Additional comments on Marijuana, Medical Marijuana, and Amotivation Syndrome

One of the most under-reported uses of EEG neurofeedback is its applications related to marijuana. 

Neurofeedback tends to spontaneously diminish marijuana use.  I and other clinicians have unexpectedly observed over the years that people who come for ADHD treatment and have been using marijuana regularly and heavily tend to stop using it. 

This surprising shift away from marijuana use is not usually an original goal of the patient (to say the least!) and has not been directly addressed during the treatment.  It just seems that people lose interest in using marijuana when their brains are working better, their minds are clearer.

I assume that the well-known "amotivation syndrome" of marijuana dependence  thus responds to EEG Neurofeedback indirectly through two mechanisms, re-turning executive function and refining self-regard, while generally increasing brain efficiency and self-regulatory capacity.

Medical Marijuana

Under federal law (the Controlled Substances Act of 1970) marijuana use for any purpose is illegal. The federal law has not stopped a number of states from enacting medical marijuana legislation. California was one of the first.

On November 5, 1996, the people of California passed Proposition 215. Through this Initiative Measure, Section 11362.5 was added to the Health & Safety Code, and is also known as the Compassionate Use Act of 1996. The purposes of the Act include, in part:

"...To ensure that seriously ill Californians have the right to obtain and use marijuana for medical purposes where the medical use is deemed appropriate and has been recommended by a physician who has determined that the person's health would benefit from the use of marijuana in the treatment of cancer, anorexia, AIDS, chronic pain, spasticity, glaucoma, arthritis, migraine, or any other illness for which marijuana provides relief..."

Despite conflict with federal law, the Medical Board of California positively sanctions medical marijuana as " an emerging treatment modality."

COMMENT: It seems to me, however, that most of the indications for medical marijuana--other than appetite stimulation and glaucoma--usually respond to neurofeedback. 

My opinion is that, for those suffering the more extreme conditions of pain, spasticity, sleep disorder and chemotherapy side-effects, most people would do well to consider neurofeedback and the  powerful LENS system before turning to medical marijuana.

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HEAD INJURY--Often Forgotten and Too Often Dismissed

Head Injuries are a common cause of many patients' problems with attention, concentration, ability to  plan  efficiently and carry out their plans.  Recent work also suggests that a substantial number of substance abusers may have had head injuries before their drug and alcohol use got out of control.  Yet, a significant number of those patients have "forgotten" their accident of injury (see Dr. Daniel Amen's many books or his web site BrainPlace.com for some helpful examples). Patients with significant lingering problems in functioning often have to be asked repeatedly whether they have had a concussion or head injury.

And it is common for patients who suffered a sharp blow to the head to have temporary impairment of consciousness or confusion--yet even those with significant problems who have been medically checked out are often dismissed because a clinical neurological examination or MRI can came out "normal" (an MRI can only reveal the anatomical disruption, not the kind of disruption that happens at the microscopic level where brain cells function--it takes a special examination of brain function such as a SPECT or PET brain scan to such injuries).  Careful neuropsychological testing would reveal cognitive impairments, but these tests require hours of examination by a specialized psychologist. (Incidentally, at our office, we have a standardized computer-based cognitive screening battery that takes an hour to complete that can document impairments in several spheres of mental functioning).

Concussions with transient loss of consciousness may be associated with an absence of memory for the injury and even a few moments before ("retrograde amnesia").  But the phenomenon of underplaying the importance of, and forgetting, head injuries seems to be a separate issue.

Len Ochs, PhD, who devised the LENS neurofeedback system, has a theory that right after minor brain injuries and other "insults" the brain sort of seals itself off--builds an inhibition network--as a self-protective device.  An analogy would be "muscle bracing" after a physical injury.  We know empirically that LENS neurofeedback is remarkably effective for reversing cognitive effects of so-called "minor" head injury (and see Stephen Larsen's book, The Healing Power of Neurofeedback for examples of recovery from more substantial injuries and stroke).

On January 30, 2008 , the Wall Street Journal ran a piece about the serious effects of long-forgotten injuries entitled, "Studies Cite Head Injuries As Factor in Some Social Ills", discussing new research indicating that hidden traumatic brain injuries can cause social or educational failure, such as alcoholism or homelessness.  Two quotes from the article highlight the significance of this issue:

• "Unidentified traumatic brain injury is an unrecognized major source of social and vocational failure," says Wayne A. Gordon, director of the Brain Injury Research Center at Mount Sinai School of Medicine in New York, where much of the research is being done. 
• In 2006, Mount Sinai's Dr. Gordon began to work with Common Ground, a New York nonprofit that builds housing for the homeless. About 70% of 100 homeless people they tested came out in the 10th percentile or lower for memory, language or attention, says the group's director of psychiatric services, Jennifer Highley. Questioning uncovered that 82% had a significant blow to the head prior to becoming homeless, usually from severe parental abuse during childhood.

