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The Postpolio Syndrome

An Overuse Phenomenon


Clinical Orthopaedics and Related Research Volume 233:145-162; August 1988
© Copyright J. B. Lippincott Co

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

* Chief, Pathokinesiology Service, Rancho Los Amigos Medical Center, and Professor of Orthopedics, University of Southern California, Los Angeles, California.
** Research Physical Therapist, Pathokinesiology Service, Rancho Los Amigos Medical Center.
*** Assistant Chief (Clinical), Pathokinesiology Service, Rancho Los Amigos Medical Center.
Supported by National Institute of Disability Rehabilitation and Research (NIDRR) grant 133AH60016.
Reprint requests to Jacquelin Perry, M.D., Rancho Los Amigos Medical Center, 7601 E. Imperial Highway, Downey, CA 90242.
Received: December 29, 1987.

Persons with good recovery of function following their initial poliomyelitis are now, more than 30 years later, experiencing new weakness, fatigue, and muscle pain. The likelihood of muscle overuse being the cause of this late functional loss was investigated by dynamic electromyography (EMG) and foot-switch stride analysis in 34 symptomatic patients. Manual testing grouped the muscles, with strong (S) encompassing Grades Good (G) and Normal (N) while weak (W) included Fair plus (F+) to zero (0). After testing quadriceps and calf strength, the patients fell into one of four classes: strong quadriceps and calf (SQ/SC) strong quadriceps and weak calf (SQ/WC) weak quadriceps and strong calf (WQ/SC) or combined weak quadriceps and calf (WQ/WC). Quantified EMG; (normalized by the manual muscle test EMG) defined the mean duration and intensity of the quadriceps soleus, lower gluteus maximus, and long head of the biceps femoris during walking. Overuse was defined as values greater than the laboratory normal (mean·+ 1 SD). Each muscle exhibited instances of overuse, normalcy, and sparing. The biceps femoris was the only muscle with dominant overuse (82%). Quadriceps overuse was next in frequency (53%). Soleus activity infrequently exceeded normal function (34%), but this still represented more than twice the intensity and duration of the other muscles. Gluteus maximus action was also seldom excessive (34%). The patients averaged two muscles with excessive use during walking. Gait velocity of the SQ/SC strong group was highest (71% of normal) while the three categories that included weak muscles had walking speeds in the range of 50% of normal. The finding of muscle overuse during a single free-speed walking test that does not attain normal velocity supports the concept of muscle overuse being the cause of the patient's dysfunction.

Poliomyelitis has been considered a self-terminating disease. That is, after the initial acute infection subsided, no further progression occurred. Recovery from the resulting paralysis generally was good and most patients assumed fully active, normal lifestyles. Only a small percentage continued with orthoses and other walking aids.

Today, 30 years or more later, many postpolio survivors who experienced good recovery are experiencing major losses of function. Some are no longer able to work, while others are losing their self-care independence and community mobility. This seemingly new phenomenon actually was first reported by Charcot over 100 years ago.[37] Since then the occasional case has been published,[9,18] but the significance was lost in the dispersion of the information among a host of individual journals worldwide. Today, these functional changes are occurring in a significant population because of the high incidence of poliomyelitis during 1935-1955.

The current problem has evolved gradually over the past ten years to become a nationwide concern. Extrapolation of the 22% incidence of late postpolio effects among the patients in the Mayo Clinic polio registry indicates that 300,000 persons in the United States would be similarly impaired.[9]

Neither the cause nor the methods of management are known. The most common complaints of the individuals are orthopedic in nature. These include muscle weakness, increasing fatigue, and pain that may be either muscular or articular. Supporting signs, however, are inconspicuous. There are no pathognomonic indicators of prior polio. Sensation is intact, motor control is precise, and reflexes are not exaggerated. Significant deformity is an infrequent finding. Atrophy, an expected sign of flaccid paralysis, is not apparent in most patients, although circumferential measurements may reveal some asymmetry. The reason for this lack of atrophy in the presence of muscle paresis has recently been identified. Muscle bulk has been preserved through the addition of sarcomeres (contracting units) to the ends of muscle fibers that are repeatedly exposed to vigorous eccentric demand. The combination of the above characteristics with a history of polio, a typical therapeutic program, and the random nature of the patient's muscle weakness support the diagnosis of the postpolio syndrome.

Several causes have been proposed. Reactivation of the virus was one suggestion but Bodian's experimental polio in monkeys confirmed the destruction of the virus within a month of the acute invasion.[6] Amyotrophic lateral sclerosis (ALS) as a late sequela of poliomyelitis was another consideration that was later rejected by the failure of the patients to follow the expected course.[7,12] The most persistent idea has been failure of the axonal sprouts that formed during the healing process. This interpretation has been based on the electromyographic (EMG) signs of increased single motor unit jitter and reduced neural transmission that were found in some patients, but the findings were not universal.[10,13,17,36] A recent control study that compared the EMG findings in "old polios" with and without new loss of function showed similar changes.[38] Hence, the electrophysiologic signs represented prior denervation rather than a recent change. That is, the EMG findings indicated old motor unit lack rather than new axonal sprout failure.

