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Post-Polio Sequelae (PPS) and Neurofeedback:
A Clinical Report
Richard R. Williams, Ph.D. and Patricia R. Williams, LMSW; BCD
Richard R. Williams is a BCIA certified clinician in private practice
in Kalamazoo, Michigan at Health Psychology / A.D.D. Institute. He was
the Founding President of the Biofeedback Society of Michigan
and also founded the Specialty Program in Holistic Health at Western
Michigan University. Patricia Tracy Williams is a Clinical Social Worker
and Director of the ADD Institute, which is a department of Health
Psychology and Medicine.
The clinical work of the authors has included treatment of a
wide range of disorders with an assortment of biofeedback modalities
over a span of 24 years. Most recently, however, we were approached
by a 52 year old woman who sought stress reduction training to
assist in her management of Post-Polio Sequelae (PPS). This was
a clinical condition which we had not encountered before. Fortunately,
the new patient was also a trained occupational therapist and
she was able to provide us with a valuable "quick course"
in PPS. Additionally, she also served as a Board Member of the
Michigan Polio Network and she was able to supply us with essential
articles and other readings which saved us much time in becoming
oriented. One of the chief problems experienced by persons with
PPS, she explained, was difficulty in managing stress. Moreover,
in addition to the physical causes and treatments for PPS, psychological
symptoms often include anxiety, depression and "type A"
behavior. Such difficulties not only contribute directly to a
decreased quality of life, they also interfere with patients making
lifestyle changes necessary to treat their PPS. During the course
of our education regarding PPS, these and other important features
of this disorder came to our attention which led us to consider
EEG biofeedback training instead of other modalities we might
have chosen if stress reduction per se had been our principal
goal.
Subsequent to the appearance of this first patient with PPS, were
approached by a second individual with a similar diagnosis. The
initial patient, the 52-year old woman had more symptomatic involvement
than the second, a man also 52 years old. The woman's problems
included neuromuscular pathology requiring the use of crutches.
She also experienced respiratory distress which began in 1983.
Tests for respiratory insufficiency showed a steady decline, reaching
a level of 70% in 1992. It was this year that she was also diagnosed
with asthma and her allergist prescribed a peak meter recording
three times a day. In 1987, she began to experience what she described
as "tongue and vocal chord fatigue"
Adding to her difficulties were the usual PPS problems associated
with disabling fatigue, concentration and memory. She had undergone
various other forms of therapy with varying degrees of success
and with varying lengths of duration. To date, nothing had provided
what could be regarded as a lasting benefit. The male patient's
principal complaints consisted of daily fatigue and great difficulties
in attention and concentration. He also had a considerable problem
in obtaining adequate sleep at night. Accordingly, daytime fatigue
would become so severe that he would be compelled to put his head
down on his desk where he worked to rest. Attention and concentration
were so extreme that he reported he could read for only brief
periods of time. He said that his house was full of books he could
not finish reading, much as one would see with adult attention
deficit disorder.
Background
Polio, one will recall, struck a number of children and adults
in the 1940's and 50's. Thankfully, the development of vaccines
has brought this crippling and often deadly disease under control.
In the 1980's, however, over half of the approximately 1.6 million
polio survivors nationwide began to experience new and unexpected
symptoms which, initially, puzzled many physicians. These symptoms
included fatigue, muscle weakness and pain. Reactions by the medical
community ranged from disbelief to thinking it was "psychosomatic"
to some kind of Amyotrophic Lateral Sclerosis (Bruno & Frick
1991). Today, PPS is a widely accepted phenomenon and appropriate
treatments in physical medicine are emerging. Despite these advances,
however, another cluster of symptoms related to PPS has only recently
received scientific attention. Moreover, the treatment of these
symptoms has received far less attention than issues of physical
rehabilitation. These symptoms include not only fatigue, but difficulties
in attention, cognition, word finding and memory (Bruno, Cohen,
Galski & Frick, 1994).
