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In patients with a history of acute paralytic poliomyelitis (APP), late progressive muscle weakness may arise, known as the progressive postpoliomyelitis muscular atrophy (PPMA). In 43 patients with PPMA, 8 were evaluated for recent or late progressive dysphagia. The mean interval between APP and onset of swallow symptoms was 27.1 years (range 23-45); the mean age of the patients was 45.4 years (range 35-52). Initial videofluorography showed signs of slight-to-moderate oropharyngeal dysfunction in 6 patients (delayed swallow reflex, diminished peristalsis of constrictor pharyngeus muscle, diminished laryngeal elevation, retention of bolus). In 2 patients, no abnormalities were found. Seven patients were reexamined after 12-36 months (mean 18). All reported subjective progression of symptoms. Videofluorography showed minor changes in 1 patient and unaltered findings in 6. No signs of aspiration were found either clinically or by video. We conclude that patients with PPMA complaining of late dysphagia do not show a significant loss in oropharyngeal function on 1-3 years follow-up.

The case of a 69 year old, male patient with slowly progressive dysphagia and an acute exacerbation is presented. He was referred to rule out an organic origin to his disorder. Apart from mild residual weakness of both legs after an acute paralytic poliomyelitis at the age of 20, the physical examination was essentially normal. No upper motor neuron pathology was found. Electromyography showed prevalent spontaneous and chronic denervation of bulbar and skeletal muscles. X-ray cinematography revealed abnormalities of bolus passage. On the basis of history and the benign clinical course over a 2 year follow-up period we assume a post-polio syndrome presenting with only dysphagia.

Poliomyelitis is an acute viral disease that attacks the brain and the ventral horn of the spinal cord. Damage to the lower motor neurons usually results in atrophy and weakness of muscle groups, perhaps paralysis and possibly deformity. A second type, bulbar poliomyelitis, infects the medulla oblongata and may result in dysfunction of the swallowing mechanism along with respiratory and circulatory distress. Minor forms of poliomyelitis result in fever, sore throat, headache, and upper body stiffness, but leave no significant atrophy or paralysis. The purpose of this paper is to review post-polio syndrome (PPS) as well as the effect of exercise on the symptoms and morphologic adaptations to PPS and where future research efforts should be directed. The most common features of PPS for over 350,000 afflicted survivors include general fatigue, weakness, and joint/muscle pain. The primary reasons for these symptoms include 1) destruction of the anterior horn cells by the polio virus, leaving fewer motor neurons to induce muscle contraction; 2) unaffected motor unit enlargement by reinnervation through terminal sprouting; and 3) defective transmission at the neuromuscular junction secondary to failure of terminal axonal sprout. Acute responses to resistive exercise suggest significant muscle strength decrements in the knee extensors compared with similar aged people without polio. However, limited training investigation indicates significant strength increases for the knee extensors following at least 6 wk of training. Acute aerobic responses also differ significantly from those observed in aged-matched control subjects. Chronic aerobic responses to limited training studies suggest significant elevations in maximal oxygen uptake.(ABSTRACT TRUNCATED AT 250 WORDS)

A new theory of how poliovirus reaches the central nervous system (CNS)--that it enters at many peripheral nerve endings with passage along nerve pathways to the CNS, with limited dispersal in the CNS--is used in making predictions of incubation periods, and these are compared with data from the literature and with predictions from other theories. The virus transit speed along the nerve of 2.4 mm/h has been used in calculating the incubation time. The calculated incubation time for Cutter vaccinees is similar to the actual times reported, and the calculated minimal and maximal incubation times in humans are similar to the published ranges. Incubation times in different animals and for different paralyses are explained. The pathology of lesions in humans and the consequent paralyses are compatible with the model. Tonsillectomy-associated poliomyelitis is reviewed and discussed in relation to possible entry of virus from peripheral nerve endings in muscle. Increased lymphocyte concentrations in the muscle may account for continuing susceptibility after tonsillectomy. Severe paralysis following exercise is explained as an effect of increased blood supply to nerves in the CNS that has already been invaded by virus. In developing countries, the phenomenon of paralysis in the injected muscle a few hours after injection in febrile children may occur in a similar fashion. The entry of poliovirus from many sites at nerve endings in muscles is consistent with clinical, experimental, and pathologic data and provides an explanation of the incubation times and related phenomena of poliomyelitis.

A 25-year-old woman is presented with hemifacial atrophy due to unilateral bulbar poliomyelitis infection. Although bulbar poliomyelitis is not an uncommon disease, it is rarely a cause of hemifacial asymmetry.

