No abstract

This case report describes carotid-cochlear dehiscence, a rare and possibly fatal condition if missed or ignored on initial work-up of several otologic procedures. Thinning of the bony plate separating the carotid canal from other anatomic structures can occur anywhere along the course of the canal, including the carotid-cochlear bony plate. This condition should be recognized by all otolaryngologists in that it can mimic other otologic pathologies. The aim of this report was to call attention to this condition and its associated mimicking symptoms and inform on its proper management. The idea for this review was formed from the case of a patient who presented with pulsatile tinnitus and was found to have carotid-cochlear dehiscence. Carotid-cochlear dehiscence is a rare anatomic variation of which the neurotologic surgeon should be aware. This condition can mimic common otolaryngologic pathologies that regularly present themselves in clinical settings. We present what we believe to be the fourth reported case of carotid-cochlear dehiscence in the literature. The patient presented having only the complaint of pulsatile tinnitus and was later diagnosed with this rare condition. We advocate a thorough preoperative work-up, including high-resolution computed tomography and careful operative planning in a case-specific manner. This is especially important when common pathologies do not become apparent after careful investigation.

Hyperplasia of middle-ear mucosa (MEM) during otitis media (OM) is thought to be partially mediated by the actions of growth factors and their receptors. The intracellular pathway leading from the small G-protein Ras to the extracellular regulated kinases (Erks) often links growth factor stimulation to cellular proliferation. This study assessed whether this pathway is involved in MEM hyperplasia during bacterial OM via the activation of Erk1/Erk2 in MEM of an in vivo rat bacterial OM model. Activation was maximal at 1 and 6 h and at 1 week after introduction of bacteria into the middle ear. Additionally, an in vitro model of rat MEM in bacterial OM was treated with farnesyl transferase inhibitor 277 or the Mek inhibitor U0126. MEM explants treated with either inhibitor demonstrated significant suppression of bacterially induced growth. These data support a role for Ras and Erk signaling in MEM hyperplasia during bacterial OM.

Hyperplasia of the middle ear mucosa contributes to the sequelae of acute otitis media. Understanding the signal transduction pathways that mediate hyperplasia could lead to the development of new therapeutic interventions for this disease and its sequelae. Endotoxin derived from bacteria involved in middle ear infection can contribute to the hyperplastic response. The p38 mitogen-activated protein kinase (MAPK) is known to be activated by endotoxin as well as cytokines and other inflammatory mediators that have been documented in otitis media. We assessed the activation of p38 in the middle ear mucosa of an in vivo rat bacterial otitis media model. Strong activity of p38 was observed 1 to 6 h after bacterial inoculation. Activity continued at a lower level for at least 7 days. The effects of p38 activation were assessed using an in vitro model of rat middle ear mucosal hyperplasia in which mucosal growth is stimulated by nontypeable Haemophilus influenzae during acute otitis media. Hyperplastic mucosal explants treated with the p38␣ and p38␤ inhibitor SB203580 demonstrated significant inhibition of otitis media-stimulated mucosal growth. The results of this study suggest that intracellular signaling via p38 MAPK influences the hyperplastic response of the middle ear mucosa during bacterial otitis media.Pathologic conditions related to otitis media include middle ear effusion, adhesive otitis, tympanic membrane perforation, tympanosclerosis, scarring of the middle ear mucosa, cholesteatoma, and atelectasis (4,24,37,38,43,46). These sequelae can lead to permanent damage of the middle ear cavity, resulting in hearing loss or impairment (1). A contributing factor to such morbidity during otitis media is the transformation of the inflamed middle ear mucosa. Normally, the middle ear mucosa consists of a simple squamous epithelium overlying a thin lamina propria that adheres to the underlying periosteum (21). This minimal mucosa ranges from 15 to 20 m thick. During otitis media the middle ear mucosa has the unique capacity to grow and proliferate to many times its original thickness, into a highly structured, pseudostratified, columnar epithelial complex (23,25,33,42). Hyperplasia of the mucosa is associated with many of the negative sequelae of middle ear infection. Production of mucus and other elements of middle ear effusions is closely linked to the production of additional mucosal cells and their transformation into a secretory phenotype (33,51

The middle ear response to otitis media includes transformation and hyperplasia of the mucosal epithelium and subepithelial connective tissue. Significant neovascularization is also noted, which occurs both to support the hypertrophied mucosa and to mediate the increased trafficking of leukocytes. We investigated the role of two known potent angiogenic growth factor families, the fibroblast growth factors (FGFs) and vascular endothelial growth factors (VEGFs), in middle ear mucosal angiogenesis. DNA microarrays were used to evaluate the expression of FGFs and VEGFs, as well as their receptors and unique signaling proteins, in the middle ears of mice undergoing a complete course of acute bacterial otitis media. In addition, a member of each family was introduced to the middle ear submucosal compartment of the normal middle ears of guinea pigs, by a continuous-release osmotic minipump system over 1 week. During the course of bacterial otitis media, a significant regulation of a number of genes important for angiogenesis was identified. Histologic evaluation of middle ear mucosa following micropump infusion of both FGF1 and VEGF-A showed significant angiogenesis at the site of infusion in comparison to control saline infusion. These results support a role for FGFs and VEGFs in the neovascularization of the middle ear mucosa during otitis media, and offer a potential avenue for therapeutic intervention.