Accumulated strain from chronic overuse may be a more likely cause for the late effects of poliomyelitis. Bennett and Knowlton termed this "overwork weakness."[4] The cause would be imbalance between the force capability of the postpolio muscle and the functional demands of a dynamic life-style. Several authors have correlated late loss of strength with aggressive activity.[4,23,24] A significant gain in weight has been identified as another cause of late onset weakness.[1] Chronic strain is implied by the patient's acceptance of low grade pain and periodic acute exacerbations as the price of having had polio.[11] They have always "pushed through it" to accomplish their vocational and home demands. Society, including physicians and therapists, has supported this approach. Today it is called "no pain no gain." The theory is that miracles can be accomplished if one tries hard enough. Today's postpolio problems indicate that we need to ask the question, "what is too hard?"

A perspective of the modern polio dilemma can be gained from a brief review of the experience at a Downey, California medical center, where a polio program began in 1949 when the increasing frequency of epidemics and improved medical care created a backlog of respiratory patients who needed a special program. In 1953 an aggressive orthopedic program was added that emphasized both intensive rehabilitation and appropriate reconstructive surgery.[28,30] With the introduction of the Salk vaccine in 1955 there was a rapid reduction in new cases throughout the United States. There was a similar precipitous drop in polio patients at the authors' medical center, and the rehabilitation-reconstructive surgical program redirected its skills to other disabilities. The respiratory program continued a maintenance service and occasionally a patient sought orthopedic assistance about bracing. Beginning in 1978 a few polio patients began appearing with complaints of decreased function, which subsequently have been identified as the late effects of poliomyelitis. The numbers have increased each year, now reaching an average of about 250 new cases annually. Among the areas of dysfunction noted, increased impairment of the lower extremities is most common.[29,38] This report focuses on increased lower extremity impairment.

To classify these new problems and develop a logical therapeutic approach, a combined clinical and laboratory research program was initiated. The purpose of the polio research program at the authors' center has been to determine if excessive effort did occur, why it was happening, and what levels of exertion would be inappropriate.


Patients included in this study were a sample of the larger clinical population who sought medical attention for their reduced function from increasing or newly acquired muscle pain, weakness, and/or fatigue. These people were referred to the pathokinesiology service for dynamic electromyography for the following reasons. The indication began as a search for a definition of the functional problem. Later patients were studied to define the level of activity that would be appropriate. A third group was tested for presurgical planning.

The patients' chief complaints, ages, polio histories, and vocational activity levels were determined at the time of the initial visit. Physical assessment included range of motion, manual testing of muscle strength, and cutaneous sensation. The patient's vocation was scored on a three-level activity scale: mild, moderate (average), and heavy. The Lovett system[24] of manual strength grading was used as it is the custom of the author's institution. This scale includes five levels above Zero (0): Normal (N), Good (G), Fair (F), Poor (P), and Trace (T). In addition, intermediary levels are designated with a plus (+) or minus (-).

There were 34 patients included in this study. All were diagnosed as having muscle dysfunction as a late consequence of poliomyelitis. A second criterion for selection was that their dynamic EMG test included the four stance-phase muscles considered significant to weight-bearing stability (vastus lateralis, soleus, lower gluteus maximus, long head of the biceps femoris).

By clinical description the patients were grouped according to their lower extremity dysfunction. Quadriceps and calf strength by manual muscle testing were the determining factors. Grades Good (G) and Normal (N) were classified as strong (S) quadriceps and calf. Strengths of Grades Fair Plus (F+) to Zero (0) were put into the weak category. The patients fell into four groups: combined strong quadriceps and calf muscles (SQ/SC), strong quadriceps and weak calf (SQ/WC), weak quadriceps and strong calf (WQ/SC), and weak quadriceps and calf (WQ/WC).

At the time of the study the patients' ages ranged between 24 and 73 years with a mean of 48.7 (±12 years). The average postpolio interval was 40.5 years (±12 years) and ranged between 19 and. 68 years. All the patients were independent ambulators and free of orthoses. Despite the wide variation in strength, the majority of the patients had a very normal appearance. Atrophy was not apparent except in the patients with extreme paralysis (primarily manual strength Grades T and P). Both contractures and joint hypermobility were uncommon and generally minor in this group of patients. All had intact sensation and lacked exaggerated reflexes.


Three techniques were used to measure the patients' functional capability. These included foot-switch stride analysis, dynamic electromyography, and electrogoniometry.

The foot-switch system includes a pair of 3-mm thick insoles containing compression-closing switches in the area of the heel, fifth and first metatarsal heads, and great toe. Switch sensitivity is 3 psi with a 2% gait cycle delay in switch closure. Each sensor is electronically coded so the pattern of foot support can be defined in addition to indicating the duration of foot contact. The insoles are of multiple sizes and designed to be inserted into the patient's shoes or taped to the sole of the bare foot. The signals from the individual sensors are transmitted by FM-FM telemetry to the Footswitch Stride Analyzer (B and L Engineering, Santa Fe Springs, California), which calculates and provides a printed record of the subjects' stride characteristics (velocity, stride length, cadence, single limb support, etc.). In addition the pattern of foot support was identified.

Dynamic electromyography recorded muscle action with a pair of fine wire electrodes (50-µm diameter with 2-mm bared tips). All data were transmitted by means of a differential input FM-FM telemetry system (common mode rejection of 58 db) to a seven-channel tape recorder for storage. The system band width was 250-2000 Hz with a gain of 1000.

An electrogoniometer was used to record knee joint motion on the instrumented limb. This single axis, sagittal plane, parallelogram type device compensates for misalignment due to joint center shifting. Rotations in the other planes are accommodated, but not measured. Recording error because of soft tissue displacement of the thigh under-reports knee motion by an average of 10%. A cable transmitted the electrogoniometry data to the recorder.


