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.
REFERENCES
