A Monthly Summary of News and Events
Vol. 2 No. 9 - October 1999
This newsletter is sponsored by EEG Spectrum International, Inc.,
a leader in providing clinical service and training professionals.
Past issues are available at www.eegspectrum.com/newsletter/
Information on how to subscribe or cancel a subscription appear at the end.
The opinions related in this newsletter reflect those of the author only.
Copyright (C) 1999 by EEG Spectrum International, Inc. All rights reserved.
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Society for Neuronal Regulation Conference Highlights
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Does generating a QEEG profile of a client improve one's neurofeedback training and subsequent outcome? Ah, there's the rub... now what is the question.
Except for notable exceptions, this year's SNR conference (held in Myrtle Beach Sep 30-Oct 3) was centered around the use of QEEG in neurofeedback training. Underlying QEEG assessment is the presumption that the goal of neurofeedback training is EEG normalization, i.e., restoring EEG (baseline) levels to a normative range. Some practitioners would disagree: neurofeedback training improves function by challenging the neuroregulatory system but without permanently altering baseline levels. Who is right?
In EEG normalization, one identifies whether an individual exhibits a deficit or surplus of activity in a frequency band (be it in amplitude, coherence or other spectral parameter) by comparing his or her topographic EEG against a normative database. Deviant spectral activity is "targetted" for training; too much beta in the right temporal lobe -- down-train beta at T4; too little alpha frontally, up-train alpha at that location. But I would argue that such a mapping between QEEG and neurofeedback protocol ignores the history (and success) of SMR training.
Until recently, most SMR training was performed almost entirely above the motor strip. This was not because motor functions were deviant or targetted, but because training the sensorimotor rhythm strongly impacted the regulatory system of the thalamocortical system -- a la the "neuroregulatory challenge" model. SMR training on the motor strip improved attention, memory, pain perception, increased cortical stability, and other forms of function across the entire neurocognitive domain. Training was performed in order to restore cortical integrity through challenge of a governing system, whereas normalization assumes direct changes in spectral activity improve behavioral and cognitive function. Which is correct (or how to reconcile the two) must await a future issue of this newsletter. For now, I turn back to the conference:
E. Roy John presented the keynote address, "QEEG and the Neurophysiology of Consciousness". John is currently working with anesthesiologists in Bean-town and Europe in order to identify QEEG correlates of consciousness: what emerges in the EEG when consciousness is lost and then found again. Notable changes were observed across the head in the theta range (3.5 Hz) using Low Resolution Electrical Tomography (LORETA); however this was not the only frequency range where changes were observed. John also describes some of the Tucson conference work (Penrose, Chalmers, etc) on consciousness, such as wave-function collapse and and the possible role played by microtubules in consciousness, ideas generated primarily out of quantum mechanics (see Toward a Science of Consciousness: The First Tucson Discussions and Debates for more info along these lines).
Barry Sterman reported covariance profiles (covariance being a time-series analysis similar to coherence) that distinguish anxiety from depression from head injury. Autism also presents a unique pattern in the QEEG. The future DSM will be EEG-based, so he quips.
Robert Gurnee argued against uptraining beta in ADD because theta is the primary problem with ADD and increasing beta can be potentially harmful given the reported correlation of elevated Beta with anxiety, alcoholism, and bipolar disorder. Conclusions such as these underlies the theoretical split in the practice of neurofeedback between those using QEEG assessment and those who don't.
Bob Thatcher reviewed the scientific foundations of EEG coherence with emphasis on the relations between EEG coherence and neural network dynamics. Using EEG coherence and fMRI measurements, he described an approach of quantifying the integrity of cortical networks, with obvious implications for assessing head injury, Alzheimer's, and other neurodegenerative diseases.
The most rousing session at SNR was the case review. During this nearly 2-hr session, a single eyes closed data file from a patient was analyzed separately using the John, Thatcher, and SKIL databases. Dualing databases, essentially. Although I may be prejudiced in my opinion (being a partner in the SKIL software development), Barry presented the most thorough review of the subject's recording, one that any clinician could follow from their seats. He began by examining the raw EEG, then the spectral activity to identify the dominant frequency for this individual. Using a number of brain maps he made a solid case about the subject's data: the patient exhibited functional disconnections between anterior and posterior systems in two frequency bands (if I recall correctly) which suggested a head injury.
