Many clinicians, even some who treat polio survivors, believe that individuals who had nonparalytic polio (NPP) cannot develop postpolio sequelae (PPS), which include fatigue, muscle weakness, joint and muscle pain, cold intolerance, and difficulty sleeping, swallowing, and breathing and which occur more than 30 yr after acute poliovirus infection.1 The common wisdom is that NPP is synonymous with "abortive polio," in which the poliovirus caused a flu-like illness but did not enter the central nervous system (CNS) and, therefore, neither damaged nor killed neurons.2 Autopsies, of course, were not performed on humans diagnosed with NPP to determine if there was damage to the CNS. However, there is significant circumstantial evidence that NPP was associated with CNS damage. For example, it was reported in 1953 that 39% of those diagnosed with NPP had measurable weakness on manual muscle testing in at least one muscle group.3 A 1954 study4 documented that 89% of polio survivors who were acutely "persuasively nonparalytic" had "very definite muscle weakness" as much as 3 yr after the diagnosis of NPP.
"Summer Grippe" and CNS Poliovirus Lesions
A less circumstantial case for the neuropathic nature of NPP came in 1947 from Cincinnati, Ohio. The previous year, 1946, had been America's worst polio epidemic to date, the death rate rising to the highest level of the century. However, from June to September of 1947, only 40 cases of polio were reported in Cincinnati, whereas there had been 167 cases during the previous summer. Coincidentally, for at least 4 wk during August and early September, pediatricians saw large numbers of children with an illness they called "summer sore throat" or "summer grippe."5 The onset of summer grippe was sudden, with fever, headache, sore throat, and muscle pain, the symptoms characteristic of abortive polio and of the first phase of a poliovirus infection of the CNS (Table 1).6 Children with summer grippe were between 1 and 10 yr of age, were not sick enough to be admitted to a hospital, and saw their physician once, if at all. The epidemic was large. Sabin and Steigman,5 at The Children's Hospital in Cincinnati, reported that there were at least "10,000 cases of this illness" and that "in some parts of the city hardly a child escaped."
Why was Sabin, a preeminent polio researcher, interested in the summer grippe? It was because some of the children had spinal or nuchal rigidity, the red flag symptoms that would lead to hospitalization and a presumptive diagnosis of "poliomyelitis." However, because summer grippe symptoms were not associated with paralysis and disappeared within a week, pediatricians were not interested in hospitalizing children; but Sabin was. He was aware that paralytic polio among American troops in the Philippines from 1944 to 1946 was accompanied by thousands of cases of "fever of unknown origin [with] pleocytosis."7 Sabin also knew of an unusually mild polio outbreak in Denmark in 1934, where although only 27 patients were paralyzed, 600 more reported having just a "slight fever."5 Sabin and Steigman5 also recalled the unusual increase in influenza in Copenhagen during August and September of 1934 that was said to be "probably due to infection with poliomyelitis virus" because the "flu" was associated with more than 100 diagnosed cases of polio. Because summer outbreaks of influenza are uncommon, Sabin wondered if a mild form of the poliovirus could have caused fever in the Philippines, the "flu" in Denmark, and the summer grippe in Cincinnati.8
From August 22 to September 9, Sabin and Steigman5 admitted to The Children's Hospital 13 children who had had a sudden onset of summer grippe symptoms. The children had fevers of approximately 103°F, almost all were listless and had headaches, and most had sore throats (Table 1).
The children had lumbar punctures and throat swabbings at the time of admission, and stool specimens were collected on 3 consecutive days. Eight children (ages 3-12; mean, 6 yr) were diagnosed as having summer grippe, three of whom had pleocytosis (40-150; mean, 98 leukocytes/mm3 of cerebrospinal fluid). One child had dysentery, another rhinitis, and a third atypical pneumonia. Two children, ages 4 and 6 yr, developed "definite nuchal-spinal rigidity for a brief period, which might have been missed if the children had remained at home," had pleocytosis (32 and 474 leukocytes/mm3, respectively), and were diagnosed as having nonparalytic polio. None of the patients was seriously ill, and they all left the hospital in approximately 9 days.
Sabin found antibodies to the type 2 (Lansing) poliovirus in five summer grippe patients, in the child with rhinitis, and in one child with NPP. However, antibodies could have been present because the children were exposed to poliovirus during the epidemic of 1946. Therefore, Sabin followed the accepted protocol for documenting that a type 2 poliovirus had indeed been present in the children: he inoculated 27 rhesus monkeys with the material collected from throat swabbings and stool specimens, observed the animals for weakness or paralysis, and killed them within 35 days.
