The Relationship between Presbycusis and Mastoid Pneumatization

Presbycusis is defined as the natural hearing loss accompanying aging, caused by degenerative changes in the inner ear. The etiology of presbycusis is uncertain. However, it would appear that a complex genetic cause is most likely. The determinants of mastoid size continue to be controversial. One of the pneumatization theories is the hereditary theory. In this study, the possible relationship between presbycusis and the extent of mastoid pneumatization was investigated. This study was carried out on 21 patients with presbycusis and 21 normal subjects of similar ages. The pneumatized volume was measured by computerized tomography. The temporal bone was scanned at 2 mm thickness intervals. Exposure (kV 130, mA105). The scan plane was parallel to the orbitomeatal line and the CT images covered the entire mastoid region. The average mastoid pneumatization in presbycusis group was 6.08 +/- 2.52 cm3 in the right ear and 6.19 +/- 2.93 cm3 in the left ear. However, in the control group it was 4.69 +/- 3.17 cm3 in the right ear (p=0.12) and 5.10 +/- 3.49 cm3 in the left ear (p=0.28). No significant difference was found between the presbycusis patients and normal subjects in terms of the volume of mastoid pneumatization.

Is the aged rat ear more susceptible to noise or styrene damage than the young ear?

Noise- and styrene-induced hearing and hair cell loss were studied in young (3 months) and aged (24-26 months) Long-Evans rats. The animals were exposed 6 h/d, 5 d/w for 4 weeks to (a) broadband noise centered at 8 kHz (92 or 97dB SPL), or b) styrene (700 ppm). Auditory sensitivity was tested by recording evoked potentials from the inferior colliculus. Histological analyses of the organ of Corti, stria vascularis, and the spiral ganglions were also performed. Aged controls showed outer hair cell (OHC) loss at the basal and apical regions of the organ of Corti, and an increase in pigmentation concomitant to a decrease in vascularization of the stria vascularis, along with elevated thresholds relative to young controls. The 92-dB noise caused similar threshold shifts in both age groups, whereas the 97-dB noise caused more threshold shifts in the aged group compared to the young group. Recovery of the hearing thresholds depended both on the intensity of the noise and on the age of the animals. Aged rats had minimal hair cell loss as a result of styrene exposure, whereas young animals showed significant OHC loss, particularly in third row. Despite significant loss of OHCs, the young subjects showed styrene-induced threshold shifts only at high frequencies. In summary, the data show that : (a) there is an influence of age on both noise-induced and styrene-induced threshold shift and hair cell loss in rats and (b) the cochlea appear to have a redundancy in the number of OHCs, thus threshold shift does not necessarily occur with significant OHC loss.