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Take steps to avoid falling!

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TAKE STEPS TO AVOID FALLING!

from the Polio Society of Washington, D.C.‘s Options

Falls, caused by balance problems, weakness and instability in walking, can cause broken bones, torn ligaments, head injuries and lacerations. Unfortunately, recovery time is longer for post-polios. Here’s some steps you can take to decrease falls:

Use kitty litter or sand to keep snowy, icy paths and steps safe. Install handrails in hallways and on both sides of stairways. Keep stair runners securely fastened. Be sure lighting is adequate, indoors and outdoors, especially at entryways and in stairways to attic and basement. Keep stairways and rooms as uncluttered at possible.

Replace throw rugs, put nonskid liners under them, or tack down their edges. Wear snug, non-skid slippers. Have working flashlights nearby in case of power outages.

From: The Torch Newsleiter, April, 1996. Albert Einstein Medical Center, Willowcrest Bldg. Orthopedics Dept., 5501 Old York Roud, Philadelphia, PA 19141

ARVES

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Polio Cold Feet

Polio Feet

There’s a reason you have cold feet – but you can keep warm and stay cool

Richard Bruno, Ph.D.

New Mobility, March 1996

The process that cause “Polio Feet” to turn blue and cold and become difficult to move when it’s only cool is the same process that caused paralysis after the original polio.

The Polio virus got into the spinal chord and either destroyed or damaged the anterior horn cell motor neurons that transmit the message to move from the brain to a muscle. When those neurons were damaged, or especially when they died, they disintergrated and the muscle fibers that used to be turned on by those cells no longer were.

There is another kind of motor neuron that was affected by the virus – the motor nerve that controls the muscle around your blood vessels. When these muscles died, there were no motor nerves to tell the blood vessel to contract; if the blood vessel cannot contract, blood ‘pools,’ especially in the veins. When the blood pools in the veins, it is going to be blue, because venous blood is not oxygenated.

Polio feet are caused by warm blood that should be in the center of your body, flowing out into the hands, arms, and especially the legs (since gravity is pulling the blood down). The warm blood pools in the surface of your skin, and because the blood vessels cannot contract, the result is “polio feet.” The venous pooling causes your blood to radiate heat into the environment. People who had polio keep the world warm, unfortunately at their own expense. The price of this is a thorough cooling of the limbs and all tissues of the limbs.

When heat leaves the veins, the motor nerves that lie near the surface of the skin start to cool. The muscles that lies just a bit below the surface starts to cool. The connective tissue that connects muscle to muscle, and muscle to bone starts to cool and stops being elastic so it is harder for it to move.

When the motor nerves aren’t functioning well, the muscles aren’t going to function well; if the muscles don’t function well, there is going to be muscle weakness. We think that muscle weakness and the loss of body heat are causing fatigue; and we think that people who lose all their body heat into the environment

are burning calories to maintain their body temperature, so there are fewer calories to keep moving.

People who had polio should dress as if it is 20 degrees colder than it actually is, but you should dress in layers so you can control your body temperature and not pass out from a rapid flow of blood away from your head as your arteries warm

The bottom line is to keep warm, stay cool and:

1. Use polypropylene socks and underwear by Gortex Thinsulate.

2. Dress in layers.

3. Never wear a skirt after Labor Day (first Monday in September) or before Memorial Day (last

Monday in May).

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Document Reference: <URL:http://www.zynet.co.uk/ott/polio/lincolnshire/library/kessler/feet.html> Created: 20th February 1997

Last modification: 30th January 2010.

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Lack of progression of neurologic deficit in survivors of paralytic polio

Lack of progression of neurologic deficit in survivors of paralytic polio: A 5-year prospective population-based study

Anthony J. Windebank, MD; William J. Litchy, MD; Jasper R. Daube, MD; and Rita A. Iverson, RN

Article abstract. We completed a prospective, population-based cohort study of polo survivors in Olmsted County, Minnesota, between 1986 and 1993. We identified 50 individuals who had had paralytic polio between 1935 and 1960, as representative of all 300 cases of paralytic polio in the county. We completed detailed quantitative clinical and electro physiologic studies at entry and after 5 years. These studies demonstrated stable neuromuscular function within the cohort, although 60% of the individuals were symptomatic. In two-thirds of the symptomatic patients, the causes of their symptoms were unrelated to earlier polio. For the 20% of patients who had unexplained muscle pain, perception of weakness, and fatigue, a mechanical disorder most likely underlies their symptoms. NEUROLOGY 1996 46:80-84

After the introduction of immunization programs in the mid-1950s, poliomyelitis was rapidly eradicated in developed nations. Patients with acute anterior poliomyelitis typically had an acute biphasic viral illness with fever, headache, and gastrointestinal symptoms followed several days later by the rapid development of limb and bulbar paralysis. This pa ralysis was caused by invasion of motor neurons by the neurotrophic polio virus, followed by neuronal death. Progression of paralysis usually stopped after 5 to 7 days. There was then a period of stability followed by some degree of gradual recovery of func tion. This recovery was caused by sprouting and re innervation of muscle by surviving motor neurons, and it progressed over months to years and was fol lowed by prolonged stability of neuromuscular func tion. During the past 10 years, late progression of symptoms and neuromuscular deficit has been re ported in persons who had paralytic polio. This has been reported for many years as a rare, late se quela of polio. In affected patients, progressive atro phy and weakness developed after at least 10 to 15 years of stable function. This change was speculated to result from age-related attrition of motor neurons from the motor neuron pool already depleted by the viral illness. This entity of late progressive weakness and atrophy has been named postpolio progressive muscular atrophy. A second type of symptom cluster in survivors of paralytie polio was described in 1987.3 Patients were identified with symptoms of progres sive muscle pain, weakness, and fatigue. This was named postpolio syndrome. The prevalence of these

symptoms is unknown but is estimated to be approx imately 70% of polo survivors.

To understand the frequency and basis of these symptoms, we used the unique resources of the Olm sted County, Minnesota, database at the Mayo Clinie. Since the early part of this century, residents of Rochester and Olmsted County, Minnesota, have received their medical care primarily at the Mayo Clinic and its affiliated hospitals. All physician con tacts resulted in a diagnosis that was coded for auto mated retrieval. Diagnoses of Olmsted County resi dents receiving medical care at other institutions or practices in Olmsted and surrounding counties were also linked for retrieval within the same system. This allowed us to identify all patients within a de fined community of 100,000 who had paralytic polia myelitis between 1935 and 1960. A representative cohort from this population was identified and fol lowed prospectively with detailed clinical and elec trophysiologic studies. Each individual was studied for 5 years. The entry characteristics of this cohort were described previously.” We now report the re sults of a 5-year followup study,

Methods. Patient population. We previously described the demographic characteristics of the study population in detail. Briefly, 608 residents with acute poliomyelitis be tween 1935 and 1960 were identified. Three hundred indi viduals met the criteria for paralytie poliomyelitis, 298 of whom were available for followup; we chose a representa tive cohort of 50 individuals for prospective, sequential Evaluations. They were chosen because they represented the whole cohort–in terms of number of limbs involved,

From the Department of Neurology. Mave Clinie and Mavo Foundation, Rochester, MN Supported by grem SGF from the Sans Gerard Foundation, Clearwater, FL Data were presented in part at the New York Academy of Sciences meeting, Bethesda, MD. April 1994. Some of the data described herein were included in a subject review Windebank AJ. Differential diagnosis and prognosis. In: Halsted L. Grimby Geds. Post-polio syndrome Philadelphia: Hanley & Belfus. 1995:69 881. Received December 7. 1994. Accepted in final form April 18, 1995. Address correspondence and reprint requests to Dr. Anthony J. Windebank. Department of Neurology. Mayo Clinie: 1501 Guggenheim Building. 200 First Street SW Rochester MN 55905. 80 Copyright © 1996 by the American Academy of Neurology

movement by decade, gender, height, weight, and side of dominance o

Function and timed tests. A battery of functional tests was performed under standard conditions at both evalua. tions Lower limb function was measured as the time to walk 100 feet as quickly as possible in the physical therapy gymnasium. The time to complete an upper limb dexterity function was assessed with two standardized pegboard tests-the Minnesota Rate of Manipulation test and the Crawford Small Parts Dexterity test.

Data analysis. This study generated more than 20,000 individual data points, enabling a large number of cross correlations. Overall, parametric statistical techniques were used unless stated. Where appropriate, Student’s ta test, analysis of variance, chi-square test, and linear re gression analysis with the method of least squares were used,

bulbar involvement, severity of involvement, likelihood of being ventilated, age at time of polio, current age, interval since polio, gender, and cerebrospinal fluid protein find ings–and not because of ongoing symptoms. All patients had detailed quantitative neurologic examinations per formed at the worst point of their acute illness.4,5 of the 50 patients, 46 completed the detailed 5-vear study. Four pa- tients declined to complete the tests but were contacted by telephone; all four reported that they were asymptomatic and did not want to participate in further detailed physio logic testing The 5-year prospective study involved repeat ing all of the tests and examinations that were done at entry.

Questorinaire. Each person completed a detailed ques tionnaire history. This was modified with additional ques tions that concerned the status of symptoms between the first and second (5-year interval) evaluations. All questions at both entry and followup were answered in a yesino format. The questionnaire contained 337 items about limb and bulbar weakness, pain, fatigue, and activities of daily living. Specific examples of the format for questions have been published. For data analysis, certain key items were extracted from this questionnaire to devise a progres sion score. For example, in response to the statement, “The arm weakness has worsened during the last 5 years,” a positive answer was assigned one point. This progression score would yield a maximum of 50 points for subjects who thought they were maximally deteriorating in every aspect of their function. The score is a simple way of adding the number of symptoms from a standardized questionnaire that allows graphic representation of symptoms without implying a linear relationship between symptom score and severity of discase.

Neurologic disability score. This scored and validat ed“ neurologic examination was performed for all pa tients. For this study, only muscle strength scores were used. A score of 0 represents completely normal bulbar, trunk, and limb muscle strength; a score of 216 represents complete paralysis of all muscles. The neurologists (AJ.W. and WJL.) completing the examinations were unaware of the symptom status of the patient and did not have the results of the first examination available when the second examination was performed 5 years later.

Electrophysiology. All patients underwent bilateral ul nar, median, and peroneal motor and ulnar, median, and sural sensory nerve conduction studies at both evalua tions, performed by the same neurologist (J.R.D.). Com pound muscle action potentials (CMAP) were recorded at identical locations by anatomic landmarks. Technique and reproducibility have been reported. We estimated the number of motor units (MUNE) present in median inner vated thenar muscles and peroneal innervated extensor digitorum brevis muscles bilaterally with a statistical mod. ification of the McComas method.

Biomechanical measurement of muscle strength. Iso metric strength was measured in the Mayo Biomechanics Laboratory. The method has been described in detail. 10 Identical techniques were used at both evaluations. Strength was evaluated bilaterally for the following joint movements: elbow flexion and extension, forearm prona tion and supination, knee flexion and extension, and ankle extension and flexion. Data were normalized for each

Results Patients. Of the original cohort of 50 subjects, 46 returned to complete the studies. Of the four who did not return, two completed the symptom questionnaire and two reported by telephone that they were doing well. No data were analyzed from the two subjects interviewed by telephone. Of the 46 subjects who returned for testing, 42 completed all studies; 4 did not complete the electrophysi Ologic ones.

Stability of symptoms. The symptom score was de signed to elicit symptoms of muscle or joint pain, fatigue, progressive weakness, or progressive muscle atrophy. Twenty-three individuals had at least one of these com plaints at the first and second evaluations, 12 had no com plaints at either evaluation, 7 had complaints at the first evaluation but did not have a complaint at the second, and 6 had no complaints at the first evaluation but did have a complaint at the second. This finding suggests a relative stability of complaints (p = 0.0055, Fisher’s exact test), When the individual types of complaints (pain, weakness, fatigue, or atrophy) were analyzed, the distribution was similar. The extent of complaints in each patient has been reported elsewhere !!

The symptoms of pain, weakness, fatigue, and atrophy make up the postpolio syndrome. However, those are non specific symptoms, especially in an aging population. At the second evaluation and in the analysis, we sought alter native explanations for the specific symptoms reported by the patients. Twenty patients had an explanation for their symptoms that was not related to failing neuromuscular function: 14 had radiologically demonstrated degenerativa joint disease that accounted for their pain and 6 had one each of diabetes, fatigue due to a 30-pound weight gain, alcoholism, depression, the residual of a motorcycle accia dent, and acute lumbar disc herniation

Neurologic disability score and timed tests of function. Neurologic disability scores (NDSs) remained stable. Re gression analysis showed that both the mean of the popu lation and the individuals within that population did not change. When NDSs after 5 years were plotted against initial NDSs, the slope of the line was 1 and the correlation coefficient was highly significant (p = 0.95). The intercept of the regression line was -2.45, indicating improvement of the population. The mean NDS improved slightly but significantly from 20.3 + 3.6 at the first evaluation to 17.1 # 3.7 (p = 0.0036, paired Student’s t-test) at the second evaluation, in parallel, the time to walk 100 feet had im

January 1996 NEUROLOGY 46 B1

2.95

0.96x;

PA2

0.83

Left Peroneal Right Peroneal

Left Median Right Median

Combined CMAP (mv) after 5 year interval

MUNE after 5 year interval

MUNE at entry

10 20 30 40 50 Combined CMAP (MV) at entry

Figure 1. Regression of summuted compound muscle ae tion potentials (CMAP) amplitudes (right and left thenar plus right and left extensor digitorum brevis muscles) at the second examination (5-vear intercal) compared with the summated CMAP amplitude at the first evaluation. The amplitudes are stable (slope = 0.96) and reproducible within individual subjeets (r2 = 0.83).