Fifteen children ranging in age from one and one-half to 14 years received intravenous polyriboinosinic-polyribocytidylic acid [poly (I)-poly (C)], an interferon inducer. The patients all had serious neurologic illness either directly or circumstatially related to viral infection. Peak titers of interferon in serum ranged from 8 to 500 units/ml in response to doses of poly (I)-poly (C) of 0.1-1.0 mg/kg. Serum interferon persisted for less than or equal to 24 hr after induction. Hyporesponsiveness to a second dose of poly (I)-poly (C) persisted for seven days after initial induction, after which time full response again occurred. The half-life of poly (I) poly (C) in plasma as measured in three patients was less than 30 min. poly (I-poly(C) appears to be safe when given intravenously, but the low titers of interferon induced may limit its clinical usefulness as an antiviral drug.

Human poliovirus infection in mice was studied to determine the similarities to human poliomyelitis, the selective vulnerability of neurons to infection, the role of the immune response in age-dependent susceptibility, and possible viral persistence. Mice inoculated intracerebrally (ic) with the Lansing type 2 poliovirus developed a disease with clinical, pathological, and age-dependent features resembling human poliomyelitis. Adult mice had a shorter incubation period (50% paralysis, Day 8 vs. Day 13) and a higher incidence of paralysis (97% vs. 79%) than newborns. Only paralyzed animals had pathologic changes in the spinal cord, and these corresponded to the degree of paralysis. Fluorescent antibody staining showed that selective infection of neurons was most intense in the anterior horn motor neurons of the spinal cord. There was no extraneural virus replication and no systemic neutralizing antibody response. Cyclophosphamide immunosuppression enhanced rather than diminished disease, indicating that maturation of immune responses did not explain the relative resistance of newborns to paralysis.

Paralytic poliomyelitis presenting with quadriparesis, transient encephalitis and bulbar symptoms in 2 patients in close contact with recently vaccinated children with trivalent live oral polio vaccine is described. Symmetrical lower motor neuron involvement of deltoid muscles with electromyographic confirmation was found. Upper motor neuron signs, with symmetrical hyperactive deep tendon reflexes developed in the lower extremities. Poliovirus Type-2 vaccine-like strain was cultured from one patient and both patients showed significant antibody titers rises to poliovirus. Attention is drawn to the possible clinical differences between vaccine associated poliomelitis and the usual features found in wild strain poliomyelitis. It is suggested that in selected cases, non-immunized contacts be given inactivated polio-vaccine when the vaccinees are immunized with the live oral-vaccine.

The mechanism of resistance of newborn mice to poliovirus-induced paralysis was studied by comparing regional virus replication in the adult and in the newborn central nervous systems (CNS) after intracerebral (ic) and intraspinal inoculation. Initial virus replication in the brains was similar in both age groups. Paralysis correlated with replication of virus in the spinal cord to a constant threshold, and this replication in newborns was delayed. Intraspinal inoculation of newborns eliminated the delay, indicating that neonatal anterior horn motor neurons were fully susceptible to infection. Cordectomy prevented the spread of virus, despite patent cerebrospinal fluid (CSF) pathways. Thus, poliovirus appeared to spread within the CNS via an axonal transport system. Known maturational changes in the fast transport system may explain the relative resistance of immature mice to poliovirus-induced paralysis.

Many of the deaths in acute bulbar poliomyelitis have been attributed to pulmonary complications, among which are listed suppurative tracheobronchitis, pneumonia, atelectasis, mediastinal emphysema, and pneumothorax. The literature so far encountered, however, fails to reveal any report correlating these lesions, roentgenologically demonstrated, with the clinical course of the disease. This study was undertaken to evaluate, if possible, the various pulmonary complications and to alert clinicians and radiologists to the possible factors which predispose to their development. It has been observed by many (2, 4, 7, 15, 17) that symptoms of cerebral involvement in bulbar poliomyelitis, heretofore considered a result of actual virus infection, have cleared completely almost immediately after establishment of an unobstructed airway. Thus, the treatment and prevention of pulmonary acidosis and anoxia (1) have emerged as a most vital adjunct to therapy. Histopathologic studies reported by Courville (3) emphasize ...

