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Post-Polio Syndrome: Pathophysiology and Clinical Management
Anne Carrington Gawne and Lauro S. Halstead

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Knowledge of the pathophysiology of acute polio is necessary to understand the possible causes for PPS and to provide a rational basis for its management. The poliovirus is a positive single-stranded RNA enterovirus belonging to the picornavirus group. The virus is relatively small (30 nm in diameter) and the poliovirus genome is about 7400 nucleotides long.[16] It lacks a lipid coat or capsule but has a protein coat shaped like a polyhedron with 20 faces.[17] There are three polio viruses, numbers 1, 2, and 3, defined by the configuration of the capsid proteins. Therefore, theoretically, a person could be infected more than once.

Wild poliovirus enters the body by oral ingestion, then replicates in the lymphoid tissue of the pharynx and ileum and spreads regionally to lymphoid tissue. It is extremely infectious and usually benign. The vast majority of infected individuals (95 to 99%) remain asymptomatic or experience a self-limited illness characterized by fever, myalgia, and gastrointestinal symptoms.[18] However, in 1 to 5% of persons, viremia may follow, with invasion of the anterior horn cells of the central nervous system (CNS). These patients usually develop a headache, stiff neck, and back pain, similar to viral meningitis. Only 1 to 2% of all those infected develop paralysis. Finally, the rate of paralysis varies with the strain of the virus and the patient's age. In children, paralysis occurs in 1/1000 cases, while in adults 1/75 develop paralysis. Asymmetric, flaccid paralysis occurs, with legs more commonly involved than arms. Severe bulbar weakness occurs in 10 to 15% of all paralytic cases. Less frequently, there is ophthalmoplegia and bladder involvement.[18] The pathological findings of acute polio consist of inflammation of meninges and anterior horn cells, with loss of spinal and bulbar motor neurons.[19] Less prominent findings include abnormalities in the cerebellar nuclei, reticular formation, thalamus, hypothalamus, cortical neurons, and dorsal horn.[19]

Once the virus has invaded the CNS, neurological and functional loss occurs as anterior horn cells are lost, and thus the muscle fibers innervated by them are "orphaned". Recovery begins in weeks and reaches a plateau in 6 to 8 months. The extent of neurological and functional recovery is determined by three major factors: (1) the number of motor neurons that recover and resume their normal function, (2) the number of motor neurons that develop terminal axon sprouts to reinnervate muscle fibers left orphaned by the death of their original motor neurons, and (3) muscle hypertrophy. The phenomenon of terminal axon sprouting makes it possible for an uninvolved or recovered motor neuron to "adopt" these orphaned muscle fibers. Stalberg has shown that a motor neuron cell can adopt five to seven additional muscle fibers commonly and occasionally, as many as 20 for every muscle cell innervated originally.[20] A single motor neuron that originally innervated 100 muscle fibers iriight eventually innervate 700 to 2000 fibers. As a result, the survivors of acute polio may be left with a few, significantly enlarged motor units doing the work previously performed by many units.[21] Figures 3, 4, 5, and 6 provide a schematic illustration of this phenomenon. Both electrophysiological evidence, including single fiber and macro-EMG and morphological data support this concept.[22-27]

In addition to this reinnervation, the remaining muscle fibers hypertrophy to increase the strength of the muscle group.[25,28] Because this mechanism of neurophysiological compensation is so effective, a muscle can retain normal strength even after 50% of the original motor neurons have been lost. Therefore, in some patients, manual muscle testing (MMT) may be normal when more than half the original anterior horn cells are destroyed.[29]

Figure 3
FIGURE 3. A normal motor unit containing the motor neuron and the muscle fibers it innervates.

Figure 4
FIGURE 4. Details of the motor unit.

Figure 5
FIGURE 5. Pathophysiological changes seen with acute poliomyelitis.

Figure 6
FIGURE 6. Reinnervation through collateral sprouting.

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This document comprises fifteen sections or subdocuments. Permission for printing copies is granted only on the basis that ALL sections are printed in their entirety and kept together as a single document. It is also available as a single 226K document, <URL:>

Document preparation: Chris Salter, Original Think-tank, Cornwall, United Kingdom.
Document Reference: <URL:>
Created: 5th June 2000
Last modification: 24th January 2010.

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