Definition of Neurofeedback

Adopted by the International Society for Neurofeedback & Research, 2009

Like other forms of biofeedback, NFT uses monitoring devices to provide moment-to-moment information to an individual on the state of their physiological functioning. The characteristic that distinguishes NFT from other biofeedback is a focus on the central nervous system and the brain. Neurofeedback training (NFT) has its foundations in basic and applied neuroscience as well as data-based clinical practice. It takes into account behavioral, cognitive, and subjective aspects as well as brain activity. Thus, it meets the American Psychological Association's definition of an evidence-based intervention since NFT is "...the integration of the best available research with clinical expertise in the context of patient characteristics, culture, and preference."

NFT is preceded by an objective assessment of brain activity and psychological status. During training, sensors are placed on the scalp and then connected to sensitive electronics and computer software that detect, amplify, and record specific brain activity. Resulting information is fed back to the trainee virtually instantaneously with the conceptual understanding that changes in the feedback signal indicate whether or not the trainee's brain activity is within the designated range. Based on this feedback, various principles of learning, and practitioner guidance, changes in brain patterns occur and are associated with positive changes in physical, emotional, and cognitive states. Often the trainee is not consciously aware of the mechanisms by which such changes are accomplished although people routinely acquire a "felt sense" of these positive changes and often are able to access these states outside the feedback session.

NFT does not involve either surgery or medication and is neither painful nor embarassing. When provided by a licensed professional with appropriate training, generally trainees do not experience negative side-effects. Typically trainees find NFT to be an interesting experience. Neurofeedback operates at a brain functional level and transcends the need to classify using existing diagnostic categories. It modulates the brain activity at the level of the neuronal dynamics of excitation and inhibition which underly the characteristic effects that are reported.

NFT has been found to be a successful intervention in modifying seizures, attention, traumatic brain injury, chronic pain, autistic behaviours, headache/migraine, depression, anxiety, addictions, and sleep problems. Also, it has been applied effectively in meeting educational goals such as resolving reading and math disabilities. Moreover, it has been used to help maximize the performance of athletes, artists, and executives. Lasting positive changes have been documented after successful NFT.

Being a self-regulation method, NFT differs from other accepted research-consistent neuro-modulatory approaches such as audio-visual entrainment (AVE) and repetitive transcranial magnetic stimulation (rTMS) that provoke an automatic brain response by presenting a specific signal. Nor is NFT based on deliberate changes in breathing patterns such as respiratory sinus arrhythmia (RSA) that can result in changes in brain waves. At a neuronal level, NFT teaches the brain to modulate excitatory and inhibitory patterns of specific neuronal assemblies and pathways based upon the details of the sensor placement and the feedback algorithms used thereby increasing flexibility and self-regulation of relaxation and activation patterns.

The International Society for Neurofeedback and Research (see www.isnr.org) is the largest group of licensed professionals involved in the practice, teaching, and research of NFT. Some members of ISNR have sought and received certification by the Biofeedback Certification Institute of America (see www.bcia.org). Members of ISNR subscribe to a code of ethics providing an added measure of accountability to the standards of their profession. Additionally, ISNR is committed to supporting new developments by publishing a professional journal and newsmagazine, by producing a well-attended annual conference, and by encouraging large studies of NFT through the ISNR Research Foundation.

This definition was ratified by the ISNR Board of Directors on January 10, 2009

Sleep, Nightmares, and REM-state Problem Solving

November 15, 2009

Recently, I noted that more people were landing on this web site from the keyword "Nightmares" than from EEG Neurofeedback, or ADHD, or marijuana (numbers 2 through 4 in popularity).  Presumably the reason is that neurofeedback and LENS are being recognised as first-line treatment for sleep disorders.  It's clear I must blog more about sleep disturbances, anxiety and nightmares.

In the meantime, I've come across an interesting study reported on the BBC web site (http://news.bbc.co.uk/2/hi/health/8090730.stm) confirming the common wisdom that "sleeping on a problem" can provide creative solutions.  In this UC San Diego study with 77 volunteers, problem solving was improved by 40% if they took a nap and demonstrated REM-stage sleep. The REM sleep was important, compared to dream-less sleep and an equal length awake period.  Lead author Sarah Mednick assumes that dream sleep enhances brain plasticity.  As the BBC reports, "The researchers believe REM sleep allows the brain to form new nerve connections without the interference of other thought pathways that occur when we are awake or in non-dream-state sleep."

