May 8, 2012

Post-poliomyelitis syndrome or Post-polio syndrome (PPS)


Post-poliomyelitis syndrome or Post-polio syndrome (PPS) is the commonly accepted term to describe the neuromuscular symptoms that may develop many years after acute paralytic poliomyelitis. The prevalence estimates of late onset neuromuscular symptoms in prior polio patients vary between 25 and 74%. PPS patients are diagnosed on the basis of a confirmed history of paralytic poliomyelitis, followed by partial to fairly complete neurological recovery and functional stability for at least 15 years. After this recovery period, new or increased muscle weakness or abnormal muscle fatigability (decreased endurance), with or without generalized fatigue, muscle atrophy, or muscle and joint pain, appear usually gradually. PPS diagnosis is made by exclusion. Laboratory tests are used to show evidence of prior polio and to exclude other diseases: electromyography (EMG) displays signs of reinnervation and denervation both in symptomatic and non-symptomatic muscles. Muscle biopsy findings include type-grouping of muscle fibres as the result of reinnervation, and hypertrophy of muscle fibres as a compensation for the loss of muscle fibres. No curative treatment is available for PPS. Management is preferably multidisciplinary and aims both at reducing muscle overuse and rebalancing muscular capacities and demands. It consists of exercise, assistive devices and life style changes. The etiology of PPS is still unclear. It is currently hypothesized that muscle fibres undergo denervation again due to distal degeneration of axons of enlarged motor units.

Expert reviewer(s)

  • Dr F. [Frans] NOLLET

Restriction of poliovirus RNA replication in persistently infected nerve cells

  1. Bruno Blondel1
+Author Affiliations
  1. Unité de Neurovirologie et Régénération du Système Nerveux, Institut Pasteur, 28 rue du Docteur Roux, 75724 Paris cedex 15, France1
  1. Author for correspondence: Bruno Blondel (e-mail and T. Couderc ( Fax +33 1 45 68 87 62.
  • Received 25 October 2001.
  • Accepted 8 January 2002.


The aetiology of post-polio syndrome may involve persistence of poliovirus (PV) in the CNS. PV persists in the CNS of infected paralysed mice for over a year after the acute phase of paralytic poliomyelitis. However, infectious PV particles cannot be recovered from homogenates of CNS from paralysed mice after the acute phase of disease, indicating that PV replication is restricted. To identify the molecular mechanism by which PV replication is limited, PV RNA synthesis was analysed by estimating the relative level of genomic (plus-strand) and complementary (minus-strand) PV RNA in the CNS of persistently infected mice. PV RNA replication decreased during the 6 months following onset of paralysis, due mainly to inhibition of plus-strand RNA synthesis. Thus, restriction of PV RNA synthesis may contribute to persistence by limiting virus replication in the mouse CNS. Interestingly, viral RNA replication was similarly inhibited in neuroblastoma IMR-32 cell cultures persistently infected with PV. This in vitro model thus shows that cellular factors play a role in the inhibition of viral RNA synthesis.


Poliovirus (PV) is an enterovirus of the Picornaviridae family and is the causal agent of paralytic poliomyelitis, an acute disease of the central nervous system (CNS). The PV genome is a single-stranded RNA of positive polarity, 7500 nucleotides long, composed of a long 5′ non-translated region (NTR) followed by a long open-reading frame and a short polyadenylated 3’ NTR. The PV genome is copied, starting from the 3’ end, to generate a complementary, negative-strand RNA that, in turn, is transcribed into new molecules of positive-strand genomic RNA. Both processes are catalysed by the RNA-dependent RNA polymerase (3Dpol) but a number of other viral proteins and cellular factors also participate in RNA replication (for review, see Xiang et al., 1997 ). RNA replication is highly asymmetric with the ratio of positive-strand to negative-strand RNA synthesis being greater than 30:1 in human epithelial cell cultures (Andino et al., 1990 ; Giachetti & Semler, 1991 ; Lopez-Guerrero et al., 1991 ; Novak & Kirkegaard, 1991 Read more
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