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Acute flaccid paralysis

急性无力肢体麻痹

Evidence-backed informationEN 4/7 applicable sections · ZH 4/7 applicable sectionsUpdated Sep 3, 2026

Acute flaccid paralysis denotes a sudden onset of limb weakness that functions as a critical clinical presentation across multiple distinct pathophysiological pathways [1]. Historically monitored as a sentinel indicator for poliovirus circulation, the syndrome now reflects a shifting etiologic landscape where declining poliomyelitis coincides with increasing contributions from non-polio enteroviruses and flaviviruses [2][3]. Clinical manifestations vary widely, encompassing both direct viral destruction of central motor neurons and immune-mediated peripheral nerve damage frequently triggered by preceding infections [4][5]. Ongoing monitoring of these diverse neurological presentations remains essential for tracking emerging viral strains and guiding regional health responses [2].

Read the full clinical and epidemiological profile5
Syndrome or outcome definition

Acute flaccid paralysis is broadly characterized as the abrupt development of flaccid weakness in the extremities and serves primarily as a standardized public health surveillance concept designed to detect undetected poliovirus transmission [1]. The terminology encompasses heterogeneous pathological conditions, notably spinal cord anterior horn cell injury driven by specific enteroviruses alongside autoimmune peripheral neuropathies such as Guillain-Barré syndrome [2][4]. To clarify anatomical distinctions between central nervous system involvement and peripheral nerve disorders, related diagnostic classifications have also been established to prevent terminological overlap [1].

Clinical criteria and consequences

Affected individuals typically present with progressive motor weakness that frequently follows an antecedent infectious illness, most commonly involving respiratory or gastrointestinal tracts [4]. Pathophysiological mechanisms diverge significantly by etiology, ranging from molecular mimicry-triggered autoantibody responses that damage peripheral nerves to direct viral invasion of spinal cord motor neurons [2][4]. Pediatric cases may additionally involve autonomic dysfunction and respiratory compromise, necessitating close clinical observation and potential intensive care admission [5]. While many patients experience partial or complete motor recovery, substantial proportions remain with permanent neurological deficits or face mortality [4].

Occurrence and burden

Sustained global eradication campaigns have drastically reduced poliomyelitis-related cases, confining endemic transmission to limited regions while anticipated vaccine-associated occurrences continue to decline [2]. Non-polio enteroviruses, particularly EV-D68 and EV-A71, have increasingly replaced polioviruses as dominant etiologic agents, with EV-D68 demonstrating genetic adaptations linked to severe respiratory and neurological disease clusters [2]. Flavivirus infections substantially contribute to the global burden, circulating widely across multiple continents and generating recurrent epidemic waves that affect hundreds of millions of individuals annually [3]. These shifting patterns highlight the dynamic nature of neurotropic viral circulation and the ongoing need for targeted regional monitoring [2][3].

Outcome surveillance

GlobalID source-data note: Japan's acute flaccid paralysis surveillance series explicitly excludes acute poliomyelitis. It is a syndrome-surveillance count for non-polio AFP and must not be used as a poliomyelitis count or as an unrestricted total of every AFP cause.

References
  1. 1Hosoya M et al. [Acute Flaccid Paralysis]. Brain Nerve. 2022 Oct. PMID: 36198640. doi: 10.11477/mf.1416202203.PubMed: https://pubmed.ncbi.nlm.nih.gov/36198640/
  2. 2Bitnun A et al. Acute Flaccid Paralysis and Enteroviral Infections. Curr Infect Dis Rep. 2018 Jun 29. PMID: 29959591. doi: 10.1007/s11908-018-0641-x.PubMed: https://pubmed.ncbi.nlm.nih.gov/29959591/
  3. 3Pierson TC et al. The continued threat of emerging flaviviruses. Nat Microbiol. 2020 Jun. PMID: 32367055. doi: 10.1038/s41564-020-0714-0.PubMed: https://pubmed.ncbi.nlm.nih.gov/32367055/
  4. 4Shahrizaila N et al. Guillain-Barré syndrome. Lancet. 2021 Mar 27. PMID: 33647239. doi: 10.1016/S0140-6736(21)00517-1.PubMed: https://pubmed.ncbi.nlm.nih.gov/33647239/
  5. 5Langille MM et al. Guillain-Barre Syndrome in Children and Adolescents. Adv Pediatr. 2023 Aug. PMID: 37422300. doi: 10.1016/j.yapd.2023.04.001.PubMed: https://pubmed.ncbi.nlm.nih.gov/37422300/
Coding Register
ICD-10
ICD-11
Key Statistics
Total cases
11K
Peak month
2023-03
Coverage
4 reporting countries · 2000-01-01 → 2026-08-30

Coverage

Reporting countries and regions

4 locations

Monthly patterns over time

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Literature links are provided for discovery and do not alter or validate the surveillance series above.

Data access

Page dataset index with source links and update metadata.

Rows1,375
Updated2026-09-01
Coverage
Partitions6
Source2 series · 459 observations
Official sourcesAuthority, cadence, notes4
Brazil

Brazil DATASUS SINAN

Brazil

Source
monthlyftp_dbc

Brazil Ministry of Health DATASUS/SINAN public DBC microdata aggregated to national monthly notification counts.

Canada

Canada PHAC CNDSS Annual

Canada

Source
ANNUALweb

Canada is the national jurisdiction; subdivision feeds are registered separately.

Japan

JP NIID Weekly

Japan

Source
weeklyweb

Japan weekly infectious disease surveillance via NIID/JIHS.

Taiwan, China

Taiwan, China CDC NIDSS

Taiwan, China

Source
monthlyopen_data_csv

Taiwan, China monthly notifiable infectious disease open-data CSV feed.

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