Figure 2. Regression of motor unit number estimates (MUNE) at the second examination (five–year interval) compared with MUNE at the first evaluation. The pero neal nerve was stimulated at the fibular head recording over the extensor digitorum breuis muscle. The median nerve was stimulated at the elbow with recording over the abductor pollicis breuis muscle.

proved slightly but significantly (from 27.6 + 1,1 to 23.6 1.3 seconds, p . 0.0001), whereas results of upper limb function tests had not changed Minnesota Rate of Manip ulation, 39.2 + 5.1 sec to 410 + 5.7 sec, p = 0.4: Crawford Small Parts Dexterity test, 52.1 + 5.0 sec to 48.3 5.1 sec, p = 0.23). Data sets have been filed with the National Auxiliary Publication Service (NAPSI.

Electrophysiology. We have demonstrated that the summation of CMAP is a clinically useful way of generat ing a single estimate of muscle function for an individual, Regression analysis of these data (figure 1) showed popula tion and individual stability when the two evaluations were compared As with the previous data set, there was a slight but significant (two-tailed test, p = 0.0195) improve ment in mean CMAP from 27.7 * 1.5 mV to 29.3 + 1.8 m V between the two evaluations. MUNE was also stable. Eleen trophysiologic data are available through NAPS.

Secondary analysis of data. Because poliomyelitis and the residua are multifocal, we were concerned that signifi cant changes in paretie limbs might be masked by stability in uninvolved limbs. To make comparisons, we considered five separate parts for each subject: bulhar musculature, right and left upper limbs, and right and left lower limbs, We then determined whether a part had been involved by the original disease process on the basis of the original record available at the height of the acute paralytic illness, The neurologic recordem was instituted in 1917 at Mayo Clinic; all patients in this study had detailed, complete records from the time of their acute illness. This analysis yielded 115 normal or unaffected limbs and 135 paretio limbs. We then compared each of our measurements (NDS CMAP, and MUNE isometric and isometrie strengths) for 82 NEUROLOGY 46 January 1996

a limb between the first and second evaluations. For each measurement, we considered only the measurements for the muscles in that limb. These comparisons showed no difference between the control and paretic limbs, except for a small but significant improvement in function of the paretic limbs (mean change in NDS for unaffected limbs, 0.15 1.0 versus 0.76 + 2.9 for paretic limbs during the 5-year interval; p = 0.046 in the direction of improve ment).

The other approach to secondary analysis was to con pare subjects who thought they were having new difficul ties with those who were not. This showed no sipnificant difference between groups (data tables filed with NAPS),

Finally, we considered the 10 patients who complained of pain, weakness, and fatigue but had no other explana tion for these symptoms. All these patients had the symp toms at the second evaluation; thus, the symptoms were stable and had been present at both evaluations or had appeared since the first evaluation. The NDS had de. creased in this group from 21.2 + 6.0 to 14.9 1 5.0 (SEM). In the control group, the NDS decreased from 19.7 4.3 to 17.7 I 4.6 (SEM). This group had either no symptoms or symptoms with an adequate explanation as described above). The improvement in NDS was significantly greater (p = 0.01) for the symptomatic group than for the controls. We made a similar comparison for the summated CMAP. This improved by 1.3 I 0.9 mV (SEM) for the control compared with 3.3 15 mV for the symptomatic group. This difference was not significant (p = 0.26). There was no significant difference for the change in MUNE between the groups. Additional analyses included regression of ICMAP, INDS, and AMUNE against age at onset of dis.

case, interval since acute disease, age at second evalua tion, maximal NDS during acute illness, and weight gain. No correlations were found.

Discussion. This prospective study demonstrated remarkable stability of neuromuscular function in a group of survivors of paralytic polio. Several at tributes of neuromuscular function actually im proved in the group during the 5-year observation period. The indications of better neuromuscular function were all small but statistically significant They are reliable indicators and are different ways of measuring muscle function: The NDS is a clinical examination, walking 100 feet is a timed test of func. tion, and CMAP is an objective electrophysiologic measure. The results raised the question of whether, even in this mature population, 35 to 50 years after the acute illness, reinnervation is still occurring. Our subjects underwent no specific therapy as a result of participation in this study.

The observation of improvement or stability raises questions about the sensitivity of the techniques used to detect change. When we designed the pro spective study, we chose the primary techniques be cause they had been validated and shown to be sen sitive to change in diabetic neuropathy, an indolently progressive neuromuscular disorder that has a time course of change similar to that of symptom reports in polio survivors, Our inability to detect deteriora tion was not likely due to a lack of sensitivity of the measuring instruments. The high degree of correla tion between measurement at the first and second evaluations further validates the measurements. Other groups that have detected deterioration on ret rospective analyses had preliminary findings that were similar to ours when they used a prospective design, 14.15

We found that symptoms reported in polio survi. vors included combinations of pain, weakness, and fatigue. These symptoms, which have been reported as being components of postpolio syndrome, were present in approximately 60% of our cohort. Twenty of the 30 patients with these symptoms had other causes that completely explained their symptoms. We believe this was an important observation. If a patient who had polio presents with one or more of these symptoms, postpolio syndrome should not be diagnosed automatically. If this group is representa tive, then in about two-thirds of symptomatie pa tients an alternative cause will be found, which has different therapeutic implications.

These findings raise questions about postpolio syndrome as a distinct clinical entity. Undoubtedly patients who had polio do have these symptoms. In our group, 20% of patients had pain, perception of progressive weakness, and fatigue with no alterna tive explanation. However, it is equally clear that the symptoms in this group are not based on progres sive neuromuscular failure. The subset of 10 patients with these symptoms had stable or improving neuro muscular function. Although the cause of these

symptoms remains unknown, they are sunilar to symptoms present in patients with chronic fatigue syndrome. This disorder is often associated with de pression, which was absent from our cohort, as de termined from evaluations with the Minnesota Mul tiphasic Personality Inventory at both visits. Depression scales were normally distributed at the first and second visits (data not shown),

Another neuromuscular disorder associated with muscle pain and perception of weakness and fatigue is tension myalgia, or fibromyalgia 17 This disorder is not usually associated with depression and involves muscle pain, usually at tendon insertion, that is worsened with and may persist after use or overuse, The disorder is common in middle-aged, decondi tioned persons. Because of the degree of similarity in symptoms between our subset of patients and those with fibromyalgia, we believe this is a reasonable alternative diagnosis. In neither case is there any evidence of intrinsic nerve or muscle disease. The incidence of fibromyalgia in the population is un known, so we cannot say whether it is more common in polio survivors. The chronic use of weak muscles or muscles acting in a compensatory fashion may well predispose persons to this type of problem. If this is the cause of postpolio syndrome, it leads di rectly to therapeutic strategies. Patients with fibro myalgia can be effectively treated with conditioning, physical medicine approaches, and tricyclic antide pressants.!? Because there was no evidence of pro gressive neuromuscular deterioration, there is no basis for the use of drugs designed to improve neuro muscular function.

The second disorder that has been associated with late-onset weakness after polio is postpolio progres sive muscular atrophy. This was originally described by Mulder et al as a rare, late complication of polio. We did not detect any case within our cohort. Each of the investigators has, however, seen patients with this disorder in their referred practice. This usually involves painless and slowly progressive weakness and atrophy in muscles that were often severely af fected by the original disease !! We would concur with Mulder et al that this is a rare disorder of sufficiently low incidence that it was not detected in a cohort of 50 persons at risk

The cohort was representative of polio survivors in the United States. The population of Olmsted County from 1935 to 1960 was of predominantly northern European descent (German, Irish, and Scandinavian). It does not represent populations of different race or ethnicity. The type of polio epidemic that occurred in the upper Midwest was similar to those occurring throughout the United States and Europe. The cohort was also representative in terms of severity of original disease and sites of involve ment. For all these reasons, we believe that our findings can be extrapolated to the whole population of polio survivors in the United States. Overall, these findings are reassuring. This group has no evidence of progressive neuromuscular failure, and rational

January 1996 NEUROLOGY 46 83

therapeutic approaches may produce substantial benefits.

Acknowledgments

The secretarial assistance of Ms. Linda A. Goldbeck and the assis. tance of Ms. Debra A. Wittrock for her data entry and analysis are greatly appreciated. The excellent technical assistance of the Mayo Biomechanics Laboratory under the direction of Drs. Ed mund Y. S. Chao and Kai-Nan An is gratefully acknowledged,

Note. Readers can obtain five pages of supplementary material from the National Auxilary Publications Service, co Microfiche Publications, PO Box 3513, Grand Central Station, New York, NY 10163-3513. Request document no. 05224, Remit with your order inot under separate cover), in US funds only: $7.75 for photocopies or $4.00 for microñche. Outside the Unted States and Canada. add postage of $4.50 for the first 20 pages and $1.00 for each 10 pages of material thereafter, or $1.75 for the first microfiche and $.50 for each fiche thereafter. There is a $15.00 inozcing charge on all orders filled before payment.

5. Windebank A., Daube JR, Litchy WJ, et al. Late sequelae of

paralytic poliomyelitis in Olmsted County, Minnesota. Birth

Defects 1987:23-27-38. 6. Dyck PJ. Kratz KM, Lehman KA, et al. The Rochester Dia

betic Neuropathy Study: design, criteria for types of neuropa thy, selection bias, and reproducibility of neuropathic tests,

Neurology 1991:41799-807 7. Daube JR. Statistical estimates of number of motor units in

thenar and foot muscles in patients with amyotrophie lateral sclerosis or the residual of poliomyelitis abstract) Muscle

Nerve 1988;11:957 958. 8. Galea V. de Bruin H. Cavasin R. McComas AJ. The numbers

and relative sizes of motor units estimated by computer. Mus.

cie Nerve 1991:14:1123-1130. 9. Wiedebank & Chnical evaluation of motor function. In: Duck

PJ, Thomas PK Asbury AK, Winegrad Al, Porte D Jr, eds. Diabetic neuropathy. Philadelphia: WB Saunders, 1987:100 –

106. 10. Morrey BF, An KN, Chao EYS. Functional evaluation of the

elbow. In: Morrey BF, ed. The elbow and its disorders. Phila

delphia: WB Saunders. 1985:73-91. 11 Windebank AJ. Prognosis and differential diagnosis. In: Halstead L. Grimby G, eds. Past-polie syndrome. Philadelphia:

Hanley & Belfus, 1995:69 – BA 12. Ahlskog JE. Aksamit Aronson AE, et al. The sensor,examination. In: Clinical examinations in neurology, 6th ed.

St. Louis Mosby-Year Book, 1991:255-275. 13. Aronson AE. Auger RG, Bastron JA, et al. Clinical examinations in neurology, 5th ed. Philadelphia: WB Saunders, 1981 14. Agre JC. Local muscle and total body fatigue. In: Halstead LS.

Grimby G, eds. Post-polio syndrome. Philadelphia: Hanley & Belfus, 1995.35-67. 15. Dalakas MC Post-polio Syndrome detinition, classification,

clinical description Ann NY Acad Sci 1995:753:68-60, 16. Windebank Ad Litchy WJ Daube JR Prospective cohort study of polio survivors in Olmsted County, Minnesota. NY

Acad Sci 1995:753:81-86. 17. Thompson JM. Tension myalgia as a diagnosis at the Mayo Clinic and its relationship to fibrositis, fibromyalgia, and myo fascial pain syndrome. Mayo Clin Proc 1990;65:12371248.

References

1 Cornil L. Sur un cas de paralysie generale spinale anterieuresubaigue suivi d’autopsie. Gaz Med (Paris! 1875:4:127-129. 2. Mulder DW. Rosenbaum RA, Layton DD Jr. Late progression

of poliomyelitis or forme fruste amyotrophie lateral sclerosis?