THE IMMEDIATE concern in any case of acute poliomyelitis is the treatment and management of two systems, namely, the cardiovascular and the respiratory. It is through the involvement of these systems that death ensues, even though the actual pathology may be confined to the central nervous system. As stated by Plum and Wolff 1 : In our experience, arrhythmias and shock due to failure of neurogenic cardiovascular regulation proved unresponsive to therapeutic measures, such as administration of the digitalis glycosides or phenylephrine (neo-synephrine®) and parenteral injection of fluids. In contrast to the discouraging prognosis offered by circulatory failure, the ill effects of respiratory insufficiency could often be prevented or reversed, and therefore the maintenance of a physiologic respiratory exchange was given primary attention. Most of the signs, characterizing what we will later refer to as the encephalitic type, could and probably do result from hypoxia (low oxygen tension) and hypercapnia (high

The provision of endobronchial pressure at the tip of an aspiration catheter, as described above, results in a more effective removal of obstructive mucus.

Cardiovascular collapse accounted for approximately one-third of the deaths from acute poliomyelitis in two epidemics. This syndrome occurred early in the disease and only in cases of bulbar involvement. In all cases there was morphologic involvement of the medulla and in 75 per cent of the cases there was a varying degree of myocarditis. There was a much smaller incidence of less severe myocarditis in the cases dying of other causes. It is suggested that the combination of sustained vasoconstriction arising as a result of the medullary lesion and the presence of interstitial myocarditis leads to circulatory failure and pulmonary edema.

The supine total lung capacity and its subdivisions has been determined in 62 patients with respiratory muscle paralysis due to poliomyelitis. The results were contrasted with those obtained using the same methods in 50 healthy subjects matched according to age, sex, and physical characteristics. A significant reduction of the total lung capacity was found in the patients. This was accounted for by reductions or alterations in the functional residual capacity and the maximum lung volume above the resting expiratory level. The frequent reduction of functional residual capacity was more marked in the patients studied after 2 years from onset of their illness. Respiratory muscle paralysis, duration of illness, thoracic deformities, and prolonged artificial respiration were considered to be contributory to these lung compartition changes.

0 NE OF THE oldest surgicaI procedures for sustaining Iife under emergency conditions is that of tracheostomy; we find it first mentioned by AscIepiades of Dithyma in 124 B.C. [I]. There is further mention of this operation in the days of Pompeii by a daring and capabIe surgeon, PauI of Agenia in 6go A.D. [2]. Coming to somewhat more modern times, Armond Trousseau was the first to perform tracheostomy in Paris, and for his brilIiant treatise on the subject, he received the coveted prize of the Academy of Medicine [3]. This procedure proved to be of such worth that American physicians were rapid to adopt its use and a number of pioneers in this country are listed in our historica writings. With this ancient background, it is obvious that the operation is no new story in medicine, nor is it our intention to suggest anything that might Iead to a comphcation of the simpIe methods of this very oId operation of opening the windpipe. Recent experience, however, pfompted the recording of present day uses of a modaIity sometimes considered appIicabIe onIy ih the direst of emergencies, as a Iast gasp procedure. The experience of ourseIves and many others [4-71 in the past decade does in no way suggest that “something new had been added,” but rather that “something oId has been expanded.” The broader use of tracheostomy in situations more Iifesustaining rather than actuaIIy Iife-saving seems worthy of consideration. The performance of this operation in the hospita1 bed, x-ray department, or in areas otherwise not surgicaIIy adapted seems to us rareIy necessary. We are not inclined to agree with recent reports in which the favored IocaIe was at the bedside [8]. Signs, symptoms and prodroma1 warnings are suffIcientIy we11 estabhshed to permit ampIe time for forma1 scheduIing of this operation in the surgica1 amphitheater where the operation can be done under idea1 surroundings and with the frequentIy needed support of our anesthesioIogy coIIeagues. This phiIosophic attitude with reference to respiratory probIems of this type admittedIy pIays a major roIe in surgica1 judgment and in the handIing of each individual patient. If, in our consuItative evaIuation of a given case, tracheostomy is a subconscious suggestion, in most instances evidence is probabIy sufficient to warrant immediate pIanned surgery. It is with these precepts in mind that we wouId Iike to present this cIinica1 experience. Our series incIudes that of the writers, thoracic surgica1 attendings, genera1 surgeons and residents in hospitaIs Iocated throughout the greater East Bay Area. These procedures were performed during a five year period from JuIy 1957 through June 1962 and totaIIed 461 cases. TabIe I, Iists the indications for which tracheostomy was performed in this series. The deaths, al1 but five of which were beIieved due to the underlying pathoIogy, wiII be discussed Iater.