It is a widely accepted observation that the polio virus induces
damage to anterior horn motor neurons (Trojan, Gendron & Cashman,
1991), thus disrupting normal neuromuscular activity. However,
such neuronal damage cannot explain problems related to psychological
functioning and fatigue (Bruno, et al 1994). Such difficulties
would suggest involvement of brain centers such as those responsible
for promoting and maintaining arousal, and histopathological studies
have, in fact, shown this to be the case. For example, Luhan (1946)
has stated that a brain stem area most uniformly involved after
poliovirus infection is the reticular formation, an area known
to be of central importance in mechanisms of arousal (Morruzi
& Magoun, 1949). Additionally, other areas found to have been
most consistently damaged include the posterior hypothalamus;
thalamus; putamen; caudate; locus ceruleus; and substantia nigra
(Bruno et al, 1994).
With this information in hand, it was our decision to approach
treatment in a manner similar to the way we would address other
problems related to weaknesses in arousal. The combination of
symptoms including fatigability and those associated with deficiencies
in attention strongly suggested this.
Evaluation and treatment
As a way of gathering additional information, and for the purposes
of obtaining therapeutic baseline data, a Quantitative Electroencephalograph
(QEEG) was performed with both patients. This involved a 19-channel
recording with our Lexicor equipment. Conditions included were
eyes closed, eyes open and cognitive challenges. Information obtained
were subjected to topographical mapping and power spectral analysis.
Also, we made a decision to compare the eyes closed portion to
the Johnston and Thatcher (1991) reference data base as we have
done with our patients presenting with potential brain traumas.
Female patient
One of the most remarkable, but not unexpected features obtained
from the QEEG of the female patient was seen in very low amplitude
readings in the entire Beta range (12-21 cps). Average amplitudes
throughout were approximately 2.5 microvolts . Also, the eyes
closed condition showed very little activity in the alpha range
(8- 12 cps) at every electrode site. The dominant activity was
seen between 0.5 and 6 cps, but in itself relatively weak; averaging
only around 20 microvolts at most. In general, the entire EEG
spectrum (0.5 - 32 cps) appeared to be lower in power and quite
slowed; a feature consistent with the aforementioned subcortical
damage. Comparison to reference database also showed relative
power elevations in the delta frequencies at every electrode site
on both hemispheres. Also an increase in coherence in both hemispheres
were characterized by delta which involved both short- and
long-run inter-electrode sites. It was easy to see why this woman
was experiencing such pervasive difficulties in fatigue, attention
and cognition. We could only guess at what the QEEG might represent
in regard to her breathing problems.
Because of these QEEG results, a neurofeedback program was written
to address the most dominant and abnormal appearing feature of
her spectral analysis; the excessive slow activity relative to
faster frequencies. She was trained under eyes closed conditions
to reduce activity between 2 and 6 cps at location Ct. This was
done because keeping her eyes open was causing distress. Approximately
20 sessions were completed at the rate of five sessions a week.
After seeing that she was able to reduce this slow frequency activity
from around 20 microvolts to around 16.5 microvolts, and a fixed
percent time from about 40% to 14%, we decided to switch to an
attempt to increase SMR from 12 to 16 cps. Out goal at this point
was not only to introduce beta training at the low end of the
beta frequencies, but to offer her an opportunity to improve her
neuromuscular status which from the abdomen down was extremely
rigid. This protocol had to be abandoned because she began to
experience headaches and fatigue during sessions. At this point,
we performed a second power spectral analysis at Ct alone to see
what changes might have occurred. We were surprise to see a quite
large increase in alpha activity during the eyes closed condition
which was almost four times greater than the initial recording.
Also, it attenuated well when she opened her eyes. At the same
time, she began to report a change in muscle tone with good improvements
noted in a Peroneus longus muscle transplant. She also noted improvements
in short-term memory. Moreover, she is a person who gives occasional
speeches regarding PPS and she began to notice feeling more poised
and relaxed during presentations.
Because of the movement seen in the alpha band, we decided to
shift to a program of training to enhance alpha. She found this
relatively easy to do, but not as easy as slow wave reduction.
Surprisingly, we saw little additional increase in alpha activity.