Lubar interpreted the data similarly using a different database. But the greatest hubbub of the conference came about from the "remontage" mantra by Jay Gunkelman. Using a local spatial averaging technique, he reported the greatest disturbance at right temporal sites, sites that all other "contestants" saw as normal. There are two strong arguments against relying on local average transformations in EEG analysis, however, and they were made at the session that day. One, performing laplacian transformations on EEG activity around the "fringe" (those sites without neighbors on all sides; i.e., Fp1, Fp2, F7, F8, T3, T4, T5, T6, O1, O2) can be noisy and artifactual; and two, unless one can train using such transformations (which is difficult and no one currently does), then one cannot follow any protocol suggested by this approach. Not unlike using metric values to calculate thrust and English values to assess one's orbital coordinates over Mars....
After four days of presentations, workshops, and mild disagreements, we did as all scientists do at a good conference: we adjourned to the hottub.
For more information including presentation abstracts, see http://www.snr-jnt.org/NewsPlus/99-sched.htm
Event-Related Desynchronization
by G. Pfurtscheller & F.H. Lopes da Silva
Clinical Disorders of the Endometrium and Menstrual Cycle
by Iain T. Cameron, Ian S. Fraser, and Stephen K. Smith
The Integrative Neurobiology of Affiliation
by Carol Sue Carter
Alternative Treatments for Fibromyalgia and Chronic Fatigue Syndrome: Insights from Practitioners and Patients
by Mari Skelly, James Lavalle, Andrea Helm, Paul B. Brown
Language and Reading Disabilities
by Alan G. Kamhi, Hugh William Catts
Psychological Effects of Cocaine and Crack Addiction
by Ann Holmes, Carol C. Nadelson, Claire E. Reinburg
Targeting Autism : What We Know, Don't Know and Can Do to Help Young Children With Autism and Related Disorders
by Shirley Cohen
CDC looks at hyperactivity as a public health issue
--The Centers for Disease Control and Prevention and the Department of Education met in Atlanta last month to discuss this mental disorder and what needs to be done in the future. ADHD costs taxpayers $3 billion a year in special education services alone. And 2 to 5 million adults are believed to have ADHD. This disorder is becoming a major health concern, especially as the primary treatment modality, Ritalin, is surrounding by questions about the safety and risks of long-term use.
Infants of depressed mothers show atypical brain activity
--Infants of depressed mothers exhibited reduced left frontal EEG activity relative to right frontal EEG activity. "Our results suggest that maternal depression may alter frontal brain activity which is associated with positive emotions," said Geraldine Dawson, PhD, head of the study. "This effect may be caused by the mother's depression increasing the child's threshold for experiencing emotions such as joy and interest."
Reading, Writing-- And Ritalin
--Ritalin, a drug so similar to cocaine "it takes a chemist to tell the difference." A 1995 Archives of General Psychiatry report states: "Cocaine, which is one of the most reinforcing and addicting of the abused drugs, has pharmacological actions that are very similar to those of methylphenidate, which is now the most commonly prescribed psychotropic medicine for children in the U.S."
NIH consensus conference: Rehabilitation of persons with TBI.
--The focus of this conference was the evaluation of rehabilitative measures for the cognitive and behavioral consequences of traumatic brain injury (TBI). Approximately 1 in 1000 persons has suffered or is currently suffering from a traumatic brain injury. TBI results in 52,000 annual deaths and lifelong impairment of physical, cognitive, and psychosocial functioning of 2.5 million to 6.5 million individuals. Mild TBI is significantly underdiagnosed and the likely societal burden is therefore even greater. Evidence supports the use of certain cognitive and behavioral rehabilitation strategies for individuals with TBI. This research needs to be replicated in larger, more definitive clinical trials and, thus, funding for research on TBI needs to be increased.
Management of PTSD: diagnostic and therapeutic issues.
--Posttraumatic stress disorder (PTSD) is not always properly diagnosed due to a high rate of comorbidity, patient denial or minimization, overly high diagnostic thresholds set by clinicians, or failure to take a trauma history. Patients with PTSD may not respond to pharmacotherapy in the same manner, and it is unclear whether this is related to gender, trauma type, or other factors.
Scientists Identify Brain Chemicals Involved In "Switching On" Cocaine Addiction
--What converts drug use into addiction? Cocaine users may take the drug from several times to several years before they become addicted. However, at a certain point, their use becomes compulsive and they have great difficulty quitting. "It seems that prolonged drug use eventually causes a 'switch' to be thrown in the brain, symbolizing the onset of addiction," says NIDA Director. One component of the switch appears to be the activation of a gene that codes for the production of a protein called delta-FosB. Another involves changes in glutamate receptors in the nucleus accumbens.

