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).

When this diffuse slowing with slower alpha is seen, a vertex or central sensory-motor strip beta training will slightly speed up the alpha and decrease the slowing seen. A frontal beta minima seen in the data may respond to a more anterior placement for the beta training.

This increased beta training should correspond to a brain stem shift in RAS activation with increased norepinephrine level’s stimulating effect and results in increasing vigilance.

When this slowing and alpha pattern is seen, but with alpha intruding frontally (occasionally with less of the slowing) , the protocol should include some parietal “high alpha”, defined as 11-16 Hz in the classical EEG literature, but usually in NT, this is from 10 or 11 to 14 Hz.

This parietal high alpha training shifts the alpha mean frequency higher, decreasing the diffuse projection system’s frontal alpha and increasing the posteriorly distributed specific projection system alpha (though at a slightly faster frequency distribution). Often it is the slower alpha frequencies that are intruding frontally, and they are reduced with this shift.

Focal slowing

Focal slowing that is not an artifact (such as a pulse, electrode, electrodermal, eye movement or other artifactual source of slowing) should be evaluated by an electroencephalographer or neurologist.

The focal slowing may be from a tumor, ischemia, stroke, trauma, inflamation or other medical condition. The etiology should be identified prior to any intervention or consideration of NT.

Should the etiology be known, generally the reduction of the slowing and enhancement of faster activity improves the brain function following NT. Slowing is reported in specific learning disabilities and sensory processing problems (Chabot et al., SSNR Aspen,1997)

Faster alpha variants, not low voltage

The alpha frequencies may be faster than usual, sometimes corresponding with anxiousness or hypervigilance. These situations can present with complaints about attentional problems, with the hypervigilance acting as a source of increased distraction, but with the process differing from more usual ADD/ADHD presentations.

The faster alpha often has increased EMG associated with it. Patients with these findings seem to respond with paradoxical increased anxiety if EMG relaxation is tried without first addressing the hypervigilance of the faster alpha. The ‘letting down of the guard’ is anxiety producing.

Training the slower end of the normal alpha band parietally seems to have a strong positive effect on these individuals, with SMR training used by some therapists. If the EMG remains, the subsequent relaxation therapy seems to work without the increased anxiety following the NF intervention.

Frontal lobe disturbances

The frontal lobes inhibit distractions and inappropriate impulsively motivated behavior, control affective mood states and attentional states. The frontal lobes also set the motor strips tone via inhibitory control loops involving subcortical structures. The frontal lobe has general regulatory control over the entire rest of the brain.

In attentional and affective disorders as well as motor dyscontrol such as hyperkinetic disturbances the locus of the dysfunction is commonly the frontal lobe.

Work recently done on ADD/ADHD and affective disorders shows a variety of frontal disturbances seen with the qEEG. These varieties include slowing in theta, alpha intrusion and even excess beta (Chabot et al, 1998 SSNR, Austin). Non- systematically replicated research showed the qEEG to predict the response of the patient to medications. The theta types responded to stimulants, with the frontal alpha, especially when the mean frequency of alpha was slowed, responding to amphetamines. Other researchers show some of the alpha types to respond to SSRI type antidepressants (such as the OCD responsive type in work by L. Prichep and the depressives with frontal alpha in work by S. Suffin and Emory).

In NT, the qEEG may be used to adjust the intervention, with frontal theta responding to beta protocols with suppression of the excessive theta. The alpha frontal types respond less well to frontal alpha downtraining than to posterior high alpha training with concurrent frontal beta training. The frontal beta type seeming to respond to normal frequency alpha training posteriorly and frontal beta suppression if the beta is still excessive (with any slowing noted suppressed as well). The frontal beta excess type is often a difficult patient in my experience.

Frontal beta minima can be seen in frontal disturbances and seem to respond well the NF intervention. Areas commonly seen are F7 in attentional problems, F8 in impulsivity and F3 or Fp1 in depression. The locus or even presence of a minima is difficult to predict behaviorally, as other disturbances of function may yield the same behaviors.

