Clinical Presentation

Polio infection remains asymptomatic in over 90 percent of cases. The majority a symptomatic polio infections involve only a minor viral illness that causes no paralysis, termed abortive polio. After an incubation period of a few days, symptoms may include fever, malaise, headache, sore throat, and gastrointestinal symptoms. Some of the patients who experience the minor viral illness, especially young children, may develop aseptic meningitis as the infection resolves. Only 1 to 2 percent of all poliovirus infections result in the major illness associated with neurologic involvement. Often there is resolution of the minor viral illness symptoms prior to development of neurologic symptoms, such that it is difficult to identify the preceding minor viral illness. Muscle pain, stiffness, and weakness during the early viral syndrome may suggest the later occurrence of paralysis. Because exercise can exacerbate the severity of the subsequent paralysis, patients with these symptoms suspected of having polio should be advised to avoid exercise.

When the major illness occurs, most commonly the spinal cord anterior horn cells are affected, causing asymmetric proximal limb weakness, especially in the legs. Spinal polio is characterized by flaccid and weak muscles, absent tendon reflexes, and fasciculations. Although pain, paresthesias, and transient sensory abnormalities are noted by polio patients, sensory deficits are usually not found on clinical examination. Maximal paralysis usually occurs within 5 days, and muscle wasting then occurs over several weeks. Autonomic dysfunction, including sweating disturbances, urine retention, delayed gastric emptying, and constipation, is commonly found. Nearly all spinal polio patients will demonstrate improved motor function, with paralysis resolution occurring within the first year after the acute infection.

Up to 20 percent of polio patients with paralysis will develop bulbar polio, which causes speech, swallowing, facial muscle, and rarely extraocular muscle dysfunction. Acute polio infection also can cause encephalitis and can disturb the reticular formation, resulting in cardiac dysrhythmias, blood pressure alterations, hypoxia, and hypercarbia. Patients who survive the acute episode of encephalitis normally will recover without residual affects.

Patients who present with postpolio syndrome complain of muscle fatigue, joint pain, worsening of skeletal deformities, or weakness in muscles that were spared during the initial viral infection. 26 These complaints can occur decades after maximal resolution of the neurologic symptoms caused by the initial polio infection. When muscle weakness is observed, atrophy, pain, and fasciculations may be noted both in previously unaffected muscle groups and in those previously involved. Patients with PPMA also may present with new bulbar, respiratory, or sleep difficulties. For example, laryngeal muscle weakness can cause progressive dyspnea, dysphagia, and/or hoarseness. Some patients complain of abnormal movements in sleep that disturb normal sleep, requiring therapy with benzodiazepines or dopaminergic drugs.27 These symptoms occur independent of any concurrent neurologic, orthopedic, psychiatric, or systemic medical illness.

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