Mave Clin Proc 1972:47:756-761. 3. Halstead LS, Rossi CD. Post-polio syndrome: chnical experience with 132 consecutive outpatients Birth Defects 1987:23.13-26. 4. Windebank AJ, Litchy WJ, Daube JR. Kurland LT Codd MB

Iverson R. Late effects of paralytic poliomyelitis in Olmsted County, Minnesota. Neurology 1991:41:501-50784 NEUROLOGY 46 January 1996

Lack of progression of neurologic deficit in survivors of paralytic polio Read More »

Post Polio Research Update

With Dr. Jacquelin Perry Reported by Mary Clarke Atwood

World renowned polio specialist Dr. Jacquelin Perry was the featured speaker at the Rancho Los Amigos Post-Polio Support Group meeting in Downey, California on December 10, 1995.

In her annual talk to this support group Dr. Perry gave an overview of some current research approaches to managing Post-Polio Syndrome (PPS) including reports of studies on nerve axon overuse, medications used for treating PPS fatigue and pain, and myoneural junction overuse. When looking at results of studies she cautioned people to look at the volume of data, not just the numbers. Dr. Perry advised survivors to avoid overuse by cutting back and realistically managing the demands of home, family, work, and play.

Diagnosis of PPS

PPS is one of the disabilities that is diagnosed only through clinical findings. Often muscle studies such as EMG, Macro EMG or biopsy are performed on weakened muscles but these studies can only reveal prior motor unit lesion, i.e., the reports may say that a person has had something like polio at one time, but not polio definitively. (A motor unit is composed of nerve cell, its attached nerve axons, and the supplied muscle fibers. Even if enlarged motor units are detected on an EMG, that single finding cannot confirm PPS.)

In a previous talk Dr. Perry said she bases a diagnosis of PPS on three things:

a history of polio 2. a period of some recovery followed by new loss of function 3. a physical examination that reveals
scattered muscle weakness (observed during an extensive manual muscle test from head to

toe) 2. normal sensations 3. reflexes that are normal (2+) for strong muscles and depressed for weak muscles

Nerve Axon Overuse

During the acute phase of polio, 95% of the patients anterior horn cells were either injured or destroyed by the polio virus. (These are the nerve cells that ultimately control muscles.) Then as recovery began new nerve axon sprouts formed to adopt orphaned muscle fibers that no longer had a nerve supply. Within a month, 12% to 91% of these cells began to recover. Although many people seemed to “recover”, the majority do not have as many motor nerve cells as normal. (The average person had only 47% recovery.)

Therefore, their motor system is not as strong as normal. So with fewer motor units, the muscles have been working harder than normal trying to meet regular demands. This results in overuse of the system and weakness develops.

Dr. Perry cited a study by Pachter with rats. (B. Pachter, Ph.D., “A Rat Model of the Post-Polio Motor Unit”, Orthopedics Vol. 14 Dec. 1991). This study demonstrated that when a muscle loses its nerve supply (as in polio) there is less muscle strength and less muscle fiber; when the nerve supply is increased there is an increase in muscle fibers and muscle strength. But, in the later life cycle of the rat those muscle fibers again decrease and the muscle strength decreases also. Dr. Perry said, “This is not good news but at least it gives you facts.” (There has been speculation about the cause of. PPS being due to the failure in the muscle, the myoneural junction, or the nerve cell body.) “This study indicates that the secondary nerve sprouts (1) are not that good, (2) cannot take strain, (3) can fail when challenged. Pachter’s conclusion is that the sprouts are degenerating from overuse.”

Manual Muscle Testing

Determining what is significant muscle weakness can be a problem because it depends on the strength of the examiner and how much pressure is exerted on a muscle. The examiner can create a great variable in manual muscle testing. Since some examiners cannot identify differences between muscle grades 3+ and 5 (normal) Dr. Perry’s current research is defining the guidelines to differentiate muscle strength within that range.

Dr. Perry advises that muscles that are less than grade 3 must be protected; grade 3+ muscles can be used gently; grade 4 and 4+ muscles can be used moderately and grade 5 muscles can be used freely. Be aware that even a grade 5 (normal) muscle for a polio survivor is still only 50% of normal.

Fatigue Seventy

Dr. Perry cited a Fatigue Severity Scale that shows:

Normal fatigue varies between 1-6 and averages 3. Fatigue in people with other neurological diseases was slightly higher, reportedly between 2-7 and averaging 4. People with PPS have the most fatigue; it was reported between 3 and 7 and averaged 5. Note that the least fatigue reported for PPS is greater than that in the other two categories!

Medications for Fatigue

Since Fatigue is a major complaint of many people with PPS and other doctors sometimes prescribe medications to counteract that fatigue, Dr. Perry investigated reports on their use and effects.

Amantadine

According to reports, the use of amantadine to decrease PPS fatigue was almost equal to the use of a placebo: 6 out of 10 people with PPS reported less fatigue with amantadine while 6 out of 13 reported less fatigue when taking a placebo.

Growth Hormone

Studies have revealed that in 113 of normal elderly people growth hormone level was reduced and activity level was also decreased. If a person has physical reasons to reduce activity, then growth hormone level might be low but it cannot be increased by taking this medication. When growth hormone was prescribed for PPS about 1/3 of these people reported a decrease in fatigue. Those who improved were mostly older, obese men who had difficulties with Activities of Daily Living (ADL). For those who reported less fatigue the results were not significant. Therefore, the level of growth hormone was not significant as a causative or a curative factor in treating PPS fatigue.

Prednisone

Cortisone type drugs have been used for many years at minimal levels to control the symptoms of arthritis. Nothing specific has been reported beneficial for PPS. 4. Mestinon

For many years Mestinon has been prescribed for myasthenia gravis patients. It functions at the nerve and muscle (myoneural) junction to improve the transmission between the nerve and the muscle. Studies of its use for PPS fatigue show that about 64% of those who used the drug felt some reduction in fatigue but no change in muscle strength.

Mestinon helps myoneural junction overuse. According to Grimsby a muscle that is grade 4+ or basically normal activates its muscle fibers 20 times per second, i.e., essentially pushes the button 20 times to make that muscle work. A weaker grade 3+ muscle must activate its muscle fibers 40 times per second or twice as fast (double timing) to get more work out of less. The duration for the normal muscle would be 100 milliseconds but for the weaker 3+ muscle it would have to be activated 500 milliseconds.

Dr. Perry concluded that: if these “borderline inadequate” muscles are all being overworked, and . if Mestinon is working at the myoneural junction, and

if the junction could be overused, maybe that is why Mestinon helps some polio survivors. There is no controlled study on who benefits from Mestinon, but Dr. Perry has observed that people with muscle grades between 2 and 3+ seem to find Mestinon helpful but people with stronger muscles seem to get little benefit from this drug. Thus myoneural junction overuse is one situation that can be helped medically

Medication for Pain

In general, Dr. Perry’s philosophy is to not use pain mediation for PPS because it acts as a mask and a person might continue over using a weak neuro-motor system. To reduce inflammation, nonsteroidal anti-inflammatory drugs (NSAIDs) are acceptable because they act at the first level of injury.

Coping

We need to protect ourselves from overuse and its consequences. Dr. Perry says, “Don’t dream of what was. That is past.”

Weigh your demands to make sure they do not exceed what you can do – at home with your family, at work, and at play.

How do you control PPS? The only way to control it is to remove the strain by cutting back,

The only key symptom of PPS is weakness. When the nerve supply to the muscle is reduced the result is a decrease in muscle strength. . When a person is not coping and facing things, anxiety and depression can be secondary effects.

In summary, since all polio survivors have less strength they also have less work capacity. So it is necessary to plan how to make less demands on your body by lifestyle modification.

Lifestyle Modification

Dr. Perry again cautioned that those people who had severe polio followed by good recovery are most at risk for neuromuscular overuse injury. Even when polio muscles appear normal on the outside, those muscles are less efficient and their motor units are most likely to decompensate. These muscles must be protected from overuse both by cutting back demands and possibly by bracing. It is necessary to learn how to control lifestyles in order to continue enjoying the pleasures of life. If a person currently has no symptoms, there is no problem. But if or when problems do appear then a person may need to adjust his lifestyle. For those people whose lifestyle currently exceeds their neuromuscular physiology, they may “bankrupt” that system unless lifestyle is modified and strain is removed. For people with joint degeneration and mechanical problems, orthoses may help protect those muscles and joints. Dr. Perry advises overweight patients to try to get rid of their “spare tire” by losing weight, thus reducing the strain on weakened muscles.

Exercise

Here in Southern California winter weather is different from many other parts of the country where it freezes, forcing people to stay indoors and get lots of rest. With the mild winters here, people remain active outdoors and muscles do not get the same amount of rest compared to muscles of people living in places that have long hard winters. Thus Dr. Perry believes that exercise is not very useful for PPS patients in Southern California because our lifestyles are very active already – leaving no extra muscle to use. In a Canadian study of exercise, there was a gain of 3% -26% in strength. But the raw data showed that only one person had a gain of 26% while the other four people showed 3%-5% gain or a slight loss. (A 26% gain in a grade 2 or 3 muscle is still not a large gain of muscle strength.)

Reduce Strain

Lifestyle modification is by far the most important. 2. Orthoses and aids (braces, canes, crutches, power wheelchairs) can help support weak muscles. 3. Exercise is not too effective – sometimes muscle strength is increased only 5%. 4. Surgery is occasionally helpful.

How to Cut Back

First of all, polio survivors need to sense what is happening to their bodies and become aware of which muscles are getting tired and which muscles are not. 2. Break up activities into pieces by working a little, rest a little, work a little, rest, etc. Sit whenever possible. Dr. Perry does not advise patients to stop everything because then muscles will atrophy from disuse.

How to Educate Your Doctor About PPS

Dr. Perry suggests that a polio survivor provide their personal physician with the briefest literature that is heir own PPS problem. Remember that you are a small portion of that doctor’s practice. If your physician does not respond, Dr. Perry advises looking for another doctor.

Conclusion

This report has focused on some of the current research approaches to managing PPS. Dr. Perry still feels that lifestyle modification is one of the most effective ways of managing PPS. Her guidelines for a safe activity level are that “polio survivors can do anything as long as it results in no pain and fatigue that lasts no more than ten minutes.”

Polio Clinic

Clinic appointments are scheduled several months in advance at (310) 401-7117

Dr. Jacquelin Perry can be contacted at: Rancho Los Amigos Medical Center Pathokinesiology Lab – Bldg. 304 7601 E. Imperial Hwy. Downey, CA 90242

Thanks to: Rancho Los Amigos Post-Polio Support Group NEWSLETTER, March 1996.

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Post Polio Breathing and Sleep Problems

POST POLIO BREATHING AND SLEEP PROBLEMS

Judith R. Fischer and Joan L. Headley, International Polio Network

New breathing and sleep problems in aging polio survivors can be insidious and often not recognized by either polio survivors themselves or health care professionals. Polio survivors who were in an iron lung or barely escaped one during the acute phase should be aware of potential problems and educate themselves in order to avoid acute respiratory failure. Polio survivors who did not need ventilatory assistance during the acute phase may also be at risk for respiratory failure and should likewise be aware of problems with breathing and sleep.

Simply stated, the major problem for polio survivors is hypoventilation (Commonly referred to as underventilation). Not enough air reaches the lungs, producing an imbalance in the gas exchange in the blood: too little oxygen, too much carbon dioxide (CO2) or hypercapnia. Hypoventilation is caused by one or a combination of the following: chest wall deformities such as scoliosis, respiratory muscle weakness due to the poliomyelitis, and sleep apnea (an interruption of breathing during sleep) which can be central obstructive, or mixed, and occurs in the general population as well. Other factors contributing to a polio survivor’s problems are a history of smok9ing, obesity, lung disease, and diminished vital capacity (VC). As aging occurs in anyone, vital capacity (VC) diminishes, but this decrease in VC is more serious in an aging polio survivor with limited musculature remaining to produce adequate ventilation. Many polio survivors had impairment of the diaphragmatic and intercostal muscles, and the normal changes due to aging may cause them to lose VC at a greater rate, thus exacerbating the development of hypoventilation. Signs and symptoms include: fatigue, daytime sleepiness, morning headaches, need to sleep sitting up, sleep disturbances (including dreams of being smothered, night mares, restless sleep, interrupted sleep), snoring, poor concentration and impaired intellectual function, shortness of breath on exertion, claustrophobia and/or feeling that the air in the room is somehow bad, anxiety, difficulty in speaking for more than a short time, quiet speech with fewer words per breath, use of accessory muscles to breath, and a weak cough with increased susceptibility to respiratory infections and pneumonias. Polio survivors experiencing more than one of the above signs and symptoms should seek a respiratory evaluation by a pulmonologist, preferably one experienced in chronic neuromuscular disorders. Pulmonary function tests should include at least: VC, air flow, MIF (maximum inspiratory force) and MEF (maximum expiratory force), and ABG (arterial blood gases). A sleep study should also be considered, however, strong anecdotal evidence from polio survivors indicates that a sleep study may miss detection of hypoventilation. A sleep study is designed to detect sleep disturbances, such as sleep apnea: it does not measure CO2. Management of breathing and sleep problems can be achieved largely through the use of nocturnal noninvasive ventilation, in the form of mouth intermittent positive pressure ventilation, nasal intermittent positive pressure ventilation ( a variety of commercial and custom nasal/face masks are available), and negative pressure body ventilators. However, polio survivors may find themselves gradually extending periods of ventilator use. In some cases, as a last resort, invasive tracheostomy positive pressure may be necessary. Medical literature regarding the management of breathing problems often includes a warning about the use of oxygen therapy. Respiratory failure in polio survivors is usually due to hypoventilation which can be aggravated by the short and long term use of oxygen. When the brain senses an excess concentration of CO2 in the blood it instructs the body to increase breathing, ridding it of the CO2 and increasing the oxygen. When oxygen is supplied, the mechanism in the brain detection the CO2 eventually turns off. Hypercapnia is best treated with assisted ventilation. Polio survivors with different problems, such as COPD or pneumonia, may benefit from short term oxygen therapy under careful supervision.

