Presbycusis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Saumya Easaw, M.B.B.S.[2], Farman Khan, MD, MRCP [3]
Pathophysiology
Examples of microscopic changes seen in this condition are hair cell degeneration of the cochlea and giant stereociliary degeneration.
Hearing loss is broadly subdivided into two categories: Sensorineural and conductive. Conductive hearing loss is characterized by the inability to mechanically transmit sound vibrations from the environment to the inner ear. Sensorineural hearing loss is caused by the inability to effectively transduce sound information into usable neural signals. Mostly sensorineural hearing loss is the result of disorders of the inner ear itself. Presbycusis is sensorineural hearing loss, in which cochlear hair cells and, to a lesser extent, the spiral ganglion cells in the vestibulocochlear nerve can be affected.[1][2]
In the histopathology classification system there are three main types of presbycusis.
- Sensory: High-frequency hearing deficit caused by loss of hair cells.
- Metabolic: Low-frequency hearing deficit caused by loss of stria vascularis.
- Neural: Variable pattern of hearing loss caused by loss of ganglion cells.
References
- ↑ SCHUKNECHT HF (1964). "FURTHER OBSERVATIONS ON THE PATHOLOGY OF PRESBYCUSIS". Archives of Otolaryngology (Chicago, Ill. : 1960). 80: 369–82. PMID 14198699. Unknown parameter
|month=ignored (help) - ↑ Cohn ES (1999). "Hearing loss with aging: presbycusis". Clinics in Geriatric Medicine. 15 (1): 145–61, viii. PMID 9855664. Unknown parameter
|month=ignored (help)