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Neural Plasticity and Neurofeedback

March 15, 2010

The neurotransmitters in the brain change rapidly, turning over in as little as 36 hours (that was established early in the 21st century); the structure of nerve connections are altered by mRNA over a 6 week time frame.  Neurofeedback specialists have long speculated that EEG biofeedback training "changes the brain"--called neuroplasticity--and now a very creative and productive group in London has demonstrated such structural change.  Dr. Tomas Ros  with Dr. John Gruzelier and others have just published Endogenous control of waking brain rhythms induces neuroplasticity in humans in the European Journal of Neuroscience.  The same group had demonstrated that surgical skills of opthamologists can be improved with neurofeedback.  Dr. Gruzelier is the researcher who demonstrated dramatic improvement in musical skills in advanced music students with neurofeedback.

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Adult ADHD

April 13, 2010

A recent story by Melinda Beck in the Wall Street Journal was important for disseminating information about Adult ADHD, but disappointing for the absence of any mention of EEG brainwave biofeedback. I wrote to Ms. Beck, "Good article BUT...why no mention of neurofeedback (EEG biofeedback)? By now the professional literature is replete with studies demonstrating that neurofeedback is comparably helpful for ADHD as stimulant medication--and that upon discontinuation the effects tend to hold much more than with medication. I've attached a current bibliography.

"Perhaps you didn't mention it because of the paucity of studies with adult ADHD. To that, I can only assert (weakly) that my clinical experience bears out the studies with childhood ADHD.

"Another interesting question to be studied is the ways in which neurofeedback and medication help different aspects of the condition. (I just reviewed an article for a journal which found that while the overall results were statistically significant and positive for neurofeedback and methylphenidate (Ritalin), methylphenidate was superior on behavioral measures of inattention and hyperactivity, but neurofeedback was superior for control of impulsivity). All such questions are confounded by the problem that what we call ADHD is an undifferentiated cluster of conditions as suggested by the genotype studies."

A current article in the Journal of Attention Disorders, 5, 524-531 studied the functioning of adults who were medicated.  Residual impairments were significant even after stimulant medication--almost all those studied were functioning half as well at work as non-ADHD adults.  To my thinking, this is a powerful argument for the addition of neurofeedback in the treatment program of adults with ADHD.

The article was nicely summarized in a recent post by David Rabiner PhD, in his newsletter, Attention Research Update, as follows.

How effective is medication treatment for adults with ADHD?

One way to answer this question is by looking at the reduction in core ADHD symptoms, i.e., difficulties with attention and hyperactivity-impulsivity, that medication treatment yields. When examined in this manner, it appears that a reduction in core symptoms of about 50% or less is what is generally obtained, although this can vary considerably from one individual to the next. This is a sufficient reduction to have a meaningful impact on daily functioning for many adults with ADHD, although it would also seem likely that significant residual difficulties related to ADHD remain for many.

A good way to get at these residual difficulties - and how impairing adults with ADHD find them to be - would be to examine adults' perception of their functioning in important life areas following ADHD medication treatment. This was done in an article published recently in the Journal of Attention Disorders [Safren et. al., (2010). Life impairments in adults with medication-treated ADHD. Journal of Attention Disorders, 5, 524-531.

Participants were 105 adults diagnosed with ADHD (55 men and 55 women) with an average age of 42, all of whom were being treated with ADHD medication. Participants completed a rating of ADHD symptom severity and were administered a semi-structured interview to assess their quality of life impairments in 4 areas: work life, interpersonal relationships, recreation, and overall life satisfaction. (Note: For adults who were in school rather than working, the work domain focused on their functioning at school.) This interview was administered to participants by a trained clinician who rated the extent to which the adults' functioning in different areas had been impaired during the past week as a result of ADHD symptoms.

- Results -

Impairment was judged to be greatest in the work domain, where the average score across the 105 participants indicated 'moderate impairment'. Overall, 73% of the sample was judged to have moderate impairment at work because of ADHD symptoms (remember, these were symptoms that were evident even though all adults were receiving medication treatment) and 98% were judged to have at least 'mild impairment'.

Interpersonal relations was the domain that received the second highest impairment ratings. Here, 50% of participants were judged to have at least some impairment because of ADHD symptoms. However, on a positive note, that means that half the adults were not felt to be impaired in their interpersonal functioning because of residual ADHD symptoms and only 17% were judged to be significantly impaired because of such symptoms.

Ratings of overall life satisfaction were similar to those found for the interpersonal domain. Fifty-nine percent were judged to have residual ADHD symptoms that compromised their overall life satisfaction but only 5% were judged to have poor overall life satisfaction because of ADHD symptoms.

Impairment from ADHD symptoms was lowest in the recreational domain where only 29% of participants were judged to have at least a moderate level of impairment.

