Real the full article here – Electroencephalographic Cerebral Dysrhythmic Abnormalities in the Trinity of Nonepileptic General Population, Neuropsychiatric, and Neurobehavioral Disorders

(The Journal of Neuropsychiatry and Clinical Neurosciences 2008; 20:7?22)

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

The two images below show the referential and sequential montage display of an active right temporal-parietal spike and slow wave focus, seen in a child clinically diagnosed with an attachment disorder. There was no history of convulsion, nor any suspicion of the actual underlying pathophysiological basis for the behavioral presentation.

The focus cortical area is normally involved in comprehension of facial expression and body language, as well as the prosodic (emotive) aspects of language. Any disturbance in that cortical area’s function generally has social contextual implications for behavior due to “prosodic blindness”. (see: Van Bloem, L. QEEG in Children with Reactive Attachment Disorder,

Journal of Neurotherapy, 4(4), 2001.

The implications for treatment option with this pathophysiological source for the behavioral presentation which could really only be discovered through the EEG are enormous. The use of an anticonvulsant or an approach with one of the proven efficacious applications of Neurofeedback in treating epilepsy can be used to target the underlying cause, rather than trying to effect some symptomatic control with antipsychotic or antidepressant medications so commonly used in these situations of severe attachment disorder. (see a review of SMR applied to epilepsy by Dr. M. Barry Sterman, Professor Emeritus, UCLA, from 2000 in Clinical Electroencephalography’s special edition on Neurofeedback)

In these images the referential focus is seen associated with the largest waveform, though in the sequential data the 180 degree phase reversal points to the focus.

EEG & Epilepsy - Referential Montage Display

EEG & Epilepsy - Sequential Montage Display

In modern neuroscience centers, the EEG is still the tool of choice in evaluation of convulsive epilepsy, as well as some other non-convulsive forms, such as staring episodes seen in “absence epilepsy” typically as a 3/second spike and wave dominant anteriorly, or temporal lobe epilepsy, which is seen as a “notched” slow wave discharge fronto-temporally.

The EEG can now be processed through algorithms, such as spike dipole localization software, to identify the “seizure focus” cortically, or spectral averaging to look for changes in the underlying EEG rhythmicity due to the disorder.

One of the difficulty with the two later categories is that they are not always identified as forms of epilepsy, and thus can be mis-diagnosed based on behavior alone as some other disorders, including ADD/ADHD in absence epilepsy “spells” where the attentional process is disturbed by the discharge taking segments of time out of the cognitive streaming of perception, or from discharge in sensory areas.  These segments being removed do not have any conscious awareness of the event for the person experiencing the blips missing from their cognitive process, and they will have trouble tracking on-going events, like driving or listening to a speech or lecture.  Imagine missing a few here and there, to tens of seconds from your awareness, and see if you don’t have “attentional deficits”.

The other major areas of misdiagnosis are of a “schizophrenic” or “psychotic” nature.  This occurs when the discharges are frontal or temporal and disturbing local cortical function, and may be seen as a range of presentations from hallucinations or emotional outbursts of rage, or even “fits of laughter” in “Gelastic seizures”.   Temporal Lobe Epilepsy (TLE) is a particularly difficult one to properly diagnose in the absence of the EEG.

The importance of these missed-diagnoses can be quite severe, with the use of medications to treat the symptoms often being contra-indicated by the epilepsy.  One example of this is TLE that is assumed to be psychosis, since antipsychotic medications lower the seizure threshold, and make the person worse, which can then be responded to with more antipsychotics, spiraling the person into a progressively worsened condition.  The use of stimulants in epilepsy is a controversial area, as the effect of stimulants for inattention in known and treated epileptics may be acceptable, though throwing a stimulant at an undiagnosed epileptic can have severe negative consequences.

The real issue is that IF YOU DO NOT LOOK, YOU WILL NOT SEE… and in epilepsy, looking requires the EEG, as the gold standard.

In surgical approaches, the EEG is used to identify whether there are multiple foci, which generally will preclude a good outcome (you remove the brain tissue and the seizures do not change).

I will post some images of the WIDE variety of morphologic presentation that epilepsy can take, so that some understanding of the task of the Electroencephalographer and Epileptologist can be better appreciated by those who think it is straight-forward.

Thanks for your attention to these obscure issues.

Jay

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

General comments:

There is a generally reciprocal effect between alpha and beta, as brain stem stimulation desynchronizes the alpha generators, beta is seen.  During states of under-arousal, this relationship is not seen, as when the subject is alerted, when both alpha and beta increase.