Following an explanation of the procedure and the signing of an informed consent, the instrumentation was applied to the patients. Utilizing Basmajian and Stecko's[2] single-needle technique, a pair of fine wire electrodes were inserted into the following four muscles: lower gluteus maximus, biceps femoris long head, vastus lateralis, and soleus. Often other muscles also were tested for additional information. Electrode placement was confirmed by mild electrical stimulation. Prior to the walking trials two baseline EMG recording series were made. A resting run with the patient lying quietly and the muscles relaxed documented the system noise level for each channel. The EMG also was recorded during a maximum manual strength test of each muscle. The standard testing techniques as described by Daniels and Worthingham[14] were followed.

For the walking test, foot switches were taped to the soles of the subject's bare feet. An electrogoniometer was aligned on the anterior surface of the thigh opposite the knee joint center and fastened with hook and loop straps as tightly as comfort allowed. Goniometric baselines were recorded with the knee in neutral alignment or maximum available extension. After all the instrumentation was applied the subjects were given an opportunity to walk about for familiarization.

The patients were positioned at one end of the walkway and asked to traverse the distance at their free (self-selected) speed. The middle 6 m of the 10-m walkway were demarcated as the data collection areas, with the ends being used for starting and stopping. Testing began with a preliminary practice walk. Then two free and two fast walks were recorded. EMG, goniometric, and foot-switch data were recorded simultaneously.

All the data were stored on seven-channel analog tape for subsequent computer analysis. In addition the data were immediately printed on light sensitive paper for visual analysis. The footswitch signals also were transmitted to the Footswitch Stride Analyzer for immediate analysis and print out. Channels failing to display gait data by muscles that exhibited activity on the manual tests were checked for electrode displacement. When this occasional complication occurred, new electrodes were inserted and the test repeated if time permitted.


Means and standard deviations for the stride data and knee joint motions were calculated for each of the four clinical groups. Velocity and single limb support were used to define the functional significance of the different patterns of muscle disability. Each stride parameter was calculated as a percent of age-matched normal values established in the pathokinesiology laboratory. The patient data were reported as a percent of normal (% N). Knee motion was analyzed for the peak flexion occurring in loading response, terminal stance, and swing.

The EMG data were digitized at 2500 samples per second on a DEC 11/34 computer and quantification was performed on a DEC VAX11/750 computer (Digital Equipment Corp., Maynard, Massachusetts). The EMG data were full wave rectified and integrated (summed for designated units of time). Baseline noise was removed where the level of activity was less than the threshold level determined from the resting run. The processed EMG from all walking tests was normalized to that obtained during the maximum effort manual test of the corresponding muscle and summed over 0.02-second intervals for subsequent processing. Results were reported as a percentage of the subject's maximum effort as determined by manual muscle testing (% MMT). Normalization excluded the variable of each electrode insertion representing an uncontrolled sample of motor units. This provided a common reference for pooling the data from multiple subjects.

To permit comparison of the EMG activity and motion achieved between subjects the gait cycle was normalized to 100%, and the stance and swing phases of the gait cycle were normalized to their average intervals. For these gait cycle normalizations initial contact and toe-off times obtained from the foot-switch record were used to define the changes from stance to swing and swing to stance. Separate files of stance and swing data were created for each muscle for all strides occurring within the 6-m data collection area. Each stance and swing table was then normalized to the average for the group before recombining into a single table for each muscle with data intervals representing each 2% of the gait cycle.

By computer analysis the number of intervals containing muscle function equal to or exceeding 5% of the muscle's manual test level were identified and the intensity of muscle action defined. Average intensity and total duration of muscle action were calculated. Because the biceps femoris has distinct functions in swing and stance these periods were differentiated. The brief terminal swing interval of the gluteus maximus and vastus lateralis were included in their stance time calculations. Stance only was identified for the soleus. Diagrams showing the combined intensity and duration qualities of each muscle for the four clinical categories were compiled. Normal data for these four muscles, developed in the pathokinesiology laboratory, were similarly diagrammed.

Statistical significance of the difference in gait velocity was calculated between the two major clinical groups, symptomatic but strong and those with obvious weakness (strengths less than F+). Analysis of variance (ANOVA) was used to determine the significance of the EMG values between groups with the location of the significant differences being identified by paired t tests. If there was a significant difference in variance (Levine test[39]) an appropriate data transformation was used for statistical analysis. To identify the incidence of excessive muscle action a manual count was made of the number of EMG values that were greater than the normal mean.


Age and gait velocity differentiated the four functional groups. The patients with "strong" quadriceps and calf muscles, as a group, were younger than the mean ages for the other three clinical categories. The differences represented a wider age span in more disabled groups, 24-74 years for the weak patients compared with 35-49 years for the stronger group (Table 1).

Gait velocity for the "symptomatic strong" patients (71% N) was significantly faster than that of the three groups with obvious weakness (53% N). Among the three groups with weak quadriceps and/or calf muscle (Fair or less), there was no significant difference in walking speed (Table 1). Single limb support time was approximately normal (90%-76% N) for all four clinical categories. Mean swing phase knee flexion also was in the normal range (64°-57°).