- Summary and Implications -

Results from this study highlight that many adults with ADHD who receive medication treatment continue to experience important functional difficulties, particularly in the work domain. In fact, nearly all experienced at least some impairment at work related to their ADHD symptoms as judged by the assessor. Residual symptoms also compromised interpersonal functioning for many participants, although the impairment in this domain was generally less problematic than in the work domain. While this is discouraging news, it is also important to recognize that a substantial percentage of medication treated adults were not experiencing impairment in these areas from ADHD symptoms.

The implications of these findings are self-evident: for many adults with ADHD, medication treatment alone will not eliminate the difficulties created by their ADHD symptoms and additional interventions to address these difficulties are required. Helping adults with ADHD develop compensatory strategies at work are especially important, as is the need to address relationship difficulties to which ADHD symptoms also contribute.

There are limitations to this study that the authors acknowledge. Most importantly, there was no control group on non-treated adults with ADHD so that impairment rates could be compared for those receiving vs. not receiving medication. The authors also did not control for other psychiatric symptoms in participants, e.g., depression, anxiety, so that the unique contribution of ADHD symptoms to life impairments after controlling for these other factors could be evaluated. Finally, it would have been helpful if the authors provided more specific information about the types of impairments that adults were experiencing at work and in relationships as a result of their ADHD symptoms.

In conclusion, while these findings do not indicate that ADHD medication is not important in the treatment of ADHD - far from it - they do highlight the limitations of such treatment. For these reasons, careful attention should be given to the development of psychosocial treatments for ADHD in adults. Unfortunately, however, research in this area is quite limited, although promising findings have been reported in several studies. In the months ahead, I will try to include reviews of such studies in Attention Research Update.

 

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Placebos, Lucky Charms, and Positive Expectancy

May 5, 2010

A useful summary of placebos in medicine is found in Olivia Judson's New York Times blog May 3.  She defines the placebo effect as, "the improvement in health that some patients experience because of the feeling that they are receiving medical care".  She adds, "the most reliable source of a strong placebo effect appears to be: the doctor. Placebo treatments are more powerful if your doctor believes in them. They are also more powerful if the doctor tells you so. In one study, for example, patients who had just come out of surgery were given a saline infusion, and — whenever they asked for it — the pain killer buprenorphine. However, some patients were told the saline infusion was a powerful painkiller, others that it might be one, while a third group wasn’t told anything. Over the course of three days, those in the “know-nothing” group asked for more buprenorphine than those in the “maybe” group, who in turn asked for more than those told they were getting a real drug."  That article is all the more valuable for the annotated bibliography she places at the end.

Positive expectancy is at the center of the placebo effect.

Consider also THE POWER OF LUCKY CHARMS in April 29 2010 Wall Street Journal by Carl Bialik. A report on a series of studies demonstrating "they really make us perform better." A study to appear next month in the Journal of Psychological Science used golf. Those who were using a "lucky ball" had a 35% improvement sinking the ball on a putting green. Other examples were more persistence in an anagram game and better performance on a memory game by 30% in those wearing a lucky charm. Of course, the lucky charms only worked when it can matter that you believe in your good fortune--they are of no help in the instances of watching a horse race on which one has bet.

UCLA psychiatrists Ian Cook and Andrew Leuchter have done a series of sophisticated studies analyzing EEG brain waves and placebo responses. Also a brain imaging studies review published in 2008 by V. Faria and colleagues concluded that effective placebo treatments exert their effects by engaging neural systems mediating reward expectancy. That is to say, the brain has complex systems wired together that harness the power of positive expectancy.

That's why placebos and lucky charms have measurably real and positive effects on self-regulation.

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Food Additives and Hyperactive Behavior

Scientific evidence is now conclusive that food additives can cause hyperactive behavior.

I say that clearly at the top, so there will be no confusion when I add:

• Food additives do not cause ADHD
• Food additives cause hyperactive behavior in only some children (my guess is that susceptible adults are more likely to suffer restlessness).
• Elimination diets are an effective intervention for some children with hyperactivity problems.

A recent study in the American Journal of Psychiatry (September 2010 by Stevenson, et al) reported specific genes responsible of that hyperactive response.  Details below.

The information is interesting in its own right, of course, but I am taken with how slowly the information has flowed into the mainstream medical community.  I suppose that organized resistance to Benjamin Feingold’s 1975 report comes from the vested interests of food technology companies pushing academic  and practitioner skepticism; established doubt is not easily displaced.

That was certainly true for myself.  I held the position that food additive sensitivities was unproved.  It was only after a few parents were able to convince me that for their child, certainly, hyperactivity diminished when food additives were restricted.  I realized that, as with many other studies, important subgroups were statistically “unnoticeable” in amalgamated group studies.