The point is that the arousal level changes the EEG responses expected, as when a stimulant is given to an under-aroused subject, increasing alpha. In a normally aroused subject, stimulants decrease alpha, and in an anxious (low voltage fast EEG variant) subject alpha will not be seen as changed by a stimulant.

Though there is a response stereotype for each medication, there are also individual responses, which vary. Mixtures of medications become too complex to evaluate each individual medication’s contribution, not to speak of synergistic effects not seen with any single medication, which may be seen in polytherapy.

The following pages represent a summary of many articles, papers, reviews and books on medications and the CNS function, and finally nearly 30 years of experience in clinical and research EEG. The difficulty in this area is the definitions of bands varies, the methods of analysis range from visual inspection of the raw EEG to quantitative measures, not all of which are clearly defined… and thus the need for a brief summary which puts this into a concise form for reference.

I will use the following definitions for the EEG bands. Delta is .5-3.5 Hz.; theta is 3.5-7 Hz, with slowing describing activity starting in the delta band, fading out in amplitude through the theta band. Alpha is 7-13 Hz, with “high alpha” being 11-15 or 16 Hz. Beta is from 13 Hz to the high frequency response of the system.

Due to the difficulty in visually detecting many of the changes reported, even small but significant changes can be missed. Don’t expect to “see” every change noted in each patient, or when using only visual inspection.

Marijuana/ Hashish/ THC:

There is increased frontal alpha, with increased frontal interhemispheric hypercoherence and phase synchrony.  These findings are reported in chronic exposures.

Effects on the evoked potentials have been noted as well.

Lysergic acid diethylamide (LSD-25):

The baseline EEG seems to determine the effect, with decreased alpha and increased beta from a normal background.  With slower EEGs, there is an increase in alpha and fast activity. The low voltage fast EEG shows little change in spectral profile with exposure.

The increase in conditioned inhibition seen with lower doses corresponds to the decrease in paroxysmal activity. The stimulant effects of this powerful drug may cause convulsions at higher doses, such as the early government studies. In these studies, milligram doses were supplanted for the microgram recommendations from Switzerland, where the LDS was produced.

PCP, Phencyclidine, or angel dust:

There is a marked increase in slow activity, with paroxysmal activity and extreme voltages noted with increased dosage. Convulsions have been reported.

Barbiturates:

Rhythmic 18 to 26 Hz activity is noted, initially frontally, spreading with time to the entire cortex. With increased dose there is an increase in slowing, with further increases the faster activity is decreased and the slowing predominates, progressing to a decreased voltage and even a recoverable iso-electric pattern, in barbiturate coma.

Morphine/Opiates/Heroin:

Shortly following administration, there is increased alpha, with slowing of alpha during the euphoric high, with increased dose there is increased slowing, and like barbiturates the EEG may go iso-electric. There is an increase in REM sleep noted with opioids.

Alcohol:

Ethanol at higher levels causes slowing to occur, with the depressant effect seen behaviorally.  In the low voltage fast type EEG (seen in anxious, nervous and in many chronic alcoholics and their family members), the initial alcohol exposure causes the sudden occurrence of alpha. With severe chronic alcoholism, there can be an abnormal pattern of periodic lateralized epileptiform discharges (PLEDS) seen with obtundation. This is not true underlying epilepsy, but rather disappears with the treatment of the alcoholism.

Neuroleptics:

“Tranquilizers” such as chlorpromazine, or it’s equivalent, increase the coherence of the EEG and decrease beta, however they increase temporal and frontal sharp morphologic theta transients. There is a reduced alpha blocking with sensory stimulation, likely corresponding to the memory disturbance reported with these medications.

In cases of dopamine receptor hypersensitivity (tardive dyskinesia) there are prolonged bursts of mixed fast/sharp transients and slowing. There is a potentiation of latent epileptiform activity, even with lower doses.

Thioridazine also increases faster activity, accounting for its commonly reported antidepressant effects.

Clozapine, or Clozaril, shows the typical neuroleptic pattern, though with an increase in epileptiform discharges and increasing possibility with duration of medication usage, reaching as high as 30% of patients with epileptogenic EEGs after 3 years of use.

Anxiolytics:

Meprobamate was the first anxiolytic, or anti-anxiety, medication. It decreases alpha and increases beta over 20 Hz, also slightly increasing theta, while not increasing epileptiform activity or paroxysms. The benzodiazapines, like Valium or Ativan also decrease alpha and increase the 20-30 Hz band, with a sinusoidal hyper-rhythmic spindling waveform. Paroxysmal and epileptiform discharges are reduced with these medications. The effect of decreasing neural has been used for its anti-epileptic qualities, especially in cases of status epilepticus, where Intravenous Valium has the apparently “comatose” patient sitting up wondering what has been happening.

