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Biomedical subjects

S N Merchant

Publications and source records attributed to S N Merchant.

12 recordsLinked to original sources
PubMed1990

Cadaver middle ears as models for living ears: comparisons of middle ear input immittance.

In vitro measurements of the middle ear input immittance in temporal bones extracted from human cadavers were directly compared with similar in vivo measurements from clinically normal subjects. The results of this comparison indicate that most otoscopically normal unfixed cadaver ears have middle ear input immittances that are indistinguishable from those of live subjects in the 0.1- to 2-kHz range--as long as they have been kept from drying and the static pressures on either side of the tympanic membrane are equal. The effects of the middle ear muscles on the measured input immittance are generally small and the cadaver ears can be maintained in the frozen state for several months with little change. Tympanometry appears to be a reliable indicator of normal middle ear immittance. Cadaver middle ears are useful models of human middle ear function.

Acoustic Impedance Tests↗
PubMed1989

Meniere's syndrome and endolymphatic hydrops. Double-blind temporal bone study.

A systematic double-blind assessment of case histories and histopathologic findings in temporal bones in the collection at the Massachusetts Eye and Ear Infirmary was performed to test the hypothesis that clinical Meniere's syndrome is associated with endolymphatic hydrops demonstrated histopathologically at death. Thirteen of 13 cases of clinical Meniere's syndrome were found to have endolymphatic hydrops not attributable to other causes. However, some patients with idiopathic endolymphatic hydrops did not exhibit clinical Meniere's syndrome as revealed in their medical records. These results challenge the dogma that endolymphatic hydrops per se generates the symptoms of Meniere's syndrome.

Aged↗
PubMed1988

Transcriptional and post-transcriptional regulation of the genes encoding cytochromes P-450c and P-450d in vivo and in primary hepatocyte cultures.

In both primary cell cultures of rat hepatocytes and in liver, polycyclic aromatic hydrocarbons (PAHs) were found to influence the accumulation of the cytochrome P-450c and P-450d mRNAs by both transcriptional and post-transcriptional mechanisms. Following treatment with PAHs, cytochrome P-450c mRNA levels increased approximately 100-fold in both hepatocyte cultures and in liver, while transcription rates, measured by run-on transcription of isolated nuclei, increased 3-fold in hepatocyte cultures and 10-fold in liver. The difference in the -fold increases of mRNA level and transcription rate suggests that post-transcriptional, as well as transcriptional, mechanisms contributed to the regulation of cytochrome P-450c mRNA levels. Following treatment with PAHs, cytochrome P-450d mRNA levels increased 200-fold in hepatocyte cultures and 70-fold in liver, while transcription rates remained unchanged in hepatocyte cultures and increased only 1.7-fold in liver. This suggests that post-transcriptional mechanisms were of primary importance in regulating cytochrome P-450d mRNA levels. The newly developed hepatocyte primary cell culture system used in these studies differs from previously reported systems in that the cytochrome P-450d gene, as well as the cytochrome P-450c gene, were expressed in response to PAHs. In this cell culture system the regulation of these two genes was quite similar, although not identical, to that found in liver. The mechanisms controlling the tissue-specific expression of the genes encoding cytochromes P-450c and P-450d were also examined. The cytochrome P-450c mRNA was found in kidney, heart, and lung, as well as in liver, of PAH-treated rats, while the mature cytochrome P-450d mRNA was detected only in liver. The substantial increase in cytochrome P-450c mRNA in kidney in response to beta-napthoflavone was not associated with a detectable change in the transcription rate of cytochrome P-450c gene, indicating that cytochrome P-450c mRNA levels must be regulated primarily post-transcriptionally in kidney. Even though mature cytochrome P-450d mRNA could not be detected in kidney, the cytochrome P-450d gene was transcribed at a substantial rate in this tissue; therefore, the lack of accumulation of mature cytochrome P-450d mRNA in kidney must have been due to post-transcriptional control.

Animals↗
PubMed1986

Experiences with the butterfly chart.

The bithermal caloric test remains, four decades after its first description, the single most valuable test of vestibular function. However, there are several variations described in the exact procedure of caloric stimulation and in the method of evaluating and representing the test results. For the past 10 years, we have followed a procedure using a constant standardized stimulus and a particular system for caloric nystagmus representation, viz., the Butterfly Chart, and have found it to be very satisfactory. This paper describes our experience with the use of the Butterfly Chart and its clinical application in over 4,500 cases.

Adult↗
PubMed1986

The caloric response in the contralateral ear in acoustic neuroma.

The caloric test response from the unaffected ear in a case of acoustic neuroma may be normal, hypoactive or hyperactive; each has a different pathophysiological connotation: a normal response is the anticipated finding; a hyperactive contralateral response is due to the presence of a large neuroma with brainstem compression; and a hypoactive response may result from several factors, such as lack of mental alertness during the test, drugs like barbiturates, raised intracranial tension, or the presence of bilateral neuromas.

Caloric Tests↗
PubMed1986

Vestibular effects of intravenous lidocaine used in the treatment of tinnitus.

Intravenous lidocaine is known to have an effect on the auditory system in that it is useful for suppressing tinnitus, albeit temporarily. We have used intravenously administered lidocaine as one of the treatment modalities for refractory, disturbing, tinnitus. Its effects on the vestibulo-ocular system were determined by electronystagmography performed before and immediately after injecting lidocaine: smooth pendular stimulus tracking was unaffected; spontaneous and positional nystagmus tended to be suppressed; directional preponderance was reduced or reversed; and the difference between the nystagmus responses in the two directions during the pendular rotation chair test was also reduced or reversed. These changes in the caloric and rotation tests were statistically significant. Lidocaine also appeared to have altered the balance between the two sides in the vestibulo-spinal system as indicated by the results of the stepping test during craniocorpography. The results lend support to the hypothesis that intravenous lidocaine acts at the level of the central nervous system rather than at the periphery.

Electronystagmography↗
PubMedDate not supplied

Histopathology of the ears, eyes, and brain in Norrie's disease (oculoacousticocerebral degeneration).

Norrie's disease is an x-linked recessive disorder characterized by progressive oculoacousticocerebral degeneration. The light and electron microscopic changes in the temporal bones, eyes, and brain of an affected 77-year-old man who suffered from bilateral profound sensorineural hearing loss, blindness, and mental retardation are described. The inner ears showed marked atrophy of the stria vascularis, severe degeneration of hair cells and cochlear neurons, and connective tissue proliferation in the spiral ganglion, osseous spiral lamina, and walls of the membranous vestibular labyrinth. The eyes showed detached retinae, dense proliferation of fibrillary glial cells in the retina and vitreous, severe atrophy of the optic nerves, and degenerative hyalinization of blood vessels. This case is the first published report of the histopathology of the inner ear in Norrie's disease.

Aged↗
PubMedDate not supplied

Vestibular atelectasis.

The temporal bone collection at the Massachusetts Eye and Ear Infirmary includes specimens from several cases in which the only reasonable explanation for vertigo is collapse of the walls of the ampullae and utricle, a disorder we have termed vestibular atelectasis. The clinical histories and temporal bone studies support the existence of a primary type that may have a paroxysmal or insidious onset, and a secondary type that occurs in association with other inner ear disorders. The principal clinical symptom is chronic unsteadiness, precipitated or aggravated by head movement, and sometimes associated with short episodes of spinning vertigo. It is presumed that the collapsed membranes interfere with the motion mechanics of the cupulae and otolithic membranes.

Adult↗