Poliomyelitis

Poliovirus infections with wild-type virus may follow 1 of several courses: inapparent infection, which occurs in 90–95% of cases and causes no disease and no sequelae; abortive poliomyelitis; nonparalytic poliomyelitis; or paralytic poliomyelitis. Paralysis, if it occurs, appears 3–8 days after the initial symptoms.

Incubation Period:

The incubation period of poliovirus from contact to initial clinical symptoms is usually considered to be 8–12 days, with a range of 5–35 days.

Abortive Poliomyelitis.

In about 5% of patients, a nonspecific influenza-like syndrome occurs 1–2 wk after infection, which is termed abortive poliomyelitis. Vomiting occurs irregularly. The physical examination may be normal or may reveal nonspecific pharyngitis, abdominal or muscular tenderness, and weakness.
Nonparalytic Poliomyelitis.
In about 1% of patients infected with wild-type poliovirus, signs of abortive poliomyelitis are present, as are more intense headache, nausea, and vomiting, as well as soreness and stiffness of the posterior muscles of the neck, trunk, and limbs. Fleeting paralysis of the bladder and constipation are frequent. Approximately ? of these children have a short symptom-free interlude between the 1st phase (minor illness) and the 2nd phase (CNS disease or major illness). Nuchal and spinal rigidity are the basis for the diagnosis of nonparalytic poliomyelitis during the 2nd phase.
Physical examination reveals nuchal-spinal signs and changes in superficial and deep reflexes. Gentle forward flexion of the occiput and neck will elicit nuchal rigidity. Head drop is demonstrated by placing the hands under the patient’s shoulders and raising the trunk. True nuchal rigidity will persist during this maneuver. In the early stages the reflexes are normally active and remain so unless paralysis supervenes. Changes in reflexes, either increased or decreased, may precede weakness by 12–24 hr. The superficial reflexes, the cremasteric and abdominal reflexes, and the reflexes of the spinal and gluteal muscles are usually the 1st to diminish. The spinal and gluteal reflexes may disappear before the abdominal and cremasteric reflexes. Changes in the deep tendon reflexes generally occur 8–24 hr after the superficial reflexes are depressed and indicate impending paresis of the extremities. Tendon reflexes are absent with paralysis. Sensory defects do not occur in poliomyelitis.
Paralytic Poliomyelitis.
Paralytic poliomyelitis develops in about 0.1% of persons infected with poliovirus, causing 3 clinically recognizable syndromes that represent a continuum of infection differentiated only by the portions of the CNS most severely affected.
These are (1) spinal paralytic poliomyelitis, (2) bulbar poliomyelitis, and (3) polioencephalitis.
Spinal paralytic poliomyelitis may occur as the 2nd phase of a biphasic illness, the 1st phase of which corresponds to abortive poliomyelitis. Severe muscle pain is present, and sensory and motor phenomena (e.g., paresthesia, hyperesthesia, fasciculations, and spasms) may develop. On physical examination the distribution of paralysis is characteristically spotty. Single muscles, multiple muscles, or groups of muscles may be involved in any pattern. Within 1–2 days, asymmetric flaccid paralysis or paresis occurs. Involvement of 1 leg is most common, followed by involvement of 1 arm. To detect mild muscular weakness, it is often necessary to apply gentle resistance in opposition to the muscle group being tested. Examination at this point may reveal nuchal stiffness or rigidity, muscle tenderness, initially hyperactive deep tendon reflexes (for a short period) followed by absent or diminished reflexes, and paresis or flaccid paralysis. In the spinal form there is weakness of some of the muscles of the neck, abdomen, trunk, diaphragm, thorax, or extremities. Sensation is intact; sensory disturbances, if present, suggest a disease other than poliomyelitis.