Specimens from four summer grippe patients caused infections in 18 monkeys: one monkey died after developing peritonitis, one was paralyzed, and the rest appeared to be healthy. When the animals were killed, 50% had spinal cord and/or brain lesions typical of poliovirus infection. Specimens from three patients damaged spinal cord motor neurons, whereas specimens from four caused lesions characteristic of the poliovirus in the midbrain reticular formation, medulla, hypothalamus, thalamus, dorsal vagal motor nuclei, vestibular nuclei, the olives, and substantia nigra.10 Specimens from only one of the two children who were diagnosed with NPP caused paralysis in the inoculated monkeys and damaged neurons in the spinal cord and medulla (Papers from The Hauck Center for the Albert B. Sabin Archives, Cincinnati Medical Heritage Center, University of Cincinnati Medical Center). However, when Sabin and Steigman5 inoculated monkeys with specimens from seven additional patients from Cincinnati who were diagnosed with NPP during August 1947, only one monkey became paralyzed and the others had no evidence of CNS damage.
Sabin concluded from these findings that a low virulence type 2 poliovirus caused the flu-like symptoms of summer grippe. However, although Sabin's low virulence poliovirus did not cause even muscle weakness in humans, it caused lesions in the monkeys' CNS nearly twice as frequently as did the virus causing typical NPP in Cincinnati during that same summer. Furthermore, Sabin's low virulence poliovirus did something that even the most virulent paralytic poliovirus did not do: sicken at least 10,000 children. At its worst, the typical poliovirus in Cincinnati had sickened only 167 children.
Sabin vs. Bodian
Yet, not everyone agreed with Sabin that a low virulence type 2 poliovirus caused the summer grippe, not even David Bodian, editor of The American Journal of Hygiene, the journal in which Dr. Sabin's article was published. Bodian informed Sabin in a letter that the evidence supporting his conclusion was "very far from being satisfactory" and that the article would be "subject to serious criticisms." Bodian, a Johns Hopkins neuropathologist, had performed dozens of postmortem examinations on humans who had contracted polio and conducted scores of autopsies on monkeys intentionally infected with poliovirus. Bodian10 discovered that damage to specific neurons in the brain stem and anterior horn of the spinal cord-the same lesions that Sabin found as a result of inoculating monkeys with specimens from summer grippe patients-is the characteristic histopathologic signature of poliovirus infection of the CNS. Bodian10 also documented that 60% of motor neurons had to be killed by the poliovirus for any muscle weakness, let alone paralysis, to be clinically apparent: "The evidence from experimental work and from human material is overwhelmingly clear on this point. Neuronal and inflammatory lesions may be regularly found in any susceptible center, including the anterior horn of the spinal cord, in individuals who have never exhibited symptoms."
Bodian should have been the one scientist to readily accept Sabin's claim that a poliovirus could cause summer grippe symptoms and kill neurons, although not enough neurons to cause paralysis, weakness, or even nuchal-spinal rigidity. However, he did not accept it. Bodian wrote to Sabin that a "causal relationship" between the poliovirus and summer grippe had not been proven, saying, "it is equally plausible to assume that the [polio] virus was found in accidental relationship with the illness." Sabin wrote back that specimens collected "during the same period" from 24 additional patients with NPP did not cause CNS lesions in monkeys, which supported his claim that there was a different poliovirus that caused summer grippe and damaged neurons in monkeys more frequently than did the NPP poliovirus. However, Sabin could not actually prove a causal relationship between a low virulence poliovirus and the summer grippe, admitting to Bodian, "It is, in fact... a matter of probable guilt by association."