Hormones:

Vasopressin, usually in the form of DDAVP (desomopressin acetate), increases the high alpha band.  Cyproterone acetate is an anti-androgen with clinical effects on premenstrual complaints, though the qEEG effects predicted its strong anti-anxiety and mood elevating side effects. The decrease in frontal alpha and increased beta are noted.

Antidepressants:

Imipramine:

This drug produces an increase in slow activity, a decrease in alpha and high alpha, with an increase in the faster beta frequencies in the mid to upper 20 Hz range and up.

Amitriptyline: This drug produces more slowing than imipramine, though the other effects are similar. This corresponds to an increased initial sedative effect and its use as a sleeping medication for sleep onset as well as the usual wakefulness effects of antidepressants. In epileptics, there are increases in paroxysmal discharges, which can be controlled normally with adjustments to the anti-epileptic medications.

Ipronazid: This drug produces a slight increase in slower activity, though it produces a marked increase in faster activity. Paradoxically, this antidepressant does not produce an increase epileptiform profile or promote convulsions, even with this beta increase.

MAO Inhibitors: These medications have a wider variation of response than the other antidepressants. Isocarboxazide increases 30-20 Hz and decreases slower and higher frequencies, similar to a stimulant profile. Nialamide and Tranylcypromine produce a more typical profile, though with more variability.

SSRIs: These more modern antidepressants, such as Prozac, Paxil and Zoloft have fewer changes in the slow activity (associated with less viscero/autonomic side-effect), with a mild fronto-central beta increase in the range of 18-25 Hz and a decrease in alpha anteriorly.

Stimulants:

Stimulants increase the activity in the RAS, with the Raphe nucleus releasing norepinephrine, decreasing the polarization in the reticular nucleus of the thalamus and thus increasing the “clocking” or peak frequency of the rhythmic alpha activity and increasing faster activity.

Amphetamines: Both dextro and methamphetamines like Dextrostat or Adderal are similar in effect, with decreased slower activity and increased beta from 12-26 Hz. There is a paradoxical increase in alpha noted in the CEEG work of Itil (Itil et al., 1980). This is likely from the increased activation effect mentioned in the opening section.

Methylphenidate: Ritalin produces a decrease in delta and theta, with a more pronounced posterior alpha increase and an increase in low beta, with effects delayed up to 6 hours, compared to the rapid effects of the amphetamines.

Caffeine: This moderate stimulant has a moderate length of effect, but has surprisingly little research on its EEG effect. A fairly current study of its withdrawal effects (Clinical EEG, Vol. 26 No.3, July 1995) shows an alpha increase frontally, with suppression following resumption. The study also shows theta increases with withdrawal, maximal the second day, resolving with resumption. The degree of change in both frequencies corresponds well to the subjective withdrawal severity.

Nicotine: This drug has similar effects to caffeine, including the withdrawal study (Itil et al., 1971).

Cocaine: The effects of cocaine differ from the amphetamines in that cocaine decreases synaptic reuptake, and amphetamines increase the release of the neurotransmitters in the dopamine/norepinephrine systems in the brain. With lower to moderate doses, there is increased alpha and beta. With increased doses there is a desynchronization of the EEG and faster activity predominates.

The alpha increase frontally is seen during the euphoric phase of the subjective report. Cocaine is a well-known epileptic potentiator. Chronic abuse causes a “burned out” dopamine system, with delta decreases and slower alpha noted with little improvement even one year later

Antimanics:

Lithium carbonate is used extensively to treat bipolar depression, reducing the manic behavior and being prophylactic to depressive recurrences and further mania. The EEG shows an increase in theta, mild decrease in alpha as well as increased faster activity, with a strong potentiation of latent epileptiform activity. This mimics the tricyclic anti-depressant profile, though with slower slows and more fast activity.

Overdoses produce a marked slowing of the EEG, with triphasic discharges reported, likely associated with the liver toxicity and the associated metabolic disturbances, similar to the findings in hepatic encephalopathies. These slower findings may be noted many weeks following discharge from the hospital. Slowing of alpha (rhythmic background that responds to eye opening) down to 4 and 5 Hz two weeks after discharge from hospitalization, with normal 9 Hz alpha in the child returning only after many months is reported in a case study (NeuroNet Neuroscience Centers, 1999).

