In the inapparent infections, and those in which there are only mild systemic symptoms with pharyngitis or gastroenteritis had been called abortive poliomyelitis. The mild symptoms correspond to the period of viremia and dissemination of the virus; they give rise in most cases to an effective immune response—a feature that accounts for the failure to cause meningitis or poliomyelitis. In the relatively small proportion of patients in whom the nervous system is invaded, the illness still has a wide range of severity from mild aseptic meningitis (nonparalytic or preparalytic poliomyelitis) to the most severe forms of paralytic poliomyelitis.
Nonparalytic poliomyelitis The prodromal symptoms consist of listlessness, generalized, nonthrobbing headache, fever of 38 to 40°C (100.4 to 104°F), stiffness and aching in the muscles, sore throat in the absence of upper respiratory infection, anorexia, nausea, and vomiting. These symptoms may subside to a varying extent, to be followed after 3 to 4 days by recrudescence of headache and fever and by symptoms of nervous system involvement; more often the second phase of the illness blends with the first. Tenderness and pain in the muscles, tightness of the hamstrings (spasm), and pain in the neck and back become increasingly prominent. Other early manifestations of nervous system involvement include irritability, restlessness, and emotional instability; these are frequently a prelude to paralysis. Added to these symptoms are stiffness of the neck on forward flexion and the characteristic CSF findings of aseptic meningitis. This may constitute the entire illness; alternatively, paralysis may follow the preparalytic symptoms.
Paralytic poliomyelitis Weakness becomes manifest while the fever is at its height, or, just as frequently, as the temperature falls and the general clinical picture seems to be improving. Muscle weakness may develop rapidly, attaining its maximum severity in 48 h or even less; or it may develop more slowly or in stuttering fashion over a week, rarely even longer. As a general rule, there is no progression of weakness after the temperature has been normal for 48 h. The distribution of spinal paralysis is quite variable; rarely there may be an acute symmetrical paralysis of the muscles of the trunk and limbs as occurs in the Guillain-Barré syndrome. Excessive physical activity and local injections during the period of asymptomatic infection were thought to favor the development of paralysis of the exercised or injected limbs.
Coarse fasciculations are seen as the muscles weaken; they are transient as a rule, but occasionally they persist. Tendon reflexes are diminished and lost as the weakness evolves and paralyzed muscles become flaccid. Patients frequently complain of paresthesias in the affected limbs but objective sensory loss is seldom demonstrable. Retention of urine is a common occurrence during the early phase in adult patients, rarely persisting. Atrophy of muscle can be detected within 3 weeks of onset of paralysis, is maximal at 12 to 15 weeks, and is permanent.
Bulbar paralysis is more common in young adults, but usually such patients have spinal involvement as well. The most frequently involved cranial muscles are those of deglutition, reflecting involvement of the nucleus ambiguus. The other great hazards of medullary disease are disturbances of respiration and vasomotor control—hiccough, shallowness and progressive slowing of respiration, cyanosis, restlessness and anxiety from air hunger, hypertension, and, ultimately, hypotension and shock. When these disturbances are added to paralysis of diaphragmatic and intercostal musculature, the patient’s survival is threatened and the institution of respiratory assistance and intensive care becomes urgent.