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

How can we live a fuller and healthier lifestyle as we get older? Perhaps keeping our body and brain engaged can help. That seems to be the case in Japan where the number of centegenarians is greater than 20,000.

THE ART OF AGING:THE LIMITLESS POTENTIAL OF THE BRAIN introduces a number of these “super-seniors” who lead healthy lives at nearly 100-years-old and, through them,searches for the “keys” to living a healthy and vital life regardless of age.

Click here to view the embedded video.

These results are from 300 seconds of linked ear EEG data, note the dominant slower alpha peak frontally…. And the raw coherence values of that linked ear data. The raw EEG file sample is also included, so you can see the waveforms these values are being drawn from.

Linked Ears

Raw Coherence Values of Linked Ear Data

Raw EEG

The same exact 300 seconds of EEG data, reprocessed now with the weighted average montage.  Note the difference in spectra, and waveform!!!  The temporal slower alpha is now seen as the source of that slower alpha content.

The alpha hypercoherence in the EEG is easily seen in this data, but not in the linked ears.

This shows that you need to find the EEG montage that shows the actual EEG data for your case first, and THEN calculate coherence.

Weighted Average Spectra

Weighted Average Waveform

Weighted Average Raw

The images below show the Spectral plot, coherence plot and raw EEGs. Just like the other montages did. The Cz coherences are so inflated with field effects they are at 0.8 across the full spectrum at some sites, obviously artifactually high.

Spectral Plot

Coherence Plot

Raw EEG

We are honored to welcome several high-profile speakers, including:

• Personalized Medicine in the Age of Technology - Vilayanur S. Ramachandran, MD, PhD; Director of the Center for Brain and Cognition and Professor with the Psychology Department and Neurosciences Program at the University of California, San Diego, and Adjunct Professor of Biology at the Salk Institute

• Regeneration and Stress at Work: Strategies for Improved Employee Health - Tores Theorell, MD, PhD; Professor Emeritus at the University of Stockholm, Sweden

• An Overview of Mind Body Healing - C. Norman Shealy, MD, PhD; founder of the American Holistic Medical Association, and past president of the International Society for the Study of Subtle Energies and Energy Medicine

• Neurotherapy in the Treatment of Traumatic Brain Injury: A Physiological Hypothesis – Paul Rapp, PhD; Professor in the Department of Military and Emergency Medicine at the Uniformed Services University of the Health Sciences

An excellent story regarding the use of Neurofeedback in sports.  The Mind Room utilizes the Thought Technology Procomp Infiniti equipment.

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.

I suggested at the time that all the emotion was merely an example of someone yelling “the sky is falling”, like Chicken Little. There was no real problem, just lots of crying out and hand wringing.

I requested in an open international forum for anyone to send me a sample of the problem, and none could be produced. I suspected there was no real problem, as the sample issue was concerning a 500 sample/second device having a time skew… though this was in comparison to a database collected on a 100 sample per second device, with the waveforms interpolated from these samples.

It was highly suspect from my technical perspective when this issue was raised, and it was even more suspect when nobody could produce actual data showing the coherence or phase issue.

Testing now has shown that the old style Mitsar, with the non-simultaneous sampling is identical in performance to the new style amplifier that has simultaneous sampling, and thus no skewing error is possible in the newest amp.  There is also an intermediate style amplifier tested, which is one of the smaller amps, but with a more current sampling design.

The data clearly show that there is no difference in coherence between these devices.

The Mitsar amplifier also has been tested with the new BranMaster  Discovery amplifier, and it also was shown to have indenticle coherence findings with the Mitsar amplifier.

Clearly there is no real issue.

Data rules…. the experimental details are below.

Jay

We performed the following experiment.

We took three different Mitsar amplifiers:

1. Mitsar-EEG-201 – old model of amplifiers with relatively large time shift between channels (1.75 ms maximum) 2. Mitsar-EEG-201M – new model of amplifiers with relatively small time shift between channels (470 microsecond maximum) 3. Mitsar-EEG-202 – 32-channels amplifiers with zero time shift between channels.

Than we take Electro-Cap and put it on the head of one subject. We used linked ears referent for EEG recording.

We sequentially connect Electro-Cap and referents to three different amplifiers and perform independent recording of EEG in eyes closed condition. The duration of recording was longer than 300 seconds.

When we reconnect Electro-Cap and referents from one amplifier to another we do not touch to electrodes on the head and ears.

The total time of out experiment was approximately 20 minutes. This means the functional state of subject remain relatively stable.

Than we remontage the EEG to average referent (very important for time  shift influence measurements), compute the coherence for all three EEG recordings using the same processing parameters and compare them. The duration of time interval for processing was the same for these EEG recording and was equal to 300 seconds.