The purpose of this paper is to present a surgical technique for the relief of complete inability to swallow resulting from poliomyelitis. Inability to swallow is of common occurrence in bulbar poliomyelitis, but most cases recover. I have observed only five cases of permanent swallowing paralysis in 4975 poliomyelitis admissions at the Elizabeth Kenny Institute in Minneapolis during the past seven years. Accurate figures as to the actual incidence of aphagia are not available, but information received from various poliomyelitis centers indicates that there are approximately 150 such cases in the United States. In 1951 Kaplan 1 reported a single case of paralytic deglutition following poliomyelitis treated by section of the cricopharyngeus muscle. In the two cases reported in this paper a new surgical technique which proved successful in both cases will be presented. Before presenting the case reports and describing the surgical technique the anatomy, innervation, physiology, and pathology

DURING the 1955 epidemic in Massachusetts more than 400 patients with poliomyelitis were hospitalized at the Massachusetts General Hospital. There were 74 adults requiring respirator management, with 17 fatal cases. Death in acute poliomyelitis that is not the result of obvious airway obstruction, ventilatory insufficiency or some other specific complication has been attributed to "circulatory collapse" secondary to involvement of the medullary vasomotor center1 , 2 and, less frequently, to "circulatory collapse" from myocarditis.3 The observations reported below appear to amend these concepts and suggest other possibilities and empirical methods of management. Presentation of the Clinical Material An analysis of these 17 . . .

Three days after her brother developed bulbospinal poliomyelitis, a 4-year-old Negro girl was examined because of fever and abdominal pain. Neurological examination was negative. Poliovirus type 1 was isolated from cerebrospinal fluid (CSF), throat swabs, and a later stool specimen, but not from serum obtained on the same day as the CSF. Although echoviruses and coxsackieviruses have been detected frequently in human CSF, poliovirus has been detected in CSF in only 7 well-documented cases. Several possible explanations for the presence of poliovirus in CSF are discussed, of which none appear to be satisfactory. The mode of entry of virus into the CSF remains unknown.

Summary Residual neurological impairment has been reviewed in a series of fifty patients seventeen to nineteen months after their acute bulbar poliomyelitis. Unexpectedly, a high incidence of persistent disability has been found. At the time of this follow-up examination 88 per cent of the observation group continued to have symptoms of cranial nerve involvement. This involvement was demonstrated at physical examination in 72 per cent of this group. The schedule of recovery from these disabilities and the circumstances of their later examination are similar to those noted in patients having persisting motor impairment after “spinal paralytic” poliomyelitis.

(1956). The Treatment of Bulbar Poliomyelitis. Postgraduate Medicine: Vol. 20, No. 2, pp. 168-176.

In bulbar poliomyelitis one of the serious complications is the inability to swallow. Not only is the patient unable to take food normally, but he is unable to dispose of his oral and nasopharyngeal secretions. These secretions are often aspirated. When this condition is combined, as it often is, with an absent or decreased cough reflex, tracheotomy is necessary so that the aspirated material may be removed by suction. Frequent attacks of atelectasis occur, requiring bronchoscopy for aspirations of the plugs. The occurrence of this condition in bulbar poliomyelitis is very common. Fortunately most of the cases improve. There are a considerable number that do not improve and are left seriously crippled. Not only do they have to be fed by nasogastric tube or gastrostomy, but they also have to wear a permanent tracheotomy tube. There are cases that overcome the difficulty in time. There have been improvements as long

Using the rapid infrared CO2 analyzer the alveolar CO2 of two major groups of patients with acute poliomyelitis were followed with almost daily observation from the day of admission for varying len...

THE DATA from which descriptions of the neurologic signs of early poliomyelitis have been derived have been obtained chiefly from occasional irregularly spaced examinations of large numbers of patients, each at some different time from the onset of the disease. It was thought that a more accurate description would result from frequent regularly spaced examinations both day and night during the early stage of poliomyelitis. Accordingly, eleven neurologists were rotated in tours of duty of six hours during the day and night for thirty days in the Municipal Contagious Disease Hospital (Chicago). Frequent examinations of each patient were made from the time of entrance to the hospital following the diagnosis or presumption of acute anterior poliomyelitis. This resulted in the examination of a pool of patients—at first, the few who were admitted on the first day and this number increased by subsequent admissions. During the period of thirty days the

WHEN patients have severe airway obstruction or swallowing difficulties, as may occur with bulbar poliomyelitis, the insertion of a tracheostomy tube may be required to ensure a clear airway, to reduce respiratory resistance and to minimize aspiration. It has been recommended that as large a tube as possible be inserted,1 to maintain the internal diameter close to that of the trachea and not to increase the resistance to breathing unduly as the patient breathes through the tracheostomy tube. When patients are weaned from tracheostomy tubes, progressively smaller tubes are inserted over a period of days or weeks. To help the . . .