Cases reported "Endolymphatic Hydrops"

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1/8. Spontaneous intracranial hypotension: a rare cause of labyrinthine hydrops.

    Spontaneous intracranial hypotension should be considered as a possible cause of cochlear hydrops. We report a case of unilateral hearing loss attributed to spontaneous intracranial hypotension on the basis of characteristic abnormalities seen on magnetic resonance imaging. The diagnostic gold standards for intracranial hypotension are lumbar measurement of cerebrospinal fluid pressure and magnetic resonance imaging. The usual treatment is an autologous blood injection into the peridural spaces. The mechanism of hearing loss is thought to involve secondary perilymph depression due to a patent cochlear aqueduct. This perilymph depression would induce a compensatory expansion of the endolymphatic compartment, with a subsequent decrease in basilar or Reissner's membrane compliance. endolymphatic hydrops can occur in the course of intracranial hypotension, and not only because of abnormal endolymph production or resorption. Hydrops can thus be classified into 1) syndromes of endolymphatic origin and 2) syndromes of perilymphatic origin, in which loss of perilymph induces compensatory expansion of the endolymphatic space.
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keywords = perilymphatic, aqueduct, duct
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2/8. Changes in the Tullio phenomenon and the fistula sign in the course of endolymphatic hydrops.

    We performed electronystagmography with caloric stimulation and studied vestibular evoked myogenic potentials (VEMPs) associated with changes in the Tullio phenomenon and the fistula sign during the clinical course of a patient with endolymphatic hydrops. The Tullio phenomenon and the fistula sign disappeared in association with a reduction in the caloric response, which implicates the ampullary function of the lateral semicircular canal. Even when no VEMP could be detected for the affected ear, the Tullio phenomenon and fistula signs were observed; thus, either these phenomena had a lower response threshold than the VEMPs, or saccular receptors were not involved in the Tullio phenomenon.
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ranking = 0.00014537748563693
keywords = duct
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3/8. Paget disease and sensorineural hearing loss associated with spiral ligament degeneration.

    HYPOTHESIS: Previously unreported cystic degeneration of the spiral ligament in cases of Paget disease. BACKGROUND: About 70% of cases of Paget disease involve the skull, with hearing affected in approximately 50% of these. The hearing impairment may be sensorineural, mixed, or, rarely, only conductive. The etiology and pathogenesis of the hearing loss are not yet understood, and reports in the literature are inconsistent regarding the pathologic changes responsible for sensorineural hearing loss. Of six pairs of temporal bones from patients with Paget disease in the temporal bone collection of a research institution, two pairs have abnormalities not previously associated with sensorineural hearing loss or Paget disease. We report the histopathologic findings in these temporal bones. methods: The temporal bones were fixed in formalin, decalcified in ethylenediaminetetraacetic acid, embedded in celloidin, and sectioned in the horizontal plane at a thickness of 20 microm. Every 10th section was stained with hematoxylin-eosin and mounted on glass slides. The sections were examined by light microscopy. RESULTS: Cystic degeneration of the spiral ligament, primarily in the basal segment, was found in both cases. endolymphatic hydrops and a small endolymphatic sac with calcification of the perisaccular tissue were found in one case. CONCLUSIONS: Cystic degeneration of the spiral ligament has not been previously reported and may be unique to Paget disease. This is consistent with recent literature showing a previously unsuspected role of the spiral ligament in sensorineural hearing loss.
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ranking = 0.00014537748563693
keywords = duct
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4/8. temporal bone findings in Cogan's syndrome.

    We report on the pathological findings in temporal bones taken from a 92-year-old man who had been diagnosed as suffering from Cogan's syndrome before death. Extensive endolymphatic hydrops was observed in the cochlea of the right ear. The saccule showed a collapse following intense dilation. Outpouching of the utricle and crus commune was found and the perilymphatic space of the posterior semicircular canal was occupied by the fibrotic tissue. The left ear showed neither hydrops nor fibrosis. There was absorption of the enchondral bone in both ears, but in the blood vessels there were no pathological changes.
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ranking = 0.67485290403185
keywords = perilymphatic
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5/8. Intratympanic gentamicin treatment: preliminary results in two patients with Meniere's disease.

