Osteogenesis imperfecta (OI), also known as Lobstein disease, is a rare inherited connective tissue disorder characterized by bone fragility and various extra-skeletal manifestations. Hearing loss is a frequent but often underestimated complication that may significantly impair quality of life.

We report the case of a 34-year-old woman with clinically established osteogenesis imperfecta type I who developed progressive bilateral conductive hearing loss over a three-year period. Audiological evaluation revealed symmetrical conductive impairment with preserved speech discrimination. High-resolution temporal bone computed tomography (CT) demonstrated diffuse otic capsule demineralization, bilateral stapes footplate thickening, and atypical crown-shaped hypodense lesions surrounding the cochlea.

Early recognition of hearing loss in osteogenesis imperfecta, combined with detailed imaging and multidisciplinary management, is essential to optimize functional outcomes.

Brucellosis is a zoonotic infection common in Mediterranean countries and the Middle East. Neurological involvement, although rare, can lead to severe complications, including sensorineural hearing loss (SNHL). This case is particularly noteworthy as it highlights irreversible auditory nerve damage in brucellosis, emphasizing the importance of early diagnosis and treatment to prevent permanent neurological consequences. The novelty of this case lies in the severity of auditory involvement despite timely treatment.

A 43-year-old male farmer of Maghrebi origin presented with neurobrucellosis complicated by severe, irreversible bilateral sensorineural hearing loss. The patient initially reported symptoms of hearing loss and dizziness, which were confirmed to be associated with auditory nerve involvement. Wright’s serology and polymerase chain reaction (PCR) testing confirmed brucellosis. Despite appropriate and prolonged antibiotic therapy, including drugs that penetrate the meningeal barrier and act intracellularly, the patient’s auditory impairment remained permanent. The patient is currently a candidate for cochlear implantation to manage his severe hearing loss. Neurological symptoms did not improve with treatment, but cochlear implantation may offer a potential solution to his hearing deficit.

This case highlights the importance of early recognition and intervention in brucellosis cases, particularly those with neurological involvement. Delayed diagnosis and treatment can result in irreversible neurological damage. It also underscores the potential for cochlear implantation in patients with severe, irreversible sensorineural hearing loss caused by neurobrucellosis. Cochlear implantation offers an important solution for patients with brucellosis-related hearing deficits, improving their quality of life despite the neurological damage caused by the infection.