REFERENCES:

*Advice for People with Polio or Other Neuromuscular Disorders by Augusta Alba, MD, and Alice Nolan, RN; Rehabilitation Gazette, Vol.23, 1980

Evaluation and Management of Post-Polio Respiratory Sequelae: Non-Invasive Options by John R. Bach, MD; Chapter 6, Post-Polio Syndrome (ISBN 1-56053-117-7) edited by Halstead and Grimby, published by Hanley and Belfus, Inc., Philadelphia PA (800-962-1982).

Suggestions for Avoiding Respiratory Complications by John R. Bach, MD; **I.V.U.N. News, Vol. 9, No. 2, Fall 1994

Severe Hypercapnia After Low-Flow Oxygen in Patients With Neuromuscular Disease and Diaphragmatic Dysfunction by Peter C. Gay, MD, and Lee C. Edmonds, MD; Mayo Clinic Proceedings, Vol. 70, pp327-330; Editorial pp403-404, April 1995.

Noninvasive Ventilation: Does It Work, for Whom and How ? By Nicholas S. Hill, MD; American Review of Respiratory Disease, Vol. 147, pp. 1050-1055, 1993.

Comparison of Commercial and Custom Nasal/Face Masks by Susan Sortor Leger, RRT; I.V.U.N. News, Vol. 9, No. 1, Spring 1995.

The Diagnosis of Underventilation Following Polio and Treatment of Underventilation by Day and by Night by G.G. Spencer, FAARCS; I.V.U.N. News, Vol. 2, No. 2, Fall 1988

*Available by sending a self-addressed #10 envelope with 32 cents postage to 4296 Lindell Blvd., #110, St. Louis MO 63108-2915.

**I.V.U.N. News, a bi-annual newsletter edited by Judith R. Fischer, links ventilator users and health care professionals. The annual subscription fee is $12. A complete set of 18 back issues is available for $25 postpaid. To order, contact G.I.N.I., 4207 Lindell Blvd, #110, St. Louis MO 63108-2915. From Polio Network News, Fall 1995, Vol. 11, No. 4 From GLEANINGS, Nebraska Polio Survivors Association, P.O. Box 37139, Omaha, NE 68137

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Using Ear Acupuncture to Treat Post Polio Pain

USING EAR ACUPUNCTURE TO TREAT POST-POLIO PAIN

Diane Baxter

Excerpted from The Polio Society Newsletter “Options”, Fall 1995

Dr. Francis H’Doubler, M.D., a Missouri thoracic surgeon, discovered the usefulness of ear acupuncture to treat his own pain and discomfort from Korean War injuries. In the last five years he has been using ear acupuncture to treat people who have chronic pain, including post-polio people. In 1990 a friend came to him for advice about his post-polio pain. Dr. H’Doubler tried ear acupuncture, and happily his friend got relief of many of his symptoms. Then, Dr. H’Doubler spoke with the local post-polio support group and did a pilot study of 12 post-polio patients to formally test ear acupuncture. The treatments generally consisted of four to fourteen one hour sessions of stimulation to various points on both ears every three to seven days. The instrument used is called the Electro-Acuscope. Patients were told to continue seeing their regular doctors and maintain their current management of symptoms. Dr. H’Doubler notes that some patients improved even after one or two sessions, reporting less fatigue and weakness and increased energy and general well-being. After the treatments, 8 out of 12 patients reported 100% symptom relief, 2 had 75% improvement and 2 had 20-40% improvement. On a two year follow-up, most reported no return of symptoms. When symptoms did recur, they were again relieved with additional treatments. Since the pilot study, Dr. H’Doubler has treated many more post-polio patients with similar success. He plans to continue the use of ear acupuncture and encourages other medical professionals to study this procedure as a way of reducing or eliminating the symptoms of PPS. From: The Torch, April, 1996. Albert Einstein Medical Center Willowcrest Bldg. Orthopedics Dept. 5501 Old York Road Philadelphia, PA 19141

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Swallowing

FRANK C. SNOPE, MD

Swallowing difficulties (dysphagia) occur in 10-15% of individuals with acute poliomyelitis and 10-20% of individuals experiencing the post-polio syndrome according to Terry Molsen a speech pathologist from Ringwood, NJ. Ms. Molsen conducted a workshop on swallowing difficulties at the recent NJ Confer on Post-Polio Syndrome.

Ms. Molsen explained that swallowing was a complex mechanism involving many muscles and nerves in and around the throat. Polio can weaken these muscles, with the result that swallowing problems can arise.

The kind of swallowing problems that can occur in post-polio syndrome are coughing and choking during and after eating, “sticking” in the throat, regurgitation of food, and difficulty managing secretions (e.g., saliva). The type of foods that cause the most problems are tough meats, nuts, popcorn, peanut butter, crisp vegetables (e.g., carrots, apples), dry breads, medications, certain cheeses, and carbonated drinks.

Ms. Molsen provided a list of things that can be done to make swallowing easier:

Chew all food well
Slow the rate of eating
Alternate food with liquids to “wash” food down
Take smaller bites
Swallow everything before the next bite
Swallow several times per bite
Eat when less fatigued
Eat in a relaxed atmosphere
Eat the most difficult food first (when swallowing muscles are less fatigued)
Avoid problematic food or prepare it in a way that is easier to swallow (e.g., peel apple, blend carrots, etc.)

In addition to these suggestions, Ms. Molsen also noted that some individuals can reduce swallowing problems by turning the head to the right or left, or tucking the chin down when swallowing.

Finally, Ms. Molsen cautioned that swallowing difficulty is a symptom, not a disease. Any persistent or unusual problems that do not respond to the suggestions given above should be discussed with one’s physician. A referral to a speech pathologist for further evaluation may be necessary to eliminate other causes of swallowing problems and to plan proper management.

New Jersey Polio Network Newsletter Fall 1995

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Post-Polio and Physical Therapy

POST-POLIO AND PHYSICAL THERAPY

Susan L Fish MAPT

During recent years, I have had the opportunity to meet and work with patients experiencing the late effects of polio. Many times I have detected some frustration and anger regarding my professionals lack of experience in treating Post-Polio patients. I write this brief article now for two reasons.

to explain and help you understand this lack of knowledge on the part of many of my colleagues. 2. to provide some guidelines regarding Do’s and Don’ts when seeking physical therapy.

Most Physical Therapists (PT’s) (Physiotherapists in UK) working today weren’t even alive during the major polio epidemics. Their formal education regarding poliomyeliitis was more historical than factual, with little more than definitions of pathology and no clinical experience. Post-Polio Syndrome is only recently being recognised and it’s existence is still questioned in some medical circles. Both acute polio and post polio syndrome present clinical pictures which are unlike any other neuromuscular condition. Without the experience of working with acute polio patients and with little documented information regarding the treatment of Post-Polio Syndrome, it is not surprising to find professionals lacking in knowledge.

Although, there may be reasons for a lack of knowledge, a responsible professional should NOT treat any condition that he or she is not confident and knowledgeable in treating. You may be able to direct a PT to appropriate resources. Please see the resources at the end of this article and I would be happy to help also.

Reasons for seeking physical therapy will vary. You may be referred to a PT to help you with your Post Polio Syndrome. You may be referred for rehabilitation following corrective surgery for a polio related condition. You may also be referred for a condition not necessarily related to polio at all such as arthritis, bursitis, tendonitis, fractures, osteoporosis, low back pain, stiff neck, etc, etc. Your physical therapist is well trained to treat these other conditions. However, your post polio status should be taken into consideration when designing a program. Here is some advice.

Do’s and Don’ts to keep in mind when going for physical therapy.

Do trust yourself and the knowledge you have gained over the years about your body. Do be willing to alter your lifestyle.

Do avoid fatigue.

Do get enough rest.

Do pace your activities rather than discontinuing them.

Do conserve energy. It may make more sense to spread your activities out, allowing for rest periods, rather than eliminating interests and activities.

Do recognise that your body is aging and some physical changes will occur which are not related to post polio. There IS a normal aging process even though post-polio may be a part of it. Do respect your feelings. This may be a difficult adjustment time for you; seeking emotional as well as physical guidance may be a wise thing to consider.

Don’t follow advice regarding physical exercise if you become fatigued while doing it. Don’t become short of breath with exercise.

Don’t do more than your body feels comfortable doing.

Don’t cause pain with activity or exercise.

Don’t gain weight.

Don’t reject using aids and assisting devices without giving them serious thought. (They are meant to conserve energy and preserve anatomical structures, i.e. joints, muscles, tendons, cartilage and ligaments.) Most are delighted and surprised by the increased endurance and energy they have with the use of canes, wheelchairs, motorised scooters or the many other easily found assisting devices.

Resources

Dean, Elizabeth. Clinical Decision Making in the Management of Late Sequela Poliomyelitis. Physical Therapy Oct 1991,Vol 71; 10 752 – 761. [PubMed Abstract]
Weiss, Marianne R. Becoming an intelligent Consumer of Physical Therapy Services, Polio Network News Winter and Spring 1993, Vol. 9 Nos. 1 and 2.

The Lincolnshire Post-Polio Network

Registered Charity No. 1064177

An Information Service for Polio Survivors and Medical Professionals

All enquiries, book requests, medical article requests, membership fees, items for newsletters and donations to

The Secretary, Lincolnshire Post-Polio Network

PO Box 954, Lincoln, Lincolnshire, LN5 5ER United Kingdom

Telephone: +44 (0)1522 888601

Facsimile: +44 (0)870 1600840

Email: info@lincolnshirepostpolio.org.uk

Web Site: www.lincolnshirepostpolio.org.uk

Document preparation: Chris Salter, Original Think-tank, Cornwall, United Kingdom.

Document Reference: <URL:http://www.zynet.co.uk/ott/polio/lincolnshire/library/usa/therapy.html> Created: 26th January 1997

Last modification: 31st January 2010.

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A Report in to the Consequences of Living With Polio for 63,500 Years

A REPORT INTO THE CONSEQUENCES

OF LIVING WITH POLIO FOR 63,500 YEARS

Peter Field

1995

Contents

Objective

The Findings

QUOTATIONS FROM SURVEY FORMS

PRINCIPAL RESPONSES

Method

The Sample

Circumstances at onset and now.

Changes since recovery

Analysis of changes since recovery

Change in overall situation.

Relationship of age at onset to probability of subsequent deterioration.

SUMMARY OF FINDINGS

Conclusion

Objective

This survey was conducted as a lay study into the impact on the lives of people who had polio earlier in life, and also to establish the frequency as well as the severity of the problems attributed to the “Late Effects of Polio”.

The problems it has highlighted are shown to be common occurrences among those who had polio 30 plus years ago.

A worthwhile outcome to this investigation would be further, more clinical, investigation with a view to drawing up a list of good practices to minimise, if not to halt, the impact on those many polio survivors around the world.

The Findings

The true impact of the findings are not distorted by the statistics. The message is loud and clear – having had polio is likely to have a recognisable impact later in life. What form or extent this impact is likely to have cannot be measured or predicted – but that there will be an impact is clear for all to see.

The survey is clear in its message that the medical profession are not familiar with the harmful effects that having had polio earlier in life are likely to have on the ageing body. They are inexperienced as to the probability of certain outcomes, which most likely leads to the dismissive attitude sometimes referred to. This, it is suspected, is a significant contributor to the trauma often described.

The production of the information sheet by the BPF for those who had polio earlier in life is confirmed as being a necessary and valuable aid to overcoming this shortfall in awareness. A condensed version of the statistical results of the survey may add weight where that is required. It is however recommended that attendant cautionary words are added clearly stating that the conditions described are not inevitable.

It is a fact that the rising average age of the population will result in an increase in the age of polio survivors. The findings of this survey provide statistical evidence of a reduction in the physical capability of the individual polio survivor and the inevitable attendant increase in the severity of disablement – polio is not going to leave the UK scene for some time to come and is likely to have a significant impact on the demands on Care in the Community.

