Intracranial infection caused by minor skin contusion associated with previous craniotomy.

Minor damage to the scalp may lead to intracranial infection. Moreover, the postoperative state of the scalp, skull and meninges is especially noteworthy with respect to invasion of pathogens into the skull. Therefore, a detailed medical history should be obtained from patients with even minor scalp injuries to avoid intracranial infection. We herein report a case of intracranial infection caused by a minor scalp injury associated with previous craniotomy, which was missed at first.

The non-steroidal anti-inflammatory drugs protect mouse cochlea against acoustic injury.

Acoustic injury is a common cause of hearing loss for people in industrial societies. Cyclooxygenase (COX) and lipoxygenase (LOX) are two important enzymes involved in arachidonic acid metabolism. Two COX isozymes are characterized, COX-1 and COX-2, that differ in terms of regulatory mechanisms of expression. Although COX-1, COX-2, and LOX are expressed in cochlea, their roles played in cochlear acoustic injury have not fully been evaluated. Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit either COX or LOX, or both. This study evaluated the effects of NSAIDs on the functional recovery of the cochlea after acoustic injury. Mice were exposed to a 4-kHz pure tone of 128 dB SPL (sound pressure level) for 4 hours and received one of the following drugs for two weeks after acoustic overexposure: indomethacin (COX-1 inhibitor), meloxicam, SC58125, and CAY10404 (COX-2 inhibitors), and nordihydroguaiaretic acid (LOX inhibitor). The hearing ability was evaluated using an auditory brainstem response (ABR) before and after overexposure. The ABR threshold shifts, defined as subtraction between ABR thresholds before and after overexposure, were compared among the control and the medication groups at one and two weeks after acoustic overexposure. Treatment of mice with either indomethacin or nordihydroguaiaretic acid decreased the ABR threshold shifts after overexposure, indicating that COX-1 and LOX inhibitors exhibited protective effects against acoustic injury. In contrast, COX-2 inhibitors, meloxicam, SC58125, and CAY10404, showed no noticeable effects on the ABR threshold shifts. These findings suggest that COX-1 and LOX are involved in the pathogenesis of acoustic injury in cochlea.

Epiglottic cyst in an infant.

Epiglottic cyst is a rare cause of stridor and respiratory distress in newborns and infants. A 2-year-old girl was referred to our department for the treatment of an epiglottic cyst causing inspiratory stridor. Flexible fiberoptic laryngoscopy and a computed tomography (CT) scan revealed a cystic lesion on the lingual surface of the epiglottis. Frequent episodes of sleep apnea accompanied by desaturation had been observed during her sleep. Endoscopic deroofing was performed under general anesthesia. After the operation, stridor and sleep apnea disappeared.

The importance of postoperative radiotherapy against polymorphous low-grade adenocarcinoma of the parotid gland: case report and review of the literature.

Polymorphous low-grade adenocarcinoma (PLGA) of the salivary gland is a disease entity that is a recently described form of adenocarcinoma. PLGA most commonly arises in the minor salivary glands. We report two cases of PLGA of the parotid gland. Case 1: A 52-year-old female visited the University of Tsukuba Hospital with a painless mass in the left parotid region. A superficial parotidectomy and postoperative radiotherapy were performed. The patient has been free from disease for 50 months. Case 2: A 55-year-old female initially noticed a painless slowly growing mass in the left parotid region. The tumor was removed with a superficial parotidectomy. The local recurrence was found 6 years after the initial surgery. The recurrent tumor was removed, and radiotherapy was administered thereafter. The patient has been free from the disease for 33 months since the last treatment. The treatment for the primary lesion is crucial for the prognosis since metastasis to the regional lymph node or to distant region is unusual in PLGA. Although surgical extirpation is the recommended modality for treatment of PLGA, wide resection with a safety margin is often difficult in the parotid gland because of the presence of the facial nerve. Our two cases were successfully treated with surgery and postoperative radiotherapy. Although our literature search revealed 32 previously reported cases of PLGA of the parotid gland, only five of the 32 cases were treated postoperative radiotherapy. We highlight the importance of postoperative radiotherapy for PLGA of the parotid gland.

Successful treatment of eosinophilic otitis media using ramatroban: report of two cases.

OBJECTIVE: The pathogenesis of eosinophilic otitis media is not yet fully understood. The purpose of this paper is to describe the clinical course of our two patients with eosinophilic otitis media and to discuss the pathogenesis and treatment of this intractable condition. METHODS: Two cases of eosinophilic otitis media were treated with ramatroban. RESULTS: The middle ear effusion has been well controlled in both patients for more than 1 year with minimal corticosteroid therapy. CONCLUSIONS: Our experience suggests that the pathogenesis of eosinophilic otitis media is related to the pharmaceutical effects of ramatroban, i.e., inhibition of the thromboxane A2 receptor (TP) and the chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2).

Dehydroepiandrosterone sulfate reduces acoustic injury of the guinea-pig cochlea.

The present study was performed to determine effects of dehydroepiandrosterone sulfate (DHEAS), a neurosteroid, on acoustic injury. Albino guinea pigs were exposed to a 2 kHz pure tone of 120 or 125 dB sound pressure level for 10 min immediately after intravenous administration of DHEAS. Statistically significant improvement in the compound action potential threshold shifts and in amplitude reduction of distortion-product otoacoustic emissions was observed 1 week after the acoustic overexposure in the animals treated with DHEAS. The present results suggest that DHEAS has a protective effect against acoustic injury of the cochlea.

Involvement of poly(ADP-ribose) synthetase in acoustic trauma of the cochlea.

We investigated effects of poly(ADP-ribose) synthetase (PARS) inhibitors on acoustic trauma. Albino guinea pigs were intravenously given 3-aminobenzamide, nicotinamide or 3-aminobenzoic acid (an inactive analog of 3-aminobenzamide) just prior to exposure to a 2 kHz pure tone of 120 dB sound pressure level (SPL) for 10 minutes. The threshold of the compound action potential (CAP) and the amplitude of distortion-product otoacoustic emissions (DPOAEs) were measured before and 4 hours after the acoustic overexposure. Statistically significant decreases in the CAP threshold shifts and significant increases in the DPOAE amplitudes were observed 4 hours after the acoustic overexposure in the animals treated with 3-aminobenzamide or nicotinamide, whereas 3-aminobenzoic acid did not exert any protective effect. These results strongly suggest that excessive activation of PARS is involved in generation of the acoustic trauma.

Determination of prednisolone in the cochlear tissue.

Although glucocorticoids are widely used to treat inner ear diseases, glucocorticoid concentration has never been determined in the cochlear tissue. The aim of the present study was to measure the prednisolone concentration in the cochlear tissue after intravenous administration. At 0.5, 1, 2, 4 or 8 h after the injection (100 mg/kg), cochlea, hepatic and brain tissue and serum were removed, and prednisolone extracted from these samples was measured using high-performance liquid chromatography. Although prednisolone was not detected in the brain tissue, it was detected in the hepatic tissue and serum, demonstrating the peak value at 30 min after administration and a rather rapid decline with time thereafter. Prednisolone was also detected in the cochlear tissue, but the uptake and elimination patterns were entirely different from other samples. The prednisolone level in the cochlea reached the peak value 1 h after administration and gradually declined. The present study shows that the prednisolone administered is gradually transported to the cochlear tissue from blood and remains at higher concentrations than in the hepatic tissue or serum over several hours. It is highly likely that this slow elimination is closely related to the therapeutic effect of steroids in inner ear diseases.