In light of the new study, I have looked into the medical literature and found the evidence has been growing for years, unrecognized by most. 

A report written for the Center for Science in the Public Interest by Jacobson and Schardt (1999) found on the web reviews 23 double-blind studies and reports that 17 of these studies found evidence that the behavior of some children are negatively affected following consumption of artificial colors or particular foods.

Elimination diets (to remove food coloring and sodium benzoate preservative) gained academic, if not clinical, respectability when a British group published a large placebo controlled study of 3 year olds in 2004 (Bateman et al).  Evidence of behavioral improvement was seen in the children who had elimination diets, whether or not they were clinically diagnosed with ADHD.  The same group (McCann et al) published a follow-up study of different children at ages 8-9 years who consumed a drink with a moderate level of additives or its placebo control.  Once again the conclusion was that the additives provoked hyperactive responses in a subset of the children.

The current study is from the same group (here, Stephens is the lead author).  This time, they studied the genetics of the responders vs. the non-responders in the two prior samples.  They studied single nucleotide proteins (SNPs) related to histamine and found “a link between histamine and ADHD symptoms in the HNMT gene moderating behavioral responses to food additives”. 

The article concludes that these gene abnormalities (polymophisms) impair histamine clearance, and a food challenge causes histamine release—essentially, an allergic response, which affects the histamine receptors known to be in the brain.

To repeat, not all ADHD children had the abnormal gene pattern, and not all of those with the abnormality had diagnosable ADHD; but reliable observation scales demonstrated that those with the abnormality had hyperactive behaviors in response to the food additives.

Here is a list of the substances that provoked hyperactive reactions in the susceptible children:

• Sodium benzoate
• FD&C Yellow No. 6 (sunset yellow)
• D&C Yellow No. 10 (quinoline yellow)
• FD&C Yellow No. 5 (tartrazine)
• FD&C Red No.40 (allura red)

Finally, I add an annoyed editorial comment.  I just read what is otherwise a good, thorough review of treatments for children with ADHD, subtitled “Current Evidence and Practice” in the Journal of Child & Adolescent Psychopharmacology, October 2008 (by Ghuman et al).  It’s a comprehensive review and has no mention of EEG neurofeedback.  Many other less helpful treatments are reviewed and, largely, dismissed (interestingly, only elimination diets for artificial colorings and preservatives are held as effective alternative interventions).  By now, the literature on neurofeedback for ADHD is solid enough that all reports should include it.

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Sports Head Injuries--more concern

Study Finds Student Athletes Without Concussion Symptoms Remain At Risk.
The Indianapolis Star (10/8, Newell) reports that a new study published online this week in the Journal of Neurotrauma has determined that high school football players "may be damaging their brains even if they have not been diagnosed with a concussion." After examining the helmets of 21 Lafayette Jefferson High School players, Purdue researchers discovered that whenever sub-clinical concussions are not recognized, "the athletes are potentially at risk for additional, more serious concussions and other brain illnesses," including early onset Alzheimer's disease, chronic depression, and chronic traumatic encephalopathy.

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Workshop:

Beta-Reset, Gamma Attunement Protocol

with Jaclyn Gisburne PhD

at UCLA

December 9 - 12, 2010

limited enrollment--professionals only

contact tbrod@ucla.edu

Thomas M Brod MD, DFAPA                                           

Associate Clinical Professor, Psychiatry                         

Geffen UCLA School of Medicine

 

Joy Lunt RN, BCIA

CEO, Brain Potential, Inc.

In cooperation with the UCLA Department of Psychiatry and Biobehavioral Science

Present

a Four-Day Workshop for Neurofeedback Practitioners

Beta Reset/Gamma Brainwave Surfing:

How to apply the new Gisburne-Harr paradigm for chronic & neurodegenerative conditions

Jaclyn M. Gisburne, Ph.D. &

Jana C. Harr, BA MRT

• WORKSHOP DATE: December 9-12, 2010

 Thursday - Saturday 9 AM – 4:30 PM ; Sunday 9 AM to 1 PM

1. WORKSHOP LOCATION:  UCLA Semel Institute (Room 28-181 NPIH)

 

Registration & Housing information at the end of this announcement

 

 

1. WORKSHOP DESCRIPTION:

 

Beta Reset is a painless, non-invasive, neurosomatosensory intervention process utilizing EEG neurofeedback technology.  Its paradoxical sequencing, site selection, and frequency bands are intended to interrupt and correct neuronal and non-neuronal dysregulation as read by sensors at the back of the head. Developed over the past four years, the process has shown promise in the neural and physiological correction of cognitive, affective, and physical pathologies.  To date we have observed remarkable outcomes with chronic and neurodegenerative conditions including, but not limited to –