We do not find any dramatic differences in coherence corresponding to different amplifiers. The small fluctuations can be explaned by amplifiers noise and non-stationarity of EEG.

Mitsar Calibration

The Mitsar system is calibrated at the manufacturer. There is no need to recalibrate the amplifier unless there is a serious problem from damage. The calibration button is so the user can run a test calibration signal to demonstrate that the channels are in fact correct and equal. If these were ever not correct (or equal) then the manufacturer would recalibrate the hardware device. It is blocked so that a user cannot accidentally mess the calibrations up. So in summary the calibration button in the software is pressed and then the button to observe EEG is pressed. Then the test calibration signal is generated and can be recorded. This is a good idea if the case is a medical or legal evaluation so that when the data is presented as evidence there is validation that a microvolt equals a microvolt.

All of these new tools will require clinical validation prior to being able to be considered standard techniques within our field’s armamentarium of efficacious techniques and clinical applications. All of these techniques offer great hope at this time with preliminary results, but careful clinical outcome studies remain to be performed.

In this brief note I will discuss Z-score feedback. This promising technique offers to set normative boundaries around the mean of many features of the EEG, and allow feedback to be controlled by these parameters. This obviously offers great hope to clinical outliers, as their Z-score divergence should be related to their pathology. One difficulty is that database Z-scores also show divergence when an adaptive or counter-balancing feature is used to cope with an abnormal finding. A crutch is not a normal finding, but you can’t walk without it if you have a broken leg.

This suggests that the selection of which Z-score features to include as feedback contingencies and which to “ignore” will become an important feature in clinical decision making using these new tools. Training away an adaptive coping mechanism is not a proper NF Z-score targeting choice.

One area which is not very well discussed in the field of qEEG is how poorly the databases are at characterizing shifts in the frequency “tuning” of the EEG. The NeuroGuide database reports peak frequency, but the calculation is not for the peak, but for a “centroid” which is more related to the Mean than the Peak frequency. Nx-link does not report the peak, but uses a mean frequency calculation. BRC database uses a peak frequency of alpha statistic, but it is constrained to looking within the alpha predefined band.

Databases report “too much” and “not enough” amplitude/magnitude/power, but they do not tell you if this value would be normal at a different frequency tuning. An example is in order to illustrate this important concept. Take a normal amount of 9.5 Hz sinusoidal alpha seen dominant posteriorly, with normal coherence relationships… let’s arbitrarily say there is 50 microvolts of amplitude in the alpha spindles. Now, take this alpha tuning and shift it 2 Hz slower, so 7.5 Hz is the sinusoidal frequency, and what does the database tell you?

Databases will say there is too much 7.5 Hz power, and that it is hypercoherent, since the database does not expect alpha at 7.5 Hz. In reality, the alpha frequency is slow, but the fact that it is 50 microvolts is not too much power for the background, and it really is not hypercoherent, it is just too slow.

Frequency tuning issues are so poorly described in databases that the databases will not do a good job of normalizing the client’s function… dropping the background’s normal power and coherence relationships is not appropriate, but the database would use these values as their contingencies for NF based on the database.

This would suggest that frequency shifted clients may comprise another group that will require special adaptations for Z-score based feedback to be properly applied.

One other area that deserves some discussion is the use of NF in non-medical applications for “peak performance”. By definition, these peak states are not a common occurrence, as they are seen in uniquely gifted athletes, scholars, and business leaders that are not that common in the first place, and then these states are not always seen in these individuals in their average states. These states that are being trained for are not statistically “Mean-oriented” states, but rather exist as a unique pattern of outliers which are not capable of being reported in univariate statistics such as Z-scores. It requires a flexible nervous system to achieve these outlier states, and a resilient nervous system to “return” or “recover” and continue to function “normally”.

These observations suggest that peak performance may not be the best application for Z-score feedback, though this is hypothetical, and requires the validation only achieved with experience over the years.

The database selected also will become an issue, as the NeuroGuide is severely restricted in the frequency range, with the amplifier response stopping at 28Hz, as seen in the FRC curve(Fig 1). It is not possible to do gamma based feedback with Z-scores of the database used does not go to gamma.

Figure 1

What is clear at this time is that Z-score feedback remains experimental until the validation studies are performed, and though it is a promising new application utility, there are areas which deserve special attention even in this early stage of the evaluation of this emerging technique, including coping mechanisms, frequency shifts, peak performance applications, and database limitations.

The vendors who promote Z-score feedback are all adamant that the Z-score feedback does not preclude the need for client evaluation, but rather that is increases the complexity of the evaluation as various features are selected or de-selected for being feedback contingencies to account for client coping mechanisms, and the various frequency shifting issues and other database inadequacies.

Welcome to the New World of high tech clinical application tools, please check your expectation that this will be “quick and easy” at the door. More on LORETA and ICA based neurofeedback later.