In research that may help construct a working model, J.W. Mason (1982) studied subjects who showed extreme values in several hormones (either high or low) were at a higher risk of developing disease than were those who had moderate values. In discussion of his finding he stated that susceptibility to disease may not be simply a function of increased or decreased levels of one hormone, but rather the net result of a complex interaction among hormones and target organs and that an unstable CNS (e.g., hypothalamus) may yield increased vulnerability to disease. In a related study, Black (1994) concluded that hypofunctioning of the HPA may be involved in autoimmune or other diseases with excessive immune system activation whereas hyperfunctioning of the HPA axis has been found in a large number of patients with major depression.
The medication lithium carbonate typically utilized as a "mood stabilizer" is prescribed prophylactically in the treatment of manic-depressive psychosis, schizophrenia, and alcoholism. The proposed mechanism of action for lithium is thought to be the stimulation of a downregulated immune system (Smith, 1991). Other medications prescribed to bring about stabilization include Tegretol, Depakote, and Klonopin. Stabilization or regulation of a disregulated system is a goal in the pharmacological treatment of psychological as well as physiological disorders.
Instability of the central nervous system is seen in seizure disorder, attention deficit disorder, and closed head injury among other central nervous system disorders currently being successfully treated with neurofeedback. Also, disregulation of brain function is thought to be the basis of certain psychological disorders (depression, mania, obsessive-compulsive disorder, anxiety, Etc) which likewise respond to neurofeedback treatment. If it is that Mason, Black, and Smith's findings are true, and medication produces stabilization within the CNS, then we have at least one theoretical model for proposing a mechanism of action for immune regulation and therefore modulation through neurofeedback. Our working hypothesis then becomes: just as seizure thresholds can be raised, attention and concentration skills can be refined, and neurons can be reeducated and/or recruited to produce beta in closed head injury, so can a disregulated, downregulated, or an unstable immune system be stabilized and/or modulated utilizing neurofeedback.
THE RELATIONSHIP OF CORTICAL EEG TO PHYSIOLOGY
At this point I will briefly summarize the theoretical and historic basis of neurofeedback as it relates to altering physiology. There is general consensus that repetitive waves recorded from the surface of the scalp (the EEG) are summed synaptic potentials generated by the pyramidal cells in the cerebral cortex. The EEG represents responses of cortical cells to rhythmic discharges from thalamic nuclei. The frequencies and sizes of the thalamic discharges, and hence the cortical potentials, are determined by the special arrangements of excitatory and inhibitory interconnections among thalamic cells. This physiology has been termed the ascending pathway of the somatosensory system (Dempsey and Morrison, 1941, Shepherd, 1983). Interaction among deep brain structures, in particular the reticular formation, disrupt or desynchronize rhythmic discharges in the thalamic nuclei thereby altering cortical EEG. This fact allows for the likely hypothesis that, since changes in deep brain structures alter cortical EEG via well-defined pathways, neurofeedback -which alters cortical EEG patterns - can have a pronounced effect upon these same deep brain structures. This proved to be true in the discovery of somatotopic maps. Neurons carrying information from the sensory periphery terminate at selected areas of the thalamus where they are arranged in a somatotopic representation of the body. These thalamic areas in turn project to selected areas of the cortex, all in very orderly fashion and with substantial reciprocal projections from the cortex.
In the 1970's and 1980's, "states of consciousness" were defined and yielded important tools for recognizing cerebral abnormalities (Sterman, 1981). As computers and instrumentation became more sophisticated, distinct event contingent changes in EEG were delineated. M. Barry Sterman (1967) defined the sensorimotor rhythm (SMR) as a unique 12-14 Hz. activity recorded over the sensorimotor cortex and went on to identify specific frequency-function relationships in the cortical EEG. It was noted that gradual depression of tonic muscular activity occurs when SMR activity is present in the EEG. Sterman went on to show that SMR can be conditioned (Wyrwicka and Sterman, 1968), thus laying the foundation for neurofeedback treatment of seizure disorder. Chase and Harper (1971), in related studies, demonstrated a marked decrease in heart rate and stabilization of respiration during SMR activity. These intriguing findings demonstrate an intrinsic connection between heart rate, respiration, muscular activity and the dynamic rhythmic activity of the brain as measured in the EEG. The discovery that CNS states can be conditioned and altered to bring about positive changes in physiology is nothing short of remarkable.