As Sabin became occupied with development of the oral polio vaccine, there is no evidence, from his publications or private papers, that he continued to argue "that in Cincinnati in 1947 there were in circulation at the same time strains of high and low virulence"5 poliovirus, the latter causing the summer grippe. However, Sabin's own research would eventually support this hypothesis. In 1949, Bodian discovered that not only the type 2 poliovirus, but also two additional distinct poliovirus immunotypes caused illness in humans.11 In 1952, Sabin12 tested specimens saved since 1947 from his paralytic polio patients (but, unfortunately, not from the summer grippe children) for the newly identified poliovirus immunotypes. Sabin discovered that all of the 1947 specimens from the paralytic polio patients were positive for type 1 (Brunhilde) poliovirus antibodies and, thus, documented that type 1 poliovirus, not type 2, was responsible for paralytic polio in Cincinnati in 1947. Still, it was not proven that a low virulence type 2 poliovirus caused the summer grippe. However, an observation with which Sabin began his article and that described the summer grippe would indicate a causal connection: when the epidemic of summer grippe was "at its peak by the end of August, there were not more than 40 reported cases of poliomyelitis."5 When the summer grippe was largely over by the middle of September, though, the number of polio cases increased, reaching a total of 170; 77% of polio cases in Cincinnati during 1947 occurred only when the summer grippe epidemic was over. It seemed that Sabin's putative low virulence, type 2 "summer grippe" poliovirus somehow prevented the children of Cincinnati from being infected with a high virulence, type 1 strain, which caused the additional 130 cases of typical polio, but only when the summer grippe virus was gone. Interference between different poliovirus immunotypes would ultimately support the hypothesis that low virulence type 2 poliovirus was the cause of the summer grippe in 1947.
Iceland Disease: Another Form of "Nonparalytic" Polio?
In September of 1948, three cases of paralytic polio were diagnosed in Akureyri, Iceland. Although not another case of polio was documented, more than 1100 additional Icelanders reported symptoms typical of paralytic polio infection (fever, neck pain, muscle weakness, and a few cases of paralysis) as well as symptoms not usually associated with polio (e.g., tingling and numbness).13 Specimens from four Icelanders were sent to Bodian's laboratory for testing, but poliovirus antibodies were not found. Yet, physicians in Iceland concluded that there were only two possible causes for what has come to be known as Iceland disease (ID): "Either a strain of [poliovirus] of low virulence was responsible for this epidemic," or "some unknown neurotropic virus has been present."13
Evidence supporting a low virulence poliovirus as the cause of ID did not come for 6 more years. In 1955, there was a large polio epidemic in Iceland caused by type 1 poliovirus and new outbreaks of ID.14 Remarkably, no cases of polio were reported in ID-affected towns, despite only 7% of the children having antibodies to type 1 poliovirus compared with 86% of the children in the polio epidemic areas. However, 100% of the children in towns with ID had antibodies to type 2 poliovirus. As Sabin thought occurred in Cincinnati, children in Iceland apparently had been exposed to a low virulence type 2 poliovirus that damaged the CNS and caused symptoms of Iceland disease but prevented infection by a high virulence type 1 poliovirus.
How could infection by one poliovirus strain prevent infection by another without protective antibodies? That answer came during the 1959 Singapore trial of Sabin's oral polio vaccine.15 Children were vaccinated with Sabin's three types of live, attenuated poliovirus. The type 2 poliovirus was always found to be dominant over the others, the only type that always entered the blood. It was concluded that the type 2 poliovirus actually interfered with other polioviruses (even the naturally occurring type 1 poliovirus that was causing the 1959 Singapore polio epidemic), stopping types 1 and 3 from entering the blood and thus preventing CNS infection even in those without poliovirus antibodies. Such interference of type 2 poliovirus with both types 1 and 3 has been documented repeatedly since 1959.16
Therefore, it seems that the reason children in Iceland in 1955 did not develop paralytic polio was because a low virulence type 2 poliovirus interfered with infection by a high virulence type 1 poliovirus, but at the price of contracting another neuropathic illness, Iceland disease. In 1947, a low virulence type 2 poliovirus apparently protected the children of Cincinnati from paralysis by preventing a high virulence type 1 poliovirus from entering the blood, but at the price of the summer grippe.