Advanced Training Courses | ||
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BETA/SMR Advanced Practicum
with Sue Othmer Topics Covered
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Alpha-Theta Advanced Practicum
Topics Covered
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| 1999 Schedule | ||
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| New York, New York | BETA/SMR Advanced Practicum | 10/12/99 Tue |
| Austin, Texas | Alpha-Theta Advanced Practicum | 11/23/99 Tue |
| Beta-SMR Advanced Practicum Limit = 20 | Alpha-Theta Advanced Practicum Limit = 15 | ||
Conferences for Neurofeedback Clinicians & Researchers | ||
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| CONFERENCE | LOCATION | DATES |
| Winter Brain 2000 | Palm Springs | Feb 4-8th, 2000
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| AAPB 2000 | Denver, CO | March 29-April 2, 2000 |
Andy Hogan Counseling & Neurofeedback Andy Hogan, MA, LCPC 126 Sixth St PO Box 584 Charleston, IL 61920 (217) 348-1086 ahogan@lincweb.com Jean Menendez, A.A. Preey Vitale, Ph.D. Assoc for Human Development P.A. 2400 N University Drive, Suite 208 Pembroke Pines, FL 33024 (954) 437-2034; Fax-436-2004 amenendez@mindspring.com Frank Schlosser, MFT 1107 So. Broadway Santa Maria, CA 93454 (805) 922-2989 Christie M Betz, RN Northwest Neurofeedback 160 Cascade Drive, Suite 215 Burlington, WA 98233 (360) 404-2005; Fax-2008 cbetz@sos.net | W. Roy Evans, M.A. Licensed Psychologist 6381 Osgood Avenue North, Bldg C Stillwater, MN 55082-6118 (651) 439-2301; Fax-7368 psyserv@pressenter.com Karen S Kiefer, MS, DO Greg Maddex, DO S.M.A.R.T. Medical 1111 S. Grand Ave Ste J Diamond Bar, CA 91765 (909) 861-2291; Fax-0194 KKieferDO@aol.com Eva Gumprecht, MSW 96 Sheridan St Jamaica Plain, MA (617) 983-1953; Fax-1954 eva@hillel.harvard.edu Mile Paelen Ungdomshjem Psychologist Sigurd Stubsjoen Leder Vidar Hald Eimerud, Postboks 122 2150 Arnes Norway 63-91-0065 |
On the Road to Damascus
In 1987 D Landsborough published an intriguing paper in the Journal of Neurology, Neurosurgery, and Psychiatry called St Paul and temporal lobe epilepsy. In this paper D argues how Paul, the great Christian missionary of the first century, may have suffered from temporal lobe epilepsy (TLE). Were his ecstatic visions, his conversion on the road to Damascus, the "light from heaven" which went off in his head, a product of TLE? Such investigations need not diminish the religious aspects of such events. In fact probing the neurological origin of religious thought may ultimately require a revision of our scientific thought. Who knows?
Of course it is always difficult to diagnose a patient, especially one who died prior to the invention of the MMPI or MRI, but Paul alludes to his illness in his writings and from this sparse evidence we may presume something about his life and his condition. Paul describes an estatic personal experience in his letter to the Church in Corinth in which he felt "caught up to paradise." He was "caught up to the third heaven. In the body or out of the body? That I do not know... and (here he) heard sacred secrets which no human lips can repeat" (Moffatt Translation). A sense of unreality in relation to one's body in space and a dreamy state of auditory hallucinations reminded Landsborough of experiences related by his TLE patients. Paul also complained about a "thorn in the flesh" -- perhaps a metaphor for an infirmity which periodically racked him such as convulsions.
Landsborough took particular interest in Paul's letter to Galatians. "(I)t was because of an illness... that I preached the gospel to you (the Galatians) on my former visit". Paul was impressed that these people did not "spurn" or "reject" him -- a translation of the literal verb "to spit out at". As Landsborough states, "Epilepsy was sometimes called morbus qui sputatur -- spitting was the superstitutious reaction of a witness to an attack of epilepsy" Thus reaching across the years as if it were yesterday a possibly spitting audience becomes a diagnosis of convulsions.
But other parallels exist between Paul and TLE patients. Hyperreligiosity is not uncommon in these patients. Religious conversion following ecstatic auras has been documented in at least six patients (Dewhurst & Beard, 1970). Perhaps much of our religious and mystical imagery comes about from limbic (self-referential) contents temporarily dominating cortical (more rationale) processes. We may never know what exactly transpired on that road to Damascus, but we do know that it changed the course of the world, eventually transforming a backwater Galilean cult into the most dominant force in history. But what interests the scientist part of me, this experience probably had a neurological origin, one when given the right circumstances could be replicated... Hmmm.
Which is not to say that on that dusty highway Paul experienced something our science can explain.
DK
More info: Landsborough (1987). St Paul and temporal lobe epilepsy. J Neurol Neurosurg Psychiatry, 50, 659-64. -- http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query?uid=3302109&form=6