After some 15 sessions of this training we shifted to a program
to train beta (15 - 18 cps) with eyes open. This was somewhat
more successful than the alpha training, but we saw changes occurring,
not in beta, but in alpha once more. It appeared that whatever
we wanted to train it was alpha that increased, unless we trained
the alpha frequency itself. Throughout the course of the work
we have done with her, reduction of slow activity (2 - 6 cps)
has been the most productive. She has now had approximately 60
sessions. Extended training is now taking place with attempts,
once again, to increase beta activity between 15 and 18 cps. It
appears that she is beginning to show an ability to enhance this
faster frequency and we are seeing some power increasing in beta
now occurring. In her case, it seemed necessary for her first
to decrease slow activity before showing an ability to enhance
faster activity.
The net results of training, to date, have been seen in reduced
fatigability; markedly improved respiration; enhanced concentration
and memory; and decreased tongue and vocal cord stress. She has
always enjoyed singing and she now reports that she has regained
the ability to smoothly change pitches. Her respiration has improved
from a measurement of one deep breath out of three, to 50 out
of 50 at, or within, a normal capacity range.
Male Patient
Power spectral analysis for this 52 year old man showed reduced
power in all frequency bands, again consistent with a disturbance
in mechanisms of arousal. Theta activity (4-8 cps) was increased
over the entire anterior cortical regions along with decreased
power in the alpha range (8-12 cps) in the posterior regions.
Central and frontal beta (12-21 cps) was reduced in both hemispheres.
His primary complaints were, again, marked fatigability; inability
to concentrate; and poor sleep.
The training protocol chosen for this patient consisted of beta
enhancement from 18 to 23 cps over the frontal area at location
Fz. After about 16 sessions he began to report improvements in
sleep quality as well as a 30% reduction in fatigue. Most recently,
he sent us a letter stating that he discovered a capacity for
a type of relaxed awareness to which he was quite unaccustomed.
For example, while attending a piano recital he noticed that..."the
ambiance just kind of flowed in, in an unusually relaxed manner.
I felt like there were no demands on me, my back didn't hurt,
I was unusually comfortable, I didn't try to analyze the performance,
I wasn't impatient, I just sat there comfortably enjoying what
was going on around me. For me, that state of mind is extremely
unusual and has never before been experienced to the degree I
experienced it last Saturday. I was distracted by it and I loved
it." He has since experienced such a form of awareness again
and attributes it to the neurofeedback training. He concluded
his letter by saying..."I have plenty of incentive to continue
with it."
Observations
To our knowledge, this is the first work reported, or perhaps
even undertaken with Post Polio Sequelae patients utilizing EEG
biofeedback training. One of the most striking features of their
QEEG's is a consistency with a "low arousal" syndrome.
As mentioned previously this is what one would expect to see if
one of the consequences of the polio virus was damage to brain
stem areas such as the reticular formation. It is quite encouraging,
therefore, that results in our ongoing work are indicating that
resulting problems such as increased fatigue, poor attentional
capacity and, perhaps, even respiratory distress can been improved
through brain activity biofeedback training. With the two patients
discussed in this article, we have seen strong evidence that this
can occur. Most importantly, the training seems to be contributing
to an improved quality of life by decreasing symptoms which, in
this population of patients, have been so resistant to treatment
through other modalities. We feel that EEG biofeedback training
offers even more potential for persons experiencing the ravages
of PPS if it would be included as an additional element in a multidisciplinary
rehabilitation program. It is our hope that others will enjoin
the effort for this to happen.
References
Bruno, R.L. & Frick, N.M. (1991) The psychology of polio as
prelude to post-polio sequelae. Orthopedics, 14:1185-1193.
Bruno, R.L., Cohen, J.M., Galaski, T. & Frick, N.M. (1994)
The neuroanatomy of post-polio fatigue. Archives of Physical Medicine
and Rehabilitation, 75, 498-504,
Trojan, D., Gendron, D. & Cashman, N.R. (1991) Electrophysiology
and electrodiagnosis of the post-polio motor unit. Orthopedics,
14:1353-1361.
Luhan, J.A, (1946) Epidemic poliomyelitis: some pathological observations
on human material. Archives of Pathology, 42:245-260.
Morruzi, G. & Magoun, H.W. (1949) Brain stem reticular formation
and activation of the EEG. EEG and Clinical Neurophysiology 1:455-473.
Johnston, J. & Thatcher, R.W. (1991) Quantitative EEG analysis
and rehabilitation issues in mild traumatic brain injury. EEG
Analysis and Rehabilitation. 23 (4): 228-232.
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