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October 21, 2009
Self-Regulation of the Immune System
By Gary J. Schummer, Ph.D.
The concept that we can modulate immune response through neurofeedback is a logical extension of currently accepted procedures and protocols.
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INTRODUCTION
The concept that we can modulate immune response through neurofeedback is a logical extension of currently accepted procedures and protocols. The extensive body of literature in psychoneuroimmunology (PNI) may lead one to wonder why this is not one of the primary areas of research utilizing biofeedback and neurofeedback. Certainly one reason must be the fact few researchers have knowledge in the disparate domains of PNI. Besides a background in biofeedback, one must have at least a rudimentary understanding of molecular biology, psychology, neuroscience, endocrinology and immunology to adequately address this field - or have access to competent individuals with whom to collaborate.
Research has elucidated extensive mediating mechanisms with a dense communication network that interfaces the central nervous system (CNS) with both the endocrine and immune systems. The brain communicates with the immune system through two known pathways, the autonomic nervous system and the hypothalamic pituitary adrenal axis - HPA (Angeli, 1994). Bullock (1985) writing in Neural Modulation of Immunity showed rather conclusively that there are autonomic nervous system fibers that go directly to the thymus where T-cells mature. More recently, Felten and Felten (1991) have demonstrated that primary lymphoid organs are heavily innervated by fibers from the sympathetic nervous system. A relatively new field called "immunoendocrinology" is uncovering numerous bilateral interactions between the immune system and neuroendocrine circuits. Researchers' Derijk and Berkenbosch writing in the International Journal of Neuroscience (1991) discuss evidence indicating that an immunoendocrine feedback loop, which they term "immune-hypothalamo-pituitary-adrenal systemâ€, is an integral part of the regulation of self tolerance. Pathology within this system is related to development of autoimmunity, a discovery that may lead to new prophylactic and therapeutic strategies.
Simply observing immune response is often proposed as key to understanding the etiology and directing the treatment of physical, psychological, and even psychosocial (Smith, 1991) disease. Many journals are dedicated to research that exposes the complex homeostatic mechanism in the immune system as it responds to stress, pathogens, trauma, pain, toxins, as
well as positive life experiences. Consequently, the application of neurofeedback techniques that reorganizes and reorients brain electrical activity can, in all probability, be utilized to modulate positively the immune response.
PERTINENT RESEARCH
An exhaustive review of the literature regarding the mind's impact on the immune system is beyond the scope of this paper, however, selected studies shall serve to illustrate this relationship. One of the most dramatic demonstrations of the intimate involvement of the brain with the immune system is drawn from a series of studies conducted by Stephen Locke of Harvard University and reported on in a book titled The Healer Within-The New Medicine of Mind and Body (1987). The researcher withdrew cancer- and virus-fighting natural killer cells from a group of depressed subjects as well as from a group of non-depressed subjects. When these killer cells were placed in contact with cancer cells, the killer cells from the non-depressed subjects surrounded the cancer cells and destroyed them while the killer cells from the depressed subjects did nothing. This might cause one to ask: How did the natural killer cells from the non-depressed subjects know what to do while the natural killer cells from the depressed subjects did not? Apparently, through complex and, as yet, not well understood mechanisms, important immune system factors can be turned on or off by the chemicals produced with certain moods. This fact caused the author to write, "Even relatively minor life stresses leave their mark on the immune system." Ruff (1984) and Pert, et al (1985) likewise reported that subjects who were made to feel helpless (a primary feature of depression) show macrophages that move more sluggishly than their counterparts from non-depressed subjects. Pert has suggested that neuropeptides are a key biochemical product of emotional expression since they appear in relatively high concentrations in the limbic system. Alteration in the production of these peptides during a depressive episode produces immune suppression through a number of pathways. One possible mechanism of this suppression that has been proposed is that corticotropin-releasing factor (CRF) a hypothalamic hormone may trigger release of adrenocorticotropin (ACTH) which stimulates the release of corticosterone - a known supressor of immune function. ACTH is secreted by the pituitary gland and acts on the adrenal gland.