Tuburculostatics:

INH, Isonicotinic acid hydrazide, is an irritant to the CNS. Large doses can hypersensitize the CNS. The EEG shows bursts of paroxysmal activity with photic stimulation.

Methanol:

The EEG shows marked slowing, which correlates with the extent of acidosis more than the blood levels of methanol. This has been shown to be quite neuro-toxic, with optic nerve blindness noted commonly in chronic abuse/exposure.

Solvents:

The EEG show slowing, though the etiology remains uncertain, it is not without possibilities. Polyneuropathy, dendritic degeneration and demyelination have been seen in industrial exposures, any and/or all of which can cause slowing.

Mercury:

With initial exposure to this neurotoxin (and many other heavy metals) there is an increase of faster activity, though with increased concentrations there is an increase in fast and slow activity, with eventual paroxysmal activity of an epileptiform nature.

Organo-phosphates:

The insecticides are known to form peripheral neuropathies, though also have central actions. The EEG shows slowing and paroxysmal bursts, though in coma there is a paradoxical spindling fast activity.

Chlorinated hydrocarbons:

Also insecticidal, these chemical compounds are fat soluble, stored and accumulating to a toxic level they are known to cause convulsions. Neurologically, there are bi-temporal sharp discharges and anterior slowing, rarely are spikes noted, with or without convulsions.

Lead, organic:

Cerebrotoxic effects are strong, with IQ points dropped significantly even with trace measurable exposure. Dementia progresses with increased exposure, with eventual convulsions. The EEG shows diffuse slowing in sub-acute exposure, with increased exposure leading to paroxysmal discharges. Inorganic lead has weak cerebrotoxicity.

Aluminum:

Commonly seen in dialysis encephalopathies, with myoclonic activity seen behaviorally. Though not well documented, the EEG shows slowing with excessive fast activity, in my experience.  At autopsy, the aluminum is found concentrated anteriorly.

Provided courtesy of Jay Gunkelman, QEEG-Diplomate, Q-Pro Worldwide

Epilepsia

Volume 43 Issue 5 Page 482 – May 2002

To cite this article: Martin C Salinsky, Lawrence M Binder, Barry S Oken, Daniel Storzbach, Carey R Aron, Carl B Dodrill (2002)
Effects of Gabapentin and Carbamazepine on the EEG and Cognition in Healthy Volunteers
Epilepsia 43 (5), 482–490.
doi:10.1046/j.1528-1157.2002.22501.x

The results demonstrate that prolonged treatment with either CBZ or GBP can have significant effects on quantitative measures derived from EEG background rhythms. Both AEDs slowed the posteriorly dominant (alpha) EEG rhythm and median EEG frequency, and increased the percentage of theta and delta power. Overall, CBZ produced significantly greater slowing than did GBP. The observed test–retest changes are not simply shifts in group mean over time, but include many individuals (10 of 11 CBZ subjects, and six of 12 GBP subjects) whose test–retest change exceeded the 95% CI based on untreated healthy controls. Long-term AED treatment also affected several objective and most subjective measures of cognition and mood as compared with test–retest normative data obtained from untreated controls.

Part 1

Part 2

Dr. George H. Green and John LeMay, MFT, have been collaborating in the area of brainwave biofeedback for several years. About a year and a half ago Cerebotix focused on using the brainwaves monitored in biofeedback to move a remote object. After hundreds of hours of development, initial test subjects were able to successfully loft a remote controlled device (BCI – Brain Controlled Interface) in the Cerebotix corporate office. Since that time, countless refinements have been made, and the initial clinical results have been excellent.

In order to control a remote object, brainwaves are measured through five electrodes placed on the head. The resulting brainwave impulses are sent to a computer where they are processed through proprietary Cerebotix algorithms into three live data streams. These data streams are converted into radio frequency signals that are then transmitted to a wireless receiver mounted on a helium-filled Mylar balloon that has been ballasted to be slightly heavier than the surrounding air. As the person’s brainwaves become increasingly organized, the Remote Controlled Object (RCO) will develop enough power to activate a propeller, ascend and start to fly. The device is entirely under the control of the individual’s brainwaves. There are no additional controls in place whatsoever. The RCO is lifting off and flying literally 100% under brain control. This is the first time in history that brain waves have been used successfully to move remote objects.

