This is the title of my dissertation for the Ph.D. degree in Psychophysiology with an emphasis in Neuroscience. My research began in 1989 and continues today. My wish is to express to the reader of this article what I have found and continue to find in studying and observing those afflicted with this illness.

Perhaps one of the best kept secrets in medicine today is that humans are developing previously unknown and frightening diseases which are emerging as distinct disease entities. Many of these illnesses present with that difficult symptom constellation of headaches, dizziness, memory loss and "black out spells." Diagnosis is evasive, but essential to proper treatment. I believe these newly emerging diseases represent a world out of balance.

There is good reason to believe that these diseases may be due to our suffering, toxic environment and the effect this environment is having on our immune systems. Hypotheses and research toward discovering causes for these illnesses have tended to focus on infectious agents, such as viruses or bacterium. Relatively little attention has been paid to the issue of susceptibility. I propose that both new viruses (this would include "old viruses" combining to form possible hybrid viruses), and susceptibility need to be explored.

As I began to focus upon this one specific illness, as well as the possibility of viruses and bacterium mutating in order to enter a susceptible host... a host who may have been previously immune to invasion, I began to understand why environmental illness is often seen in patients with CFIDS. The sensitivity to odors which often causes exacerbation of all symptoms may be explained by a dysregulation of the part of the brain known as the piriform cortex. Unusual sensitivity to other substances may be explained by limbic antigen presentation which is now known to occur in stressed rats and also by direct transport of substances from the oropharynx to the brain. In fact, some CFIDS patients have been diagnosed by their physicians as having "Chemical Sensitivity Syndrome (CSD)." It is almost a matter of semantics when these same physicians take an adamant stance against the diagnostic term of CFIDS.

My only explanation for this bias on naming an illness is that CFIDS has become a medical/ethical/political illness. I propose that for the care of the many afflicted, clinicians take care in regards to "owning a disease" and in making claims as to cures.

If CFIDS is a discrete disease, it should have some symptoms that are not explicable through the concept of somatization and depression. Symptoms appear to differ from symptoms of somatization/depression, including muscle weakness specifically in response to exercise ( as opposed to general lethargy associated with depression). As Abbey and Garfinkle put it, "abnormalities in muscle metabolism remain as one of the most persuasive arguments in favor of the existence of CFIDS as a bone fide discrete disease."

For my first study towards finding a diagnostic marker, I studied various neurological and psychological illnesses such as organic brain syndrome, Alzheimer's disease, multiple sclerosis, chemical sensitivity syndrome, closed head injury, stroke patients, manic-depressive disorder, bipolar personality disorder, attention deficit disorder, and chronic depression. I utilized quantified electroencephalograph (QEEG commonly referred to as "brain mapping") in conjunction with specific cognitive tests. Once I had established a brainwave signature (a unique EEG pattern) for each illness studied other than CFIDS, I then included 10 CFIDS patients diagnosed through the CDC criteria and by Dr. Paul Cheney.

Next, I studied the brainwave patterns of CFIDS patients and compared their QEEG results to controls and to patients known to have neurological and psychological disease. My objective was to see if I could find a brain abnormality which was subtle (and therefore missed by MRI, SPECT, PET and BEAM) through QEEG and to develop that brain wave into a signature which would be sensitive and specific to CFIDS, thus establishing a diagnostic marker for the disease.

After carefully analyzing the data, it was clear that patients showed an abnormal increase in slow wave activity compared to controls who demonstrated normal EEG patterns. This slow wave activity was not seen in the resting state of most patients, which could explain why conventional EEG testing has failed to pick up these abnormalities (conventional EEG is usually done in the sleep-deprived state, while the patient is instructed to close their eyes and relax). Patients demonstrated increasing abnormal slow wave activity with tasks of increasing cognitive difficulty which was not seen in controls.

Increased and generalized slow wave activity is consistent with a metabolic encephalopathy which may include slow viral infection as a subset of the metabolic encephalopathies.