In another study, Bartrop and associates (1977) found that bereaved spouses had ten times lower T-cell function after the loss of their loved one than non-bereaved individuals. In this case, T-cells, lymphocytes originally derived from the thymus gland, mediate cellular reactivity. This modulation is accomplished by delicate feedback loops involving neurotransmitters such as catecholamines, prostaglandin, somatostatin, histamine, and insulin. Autonomic changes that accompany anxiety and depression (common sequelae during bereavement) thereby play a role in immune regulation. Bartrop's findings were confirmed by M. Stein's (1981) study wherein lymphocytes of men whose wives died of cancer failed to respond to activating agents. This led the author to conclude that suppression of mitogen-induced lymphocyte stimulation appeared to be a direct consequence of bereavement - a finding he later extended to depressed individuals. Functional activity of the lymphocyte and the number of immune competent cells are decreased in clinically depressed patients.
Other studies indicate that natural killer cell activity, which is mediated by T-cells, is significantly decreased in "stressed-out" college students who are not coping well with the demands of school (Rogers, 1979). Here it is thought that epinephrine and norepinephrine, the primary stress response syndrome hormones, decreases immune response. These studies, as well as a myriad of others, point to the fact that the immune system - at the cellular level - can be profoundly modulated by inner subjective experience (i.e., depression, bereavement, stress) as effectively as by pathogens or toxic exposure. A bidirectional circuit exists between the CNS and the immune system since activation of the immune system results in the elaboration of cytokines as well as inflammatory mediators; these mediators induce hypothalamic CRF, which stimulates the release of the same immunosuppressive molecules that mediate the response to stress (Black, 1994). To date, approximately 20 hormones and neurotransmitters have known immunological modulation potential (Khansari, 1990). These either increase or decrease in response to stresses. This indicates that the full neurochemical consequence that would have an impact on immune function is, most likely, extraordinarily complex.
There is little argument that the immune system is activated by pathogens that go on to produce global cognitive, behavioral, and physical pathology. However, this reality is but one thread in a complex feedback system that may be modulated by multiple factors. As the above studies demonstrate, the immune system exists in dynamic relationship to both interior psychological states as well as exterior environmental conditions. Through a variety of pathways the immune system is modulated by such diverse factors as: personality (Rosenman, 1964, Temoshok, 1992), odors (Cocke, 1993), exposure to humor (Dillon, 1985), physical fitness (Roth, 1985), left or right handedness (Searleman, 1987, Chengappa), seasonality and light (Kasper, 1991), and marital conflict (Kiecolt-Glaser, 1993).
THE CNS - IMMUNE SYSTEM FEEDBACK LOOP
At this point in time, the earlier supposition that the immune system acts independently of the brain has been permanently laid to rest. The discoveries from the emerging field of psychoneuroimmunology have demonstrated the close links between mental state and immunological reaction (Vollhardt, 1991). In the 1960's Russian researcher Elena Korneva produced changes in the immune system by selectively damaging different parts of the hypothalamus. George Soloman repeated her experiments and became one of the first American researchers to suggest that the central nervous system played an important role in the immune system. His work has been extended by individuals such as Marvin Stein (1981) who demonstrated that lesions of the anterior hypothalamus reduce cellular and antibody-mediated immune responses to antigenic substances. French researcher Gerard Renoux discovered immune suppression in subjects having severe brain damage to their neocortex, the brain's gray outer layer. He extended his research to brain laterality, i.e., different sides of the brain have different expressions of immune suppression, the left hemisphere having a more direct impact on the immune system.
Not only does the nervous system influence immune responses but immune responses alter nerve cell activities. Cells in the immune system function in a sensory capacity, relaying signals to the brain about such stimuli as invading pathogens (Besedovsky, 1981, 1983; Smith, 1982, 1991). In 1985, Hall coined the term "immunotransmitters" which are substances (i.e., thymic peptides, lymphokines, Etc) produced by immune cells that communicate back to the hypothalamus and the autonomic and endocrine systems. Immune cell cytokines, via direct action on the CNS, alter sleep, pain perception, and appetite level. The most potent example of the intimacy between the immune system and the brain can be seen in cases of brain injury. Immune cells secrete substances called interleukins. These cross the blood-brain barrier, gather at the site of the brain injury and stimulate the growth of glial
cells. These glial cells in turn secrete substances that help injured nerve cells to survive and grow new dendritic branches that at least partially compensate for lost nerve cells. It would seem that activated leukocytes cross the blood-brain barrier at very low levels under normal conditions and in much higher numbers during neuropathological disorders like multiple sclerosis or retroviral infections as well as in brain trauma (Couraud, 1994). The dedicated work of many psychoneuroimmunologists in their search for neuromodulatory mechanisms has led us to conclude that the immune system and the central nervous system is a hard-wired two-way feedback loop.
