Published online Feb 28, 2013. doi: 10.5319/wjo.v3.i1.1
Revised: January 28, 2013
Accepted: February 5, 2013
Published online: February 28, 2013
The etiology of sudden deafness or idiopathic sudden sensorineural hearing loss (ISSHL) remains unclear. Over the past 15 years, we have investigated the mechanisms of ischemic-induced hearing loss using a gerbil model of transient cochlear ischemia. In the gerbil, cochlear ischemia can be induced by occluding the bilateral vertebral arteries simultaneously at the neck, because the posterior communicating arteries of the Circle of Willis close spontaneously around 1 mo after birth. When 15 min ischemia was loaded on this animal, permanent hearing loss of about 25 dB and the death of hair cells, especially inner hair cells were induced. These pathological changes were mainly due to lack of an energy source, glutamate excitotoxicity, and the production of free radicals, especially superoxide and nitrous oxide species. Ischemic damage could be prevented by various procedures, such as cooling the cochlea, intratympanic administration of insulin-like growth factor 1 or AM-111 (an anti-apoptotic agent), and systemic administration of prednisolone (steroid), edarabone (free radical scavenger), ginsenoside Rb1 (Kanpo), hematopoietic stem cells, glia-cell derived neurotrophic factor, and liposome-encapsulated hemoglobin (artificial red blood cells). We also found that the cochlea was protected by the ischemic tolerance, indicating that minor cochlear ischemia alleviates or prevents inner ear damage in subsequent severe cochlear ischemia. As ISSHL usually occurs suddenly, with no preceding sign or symptom, we suggest that most ISSHL cases are caused by circulatory disturbance, probably at the stria vascularis.