TABLE 1. Postpolio Syndrome Patient Demographics
Group Sex* Age**
Velocity %
SQ/SC 6 5 42 (5) 35 (5) 71 (13)
SQ/WC 3 7 53 (14) 39 (11) 54 (16)
WQ/SC 2 1 62 (11) 44 (35) 63 (12)
WQ/WC 8 2 53 (11) 43 (14) 50 (12)
TOTAL 19 15 53 (12) 40 (16) 60 (13)
* Sex data represent the number of men and women patients in each group.
** The data on age, postpolio interval, and velocity are means with the standard deviations in parentheses.

The EMG records showed the four muscles studied responded differently to the demands of walking. These data also demonstrated a pattern of overuse. Whether intensity, duration, or total effort was considered, the majority of the group means (75%, 81%, and 81%, respectively) for the different muscles were higher than the normal average. Few means were below normal (6%, 12%, 0%). There was, however, wide individual variability in the patients' intensity and duration of muscle action. For most of the categories the patients showed mixtures of reduced, average, and excessive use of each muscle. The dominance of one mode of muscle action over the other varied with the clinical category.

Normal. The quadriceps, biceps femoris, and gluteus maximus had comparable intensity and duration levels(Fig. 1). Vastus lateralis intensity of action averaged 13% of the manual muscle test grade (% MMT), and the mean duration was 23% of the gait cycle (% GC). Biceps femoris action averaged 12% MMT intensity and 21% GC duration. The duration of biceps femoris activity was greater in swing (12% GC) than stance (9% GC), with similar intensities. Lower gluteus maximus activity had an average intensity of 19% MMT, and the duration was 15% GC. Only the soleus muscle exhibited prolonged action, averaging 39% GC. Its mean intensity also was greater, 35% MMT (Fig. 1).

Fig 1 Graph
FIG 1. Normal intensity and duration of muscle action during walking. End of diagonal indicates the mean value. (% MMT, measure of intesity as a percent of the maximum muscle test EMG; % Gait Cycle, measure of duration as a percent of the gait cycle.)

Symptomatic Strong: Strong Quadriceps/Strong Calf (SQ/SC). Vocationally these were active people (level 2 on the three-level scale). All 11 were employed, and their major complaint was difficulty maintaining the needed level of activity because of muscle soreness and/or fatigue. Walking speed for this group averaged 71% (±13%) of normal (Table 1). During stance they had a normal loading response knee flexion (18°) and 7° flexion persisted in terminal stance.

On manual testing the strength of these patients' extensor muscles were between Grade Fair Plus (F+) and Normal (N) (Table 2). All the subjects were graded Good to Normal in their quadriceps, gastrosoleus, and biceps femoris muscles. The lower gluteus maximus registered F+ in three patients.

The EMG data demonstrated neither notable nor significant difference in the mean intensity and duration values for the four muscles studied (Table 3). Analysis of the incidence of excessive and sparing muscle activity revealed differing responses. Excessive use of the vastus lateralis and soleus occurred in one half of the patients (six of 11) (Table 4). This was an infrequent finding in the lower gluteus maximus (three of 11). There was almost a universal pattern of excessive biceps femoris action with increased intensity being the dominant finding (ten of 11 subjects). The mean intensity of 29% MMT was more than double the normal level, a difference of statistical significance (p < 0.02). Prolongation of biceps femoris action also occurred in half of the subjects (Fig. 2).

Fig 2 Graph
FIG 2. Strong quadriceps, strong calf (SQ/SC) patients' muscle action pattern during walking. End of the diagonal indicates the mean value. Both the soleus and biceps femoris displayed increased intensity of muscle action. (% MMT, intensity, % Gait Cycle, duration.

Strong Quadriceps/Weak Calf (SQ/WC). The ten people comprising this group were more varied in their vocational intensity Half of the group was Level 1 and the other half was Level 2. Their gait velocity was significantly limited, with a mean of 52% N (Table 1). During the stance phase knee flexion was increased. This was true for both the loading response (23°) and terminal stance(13°).

Manual strength grades for the quadriceps continued to be in the Good Minus (G-) to Normal (N) range (Table 2). Soleus strength, however, was between Fair (F) and Poor (P), with the latter value dominating. Gluteus maximus and biceps femoris strength also was reduced; only one person registered a normal grade.

In the majority of the patients the quadriceps (6/10) and biceps femoris (7/10) assumed the added burden imposed by walking with a weak calf (Table 4). Vastus lateralis intensity increased to 32% MMT and the duration of action was also lengthened (38% GC) (Table 3, Fig. 3). Biceps femoris activity was both excessively intense (25% MMT, p < 0.02) and prolonged (41% GC, p < 0.01). Stance phase activity exceeded that occurring in swing. Soleus intensity was greater than normal in only three patients, but their effort introduced a high mean value (48% MMT). The duration (41% GC) of the soleus action was either normal or curtailed in most instances. Action of the gluteus maximus was insignificantly prolonged (22% GC) while the intensity was normal(15% MMT).

Fig 3 Graph
FIG 3. Strong quadriceps, weak calf (SQ/WC) patients' muscle action pattern during walking. End of the diagonal indicates the mean value. Vastus lateralis and biceps femoris muscles displayed marked increase in duration and intensity of action. (% MMT, intensity; % Gait Cycle, duration.)

Weak Quadriceps/Strong Calf. The three patients in this group only reflect a trend. Their gait velocity was 63% N. Two of the group were in light-demand vocations and the third was not working. Two patients avoided loading response knee flexion and moved into slight hyperextension (10°) for limb stability. The other patient had knee flexion in both stance phases, with a 18° loading response and persistent 13° flexion through terminal stance.