New Muscle Weakness and Nonparalytic Polio
Sabin's finding that there is a "mild" type 2 poliovirus that damages neurons in the spinal cord and brain without causing nuchal rigidity or paralysis and evidence that a type 2 poliovirus of low virulence was responsible for the ID outbreaks are important as we try to understand the pathophysiology of PPS today. As early as 1941, Bodian and Howe17 cautioned that "the clinical diagnosis of a nonparalytic case [of polio] may rest on the failure to detect minimal degrees of muscle weakness," predicting the 1953 finding that at least 39% of those diagnosed with NPP in fact had demonstrable muscle weakness3 Bodian showed that paralytic and nonparalytic polio are not separate entities but a single process whose pathophysiology and clinical manifestations lie on a continuum. He reported that the occurrence of paralysis and its severity increased as the percentage of motor neurons that were killed increased; rhesus monkeys could have apparently normal muscle function with only 40% of their anterior horn cells remaining (Fig. 1).18
In 1997, McComas et al.19 corroborated Bodian's findings, documenting that the "limbs not considered to have been involved" in paralytic polio survivors had lost, on average, 40% of their motor units. These findings contradict the common wisdom that the absence of paralysis is synonymous with the absence of CNS damage and the notion that NPP survivors' motor neurons could not be experiencing metabolic failure and death, to which late onset muscle weakness has been attributed.19
New Fatigue and Nonparalytic Polio
The principle focus of PPS research during the past 15 yr on new muscle weakness has ignored the most frequently reported and most disabling late onset symptom: fatigue.1 Certainly brain fatigue, with its associated cognitive symptoms, cannot be attributed to spinal motor neuron damage.20
Bodian made scores of postmortem comparisons between poliovirus-induced spinal cord and brain lesions. In animals without paralysis, he found that "lesions in the brain are more extensive and numerous than in some monkeys which did develop paralysis" and that some "animals with non-paralytic poliomyelitis do not have any lesions in the spinal cord but have a characteristic distribution of lesions in the brain."21, 22 (Notably, the brain lesions Bodian documented were in the same areas damaged in monkeys that were inoculated with specimens from Sabin's summer grippe patients.) Bodian and Howe17 stated that "although nonparalytic infection may be associated with severe neuronal damage in the spinal cord," the poliovirus "is capable of producing an encephalitis, with or without associated clinical symptoms, in the absence of any pathological change in the spinal cord" (italics Bodian and Howe's). Bodian18 also found that the "degree of involvement of brain centers" in humans who have paralytic polio is comparable with the brain lesions in animals with nonparalytic polio. Bodian22 concluded that "all available evidence shows conclusively that every case of poliomyelitis, human or experimental, exhibits lesions of the brain," and that, "As far as the pathologist is concerned, all cases of poliomyelitis are 'encephalitic'."
The finding that lesions in the reticular activating system can be the only damage resulting from poliovirus infection may explain the following: (1) why fatigue is reported more frequently than is muscle weakness in both paralytic and nonparalytic polio survivors; (2) the lack of correlation between the severity of late onset fatigue and the number of limbs paralyzed, hospital admission or length of hospital stay, and impaired breathing or use of respirator during the acute polio episode; (3) the neuropsychologic, neuroendocrine, neuroanatomic, and electroencephalographic abnormalities associated with postpolio fatigue; and (4) the occurrence of central sleep apnea and abnormalities of sleep architecture in polio survivors.1, 20, 23-28 With the occurrence of late onset fatigue, we are seeing today what Bodian10 predicted in 1949: that symptoms resulting from "lesions in the central gray of the mid-brain and hind-brain and in the mid-brain tegmentum and reticular formation" would be more often observed if they were not overshadowed by "paralysis of skeletal muscles."
Prevalence of Poliovirus-Induced Illness
Unfortunately, it is impossible to know how many Americans had CNS damage resulting from poliovirus infection that sets the stage for PPS. Although infectious disease texts state that there is a 1:10:50 ratio of paralytic polio, nonparalytic polio, and a minor illness with symptoms identical to the summer grippe, the data do not support this claim.2, 29 In Cincinnati during 1947, the ratio of paralytic to nonparalytic cases was 1:1.2, whereas the ratio of paralytic polio patients to summer grippe cases was at least 1:106.5, 7 Across the United States, the incidence of reported NPP cases varied widely depending on location and year, ranging from 0% to 80% of cases during the 1940s (mean ratio of paralytic to nonparalytic cases, 7:3) and 25% to 65% during the 1950s (mean ratio of paralytic to nonparalytic cases, 1:1) (R. Bruce, Centers for Disease Control, personal communication).4, 7 Several factors, listed below, caused the marked variability in reported cases of paralytic and nonparalytic polio.