QUOTATIONS FROM SURVEY FORMS

The following are a sample of quotations extracted verbatim from the completed forms which in themselves paint perhaps the most important picture to emerge from the whole survey. A Doctor can hardly be expected to interpret a set of circumstances presented at one moment in time, particularly when change has in all probability taken months if not years to manifest itself with little or no clinical precedent or in many cases medical logic. They non the less express the feelings, findings and experiences of a cross section of the respondents. They have been analysed into the summary of findings, such is their importance.

It is worth while pointing out that great emphasis was placed on these descriptive responses, setting aside the emotion that appeared in quite a few, they are the best measure of the overall impact on the lives of those who actually had polio. They are not dreamed up. They were not expressed in a medium which would elicit a sympathetic response. Many are factual reporting of a very real situation, most without question carry an important humanitarian message for the medical profession.

Q1. “Now that I have MS it’s difficult to assess which may be late effects of polio or the MS” Female, born 1957, polio at 9 months.

Q2. ” At 39 years (of age) a rapid decrease in mobility, an increase in fatigue, weakness and tiredness and now I have constant severe pain. Up to three years ago I never considered myself as having a disability……….I was always on the go…….so when this happened to me 3 years ago it was like a nightmare. I now cannot walk at all. I would never ever believe that I would deteriorate so rapidly and feel so ill as I do now”. Female, born 1953, polio at 2 1/2 years.

Q3. “Condition static for 26 years, worse after fractured leg in 1982, much worse in last 18 months” Male retired Doctor, born 1927, polio at 28 years

Q4. “Diagnosed at National Hospital for Nervous Diseases (London) in 1989 as suffering from “Post polio

muscular atrophy” (LEP) Informed – no treatment, no cure, no prognosis! This was as a result of marked loss of muscle and range of movement during late 1980’s. Initially told my muscles needed building up – therefore 3 years of physiotherapy, ( I did not accept this explanation as I had always been very physically active). Result of physio – increase loss of muscle power and range. Was told later I should have rested not exercised. Too late! Left me very frightened for the future, – will I end up with no use of either arm?” Female, born 1947, polio at 18 months.

Q5. “I felt as fit as a fiddle till I reached forty, My back and joints started to give me pain. By the time I was 43 I realised that I couldn’t do half the things I had always taken for granted.” Female, born 1948, polio at 6 months.

Q6. “Have horrendous tiredness/fatigue problems – for me the answer is to lie down for an hour at least to let the body recover. I dread the cold.” Female, born 1945, polio at 4 years.

Q7. “Recovery was so good I was able to become a District Nurse, with all that entails. In 1986 I was visiting a client and found I couldn’t negotiate the outside path and steps without arm support. Subsequent neurological investigation revealed LEP. My strength has deteriorated to the extent that I had to retire completely last year after having gone on part time and then changing career completely.” Female, born 1941, polio at 20 months.

Q8. “I find exhaustion is a problem – acute tiredness – it’s awful – functioning but feeling only half alive. I can go to bed feeling “alive” and wake up feeling so very heavy and awful. My shoulders are now giving great concern – they have had enough of being used as hips, and my arms are tired of being used as legs.” Female, born 1946, polio at 6 yrs.

Q9. “This extreme fatigue is what worries me most” Female, born 1925, polio at 26.

Q10. “I have been unable to get downstairs for 8 years, only twice lately when I had to slide down each step on my behind, but I couldn’t get back up again so had to call an ambulance to get me up into a chair. My social worker has put in for a stair lift for me a long time ago. But they say there is a long waiting list.” Female, born 1926, polio at 16 months.

Q11. “Noticed weakness in legs after major operation for gall bladder removal 10 years ago. Now I get tired and unable to walk outside without escort. Stairs and steps I cannot manage.” Female, born 1920, polio at 7 years.

Q12. “I feel I am fortunate to have held fairly steady physically – long may it last, I couldn’t afford to loose a lot! If I have an illness – flu cold etc., it takes a long time for me to get back to normal” Female, born 1939, polio at 17 years.

Q13. “I find gentle activity is more beneficial than staying in bed or inactive which only increases pain. Painkillers taken every day seem to increase problems.” Female, born 1939, polio at 12 years.

Q14. “I worked hard in a large house and did get excessively tired and crotchety and had much shoulder, elbow and knee problems (crutches) – but now in retirement using a chair – and no one else to worry about, I can pace myself, rest when I feel like it and feel I’m a much calmer, nicer person. If only the great value of rest at regular intervals was stressed in rehabilitation to ones relatives as well perhaps the value of wheelchairs suggested, I might have enjoyed life more.” Female, born 1927, polio at 25.

Q15. “After reading in the newspaper the late effects of polio, I could think of many things over the last 30 years, many falls also the feeling of desperate tiredness…..my GP always said it was old age.” Female,

born 1920, polio at 1 year.

Q16. “I improved quite well until 7 years ago when I had a flu like attack, since then my walking has deteriorated very badly.” Female, born 1929, polio at 28.

Q17. “In 1982 at age 54 I had, quite suddenly, very severe Thyrotoxicosis. After this my muscle power diminished so much I could not recover my strength and need a powered scooter to go anywhere except around the house.” Female, born 1927, polio at 18 years.

Q18. “About 2 1/2 years ago I started to become very tired and fatigued, and had a small lump on the left side of my jawbone, which was not painful. After 8 months and three biopsies later I was told I had an illness called Histiocytosis X. I asked if this was anything to do with having had polio: was told definitely not. Reading your bulletin last year on post polio syndrome I’ve been getting all those symptoms so I was surprised to be told polio had nothing to do with it.” Male, born 1950, polio at 3 years.

Q19. “Condition deteriorated markedly so in 1988; markedly indeed since 1992.

10 years ago could walk 5 miles

5 years ago could walk 2 miles

1 year ago could walk 300 yards

now can walk 100 yards.

10 years ago could manage 5 flights of stairs

now can manage only one.

The orthopaedic problems are bad enough; the systematic exhaustion is harder to predict and thus to compensate for” Male, retired doctor, born 1942, polio 8 years.

Q20. “I did recover from it (polio) to the extent that for several years I was a heavy goods vehicle driver, doing long distance work. But now the only use I have in my right arm is the wrist and fingers.” Male, born 1940, polio at 5 years.

Q21. “I am at odds with the medical profession. I maintain that my troubles are connected with polio, particularly LEP, but hospital state the cause is spinal stenosis.” Male, born 1932, polio at 20 years.

Q22. “As well as polio I have developed MS since 1977 after my third child. I have arthritis in most of my joints and I have bronchial asthma.” Female, born 1946, polio at 18 months.

Q23. “The LEP was more noticeable from four years ago when I had a bad fall. I spent three weeks resting in hospital and never got back to the previous mobility (as before the fall).” Male, born 1931, polio at 14 years.

Q24. “The GP treatment of polio patients leaves a lot to be desired…….it is time to respectfully ignore BMA opinions!!!! There are many polio persons who are not BPF members consistently deriving benefit from Chiropractic treatment.” Male, born 1931, polio at 11 years.

Q25. “By the time I was 16 I was in full time employment in the engineering trade. In robust health and stronger than most boys of my age. This trend continued until I was 32 when through the effects of polio the part of my central nervous system that controls the breathing deteriorated…..I require a respirator to live…..(apart from my breathing) I consider my condition at the age of 64 as good as most people, only my breathing holds me back.” Male, born 1930, polio at 7 years.

Q26. “I think I may be following the general pattern of ‘LEP’, loss of strength, weakness and fatigue over the past 18 years which brings on such frustration when you look back and think of what you were once capable of doing without pain even though it was limited.” Male, born 1928, polio at 17 years.

Q27. In response to the question as to whether the disability has changed “Yes, whole body now diagnosed by hospital as post polio syndrome.” Male, born 1921, polio at 36 years.

Q28. “Retired from work at age of 60 – found journey to work exhausting. Last six years have needed ventilator at nights to clear blood gases.” Male, born 1921, polio at 31 years, was on respirator.

Q29. “By my late teens I had reached 80% normal physical ability. At this stage I had no need for any aids and I led a normal active life until I reached my late thirties, when there began a marked and rapid deterioration in my condition for no apparent reason. There was no medical reason for this until I discovered the condition of post polio syndrome. I continued to deteriorate and would not be able to function without the constant aid of my wife and mobility aids. I would consider that my capabilities are now about 30% and still falling.” Male, born 1942, polio at 3 years, was on respirator.

PRINCIPAL RESPONSES

DESCRIPTION		NUMBER PERCENT
HOSPITALISED FOR OVER ONE MONTH AT ONSET	917	79%
HAS NOTICED DETERIORATION SINCE RECOVERY	895	77%
REPORTED LOW STAMINA/HIGH FATIGUE	774	66%
REQUIRES MORE HELP NOW FOR DAY TO DAY TASKS	702	60%
GENERAL WEAKNESS	671	57%
USES WHEELCHAIR ON REGULAR BASIS	652	56%
USES WALKING STICKS	491	42%
USES CALIPERS ON ONE OR BOTH LEGS	425	36%
HAD TO LEAVE WORK DUE TO WEAKNESS	364	31%
ATTENDS ORTHOPEADIC HOSPITAL	321	28%
GENERAL PAIN	313	27%
IS UNDER REGULAR TREATMENT BY GP	274	23%
WAS ON RESPIRATOR AT ONSET (OR NOW)	225	19%
BREATHING DIFFICULTY	189	16%
HAS SCOLIOSIS	195	17%
USES CRUTCHES, SHOULDER OR ELBOW	190	16%
HAD TO LEAVE WORK DUE TO PAIN	187	16%
ARM/SHOULDER PROBLEMS DUE TO USING CRUTCHES	185	16%
HAS DEVELOPED ARTHRITIS	181	16%
HAS HAD GENERAL SURGERY	178	15%
REPORTED POOR BALANCE	174	15%
ATTENDS GENERAL HOSPITAL	172	15%

ATTENDS SPECIAL UNIT	109	9%
FEELS THE COLD	78	7%
ATTENDS PAIN CLINIC	62	5%
REPORTED P&N HANDS	59	5%
REPORTED HEART PROBLEM	51	4%
HAS OSTEOPOROSIS	47	4%
ATTENDS REHABILITATION UNIT	44	4%
MENTIONED ME/MYASTHENIA GRAVIS	8	1%
TOTAL SURVEY FORMS	1167

Method

The statistics were compiled from the returns of all those who responded to a random mailing of questionnaires in the BPF magazine and some that were handed out at rehabilitation centres. It was not an easy questionnaire to complete, covering as it did aspects of pain and sleep, in addition to the main questions related to the residual effects of the polio.

Quite obviously without a progressive and standard measure of muscle power over the years it is not possible to paint a true picture of the impact of ageing on such a large number of people. The survey results are non the less a view of how the respondents have lived, and are continuing to live with the after effects.

The purpose of the survey was to establish if changes do take place, if there is any consistency as to the type changes that are being experienced, and what the most common changes are.

The survey tried to avoid leading questions, in so doing some information has undoubtedly been left out. It also proved impossible for many to give details of the state of recovery immediately after the onset simply as they were so young at the time. However it was possible to reconstruct some of the missing data by reading the responses carefully.

Only 45 forms out of the 1220 returned were unusable in the statistical review, which is a very commendable result. Only eight were unusable for the date of birth and age at onset review.

The Sample

Survey forms were returned by 1212 people with an average age of 60.1 years. Of the 1212, 782 or 65% female and 430 or 35% male. The age of the respondents shows that only 29% of the males were born before 1939 as opposed to 37% of the women, in fact only 7 men were over the age of 80 as opposed to 36 women. This trend surprisingly evens out at the end with the average age of all the females at 60.4 years and 59.6 years for the men. Finally the years since onset provide some remarkable figures as to the longevity of ex polio’s. Of all the respondents, 674 or 56% are this year over 60 years of age. This endorses what has been said about polio not going away for some time to come.

	BIRTH		ONSET
	No	%	No	%
1909 to 1914	84	7%	43	4%

1915 to 1924	265	22%		122 10%
1925 to 1934	308	25%		148 12%
1935 to 1944	216	18%		193 16%
1945 to 1954	288	24%		484 40%
1955 to 1985	51	4%		222 18%
TOTAL	1212		1212

Fig 1. Gives the number of births in ten year brackets, together with the number of cases of polio infection in the same years

It must be born in mind when looking for significant trends that these figures are of survivors not total cases, it follows that they cannot reflect the average situation during any one period. This is also true of the seriousness of cases in so much as it would be reasonable to assume that the more seriously effected would have enjoyed less chance of survival during the earlier part of the century.

	AGE AT ONSET
YEARS	No	%
UP TO 1	173	14%
1 TO 3	353	29%
4 TO 6	177	15%
7 TO 12	164	14%
13 TO 20	129	11%
21 TO 30	170	14%
31 UP	46	4%
TOTAL	1212

Fig 2. Is the age of respondents at the time they contracted polio

The age at onset is recorded in Fig. 2, but shows no significant variance between the sexes.

