gramicidin-a and Deafness

Although rare, ototoxicity from the use of aminoglycoside drops is well recognized. Ototoxicity has not been described with the use of combination aminoglycoside-steroid-antifungal creams or ointments. We present the case of a 60-year-old man with a perforated tympanic membrane who suffered a total hearing loss after the instillation of cream containing triamcinolone, neomycin, gramicidin and nystatin (Tri-Adcortyl cream) into his ear canal. On balance, we believe that a number of potentially ototoxic constituents in this cream were responsible. Other possible causes of sensorineural hearing loss and the possible mechanisms of ototoxicity of this cream are discussed. The reasons why such creams may be particularly ototoxic, compared with drops, are also considered. The authors caution against the use of such creams or ointments in the ear if there is any suspicion of a tympanic membrane perforation.

Topics: Administration, Topical; Anti-Bacterial Agents; Anti-Inflammatory Agents; Deafness; Drug Combinations; Drug Therapy, Combination; Gramicidin; Humans; Male; Middle Aged; Neomycin; Nystatin; Triamcinolone Acetonide; Tympanic Membrane Perforation

To determine whether afferent innervation regulates the strength of inhibitory connections in the gerbil auditory midbrain, both cochleas were surgically removed in postnatal day 7 animals, before sound-driven activity is first observed. Inhibitory synaptic currents were measured in a brain slice preparation 1-7 d after the ablations. Whole-cell and gramicidin-perforated patch recordings were obtained from inferior colliculus neurons, and IPSCs were evoked by stimulation of the commissure of the inferior colliculus (CIC) or the ipsilateral lateral lemniscus (LL) in the presence of kynurenic acid. Deafferentation led to a 24 mV depolarizing shift in the IPSC equilibrium potential within 1 d of deafferentation. As a consequence, there was a large reduction of IPSC amplitude at a holding potential of -20 mV in neurons from bilaterally ablated animals. Furthermore, both afferent pathways displayed a 50% reduction of the inhibitory synaptic conductance after deafferentation, indicating that driving force was not solely responsible for the decline in IPSC amplitude. When paired pulses were delivered to the LL or CIC pathway in control neurons, the evoked IPSCs exhibited facilitation. However, paired pulse facilitation was nearly eliminated after deafferentation. Thus, normal innervation affects inhibitory synaptic strength by regulating postsynaptic chloride homeostasis and presynaptic transmitter release properties.

Topics: Animals; Anti-Bacterial Agents; Auditory Pathways; Bicuculline; Cesium; Cochlea; Deafness; Denervation; Excitatory Amino Acid Antagonists; GABA Antagonists; gamma-Aminobutyric Acid; Gerbillinae; Gramicidin; In Vitro Techniques; Inferior Colliculi; Kynurenic Acid; Membrane Potentials; Neural Inhibition; Neurons, Afferent; Patch-Clamp Techniques; Receptors, GABA-A; Receptors, Glycine; Synaptic Transmission

We describe a patient with a polyethylene tube to the middle ear who developed severe deafness and vertigo after treatment with ear drops where neomycin B was considered to be the most likely offending agent. High concentration of this antibiotic in the ear drops and access of the solution to the round window membrane in the absence of inflammatory edema and secretion may have been significant factors contributing to this serious side effect. Less ototoxic preparations should be used in patients with perforated tympanic membranes or grommets.

Topics: Deafness; Dexamethasone; Drug Combinations; Female; Framycetin; Gramicidin; Humans; Middle Aged; Vertigo