These results were so promising that a second study was designed to increase the credibility of this original inquiry. The objective of this second study was to be able to differentiate CFIDS patients from controls in a blinded fashion. To differentiate the two populations, I utilized an EEG pattern which was present in approximately 280 CFIDS patients which had been in the original study. This brain abnormality was not present in other patient populations.

In this second study, patients were correctly identified with 80% sensitivity and 82% specificity compared to healthy controls. The specificity could be argued to the 90th percentile as, following testing, one of the controls confessed to having prolonged fatigue for a duration of greater than 6 months, as well as short term memory impairment significant enough to have jeopardized her job performance. Perhaps this individual represents a subclinical patient. This individual may have been untruthful in her screening process in order to receive a medical work-up for her own health concerns. The four duplicated files utilized as an internal control were selected with 100% accuracy.

At the present time. well over 400 CFIDS patients have been evaluated in this way. Primarily for purposes of documenting cognitive decline for purposes of receiving disability and for a method of tracking treatment efficacy.

Contrary to the belief among some physicians and insurance companies, this evaluation is no longer considered experimental. We have seen a better than average percent of insurance reimbursement for this evaluation. Since advancing technology implies change in the way a physician must "do business", a skeptical doctor may be most interested in keeping the patients coming through his/her door while continuing to use their existing equipment and knowledge.

Because I am primarily interested in treatment, I began to utilize my new knowledge of the brain to develop a symptomatic relief for CFIDS patients using the principles of operant conditioning as a treatment modality.

This treatment is called "neurofeedback" so as to differentiate it from conventional biofeedback, which implies behavioral change for the patient as a part of the effectiveness.

Neurofeedback does not utilize behavior change to achieve results; rather, the goal in this form of treatment is to bring order to a disordered brain physiology through operant conditioning. Neurofeedback should be thought of as a technique of rehabilitation, a type of physical therapy for the brain. Imagine a physical therapist using various modalities and instruments to rehabilitate an injured or paralyzed muscle in order to restore function to that muscle. This is the exact rationale behind the utilization of EEG neurofeedback for CFIDS patients.

Following a study of treatment efficacy, 100 patients learned to change their abnormal brain waves in various parts of their brain in the direction of either greater or lesser activation. The goal was to achieve as near-normal an EEG pattern as possible. This treatment study suggests that the impairment of the CFIDS brain is not due to an unchangeable pathological structural process, but rather to demonstrate that CFIDS patients are capable, after intensive training, of achieving a certain amount of modulation through operant conditioning of brain wave states via neurofeedback. There is a direct correlation with a reduction of frequency and intensity of symptoms and regulations of these EEG patterns. Furthermore, the changes seem to become permanent without continued treatment.

The first 100 subjects treated in this way are currently in long term follow-up: It has been five years since their treatment was completed. The reports of maintenance of symptom relief are very promising. Initial results confirm that regulation of low brain potential is impaired in chronic fatigue patients. This would suggest that the myriad of symptoms may be due to a change in brain function, not structure. If this is true, this illness may be reversible if the pathophysiology could be discovered and treated.

This long-term continued improvement suggests that it is unlikely these results would be merely placebo effect.

Neurofeedback is not considered experimental and is often covered by medical insurance. The first application of neurofeedback was in 1957 as a treatment for epilepsy. Neurofeedback is now used for many disorders including epilepsy, anxiety, stress reduction and attention deficit disorders.

Plans are in the making to get this information our to the medical community at large. Quite a bit of interest has been shown by physicians who have previously denied the presence of any definite physical findings in CFIDS patients. Besides treating and evaluating patients in Charlotte, plans are in the works for starting a clinic in Great Neck, New York for the evaluation and treatment of CFIDS patients. We in my office are hoping to make these resources available to CFIDS sufferers everywhere by getting clinicians from every state to learn and implement these techniques.