Manual strength grades for the quadriceps were Zero (0), Trace (T), and Fair (F). All had a Grade Good (G) or Good Minus (G-) soleus, gluteus maximus, and biceps femoris (Table 2).

All four of the muscles tested registered an increase in both intensity and duration of action. Vastus lateralis intensity rose to 38% MMT and the duration extended to 30% GC, despite this being the weakest muscle (Table 3). The soleus was most active. Its intensity increased to 69% MMT and the duration of activity approximated normal timing (45% GC). Both hip extensor muscles exhibited excessive use. The gluteus maximus had a marked increase in both intensity (46% MMT) and duration (32% GC). Biceps femoris action showed increased intensity (30% MMT) and normal timing (24% GC) (Fig. 4).

Fig 4 Graph
FIG 4. Weak quadriceps, strong calf (WQ/SC) patients' muscle action pattern during walking. End of the diagonal indicates the mean value. All four muscles demonstrated increased intensity of their activity. (% MMT, intensity; % Gait Cycle, duration.)

Weak Quadriceps/Weak Calf. Among this group of nine patients only two had been forced to cease working because of their lost strength. Three were in light vocations (Level 1), and the others were at the moderate level (Level 2).

All of the patients with this pattern of muscle weakness had a significant reduction in their gait velocity. Their mean of 50.3% normal related to a range from 36.8% to 69.1% N. (Table 1) Stance phase knee posture was persistent flexion. The loading response averaged 15° and terminal stance remained at 10°. Only two used mild hyperextension (5°) for limb stability.

While strength of both target muscles was limited the vastus lateralis was stronger than the soleus in all but one instance. Strength of these muscles ranged between Fair Plus (F+) and Zero (0) (Table 2). Gluteus maximus strength among the individual patients was at least a one-half grade lower than that of the biceps femoris in all but the one person with equal values. Good Plus (G+) to Poor (P) was the range for the gluteus maximus. Biceps femoris strength ranged between Good Plus (G+) and Fair Minus (F-).

During walking the weak quadriceps displayed the greater increase in intensity (38% MMT), while duration was normal(25% GC) (Table 3). The incidence of excess and reduced vastus lateralis action was about equal (Table 4). Soleus action most commonly was reduced in intensity (21 of 34 patients) although the mean value approximated norma1(33% MMT). The duration of soleus muscle activity (49% GC) was divided equally between prolonged and curtailed. Gluteus maximus action was both increased in intensity (32% MMT) and duration (39% GC). Consistency of this effort (14 of 34 patients) resulted in statistical significance at the p < 0.01 level. The biceps femoris displayed a dominant pattern of excessive action in intensity (28 of 34 patients) that led to a mean value (23% MMT) that also carried statistical signiffcance (p < 0.01). Duration (32% GC) also was generally prolonged (27 of 34 patients) (Fig. 5).

Fig 5 Graph
FIG 5. Weak quadriceps, weak calf (WQ/WC) patients' muscle action pattern during walking. End of the diagonal indicates the mean value. Vastus lateralis intensity was increased. Biceps femoris action was markedly prolonged. (% MMT, intensity; % Gait Cycle, duration.)


The patients in each disability category displayed mixtures of reduced, average, and excessive muscle activity compared with normal. It thus was necessary to look beyond direct statistical calculation to identify the basis of the patients' symptoms of disability.

The few patients included in the weak quadriceps/strong calf group (WQ/SC) represent an exception to the usual clinical picture. Throughout stance their knee remained in flexion. Far more common to this pattern of muscle paresis is a significant degree of knee hyperextension. It was the patients' unusual limb posture that warranted a dynamic EMG investigation to define their impairment.

In considering the activity patterns of the four muscles, attention will be directed to the three larger patient groups. Eighty-five percent of the patients displayed excessive activity in at least two muscles. For the symptomatic strong, the extent of muscle overuse ranged from two to three muscles. The other groups ranged from one to four. The individual patterns of excessive activity were consistent with the contribution each muscle makes to the mechanics of walking.

Quadriceps action most commonly displayed a pattern of overuse (18 of 34 patients). Excessive activity was evident in each group with the incidences being similar (54%-60%). Increased intensity and prolonged duration were equally frequent, although both mechanisms were not combined commonly. As a result total effort was greater than normal in only 45% of the muscles recorded (Table 3).

Among the patients having at least Good (G) strength in both the quadriceps and calf (SQ/SC), mean vastus lateralis function did not exceed the normal value. Half of this patient group, however, showed excessive intensity and one third registered prolonged use. Hence, there were two modes of accommodation. Some patients transfer the demand to other muscles rather than imposing an excessive demand on their quadriceps. Associated weakness of the soleus led to a notable increase in intensity of quadriceps action, although the incidence remained 60%. Activity was about equally prolonged (18/34) and curtailed, resulting in a normal mean time. Combined weakness of the quadriceps and calf musculature reduced the opportunity for overuse. Mild knee hyperextension was substituted.

The role of the quadriceps is to stabilize the knee during limb loading at the onset of stance. This is a critical event that determines whether the person can walk. Floor contact with the limb ahead of the trunk and body weight in a free fall creates a significant flexion torque on the knee. Direct restraint of this flexion torque by quadriceps activity is essential unless the demand can be removed either by knee hyperextension or marked forward lean of the trunk. Alternate sources of knee stability exhibited by the patients in this study were increased intensity of soleus muscle action and both premature and prolonged action of the biceps femoris. Both of these muscles would facilitate using a trunk alignment to reduce quadriceps demand. The increased activity displayed by the other extensor muscles showed that this substitution was common.