Patients Did Not Present for Diagnosis. Failure to present for diagnosis may have resulted from symptoms being very mild or not being seen as indicative of poliovirus infection and from patients, especially those who were poor, not having access to or being financially unable to travel for medical care. A study of polio diagnoses in a San Francisco city hospital from 1950 to 1953 and the reported cases of polio in Cincinnati during 1947 show that 15% more paralytic and 121% more nonparalytic polio cases were diagnosed among patients living in the city vs. those living in outlying areas.4, 7 Urban patients were thought to be more likely to present for diagnosis, being nearer to hospitals, than were those living in areas where they had to travel for medical care. However, those with mild symptoms-as in the summer grippe, nonparalytic polio, or even mild paralytic polio, especially in infants and young children-may never have presented for diagnosis. The number of cases of both paralytic and nonparalytic polio presenting to rural hospitals would have been underestimates of the true incidence.
Paralytic Polio Was Underdiagnosed. Studies document the underdiagnosis of paralytic polio.3, 4 Shaw and Levin4 reported that "mild degrees of muscle weakness may be easily overlooked" if manual muscle testing were employed without a functional assessment of strength: "Many patients who are eager for activity, who can readily walk out of the hospital, and who are persuasively non-paralytic will thus be found to have very definite muscle weakness which cannot be detected while they are recumbent in bed." The failure to detect muscle weakness was also attributed to "too short a period of observation without opportunity for follow-up"; 18 mo to 6 yr after having been diagnosed with nonparalytic polio, 39% of patients were found to have weakness in at least one muscle group.3, 4
Polio Cases Were Not Reported. Although diagnosis may have been more accurate and reporting to public health authorities more likely at city hospitals, the number and severity of polio cases during the epidemics may have prevented overwhelmed physicians from reporting the occurrence of polio, especially NPP, to local public heath authorities. This occurred even at Sabin's hospital in Cincinnati (J. Englert, personal communication). Even if polio cases were reported locally, between 1915 and 1934 a varying number of states failed to report cases to the federal government, thereby preventing documentation of the true incidence of polio and even of the extent of large polio outbreaks, such as the 1916 epidemic.7 Furthermore, the Centers for Disease Control did not separately tabulate cases of nonparalytic and paralytic polio until 1951 and did not require the reporting of polio cases until the late 1950s (R. Bruce, Centers for Disease Control, personal communication).
These factors not only have caused inaccuracies in archival polio incidence and prevalence data, but also have impaired the ability of recent surveys to accurately estimate the actual number of living polio survivors. For example, the 1987 National Health Interview Survey30 relied on respondents to report whether they had had polio and, if so, whether it was paralytic or NPP. The National Health Interview Survey estimated that there are 641,416 living American paralytic polio survivors, 832,852 NPP survivors, and 159,919 who reported that they had had polio but did not know whether they had been paralyzed. This survey documented one paralytic case for every 1.3 nonparalytic cases, a ratio similar to that reported during the 1950s but much lower than the 7:3 ratio of paralytic to nonparalytic cases reported during the 1940s. The fact that 10% of the National Health Interview Survey respondents did not know whether they had been paralyzed makes clear that retrospective surveys, which rely on patient reports of early life symptoms and diagnoses, may not be able to accurately determine the prevalence of paralytic polio, much less the prevalence of NPP or a minor illness such as the summer grippe.
"Polio Suspects" and PPS
It may be possible to control for the sources of diagnostic and reporting error described above, to estimate the number of living Americans who did have a minor illness, and thereby to estimate the total number of polio survivors who had CNS damage and who, therefore, are at risk for PPS today. As early as 1935, the Mayo Clinic's centralized records-linkage system recorded not only cases of paralytic and nonparalytic polio, but also what were called "polio suspects," a term used by the physicians in polio epidemic years to describe persons with an acute fibrile illness suspiciously similar to polio but without paresis or evidence of central nervous system involvement from clinical history and/or cerebrospinal fluid examination. Many of these persons were family members and contacts of cases. Some may have had abortive polio and may constitute the 'tip of the iceberg,' because so many cases of polio never came to the attention of the physician."31
Although the population-based Mayo data are not representative of polio incidence in other regions of the country, especially in urban centers, they do significantly reduce, if not eliminate, errors resulting from improper diagnosis and underreporting. Between 1935 and 1955, for each paralytic polio patient, 0.65 polio suspects were recorded in the Mayo system. Applying this ratio to the National Health Interview Survey estimate of 641,416 paralytic polio survivors, there would be at least 416,920 living polio suspects who had had symptoms similar to those of the summer grippe. Because 38% of Sabin's summer grippe patients had pleocytosis, indicating CNS involvement, 158,430 Americans would be at risk for PPS, in addition to the estimated 1.63 million paralytic and nonparalytic polio survivors.
