Section: Institute Information -> Health Psychology -> A Clinical Report

 

   

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.