Right frontal training and frontal symmetry

The commonly held belief that in NF the right frontal lobe should be avoided needs to be explored and understood before discarding it.

Frontal alpha and beta interhemispheric ratios seem to correspond well with the perceptual style of the subject. Right hemispheric dominant (more beta and less alpha than the left) subjects have a “glass is half empty” perception and a lower mood state, or more depression.

NF with the frontal lobes needs to keep the dominance on the left, or to establish such a dominance to avoid deteriorating mood states and perceptual styles in the client.

This has led some to avoid the right frontal training, or frontal training in general. This would be a drastically limiting elimination of potentially efficacious NF intervention on brain function, given the importance in brain pathophysiology and functional regulation of the frontal lobes.

If care is taken to measure and assure the desired lateral symmetry, it is my experience that the frontal lobe training on either side may be done without significant difficulty. Without this knowledge and care applied to protocol considerations, it could be a large source of client dissatisfaction.

Spindling excessive beta

This pattern has been reported to be associated with ‘cortical irritability’, viral or toxic encephalopathies and in epilepsy. It has a classically defined higher voltage beta occasionally even exceeding 20 microvolts. This abnormal beta is seen in waxing and waning spindles over the effected cortex. This pattern is seen in less than 10% of the ADD/ADHD and affective disordered population, but when seen, it is an important finding.

I have seen this excessive spindling beta in areas associated with pre-epileptic auras. In one case it was seen occipitally during visual auras and in another fronto-temporally with auras effecting the client more subtly as a smell or even a remembrance.

This pattern responds very badly to any beta training, exacerbating the symptom complex. Beta training is strongly contraindicated.

Beta suppression directly in the area of concern has shown good clinical response. The band of frequencies to be suppressed should be selected based on individual profiles, not by standard bands. I have seen broader bands like14-22 Hz or bands as narrow as 14-16 Hz in excess, with higher 20-30 Hz beta occasionaly involved as well, with many variations.

The customizing of these interventions would be very difficult, if not impossible without the qEEG to provide location, distribution and frequency range information to the NF practitioner.

The EEG can be seen with areas of decreased amplitude, not just a beta minima, an area of general amplitude minima. This phenomenon is seen well in mapping and has been reported in areas of cortical dysfunction.

The EEG requires the generation of alternating currents for any voltages to be measured in the EEG. This requires the activity of neurons in an area with the increased blood flow and glucose metabolism associated with these cellular processes. The flowing of blood in the brain is regulated by the concentration of bicarbonate ion measured as PCO2, a metabolic by-product of the burning of glucose and the generation of energy within the Krebbs cycle. The ADP/ATP cycle within the mitochondria is the site of this electro-chemical interplay.

In careful work done by Pribram, the time frame for these events has been studied, with the slower DC activity preceding the cellular action potential. This DC system has been used since the 1970’s in Europe in NF, showing that the shift to electro-positivity can even stop an epileptiform discharge from occurring (N. Birbaumer).

This phenomenon also can be seen in qEEG as an area of decreased voltages in all bands, progressing from beta through alpha to the slower frequencies. The area is effectively shut down and is not functioning. When the brain’s electropositivity increases enough, the AC activity seen in the EEG is inhibited.

These areas have been observed frontally in attentional and affective disorders (Gunkelman, SSNR1997), and are reported in observations of individuals who have been brain washed and have given the locus of control over to others (personal communication with Brownback, Mason and associates).

Training these frequency “dead areas” is something newer in the field, but it seems to respond to beta training, suppressing any slower frequencies that may be still present. Beta is correlated highly with PET measurements of metabolic activity (I.A. Cook, A. Leuchter et al, 1998 UCLA)

Generally low magnitudes

The occurance or a low voltage EEG is considered a normal variant when it is a low voltage fast EEG. When the low voltages appear slow however, it is a diffuse and non-specific abnormality. The difference between the two patterns is somewhat more qualitative than quantitative. The morphologic presentation differs more significantly than the magnitude differences in the quantitative analysis.

