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 neurosciencebased 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
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.