Characterization of facial paresis in hemifacial microsomia

Jay M Cline1, Katherine E Hicks, Krishna G Patel

  • 1Medical University of South Carolina Medical School, Charleston, South Carolina, USA.

Abstract

Insights

Facial paresis occurs in 10-45% of patients with hemifacial microsomia, often affecting all or lower facial nerve branches. Temporal bone dysmorphogenesis is the likely cause.

Area of Science:

  • Craniofacial anomalies
  • Neurology
  • Genetics

Background:

  • Hemifacial microsomia (HFM) is a congenital condition characterized by underdevelopment of one side of the face.
  • Facial nerve (CN VII) involvement, leading to facial paresis, is a recognized complication in HFM.
  • The oculo-auriculo-vertebral (OAV) spectrum encompasses HFM and related anomalies.

Purpose of the Study:

  • To review the incidence, characteristics, and proposed etiologic mechanisms of facial paresis in HFM.
  • To synthesize current knowledge on facial nerve dysfunction within the OAV spectrum.

Main Methods:

  • Comprehensive literature review of English-language studies.
  • Searched PubMed database without date restrictions.
  • Identified studies focusing on incidence, characterization, and etiology of facial paresis in HFM/OAV spectrum.

Main Results:

  • Prevalence of facial weakness in HFM/OAV spectrum ranges from 10% to 45%.
  • Facial nerve involvement typically affects all branches or exclusively lower branches.
  • Associated anomalies commonly include mandibular and auricular malformations.
  • Temporal bone dysmorphogenesis impacting the facial nerve is the most probable cause.

Conclusions:

  • Facial nerve presentation in HFM/OAV spectrum is highly variable with unclear etiology.
  • Understanding presentation and etiology can lead to improved management strategies for facial weakness.
  • Further research is needed to elucidate specific etiologic pathways and refine treatment approaches.

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