Feasibility of Preoperative Video Head Impulse Test to Predict the Nerve of Origin in Patients with Vestibular Schwannomas.

Vestibular schwannoma (VS) originates from Schwann cells in the superior or inferior vestibular nerve. Identifying the precise origin will help in determining the optimal surgical approach. We retrospectively analyzed the preoperative vestibular function test according to VS origin to determine whether the test is a valuable indicator of tumor origin. Forty-seven patients with VS (male:female = 18:29, mean age: 54.06 ± 13.50 years) underwent the cochleovestibular function test (pure-tone audiometry, caloric test, video head impulse test (vHIT), cervical and ocular vestibular-evoked myogenic potential, and posturography). All patients then underwent surgical removal of VS, and the schwannoma origin was confirmed. The tumor originated from the superior vestibular nerve (SVN group) in 21 patients, the inferior vestibular nerve (IVN group) in 26 patients, and an undetermined site in eight patients. The only value that differed significantly among the groups was the gain of the vestibular-ocular reflex (VOR) in the ipsilesional posterior canal (iPC) during the vHIT. Our results indicate that VOR gain in the iPC may be used to predict the nerve origin in patients with VS. Other cochleovestibular function tests have limited value to discriminate nerve origins, especially in cases of medium to large VS.

NLRP3 inflammasome activation in human vestibular schwannoma: Implications for tumor-induced hearing loss.

Vestibular schwannoma (VS) is the fourth most common intracranial tumor, arising from neoplastic Schwann cells of the vestibular nerve and often causing debilitating sensorineural hearing loss (SNHL) and tinnitus. Previous research suggests that the abnormal upregulation of inflammatory pathways plays a highly significant, though infrequently described role in VS pathobiology, and that VS-associated SNHL is due not only to mechanical compression of the auditory nerve but also to differences in the intrinsic biology of these tumors. We hypothesize that patients who present with poor hearing associated with VS experience a more robust inflammatory response to this tumor than VS patients who present with good hearing. To investigate this hypothesis, we conducted a comprehensive pathway analysis using gene expression data from the largest meta-analysis of vestibular schwannoma microarray data, comprising 80 tumors and 16 healthy peripheral nerves. We identified the NLRP3 inflammasome as a novel target worthy of further exploration in VS research and validated this finding at the gene and protein expression level in human VS tissue using qRT-PCR and immunohistochemistry. To date, NLRP3 inflammasome activation has not been reported in VS, and this finding may represent a new and potentially significant therapeutic avenue. Notably, after analysis of 30 VSs, we observe that overexpression of key components of the NLRP3 inflammasome is preferentially associated with tumors that produce increased hearing loss in VS patients. Therefore, therapeutic development for VS should include considerations for minimizing NLRP3-associated inflammation to best preserve hearing.

Terahertz otoscope and potential for diagnosing otitis media.

We designed and fabricated a novel terahertz (THz) otoscope to help physicians to diagnose otitis media (OM) with both THz diagnostics and conventional optical diagnostics. We verified the potential of this tool for diagnosing OM using mouse skin tissue and a human tympanic membrane samples prior to clinical application.

A case of sudden hearing loss during treatment with decitabine for chronic myelomonocytic leukemia.

Chronic myelomonocytic leukemia (CMML) was initially classified in the category of myelodysplastic syndrome (MDS), but it is now categorized by the 2001 World Health Organization (WHO) classification in a separate nosological group of MDS. Unlike chronic myeloid leukemia (CML), the bone marrow morphology in CMML demonstrates prominent dysplastic changes in at least two of the three myeloid lineages. A 73-year-old male patient was brought to division of hematology for evaluation of leukocytosis. He was diagnosed with CMML and treated with decitabine. The hearing impairment had arisen during the third cycle of decitabine. To our knowledge, this is the first case that idiopathic sudden hearing loss (SHL) occured in CMML patients during treatment with decitabine.