Neurotherapy using slow cortical potentials also shows promise in the treatment of epilepsy (Kotchoubey et al., 2001; Birbaumer et al., 1981; Sterman, 2000). Neurotherapy has also been used for ADD/ADHD (Monastra, Monastra, & George, 2002) depression (Rosenfeld, 1997), anxiety (Vanathy, Sharma, & Kumar, 1998), fibromyalgia (Donaldson, 2002), and for cognitive enhancement (Budzynski, 2000; Klimesch, et al.). Commonly reported success rates of 60 to 90% are reported  (Wright & Gunkelman, 1998).

Neurofeedback is an emerging neuroscience based clinical application based on the general principles of biofeedback or cybernetics. The Neurofeedback process involves training and learning self regulation of brain activity. Understanding the underlying principles of this process allows the therapist to provide referrals or treatment to their clients with some added understanding, and provides clients with  a framework for understanding the neurofeedback process. The following short paper will provide a quick review of the brain’s function, and the underlying process involved in neurofeedback, a technique  that will allow the client to better regulate and operate their brain.

The brain controls its own blood supply through the dilation and constriction of the blood vessels, and the blood flow is directed to areas that are more active through this self-regulation. The blood supply’s flow, along with the utilization of the oxygen and glucose the blood carries is measured as “perfusion,” a measure that is clearly seen in some of the modern imaging techniques, such as Positron Emission  Tomography (PET) and SPECT technology. Though these techniques are invasive, requiring the injection of small amounts of very short half-life radioactive materials, they do give good resolution of the perfusion due to the emission of the positrons, which are emitted from where the brain utilizes the oxygen and burns the glucose carried by the blood flow.

A research project performed at UCLA’s Neuropsychiatric Institute (Cook, O’Hara, Uijtdehaage, Mandelkern, & Leuchter, 1998) showed that the brain’s electrical activity, or electroencephalogram (EEG), had specific correlates of the brain’s perfusion. This is useful in that the EEG is capable of showing when the perfusion is low, such as  seen frontally in ADD/ADHD. In these situations, the EEG shows a resting or idling rhythm of alpha (8–13 Hz) and/or theta (4–7 Hz), frequency patterns in the EEG that have rhythmic waveforms.
(For a general review of electroencephalography see Niedermeyer & Lopes Da Silva, 1999).

In ADD/ADHD a study of over 400 participants using a neurometric approach (see Prichep & John, 1992; Prichep et al., 1993) showed that there were generally findings of excess alpha and/or theta in the frontal lobes (Chabot & Serfontein, 1996), which corresponded to the frontal hypoperfusion seen in ADD/ADHD with the PET or SPECT perfusion studies. The frontal lobes are executive areas in the  brain, which control attention, emotions (affect) and impulsivity, as well as regulate (inhibit) the motor areas of the brain. The Chabot study (1996) also showed that the EEG could be used to differentiate those with ADD/ADHD from normal clients, as well as differentiating ADD/ADHD from those participants with a learning disability (LD). The LD population was shown to have a slower pattern, with excess activity in the delta frequencies (1–3.5Hz) over the central and parietal lobes (posteriorly at the crown of the head). These areas are responsible for integrating raw sensory stimuli into perceptually interpretable activity.

More recently, a comparison of children and adults seen in a single neurofeedback practice specializing in ADD/ADHD was performed (Gurnee, 2000). This study showed that unlike the children’s study, which showed theta to be the dominant pattern, the adults had an alpha dominance, likely due to maturational changes that have increased the frequencies. In the children the excess theta group is over 50% of the cases, with the adult group showing excess theta to only comprise about 25% of the incidence.

The qEEG data may also be used to select specific medications if a pharmacotherapeutic approach is preferred. The qEEG pattern of frontal theta responds better to stimulants such as methylphenidate (Ritalin), whereas the frontal alpha type responds better to antidepressants. If a specific statistical measure called ‘coherence’ is deviant (too high or too low), the participant may require an anticonvulsant (Suffin & Emory, 1995). These patterns also may coexist such that an individual may require two or more types of medication.

Physicians generally use behavioral indicators in choosing psychoactive medication. However, it was clear from the work of Suffin and Emory that neurophysiological profiles can be used to guide prescription, even in populations of patients with similar behavioral disturbance (e.g., attentional or affective disorders as defined by DSM). Most physicians generally find the proper medication the old fashioned way . . . by trial and error. The “best guess” medication selection method requires more doctor office visits, medication trials, and has the possibility of significant side effects. All this is generally avoided with the more objective qEEG based method, which is based on the person’s physiology, not the behavior. It is not difficult to see why this is the case. The medication treats the physiology, hoping to affect the behavior. The measurement of the physiological indicators should logically be more related to the proper medication choice, since this is what is actually being treated.