Soleus activity deviated from its normal pattern only when this muscle had good strength and the quadriceps was weak; in this situation the intensity doubled. There are three reasons for this limited response to disability. First is the normally lengthy activity period for the soleus, averaging 39% of the gait cycle. The action starts during the loading response and continues into preswing. This leaves premature action in swing to contribute tibial control at the onset of stance as the only mechanism for improving knee stability. Continued activity in preswing would not be useful as weight has been transferred to the other limb. Second, the normal intensity of muscle action (35% MMT) leaves only a narrow margin below the 50% level where inefficient anerobic energizing would become dominant. Third, a useful contracture that limits passive dorsiflexion range to no more than zero was common (30% in the study patients). Tension on the intramuscular fibrous sheaths by body weight moving forward of the ankle would provide the desired tibial stability without additional soleus muscle action. Both groups of patients with a "strong" soleus had the better gait velocities (71% and 63% N). This strength would allow better use of the forefoot rocker in terminal stance and consequently a longer stride.

Lower gluteus maximus activity was increased in two disability groups. The muscle's mean intensity was greater than normal only when there was notable quadriceps weakness (WQ/SC and WQ/WC). Activity was prolonged only in the weakest group (WQ/WC). The hip extensor action of the lower gluteus maximus contributes to knee stability through two mechanisms. It allows the trunk to lean forward and, thereby, advance the body vector close to or beyond the center of the knee joint. This action reduces the flexion torque that normally occurs during limb loading at the onset of stance. The second effect of the hip extensor action of the gluteus maximus is indirect knee extension by a posterior pull on the femur once the trunk is forward.

The biceps femoris proved to be a ready supplement for quadriceps and calf muscle weakness. The intensity of biceps femoris activity was greater than normal in 85% of the patients. It occurred about equally in all four groups. For the patients with notable weakness of both the quadriceps and calf (WQ/WC) the increased biceps femoris activity approached statistical significance (p < 0.1). Among the patients with dominant calf weakness (SQ/WC), biceps femoris activity was prolonged significantly (p < 0.01). Increased intensity in swing would accentuate limb deceleration and lead to more complete knee extension at the time of initial floor contact. This also would minimize the flexion thrust during limb loading. Increased stance phase activity by the biceps femoris contributes additional hip extensor support. The greater response displayed by the biceps femoris suggests it is more versatile functionally than the gluteus maximus. As mentioned earlier strong hip extensor support allows a forward trunk lean to minimize the loading response flexion torque at the knee. Having the biceps femoris serve in this capacity, however, also introduces active knee flexion that threatens knee extensor stability. Excessive stance phase knee flexion was present in all but a few patients (7°-13°). Frequently there was a mild (10°) flexion contracture. Only the small group with the combination of weak quadriceps and strong calf tended toward slight hyperextension (10°).

Despite the excessive muscle action displayed by the four groups, mean free gait velocity was significantly less than normal (71%-50% N). A person's walking speed represents that which utilites the least energy.[22] Functional demand and muscular response are balanced optimally. Walking faster increases the muscular effort required to decelerate falling body weight during stance and advance the limb in swing. Subnormal slowness increases the duration of the muscular activity required to meet the same mechanical demands of limb control. One's self-selected (free) gait velocity is relatively constant, varying only 7% on repeat testing over three weeks.[35] Gait velocity has been found to relate inversely to disability, i.e., slowness represents physical impairment. The finding of greater than normal muscular effort in the presence of a reduced walking speed among the symptomatic postpolio patients implies that their particular pattern of muscular strength was inadequate to meet the normal demands of walking, even in the group with at least Good (G) quadriceps and calf musculature.

This assumption of muscular inadequacy immediately questions the definition of weakness. The patients in the group classified as "symptomatic strong" had muscle grades of Good (G) and Normal(N) by manual testing. Only the gluteus maximus had a few Fair Plus (F+) grades. Experience in a large rehabilitation center with many paralytic patients has revealed that both therapists and physicians interpret Grades N and G as being similar. Both grades take strong resistance on manual testing. The F+ grade often is included in this index of functional adequacy as it, too, accepts a notable amount of the examiner's force.

This apparent conflict in clinical interpretation of muscle strength grading and the patient's ability to function lies in the limitations of manual testing. Beasley's[3] dynamometer comparisons of polio patients' strength with an age-matched population of normal subjects showed the manual grades markedly overestimate paretic muscle strength. The clinical grade of Normal (N) for the quadriceps, hip extensors, and ankle plantar flexors was only 54%, 65%, and 81%, respectively, of the strength of nonpolio, normal subjects. It also should be noted that in this study a standing test was used for ankle plantar flexion (manual resistance can only approximate a Poor (P) grade).

Beasley's findings concerning the limitations of the N and G grades have been confirmed coincidently by two other studies. Functional assessment of postpatellectomy patients revealed their manually N quadriceps strength equaled only 60% of the torque registered by the sound limb during static testing on an isokinetic machine (Cybex Lumen, Ronkonkoma, NY).[21] Sharrad,[33] in his postmortem study of anterior horn cell (AHC) distribution found the clinicians had not identified any muscle weakness, i.e., Grade Good (G) until more than half of the AHC cells had been destroyed. These findings strongly imply that the convenient manual testing of muscle strength must be put in the proper perspective.