The magnitudes are all low, and in relative terms the power will look slowed in both cases, though the faster morphologic pattern is a normal variant. When a low voltage slow pattern is seen and is confirmed not to be drowsing, it should be evaluated for metabolic, toxic or other diffuffuse encephalopathies such as degenerative or post hypoxic etiologies.

The low voltage slow type is reported in dementias as an early EEG change. This seems to respond to high alpha training from 10 or 11 to 14 Hz. This is the same EEG effect as nootropic medications (smart drugs) will provide.

The low voltage fast type usually corresponds with anxious, nervous and hypervigilant individuals. Though not pathognomonic, it is commonly seen in alcoholism and alcohol free members of families of alcoholics with a strong family history.

Interestingly, in research on this pattern, it is shown to respond to alcohol by suddenly having alpha that is well formed. The alpha will slow and rhythmic slower activity will increase if higher doses are given. The state is reported in euphoric terms by the research subject. This euphoria is also reported associated with alpha induced by opiates.

The low voltage fast pattern responds well to alpha training with a normal alpha distribution of 8-12 or 9-11 Hz. The learning curve for this is well established, having a fifth order curve fit. The phases of the experience are well defined by the curve.

There is an initial increase in alpha due to the habituation to the clinical setting, with subsequent decreases in alpha during the active attempts at controling the alpha. These phases are followed by the release of the active attempts and a return to the habituated level. This is followed by passive volitional attempts and the eventual acquisition of voluntary control seen as the exponential increase at the end of training.

The subsequent alpha/theta training is commonly used by neurotherapists in these cases when there is a concurrent addiction or intense life stress or trauma by history.

Temporal lobe alpha

When alpha is seen in the temporal lobe, it can be from a variety of causes, indicating that a more complex neurofeedback protocol response may be needed.

The alpha from old head trauma is usually a faster alpha variant, adjusted for the individuals alpha ‘tuning’. This is seen over a year or 2 from the time of the trauma, after the acute healing and swelling have long dissipated. It replaces the slowing which may be seen initially.

Temporal alpha may also be an effect seen in response to a decrease in ipsilateral frontal lobe activity. The decrease in uncinate fasciculus or inferior longitudinal fasciculus stimulation from the frontal lobe allows the temporal lobe to be idle. This usually will be seen with one of the frontal lobe patterns discussed earlier.

The temporal idling may be cleared up with the direct frontal work discussed earlier, but may require lower band beta training directly on the temporal site.

Strong alpha at T5 or T6 can contaminate the ear references, yielding a false image of frontal alpha in the qEEG. The ears, having alpha present and the frontal lobes without alpha are compared in the differential amplifier. The amplifier will show alpha in the frontal channel falsely, which has to be controlled for by using a variety of montages in reviewing the data. The frontal alpha will not be seen with sequential or non-contaminated reference montages, such as Cz or in more sophisticated equipment the ‘common average’ or even the ‘Hjorth’ montage may be used to give a more pure look at the data.

The temporal lobes seem sensitive to excessively fast beta training, with 14 Hz training, 12-15 Hz, 14-16 Hz or other lower band beta used more commonly than a higher frequency intervention due to this sensitivity. In my experience, these bands seem to be best adjusted based on clinical response, not to any obvious spectral loss in the CSA or amplitude mapping.

The post traumatic faster alpha seems to respond to coherence training, seemingly reconnecting the functional relationships. This requires the use of qEEG coherence measurements, as without this, the training sites and bands would not be evaluated or selectable based on any objective criteria.

A note on coherence and phase

The cortex is full of neural connections, all electrically active, though not all seen with the EEG. The EEG is measuring summations of radially generated action potentials from pyramidal cells, not the laterally oriented cortical-cortical tracts.

The raw EEG is blind to nearly 2/3 of the electrical activity of the cortex. Much of which is seen by the Magnetoencephalography (MEG), a measure of the “magnetic” activity of the brain (actually lateral current flow of intracellular activity). The MEG is however blind to the extracellular potentials arranged radially which comprise the EEG.

