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BACKGROUND: This study aimed to clarify the quantitative threshold of intraoperative radiological parameters for suspecting posterior malposition of the oblique lumbar interbody fusion (OLIF) cage triggering contralateral radiculopathy. METHODS: We measured the sagittal center and axial rotation angle (ARA) of the cage using postoperative computed tomography (CT) in 130 patients (215 cages) who underwent OLIF. The location of the cage tip was determined from axial magnetic resonance imaging in selected cases based on CT simulations to assess whether the cage was in contact with the contralateral exiting nerve or whether the surgical instruments could contact the nerve during intradiscal maneuvers. RESULTS: The sagittal center of the cages was on average 41.5% from the anterior edge of the endplate (shown as AC/AP value: anterior end plate edge-cage center/anterior-posterior endplate edge ×100%), and posterior cage positioning ≥50% occurred in 14% of the cages. The ARA was -2.9°, and posterior oblique rotation of the cages ≥10° (ARA ≤ -10°) was observed in 13%. CT simulation showed that the cage tip could directly contact the contralateral nerve when the cage was placed deep in the posterior portion ≥50% of the AC/AP values with concomitant posterior axial rotation ≥10° (ARA ≤ -10°), or deep in an extremely rare portion ≥60% of the AC/AP values with posterior axial rotation ≥0° (ARA ≤ 0°). Six percent of the cages (13/215) were placed in these posterior oblique areas (potential contact area: PCA). Three cages in the PCA were in direct contact with the contralateral nerves, and 9 were placed deep just anterior to the nerves. Symptomatic contralateral radiculopathy occurred in 2 cages (2/13/215, 15.3%/0.9%). CONCLUSIONS: Two intraoperative radiological parameters (AC/AP and ARA) measurable during OLIF procedures may become practical indicators for suspecting cage malposition in PCA and may be available when determining whether to consider cage revision intraoperatively to a more ventral disc space or anteriorly from the opposite endplate edge.

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Giant cell tumor (GCT) is a benign neoplasm arising most commonly in the long bones. GCTs of the larynx (GCTL) are relatively rare, and only individual case reports are documented in the literature. Patients with such tumors may present with hoarseness and anterior neck swelling. We present a 59-year-old man with hoarseness and enlarging anterior neck mass for 3 months. A fiberscopy revealed a submucosal swelling of the left subglottic trachea. Computed tomography and magnetic resonance imaging of the larynx demonstrated a large, well-defined, inhomogeneous enhancing mass at the left thyroid cartilage, which was obstructed entirely. The anterior neck mass was biopsied for histopathological analysis, which showed multinodularity with intervening vascularized connective tissues. The mass was made up of mononuclear cells and distributed multinucleated giant cells. The mitotic activity of the mononuclear cells was as high as 6 per 10 high-power fields. Pathologic consultation resulted in a diagnosis of giant cell tumor. The patient underwent total laryngectomy and, postoperatively, he did well without recurrence or metastasis for two and a half years.

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An extraskeletal chondroma is a rare benign cartilaginous tumor that develops in soft tissue. Histologically, it is a lobulated nodule surrounded by a fibrous capsule; the inside consists of mature hyaline cartilage containing a few normal chondrocytes. We present a rare case of extraskeletal chondroma in the preauricular region. A 43-year-old man presented with a 2-cm-diameter right preauricular tumor that had been developing for 1 year. Magnetic resonance imaging showed a solid lobulated tumor in the right preauricular region, which was proximate to the capsule of the right temporomandibular joint (TMJ). This was subsequently resected under general anesthesia. The tumor was not in contact with the TMJ capsule and had not invaded the surrounding tissue, facilitating en bloc excision. Histopathologically, the tumor comprised mainly of hyaline cartilage containing chondrocytes with chondrocytic lacunae and was diagnosed as a chondroma. The postoperative period was uneventful, and there was no evidence of recurrence at the 2-year followup. We describe the clinical characteristics of our case and review the literature, emphasizing the differential diagnosis.

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Noise, ototoxic substances and various genetic factors are common causes of profound hearing loss. Cochlear implants can often restore hearing in these cases, but only if a sufficient number of responsive auditory nerve fibers remain. Over time, these nerve fibers degenerate in the damaged ear, and it is therefore important to establish factors that control neuronal survival and maintain neural excitability. Recent studies show that neuregulins and their receptors are important for survival and proper targeting of neurons in the developing inner ear. A role for neuregulins as maintainers of the neuronal population in the mature inner ear was therefore hypothesized. Here, this hypothesis was directly tested by chronic local application of substances that block neuregulin receptors. Using auditory brainstem response measurements, we demonstrate that such receptor block leads to a progressive hearing impairment that develops over the course of weeks. This impairment occurs despite a normal number of auditory neurons and preserved outer hair cell function. Real-time quantitative reverse transcriptase-polymerase chain reaction shows alterations in neurotrophin-3 expression, suggesting that this growth factor participates in regulating cochlear sensitivity. The present work demonstrates the critical importance of neuregulin/erbB signaling in long-term functional regulation in the mature guinea pig hearing organ.

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The effects on distortion product otoacoustic emissions (DPOAEs) during the late phase of ischemia/reperfusion injury in the cochlea were studied. Ischemia/reperfusion injury was induced in a gerbil model by occluding both vertebral arteries for 15min. Hearing was assessed by recording compound action potentials (CAPs) before, during, and 7 days after ischemia. The histological changes in the hair cells were evaluated in specimens stained with rhodamine-phalloidin and Hoechst 33342. The average increase in CAP threshold 7 days after ischemia was 16.3+/-8.0dB at 8kHz. In contrast, interruption of the blood supply to the cochlea decreased the DPOAE amplitudes to the noise floor; this usually recovered to the same level as that seen under pre-ischemic conditions 7 days after ischemia. Histologically, the mean respective losses of inner and outer hair cells (IHCs and OHCs, respectively) of the inner ear were 26.5% and 3.3% in the basal turn, respectively. These results indicate that in gerbils OHCs are tolerant to ischemia/reperfusion injury pathologically and physiologically because DPOAE is closely related to the active process of OHCs and is a useful test to examine OHC function.