Nonparalytic Polio and Postpolio Syndrome
The diagnostic criteria for PPS reflect the principal clinical concerns of the 1950s and the 1980s: acute paralysis and new muscle weakness, respectively. Postpolio syndrome criteria require the "onset of new weakness" in an individual with a "prior episode of paralytic polio confirmed by history, physical exam," as well as electromyelographic changes "consistent with prior anterior horn cell disease."32 Unfortunately, these criteria do not take into account the studies described above, which make clear that nonparalytic polio and even a minor illness such as the summer grippe can be associated with the death of neurons in the spinal cord and brain, which set the stage for late onset symptoms.
Recent studies make clear that NPP survivors do have late onset symptoms. A population-based study of 828 polio survivors found that new muscle weakness and fatigue were reported, respectively, in 38% and 34% of those who had been paralyzed and in 14% and 21% of those who had had NPP.23 A study of 34 sets of twins found PPS symptoms in 71% of the twins who had had paralytic polio and "PPS-like symptoms" in 42% who had had no symptoms of paralysis.33 The presence of PPS-like symptoms, as well as muscle biopsies "showing long-standing signs of denervation" in some of the nonparalyzed twins, caused the authors to conclude that the acutely nonparalyzed twin "had also suffered subclinical nonparalytic polio [and that] symptoms of PPS might also be sequelae of nonparalytic polio."33 Indeed, 13% of the nonparalyzed twins had been acutely diagnosed as having "non-paralytic polio."34
Furthermore, the 1987 National Health Interview Survey30 found that 28% of NPP survivors reported new health problems related to polio. NPP polio survivors reported 46% more limitation in life activities than did the general population, whereas 45% more paralytic polio survivors reported limitations as compared with those who had had NPP (Table 2).
Electromyographic changes indicative of denervation may not be present in those who had summer grippe, NPP, or even transient paralysis acutely. Sabin and Ward35 stated that "transitory" and reversible paralysis may be seen because "not all nerve cells attacked by the poliomyelitis virus are irreversibly damaged." Bodian10 documented that motor neurons did recover function after poliovirus infection, even if all of the intracellular organelles, except for the nucleus, had been destroyed. Thus, an individual could have been acutely paralyzed without neuronal death or axonal degeneration, the poliovirus-infected neurons recovering and restoring muscle function without electromyelographic evidence of chronic denervation. Such a scenario would be more likely in those who had been weakened or mildly paralyzed acutely and especially in those who had NPP or summer grippe.
However, it is important to note that neurons that recovered from poliovirus infection were internally damaged, their cellular apparatus for oxidative metabolism, protein synthesis, neurotransmitter packaging, and axonal transport likely having been significantly impaired36, 37 Bodian38 suggested that such poliovirus-damaged neurons "may be vulnerable for life to metabolic factors such as changes of senescence"; this vulnerability and eventual metabolic failure are thought to be the likely causes of late onset muscle weakness and fatigue in polio survivors with or without acute evidence of paralysis or electromyographic evidence of denervation.19, 26, 39, 40
Therefore, "postpolio syndrome" should not be used as the generic descriptor for late onset problems in polio survivors, because its diagnostic criteria exclude those without a history of paralysis, electromyographic evidence of denervation, and new muscle weakness. The postpolio syndrome definition either should be modified to include other frequently reported and disabling symptoms, especially fatigue, or its name should be changed to "postpolio muscle weakness syndrome." In either case, the requirement of a history of paralytic polio and electromyelographic evidence of denervation should be removed.
Clinicians need to explain to their patients that NPP, and possibly even a poliovirus-induced minor illness such as the summer grippe, can be associated with CNS damage and late onset symptoms. Nonparalytic polio survivors with PPS symptoms should apply the conservative techniques found to be successful in managing paralytic polio survivors' PPS: reducing physical and emotional stress, using appropriate assistive devices, conserving energy, getting adequate rest, and pacing activities.41-45
I gratefully acknowledge the support of Ruth Bridgens for alerting me to the summer grippe, the suggestions of Greg Seaton, and the efforts, expertise, and good humor of Maggie Yax and Anna Truman of The Hauck Center for the Albert B. Sabin Archives, Cincinnati Medical Heritage Center, University of Cincinnati Medical Center.
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