The mammalian inner ear processes sound with high sensitivity and fine resolution over a wide frequency range. The underlying mechanism for this remarkable ability is the "cochlear amplifier", which operates by modifying cochlear micromechanics. However, it is largely unknown how the cochlea implements this modification. Although gradual improvements in experimental techniques have yielded ever-better descriptions of gross basilar membrane vibration, the internal workings of the organ of Corti and of the tectorial membrane have resisted exploration. Although measurements of cochlear function in mice with a gene mutation for alpha-tectorin indicate the tectorial membrane's key role in the mechanoelectrical transformation by the inner ear, direct experimental data on the tectorial membrane's physical properties are limited, and only a few direct measurements on tectorial micromechanics are available. Using the hemicochlea, we are able to show that a tectorial membrane stiffness gradient exists along the cochlea, similar to that of the basilar membrane. In artificial perilymph (but with low calcium), the transversal and radial driving point stiffnesses change at a rate of -4.0 dB/mm and -4.9 dB/mm, respectively, along the length of the cochlear spiral. In artificial endolymph, the stiffness gradient for the transversal component was -3.4 dB/mm. Combined with the changes in tectorial membrane dimensions from base to apex, the radial stiffness changes would be able to provide a second frequency-place map in the cochlea. Young's modulus, which was obtained from measurements performed in the transversal direction, decreased by -2.6 dB/mm from base to apex.

Lingual hematoma is a rare but potentiallyfatal cause of upperairwayobstruction.Patients receiving anticoagulants such as heparin can sufferfrom significant complications of these medications. Not only does heparin exert effects directly on thecoagulation cascade,but it hasthepotential to cause thrombocytopenia by stimulating formation of antibodiesagainstplatelets. Wepresentthecase ofapatient beingtreatedwith heparinfora deep-vein thrombosis, who subsequentlydeveloped heparin-inducedthrombocytopenia and lingual hematoma, necessitating tracheotomy.