The exact mechanism of action of the above mentioned immune modulating feedback loops await further research, however they will become more and more important in describing how neurofeedback can enhance the immune systems ability to either maintain health or ward off disease. Our ability to describe an exact mechanism is limited by our elementary understanding of how the immune system communicates with the brain at the electrical and biochemical level. Currently, immune disregulation is in the forefront of contemporary research due to the unfortunate and truly frightening pandemic infection with the human immunodeficiency virus (HIV) and its subsequent disease, acquired immunodeficiency syndrome (AIDS), as well as increases in the rates and types of cancer.
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).
Subjects with HIV have been utilized in many of these studies. Individuals with HIV are excellent candidates for study since the virus invades the body and begins to destroy the immune system. As it progresses, opportunistic illness become increasingly serious and debilitating. A key immune system component, the T-4 (thymus-derived) helper cell (also called CD4 or leu-3) is taken over by the virus. The infected helper cells attach to each other forming giant clusters known as synctial cells. These synctial cells infect other T-4 cells. Over time, the T-4 number declines and the immune system deteriorates. The so-called "T-cell test" or T-cell subset count is widely utilized as a primary measure for monitoring the health of the HIV+ or AIDS patient. The number of T-cells is expressed per cubic milliliter and the normal range is 1000-2000; the unhealthy range is from 400-1000; the abnormal range is 0-400. Since the disease is continuous and progressive, increases in T-4, especially in grouped data, would be highly unlikely and have to be due to a treatment that strengthens of the immune system.
As early as 1977 Hugo Besedovsky found more than a 100 percent increase of brain electrical activity in the brains of rats injected with virulent antigens. Besides supporting the hypothesis that information from an activated immune system is communicated to the hypothalamus, brain electrical activity was found to be significantly altered post infection. Extending this research to HIV, Turan (1990) found that computer-analyzed EEG's and dynamic brain mapping evaluations of HIV+ individuals more closely resemble those of patients diagnosed with mild dementia than age-related normals. These researchers also found that, as the disease progressed to AIDS, there was a deterioration in the EEG that matched the profiles of severely demented patients. More recently Norman Moore (1991) found that brain electrical abnormalities (endogenous auditory P300 ERP components) were found in HIV+ patients whose encephalopathy had not yet progressed to the point where cognitive impairment was clinically evident. From these studies there is ample evidence that brain disregulation occurs with HIV infection and this disregulation progresses as the disease deteriorates the immune system and AIDS evolves. This leads us to ask: can neurofeedback alter this process?
A single case study was presented at the Society for the Study of Neuronal Regulation conference in 1994 by Ellen Saxby. In this study she recruited a HIV+ subject and utilized 14 Hz. enhancement of C1-C2 utilizing the Roshi neurofeedback instrument from Talos/4 Mindwork alternating with EEG-driven photostimulation. She applied the training over a period of five sessions in three weeks. By the end of the experimental phase the subject increased T-4 absolute count from 110 to 264 - a 140% increase. Saxby's results are suggestive but the single case design is scientifically inconclusive and limits generalization.
A
study that is in progress was conducted by me along with
co-investigators: Martin Crane, Luis Wong, and Concepcion Aguirre. It
is a pilot study titled "The effect of alpha and theta neurofeedback
and alpha-stim treatment on immune function, physical symptoms, and
subjective stress within a group of HIV+ subjects, a controlled
study". As of the writing of this paper we have completed
approximately two-thirds of the study. Due to an absence of studies in
this important area I will summarize the results we have to date.
We are investigating the effects of neurofeedback training (8-12 Hz, 6-8 Hz) and Alpha-Stim therapy on 40 subjects with HIV. The goal of the study is to document previously observed changes and to justify the utility of further investigation. The 40 subjects were assigned to one of three treatment conditions and one control group as follows: I. Control - no treatment; II. Alpha-Stim treatment only; III. Neurofeedback training - alpha or theta enhancement with daily home practice; IV. Alpha-Stim treatment and Neurofeedback training with daily home practice.
Initially, all subjects had T-cell counts (T-4) between 200-500 and ranged in age from 18-55. Subjects were willing to provide results of blood work before treatment, at the two month mark, and at the four month mark. The subjects received the treatments over a four month period of time.
