In order to obtain information about the sequence of events leading to degenerative changes in the cochlea after acoustic trauma, a systematic LM study was performed in the guinea pig organ of Corti. The results were correlated with measurements of CAP N1 thresholds from the same animals. Twenty pigmented guinea pigs were used in the study. Ten of these animals were exposed to a 3.85 kHz pure tone with an intensity varying between 108 and 120 dB SPL for 22.5 to 360 min and were sacrificed after 4 weeks. Eight animals were exposed to 120 dB SPL for 22.5 min and sacrificed at regular intervals after exposure, viz. 5 min, 4, 24 h and 5 days. Prior to sound exposure the animals in the 4-week group were implanted with a permanent round window electrode for measurements of CAP N1 thresholds. The study indicates that the degeneration and reparative processes are not entirely completed after 4 weeks. The development of holes in the reticular lamina may result in further degeneration of cells bilateral to the initial maximum damage. Darkly stained cells seem to be activated in the reparative process in the organ of Corti. Local appearance of dendritic macrophages in the organ of Corti indicate the existence of a local mechanism for disposal of degeneration products from the organ of Corti. The retrograde degeneration of radial nerve fibres seems to be closely associated with that of the pillar cells. A close correlation between structural hair cell damage and CAP N1 threshold shift was found in the region of the organ of Corti corresponding to the exposure frequency. The TS 5 min, 4 h and 24 h after exposure showed a close correlation with swellings in the afferent nerve endings below the IHC in the area of maximum damage and basalwards.
The presence of carbohydrates was investigated in the vestibular end organs of the guinea pig using FITC-lectins. The following sugars have been identified: N-acetyl-glucosamine, galactose, mannose and fucose. In contrast, N-acetyl-galactosamine was not clearly detected. These sugars were suggested to be closely related to the formation and maintenance of otoconia as well as of the cupula. N-acetyl-glucosamine was considered to be the major component of the glycocalyx and also suggested to have a function as an anchoring structure between the epithelial cell and the otolithic membrane or the cupula.
The incidence of clinical otosclerosis was 5.67 patients/100,000 inhabitants/year. The calculated prevalence was 0.287%. The number of cases increased progressively during the study period (p<0.001). The 15-45-year age group was the largest (62.2%) and 68.4% of patients were females. The most frequent type of otosclerosis was estapediovestibularis (fenestral), non-obliterative (91.8%). Only 48 cases (2.3%) of cochlear and 45 (2.2%) of obliterative otosclerosis were reported. The most frequently employed therapeutic procedures were stapedectomy and stapedotomy (75.70%). The average total and preoperative lengths of stay were 3.59 and 1.04 days, respectively. There were significant differences between the different types of otosclerosis. Improvement in the air-bone gap was 15.37+/-1.19 dB (n=164) and the overclosure or operative damage was 0.49+/-0.85 dB (n=164). A gap improvement of 10-40 dB was observed in 61.4% of patients. The > 65 years age group showed the best gap improvement but the largest variability. The quality of hearing measured by the QHQ showed that, in general, a better gap improvement was associated with a higher quality of hearing (Pearson correlation r=0.183; p<0.05). The 15-45-year age group had the worst gap improvement but, in contrast, the better quality of hearing.
The biochemical effects of experimental renal insufficiency produced by bilateral nephrectomy on perilymph were studied. Rats were used for the experiments; measurements were carried out at various intervals after nephrectomy. Statistically significant changes in perilymph (osmolality, Na, K, Cl, and urea), and serum (osmolality, urea and creatinine) were found. These findings represent a marked labyrinth alteration, and may partly explain the pathophysiology of labyrinthine disturbances in chronic renal disease.
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