Fig 3. Shows the number of cases per year, with the average summer temp shown in the heavier line.

The date of onset is of some academic interest if only because it confirms the relationship between the number of cases and the average peak daily temperature during June, July and August each year. Hot summers contributed to a rise in the number of polio cases. The earlier information is obviously less dramatic, but the pattern in the late forties is very clear with the number of cases rising with peaks in summer temperatures as shown in figure 3.

Reverting to the question of age and its relevance to the following information, the evidence is that there is very little, if any, significance between the sexes or the age at which polio was acquired.

	AVERAGE AGE/YEARS FROM ONSET
	No	%	AVE/AGE	FROM ONSET
MALE	430	35%	59.57	50.81
FEMALE	782	65%	60.39	53.36
ALL	1212		60.14	52.45

Fig 4. Male/Female, age and years from onset

In keeping with the previous statistics Fig 4. shows that the average age of the female respondents was slightly greater than the males, they also had polio at a marginally earlier average age. However it is felt that the difference between the statistics for the sexes again indicates that there is no significant difference, or at least not sufficient difference to warrant recording in the results.

		YEARS SINCE ONSET
	MALE	%	FEMALE	%	ALL	%
80 PLUS	7	2%	36	5%	43	4%
70 TO 79	35	8%	87	11%	122	10%
60 TO 69	51	12%	97	12%	148	12%
50 TO 59	67	16%	126	16%	193	16%
40 TO 49	180	42%	304	39%	484 40%

30 TO 39	90	21%	132	17%	222	18%
TOTAL	430		782		1212

Fig 5. Details of years since onset by sexes and total

This feature is brought about by the higher percentage of onset in the 30 to 40 years since onset sample among the males rather than any other significant factor. This was taken as further evidence that the sex of the respondents does not appear to contribute in any meaningful way to the results and thus justifies ignoring the sex of the respondents in the rest of the analysis of the information.

Of passing interest only is the magnitude of the experience of living with polio among the respondents, it amounts to a total of 63,574 years. Let nobody discount the contents because this study was not conducted under clinical conditions. The quotations speak for themselves.

Of the total forms returned, 1167 contained information that was used in the analysis that appears in the following pages. Memory must play a part in the accuracy of the first two responses in Fig 6., many were not able to remember if they were on a respirator or indeed whether they were hospitalised.

Again no purpose could be detected in favour of splitting the sexes for tabulating the statistics.

The intention was to isolate the reason for any type of treatment to those conditions directly attributable to the after effects of the polio, some of the responses make this area reliant to some degree on a subjective interpretation.

Circumstances at onset and now.

	AT ONSET
Hospitalised for over one month at onset		917	79%
On a respirator at onset		225	19%
	MOBILITY AIDS – NOW
Uses wheelchair regularly		652	56%
Uses walking sticks		491	42%
Uses callipers on one or both legs		425	36%
Uses crutches		190	16%
	TREATMENT FOR EX POLIO CONDITION – NOW
At orthopaedic hospital		321	28%
By GP		274	23%
At general hospital		172	15%
At special unit		109	9%
At pain clinic		62	5%
At rehabilitation unit		44	4%

Fig 6. Information about the onset and conditions now.

Changes since recovery

The number of cases which reported a marked change in condition was very high, Fig 7 reflects the broader topics, followed by more specific conditions in Fig 8.

CHANGE SINCE RECOVERY
Reported deterioration since recovery plateau	895	77%
Requires more help for day to day activities	702	60%
Had to leave/change work due to condition	364	31%
Had to leave/change work due to pain	187	16%

Fig 7. The principal changes since recovery.

Responses in Fig 7. were made against specific questions, whereas Fig 8. and 9. represent conditions reported in the general supporting text and do not reflect the prompting of a leading question, it is reasonable to suppose therefore that they reflect a greater concern to the individual reporting them.

The only exception to this is the first response in Fig 8. The section on sleep offered a response on fatigue while carrying out day to day activities, this was used together with the oft repeated endorsement of fatigue as being one of the most debilitating features of the whole condition. (See Q8/9) If this response is added to the next one in order of magnitude, the level of general overall weakness which can be difficult to differentiate from fatigue, then the importance of this area of effect on the individual and their lifestyle is obvious.

SPECIFIED CHANGES SINCE RECOVERY
Mentioned low stamina/high fatigue more than once	774	66%
General weakness reported as overwhelming effect	671	57%
General pain both muscular and joints reported	313	27%
Poor balance specifically mentioned	174	15%
Reported feeling the cold as a major feature	78	7%

Fig 8. Most frequent specific change mentioned

Some of these reports have to be interpreted with a degree of caution. For instance, poor balance in all probability refers to a lack of the ability to make corrective movements with the legs in many cases, rather than any impairment to the balance mechanism. There is also a lack of definition between stamina/fatigue/weakness, and no doubt a degree of overlap has been included. That caveat must not be allowed to detract from the importance of this singularly authoritative message.

Pain is also to some extent derived from, or a product of fatigue, but many individuals reported pain unrelated to any particular activity or specific cause. The high frequency of arthritis and its associated pain must be a contributing factor in this response.

SPECIFIC CONDITIONS REPORTED
Breathing problems, not all requiring assistance	189	16%
Scoliosis	195	17%

Arm/shoulder problems due to using crutches	185	16%
Arthritis	181	16%
Had surgery to correct polio defect	178	15%
Reported frequent pins & needles in hands	59	5%
Reported heart problem	51	4%
Has osteoporosis	47	4%
Has been diagnosed ME/Myasthenia Gravis	8	1%

Fig 9. Other specific conditions/problems mentioned voluntarily

The reports of damage to upper arms and shoulders due to the prolonged use of crutches must be qualified by comparison with other factors. For instance only 64 or 34% of those who currently use crutches reported these problems as opposed to the 141 or 74% who reported the problem but now use a wheelchair. This probably indicates that acknowledging that the use of crutches can cause damage to upper limbs may lead to the adoption of a wheelchair as a more appropriate mobility aid. It is felt that this whole area is probably understated. There are many reports of respondents having to resort to the use of a wheelchair with loss of power in upper arms also mentioned, but the two situations are not linked. No assumptions were made in these cases, although one can remain suspicious.

Some of these responses need explanation which can be derived from the context in which they were made. For instance in most of the 8 cases when ME or Myasthenia Gravis was mentioned it was reported in the context of it having been given as a possible reason for certain symptoms rather than a positive diagnosis. In some cases it was reported as having been given to the patient in a dismissive manner as if to justify the view that the doctors time was being wasted!

The mention of heart problems can in all probability be dismissed as being in line with the rest of the population. In fact most of the reports were in connection with another condition such as persistent ulcers or general circulation problems, and as such have been ignored.

The incidence of breathing difficulty has a significant message. Of the 16% who mentioned this problem specifically, only 76, or one third had required a respirator at the onset, thus leaving 113 whose breathing has deteriorated to such an extent that they felt they had to report it. The significance is that these are the only involuntary muscles that are measurable in the survey, and therefore in some way the least subjective

of all the evidence of deterioration in muscle power. See quotation Q25.

Analysis of changes since recovery.

In an attempt to predict the probability of deterioration taking place, Fig 10 looks at the number of reports by date of birth and Fig 11 is the same information but sorted by date of onset.

	BIRTH		DETERIORATION
	No	%	No	%
1909 to 1914	84	7%	60	71%
1915 to 1924	265	22%	208	78%
1925 to 1934	308	25%	231	75%
1935 to 1944	216	18%	166	77%

1945 to 1954	288	24%	208	72%
1955 to 1985	51	4%	22	43%
TOTAL	1212		895

Fig 10. The proportion of those reporting deterioration by the date of birth.

	ONSET		DETERIORATION
	No	%	No	%
1909 to 1914	43	4%	27	63%
1915 to 1924	122	10%	92	75%
1925 to 1934	148	12%	112	76%
1935 to 1944	193	16%	139	72%
1945 to 1954	484	40%	368	76%
1955 to 1985	222	18%	157	71%
TOTAL	1212		895

Fig 11. The proportion of those reporting deterioration by the date of onset

The figures in both charts are remarkably consistent, leading to the conclusion that the probability of deterioration occurring is neither age related or related to the elapsed time since onset, but to other factors. The only deviation from the consistent pattern in these sets of statistics is the lower percentage reporting deterioration among those born after 1955, but even this is in all probability cancelled out by the consistency of the data presented in Fig.11.

178 reported that they had had surgery to correct defects related to polio, many were vague as to the nature of the corrective action so a detailed analysis was felt to be of little use. Of those who had surgery 149 or 83.7% also reported deterioration, see charts in Fig 8 & 9, as opposed to 76.7%. The difference could be explained by the need for surgery indicating more serious effect in the first place.

To establish if there is any correlation between deterioration and the age at which the respondent contracted polio a detailed study was carried out, see Fig 14.

Change in overall situation.

A functional abilities chart was included in the survey form which although difficult for many to complete in detail due not the least to the passage of time, helped considerably in arriving at Fig 12. This shows the change in muscle perceived by the respondent at three points in time. First as close to the recovery period as can be remembered, second at the very peak of recovery or muscle power, and third as perceived today.

All 1167 assessments were narrowed down to the relative position of 1 being the least affected through to 6 being the most severely affected. While the categorisation is somewhat subjective, in the main level 1 means no one limb completely affected, while 6 would represent total incapacity and full reliance on a respirator all night and a major part of the day as well. The shadings used are black “at recovery”, grey at mid term or “best” and ladders representing the situation “now”. To establish the degree of change for example from “best” to “now” look at the change from the number of yellow to red cases at each level (1 to 6). The bias toward blue, or “at recover” cases at the lower end of the 1 to 6 scale is obvious when

compared to the red “now” cases.

Fig 12. Chart plotting severity where 1 is best and 6 is most severe.

The actual numbers portrayed in this chart are shown in Fig 13. It could be said that the table should only contain those who reported a deteriorating condition leaving out the 23% reporting a stable situation. It was felt that this way the pattern across all respondents demonstrates the gravity of the situation more graphically.

	No	%	No	%	No	%	No	%	No	%	No %
SEVERITY	ONE		TWO		THREE		FOUR		FIVE		SIX
AT RECOVERY	50					4% 343 29% 432 37% 236 20%			85	7% 21 2%
AT BEST	226					19% 501 43% 297 25% 107		9%	30	3%		6 1%
NOW	28					2% 158 14% 396 34% 382 33% 180 15% 23 2%

Fig 13. Number and % of cases shown in Fig 12

Relationship of age at onset to probability of subsequent deterioration.

Fig 14 was compiled in order to determine whether there is any correlation between the age of respondents at the onset of the acute phase and the probability of loss of muscle power, or any of the other unspecified symptoms of general deterioration. This is a detailed analysis of the cases of onset during the year 1950 using the three most common unspecific reports of signs of a condition existing which would point to the fact that deterioration was taking place, plus the unsolicited mention of unspecified pain.

		A		B		C		D
D o B	CASES No		%	No	%	No	%	No	%
UP TO 1925	11	8	73%		8 73%		9 82%		3 27%
1926 – 1935	13	11	85%		4 31%		9 69%		5 38%
1936 – 1945	24	20	83%		18 75%		16 67%		6 25%
1946 -1950	28	21	75%		18 64%		14 50%		7 25%
ALL 1950	76	60	79%		48 63%		48 63%		21 28%

ALL SURVEY

1167

895

77% 774 66% 671 57% 313 27%

Fig 14. Analysis of onset during 1950. Where: A – Deterioration. B – Reduced Stamina. C – General Weakness. D – General Pain.

The remarkably consistent pattern of the results in Fig 14 indicates that there is no relationship between age at onset and the likelihood of deterioration occurring in later life. Given the span of age at onset, with 11 over the age of 27 years, 5 between 20 and 24 years, and the rest falling between year of birth and 19 years, within the group studied, 1950 is considered to be a representative year as well as being the most prolific for polio among those who contributed to the survey.

If any further confirmation were needed, 1950 compares well with the statistics for the whole study, with a maximum deviation of 6% in the number of reports of General Weakness, which also happens to be the response with the greatest variation in the analysis of the 1950 figures.

SUMMARY OF FINDINGS

The summary of findings are taken largely from the set of quotations detailed under that heading. However they are also substantiated within the statistical analysis. There are eleven important messages contained in the summary, as explained in the introduction to the quotations, these are considered to be the most important outcomes from the study.

