A Case of Varicella-Zoster Meningoencephalitis Presented by Ramsay Hunt Syndrome.

Varicella-zoster virus (VZV) reactivation can cause meningoencephalitis. Ramsay Hunt syndrome is the reactivation of VZV in facial nerve, consisting of ear pain, facial nerve paralysis, and auricular rash. We present a case of VZV meningoencephalitis presented with Ramsay Hunt syndrome. Early clinical suspicion was beneficial in starting aggressive treatment.

Preoperative computed tomography may fail to detect patients at risk for perilymph gusher.

Perilymph gusher (PG) is a very rare occurrence that can lead to an adverse outcome during inner ear surgery. In the absence of a family history of X-linked mixed deafness syndrome, surgeons may have difficulty determining if a patient is at risk preoperatively. Radiographic imaging is often performed in an attempt to identify such a possibility, but there are few data to support the value of negative studies. We conducted a retrospective study of 3 cases of PG in which findings on preoperative high-resolution computed tomography (CT) of the temporal bone had been interpreted as normal. We reviewed these CTs to discern if they did in fact demonstrate any abnormalities that might have indicated a risk of PG, and we found that the original radiologist had missed a dilated internal auditory canal and a deformity of the cochlear modiolus in the affected ear of 1 of these patients. No abnormality was detected on review of the CTs of the other 2 patients. Therefore, we conclude that negative CT findings do not necessarily rule out a risk of PG.

Tympanic membrane metalloproteinase inflammatory response.

OBJECTIVE: The goal of this study was to determine whether expression of matrix metalloproteinases (MMP) in tympanic membranes (TM) is stimulated by host tumor necrosis factor-alpha (TNF-alpha) and bacterial toxin (lipopolysaccharide, LPS), which may play a role in the pathogenesis of cholesteatoma. STUDY DESIGN: Gerbil TMs (n = 48) were cultured in the presence of either TNF-alpha or LPS. Quantitative analysis of TNF-alpha and MMPs was performed on both the homogenized TMs and the culture media supernatant. RESULTS: Levels of TNF-alpha and MMPs did not increase significantly in TMs with exposure to inflammatory mediators. TNF-alpha levels in supernatant were elevated (P < 0.007) with more concentrated LPS exposure. Supernatant levels of MMP2 were increased (P < 0.007) at most concentrations of LPS and TNF-alpha. CONCLUSION: Cultured TMs expressed MMPs in response to bacterial and host inflammatory mediators. These findings support a link between inflammation and the secretion of potentially destructive MMPs in the TM, which may contribute to the pathogenesis of cholesteatoma.

Matrix metalloproteinases in a gerbil cholesteatoma model.

OBJECTIVE: The goal of this study was to determine whether expression of matrix metalloproteinases (MMP) and tumor necrosis factor-alpha (TNF-alpha) occurs in a gerbil cholesteatoma model, which may be involved early in the pathogenesis of cholesteatoma. Study design Atelectasis was induced by transpalatal, bilateral Eustachian tube obstruction on gerbil ears (n = 60). Tympanic membranes were removed at days 0, 3, 7, 14, 28, 56, and 84, and quantitative analysis of TNF-alpha and MMPs was performed. RESULTS: Atelectasis and middle ear inflammation increased with time. TNF-alpha and MMP levels increased (P < 0.0083) with time, inflammation, and atelectatic stage with some variability seen between different MMPs. CONCLUSION: Elevation of TNF-alpha and MMPs associated with progressive tympanic membrane atelectasis suggests a possible role for these inflammatory mediators in the pathogenesis of cholesteatoma.

Inhibition of matrix metalloproteinases in gerbil cholesteatoma: preliminary findings.

OBJECTIVES: This study was conducted to examine the role of matrix metalloproteinases (MMPs) and the impact of a topical MMP inhibitor, ilomostat, on the development of tympanic membrane (TM) atelectasis in the gerbil model. METHODS: Eustachian tubes were cauterized bilaterally in 19 gerbils. Thereafter, both TMs received once-daily topical treatment for 8 weeks with ilomostat or vehicle or no treatment (n = 6 or 7 per group). TM atelectasis was serially graded, and TMs were harvested at 8 weeks. Gelatin zymograms were performed to determine MMP activity. RESULTS: The mean activity levels of proenzyme and active MMP-9 and MMP-2 and degree of atelectasis did not differ between groups. TM atelectasis did not correlate to levels of enzymes across individual samples. CONCLUSIONS: Topical application of an MMP inhibitor did not significantly prevent the development of TM atelectasis. It remains to be determined whether the use of MMP inhibitors may prevent the progression of atelectasis in humans.