The stimulant medications typically decrease appetite, with weight loss commonly noted, as are sleep problems. Long-term use of stimulants have been known to cause teeth grinding (Bruxism), cardiac rhythm changes, blood pressure increases, weight loss, changes in sleep patterns, anxiety/nervousness and even “psychotic” symptoms (such as hearing voices or other sensory hallucinations). There are also those with medical contraindications for stimulant use, such as heart problems, gastro-intestinal and blood pressure problems and other more rare complications that preclude prescribing them. In these individuals, as in those with complications from taking the medications, the presence of an alternative treatment is essential for proper behavioral adjustment and scholastic achievement. For those individuals uncomfortable with using potent medications, or those with adverse side effects, it is fortunate that a non-medication intervention is available.

The choice of medicating the client requires continued treatment, as it is merely a temporary change, due to the drug’s effects. Neurotherapy is a treatment, which changes the way the brain works, and once the skill is learned, (unlike medication) it appears to be persistent. Follow-up studies show long-term change in the brain’s function following neurotherapy (Monastra, 2003). Both of these methods (medication and neurotherapy) improve the client’s attentional and behavioral states. The choice of which method to use is merely a personal choice. Medications, when used long term, may end up being more expensive than Neurotherapy. Neurotherapy has less likelihood of having side effects than does the medication, but it takes a number of training sessions before the effect is noted and becomes more persistent.

It is no surprise that the brain can learn, but what may surprise some is that the brain changes structurally when it learns. This morphologic change is microscopic, the forming and reinforcing of small connections between a part of a neuron, called “dendrite,” but it is a structural change, nevertheless. This highly changeable connective nature is referred to as “neural plasticity,” based on the original definition of plastic, not as a substance, but as a descriptor of the malleability or change—ability of materials or structures.

The brain has a method of developing and expanding the pathways that are used, and “pruning” the connections that aren’t utilized. This process is most dramatic early in life, but continues throughout life. We are born with about twice as many neurons as are present when we become young adults. The pathways that are more consistently utilized are protected from the pruning process through a mechanism still unknown to science, though the fact of the change is irrefutable.

Another time when this process of plasticity is evident is following damage, such as head injury, or disuse of an area, due to “deafferentation,” such as when hearing is lost. In these situations the surrounding functions may take over an area not utilized, occasionally causing some subjective changes, which may be uncomfortable. One example of this is tinnitus, or ringing in the ears, following loss of hearing; another is “phantom pain” when a limb is severed and is no longer present, but sensations seeming to come from the missing limb are felt. The functions adjacent to these areas in the brain merely intrude into the area and the person misinterprets these new
signals as the older inputs.

These examples are dramatic, but “growththrough-utilization” is the underlying process we want to focus on. This process is how we build additional capacity for the nervous system to do its work. Analogous to exercise building muscle mass, the utilization of the brain builds the mass of the brain’s dendritic connections.

Certain intense negative experiences may change the body’s chemistry, increasing the stress hormone released from the adrenal cortex of the kidneys. This chemical, cortisol, is a healthy response to stress, though with chronic or overly intense stressors, the cortisol has deleterious effects on the brain, specifically attacking a temporal lobe structure, the hippocampus, which has immune receptors. This structure has important non-immune system functions as a memory comparator, required for both comprehension and recall. The implication for this latter process where stress deteriorates the brain’s ability to comprehend and recall has large implications for education. A person with a stressful existence may never reach his or her true potential due to the damaging effects of the stress hormones. If the stress was experienced during pregnancy from the mother’s hormonal balance, the newborn will have a disproportionately intense reaction to stress, causing inordinately large amounts of strain (and thus more cortisol) and ultimately more extensive deterioration of the brain’s capacity.

The ability to teach a new response to the situational stressors can change the life course for these individuals, creating a much more favorable outcome. The operant conditioning technique, Neurotherapy, mentioned earlier is one such method of intervention. Similarly to the stress response, there is a relaxation response, which can be trained to counteract these deleterious effects.

The brain’s electrical patterns are a form of behavior, which is subject to behavior modification through “operant conditioning,” a fact discovered in research done in the late 1960s by Dr Barry Sterman, now a professor emeritus at UCLA. The operant conditioning of the EEG was first demonstrated in cats, where placebo effects are assumed to be absent. Sterman’s original work with animals was replicated in humans starting in the 1970s (Sterman, 2000).