The longitudinal myelinated fiber tracts are the high speed web of the cortex, not the organized subcortical radiations of the thalamo-cortical systems or other subcortical-cortical projection pathways. This network of local arcuate, longitudinal, fronto-temporal (uncinate) and interhemispheric collosal tracts are invisible to the raw EEG.

The activity of this invisible network, however, can be inferred from the coherence and phase relationships between areas “hooked up” by the network. This spatial distribution, “connectivity” reflection of the subsurface activity is obviously quite complex. The covariance of power at two sites (coherence) or their covariance in time (phase) give measure within the EEG to activities within this invisible network.

The view of the raw coherence and phase data yields little to the non-expert. When compared to an age and sex matched normative database, displayed as a Z-score, the magnitude and direction of variance, including the significance of the variance become much more evident.

There are two types of phase relationships seen in qEEG, conducted phase differences and propogated phase differences. The propogated phase is seen where a focal phase reversal indicates the source of an EEG phenomenon. The conductive phase is simply the time delay due to propogation along neural pathways.

The phase measurement reflects the correlation of covariance in time of activity at two sites. This temporal relationship can be slowed by damage to tracts due to demyelinating, structural or toxic/metabolic influences. The phase relationship may be faster with increased nerve conduction velocity, or by volume conduction through fluids and as a field effect.

The simultaneous projection to various cortical locations of synchronized volleys from thalamo-cortical radiations seen during thalamic activity paced by the ventral-medial or reticular nucleus is a “highly connected” state, with high phase synchrony. This unique synchronized state is predictive of meditative expertise in Zen meditators (Gevins et al.). It involves progressively generalizing increased phase synchrony in alpha, followed by increases in theta synchrony (possibly representing slowed alpha).

Similar findings have been seen in Yogic meditators, though with differences in habituation to repetitive sensory stimulation. The Yogic meditators habituated faster than normal and the Zen meditators failed to habituate. Interestingly, this reflects the philosophical views of the two meditative techniques. The Zen meditation aspires to novelty of experience while the Yogic traditions emphasize the imaginary nature of the external reality.

The phase relationship is measured as difference in the degree of arc of tangents of two waveforms, measured at a point in time. This is reported as degrees of phase shift from 1-180 degrees, or time synchrony of the waveforms, reported in milliseconds.

Often confused with phase is the EEG measure of coherence. The confusion comes from the use of the term “coherence” as an adjective descriptor for phase. This misuse of a technical term as a descriptor in the same field of interest is problematic. The term “phase coherence” should be eliminated and replaced by “phase synchrony” or, most properly, by specifying a phase relationship from 0-180 degrees of phase shift or by giving the Z-score deviation from normal. Please retain the use of coherence for it’s technically proper role within this field.

Coherence is the cross correlation of the power (or amplitude) of activity at two sites. Sites that covary highly are presumably processing related cortical/subcortical volleys or have a high “connectivity”. This is reported as a value from 1 to 0 (on some older equipment, as a value from 100% to 0% coherence).

The cortical-cortical long fiber connections compete with the shorter connections. As Bob Thatcher says, “The close siblings can speak to each other, but not to their distant cousin at the same time.”. This is called the two compartmental model of coherence.

There is a third compartment I believe, the subcortical-cortical compartment, which would explain the observation of high coherence locally having decreased connections locally. The coherence is from the subcortical source being connected to both sites, not the cortical-cortical compartment’s connectivity.

Coherence is most easily viewed as morphological similarity, with correction for absolute magnitude and is irrespective of the time synchronization. When two waveforms are shifted in time until maximal coherence values are attained, the time base shift is the phase delay of the waveforms.

Structural damage produces reliable, consistent patterns of change in phase and coherence patterning in the qEEG, though functional influences account for variable findings. This variance makes interpretation of the data subject to having to rely only on strong patterns of variance, not isolated findings.

The proper conservative interpretation of these data must also be viewed in the context of the entire constellation of findings from the rest of the patients EEG, qEEG and clinical presentation.

When training changes in coherence or phase using neurofeedback, over-training (shifting beyond a normal relationship range) needs to be avoided. This requires merely setting a proper normalized goal or value as a training target.

