Introduction <p>Conductive hearing loss (CHL) with an intact tympanic membrane is often attributed to otosclerosis. However, a subset of patients explored surgically for presumed otosclerosis is found to have no disease or alternative non-otosclerotic pathology. Recognition of these mimics is crucial to avoid unnecessary surgery and optimize management.</p> Objective <p>To review the spectrum of non-otosclerotic causes of CHL; outline distinguishing clinical, audiologic, and radiologic features; and summarise current evidence on management strategies.</p> Methods <p>This clinical narrative review is based on a comprehensive literature search conducted in PubMed, examining ossicular chain abnormalities and third-window lesions that present with conductive hearing loss (CHL). Particular emphasis is placed on the differential diagnosis, imaging characteristics, and reported treatment outcomes associated with these conditions.</p> Results <p>Non-otosclerotic etiologies include congenital or paediatric stapes fixation, tympanosclerosis, ossicular discontinuity or fixation, temporal bone trauma, and third-window lesions such as superior semicircular canal dehiscence (SSCD) and enlarged vestibular aqueduct (EVA). Distinguishing clues include preserved stapedial reflexes, symptoms of autophony or sound-induced vertigo, and high-resolution CT findings. Surgical outcomes vary widely: while stapedectomy offers favourable results in juvenile otosclerosis, outcomes in congenital fixation and tympanosclerosis are less predictable. In third-window lesions, management focuses on vestibular rather than auditory symptoms.</p> Conclusion <p>Non-otosclerotic CHL encompasses diverse pathologies that can closely mimic otosclerosis. A systematic diagnostic approach—integrating clinical assessment, acoustic reflex testing, and targeted imaging—enables accurate differentiation and tailored management. Awareness of these entities prevents negative explorations and enhances patient outcomes.</p>

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Non-otosclerotic conductive hearing loss: diagnostic challenges and management

  • Ashish Varghese,
  • Khalil Macki,
  • Ismaili Salim

摘要

Introduction

Conductive hearing loss (CHL) with an intact tympanic membrane is often attributed to otosclerosis. However, a subset of patients explored surgically for presumed otosclerosis is found to have no disease or alternative non-otosclerotic pathology. Recognition of these mimics is crucial to avoid unnecessary surgery and optimize management.

Objective

To review the spectrum of non-otosclerotic causes of CHL; outline distinguishing clinical, audiologic, and radiologic features; and summarise current evidence on management strategies.

Methods

This clinical narrative review is based on a comprehensive literature search conducted in PubMed, examining ossicular chain abnormalities and third-window lesions that present with conductive hearing loss (CHL). Particular emphasis is placed on the differential diagnosis, imaging characteristics, and reported treatment outcomes associated with these conditions.

Results

Non-otosclerotic etiologies include congenital or paediatric stapes fixation, tympanosclerosis, ossicular discontinuity or fixation, temporal bone trauma, and third-window lesions such as superior semicircular canal dehiscence (SSCD) and enlarged vestibular aqueduct (EVA). Distinguishing clues include preserved stapedial reflexes, symptoms of autophony or sound-induced vertigo, and high-resolution CT findings. Surgical outcomes vary widely: while stapedectomy offers favourable results in juvenile otosclerosis, outcomes in congenital fixation and tympanosclerosis are less predictable. In third-window lesions, management focuses on vestibular rather than auditory symptoms.

Conclusion

Non-otosclerotic CHL encompasses diverse pathologies that can closely mimic otosclerosis. A systematic diagnostic approach—integrating clinical assessment, acoustic reflex testing, and targeted imaging—enables accurate differentiation and tailored management. Awareness of these entities prevents negative explorations and enhances patient outcomes.