Recording and analysis of EEG has been shown to yield reliable results (Fein, Galin, Yingling, Johnstone, & Nelson, 1984). Further, those studies done with control groups have shown the neurotherapy technique to be a robust and valid intervention. Many more studies are of a case series variety, without control groups. Though this latter category is not held in high regard, perhaps this is changing. A recent issue of the New England Journal of Medicine reviews of research design have cast doubt on the need for placebo-controlled designs. Their review has shown that when there is a preponderance of case series reports, the concordance between those results and those of the “gold standard” (double blind placebo-controlled studies) was very high. Many in the field are now arguing against doing a double blind study due to the lack of proper humane treatment of those in the control group (receiving no treatment), an approach which is also now considered unethical by the World Health Organization when known treatments exist. Interestingly, recent work with placebo effect has elucidated brain mechanisms underlying placebo response that were different than those mediating medication response (Leuchter, Cook, Morgan, Witte, & Abrams, 2002).

With the neurotherapy approach, the brain frequencies that are in excess are reduced, and those with a deficit are increased. The technique uses the EEG, amplified from the minute voltages and hooked up with special instruments to control a computer game. The person’s EEG is the “joystick” they use to operate the game. Over a series of sessions the person learns to use the EEG to control the game. The clinician slowly adjusts criteria for reward presented to the individual, and thereby “shapes” the behavior of the participant’s brain into a more normal pattern.

The neurotherapy technique requires time to learn, and varies depending on the initial condition the individual starts with. In general, the more severe the starting condition, the more learning has to occur to correct the state. Simple relaxation may take as few as 10 sessions to learn; although with more severe cases, a longer training course may be needed, such as with generalized anxiety disorder, or panic attacks. The important point is that the learning is internalized so that the benefit of the training persists, and does not require on-going training. This is unlike the use of medications where symptoms typically reappear after discontinuing medication.

The learning curve for EEG has been described in research done at Langley Porter Neuropsychiatric Institute, at the University of California, San Francisco. The research showed that the curve is a fifth-order curve, which contains an initial increase, followed by a dip, a second increase, followed by the exponential increase at the end of the training (Hardt, 1975). This corresponds to the subjective states reported in some individuals. They are initially presented in a slightly anxious state, which gets better when they habituate to the training situation, corresponding to the initial increase in the curve. The individuals then report that they “try hard to relax,” a counterproductive attempt, which corresponds to the dip. They give up trying hard (active volitional attempts), corresponding to the second increase, which is then followed by the learning of the passive volitional state, which is the final exponential increase.

In some cases, the individuals may need more peripheral forms of biofeedback-based intervention, such as muscle relaxation or training of temperature or the electrodermal responses. These will depend upon whether their individual response profile shows their stress in these areas as well. The peripheral training often requires less training time, though the source of the difficulty is universally central, as these modalities are all under the control of the central nervous system. Training peripherally may be all that is required in more mild cases, but in many individuals, the central training is the only method that will have a persistent result. In our clinical experience with these more severe cases there may be symptom substitution without the central intervention. In cases with mild stress, the peripheral intervention is often a complete intervention, though when additional complaints such as attentional problems, depression, or hyperactivity are noted, the central intervention is usually the first choice, to minimize the total number of sessions, by getting directly to the common source
of the problem.

Prior to starting work with an individual, and in order to design an appropriate operant conditioning intervention, their existent brain function must be known. Optimally, this would entail a full recording of their EEG, with quantitative analysis and comparison of the individual’s brain activity to an age matched database. These databases are commercially available from a number of sources, and are described in a recent Journal of Neurotherapy special edition (Vol. 7, No. 3 and 4, 2003). Following such a comparison, areas that deviate from normal may be identified, as well as the direction of the deviation from normal. This shows whether an excess or a deficit of any frequency pattern exists, as well as the location of the deviation. Specific individualized patterns of results are used to guide intervention with neurotherapy.

Following this evaluation, an appropriately customized operant training may be designed which optimizes the training time by focusing on the areas of deviation. The training will take time, with 30 to 40 sessions being quite common before a permanent result is established, and even more are required for more severe or complex cases such as Asperger’s/Autism (Thompson & Thompson, 2003). There are commonly reported behavioral changes long before this end point of training is reached, with the early signs of change showing themselves at 5–10 sessions for most individuals, though some have strong changes even after their initial session. It is also common for an individual to not notice the change, as they are occasionally not self-aware, though the changes are easily seen in objective testing and reported by those observing the individual’s behavior.