Subjects receiving neurofeedback had two, one-half hour sessions per week in the office utilizing either Neurodata or the CapScan VEEG3 neurofeedback instruments. During each session, they were provided two, ten minute practice periods during which time they received monopolar alpha (8-12 Hz) training at O-z (according to the international 10/20 system) for two to three months followed by monopolar theta (6-8 Hz) training at O-z for the remainder of their time in the study. Auditory reward was given when the subject exceeded the amplitude threshold set for that subject on that day. In accordance with standards of reward contingency factors to optimize training we maintained the reward rate within a window of 60-80%. The decision to switch from alpha training to theta training was made when the subject was able to produce steady, rhythmic alpha. To facilitate consistency in developing the ability to produce the desired frequencies, they were instructed to practice daily for 20 minutes at home what they were learning in the neurofeedback training. Subjects utilizing the Alpha-Stim unit had home training devices and practiced for 20 minutes per day at home.
The dependent variables for this study included the subject's T-4 absolute count (measured at the beginning of the study, at the two month mark, and four month mark), as well as changes in physical symptomotology as measured by the Symptom Check List (SCL-90-R), and a stress audit test designed to measure subjective stress levels. Both the SCL-90 and stress audit were administered weekly for the four months. The above dependent variables are being analyzed utilizing standard statistical techniques.
As of the date of this writing, in 10 subjects given only neurofeedback therapy, the group averaged a 31% increase in T-4 level over the four months of treatment (eight increased significantly, two stayed the same). In the subjects who were given neurofeedback and Alpha-Stim, we have eight subjects who have completed the four months. This group currently has averaged a 34% increase in T-4 level. All the subjects reported a significant decrease in physical symptoms and subjective stress within the first month of the study. The research is currently being completed and will have a control group and Alpha-Stim only group (10 subjects each). The results thus far have been extremely compelling in favor of positive immune modulation with neurofeedback. We would like to see this study replicated by interested researchers as we believe it has the potential of helping many people with HIV as well as other immune problems.
Future studies, if funded, will have better measures of immune function. Pharmaceutical companies are utilizing blood tests that actually assay viral activity or viral load and are far superior than utilizing T-4 absolute values. Also, I would recommend utilizing central or frontal placement for the electrodes based upon what we know about the thalamocortical network. A logical extension of the work done by Sterman, Lubar, Othmer and others indicate that higher cortical regions can regulate and perhaps stimulate lower, primary input areas (Schummer, 1989). Extending this recommendation farther, Kang, et al (1991) showed significant differences in natural killer cell activity inversely correlated with right frontal activation. This finding supports the hypothesis that there is a specific association between frontal brain asymmetry and certain immune responses. These factors would indicate that an electrode placement over the central or frontal cortex would probably yield more significant results than the occipital region. Further study is necessary to confirm this hypothesis.
CONCLUSION AND A VIEW TOWARD THE FUTURE
As the complexity involved in the interaction between the central nervous, immune, and the endocrine systems become better understood many questions will be resolved. Certainly the immune system has a level of sophistication and organization that we are just beginning to appreciate. Neurofeedback as a science is still in its infancy because so little is known about how changes in cortical EEG affect deeper brain structures (the thalamus, hypothalamus, etc.). It is the interface between these deeper brain structures with the immune and endocrine systems wherein lays the possibility for true enhancement of the immune response.
At this point in time there are many more questions than answers. However, as more knowledge presents itself regarding neural pathways for the propagation of positive modulation of the immune system we can correlate these changes with cortical EEG patterns utilizing sophisticated EEG brain mapping technology. Once correlations are established and quantified between the EEG and immune function, research can be designed to change cortical EEG utilizing the operant conditioning paradigm of neurofeedback. Advances in computer technology and application of such to neurofeedback in the form of photic stimulation as well as virtual reality feedback will yield better and quicker learning curves to reorganize and reorient brain electrical activity to match desired frequency/amplitude patterns. The good news is that the evolution of this technology is within our grasp today. Hopefully the discipline inherent in the scientific method will continue to be applied so that the results we see will be real and stand up to replication. Neurofeedback is perhaps one of technology's greatest gifts to humankind. As stated above, we can look forward to freedom from autonomic control that will let us maximize human physiology. The new frontier of neurofeedback will allow for immune enhancement as well as application and refinement of the various disorders of the central nervous system already under investigation. Ultimately neurofeedback can, and undoubtedly will, facilitate the growth and development of human potential, communication, and consciousness.
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