Biomedical subjects

F Suga

Publications and source records attributed to F Suga.

At least 19 recordsLinked to original sources

PubMed1976

Sensorineural deafness due to osteitis fibrosa.

A 91-year-old woman with deafness died from renal failure. Autopsy revealed osteitis fibrosa cystica generalisata, chronic myeloid leukemia, renal atrophy, and hyperplastic parathyroid glands. The temporal bones showed senile osteoporosis, osteitis fibrosa, and chronic myeloid leukemia. The inner ears showed extensive degeneration of cochlear sensorineural elements. The perilymph showed a general increased staining reaction with hematoxylin-eosin that was most evident in localized areas, where marrow spaces of osteitis fibrosa communicated directly with perilymph. It appears that the active diseased marrow exerted a toxic effect on the sensorineural elements of the cochlea by diffusion through the perilymph.

Aged↗

PubMed1976

Hereditary progressive sensorineural deafness.

Progressive sensorineural hearing losses found in seven members of three families are presented. Genetic transmission patterns in the study appeared to be autosomal dominant in two families and recessive in one family. The common audiological features of these cases include bilaterally symmetrical audiometric configuration and fairly good speech discrimination. The hearing losses of most of the cases appeared to begin at high frequencies progressing later to involve lower frequencies. The main histopathological changes in the temporal bones of one of the cases were degeneration of the organ of Corti and of the spiral ganglion in the lower cochlear coils and cystic degeneration of the stria vascularis in the upper coils.

Adult↗

PubMed1976

Labyrinthine anomalies in trisomy 13 mosaicism.

The temporal bone histopathology of a 2-month-old male with a bilateral cleft palate, cleft lip and polydactylia due to trisomy 13 mosaicism was studied. Anomalies in the ear involved a partial absence of the superior semicircular canal, an abnormally wide lateral semicircular canal, underdeveloped cochlear coils, an abnormally broad modiolus, an undeveloped organ of Corti and an underdeveloped basilar membrane in the basal turn of the cochlea, an unusually wide cochlear aqueduct, and deformed stapedial crura.

Adult↗

PubMed1976

Paget's disease and sensori-neural deafness: temporal bone histopathology of Paget's disease.

Four cases with Paget's disease of the temporal bone are presented to illustrate the pathogenesis of the associated deafness. One case illustrates the combination of severe deafness due to bilateral otosclerosis with probably asymptomatic bilateral Paget's disease. One case with advanced Paget's disease presents features to explain early stages of sensori-neural deafness before actual cellular invasion of the inner ear. One case of profound deafness due to Paget's disease presents a different stage of cellular invasion of the inner ear by the disease on each side. One case illustrates invasion of the internal auditory meatus by Paget's disease with infiltration of the acoustic division of the nerve and profound deafness.

Adult↗

PubMed1975

Control of the microcirculation of the inner ear.

In general, many similarities are seen between cerebral blood flow and cochlear blood flow in response to vasodilating drugs. Cochlear vessels appear to be weakly controlled by the adrenergic nervous system. Cholinergic agents dilate cochlear vessels, although the vasodilation in the cochlea does not necessarily cause an increase in cochlear blood flow because of the associated hypotension. The effect on the systemic circulation is too profound to make these agents clinically useful. Papaverine, dipyridamole, amyl nitrite, and the plasma kinins produce transient increases in cochlear blood flow. Ten per cent carbon dioxide and 90 per cent oxygen product progressive vasodilation as long as the mixture is inhaled. Hydralazine produces too profound an effect on systemic blood pressure. Histamine and betahistine increase cochlear blood flow but only in doses that produce bronchiospasm in the guinea pig. Nicotinic acid and nicotinyl tartrate have no effect on cochlear blood flow. If one considers safety and efficacy as well as patient tolerance, papaverine appears to be the drug of choice for increasing cochlear blood flow clinically. Histamine and betahistine appear to be acceptable alternatives. Betahistine is no longer available for clinical use because of the failure to demonstrate clinical efficacy of therapy.

Cochlea↗

PubMed1974