Commonly reported success rates of 60 to 80% are seen in the scientific literature, with up to 90% reported in qEEG based intervention (Wright and Gunkelman, 1998). Using strict criteria (total remission of complaint) the percentage range from 50 to 60%, with those reporting positive results, though with less stringent measurements of success, such as “feeling like you got a positive benefit,” ranging in the 80 to 90% rate.

Many therapists are not aware of neurofeedback as an application of operant conditioning, being familiar with more easily observable behavioral operant training than the operant training of “internal states.” The neurofeedback literature is most well accepted in the area of operant training of EEG in epilepsy. Well-controlled studies show that the technique can assist in cases where medication alone was shown to be inadequate at controlling the electrical discharges associated with the epilepsy. A review of this application is published in a special edition of Clinical EEG, in the January 2000 issue (Sterman, 2000). Neurotherapy using slow cortical potentials also shows promise in the treatment of epilepsy (see, Kotchoubey et al., 2001; Birbaumer et al.,1981).

Since the EEG in epileptics can be taught to stop the abnormal discharges, leading to the elimination of the behavioral manifestations of the epilepsy, the neurotherapy technique has also been applied in less severe neurological disorders such as ADD/ADHD (Monastra et al., 2002) depression (Rosenfeld, 1997), anxiety (Vanathy et al., 1998), and fibromyalgia (Donaldson, 2002). Budzynski (2000) used neurofeedback to reverse cognitive decline in an elderly population (see also the work of Klimesch et al. for studies of EEG related to memory performance). For recent reviews of neurobehavioral disorders noted to respond to this emerging technologically based operant training technique see Yucha and Gilbert (2004), and Nelson, (2003).

There are two international professional organizations dedicated to the study of this technology and these applications: the Association of Applied Psychophysiology and Biofeedback (AAPB), and the International Society for Neuronal Regulation (ISNR). Both of these societies have annual conferences and often sponsor additional regional workshops. There are also many state and regional organizations, often affiliated with one of these international organizations. ISNR also has international chapters in other countries. Both organizations have web sites (www.aapb.org and www.isnr.org), and both sponsor a professionally published journal with material focused on Neurofeedback: The Journal of Neurotherapy (ISNR), and Applied Psychophysiology and Biofeedback (AAPB).

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1Q-Metrx, Inc., Burbank, CA.
2Department of Psychology, University of California, Los
Angeles, CA.
3To whom correspondence should be addressed at Q-Metrx, Inc.,Burbank, CA

Neurofeedback is a treatment where real-time feedback is provided for specific brain activity (most often EEG) in order to learn the brain to suppress or produce specific brain activity. This method was initially discovered for the treatment of Epilepsy and from 1976 investigated further for the treatment of ADHD. This technique has become more popular by clinicians worldwide, and is currently provided for the treatment of several disorders. Critics have often questioned the efficacy of Neurofeedback and whether it can be considered an Evidence Based treatment or not.

In collaboration with researchers from Tübingen University (Germany), Radboud University (Nijmegen, the Netherlands), Brainclinics and EEG Resource Institute a so-called meta-analysis was conducted on all published research about Neurofeedback treatment in ADHD. This meta-analysis included 15 studies and 1194 ADHD patients. Based on this study – which will be published in the July issue of EEG and Clinical Neuroscience – it could be concluded that Neurofeedback can indeed be considered an Evidence-Based treatment for ADHD. The results show that neurofeedback treatment has large and clinically significant effects on Impulsivity and Inattention and a modest improvement of Hyperactivity.

These findings apply to Neurofeedback treatment for ADHD, but do not automatically imply that Neurofeedback can be considered evidence based for any disorder. The efficacy of Neurofeedback has to be assessed separately for each disorder. For example, a meta-analysis of EEG biofeedback in Epilepsy is published in the same issue of EEG and Clinical Neuroscience demonstrating clinical efficacy in the treatment of epilepsy.

Interested clients are advised to make an informed choice regarding Neurofeedback therapists, since there is a large heterogeneity in neurofeedback treatment approaches and clinicians. It is advised to look for psychologists or physicians who are at least a member of a professional organization such as the International Society for  Neurofeedback and Research (ISNR: www.isnr.org) or other professional organizations and who use investigated methods.

Literature Arns, M., de Ridder, S., Strehl, U., Breteler, M. & Coenen, A. Efficacy of Neurofeedback Treatment in ADHD: The effects on Inattention, Impulsivity and Hyperactivity: a Meta-Analysis. EEG and Clinical Neuroscience; 40(3), 180-189.