The paralytic phase of poliomyelitis is extremely variable; some patients progress during observation from paresis to paralysis, whereas others recover, which may be slow or rapid. The extent of paresis or paralysis is directly related to the extent of neuronal involvement; paralysis occurs if more than 50% of the neurons supplying the muscles are destroyed. Paralysis of the lower limbs is often accompanied by bowel and bladder dysfunction ranging from transient incontinence to paralysis with constipation and urinary retention.
The onset and course of paralysis are variable in developing countries. The biphasic course is rare and typically presents as a single phase in which prodromal symptoms and paralysis occur in a continuous fashion. In developing countries, where a history of intramuscular injections precedes paralytic poliomyelitis in about 50–60% of patients, patients may present initially with fever and paralysis (provocation paralysis). Occasionally spasm and increased muscle tone with a transient increase in deep tendon reflexes occur in some patients, whereas in most patients flaccid paralysis occurs abruptly. Once the temperature returns to normal, progression of paralytic manifestations stops. Lack of improvement from paralysis within the 1st several weeks or months after onset is usually evidence of permanent paralysis.
Bulbar poliomyelitis may occur as a clinical entity without apparent involvement of the spinal cord. Infection is a continuum, and designation of the disease as bulbar implies only dominance of the clinical manifestations by dysfunctions of the cranial nerves and medullary centers. The clinical findings seen with bulbar poliomyelitis with respiratory difficulty (other than paralysis of extraocular, facial, and masticatory muscles) include (1) nasal twang to the voice or cry caused by palatal and pharyngeal weakness (hard-consonant words such as “cookie” or “candy” bring this out best); (2) inability to swallow smoothly, resulting in accumulation of saliva in the pharynx, indicating partial immobility (holding the larynx lightly and asking the patient to swallow will confirm such immobility); (3) accumulated pharyngeal secretions, which may cause irregular respirations that appear interrupted and abnormal even to the point of falsely simulating intercostal or diaphragmatic weakness; (4) absence of effective coughing, shown by constant fatiguing efforts to clear the throat; (5) nasal regurgitation of saliva and fluids as a result of palatal paralysis, with inability to separate the oropharynx from the nasopharynx during swallowing; (6) deviation of the palate, uvula, or tongue; (7) involvement of vital centers in the medulla, which manifest as irregularities in rate, depth, and rhythm of respiration; as cardiovascular alterations, including blood pressure changes (especially increased blood pressure), alternate flushing and mottling of the skin, and cardiac arrhythmias; and as rapid changes in body temperature; (8) paralysis of 1 or both vocal cords, causing hoarseness, aphonia, and ulti mately asphyxia unless this is recognized by laryngoscopy and managed by immediate tracheostomy; and (9) the rope sign, an acute angulation between the chin and larynx caused by weakness of the hyoid muscles (the hyoid bone is pulled posteriorly, narrowing the hypopharyngeal inlet).
Uncommonly, bulbar disease may culminate in an ascending paralysis (Landry type), in which there is progression cephalad from initial involvement of the lower extremities. This kind of bulbar disease may be rapidly fatal.
The course of bulbar disease is variable; some patients die as a result of extensive, severe involvement of the various centers in the medulla; others recover partially but require ongoing respiratory support, and others recover completely. Cranial nerve involvement is seldom permanent. Atrophy of muscles may be evident, patients immobilized for long periods may develop pneumonia, and renal stones may form as a result of hypercalcemia and hypercalciuria secondary to bone resorption.
Seizures, coma, and spastic paralysis with increased reflexes may be observed. Irritability, disorientation, drowsiness, and coarse tremors are often present with peripheral or cranial nerve paralysis that coexists or ensues. Paralytic poliomyelitis with ventilatory insufficiency results from several components acting together to produce ventilatory insufficiency resulting in hypoxia and hypercapnia. Because respiratory insufficiency may develop rapidly, close continued clinical evaluation is essential. Despite weakness of the respiratory muscles, the patient may respond with so much respiratory effort associated with anxiety and fear that overventilation may occur at the outset, resulting in respiratory alkalosis. Such effort is fatiguing and contributes to respiratory failure.
Pure spinal poliomyelitis with respiratory insufficiency involves tightness, weakness, or paralysis of the respiratory muscles (chiefly the diaphragm and intercostals) without discernible clinical involvement of the cranial nerves or vital centers that control respiration, circulation, and body temperature. The cervical and thoracic spinal cord segments are chiefly affected. Pure bulbar poliomyelitis involves paralysis of the motor cranial nerve nuclei with or without involvement of the vital centers. Involvement of the 9th, 10th, and 12th cranial nerves results in paralysis of the pharynx, tongue, and larynx with consequent airway obstruction. Bulbospinal poliomyelitis with respiratory insufficiency affects the respiratory muscles and results in coexisting bulbar paralysis.


The clinical findings associated with involvement of the respiratory muscles include (1) anxious expression; (2) inability to speak without frequent pauses, resulting in short, jerky, “breathless” sentences; (3) increased respiratory rate; (4) movement of the ala nasi and of the accessory muscles of respiration; (5) inability to cough or sniff with full depth; (6) paradoxical abdominal movements caused by diaphragmatic immobility due to spasm or weakness of 1 or both leaves; and (7) relative immobility of the intercostal spaces, which may be segmental, unilateral, or bilateral. When the arms are weak, and especially when deltoid paralysis occurs, there may be impending respiratory paralysis because the phrenic nerve nuclei are in adjacent areas of the spinal cord. Observation of the patient’s capacity for thoracic breathing while the abdominal muscles are splinted manually indicates minor degrees of paresis.