Faculty Bibliography

Polarization between proponents of intact canal wall tympanoplasty and radical (modified) mastoidectomy in the treatment of cholesteatoma and other irreversible temporal bone lesions can be avoided in many cases by the use of one or more special techniques. These include (a) Gelfilm (no-graft) induction of tympanic membrane regrowth; (b) the use of tragal cartilage and perichondrium in columellization and in Type III neomyringostapediopexy; (c) the use of laboratory-prefabricated ossicular homografts to correct malleal-capitulum and malleal-footplate discontinuities more precisely; and (d) the circumferential approach (circumnavigation of patient's head) and anterior position of the surgeon in order to visualize the sinus tympani, retropyramidal, and retrofacial areas, obviating extensive posterior tympanotomy bone dissections. These techniques make possible a third alternative to the choice of either combined-approach tympanoplasty or radical or modified radical mastoidectomy in the treatment of a number of advanced temporal bone lesions.

Although the cochlear toxicity of dihydrostreptomycin (DHSM) is well-recognized in man, it has always proved difficult to demonstrate in animals. Hearing thresholds in M. nemestrina monkeys remained essentially unchanged after DHSM 100 mg/kg im daily for 8 months, but E. patas monkeys were severely deafened by DHSM 20 mg/kg for 90 days, a regimen formerly used in treating human tuberculosis. The patas monkey may prove to be the animal model of choice for evaluating aminoglycoside ototoxicity.

For hundreds of years various types of sutures and threads have been placed in the human body by surgeons. The technique of thread augmentation involves the use of colorless absorbable (Vicryl) and non-absorbable (Neurolon) suture material on a long, straight Keith needle tunneled subdermally beneath prominent facial wrinkles in an effort to make the deep grooves less severe and to augment atrophic areas about the lips and oral commissures. This may be done as an isolated procedure or as an ancillary procedure at the time of a blepharoplasty or cervicofacial rhytidectomy.

Various forms of sensorineural degeneration patterns related to noise exposure are illustrated in six pairs of temporal bones selected from a group of 33 male patients with histories of noise exposure. For the entire group the commonest form of lesion, associated with a 4-kHz dip in the audiogram, was a relatively diffuse degeneration in the second quadrant of the basal turn, in the 9-13 mm area. An advanced form of this lesion had a wide gap of more or less complete sensorineural degeneration affecting the entire second quadrant and displaying various degrees of extension toward the apex and base. The pattern associated with an "abrupt high-tone loss," with more or less complete hair cell and nerve degeneration in both the second and first quadrants and extending to the basal end of the cochlea, was rare. In one case this pattern appeared to have evolved from the first type of lesion as the remaining nerve fibers in the first quadrant had degenerated. The protective effect of the acoustic shadow of the head for the right ear, in shooting from the right shoulder, is demonstrated for the higher frequencies. Two almost identical cases of sharply-circumscribed single areas of degeneration in the first quadrant and one case with two such areas represent the third type of lesion. In one of these cases there was a history of firearm usage. It is postulated that this type of lesion is caused by impulse noise. In most of the material the degeneration pattern differed markedly from the diffuse degeneration seen with presbycusis. Degeneration patterns with knife-sharp transitions between completely degenerated and apparently undamaged areas appear to be characteristic of noise-induced injuries.

Sixteen children with anomalies of the auricle and/or middle ear who presented malformations of the face, mouth, upper airway, spine, limbs, heart, gastrointestinal (GI), and/or genitourinary (GU) systems, were described. While clusters of anomalies suggested syndromes such as the oculo-auriculo-vertebral syndrome of Goldenhar, hamifacial microsomia, mandibulo-facial dysostosis (Treacher Collins syndrome), Pierre Robin, Klippel-Feil, Moebius, Duane, and/or VATER syndromes, many children did not fit what are usually considered even minimal criteria for these syndromes. Several children had malformations which fit the description of more than one syndrome. The importance of investigating the children for unsuspected anomalies, especially of the GU system, was emphasized. Life threatening problems in this group consisted of airway problems, congenital heart disease, and major anomalies of the GI and GU systems. Better management of sucking, swallowing and airway problems might have decreased the early morbidity and mortality (3/16) in this group. Children with multiple defacing anomalies may not be mentally retarded so that aggressive management of their visceral anomalies and hearing problems, and early educational intervention are mandatory. Delay in development may be due to hearing loss, vestibular impairment, ataxia, the consequences of early malnutrition, and multiple hospitalizations rather than to mental retardation. A pessimistic attitude in infancy is unwarranted since it is impossible to predict which children will end up competitive individuals.

The inner ear is unique in the number and variety of specialized microvascular networks that furnish blood to its parts. Four distinct capillary networks arranged in parallel supply the structures of the outer wall, and four others those of the spiral lamina. Most of the capillaries are surrounded by pericapillary spaces favoring filtration and reabsorption of fluid. In the guinea pig those of the spiral prominence and outer sulcus show a special pericapillary tissue. The strial capillaries are larger in diameter and are closely invested by strial cells. The blood within them has a higher hematocrit and flows more slowly than elsewhere in the labyrinth. The arcades of the tympanic lip and basilar membrane receive occasional innervation by fine unmyelinated nerve fibers. A possible role of prostaglandins in controlling the tone of the cochlear microvasculature is suggested. Although it appears unlikely that vascular lesions within the labyrinth could be responsible for the hydrops of Meniere's syndrome, devascularization and atrophy of the endolymphatic sac might be contributory factors.