A lumbar drain is not routinely necessary for successful closure of CSF rhinorrhea of any size. Smaller dural defects may be safely performed on an outpatient basis without complications.

To determine the efficacy of topical antiischemic drug therapy in the salvage of failing, randompattern skin flaps.

Mitomycin C may be useful as an adjunct for preventing myringotomy closure.

No abstract

The present study used distortion-product otoacoustic emission (DPOAE) suppression tuning curves (STCs), DPOAE onset latencies (OLs), and DPOAE amplitude correlations to investigate the locus of generation of the 2f1-f2 DPOAE versus the 2f2-f1 DPOAE in humans. The results of the tuning study revealed that, for the 2f1-f2 DPOAE, the tips of the STCs tuned consistently below the geometric-mean (GM) frequency of the primary tones. In contrast, for the 2f2-f1 DPOAE, STCs tuned above the GM of the primaries, with 50% of the tip frequencies at, or above, the 2f2-f1 frequency place. When the average ratio of the 2f2-f1 to the 2f1-f2 tip frequencies was computed, a factor of 1.44 provided an estimate of the frequency shift needed to align the two DPOAE generation sites. Other results showed that OLs for the 2f2-f1 DPOAE were uniformly shorter than those for the 2f1-f2, with differences at the low frequencies amounting to as much as 6-7 ms. Further, for both DPOAEs, curves describing latency decreases as a function of increasing GM frequencies were best fit by power functions. Shifting the GM frequency producing the 2f2-f1 DPOAE by a factor of 1.6 caused the latency distributions for both DPOAEs to overlap thus resulting in a single function that described cochlear delay as a function of GM frequency. Finally, for each GM frequency in the DP-gram, sliding correlations from 108 normal ears were performed on both DPOAEs by holding the primaries producing the 2f1-f2 DPOAE constant, while all 2f2-f1 DPOAE amplitudes were successively correlated with the 2f1-f2 amplitudes. This procedure demonstrated that, for a given GM frequency producing the 2f1-f2, the correlations between the two DPOAEs peaked when the primaries of the 2f2-f1 were at a GM frequency that positioned the 2f2-f1 frequency place near the GM of the primaries that produced the 2f1-f2 DPOAE. As a whole, the above findings strongly suggest that the 2f2-f1 DPOAE in humans is generated basal to the primary-tone place on the basilar membrane.