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Recognition and Management of Acute Flaccid Myelitis in Children
Gary R Nelson1, Joshua L Bonkowsky1, Elizabeth Doll1
1Division of Pediatric Neurology, Department of Pediatrics, University of Utah School of Medicine, Salt Lake City, Utah.
Insights
Acute flaccid myelitis outbreaks in children caused spinal cord gray matter lesions. Most patients experienced lasting motor deficits despite treatment, highlighting the need for early diagnosis and management.
Area of Science:
- Neurology
- Pediatrics
- Infectious Disease
Background:
- An outbreak of acute flaccid myelitis (AFM) occurred in US pediatric patients during 2014-2015.
- A key characteristic of AFM cases was spinal cord gray matter localization.
Purpose of the Study:
- To describe the clinical presentation and outcomes of pediatric patients with acute flaccid myelitis.
- To inform clinicians on diagnosis, treatment, and prognosis for AFM.
Main Methods:
- Retrospective case series of 11 children (13 months to 14 years) in the Intermountain West.
- Clinical evaluation, neurological examination, and magnetic resonance imaging (MRI) of the spinal cord.
- Assessment of treatment response to intravenous immunoglobulin, corticosteroids, or plasma exchange.
Main Results:
- All 11 children presented with acute paralysis, with 10 showing spinal cord localization.
- MRI revealed spinal gray matter lesions consistent with acute myelitis in all patients; no infectious cause was identified.
- Despite treatment, 90% of children had residual motor deficits at follow-up.
Conclusions:
- Early recognition of AFM is crucial for appropriate diagnostic imaging and laboratory testing.
- Treatment initiation and accurate prognostic information are vital for affected families.
- Unlike other causes of acute flaccid paralysis, AFM frequently results in persistent neurological deficits.
Background:
In 2014-2015, several regions of the United States experienced an outbreak of acute flaccid myelitis in pediatric patients. A common, unique feature was disease localization to the gray matter of the spinal cord.
Methods:
We report 11 children, ages 13 months to 14 years (median 9 years), in the Intermountain West who presented with extremity weakness (n = 10) or cranial neuropathy (n = 1) of varying severity without an apparent etiology.
Results:
All children experienced acute paralysis, and 10 had symptoms or signs that localized to the spinal cord. Maximum paralysis occurred within 4 days of onset in all patients. All had spinal gray matter lesions consistent with acute myelitis detected by magnetic resonance imaging; no single infectious cause was identified. Despite therapy with intravenous immunoglobulin, corticosteroids, or plasma exchange, nine of 10 (90%) children had motor deficits at follow-up.
Conclusions:
Recognition of this disorder enables clinicians to obtain appropriate imaging and laboratory testing, initiate treatment, and provide families with accurate prognostic information. In contrast to other causes of acute flaccid paralysis in childhood, most children with acute flaccid myelitis have residual neurological deficits.
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