The stapediovestibular joint: normal structure and pathogenesis of otosclerosis.
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Biomedical subjects
Publications and source records attributed to R Gussen.
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A temporal bone specimen demonstrating endolymphatic hydrops 13 years after fenestration of the lateral semicircular canal is presented. Fibro-osseous tissue extending from the lateral semicircular canal and reaching the vestibule produced fixation of the membranous wall of the utricle to the bony wall. Fixation and retraction of the utricule appears to have resulted in a permanently open utriculo-endolymphatic valve leaflet. Similar findings of fibro-osseous changes arising from the area of the crus commune and an open valve were found in a Meniere's disease specimen. The implications of these findings on the function of the valve are discussed.
A histologic study of sudden deafness resulting from rupture of cochlear membranes, first in the left ear, and then, three years later, in the right ear, in a patient with vertebro-basilar arteriosclerosis is reported. Two healed ruptures were demonstrated on the right side, one in the hook portion of the cochlea, and one in the area of the promontory. The latter was adherent to the saccule, distorting it inferiorly. In the left temporal bone, a healed rupture was demonstrated approximately 5 mm distal to the labyrinthectomy obliteration. Although the patient's vertebro-basilar artery disease and her sudden deafness syndromes are considered separate entities, one must at least consider whether such longstanding vascular insufficiency might predispose to more readily ruptured membranes with sudden pressure changes in the inner ear.
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Temporal bone changes are described in a 57-year-old man who had sudden onset of dizziness and unilateral deafness two months before death. The patient suffered from hypertension, and congestive and renal failure. At autopsy, subarachnoid hemorrhage with punctate cortical hemorrhages and arteriolar thickening involved the right superior cerebellar hemisphere. The pathological changes involved primarily the right cochlea, saccule and posterior ampulla, and were consistent with vascular embarrassment of the temporal bone of two months duration. The cochlea demonstrated total loss of the organ of Corti and severe degenerative changes of the stria vascularis, spiral ligament, outer sulcus cells and distal cochlear nerve fibers. The saccule demonstrated loss of its macula and nerve fibers. The posterior ampulla showed evidence of previous rupture of its membranous wall with fibrosis and beginning bone formation. Fresh hemorrhage, present in some areas of both temporal bones, was related to the patient's terminal subarachnoid hemorrhage.
The pathogenesis of Bell's palsy is presented as retrograde epineurial compression edema with ischemia of the facial nerve. Although the etiology is unknown, an attractive theory is vasospasm, from any cause, along any facial nerve branch, with the chorda tympani, perhaps, the usual primary involvement. Retrograde vascular distension and edema, within the epineurium of the bony facial canal, compresses the nerve from outside its perineurial sheath. The compression force may be mild or severe, resulting in varying degrees of reversible or irreversible ischemic degeneration of myelin sheaths and axons, with varying degrees of cellular reaction to myelin breakdown. The edema may be resorbed, leaving reversible or irreversible nerve damage, or may stimulate collagen formation within the epineurium, with persisting fibrous compression (entrapment) neuropathy of the facial nerve. This concept is consistent with the varying results of Bell's palsy, and depends on the severity and duration of edema, and whether fibrosis occurs within the epineurium of the facial canal. Epineurial fibrosis also results in disturbance of metabolic exchange through the epineurial-perineurial-endoneurial tissues, and may ultimately result in obliteration of vascular drainage. Two temporal bone cases of Bell's palsy, one occurring ten years before death, with residual paralysis, and one two years before death, with clinical recovery, are added to the previously described four cases in the literature, three of early Bell's palsy, and one of remote palsy with almost complete recovery.
One hundred fourteen human temporal bones from 64 individuals were studied for the presence of melanized melanocytes about the endolymphatic duct and sac. Specimens were from Caucasians (104), Orientals (6) and Negroes (4). Of the specimens from people above nine years of age 79% demonstrated melanized melanocytes about the endolymphatic duct and sac, as well as occasionally about blood vessels in the adjacent bone. These represented 74% of the Caucasian and 75% of the Negro and Oriental individuals. Pigment granules were noted in occasional epithelial lining cells and in macrophage-type cells within the lumen. Heavily melanized melanocytes were noted in five of six specimens of Ménière's disease (all from Caucasian individuals), five of five specimens with previous labyrinthitis (two of which were from a Negro woman), and in occasional specimens from patients with presbycusis, metastatic carcinoma (three of the four adult Oriental patients), chronic otitis media, otosclerosis and lymphoma, as well as in several apparently normal specimens. No clear cut correlation of degree of melanization with specific disease processes can be discerned.
Unilateral endolymphatic hydrops is described associated with absence of the vein in the paravestibular canaliculus (PVC), and with decreased vascularity of the vestibular aqueduct and endolymphatic sac. The venous return from the vestibule was normal as far as the junction of the branches forming the PVC vein. At this junction, a blind venous loop was formed with no continuation of venous drainage through the PVC. This probably represents a developmental anomaly. The decreased vascularity of the endolymphatic sac may be related to the absence of the PVC vein. However, anatomical and functional relationships of these vessels are not clear and need further study. Perisac fibrosis and endosteal bone formation are possibly secondary to the decrease in vascularity. A large chronic rupture of the inferior saccule wall probably accounts for the absence of vertigo and the relatively mild degree of cochlear endolymphatic hydrops.
Mucormycosis of the temporal bone is described in a 60-year-old female with uncontrolled diabetes mellitus whose symptoms related to cranial nerve palsies and hearing loss, following spread of infection from the nasopharynx. The infection spread along the eustachian tube and tensor tympani muscle to the base of the skull, involving the internal carotid artery with mycotic thrombosis and rupture. Subsequent spread occurred from this area predominantly along nerve pathways and as mycotic emboli in blood vessels of the labyrinth and middle ear. Infection also spread from the anterior middle ear wall through the oval window into the vestibule. The temporal bone changes were those of granulomatous inflammation with necrosis and ischemic infarction.
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