periteneal) which drains the cerebrospinal fluid accumulation
into the abdominal cavity where it is absorbed.

One other EEG finding that has a virtually diagnostic EEG signature is a
hepatic encephalopathy, where the classic EEG pattern was called a “liver
wave”. This is a triphasic slow wave, with an anterior-to-posterior phase
lead of 100-150 milliseconds. The reason I said “virtually” is that some
with less experience have mistaken triphasic slowing s from anoxia/hypoxia,
and the previously noted periodic and multifocal forms of triphasic slowing,
but this doesn?t have the phase change anterior-posteriorly seen with the
hepatic related findings.

Some point to qEEG measures of “theta” correlating with more severe AD in
the older qEEG literature, but it is really slowed alpha that shows up as
theta in broad band databases… see the work on AD by Brain Resource
Company (BRC)… increased delta with advanced severity, also with decreased
faster activity, and most importantly slowing of the alpha peak which is
more severe with advancing AD.

The EEG is very useful in dementia, but only in the hands of those expert
enough to have seen these patterns in the clinical EEG in full detail.

Jay