Immunohistochemical localization of cyclooxygenase isoforms in the organ of Corti and the spiral ganglion cells of guinea pig cochlea.

Prostaglandins have been used in experimental models and clinical studies for the therapy of sudden hearing loss and tinnitus with conflicting results. However, little is known about the rate-limiting enzymes of prostaglandin synthesis in the inner ear, the generally constitutively expressed cyclooxygenase 1 (COX-1) and the distress-inducible cyclooxygenase 2 (COX-2). To extend our knowledge concerning the physiological expression and localization of these two enzymes, immunohistochemical stainings of the guinea pig cochlea were performed. Light microscopical analysis revealed a homogenous distribution of COX-1 within nearly all cell types of the organ of Corti, but no COX-1 expression in the cuticular plates of pillar cells. COX-2 was found to be expressed in all cell types, with much stronger expression in Hensen cells, neighboring Deiters cells and cuticular plates of outer hair cells. Both COX-1 and COX-2 immunoreactions were also found in the spiral ganglion. We conclude that both COX subtypes are expressed in the guinea pig cochlea under physiological conditions. The prominent expression of the distress-inducible COX-2 isoform in cell types under mechanical stress during noise reception might support the hypothesis of a cytoprotective function of COX products in hearing and in cellular stress situations like intense noise exposure.

[Epidemiological data of patients with sudden hearing loss -- a retrospective study over a period of three years]. / Epidemiologische Daten des Hörsturzes -- eine retrospektive Studie über drei Jahre.

In this retrospective study data of 257 patients (11- 6 years; 52 % male, 48 % female) admitted during the last three years for treatment of sudden unilateral hearing loss are statistically evaluated. No correlation with coexisting disease like hypertension, coronary heart disease, hypercholesteremia, arthropathy of the cervical spine, diabetes, thyroid disorders or nicotine abuse were evident. In 194 patients (75 %) total remission was achieved after rheological therapy. Patients additionally treated with steroids had a significant better outcome. Younger patients had higher remission rates. The best prognosis was found for patients with hearing loss in the lower frequency range. There were no differences in remission rates for patients with preexisting sensorineural hearing loss or chronic otitis media. Also patients suffering from recurrent episodes of sudden hearing loss had a similar outcome also.

[Bilateral progressive hearing loss as the first manifestation of metastatic carcinoma of the head of the pancreas. Case report]. / Beidseitige progrediente Hörminderung als Erstmanifestation eines metastasierenden Pankreaskopfkarzinoms. Kasuistik.

We report the history of a patient who presented first with a progressive unilateral hearing loss and later with a bilateral deafness and an unilateral facial nerve palsy as first and only symptoms of a pancreatic adenocarcinoma. By means of magnetic resonance tomography tumor-suspect lesions in both internal auditory canals were detected. Referring to the results of further examinations these intracanalicular lesions are most probably due to rarely seen bilateral metastasis of a pancreatic adenocarcinoma in the temporal bone. In addition to this rarely diagnosed localisation of metastasis it is rather uncommon that this kind of primary malignoma had not been detected because of gastrointestinal symptoms or extracranial metastasis.

[Therapy of hyperacusis in patients with tinnitus]. / Therapie der Hyperakusis bei Patienten mit Tinnitus.

BACKGROUND: Patients with tinnitus very often suffer from hyperacusis also. METHODS AND PATIENTS: In the present study a possible treatment for patients with bilateral hyperacusis is introduced and the therapeutical results of 41 patients suffering from bilateral hyperacusis combined with a uni- or bilateral tinnitus are discussed. Twenty-one of them also had a cochlear hearing loss. By means of white noise generators or hearing aids and a specific acoustic training the auditory input to the central nervous system was increased. All patients were taught a method to reduce stress (Progressive muscle relaxation according to Jacobson). Uncomfortable loudness levels were analysed before as well as 3 weeks and 6 months after beginning of the treatment. RESULTS: By the time of 3 weeks the discomfort from ordinary sounds was distinctly reduced and the reduction progressed further after 6 months of treatment. In more than 50% of the participants the uncomfortable loudness levels could be raised to a normal range. Interestingly the improvement of hyperacusis was independent of an existing hearing loss. CONCLUSIONS: The described method of treatment seems to be helpful for patients with hyperacusis and will be compared to other therapeutical regimes.

Secondary hyperalgesia to punctate mechanical stimuli. Central sensitization to A-fibre nociceptor input.

Tissue injury induces enhanced pain sensation to light touch and punctate stimuli in adjacent, uninjured skin (secondary hyperalgesia). Whereas hyperalgesia to light touch (allodynia) is mediated by A-fibre low-threshold mechanoreceptors, hyperalgesia to punctate stimuli may be mediated by A- or C-fibre nociceptors. To disclose the relative contributions of A- and C-fibres to the hyperalgesia to punctate stimuli, the superficial radial nerve was blocked by pressure at the wrist in nine healthy subjects. Secondary hyperalgesia was induced by intradermal injection of 40 microg capsaicin, and pain sensitivity in adjacent skin was tested with 200 micron diameter probes (35-407 mN). The progress of conduction blockade was monitored by touch, cold, warm and first pain detection and by compound sensory nerve action potential. When A-fibre conduction was blocked completely but C-fibre conduction was fully intact, pricking pain to punctate stimuli was reduced by 75%, but burning pain to capsaicin injection remained unchanged. In normal skin without A-fibre blockade, pain ratings to the punctate probes increased significantly by a factor of two after adjacent capsaicin injection. In contrast, pain ratings to the punctate probes were not increased after capsaicin injection when A-fibre conduction was selectively blocked. However, hyperalgesia to punctate stimuli was detectable immediately after block release, when A-fibre conduction returned to normal. In conclusion, the pricking pain to punctate stimuli is predominantly mediated by A-fibre nociceptors. In secondary hyperalgesia, this pathway is heterosynaptically facilitated by conditioning C-fibre input. Thus, secondary hyperalgesia to punctate stimuli is induced by nociceptive C-fibre discharge but mediated by nociceptive A-fibres.