|
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.
The
application of neurofeedback techniques that
reorganize and reorient brain electrical activity can, in all probability, be utilized to
modulate positively the immune response.
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 Intemational
Joumal of Neuroscience (1991) discuss evidence
indicating that an immunoendocrine feedback loop,
which they term "immune-hypothalamo-pituitary-adrenal
system" 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.
"Even
relatively minor life stresses leave their mark on the immune system."
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
reorganize and reorient 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. The obvious question arises: now 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 suppressor 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.
Natural
killer cell activity, which is mediated by T-cells, is significantly
decreased in "stressed-out" college students.
Other
studies indicate that natural killer cell activity, which is mediated by
T-cells, is significantly decreased in "stressedout"
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 been shown to have
immunological modulation potential (Khansari,
1990). Many of 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.
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.
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).
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.
Individuals
who utilize neurofeedback state that they perceive reality with greater
clarity as well as acquire greater control over fluctuations in mood.
The
exact mechanism of action of the above mentioned immune modulating feedback
loops awaits further research, however they will become more and more
important in describing how neurofeedback can enhance the immune system's
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 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 andlor
recruited to produce beta in closed head injury, so can a disregulated,
downregulated, or an unstable immune system be
stabilized andlor 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 (Wynvicka 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.
Neurofeedback
may 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.
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 (selfregulation). 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 and theta neurofeedback training allows
the addict to more easily escape unwanted behavior patterns such as chemical
addiction, compulsive behaviors, and cravings (Peniston).
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,
ct 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).
This
research indicated that biofeedback may have helped increase the ability of
circulating lymphocytes to divide. 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 4001000; 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 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 an
HIV+ subject and utilized 14 Hz enhancement of C1-C2 utilizing the Roshi neurofeedback instrument from Taloslrl
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.
Ten
subjects given only neurofeedback therapy, the group averaged a 31% increase
in T-4 level over the four months of treatment.
We
are investigating the effects of neurofeedback training (8-12 Hz, 6-8 Hz) and
Alpha-Stim (microcurrent
cranial electrical stimulation) 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. AlphaStim 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 0-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 6080%. 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.
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.
The
dependent variables for this study included the subject's T-4absolute count
(measured at the beginning of the study, at the two month mark, and four
month mark), as well as changes in physical symptomatology
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 T4 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 effect 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 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.
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
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.
|