Overwhelming fatigue is the most common and often the most debilitating condition. (See page 12, Fig 8 and Quotations 8/9)
There is a statistically high probability that some deterioration, over and above normal ageing, will occur to those who had polio earlier in life. (See page 11, Fig 7 and Q. 19)
There is evidence of deterioration in the breathing muscles controlled by involuntary action. (See page, 12 Fig 9 and text para. 2, page 13 and Q. 25)
The demographic increase in age of the population will result in more polio survivors becoming increasingly disabled as they live longer, this will have an impact on the usage of and dependence on equipment provided by Health and Social Services. (See Q. 2/5/10)
There is evidence of further lasting damage to already weakened muscles if they are subjected to enforced rest or immobilisation. (See Q. 11/23)
There is evidence to suggest damage will result to upper arms and shoulders through prolonged use of crutches. (See page 12, Fig 9, and Q. 8/14)
There are many cases of a dismissive attitude being adopted by medical professionals toward the symptoms experienced by “old polio’s” (See text foot of page 12 and Q. 15)
There is a general lack of awareness within the medical profession of the implications of living with the after effects of polio. (See Q. 1/15/21/24)
There is some support for the theory that hard exercising can do lasting damage to muscles already weakened by the effects of polio. (See Q. 4)
There is evidence of excessive recovery times after relatively mild illnesses. (See Q. 12/16) 11. Many respondents find if they pace themselves between tasks they can achieve more. (See Q. 6/14) 12. The pattern of referrals must call for some comment. A high incidence of attendance’s at

Orthopeadic Hospitals, 321, is not supported by a corresponding number of operations, 178. There is also suspicion over the number of those attending rehabilitation centres and special units. Most probably brought about by terminology rather than a definable pattern. (See page 7)

Conclusion

The summary of findings offers twelve significant points for possible further study. The mere fact that there are so many indicates that this is not a straight forward case of a consistent pattern of events that will occur at a predictable period after the initial onset.

There is no one conclusion to be drawn from the data revealed in this study, but if an overall prediction had to be made it would be that the message repeated throughout the survey is that deterioration, without doubt, can take place in later life. The pattern of the probability of the effect on individuals varies slightly, but there is a consistency which would attribute the chances of some deterioration becoming apparent at around 80%.

However the cause of the probable deterioration can still be called into question. That deterioration to muscular and skeletal strength does take place as a result of normal ageing cannot be questioned. To what extent that ageing process is accelerated within a body already damaged by polio earlier in life certainly has not been pinpointed in the findings.

A further complication encountered when analysing the data is the impact that other possible causes of deterioration will have on the same, already weakened body. Such symptoms as slight neuropathy brought about by diabetes could well be overlooked by the normal body, but have a quite devastating effect on an ex polio.

Is there any linkage between the incidence of arthritis and earlier polio. How does the 16% of cases reported compare with the national average at the same average age? The average age of those reporting the condition was 63.5 years, at an average of 55.3 years from onset. These figures are conveniently 3 years higher than those of all respondents.

Osteoporosis is commonly associated with loss of muscle power in the immediate area. At only 47, or 4% this seems remarkably low. Is this because of a general lack of awareness of the condition or does it imply that this is not a problem condition.

There is much food for thought for all who had polio some time ago.

PETER FIELD

The Lincolnshire Post-Polio Network

Registered Charity No. 1064177

An Information Service for Polio Survivors and Medical Professionals

All enquiries, book requests, medical article requests, membership fees, items for newsletters and donations to

The Secretary, Lincolnshire Post-Polio Network

PO Box 954, Lincoln, Lincolnshire, LN5 5ER United Kingdom

Telephone: +44 (0)1522 888601

Facsimile: +44 (0)870 1600840

Email: info@lincolnshirepostpolio.org.uk

Web Site: www.lincolnshirepostpolio.org.uk

Document preparation: Chris Salter, Original Think-tank, Cornwall, United Kingdom.

Document Reference: <URL:http://www.zynet.co.uk/ott/polio/lincolnshire/library/uk/survey.html> Created: January 1997

Last modification: 31st January 2010.

A Report in to the Consequences of Living With Polio for 63,500 Years Read More »

Findings in Post-Polio

Findings in Post-Poliomyelitis Syndrome

Weakness of Muscles of the Calf as a Source of Late Pain and Fatigue

of Muscles of the Thigh after Poliomyelitis*

BY JACQUELIN PERRY, M.D.**, JAMES D. FONTAINE, M.D.***

AND SARA MULROY, PH.D., P.T.*, DOWNEY, CALIFORNIA

Investigation performed at the Pathokinesiology Service, Rancho Los Amigos Medical Center, Downey

Lincolnshire Post-Polio Library copy by kind permission of Dr. Perry

ABSTRACT: The purpose of this study was to identify overuse of muscles and other alterations in the mechanics of gait in twenty-one patients who had muscular dysfunction as a late consequence of poliomyelitis. All of the patients had good or normal strength (grade 4 or 5) of the vastus lateralis and zero to fair strength (grade 0 to 3) of the calf, as determined by manual testing.

Dynamic electromyography was used, while the patients were walking, to quantify the intensity and duration of contraction of the inferior part of the gluteus maximus, the long head of the biceps femoris. the vastus lateralis, and the soleus muscles. Patterns of contact of the foot with the floor, temporal-spatial parameters, and motion of the knee and ankle were recorded.

The principal mechanisms of substitution for a weak calf muscle fell into three groups: overuse of the quadriceps (twelve patients) or a hip extensor (the inferior part of the gluteus maximus in eight patients and the long head of the biceps femoris in four), or both; equinus contracture (twelve patients); and avoidance of loading-response flexion of the knee (five patients). Most patients used more than one method of substitution.

These obervations support the theory that postpoliomyelitis syndrome results from long-term substitutions for muscular weakness that place increased demands on joints, ligaments, and muscles and that treatment — based on the early identification of overuse of muscles and ligamentous strain — should aim at modification of lifestyle and include use of a brace.

After thirty years or more of good function after recovery from acute poliomyelitis, survivors now are experiencing new weakness, fatigue, and pain[11,12,21]. At the end of an active day, the muscles of the thigh often ache and may cramp at night. Anatomical [14], clinical[1,4], and electromyographic investigations[23,24] have implicated overuse as the source of post-poliomyelitis symptoms.

It is well known that the quadriceps stabilizes the knee as the limb is loaded: less recognized is the action

of the muscles of the calf particularly the soleus in providing indirect stability of the knee as body weight advances over a restrained tibia[20]. This action allows the quadriceps to relax. When the calf muscles lack the strength to provide tibial stability, the quadriceps must continue to support the knee actively and overuse can occur.

We found that susceptibility to overuse may not be obvious in a patient in whom manual tests show grade 4 or 5 muscle strength and who seems to move normally; there may be no conspicuous indication of any weakness of the calf muscles because of subtle substitution and a mild contracture. We therefore performed a dynamic electromyographic study of gait in patients who had post-poliomyelitis syndrome, weak calf muscles, and good quadriceps strength.

Materials and Methods

Patients who attended the Polio Clinic of Rancho Los Amigos Medical Center were referred to the Pathokinesiology Laboratory for instrumented gait analysis when dynamic electromyography was indicated to clarify the pattern of muscular activity during walking, for the planning of treatment or substantiation of a disability claim. Patients were included in this study if the strength on manual muscle testing of the vastus lateralis was good (grade 4) or normal (grade 5) and that of the soleus was zero to fair (grades 0 to 3). The study group comprised twenty-one patients (eleven women and ten men). The mean age (and one standard deviation) was 50 ± 11 years, and the mean interval after the onset of the acute poliomyelitis was 39 ± 8 years. All of the patients had symptoms characteristic of post-poliomyelitis syndrome — that is, pain, fatigue, and increasing weakness in the muscles of the calf or thigh.

Four weight-bearing muscles were studied: two hip extensors (the gluteus maximus and the long head of the biceps femoris), one component of the quadriceps (the vastus lateralis), and the major plantar flexor of the ankle (the soleus). Muscle strength was measured with both manual testing and a static dynamometer (Cybex II; Lumex, Bay Shore, New York). Activity of the muscles was recorded with intramuscular dynamic electromyography while the patients walked at their customary (free) speed. A pair of fine-wire electrodes (fifty micrometers in diameter with a two-millimeter bared tip) was inserted, with a single needle used as a cannula, into the belly of each designated muscle. The accuracy of the placement of the electrodes was confirmed with light electrical stimulation.

The bandwidth of the electromyographic recording was 150 to 1000 hertz. The electromyogram of each muscle was sampled 2500 times per second, rectified full-wave, and integrated for each 1 per cent of the gait cycle. The electromyographic values during gait were normalized to the levels of the electromyogram that had been recorded during manual testing, The total effort of the individual muscles was calculated as the product of intensity and duration. These values were compared with similar data from normal controls who were twenty to twenty-five years old. The soleus was tested in fourteen normal controls; the vastus lateralis, in twenty-eight; the biceps fcmoris, in twenty-eight; and the inferior part of the gluteus maximus, in twenty-five. Overuse or underuse of the muscle was designated if the activity differed from the normal mean by more than two standard deviations.

Motion of the knee and ankle joints was determined with the use of single-axis goniometers. The parallelogram construction and slight rotatory-axis mobility of the goniometers accommodated for minor deviations in the alignment of the joint center. The stride characteristics were recorded by a Footswitch Stride Analyzer (B and L Engineering, Santa Fe Springs, California). All data regarding gait were collected as the patients walked along a vinyl-tiled, ten-meter-long walkway. Photoelectric cells defined the middle six meters as the segment for the collection of data.

Results

Manual testing confirmed that all of the patients who had post-poliomyelitis syndrome had grade-4 or 5 strength of the vastus lateralis (Table I). Quantified torque-testing showed that grade 5 indicated 59 ± 19.8 per cent (mean and standard deviation) (range, 41 to 77 per cent) of normal strength and grade 4 indicated 41 ± 20.2 per cent (range, 17 to 67 per cent) of normal strength. Hence, all of the patients had substantial weakness of the vastus literalis.

TABLE I Muscle Strength*
Muscle	Grade on Manual Muscle-Testing[15,16]**	No. of Patients	Percentage of Normal Torque***
Vastus lateralis
	5	2	59 ± 19.8
	4	19	41 ± 20.2
	3	0
	2	0
	0	0
Soleus
	5	0
	4	0
	3	8	25 ± 13.3
	2	10	17 ± 12.6
	0	1	7
Inferior part of the gluteus maximus
	5	1	78
	4	9	55 ± 13.3
	3	10	32 ± 10.6
	2	0
	0	0
Long head of the biceps femoris
	5	1	78

	4	11	42 ± 21.6
	3	5	41 ± 15.6
	2	1	26
	0	0
The strength of the vastus lateralis was tested in twenty-one patients; that of the soleus, in nineteen; that of the inferior part of the gluteus maximus, in twenty; and that of the long head of the biceps femoris, in eighteen. Grade 5 indicates normal muscle strength; grade 4, good muscle strength; grade 3, fair muscle strength; grade 2, poor muscle strength; and grade 0, no muscle strength. **The values are given as the mean and the standard deviation.

The findings for the hip extensors were similar. The strength of the inferior part of the gluteus maximus was tested in twenty patients, and the strength of the long head of the biceps femoris was tested in eighteen. On manual muscle-testing, the mean grade for both the inferior part of the gluteus maximus and the long head of the biceps femoris was 4, although individual strengths ranged from grade 2 to grade 5 (Table I). The mean strength of the hip extensors was 44 ± 20 per cent (range, 17 to 84 per cent) of normal. Quantified torque was not recorded when the muscle could not produce an active contraction or electromyographic activity could not be elicited.

Of the nineteen patients for whom it was tested, eight had grade-3 strength of the soleus muscle; ten grade-2; and one, grade-0 (Table I). The mean quantified strength of the grade-3 muscles was 25 ± 13.3 per cent (range, 17 to 51 per cent) of normal, and that of the grade-2 muscles was 17 ± 12.6 per cent (range, 4 to 37 per cent).

Overuse during walking (a total effort of more than two standard deviations more than normal) was found in all four muscle groups. Overuse was most common in the quadriceps, but it also was frequent in the inferior part of the gluteus maximus (Tables II and III). Overuse was less common in the long head of the biceps femoris and was infrequent among the weak soleus muscles.

TABLE II Electromyographic Pattern of Muscle Use
	Total Effort
Muscle	Normal Controls*	Muscles Showing Overuse*	Percentage of Normal**
Vastus lateralis	414 ± 218	2148 ± 1370 (n=12)	519
Soleus	1719 ± 594	4707 ± 594 (n=3)	274
Inferior part of the gluteus maximus	242 ± 140	1316 ± 705 (n=8)	544
Long head of the biceps femoris	399 ± 357	1692 ± 370	424

(n=4)

*The total effort was the intensity (the percentage of the manual-muscle-test level) multiplied by the duration (the percentage of the gait cycle). The values are given as the mean and the standard deviation. **For the muscles showing overuse.

The quadriceps displayed three patterns of effort: overuse, normal, and underuse. Overuse was identified in twelve of the twenty-one patients (Table III). Both the intensity and the duration of activity exceeded the normal mean by more than two standard deviations. A flexion contracture of the knee was found in five patients, four of whom displayed overuse of the quadriceps.