• Neurofibromatosis Type 1
• Normal Pressure Hydrocephalus
• Parkinson’s Disease Levels 1-5
• Multiple Sclerosis
• Scoliosis
• Fibromyalgia
• Chronic Fatigue Syndrome
• Rheumatoid & Osteoarthritis
• Child-onset Polio
• Accident/Injury-induced Pain
• Peripheral Neuropathy
• Barometric Sensitivity
• Issues of Aging – Balance, gait, mobility, incontinence, dementia
• Chemical Induced Issues – “brain fog,” memory loss, numbness, loss of equilibrium and/or feeling
• Stroke
• Anxiety, panic attacks, PTSD
• Depression
• Occular misalignment
• Quinoline Toxicity

 

 

While its applications, limitations, and the understanding of its neurological potentials continue to be explored by individuals and groups specializing in particular disorders, the purpose of this workshop is to both present and teach this process and the paradigm and optimizes outcomes.  In addition several adjunct modalities that produce additional positive outcomes as interventions that interrupt and/or reverse the systemic activities associated with chronic and neurodegenerative disorders will also be taught and practitioner certification will be available. Therapists will learn how to effectively disengage problematic implicit and explicit encoded memories that are often precipitating and/or a hindrance to the treatment and recovery from these and other chronic condition. 

 

This will be a theoretical and experiential workshop with demonstrations and sufficient hands-on practice to ensure participant proficiency by the end of the workshop.  Participants will have time for client and condition specific questions and answers throughout the four days. 

 

We will begin by discussing the role of gamma wave potentials, which naturally emanate from the occipital and parietal regions, and how we surmise its evoked and induced potentials are instrumental in the restoration of more normal frequency distribution throughout the brain.  We will present and discuss several case studies that reflect the resetting activities as evidenced by the significant reduction or alleviation of symptoms.  We will also discuss briefly the role of stress/trauma in the development of pathologies and several adjunct modalities that help the clients resolve these entrenched and often encapsulated experiences.

 

This workshop is designed for experienced EEG neurofeedback users who are open to working with stress and/or trauma event reconciliation with adjunct modalities. Participants are encouraged to bring their laptop systems in order to gain some experiential practice. 

 

1. Main points of workshop.

• The workshop provides an immersion experience of Phase One: Reregulation allowing the participant to both see and experience the efficacy of the Beta Reset paradigm and process
• Common to all chronic and neurodegenerative disorders is neuronal and/or non-neuronal dysregulation
• Beta Reset capitalizes on the brain’s unique and reliable response to novelty, suppressing and rebounding alpha, beta, and gamma frequencies into more regulated state, synchronizing and reregulating the brain globally
• An all inclusive three-phase paradigm will be introduced.  This is a drill-down approach working globally, regionally, and then site-specific. This paradigm provides a comprehensive frame of reference for optimization of traditional modalities and protocols, addressing the neurological, physiological, psychological, behavioral, and social needs of the client/patient. In addition, it provides continuity for client progress and wellness.
• Reviews the gamma wave research literature relevant and consistent with the outcomes of the Beta Reset process.
• Discussion on condition-specific variation of the process, limitations, expectations, and effective management of the Beta Reset process to optimize client outcomes.
• Workshop is structured as a hands-on experience of the Beta Reset process
• Select attendees will participate in pre and post QEEG research data collection to demonstrate process potentials.

 

1. LEARNING OBJECTIVES:

 

• Articulate at least three differences between Beta Reset is and traditional neurofeedback 
• Articulate the rationale for Phase One: Reregulation of the 3-Phase intervention and treatment paradigm
• Describe the uses, role, and limitations of Beta Reset process and gamma wave activities in general
• Describe the role and differences between evoked (phaselocked w/theta) and induced (non-phaselocked) gamma wave functions, and ERP
• Name and describe at least three neurodegenerative disorders (NDD) from a broad spectrum of neurodegenerative disorders and articulate what we surmise are the reasons Beta Reset Process works
• Articulate the difference between fibromyalgia and arthritis based on dynamic, stories, and as observed in Beta Reset Process
• Articulate the six most likely observable outcomes related to the brain’s resetting with Beta Reset Process
• Articulate the site selection & sequencing of the Beta Reset Process intervention protocol
• Articulate the rationale for the use of Beta Reset Process and/or other intervention protocols
•  Articulate 3 factors for determining how and when to transition from intervention to stabilization protocol and which frequency-based protocol is most appropriate
• Gain an understanding on resetting functions of Beta Reset Process, e.g., alpha/beta suppression and rebounding, REM sleep, outcomes

