Neurofeedback and the Brain

Neurofeedback is an emerging neuroscience based clinical application, and understanding the underlying principles of neurofeedback allows the therapist to provide referrals or treatment, and provides clients with a framework for understanding the process. The brain’s electrical patterns are a form of behavior, modifiable through “operant conditioning,” with the excessive brain frequencies reduced, and those with a deficit are increased. The learning curve for EEG has been described (Hardt, 1975).

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.

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Thalamic Involvement in the Generation of the Alpha Rhythms

Alpha… it’s not a simple idling rhythm… let’s look at alpha generators:

The thalamic involvement in the generation of the alpha rhythm is being under-valued when looking at the LORETA images of alpha current source generators. The alpha power may come from the sources that LORETA identifies, but the thalamus is intimately involved in alpha rhythm generation, and this is not part of the LORETA image of the sources.

The polarization within the thalamus sets the base frequency of the alpha, but the cortical rhythm requires a complex multi-layer feedback loop from the thalamus to the cortex, and back to the thalamus. Without the cortex, there is a total disruption of the normal spatio-temporal distribution of the alpha wave’s spike trains within the thalamus, and cortical damage often disturbs coherence due to this mechanism.

The thalamus distributes the alpha posteriorly via specific sensory relays, which have a simple return circuit. Like the white matter relay from the lateral geniculate of the thalamus to the occipital lobe’s primary visual areas, and directly back. This thalamo-cortical-thalamic loop is relatively faster than the loop seen frontally. The frontal return circuitry is not simple, but the descending routes are complex and somewhat circuitous, taking more time, and thus it is common for the frontal lobe’s alpha to be at the slower end of the individual’s alpha frequency range. The frontal lobe has a return path through the striatum.

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Neurofeedback Foundation Award 2009

In his role as the Managing Director of the Foundation for Neurofeedback and
Applied Neuroscience
John Fisher recently announced the Foundation’s selection of a recipient of the Neurofeedback Foundation Award.

The Foundation gives an award to the author(s) of the publication which has
“contributed the most to furthering the field of neurofeedback” during the
past year. Past recipients have included Drs Rob Coben, John Gruzelier, as
well as Johan Levesque and Mario Beauregard.

This year the Foundation has chosen Professor Dr. Juri Kropotov as recipient
of this years award, based on his book and the body of work Juri has
contributed over the years.

This award selection was announced recently at the EEG Spectrum Clinical
Interchange Conference in Los Angeles.  The award includes a gorgeous plaque
as well as an honorarium.

We salute both the Foundation for helping promote the fiend of NF, as well
as all the award recipients for their publications and the substantial
contributions they all have given to our field.

Sensory + Motor Homunculus

The homunculus is a spatial representation of the cortical topography of the
somato-motor strip which is dedicated to either motor or sensory function.
The two have different structural details, since there are sensory inputs
from non-motor areas.

Some people have tried to create 3D creatures which show the spatial
distortions, with the enlarged surface proportionate to the motor expression or sensory sensitivity, with varied results.

See if you can identify the differences between the sensory and motor
version, and also critique the accuracy of the artist’s rendition of these
various versions.

Have fun with the exercise!

Jay

In Memory of E. Roy John PhD – World Renowned Neuroscientist

Life offers us many teachers, and we generally only learn a small sliver of what they have to offer from the breadth and depth of their experience.

One such teacher was E. Roy John, who most knew as a brain researcher, though he had so much more to offer… did you know he was “blacklisted” as a liberal, or that he worked on the Manhattan Project making Plutonium? Did you know he is considered the grandfather of Cuban Neuroscience? How about his love of boating…

Perhaps a quick look through his obituary will make us all appreciate just a bit more the actual magnitude of our loss from his passing…. And then you can look over the diagram of the brain and see some of the complexity of the models Roy passed on to those who now have to carry on without his wise counsel.

Joyful in having known him, and saddened by our loss,

Jay

In Memory of E. Roy John PhD

Brain Functional Diagram from Roy John PhD

qEEG Artifacting

The qEEG represents the statistical manipulation of the raw EEG, so an understanding of these manipulations should precede any discussion of the qEEGs clinical indications for protocols. Without such knowledge any given finding may be misinterpreted.

Following the careful recording of the EEG, the quantitative analysis is begun with the sampling of the data to be used in the analysis by the Fourier transform. The Fourier analysis assumes there are no transients (epileptic discharges, episodic voltage changes etc.) or state changes (light sleep, drug effect, mental task, etc.), so these must be avoided when selecting data for analysis in qEEG for eyes closed resting database comparison. There are some eyes open and task databases available more recently (Hudspeth, Sterman, Duffy etc.)

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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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Dementia & Alzheimer’s Disease (AD)

I often get questions about Alzheimer’s Disease (AD) and the EEG.

Whenever a client presents with the question of dementia, all other forms of
dementia need to be ruled out before you are left with the diagnosis of AD.
There are many EEG signatures of various forms of dementia, all of which are
helpful in evaluating a client’s presentation of dementia.

Done by experts in EEG in dementia, the EEG and qEEG may be of substantial
additive value in the differential diagnosis puzzle that all cases of
dementia represent clinically.

One EEG pattern seen in dementia is the presence of periodic triphasic
slowing in the EEG, which is actually diagnostic of subacute sclerosing
panencephalitis (SSPE). SSPE is a “spongiform encephalopathy” where the
brain becomes like “Swiss cheese”, with holes scattered throughout. This
periodic triphasic finding is differentiated from MULTIFOCAL triphasics
which are diagnostic of Crutzfeld-Jacob Syndrome (CJD), which in lay terms
is a form of mad cow disease in humans.

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