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PURPOSE: Acoustic neuroma tumor size may be evaluated using several methods. Here we investigate the variations among measuring techniques. MATERIALS AND METHODS: A retrospective analysis of pre- and posttreatment magnetic resonance (MR) scans was performed on 15 acoustic neuroma patients with a history of stereotactic radiosurgery who had been followed for more than 2 years. Tumor size was measured on each MR scan using three methods, where the extracanalicular (EX) and intracanalicular (IN) portions were measured separately. We collected data on the largest diameter (M1), the square root of the product of the maximum anteroposterior and mediolateral diameter (M2), and the average for the maximum anteroposterior, mediolateral, and superoinferior diameters (M3). Size differences between follow-up MR scans separated by more than 2 years were calculated for each method, and we evaluated whether the tumors progressed, remained stable, or regressed. RESULTS: A total of 154 follow-up pairs of EX and 115 follow-up pairs of IN showed a statistically significant difference for the number of each category among the three methods (P = 0.03, P < 0.01, respectively). The greatest category agreement was observed between the M2 and M3 methods. CONCLUSION: A significant difference between the tumor size measuring methods was observed. To strengthen specificity when evaluating tumor size difference, a measuring method using two or more parameters is recommended.

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We conducted a retrospective study to identify the clinical features and surgical observations of congenital cholesteatoma. Sixty patients were diagnosed and underwent surgery for congenital cholesteatoma between April 1987 and May 2002. All diagnoses were made on the basis of two operative findings: 1. the tympanic membrane manifested neither retraction, perforation, nor granulation. 2. the tympanic membrane was not continuous with the cholesteatoma. In this series, congenital cholesteatoma accounted for 7% of all cholesteatomas (853 ears). The patient age ranged from 2 to 48 years. The male to female ratio was 4:1. Seventeen patients had multiple cholesteatoma. Fifty-three patients exhibited closed-type cholesteatomas, while the remaining 7 patients had open-type cholesteatomas that had formed as a flat surface of the epidermis. Patients with open-type cholesteatomas presented with a much more pronounced conductive hearing loss and ossicular erosion or malformation. Twenty-two patients with relatively small cholesteatomas were analyzed to estimate the origin of their cholesteatomas. Of the 22 patients, 13 had anterior superior quadrant (ASQ-type) and 9 had posterior superior quadrant (PSQ-type) cholesteatomas. The mean age at the time of detection was older in the PSQ-type group than in the ASQ-type group and the frequency of ossicular erosion or malformation was more prominent in the PSQ-type group than in the ASQ-type group. The primary site of origin was thought to be the portion between the tympanic ostium of the auditory canal and the semicanal for tensor tympani in the ASQ-type group and near the incudostapedial joint in the PSQ-type group. A planned staged procedure was performed in 29 patients, 15 patients (52%) had residual lesions situated mostly on the oval window, the round window, an exposed facial nerve or an exposed lateral semicircular canal. The frequency of residual lesions in patients who presented with extended, multiple cholesteatoma and those with ossicular malformation was comparable to the frequency of patients who did not present with these features.

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To elucidate whether ischemia-reperfusion can cause delayed cell death in the cochlea, the effects of transient cochlear ischemia on hearing and on neuronal structures in the cochlea were studied in Mongolian gerbils. Ischemia was induced by bilaterally occluding the vertebral arteries for 5 minutes in gerbils, which lack posterior cerebral communicating arteries. In gerbils, the labyrinthine arteries are fed solely by the vertebral arteries. Occlusion of the vertebral arteries caused a remarkable increase in the threshold of compound action potentials (CAPs), which recovered over the following day. However, 7 days after the onset of reperfusion, the threshold began to increase again. Morphologic changes in the hair cell stereocilia were revealed by electron microscopy. The number of nuclear collapses was counted in cells stained for DNA and F-actin to evaluate the degree of cell death in the organ of Corti. Changes in spiral ganglion cell (SGC) neuron number were detected, whether or not progressive neuronal death occurred in the SGC. These studies showed that sporadic fusion of hair cells and the disappearance of hair cell stereocilia did not begin until 4 days after ischemia. On subsequent days, the loss of hair cells, especially inner hair cells (IHCs), and the degeneration of SGC neurons became apparent. Ten days after ischemia, the mean percentage cell loss of IHCs was 6.4% in the basal turn, 6.4% in the second turn, and 0.8% in the apical turn, respectively, and the number of SGC neurons had decreased to 89% of preischemic status. These results indicate that transient ischemia causes delayed hearing loss and cell death in the cochlea by day 7 after ischemia.

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The mechanisms of cochlear hair cell death following exposure to transient inner ear ischemia were investigated in gerbils histologically. The animals were subjected to ischemic insult by occluding both vertebral arteries for 15 min. Hoechst 33342 nuclear staining showed that inner hair cells (IHCs) underwent sporadic degeneration via nuclear condensation, which peaked 12 hours after the ischemia. Furthermore, nuclear DNA fragmentation was noted by the terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP)-biotin nick end labeling method. Transmission electron microscopy revealed morphological changes in the IHCs characteristic of apoptosis, including karyopyknosis, chromatin condensation. These findings suggest that apoptotic cell death is the major process in hair cell degeneration in this animal model.

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