The fate of an ossicular allograft in tympanoplasty.

Correction of ossicular defects in tympanoplasty most commonly involves the use of commercially available prostheses or preserved allograft ossicles. Incus autografts and tragal cartilage autografts are also used by many surgeons. Presculptured preserved allograft ossicles have not been used widely, but are used almost exclusively by our clinic. The fate of ossicular grafts has been reported by a number of in investigators with evidence obtained at revision surgery. In this paper we will be able to trace the fate of a presculptured preserved autograft ossicle clinically and pathologically. The unique aspect of this study is the demonstration of the ossicular status in post mortem temporal bone dissection followed by histopathological serial section studies.

Surgical trauma to the lateral semicircular canal with preservation of hearing.

Surgical trauma to the lateral semicircular canal (LSC) is a rare complication which does not always result in cochlear damage. The authors present six such cases, discuss the histopathological findings of one case, and review 12 previous reports. Transient cochlear depression with normalization of function within 6 weeks of trauma occurred in most instances. Vestibular symptoms were pronounced and, although compensation was not delayed, positional dizziness and instability usually persisted for several months and occasionally for a year or more. Histopathological findings (two specimens) were significant for obliterative scarring of the LSC at the site of injury and for the structural integrity of the labyrinth and cochlea. The mechanism of cochlear protection in these cases remains obscure; however, clean injuries away from the ampullary end of the canal occurring in patients without preexisting inner ear disease appear to have a better prognosis. Intraoperative closure of the defect, postoperative bed rest, and antibiotics are the basic elements of management.

Vascular mechanisms in Meniere's disease.

Normal venous drainage of the vestibular organs through the vein of the paravestibular canaliculus (PVC) may be crucial to inner ear fluid mechanics. It is proposed that increased venous pressure, with resultant venous insufficiency of the vestibular organs, may result in endolymphatic hydrops unless collateral venous circulation develops. Certain variations in pattern of venous drainage where the vestibular organs drain predominantly through the PVC vein may be a predisposing factor. In patients with Meniere's disease, different mechanisms can cause venous insufficiency. One suggested mechanism is morphologic change in the microcirculation of the intermediate portion of the endolymphatic sac. Microcirculation changes may be associated with fibrosis of the perisac tissues or shortening of the intermediate sac region or might be physiologically determined. Venous insufficiency may also result from anomalies of the PVC vein.

Endolymphatic hydrops with absence of vein in paravestibular canaliculus.

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.

Melanocyte system of the endolymphatic duct and sac.

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.

Sudden deafnfess of vascular origin: a human temporal bone study.

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.

Pathogenesis of Bell's palsy. Retrograde epineurial edema and postedematous fibrous compression neuropathy of the facial nerve.

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.

Mucormycosis of the temporal bone.

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.