The overly generous functional interpretation of the manual muscle test grades exercised by most clinicians has complicated the postpolio patients' ability to generate medical acceptance of their complaints. Being unaware of this limitation in manual muscle testing, the patients' physicians have failed to find any significant weakness. As a result the general medical reaction, being reported by the patients, has been to attribute the weakness and fatigue either to inadequate exercise or psychological difficulties at work or home.

The problem of overuse also is poorly understood. It commonly is assumed that fatigue develops only after sustained, vigorous effort. Subclinical elements of fatigue, however, begin accumulating soon after the onset of activity. Endurance is determined by the ratio between intensity and duration of the muscular effort. Time tolerance exponentially declines as the effort exceeds 15% maximum strength.[16,27] This is true for both sustained and intermittent function. The latter, by allowing periods of uninterrupted circulation, delays the onset of fatigue.[5]

Recent application of nuclear magnetic resonance to the analysis of muscle function has identified the basis of mechanical fatigue.[15] Reduced force production (maximum voluntary contraction, or MVC) is related to a decrease in fuel. The critical fuel is phosphocreatine (PCr), which serves as the buffer source to maintain the supply of ATP essential for muscular contraction. Two factors proved significant in the development of fatigue: the rate of PCr depletion and its recovery time. Depletion rate was proportional to the intensity and persistence of the muscular effort and recovery occurred as two stages. Partial replenishment was immediate (two minutes) but full replacement was delayed. A four-minute maximal effort required one hour.[26]

Studies of exhaustive exercise also have demonstrated significant muscle pathology.[34] Edema, inflammatory cells, and enzyme changes were followed by muscle fiber degeneration. Later there was fiber regeneration. During sustained moderate effort (<50% V02max) the slow twitch fibers are depleted of glycogen before much impairment of the fast twitch fibers.[32] This pattern of fiber selectivity could be the basis for the poor endurance of patients who still register Good (G) and Normal (N) strength on manual testing.

Experimental overuse that mimics late poliomyelitis more closely was seen in a study that imposed intense gait demands on a partially denervated rat soleus muscle. Fiber damage and a corresponding loss of strength resulted.[19,20] The gait data of the polio patients in this study demonstrated a major increase in total muscle demand compared with normal function. Most patients registered overuse in at least two muscles. A similar picture of progressive functional decline following obligatory, cyclic, submaximal yet excess muscle use has been identified in patients with chronic respiratory pathology.[25]


The polio patients' display of excessive muscle action during walking combined with the physiologic evidence of fuel depletion and muscle tiber damage with overuse indicates the therapeutic approach should be reduction of relative muscular demand. There are four possible directions for patient management: muscle strengthening, shortening the duration of effort, substitute devices in the form of orthoses and walking aids, and reconstructive surgery.

Exercise has been the traditional means of overcoming fatigue. The underlying premise is that the muscles have an unused functional reserve. This is true for symptomatic postpolio patients only if they have reduced their activity below their full potential. Most of the patients seen in the authors' clinic already have tried the standard forms of exercise, including aerobic exercise, and found their symptoms increased. For patients who complain of fatigue or weakness but not muscle pain, a nonfatiguing program for muscle strengthening has been-tried at the authors' center. It consists of short duration and moderate intensity (60% maximum with five to ten repetitions). Documentation of the effect of a nonfatiguing, strengthening exercise program in 23 patients showed improved endurance and the recovery of some lost function in half of the group.[31] The others either experienced no gain or increased symptoms. Only half of the functionally improved patients registered a gain in strength on manual testing, and that improvement was less than a full grade. The conclusion was that few patients had an untapped reserve. A clinical trial with this type of a fatigue-avoiding strengthening program continues to be used in combination with a strong precaution to stop promptly if symptoms are increased. Muscle pain is a contraindication to any therapeutic exercise.[31]

Life-style modification to reduce the demand on symptomatic muscles has proved to be the most important therapeutic program. Even in the patient group profiting from exercise, 91% also required modification of their life-style. There are two basic rules. The first is to shorten the duration of effort, interspersing activity with frequent rest periods. The second is to avoid strenuous demands. For homemakers this involves having others do the heavy housework. Employed persons must find ways to modify the way in which they do their job or change their vocation.

Orthoses, walking aids, and wheelchairs offer a means of reducing muscular demand while preserving function. The most commonly needed orthosis is a dorsiflexion-stop ankle-foot orthosis (AFO) to supplement weak calf musculature. To avoid introducing additional strain on the quadriceps the orthosis also must have free plantar flexion.[8] Both of these characteristics are·essential. Consequently the orthosis requires a freely moving hinge. Persons with combined weakness and knee flexion contractures need a locked knee-ankle-foot orthosis (KAFO). Hip abductor and/or extensor muscle weakness require crutches. When there is insufficient shoulder or arm strength or these joints have become painful the patient must progress to a wheelchair. Electric carts are a useful intermediary means of travel that preserve both shoulders and lower limb muscles. Once one requires an electric wheelchair, a van and lift also are necessary for community travel; locomotion then becomes very expensive.

