Technology Helps Explain Medication Failure

In almost every area of medicine, doctors can order tests to provide objective physical data to guide their medication selection. However, the practice of psychiatry is most often based on observation, self-report and psychological testing. It appears that we are better at measuring impairment than we are at identifying the source and prescribing an effective medication. Is there a way we can do better?

The director of the National Institute of Mental Health, Tomas Insel, suggests there are many medicines, but they are not working adequately. This is because the symptoms of mental illness are too illusive and are shared by many diagnoses. Insel (2012) says, “It’s much harder to fix something if you don’t know what is going wrong.” Medications are being prescribed to treat a set of symptoms suggestive of a specific disorder without any objective evidence of the cause. Additionally, the practice of polypharmacy has become way too common in children and adolescents.

Pharmaceutical industry advertising promotes adding a medication when the first medication fails to produce the desired results (i.e., adding Abilify to your antidepressant). The message is that when one medication fails, keep adding more in an effort to address the additional symptoms. Each additional medication increases the risk of side effects. It is not uncommon for children to come to us with several medications prescribed. Last month, for example, we saw a 9-year-old female with prescriptions for Olanzapine three times a day, Lithium Carbonate daily and Amphetamine Salts three times a day. Also, a 10-year-old male came to us on Focolin three times a day, Seroquel twice a day, Lexipro daily and Zyprexa daily. If there was a way to determine why a medication failed, would it not be prudent to investigate why? If current technology could help?

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International Society for Neurofeedback & Research (ISNR) 18th Annual Conference

International Society for Neurofeedback & Research (ISNR) 18th Annual Conference
Denver, Colorado Sept 30-Oct 3, 2010

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.

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First Direct Evidence of Neuroplastic Changes Following Brainwave Training

The scientific and academic press is now considering Neurofeedback as one of the ways neural plasticity can be induced/enhanced. The paper below shows the NF training changing the brain’s plasticity measurably within a single feedback session.

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!


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

Drug exposure and EEG/qEEG findings

A technical guide by Jay Gunkelman, QEEG-D

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.

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Neurofeedback Impacts on Addiction

According to the U.S. Substance Abuse and Mental Health Services Administration, addiction is currently one of the most significant health and social problems in America, affecting ~12.5% of the population. Medical costs can be up to 300% higher for an untreated alcoholic than a treated alcoholic. Other costs to society have reached almost $500 billion, taking into account unemployment, lost productivity, increased crime and justice system/incarceration costs, health care system strain, increased insurance costs, child abuse/neglect and even workplace violence. It is estimated that every dollar spent on treatment saves $4–$7 in costs from drug-related crime and can help reduce the spread of infectious diseases.

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Why do a qEEG for Neurotherapy?

There are many in the field of Neurotherapy who do not perform qEEGs prior to designing a clinical intervention. These people are currently practicing well within the standard of practice for this rapidly evolving field. Many within this group have standard protocols which are used on all clients, with various alterations to respond to the client’s reported experiences during the treatment.

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Patterns seen in the qEEG and their indicated interventions

Diffuse slowing, with slower alpha

The ascending reticular activating system stimulates the diffuse thalamic projection system and sets the general arousal level of the brain. With an increase in the CNS arousal level, there is an increase in the mean frequency of alpha and a decreased slowing. With decreases in arousal there is a slowing of the alpha, as well as eventually an increase in diffusely distributed slowing ( a mixture of diffuse lower voltage delta and theta, usually with a weak vertex prominence in linked ear montages).

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EEG Biofeedback as a Treatment for Substance Use Disorders: Review, Rating of Efficacy, and Recommendations for Further Research. Part 2

P300 Abnormalities in Cocaine, Methamphetamine, Heroin Addiction, and Alcoholism

The P300 component of the ERP, occurring 300–600 ms post-stimulus, is the most widely used ERP in psychiatry and other clinical applications (Polich et al. 1994; Polich and Herbst 2000; Pritchard 1981, 1986; Pritchard et al. 2004). The amplitude of the P300 reflects the allocation of attentional resources, while the latency is considered to reflect stimulus evaluation and classification time (Katayama and Polich 1998; Polich and Herbst 2000). The P300 is usually obtained in an oddball paradigm, wherein two stimuli are presented in a random order, one of them frequent (standard) and another one rare (target) (Polich 1990). A modification of the oddball task has been used where a third, also rare stimulus (distracter), is presented along with standard and target stimuli. It was reported that these infrequent distracters elicit a frontocentral P300, so called P3a, whereas the rare targets elicit a parietal P300, so called P3b (Katayama and Polich 1996, 1998). The P3a is recorded at the anterior scalp locations and has been interpreted as reflecting frontal lobe activity (Gaeta et al. 2003; Knight 1984). Though the P300 response in general is thought to represent ‘‘context updating/closure,’’ in a three-stimuli oddball task the P3a is interpreted as ‘‘orienting,’’ and the P3b is viewed as an index of the ability to maintain sustained attention to target (Na¨a¨ta¨nen 1990). The anterior P3a indexes the contextual salience of the rare stimuli, whereas the posterior P3b is indexing task-relevance of the stimuli (Gaeta et al. 2003).

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EEG Biofeedback as a Treatment for Substance Use Disorders: Review, Rating of Efficacy, and Recommendations for Further Research. Part 1

T. M. Sokhadze – email:
Department of Psychiatry and Behavioral Sciences, University of Louisville School of Medicine, Louisville, KY, USA

R. L. Cannon – email:
Department of Psychology, The University of Tennessee, Knoxville, TN 37996, USA

D. L. Trudeau – email:
Department of Family and Community Health, School of Health Sciences, University of Minnesota, Minneapolis, MN, USA


Electroencephalographic (EEG) biofeedback has been employed in substance use disorder (SUD) over the last three decades. The SUD is a complex series of disorders with frequent comorbidities and EEG abnormalities of several types. EEG biofeedback has been employed in conjunction with other therapies and may be useful in enhancing certain outcomes of therapy. Based on published clinical studies and employing efficacy criteria adapted by the Association for Applied Psychophysiology and Biofeedback and the International Society for Neurofeedback and Research, alpha theta training—either alone for alcoholism or in combination with beta training for stimulant and mixed substance abuse and combined with residential treatment programs, is probably efficacious. Considerations of further research design taking these factors into account are discussed and descriptions of contemporary research are given.

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