There is currently what I believe to be an inappropriate practice in coherence NT. This is the use if a single channel EEG machine used sequentially (old term bipolar) with the assumption that this will feed back coherence. This assumption suggests that increased highly coherent activity cancels, thus decreasing the amplitude of the channel. Thus training amplitude could train coherence.

This is a grossly false model of coherence feedback. This model assumes the phase of the activity to be synchronous. It also assumes that the synchronous activity has amplitude equivalence. In reality the coherence calculation equally weights amplitudes, correcting for asymmetries, the amplifier does not. The calculation of coherence is not time locked, measuring covariance independent of the time locked nature of the amplifiers response.

I believe we are not yet in the presence of enough information about the clinical impacts and needed protocol controls to make full use of the clinical application of these types of training. The clinical application of these techniques is highly fruitful ground, needing systematic clinically valid research and protocol development.

More fully conclusive research is needed based on the ongoing application of this training before rules for intervention are presented.

I have nothing against the careful clinical use of coherence or phase training. When the more “traditional” neurofeedback applications fail, these phase and coherence based interventions should be empirically tried. With more trials using the proper measures, design and controls, advances will be made.

The departing caveat

Now that I have completed this codification of some of the interventions seen currently in qEEG based NT, I can say without question that this will be a source of future embarrassment. To capture a snapshot during a field’s rapid development stage is a guaranteed red face in the future. If you don’t believe this, look at your own childhood photographs!

So, please be gentle with your ridicule, and don’t mistake this art to be a science… not just yet.

9 thoughts on “Patterns seen in the qEEG and their indicated interventions

  1. Jay, As you may recall, you reviewed my system of “types”, which I call brain activation patterns, several years ago. Very helpful to me. I am interested in a specific problem I’ve seen recently that I’m not sure how to fit into your system (or mine), though I recall having heard you speak of it in the past: Clients who appear to have excessive alpha, especially which fails to block, that is actually probably the Mu rhythm. So far training alpha down or beta up have had little effect. These do tend to show the low-empathy pattern suggested by mirror neuron work. I recall many years ago you indicated that Mu was related to extreme frontal slowing, and I seem to recall a more recent comment from you regarding training gamma to block Mu. I’d love to hear how you would fit this pattern into your phenotypes and, most especially, your recommended training approaches. Thanks, Pete

  2. Mu is an effect of a frontal lobe disturbance, commonly seen in ADHD as well as in PDD as a “mirror Neuron” system disturbance of the fronto-striatal-thalamo-motor regulatory loop. Mu is seen when the loop is not engaged, and generally you will see a frontal lobe disturbance making this problem.

    Commonly either a slow pattern, alpha excess, or a beta spindle… but the frontal lobe regulation of the motor strip will be compromised by whatever pattern it is, and often hypocoherence fronto-centrally (or Sterman’s fronto-central disconnect) will be seen in the “connectivity, though it is obviously not a cortical-cortical connection, but a cortical subcortical-cortical loop.

  3. Jay, I have a young boy, age 15, who has a 7 hz and 14 hz pattern frontally, most dominant over central electrodes. Niedermeyer states that this pattern is a normal variant in adolecents, but this boy does have attentional and emotional issues. Is this a normal variant, or just normal as in no epileptic form, but a faillure of the frontal cortex or singulate? Thanks! Dagmar Timmers.

  4. Dagmar,

    It was good that you question the opinion of normalcy of “14 and 6” but unless I see what you actually have recorded, I’m not sure you actually have “14 and 6 positive spikes” You report an atypical “14 and 7” and do not discuss the distribution ir polarity of the spike portion…. So I am not really confident what you have identified.

    I can’t comment on the specifics in your case due to this uncertainty… however, in general what Niedermayer is saying is that there is no specific pathology… no epilepsy, nop strokes, tumors, vascular lesions, demyelination, etc…

    The importance of this difference in what “normal” means was the basis for the split in the field of EEG and the AES splinter group forming AMEEGA (now ECNS) by Gibbs and Gibbs, Duffy, Hughes and others.

