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Biomedical subjects

T Egami

Publications and source records attributed to T Egami.

69 records · Page 4Linked to original sources

Inner ear hemorrhage and endolymphatic hydrops in a leukemic patient with sudden hearing loss.

Several significant histopathological findings were noted in a case of sudden hearing loss in a patient with chronic lymphocytic leukemia. The major pathological findings were leukemic hemorrhage into both perilymphatic and endolymphatic spaces in the cochlear and vestibular systems, endolymphatic hydrops in the cochlea and sacculus, and a relatively narrowed and straightened vestibular aqueduct and endolymphatic sac. Additional interesting findings include: loss of hair cells in the organ of Corti and vestibular end-organs; destruction of the stria vascularis (possibly the origin of the blood); fibrosis in the perilymphatic spaces in the cochlea and the vestibule, and in the endolymphatic space in the vestibule; and new bone formation in the perilymphatic spaces in the vestibule. The leukemic infiltrate observed in both the cochlea and the vestibule was not considered to be significant. Hemorrhage into the cochlea is thought to be the most reasonable cause of the sudden hearing loss in this case. Also discussed are fibrosis and osteogenesis as a late consequence of hemorrhage, and the coexistence of endolymphatic hydrops with an anomaly of the vestibular aqueduct and endolymphatic sac.

Aged↗

Noise-induced hearing loss. A human temporal bone case report.

The histopathology of a case of profound hearing loss which seemed to be induced by noise exposure (explosions and drillings in a gold mine) is reported. The patient's only residual hearing was 250 Hz at 90 dB SPL in the right ear. The major histopathological findings were as follows: Bilateral absence or collapse of Corti's organ was observed in the middle and basal turns of the cochlea; however, in the remaining area (approximately 6.0 mm in range in the apical portion of the cochlea) Corti's organ was well-preserved with a moderate loss in number or atrophy of the hair cells. Bilateral marked decrease of the cochlear nerve was noted in the middle and basal turns; however, the nerve was well-preserved in the remaining apical portion (approximately 6.0 mm in range) of the cochlea. These pathological findings were somewhat less severe in the right cochlea than in the left. In general, there was good correlation between the profound hearing loss and the extensive pathological findings in Corti's organ. The residual hearing in the right ear would seem to be explained by the less severe pathological changes found in the apical portion of the right cochlea than in the left cochlea. In addition to noise exposure, other possible etiological factors contributing to this hearing loss are discussed. These include diabetes mellitus and presbycusis.

Aged↗

Course and contents of the paravestibular canaliculus.

The purpose of this study is to describe the anatomy of the paravestibular canaliculus (PVC) in detail, especially its course in relation to the vestibular aqueduct (VA) and its vascular contents. Serial horizontal sections of 20 normal human temporal bones were stained either with hematoxylin and eosin, by Verhoeff-van Gieson's method, or by Mallorys method, and studied under the light microscope. Graphic reconstruction of the VA and the PVC was performed in some of the cases. In this study, the following new anatomical information on the common course and vascular contents of the PVC was obtained: 1) two PVC are present in the area near the vestibular orifice of the VA; 2) the PVC merges with the VA in the area near its cranial orifice without any particular branching, and does not enter the posterior cranial fosa; 3) veins course through the entire length of the PVC whereas arteries course only through the posterior cranial fossa side of the PVC. It appears that veins are the major contents of the PVC and that these veins represent the main venous drainage system from the vestibule. It also appears that arteries in the PVC supply the blood from the posterior cranial fossa mainly to the PVC itself.

Arteries↗

Hypoplasia of the vestibular aqueduct and endolymphatic sac in endolymphatic hydrops.

Four temporal bones from three previously reported cases showing endolymphatic hydrops and pathology of the vestibular aqueduct (VA) and endolymphatic sac (ES) were investigated further. Pathology of the VA and ES was studied by measuring the sizes of the VA and ES, paying particular attention to the proximal rugose portions. A medial-view graphic reconstruction was created to delineate the course and size of the VA, as well as its correlation with neighboring structures (posterior canal and cochlea). In addition, 20 control temporal bones were selected and measured for quantitative study of the sizes of the VA and ES. The four pathologic temporal bones were shown to have small, simple, tube-like VA and ES, without surrounding bony pathology. This appeared to be congenital hypoplasia characterized by hypoplastic funnel-shaped dilatation of the VA and hypoplastic rugose portion of the ES. Anterior dislocation of the distal portion of the VA and poorly developed periaqueductal air cells were also noted in the pathologic bones.

Adolescent↗

Experimental study of nystagmus induced by injecting various solutions into the middle ear cavity.

Injecting of various solutions into the middle ear cavity of cats and rabbits provoked certain characteristic types of nystagmus which resembled caloric nystagmus or clinical cases of peripheral vestibular disorders. Solutions with different degrees of specific gravity, osmotic effect and ion composition were used in this study. Direction-changing positional nystagmus, irritative nystagmus, and paralytic nystagmus were elicited according to the physical or chemical properties of each solution. Histological findings showed mild changes in the perilymphatic space and/or in the endolymphatic space in the period with some characteristic types of nystagmus. Infiltration of the substances into the inner ear fluids from the middle ear cavity via a round window membrane were probably responsible for these types of nystagmus.

Animals↗