Remember, proponents of the vascular theory are seeking a smoking gun: a direct linkage between some vascular event such as ischemia or infarction and deﬁnite changes associated with hearing loss. Changes in the temporal bones, such as labyrinthine ossiﬁcation, if consistently found in patients with SSNHL, would be such a smoking gun. Saumil N. Merchant, ., and his colleagues at my institution, the Massachusetts Eye and Ear Inﬁrmary, recently reviewed specimens of temporal bone in the Inﬁrmary’s collection from 17 cases of SSNHL. 3 Only one specimen showed any evidence of new bone formation—the vascular theorists’ hoped-for smoking gun. Another strike against the vascular theory is the relationship of SSNHL prognosis to the site of cochlear injury. The cochlear artery runs from the base of cochlea, where high-frequency sounds are detected, to the apex, where low-frequency sounds are detected. Since there is no collateral blood supply to the cochlear apex, blockage of the cochlear artery should cause the most severe damage to low-frequency hearing. But clinical reports show exactly the opposite: SSNHL affecting low-frequency hearing of the cochlear apex actually has a better prognosis than SSNHL affecting high-frequency hearing in the cochlear base. Another difﬁculty is that if the labyrinthine artery itself were affected by some vascular event, both auditory and balance functions should be impaired, but only a few patients with SSNHL experience severe or sustained vertigo.
The injections are performed with the patient lying down and using the office microscope. The ear is first cleaned of wax. A small area of the eardrum is numbed with a drop of medication. A small needle and syringe are then used and the needle is passed through the eardrum at the site that is numbed so that the tip is in the ear, near the round window. This is a membrane where drugs are absorbed in to the cochlea. The fluid is injected in to the middle ear and the patient stays lying down for 20-30 minutes during which he does not swallow or sniff. The drug sits against the round window and is absorbed in to the inner ear. The patient then sits up slowly and leaves the office. Patients should not drive for a few hours after this procedure. Water is kept out of the ear until it is confirmed that the tiny hole has healed.
Most of the existing studies focus on exogenous administration of antioxidants. Pharmacological activation of intrinsic defence mechanisms against oxidative stress in the inner ear caused by cisplatin therapy also proved helpful as showed by an experimental animal study using systemic administration of thiamine pyrophosphate (TPP). Thiamine pyrophosphate functions as coenzyme for peroxisomes being a crucial factor for energy metabolism, antioxidation, and myelinisation of nerve cells. Its intraperitoneal injection increased the level of natural antioxidants like glutathione and antioxidant enzymes (superoxide dismutase, glutathione peroxidase and glutathione reductase) and reduced the content of malonildialdehyde, an indicator of lipid peroxidation following increased levels of oxygen reactive species resulting from cisplatin toxicity. The histologic evaluation of cochleae harvested from TPP treated animals showed preservation of the morphology of the organ of Corti and outer hair cells and no destruction of spiral ganglion cells and stria vascularis following cisplatin therapy [ 5 ].