Normal function of the quadriceps was seen in seven patients (Table III). Four of these seven showed overuse of the inferior part of the gluteus maximus or the biceps femoris, or both. In the six patients in whom the soleus was also tested, two demonstrated overuse of that muscle.

Underuse of the quadriceps was seen in two patients (Table III), and overuse of the inferior part of the gluteus maximus (which we assumed was compensatory) was found in one of them. A related gait pattern was loading-response extension of the knee r eplacing normal flexion. This was exhibited by five patients; all had evidence of underuse of the quadriceps but the activity of the muscle differed from the normal mean by more than two standard deviations in only two.

Ten of the twenty-one patients had overuse of the hip extensors. Eight of the twenty gluteus maximus muscles tested showed overuse as prolonged duration, and four of the seventeen biceps femoris muscles tested showed overuse as increased intensity and duration. (Both extensors were not tested in every patient.)

The effort of the soleus was within two standard deviations of the normal mean in twelve of the nineteen patients in whom it was tested. Three patients had overuse and four had underuse. Related to this pattern of function was the relatively frequent occurrence of an equinus contracture, which was present in twelve

of the twenty-one patients in the study. Only one of these twelve exhibited overuse of the soleus, seven had normal function, two had und eruse, and the soleus was not tested in two because of the absence of function. The maximum passive dorsiflexion of the ankle in eleven of these twelve patients ranged from 0 to -15 degrees. The remaining patient had a severe contracture with maximum passive dorsiflexion to -35 degrees; the ankle remained in -35 degrees of dorsiflexion. Most of the contractures stretched at least partially from the effect of body weight during walking; nine of the twelve patients had substantial dorsiflexion of the ankle (mean, 7 degrees) in terminal stance. Two patients maintained slight equinus (-3 degrees of dorsiflexion) in terminal stance. For the nine patients who did not have an equinus contracture, maximum passive dorsifexion of the ankle ranged from 5 to 10 degrees, and dorsiflexion of the ankle in terminal stance averaged 12 degrees. A linear correlation (r=0.47, p < 0.03) was found between the intensity of maximum activity of the quadriceps, as recorded electromyographically, and the magnitude of dorsiflexion of the ankle in terminal stance (-15 to 10 degrees). The patient who had a severe equinus contracture (35 degrees) was excluded from the correlation.

TABLE III

Electromyographic Patterns of Muscle Use*

Case	Vastus Lateralis	Soleus	Inferior Part of the Gluteus Maximus	Long Head of the Biceps Femoris
1	Overuse	Normal	Overuse	Normal
2	Overuse	Normal	Overuse	Normal
3	Overuse	Normal	Overuse	Normal
4	Overuse	Normal	Overuse	Normal
5	Overuse	Normal	Overuse	Overuse
6	Overuse	Overuse	Underuse	Normal
7	Overuse	Not Tested	Normal	Not Tested
8	Overuse	Normal	Not Tested	No rm al
9	Overuse	Normal	Normal	Normal
10	Overuse	Normal	Underuse	Normal
11	Overuse	Underuse	Normal	Underuse
12	Overuse	Underuse	Normal	Not Tested
13	Normal	Normal	Overuse	Normal
14	Normal	Normal	Normal	Overuse
15	Normal	Underuse	Normal	Overuse
16	Normal	Overuse	Overuse	Overuse
17	Normal	Overuse	Normal	Normal
18	Normal	Not Tested	Normal	Normal
19	Normal	Underuse	Normal	Normal
20	Underuse	Normal	Normal	Not Tested
21	Underuse	Normal	Overuse	Not Tested
*Overuse and underuse were considered to differ from the normal mean by more than two standard deviations.

Discussion

Weakness is the basic abnormality of the post-poliomyelitis syndrome. Bodian, in a study of acute poliomyelitis, found that the virus had invaded 95 per cent of the anterior horn cells within the nervous system and that, on the average, 47 per cent (range, 12 to 91 per cent) recovered. Other studies showed that additional function was regained through the adoption of denervated muscle fibers by axons that sprout[28,29] and by compensatory hypertrophy of partially denervated muscles[8-10]. By these mechanisms, most survivors of acute poliomyelitis regained the ability to walk in an apparently normal manner and to have an active lifestyle. The neuromuscular system being used, however, has a sub-normal number of motor units and enlarged muscle-fiber pools[27]. As a result, these patients had a limited tolerance for chronic strain. Now, more than thirty years after the acute disease, many survivors have symptoms of new weakness, fatigue, and pain[11,12,21].

It is a clinical challenge to identify the specific residual weakness in a patient who has a very efficient substitution system. When patients who have had poliomyelitis have normal motor control and normal proprioception, they can readily and subtly modify muscular activity to compensate for areas of dysfunction[19]. For example, they can compensate for weak calf muscles when walking.

Weakness of the muscles of the calf, and the limited ability of a so-called good quadriceps to compensate, are rarely appreciated in patients who have had poliomyelitis because the signs of impairment are subtle. Although Beasley demonstrated, more than thirty years ago, that an examiner using manual testing cannot sense the full strength of large muscles such as the quadriceps, grade 5 continues to be interpreted as representing normal function. Beasley found that strength rated grade 5 on the basis of manual testing in patients who had had poliomyelitis was equivalent to 53 per cent of the strength in normal controls. In the present study, grade-5 strength of the quadriceps muscle in patients who had had poliomyelitis was equivalent, on the average, to only 59 per cent of the strength in normal controls. Grade-4 strength also tends to be considered to be closer to normal than it is. Both the study by Beasley and the present study showed that the mean strength of the grade-4 muscles w as approximately 40 per cent of normal (in the present study, the quadriceps was 41 per cent of normal and the hip extensors, 44 per cent of normal). Muscles with grade-5, 4, or even 3+ strength allow a person to move normally; the greater intensity of effort is unrecognized. When clinical treatment is being planned, the strength of a quadriceps that was given a grade of 4 or 5 on manual testing should be quantified more precisely with a static dynamometer such as a Cybex II device.

An additional diagnostic complication is the difficulty involved in the determination of the strength of the plantar flexors of the ankle. Manual testing challenges only 20 per cent of normal strength[3,18]. The forefoot is not long enough to give the examiner sufficient leverage to simulate the demand that the weight of the body places on these muscles with each stride. Multiple heel-rises have been used as a basis for grading, but the standard number of heel-rises has ranged from one[3] to ten[13]. Recent research has revealed that the mean normal endurance is twenty[18].

Walking presents a rapid demand on the quadriceps to control a passively flexed knee during weight acceptance in stance. The prompt response of the four parts of the quadriccps generates a peak intensity (25 per cent of maximum effort as evidenced by manual muscle-testing) within the first 5 per cent of the gait cycle[20]. Once the forefoot contacts the ground and the mechanics of knee flexion have subsided, the activity of the quadriceps is reduced until it becomes silent by the 20 per cent point in the gait cycle. This is a non-fatiguing level of activity for normal muscles and thus can be repeated indefinitely[17]. A grade-5 quadriceps with strength that is 59 per cent of normal must create a peak inten sity of 42 per cent of the manual-muscle-test level to control the flexing knee. When the strength of the quadriceps is grade 4, the peak effort during the weight-acceptance period of each stride represents 60 per cent of the

capability of the muscle. The anaerobic stage of contraction has been entered[2], and endurance is substantially reduced. This disability is masked by the patient’s ability to move in a normal manner by increasing the intensity of effort to a point of overuse[22].

The muscles of the calf (the soleus and gastrocnemius) make a major contribution to the stability of the knee during the period of single-limb stance. As the weight of the body is drawn forward over the supporting foot by the momentum of the swinging limb, the soleus and gastrocnemius create a force of plantar flexion of the ankle to decelerate the rate of tibial advancement[20]. This provides passive stabi lity of the knee as soon as the body-weight line (vector) moves anterior to the knee (mid-stance). The knee progressively extends as the limb advances, but quadriceps action is not needed. The normal pattern of action of the muscles of the calf is one of high intensity and prolonged duration. Soleus action begins in the latter part of the loading response (the 5 per cent point in the gait cycle) and continues throughout

terminal stance for a total period of activity equaling 45 per cent of the gait cycle. The intensity of soleus action increases rapidly to 30 per cent of the manual-muscle-test level through mid-stance as the limb advances over the flat foot and then progressively increases after heel-rise to a peak intensity of 80 per cent of the manual-muscle-test level during terminal stance. The action of the gastrocnemius is similar.

Weakness of the muscles of the calf allows the tibia to fall anteriorly in an unconstrained manner, and the opportunity to stabilize the tibia passively is lost[25]. Flexion of the knee persists throughout stance[26], and continued quadriceps action is required to preserve weight-bearing stability[20]. This is the basis of the increased duration of activity that results in overuse of the quadriceps.

The signs of late weakness of the muscles of the calf in a person who has had poliomyelitis are subtle. An inability to accomplish twenty full-range heel-rises on one side is an indication of muscular weakness. Fewer heel-rises indicate an even greater loss of strength. When a patient is walking, persistent heel contact during the second half of the single-stance period (terminal stance) is a basic indication of weakness. The patient lacks the strength to support the weight of the body on the fore-foot before the other foot strikes the ground. Increased dorsiflexion of the ankle becomes visible. The length of the stride is shortened. Flexion of the knee in mid-stance and terminal stance occurs when weakness of the soleus is more marked. Avoidance of loading-response flexion of the knee and sustained contraction of the quadriceps is an alternate mechanism of substitution.

Figure 1. Photograph of an ankle-foot orthosis with a

hinged ankle joint, showing free plantar flexion.

Contractures can have an adverse or beneficial influence on gait. A flexion contracture of the knee prevents the knee from reaching the stable position of passive extension. As a result, persistent quadriceps activity is required throughout the weight-bearing phase of gait, and either an early heel-rise or greater dorsiflexion of the ankle is required. In contrast, an equinus contracture of the ankle can be a useful substitute for weak calf muscles. Tension of the fibrous-tissue elements within the soleus and gastrocnemius provides the tibial restraint needed for indirect stabilization of the knee. The demand on the quadriceps is proportionately reduced.

Overuse of the hip extensors represents a substitutive effort to reduce the demand on the quadriceps. The action of the hip extensors is increased to support the anterior lean of the trunk. This posture moves the body vector closer, or even anterior, to the center of the knee joint. The flexor moment at the knee is correspond ingly shortened, and less quadriceps force is required[5]. Each of the hip extcnsors has a direct effect at the knee as well. The gluteus maximus, through its insertion into the iliotibial band, can produce extension of the knee directly. When the knee is flexed less than 30 degrees, the tibial insertion of the band lies anterior to the axis of the knee joint and thus is an extensor. In contrast, the tendon of the biceps femoris, by inserting on the head of the fibula, is consistently aligned to induce flexion of the knee. As a result, the anterior posture of the trunk, being supported by the hamstring muscle group, also creates slight flexion of the knee. The differing effects at the knee most likely account for the more frequent overuse of the gluteus maximus.

The most expedient way to reduce symptoms in the thigh caused by overuse of the quadriceps and hamstring muscles is use of an ankle-foot orthosis that supplants the weak calf muscles[7] and also protects the quadriceps. As the orthosis has two critical functions, a simple solid shell is inappropriate. In normal gait, a small but essential arc of 10 degrees of plantar flexion of the ankle follows heel-strike. This loading-response reduces the tibial acceleration of the heel lever[20]. As a result, flexion of the knee lags behind the rate of foot-drop, and the potential demand on the quadriceps is reduced approximately 50 per cent. Freedom of plantar flexion of 15 or 20 degrees also allows a patient who has had poliomyelitis to attain flat-foot contact with the floor while the knee is fully extended. Thus, all demand for use of the

quadriceps can be avoided. During late mid-stance and terminal stance, tibial restraint must be provided by a dorsiflexion stop. Eleven of our twenty-one patients wore a hinged ankle-foot orthosis with a dorsiflexion stop. Nine of them reported subjective relief of symptoms, o ne was un sure if there had been any improvement, and one was lost to follow-up.

The appropriate orthosis for a patient who has weakness of the muscles of the calf and quadriceps strength that is less than truly normal (even though it may appear normal on manual testing) must have three qualities; it must be articulated (hinged); it must allow free plantar ncxion of 15 or 20 degrees (Fig. 1); and it must have an adjustable dorsiflexion stop to restrain the tibia (Fig. 2). The mean setting to restrain excessive tibial advancement is 5 degrees of dorsiflexion; stronger patients, who are capable of longer strides, prefer 10 degrees of dorsiflexion. Rarely is 0 degrees of dorsiflexion or a plantar-flexed setting appropriate because these inhibit advancement of the weight of the body over the forefoot and induce a hyperextension thrust on the knee.

Figure 2. Photograph of an ankle-foot orthosis with a

dorsiflexion stop, showing limited dorsiflexion.

References

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No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. Funds were received in total or partial support of the research or clinical study presented in this article. The funding source was National Insitute of Disability and Rehabilitation Research Grant 133 AH60016.

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