12. Understand role of gamma induction and beta attunement (Beta Reset Process) as an intervention strategy, the "resetting" functions and the role of REM sleep

13. Understand the significance of “stories” and the emergence of trauma-event(s) memories, and introduce research on significance of this “window of opportunity” and reconsolidation of memories

14. Learn what to be aware of if protocol doesn’t work and list at least three psychological factors that might inhibit a client’s progress of recovery

15.  Learn and articulate three types of client “resourcing” and at least two adjunct modalities and their role in resourcing the client

16.  Successfully execute the basics of at least one of the adjunct modalities 

 

• FACULTY INFORMATION: Jaclyn M. Gisburne, Ph.D. & Jana C. Harr, BA MRT

Rocky Mountain NeuroAdvantage

Co-founders, co-developers of Beta Reset Process and 3 Phase Intervention & Treatment Paradigm

 

 

 

1. BIBLIOGRAPHY

 

REFERENCES

 

Axmacher N, Henseler MM, Jensen O, Weinreich I, Elger CE, and J Fell. (2010, February 10). Cross-frequency coupling supports multi-item working memory in the human hippocampus. The Journal of Neuroscience , 2150-2159.

 

Bauer M, Oostenveld R, Peeters M, and P Fries. (2006). Tactile spacial attention enhances gamma-band activity in somatosensory cortex and reduces low-frequency activity in parieto-occipital areas. The Journal of Neuroscience , 26 (2), 490-501.

 

Belmonte MK, Allen G, Beckel-Mitchener A, Boulanger LM, Carper RA, Webb SJ. (2004). Autism and abnormal development of brain connectivity. Journal of Neuroscience 24(42) , 9228-9231.

 

Bibbig A, Traub RD, and MA Whittington. (2002). Long-range synchronization of gamma and beta oscillation and the plasticity of excitory and inhibitory synapses: A network model. Journal of Neurophysiology , 1634-1654.

 

Börgers C, Epstein S, and NJ Kopell. (2005). Background gamma rhythmicity and attention in cortical local circuits: A computational study. PNAS , 102 (19), 7002-7007.

 

Canolty RT, Edwards E, Dalal SS, Soltani M, Nagarajan SS, Kirsch HE, Berger MS, Barbaro NM, and RT Knight. (2006, September 15). High gamma power is phase-locked to theta oscillation in human neocortex. Science , pp. 1626-1628.

 

Compte A, Reig R, Descalzo VF, Harvey MA, Puccini GD, and MV Sanchez-Vives. (2008). Spontaneous high-frequency (10-80 Hz) Oscillations dudring up states in the cerebral cortex in vitro. The Journal of Neuroscience , 28 (51), 13828-13844.

 

Demiralp T, Herrmann CS, Erdal ME, Ergenoglu T, Keskin YH, Ergen M, and H Beydagi. (2007). DRD4 and DAT1 polymorphisms modulate human gamma band responses. Cerebral Cortex , 17, 1007-1019.

 

Dickson CT, Biella G, and M de Curtis. (2000). Evidence for spactial modules mediated by temporal synchonization of carbachol-induced gamma rhythm in medial entorhinal cortex. The Journal of Neuroscience , 20 (20), 7846-7854.

 

Doesburg SM, Roggeveen AB, Kitajo K, and LM Ward. (2008). Large-scale gamma-band phase synchronization and selective attention. Cerebral Cortex , 18, 386-396.

 

Fiebach CJ, Gruber T, and GG Supp. (2005). Neuronal mechanisms of repetition priming in occipitotemporal cortex: Spatiotemporal evidence from functional magnetic resonance imaging and electroencephalography. Journal of Neuroscience , 25 (13), 3414-3422.

 

Fries P, Scheeringa R, Oostenveld R. (2008). Finding Gamma. Neuron 58 , 303-305.

 

Grossman T, Johnson MH, Farroni T, and G Csibra. (2007). Social perception in the infant brain: gamma oscillatory activity in response to eye gaze. SCAN , 2, 284-291.

 

Howard MW, rizzuto DS, Caplan JB, Madsen JR, Lisman J, Aschenbrenner-scheibe R, Schulze-Bonhage A, and MJ Kahana. (2003). Gamma oscillation correlates with working memory load in humans. Cerebral Cortex , 13 (12), 1369-1374.

 

Jokisch D & O Jensen. (2007). Modulation of gamma and alpha activity during working memory task engaging the dorsal and ventral stream. The Journal of Neuroscience , 27 (12), 3244-3251.

 

Kahana, M. (2006). The cognitive correlates of human brain oscillations. the Journal of Neuroscience , 26 (6), 1669-1672.