    Meniere's disease is a vestibular disturbance characterized by episodic vertigo, tinnitus, and fluctuant hearing loss. The long-term effectiveness of available medical and nonablative surgical treatments has been variable, with frequent symptom recurrence. Vestibular neurectomy and labyrinthectomy, surgically ablative techniques, provide more permanent relief from vertiginous attacks. However, these procedures pose possible morbidity and cochlear risk. In this paper, preliminary results are presented for two patients who underwent intratympanic gentamicin application. Like surgical labyrinthectomy, intratympanic use of gentamicin is intended as an ablative procedure, but with potentially less risk to hearing. More vestibulotoxic than cochleotoxic, gentamicin initially disrupts the endolymph-secreting vestibular dark cells, thereby preventing endolymphatic hydrops development. Following gentamicin application, both patients demonstrated a significant change in peripheral vestibular function, as characterized by a reduction of caloric response, impaired posturography performance, and reduced low-frequency gain on rotary chair testing. Posturography performance subsequently improved, confirming functional compensation. Both patients reported relief from vertiginous attacks. However, word recognition ability was significantly worse in one of these two patients. Changes in pure-tone thresholds were minimal.
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ranking = 0.00014537748563693
keywords = duct
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6/8. shy-drager syndrome presenting as Meniere's disease.

    A 59-year-old patient with a history of Meniere's disease is presented. She developed signs of progressive autonomic failure suggesting a diagnosis of shy-drager syndrome, a rare degenerative neurologic condition of unknown etiology. The most common otolaryngologic presentation of this syndrome is with stridor attributable to abductor paralysis of the vocal cords. The association with endolymphatic hydrops has not been previously described.
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ranking = 0.00014537748563693
keywords = duct
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7/8. Traumatic endolymphatic hydrops.

    Traumatic endolymphatic hydrops is an accumulation of endolymph in the cochlear duct caused by traumatic insult. The causative mechanisms are: (1) fistulization of the bony labyrinth, which causes a disturbance in the normal perilymph-endolymph pressure relationship; (2) direct injury to the membranous labyrinth, which may be just a collection of fluid in the cochlear duct from irritation, resulting in endolymphatic hydrops that may not be progressive and may subside in a short period of time after injury and hearing loss may occur; and (3) injury to the endolymphatic fluid drainage system, including a temporal bone fracture in which the fissure happens to extend through the vestibular aqueduct, causing fibro-osseous blockage of the endolymphatic duct and surgical injury to the saccule with obstruction of the longitudinal flow of endolymph, resulting in endolymphatic hydrops that may be delayed in onset and is usually persistent. The diagnosis of traumatic endolymphatic hydrops is made by a history of trauma, such as barotrauma, a blow to the head, or perhaps a previous ear operation, such as stapedectomy; the presence of typical symptoms of endolymphatic hydrops, including fullness, tinnitus, fluctuant hearing loss, and episodic vertigo; and an elevated negative summating potential and an increased summating potential:action potential ratio by electrocochleography. Three patients are presented to demonstrate this clinical entity.
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ranking = 0.32543785093942
keywords = aqueduct, duct
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8/8. endolymphatic hydrops associated with otosclerosis.

    endolymphatic hydrops (EH) associated with otosclerosis has been noted for many years. However, the causal relationship of these two entities remains controversial. Having reviewed the records of patients with otosclerosis describing fluctuant hearing loss and vertiginous symptoms, the authors found the EH may coexist with otosclerosis preoperatively; they may be two separate diseases that exist coincidentally; or EH may be caused by the otosclerotic process. Secondly, EH may occur with a fistula after surgery. Occurring after stapedectomy, EH may be caused by fistulization of the bony labyrinth, which is effectively treated by surgery to seal the fistula, which may cause EH to subside and hearing to improve. Thirdly, delayed EH may occur months or years after stapedectomy, possibly as a result of otosclerotic foci or surgical insult to the labyrinth. dexamethasone, diuretics, and a room air rebreather can be used in the treatment of delayed EH. Hearing may be maintained or may deteriorate, but there usually is no dizziness. The clinical manifestations of EH associated with otosclerosis include a conductive or mixed type of hearing loss; the presence of fullness, tinnitus, fluctuation of hearing, episodic vertigo, an elevated negative summating potential (SP), and an increased summating potential:action potential (SP:AP) ratio shown by ECoG. This report presents five cases of EH associated with otosclerosis.
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ranking = 0.00014537748563693
keywords = duct
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