A Case of Carcinoid Tumors in the Ear Canal With Long-Term Postoperative Follow-Up.

Carcinoid tumors in the ear canal are very rare. In this report, we experienced a case of carcinoid tumor of the ear canal that underwent total tumor resection. This study included a 39-year-old man presented with a chief complaint of right-sided hearing loss. Computed tomography scan showed a shadow from the ear canal to the right tympanic chamber. There were no suspicious findings of metastasis in the cervical lymph nodes or other organs. At the time of surgery, the tumor was simply removed because it was small and there was no adhesive invasion. Postoperatively, the patient has been under observation for 11.5 years without any recurrence. Carcinoid tumors in the ear canal can rarely metastasize or recur after more than 10 years. It is important to follow up with the patient for a long time after surgery, using the Ki-67 index of the removed tissue as a prognostic reference.

[Eight Cases of Small Cell Neuroendocrine Carcinoma of the Head and Neck].

Small cell neuroendocrine carcinoma of the head and neck is a rarely occurring poorly differentiated and high-grade malignant neoplasm characterized by highly active proliferation of neuroendocrine tumor cells. There are no established therapies for this disease. To clarify the clinical course and develop effective treatment(s) for the carcinoma, we reviewed the data of 8 patients of small cell neuroendocrine carcinoma of the head and neck treated by us between 2006 and 2014 at the Department of Otolaryngology, Gifu University School of Medicine and our affiliated hospitals. The patients consisted of 3 men and 5 women, ranging in age from 38 to 84 years old (mean : 60.9 years). The tumor arose from the nasal cavity or the paranasal sinuses in 3 cases, from the parotid grand in 2 cases, from the oropharynx in 2 cases, and from the hypopharynx in 1 case. The tumor that arose from the hypopharynx was a combined small-cell carcinoma with squamous cell carcinomas, and the one that arose from the oropharynx had already metastasized to the brain. Most of the patients were treated by chemotherapy and radiotherapy based on the treatment employed for small cell carcinoma of the lung. Only the patient in whom the tumor arose from a paranasal sinus was treated by surgery despite the definitive diagnosis of small cell carcinoma. We selected CPT-11 and a platinum agent for 4 patients, and VP-16 and a platinum agent for 3 patients as the first-line chemotherapy. Although two patients showed carcinoma-free survival, one died of recurrence of the regional lymph node metastases and five died of distant metastases despite the absence of locoregional recurrence. The 5-year survival rate was a dismal 25%, suggesting that we need to establish effective treatment(s) for the control of distant metastases in cases of the small cell neuroendocrine carcinoma of the head and neck.

Treatment for Progressive Hearing Loss Due to Paget's Disease of Bone - A Case Report and Literature Review.

Paget's disease is a common bone remodeling disorder that typically begins with excessive bone resorption in the elderly. Bilateral progressive hearing loss is the most frequently encountered complication of Paget's disease. The types of hearing loss identified by audiometry are conductive, sensorineural, or both. However, the precise mechanism of hearing loss remains unclear, and the treatment has been controversial. We present a 73-year-old man who suffered from bilateral progressive hearing loss due to Paget's disease. Potent bisphosphonates, oral risedronate in daily adjusted dosages for 6 months, did not decrease or suppress the worsening of the hearing loss. The Nucleus CI24 Contour electrode array was successfully inserted on the left side without surgical and postoperative complications. The Japanese open set monosyllable word recognition test in a sound field at 65 dB had a result of 74%. This cochlear implantation can be an indication for cases of profound hearing loss due to Paget's disease.

Efficacy and toxicity of concurrent chemoradiotherapy with nedaplatin and S-1 for head and neck cancer.

OBJECTIVE: We investigated the efficacy and toxicity of concurrent chemoradiotherapy with nedaplatin and S-1 for head and neck cancer, as an alternative to cisplatin and 5-fluorouracil. METHODS: A total of 31 patients were enrolled in this study. S-1 was administered orally twice a day for 14 days followed by a 2-week rest. Nedaplatin was intravenously administered on day 4. If possible, two courses of chemotherapy were performed. The radiotherapy was started concurrently with the administration of S-1. RESULTS: The overall complete response rate was 81%. The 2-year overall survival rate was 96%. The 2-year relapse-free survival rate was 94%. The main adverse events were hematological toxicity, mucositis and dermatitis. CONCLUSIONS: Our findings suggest that this therapeutic regimen has either an equal or lower toxicity than the conventional cisplatin and 5-fluorouracil, and that it has equal efficacy with regard to the clinical response and short-term outcome. Moreover, it is possible to successfully perform this treatment in an outpatient setting.

Ruptured pseudoaneurysm of the petrous internal carotid artery caused by chronic otitis media.

A 60-year-old man presented with a rare case of pseudoaneurysm in the petrous internal carotid artery (ICA) caused by chronic otitis media manifesting as right otorrhagia after the earpick procedure. Computed tomography showed the destroyed petrous bone; the ICA and the aneurysm, which were exposed to the right middle ear; and a massive hematoma in the right middle ear. Right carotid angiography revealed a pseudoaneurysm arising from the ICA coursing through the middle ear. Two weeks later, the right ICA was trapped after external carotid artery-middle cerebral artery bypass surgery using a vein graft. A biopsy specimen was obtained from the middle ear and the histological diagnosis was inflammatory disease. Pseudoaneurysm often causes sudden massive aural bleeding. The appropriate management strategy may be exclusion of the pseudoaneurysm with revascularization to avoid leaving foreign material in the infected middle ear.