Correlation of EEG patterns with behavior, cognition, and emotion are now being intensely studied and defined. Equipped with newer and better instrumentation that is reliable, immediate, and "user friendly," data are indicating that subjects may learn to control previously uncontrollable physiology (self-regulation). Furthermore, individuals who utilize neurofeedback state that they perceive reality with greater clarity as well as acquire greater control over fluctuations in mood. In the addiction recovery realm, the addition of alpha neurofeedback training allows the addict to more easily escape unwanted behavior patterns such as chemical addiction, compulsive behaviors, and cravings. Improved concentration and attentional skills come with the beta enhancement and theta suppression as documented in the attention deficit disorder literature. Some researchers are going as far as to state that neurofeedback will eventually allow humanity to transcend our present limited consciousness as we experience true liberation from automatic stress responses, addiction, chronic pain, anxiety, depression, and a variety of other cognitive, emotional, and physical limitations (Hardt, 1994).
BIOFEEDBACK AND THE IMMUNE SYSTEM
In the area of biofeedback and the immune system Peavy, et al (1985) collected correlation data that indicated that there is a significant relationship between higher stress and decreased immune function. He went on to administer EMG and thermal biofeedback with relaxation training to a group of subjects and found significant increases in phagocyte activity comparing pre and post treatment blood work. Peavy concluded that biofeedback may help individuals to develop cognitive and behavioral skills to cope with, or adapt to, stressful environments. Biofeedback with meditation was utilized in successful treatment of psoriasis, a stress-related disease, in a study conducted by Farber (1993).
Gruber, et al (1988) conducted two studies involving metastatic breast cancer. The first, a pilot study, involved 10 subjects given biofeedback and guided imagery over a one year period. Blood samples taken monthly indicated significant increases in PHA mitogen response, CON-A mitogen response, mixed lymphocyte response, interlukin 2, natural killer cell activity, erythrocyte-rosette assay, IgG, and IgM. In 1993 Gruber, et al, reported on an 18 month study of immune system and psychological changes in stage 1 breast cancer wherein subjects were given biofeedback, guided imagery, and relaxation training. Significant positive changes were found in natural killer cell activity, mixed lymphocyte responsiveness, concanavalin A as well as the number of peripheral blood lymphocytes. Reductions were also noted in levels of anxiety on psychometric scales. McGrady, et al (1992) reported increased blastogenesis as well as decreased white blood cell count (due to decreased neurophils) in fourteen subjects trained with biofeedback-assisted (EMG and thermal) relaxation for four weeks. The author also reported that the subjects with lower initial anxiety scores and forehead muscle tension levels showed larger increases in blastogenesis and larger decreases in neutrophils than subjects with higher initial anxiety and muscle tension levels. This research indicated that biofeedback may have helped increase the ability of circulating lymphocytes to divide. Since blastogenesis is known to decrease in the early states of HIV infection, and even more significantly in the later stages of AIDS, this suggests a potential benefit of biofeedback to individuals with HIV.
Auerbach, et al (1992) conducted a study on 26 HIV+ males who were assigned to either a treatment group, consisting of thermal biofeedback, guided imagery and hypnosis or a wait list control. Subjects met in a group once per week for eight weeks. Although no significant changes were found in T-4 level in the treatment condition, significant decreases were noted in HIV related symptoms (fever, fatigue, pain, headache, nausea, and insomnia) as well as increases in vigor and hardiness. For a further understanding of relaxation, imagery and biofeedback-assisted strategies as well as the use of humor, emotional factors, hypnosis and conditioning paradigms, the reader may reference an article titled, "Self-regulation of the immune system through biobehavioral strategies" in Biofeedback and Self-Regulation (March, 1991).
NEUROFEEDBACK AND THE IMMUNE SYSTEM
In the realm of immune enhancement with neurofeedback there are currently very few studies. Michael Tansey (1994) published the first peer reviewed article as to the curative effect of 14 Hz. EEG neurofeedback on multiple cases of Chronic Fatigue Syndrome (CFS). Fran Lowe (1994) likewise reported positive effects on five subjects with CFS utilizing 13-14 Hz. beta training. Both Tansey and Lowe measured improvement on psychometric measures rather than direct measurement of immune system factors (i.e., Ebstein-Barr virus).