Kaiser J, H. I. (2005). Hearing lips: Gamma-band activity during audiovisual speech perception. Cerebral Cortex , 15, 646-653.

 

Kaiser J, Heidegger T, Wibral, Altmann CF, and W Lutzenberger. (2008). Distinct gamma-band components reflect the short-term memory maintenance of different sound lateralization angles. Cerebral Cortex , 18, 2286-2295.

 

Kaiser J, Lennert T, and W Lutzenberger. (2007). Dynamics of oscillatory activity during auditory decision making. Cerebral Cortex , 17, 2258-2267.

 

Kaufman J, Csibra G, and MH Johnson. (2005). Oscillatory activity in the infant brain reflects object maintenance. PNAS , 102 (42), 15271-15274.

 

Keil A, Muller MM, Ray WJ, Gruber T, and T Elbert. (1999). Human gamma band activity and perception of a gestalt , 19 (6), 7152-7161.

 

Kobayashi M and A Pascual-Leone. (2003). Transcranial magnetic stimulation in neurology. The Lancet Neurology , 2, 145-156.

 

Landau AN, Esterman M, Robertson LC, Bentin S, and W Prinzmetal. (2007). Different effects of voluntary and involuntary attention on EEG activity in the gamma band. (11986-11990, Ed.) The Journal of Neuroscience , 27 (44).

 

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Luo Q, Mitchell D, Cheng X, Mondillo K, Mccaffrey D, Holroyd T, Carver F, Coppola R, and J Blair. (2009). Visual awareness, emotion, and gamma band synchronization. Cerebral Cortex , 19, 1896-1904.

 

Lutz A, Greischar LL, Rawlings NB, Ricard M, and RJ Davidson. (2004). Long-term meditators self-induce high-amplitude gamma synchrony during mental practice. PNAS , 101 (46), 16369-16373.

Maeda F and A Pascula-Leone. (2003). Transcranial magnetic stimulation studying motor neurophysiology. Psychopharmacology , 168, 359-376.

 

Medendorp WP, Kramer GFI, Jensen O, OOstenveld R, Schoffelen JM, and P Fries. (2007). Oscillatory activity in human parietal and occipital cortex shows hemispheric lateralization and memory effects in a delayed double-step saccade task. Cerebral cortex , 17, 2364-2374.

 

Pavlova M, Lutzenberger W, Sokolov A, and N Birbaumer. (2004). Dissociable cortical processing of recognizable and non-recognizable biological movement: analysing gamma MEG activity. Cerebral Cortex 14 (2) , 181-188.

 

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Van Der Werf J, Jensen O, Fries P, and WP Medendorp. (2008). Gamma-band activity in human posterior parietal cortex encodes the motor goal during delayed prosaccades and antisaccades. The journal of Neuroscience 28(34) , 8397-8405.

 

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Registration Form-- Introduction to Beta Reset: Gisborne & Harr

 

Advanced Registration                $795 (must be received before November 15, 2010)

General Registration                            $995

 

Students                                          $500  (waived for UCLA Dept of Psychiatry trainees)

 

Continuing Education Credit may be available at extra cost.  Please Inquire.

Parking at UCLA, $11 daily (paid at UCLA kiosk)

Make checks payable to               Thomas M Brod, MD

                                                        12304 Santa Monica Blvd #210

                                                        Los Angeles CA 90025  (tel) 310.207-3337

 

Name:­­­­­­­­­­­­­­_______________________________________________________________________________

Address: _____________________________________________________________________________

City, State, Zip: _______________________________________________________________________

Email: ________________________________________________________________________________

Professional Discipine: ________________________________________________________________

(If graduate student, please indicate where) __________________________________________

 

NOTE: Participants are encouraged to bring their own laptop EEG feedback systems in order to gain experiential practice. This is not necessary for admission.

 

For more information,   email:      tbrod@ucla.edu     

Online: http://tbrod.bol.ucla.edu   www.EEGym.com  

 

 

REFUND POLICY: Refunds, less a $75 administrative fee, will be made if cancellation notification is phoned or postmarked seven (7) business days in advance of this program.  Full refunds are made in the event the program must be cancelled. 

Important Disclosure:  Information for all learners: None of the planners or presenters of this program have any relevant financial relationships to disclose.

 

 

Housing Information

 

 

UCLA Guest House.  310.825-2923. They close on Dec 12 but will accept people through Saturday night. Rate is $143-148/nite. UCLA Guest House.  Mention you are coming in for a conference at UCLA. Pleasant, without hotel amenenities.

 

Palomar Hotel  310.475-8711.  They are a 4 Star/4 Diamond hotel in the Klimpton chain (click on the link for pix).  Rate is $159, ask for the UCLA corporate rate.

 

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