Futoshi Watanabe

Hearing loss and glutamate efflux in the perilymph following transient hindbrain ischemia in gerbils

The mechanism underlying ischemia‐induced hearing loss was studied in gerbils with transient hindbrain ischemia. Occlusion of the vertebral arteries caused an increase in the concentration of glutamate in the perilymph and elevated the compound action potential (CAP) threshold to 24.6 dB at 5 minutes. the CAP threshold subsequently recovered on reperfusion, gradually reaching 8.3 dB 120 minutes after reperfusion. Under electron microscopy, afferent dendrites of the cochlear nerve in contact with inner hair cells exhibited abnormal swelling 5 minutes after ischemia/reperfusion. These morphological changes were not observed in cochleas treated with an alpha‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole propionic acid (AMPA)/kainate‐type glutamate receptor antagonist, 6‐7‐dinitroquinoxaline‐2,3‐dione (DNQX), before hindbrain ischemia; an N‐methyl‐D‐aspartate (NMDA)‐type receptor antagonist, D‐2‐amino‐5‐phosphonopentanoate (D‐AP5), was ineffective. Moreover, the histopathological alterations noted 5 minutes after reperfusion were spontaneously ameliorated 120 minutes after ischemia/reperfusion. These findings suggest that the ischemia‐induced increase in extracellular glutamate concentration with subsequent activation of AMPA/kainate receptors is responsible for neurite degeneration and hearing loss in the early stages following transient hindbrain ischemia. J. Comp. Neurol. 418:217–226, 2000.

Transient cochlear ischemia causes delayed cell death in the organ of Corti: An experimental study in gerbils

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. J. Comp. Neurol. 456:105–111, 2003.

Hypothermia prevents hearing loss and progressive hair cell loss after transient cochlear ischemia in gerbils

The effects of hypothermia on ischemia-reperfusion injury of the cochlea were studied in gerbils. Hearing was assessed by sequentially recording compound action potentials before, during and after the ischemia. The degree of hair cell loss in the organ of Corti was evaluated in specimens stained with rhodamine-phalloidin and the dye Hoechst 33342. Ischemic insult was applied to the animals by occluding the bilateral vertebral arteries for 15 min under normothermic or hypothermic (rectal temperature 32 degrees C) conditions. Interruption of the blood supply to the cochlea caused a tremendous increase in the compound action potential threshold, which usually recovered to some extent with reperfusion. In the ischemia/normothermic group, the threshold did not return to the pre-ischemic level. The average increase in the threshold seven days after ischemia was 20.0 dB. Histologically, the hair cell loss increased gradually until four days after the ischemic insult. On the seventh day, the mean loss of inner and outer hair cells at the basal turn was 31.1 % and 2.4 %, respectively. In the ischemia/hypothermic group, the threshold returned to the pre-ischemic level within 30 min after reperfusion and remained stable thereafter. The mean loss of inner and outer hair cells on the seventh day was 0.1 % and 0.2 %, respectively. These results indicate that hypothermia can prevent inner ear damage, which otherwise occurs after transient ischemia of the cochlea.

Hypothermia reduces glutamate efflux in perilymph following transient cochlear ischemia.

The effect of hypothermia on ischemic injury of the cochlea in gerbils was studied with particular regard to glutamate efflux in the perilymph. Under normothermic conditions interruption of the blood supply to the cochlea for 15 min caused a remarkable elevation of the compound action potential (CAP) threshold, and an increase in perilymphatic glutamate. The CAP threshold recovered to some extent with reperfusion, but not to preischemic levels. CAP thresholds, under hypothermic condi- tions and with reperfusion, recovered promptly to near pre-ischemic levels, while glutamate concentration did not change. These results, together with electron microscopy studies, suggest that hypothermia prevents hearing loss primarily through reduction of glutamate efflux at the synopses between inner hair cells and primary afferent auditory neurons.

Extraskeletal Chondroma of the Preauricular Region: A Case Report and Literature Review

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.

Laryngeal Giant Cell Tumor: A Case Report and Review of the Literature

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.

Measurement of DPOAE after ischemia/reperfusion injury of the cochlea in gerbils

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.

A Case of Child Abuse Manifesting Foreign Bodies in External Auditory Canals

A case is presented of an infant who presented with foreign bodies in bilateral external auditory canals. Battered child syndrome was defined in 1962 by Kempe et al. as nonaccidental attack or injury repeatedly inflicted upon children by persons caring for them. Otolaryngologists are rarely in a position to diagnose and initiate management of child abuse presenting as injury to the head and neck area. The number of reported cases of child abuse has increased dramatically over the past several years and it is likely that physicians will examine such cases and be unaware of the fact that the child is being abused.

A Case of Postoperative Ossicular Fixation Caused by Bone Pate.

We report a case of ossicular fixation caused by bone pâte. A 57-year-old woman underwent staged tympanoplasty for right middle ear cholesteatoma. Bone pat6 was used for reconstruction of the scutum and for the prevention of the extrusion of an artificial ossicle at the second-stage operation. Although right hearing initially improved postoperatively, it gradually deteriorated 4 months after the operation. Revision surgery performed 1 year after the second-stage operation showed that the bone pâte used for scutumplasty had been incorporated with that used for eardrum augmentation, which resulted in ossicular fixation. After the removal of the part of the bone pat6 that was fixed to the artiflcial ossicle, both the mobility of the ossicle and right hearing markedly improved.

Effects of Hypothermia on Prevention of Hearing Loss Produced by Transient Cochlear Ischemia in Gerbils.

Using gerbils, the effects of hypothermia on ischemia-reperfusion injury of the cochlea were studied. Under normothermic or hypothermic (rectal temperature 32°C) conditions, cochlear ischemia was created by occluding the bilateral vertebral arteries for 15 minutes in gerbils, which lack the posterior cerebral communicating arteries since the labyrinthine arteries are nourished solely by the vertebral arteries. Hearing was evaluated by recording cochlear compound action potentials (CAPS) following the ischemia. Occlusion of the arteries caused a marked increase in the CAP threshold, which usually recovered to some extent with reperfusion. In the ischemia-normothermic group, the CAP threshold did not return to the pre-ischemic level. The mean increase in the threshold 7 days after ischemia was 16.3dB. In the ischemia-hypothermic group, the CAP threshold returned to the pre-ischemic level within 30 minutes after reperfusion, and remained stable thereafter. Histologically, the degree of hair cell death in the organ of Corti was evaluated by F-actin and DNA staining methods. In the ischemia-normothermic group, the hair cell loss increased gradually until 4 days after the ischemic insult. On the 7th day, the mean loss of inner and outer hair cells (IHCs and OHCs) at the basal turn was 26.4% and 2.9%, respectively. On the other hand, the mean losses of the IHCs and OHCs after the ischemia were less than 0.3% in the ischemia-hypothermic group. These findings suggest that hypothermia completely prevented the hearing loss caused by ischemia-reperfusion injury of the cochlea.