Neomycin-induced deafness in neonatal mice.

BACKGROUND: Hearing impairment is a rising public health issue, and current therapeutics fail to restore normal auditory sensation. Animal models are essential to a better understanding of the pathophysiology of deafness and developing therapeutics to restore hearing. NEW METHODS: Wild-type CBA/CaJ neonatal mice P2-5 were used in this study. Neomycin suspension (500 nl of 50 or 100 mg/ml) was micro-injected into the endolymphatic space. Cochlear morphology was examined 3 and 7 days after injection; hair cell (HC) loss, supporting cell morphology, and neurite denervation pattern were assessed with whole-mounts. At 2 and 4 weeks post-injection, the spiral ganglion neuron (SGN) density was analyzed with cryostat sections. Audiometric responses were measured with auditory brain response (ABR) at 4 weeks. RESULTS: Rapid and complete degeneration of the inner and outer HCs occurred as early as 3 days post-injection. Subsequently, time- and dose-dependent degeneration patterns were observed along the axis of the cochlear membranous labyrinth forming a flat epithelium. Likewise, the SGN histology demonstrated significant cell density reduction at 2 and 4 weeks. The ABR threshold measurements confirmed profound deafness at 4 weeks. COMPARISON WITH EXISTING METHODS: Compared to previously described local and systemic aminoglycoside injections, this method provides a reliable, robust, and rapid deafening model with a single infusion of neomycin in neonatal mice. This model also allows for investigating the effects of inner ear damage during auditory maturation. CONCLUSIONS: A single injection of neomycin into the endolymphatic space induces robust HC loss and denervation in neonatal mice.

Neuralgia and Atypical Facial, Ear, and Head Pain.

Though there have been considerable strides in the diagnosis and care of orofacial pain disorders, facial neuralgias, and myofascial pain dysfunction syndrome remain incredibly cumbersome for patients and difficult to manage for providers. Cranial neuralgias, myofascial pain syndromes, temporomandibular dysfunction (TMD), dental pain, tumors, neurovascular pain, and psychiatric diseases can all present with similar symptoms. As a result, a patient's quest for the treatment of their orofacial pain often begins on the wrong foot, with a misdiagnosis or unnecessary procedure, which makes it all the more frustrating for them. Understanding the natural history, clinical presentation, and management of facial neuralgias and myofascial pain dysfunction syndrome can help clinicians better recognize and treat these conditions. In this article, we review updated knowledge on the pathophysiology, incidence, clinical features, diagnostic criteria, and medical management of TN, GPN, GN, and MPDS.