Neurological events related to influenza A (H1N1) pdm09

Abstract

Objectives: To review neurological complications after the influenza A (H1N1) pdm09, highlighting the clinical differences between patients with post-vaccine or viral infection.

Design: A search on Medline, Ovid, EMBASE, and PubMed databases using the keywords “neurological complications of Influenza AH1N1” or “post-vaccine Influenza AH1N1.”

Setting: Only papers written in English, Spanish, German, French, Portuguese, and Italian published from March 2009 to December 2012 were included.

Sample: We included 104 articles presenting a total of 1636 patient cases. In addition, two cases of influenza vaccine-related neurological events from our neurological care center, arising during the period of study, were also included.

Main outcome measures: Demographic data and clinical diagnosis of neurological complications and outcomes: death, neurological sequelae or recovery after influenza A (H1N1) pdm09 vaccine or infection.

Results: The retrieved cases were divided into two groups: the postvaccination group, with 287 patients, and the viral infection group, with 1349 patients. Most patients in the first group were adults. The main neurological complications were Guillain-Barre syndrome (GBS) or polyneuropathy (125), and seizures (23). All patients survived. Pediatric patients were predominant in the viral infection group. In this group, 60 patients (4.7%) died and 52 (30.1%) developed permanent sequelae. A wide spectrum of neurological complications was observed.

Conclusions: Fatal cases and severe, permanent, neurological sequelae were observed in the infection group only. Clinical outcome was more favorable in the post-vaccination group. In this context, the relevance of an accurate neurological evaluation is demonstrated for all suspicious cases, as well as the need of an appropriate long-term clinical and imaging follow-up of infection and post-vaccination events related to influenza A (H1N1) pdm09, to clearly estimate the magnitude of neurological complications leading to permanent disability.

Figure 1

(A–C) MRI on axial Fast-FLAIR sequence shows demyelinating areas involving gyri rectus, mesencephalon, and pons. (D–F). Control MRI performed 15 months after initial symptoms shows improvement in demyelinating lesions and secondary cortical atrophy.

Figure 2

(A–C) MRI on diffusion, Fast-FLAIR, and T2-weighted sequences show extensive demyelinating areas involving subcortical white matter (bilateral centrum semi oval). (D–F) Control MRI performed 4 months after initial symptoms shows ostensible improvement of lesions and secondary subcortical atrophy.