Comparative effects of ultra-short-acting beta1-blockers on voltage-gated tetrodotoxin-resistant Na+ channels in rat sensory neurons.

BACKGROUND AND OBJECTIVE: To examine a possible mechanism for their antinociceptive actions, we compared the effects of two clinically used ultra-short-acting beta1-blockers, landiolol and esmolol, on tetrodotoxin-resistant sodium (TTX-r Na) channels in rat dorsal root ganglion neurons, which are important for nociception. METHODS: In small (<30 microm) dorsal root ganglion neurons from Sprague-Dawley rats, recordings of whole-cell membrane currents were made using the patch-clamp technique. To examine the effects of landiolol and esmolol on TTX-r Na currents, whole-cell membrane Na currents were evoked every 10 s by stepping for 50 ms from a holding potential of -70 to -10 mV. Each drug was applied at stepwise-increased concentrations every 2 min. The voltage dependence of the steady-state inactivation of the TTX-r Na current was investigated by using a conventional double-pulse protocol. To test for use-dependent blockade of TTX-r Na channels by beta-blockers, trains of depolarizing pulses (to -10 from a holding potential of -70 mV) were applied at one of three frequencies (0.2, 5 or 20 Hz) in the absence or presence of drug (landiolol 8 mmol l, esmolol 140 micromol l). RESULTS: Esmolol blocked TTX-r Na currents in a dose-dependent and use-dependent manner, but a very high concentration of landiolol was required to block TTX-r Na channel activities. The half-maximal inhibitory concentrations (IC50) for the TTX-r Na current were (holding potential, -70 mV) landiolol 7.66 +/- 0.62 mmol l (n = 6) and esmolol 145 +/- 7.5 micromol l (n = 6), and the Hill coefficients were landiolol 1.06 +/- 0.09 (n = 6) and esmolol 0.96 +/- 0.05 (n = 6). CONCLUSION: Esmolol, but not landiolol, may have useful effects against pain related to TTX-r Na channel activity.

Intrathecal neostigmine prevents intrathecal clonidine from attenuating hypercapnic cerebral vasodilation in rabbits.

We previously demonstrated that lumbar intrathecal alpha(2) agonists attenuate hypercapnia-induced cerebral vasodilation. The combination of intrathecal clonidine and neostigmine is being investigated as pain therapy. The effects of their combination on cerebrovascular reactivity are unknown. We allocated rabbits anesthetized with pentobarbital to two groups: (a) clonidine (normal saline followed 30 min later by clonidine 2 microg/kg, both into the lumbar intrathecal space; n = 6), and (b) neostigmine-pretreatment (neostigmine 2 microg/kg followed 30 min later by clonidine 2 microg/kg, both into the lumbar intrathecal space; n = 6). We then evaluated the hypercapnia-induced changes in pial arteriolar diameter in these two groups using the closed cranial window preparation. The pial arteriolar dilator response to hypercapnia was significantly attenuated in the clonidine group (14% +/- 4%, 4% +/- 4%, 6% +/- 6%, and 5% +/- 7% for before and 30, 60, and 90 min, respectively). Neither normal saline nor neostigmine alone induced any change in the cerebral reactivity to hypercapnia. Pretreatment with neostigmine completely prevented the clonidine-induced attenuation of the hypercapnic cerebral vasodilation attenuated by intrathecal clonidine (16% +/- 7%, 15% +/- 6%, 12% +/- 6%, and 16% +/- 8%, respectively).

The effects of class Ic antiarrhythmics on tetrodotoxin-resistant Na+ currents in rat sensory neurons.

IV or oral administration of antiarrhythmics has been reported to be effective for relieving neuropathic pain. Recent reports have indicated that tetrodotoxin-resistant (TTX-R) Na(+) channels play important roles in the nerve conduction of nociceptive sensation. In the present study, we investigated the effects of flecainide, pilsicainide (class Ic antiarrhythmics), and lidocaine (a class Ib drug) on TTX-R Na(+) currents in rat dorsal root ganglion neurons using the whole-cell patch-clamp method. Flecainide, pilsicainide, and lidocaine reversibly blocked the peak amplitude of TTX-R Na(+) currents in a concentration-dependent manner with half-maximum inhibitory concentration values of 8.5 +/- 6.6 microM (n = 7), 78 +/- 6.9 microM (n = 7), and 73 +/- 6.8 microM (n = 7), respectively. Each drug shifted the inactivation curve for the TTX-R Na(+) currents in the hyperpolarizing direction and caused a use-dependent block. We also studied an interaction between these antiarrhythmics on TTX-R Na(+) channels. Additional application of flecainide or pilsicainide to lidocaine resulted in an additive increase of tonic and use-dependent block. These results suggest that the inhibition of TTX-R Na(+) currents of dorsal root ganglion neurons by such antiarrhythmics is attributable, at least partly, to their antinociceptive effects.