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Post-polio syndrome

Laura Simionescu, MD
Burk Jubelt, MD
Section Editors
Jeremy M Shefner, MD, PhD
Ira N Targoff, MD
Deputy Editor
John F Dashe, MD, PhD


Paralytic poliomyelitis was a major cause of morbidity and death throughout the world during the first half of the 20th century. In 1952, shortly before the introduction of the polio vaccine, more than 20,000 cases were reported in the US. Introduction of the inactivated polio vaccine in 1954 resulted in a dramatic decline of new polio cases. (See "Polio and infectious diseases of the anterior horn", section on 'Poliovirus and poliomyelitis'.)

Although polio no longer poses a major public health threat in developed nations, a 1987 survey estimated that there were 640,000 Americans living with the sequelae of paralytic polio [1]. These sequelae are static for many and reflect the state of recovery reached after the initial disease. Although not well studied, most polio survivors experience a modest decline in function and muscle strength over many years that may reflect the natural history of old polio [2].

Other patients, however, experience a syndrome of new or progressive disability, usually occurring decades after the disease itself. These new symptoms are quite variable, and include increased muscle weakness, focal or generalized muscle atrophy, fatigue, pain, and decreased ambulatory abilities. It has become clear that this condition, called post-polio syndrome (PPS), has both neurologic and non-neurologic components.

The clinical findings, etiology, and treatment of PPS will be reviewed here. Issues regarding polio vaccination are discussed separately. (See "Poliovirus vaccination".)


The cause of progressive neurologic deterioration in PPS is unknown. The main theories of pathogenesis involve progressive degeneration of reinnervated motor units, persistence of poliovirus in neural tissue, and induction of autoimmunity with consequent destruction of neural structures.

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Literature review current through: Nov 2017. | This topic last updated: Dec 08, 2016.
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