There are selected instances in which surgery is the most effective means of improving the patients walking ability. Correction of obstructive contractures is basic. Lengthening of the tendo Achillis, however, should only recover neutral dorsiflexion to preserve passive tibial stability. Release of paralytic knee flexion contractures that include intra-articular surgery is contraindicated as a severe loss of mobility will result. The weak muscles cannot provide sufficient action to preserve connective tissue flexibility. Occasionally, tendon transfers offer a means of gaining dynamic stability. To utilize the extensor action of the biceps femoris and avoid its knee flexion role, anterior transfer of the hamstring in the presence of quadriceps insufficiency is being used in selected instances. Transfer of strong perimalleolar muscles to the os calcis can reinforce an inadequate triceps surae.

The postpolio syndrome of newly acquired fatigue, weakness, and/or muscle pain 30 or more years after having had poliomyelitis represents true pathology. Manual grades of Fair Plus (F+) and Good (G), while accepting notable amounts of examiner force, actually represent significant loss of muscle strength. The manual grade of Normal (N) also is not indicative of sound musculature.

Gait analysis has confirmed the incidence of excessive muscle action even during the patients' free walking pattern. These data demonstrate one mode of functional loss, i.e., accumulated strain from chronic overuse by highly motivated persons. The primary therapeutic principle is to reduce the strain by life-style modification, orthoses and other assistive devices, and occasionally, surgery. Exercise has a limited role and should be kept to brief strengthening exercises that induce no pain or lasting fatigue.

TABLE 2. Muscle Strength Patterns
N G- F+ G-
G G F+ G-
N G G G-
G G F+ G
G+ N G- N
N N G- G
G+ G+ G N
N G+ G+ N
N P+ N N
G+ F- F F
G F F+ G-
G- P G F
G+ F- G G-
N P+ N N
T G- F+ G-
0 G F+ G
P T F+ G
F- P F+ F+
F+ 0 P+ F-
F+ F F F
F+ T G- G
F+ P G+ G+
0 F+ F+ G
P P- G- G
T P+ F+ G-
Data indicate the subjects' muscle strength grades by manual testing.
VL, (vastus lateralis); SOL, (soleus); LGMx, (lower gluteus maximus); BFLH, (biceps femoris, long head).
N, (Normal); G, (Good); F, (Fair); P, (Poor); T, (Trace); 0, (Zero).

TABLE 3. Muscle Strength Patterns
EMG (% MMT) NOR 13.2 (3.3) 35.0 (6.1) 18.5 (6.3) 11.7 (6.0)
SQ/SC 16.8 (12.0) 48.1 (8.8) 18.6 (10.8) 29.2 (19.8)
(p < 0.01)
SQ/WC 32.2 (28.1) 37.3 (16.2) 14.9 (10.0) 24.7 (12.3)
(p < 0.05)
WQ/SC 35.3 (41.6) 68.9 (7.6) 45.9 (38.2)
(p < 0.05)
30.0 (12.7)
WQ/WC 38.4 (40.3) 32.3 (11.6) 32.0 (25.6) 23.3 (17.7)
(p < 0.1)
DURATION (% GC) NOR 22.8 (4.6) 39.1 (6.1) 15.1 (5.2) 20.9 (10.4)
SQ/SC 19.8 (14.7) 36.7 (8.7) 20.2 (15.3) 25.5 (10.8)
SQ/WC 38.2 (19.0)
(p < 0.05)
41.3 (16.2) 22.0 (16.8) 41.1 (16.2)
(p < 0.05)
WQ/SC 29.0 (21.2) 44.7 (7.6) 16.3 (10.5) 23.7 (15.8)
WQ/WC 25.3 (21.3) 49.4 (11.6) 38.6 (19.4)
(p < 0.01)
31.8 (20.0)
(p < 0.01)
TOTAL EFFORT (Intensity x Duration) NOR 308 (133) 1357 (473) 293 (141) 255 (168)
SQ/SC 411 (328) 1860 (1102) 447 (398) 788 (528)
SQ/WC 1581 (1690)
(p < 0.05)
1669 (1174) 444 (572) 1032 (719)
WQ/SC 1464 (1954) 2937 (1605) 829 (681) 609 (272)
WQ/WC 1488 (1841) 1731 (1679) 1605 (1791) 787 (570)
(p < 0.01)
Data represent the EMG mean (and standard deviation) of each muscle in the clinical groups.
NOR, (normal); SQ/SC, (strong quadriceps, strong calf); SQ/WC, (strong quadriceps, weak calf); WQ/SC, (weak quadriceps, strong calf); WQ/WC, (weak quadriceps, weak calf).

TABLE 4. EMG Deviations from Normal Mean
  Relation to normal mean: VL SOL LGMx BFLH
Less than or equal to Greater than Less than or equal to Greater than Less than or equal to Greater than Less than or equal to Greater than
Intensity SQ/SC 5 6 5 6 8 3 1 10
SQ/WC 4 6 7 3 8 2 3 7
WQ/SC 2 1 1 2 1 2 0 3
WQ/WC 5 5 8 2 4 2 2 8
Total 16 18 21 13 21 13 6 28
Overuse   53%   38%   38%   82%
Duration SQ/SC 7 4 8 3 6 5 1 10
SQ/WC 2 8 5 5 4 6 1 9
WQ/SC 2 1 1 2 2 1 2 1
WQ/WC 5 5 3 7 2 8 3 7
Total 16 18 17 17 14 20 7 27
Overuse   53%   50%   59%   79%
Data represent the number of subjects in each category. Percentage values indicate the incidence of increased intensity or duration (overuse) by each muscle.


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