    The actual 14 and 6 is identified as a non-specific marker in behaviorally disordered children according to the Gibbs and Gibbs view… not a form of epilepsy, though that is a group in which it was originally seen as well…

    I hope this note helps… even if I can’t comment on the case itself directly due to the lack of an EEG to review.


  5. Jay, I recall having heard you speak of high alpha power secondary to head injury but can’t recall if that is following gray or white-matter damage. Does training to reduce it/increase beta help with cognitive function improvement.

  6. Pete,

    Gray matter damage decreases alpha initially, and also has beta and gamma decreases. as the very neuroplastic gray m atter heals and is not re-engaged with function, the alpha will return and even be seen as an excess idling of the cortical area… until it is re-engaged in function, when the beta and gamma will return and the alpha will regain a normal dynamic, and no longer be in excess.

    White matter damage increases slowing due to a decreased inhibition of the sheet dipoles due to the lack of (or decrease in) cortical input.

    I hope this helps clarify the issue for you… let me know if you need a more in-depth answer.


  7. Jay,
    Thanks. That reinforces and deepens whaat I had recalled.
    I’ve been hearing a great deal of late about the Othmer’s infra-low frequency training but couldn’t find much about it beyond the SCP work I’ve heard you speak of previously–and that didn’t seem to be about training in bands from 0-0.01 Hz. A friend recently sent me the link to some work by Marcus Raichle at WU ( ) which she clearly thought was about infra-low, but the more I read of the article, the more it sounded like SCP. I’ve tried to find anything about the infra-low stuff in Rhythms of the Brain and Neocortical Dynamics, but can’t find anything I recognize in either. What is your take on infra-low training as the Othmers are practicing it?

  8. Pete,

    My 2 cents: Their approach is an experimental technique without any efficacy literature to support it, and those who are doing the technique need to get their approach into the efficacy literature before we can actually start to tease out the underlying factors and mechanisms.

    There are only semantic differences between SCP, infra-slow EEG and cortical DC field potential recordings, as they all are part of the same phenomenon.

    I’d be happy to discuss the Othmer’s work, but their outcomes have not been published in peer reviewed material to actually start to be able to really evaluate what their work actually is. Their explanation of the effect has changed over time from a coherence phenomenon to phase shifts… they need to get their story illustrated with real outcome data and EEG recordings to identify the actual effect before teaching classes about it as though it is a standard approach in NF. It is experimental.

    The recent edition of NeuroConnections has a good discussion of the factors influencing the DC or infra-slow activity, and I’d point you there for any current discussion bsed on actual EEG data and not just theory.

    Once they actually get their material researched with data being published, then we will be able to discuss what it is they are doing. Right now they teach theories about how it works, but the data doesn’t support their conclusion, as the signals change due to coherence, power and phase changes when it is actually examined by Richard Souter with real data and not just a thought experiment.

    I’m fine with thought experiments when actual data collection is not feasible (like the train at the speed of light experiements by Einstein), but when we can easily collect real EEG data so easily for actual data analysis, thought experiments are inexcusable.

    The slow activity could be skin contact shifting, electrode drift, thermal drift, amplifier drift, pulse artifact, respiratory artifact, eye movements, or even actual EEG activity… but until it is researched with appropriate designs to make efficacy claims, it is experimental and merely based on anecdote.

    Good luck in your search!


  9. Jay,
    I’ve just started working with a blind psychologist–lost his sight through a series of operations for glaucoma around the age of 14, so there are some trauma issues as well. He says he sees a sensation of light with eyes open, but no details or images. I’m interested in what you would expect to see vis-a-vis alpha in such a case. He shows high amplitudes of 6-8 Hz eyes-open and eyes-closed which drop significantly at task in the parietals. Centrals and Frontals also show dominance in that band, but it doesn’t change much at task. In the 8-10 and 10-12 bands he shows little activity and no typical alpha activation with eyes closed. Any special suggestions relative to training someone who is blind (other than not to count much on visual feedback)?

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