Cases reported "Hearing Loss, Sudden"

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1/26. Sudden hearing loss in a patient hepatitis c virus (HCV) positive on therapy with alpha-interferon: a possible autoimmune-microvascular pathogenesis.

    Alpha interferon (alpha-IFN) is used for the treatment of various systemic disorders. Side-effects of alpha-IFN therapy can involve numerous organ systems, but sudden hearing loss has only once been recorded. We report a case of sudden hearing loss occurring in a patient with chronic hepatitis c treated with alpha-IFN and recovered five days after the discontinuation of this agent. This is the first record of anti-endothelial cell antibodies detection in a patient with sudden hearing loss. The finding of anti-endothelial cell antibodies suggests an association between sudden hearing loss and microvascular damage during interferon therapy.
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2/26. Sudden unilateral hearing loss with simultaneous ipsilateral posterior semicircular canal benign paroxysmal positional vertigo: a variant of vestibulo-cochlear neurolabyrinthitis?

    We describe 4 patients who all simultaneously developed a sudden total or partial unilateral sensorineural hearing loss and an unusual acute peripheral vestibulopathy in the same ear characterized by posterior semicircular canal benign paroxysmal positional vertigo with intact lateral semicircular canal function. Two patients also had ipsilateral loss of otolith function. The vertigo resolved in all 4 patients after particle-repositioning maneuvers. The findings of audiometry and vestibular tests indicated that the lesion responsible for this syndrome was probably located within the labyrinth itself rather than within the vestibulocochlear nerve and that it was more likely a viral vestibulocochlear neurolabyrinthitis than a labyrinthine infarction.
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3/26. Enhancement of the eighth cranial nerve and labyrinth on MR imaging in sudden sensorineural hearing loss associated with human herpesvirus 1 infection: case report.

    The case of a 61-year-old woman who presented with herpes labialis, subclinical meningitis, and sudden onset of bilateral sensorineural hearing loss is presented. Contrast-enhanced MR imaging showed marked bilateral enhancement of the intracanalicular portion of the eighth cranial nerve, right cochlea, and left vestibule. polymerase chain reaction was positive for human herpesvirus 1 obtained from the cerebral spinal fluid, which suggested the diagnosis of viral neuritis.
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4/26. Malignant melanoma presenting as sudden onset of complete hearing loss.

    The authors describe a rare case of rapidly progressive bilateral hearing loss associated with carcinomatous meningitis secondary to a primary malignant melanoma of the lower limb 6 years previously. Carcinomatous meningitis is a relatively rare diagnosis, with the involvement of the eighth cranial nerve being present in only a small proportion of patients. diagnosis relies on clinical suspicion (when multiple cranial nerve lesions occur), magnetic resonance imaging, and cerebrospinal fluid cytology.
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5/26. Transient locked-in syndrome resulting from stellate ganglion block in the treatment of patients with sudden hearing loss.

    stellate ganglion blockage (SGB) is a local anesthetic procedure intended to block the lower cervical and upper thoracic sympathetic chain and is one of the treatment modalities for a wide range of disorders such as sudden hearing loss, Menier's disease, stroke, sudden blindness, shoulder/hand syndrome and vascular headache. The complications of SGB are recurrent laryngeal or phrenic nerve block, pneumothorax, unconsciousness, respiratory paralysis, convulsions and sometimes severe arterial hypotension. We present a case with transient locked-in syndrome following SGB for the management of sudden hearing loss. The risk of an intra-arterial injection can be eliminated by rotating the needle, as is described in this report.
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6/26. Reversible cochleo-vestibular deficits in two cases of jugular foramen tumor after surgery.

    Primary jugular foramen (JF) tumor, such as glomus jugular tumor or JF schwannoma, may manifest as a lower cranial nerve deficit; in addition, it can be accompanied by deafness or vertigo if it affects the cranial nerve (CN) VIII. Recently, we encountered JF schwannoma 1 and glomus jugulare tumor 1. Both cases invaded the adjacent cerebellopontine angle, leading to cochleo-vestibular deficits prior to the operation. After surgery, recovery of the audiovestibular function, including hearing, auditory brainstem response and caloric response, was anticipated in both patients. Therefore, cochleo-vestibular deficits in JF tumors can be attributed to compression neuropathy, rather than tumor infiltration.
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7/26. Sudden hearing loss as a first complication of long-standing Type 1 diabetes mellitus: a case report.

    The term 'sudden hypoacusis' describes a hearing loss of a rapid onset and unknown origin that can progress to severe deafness. Its pathophysiology is still unknown, the proposed aetiological mechanisms being vascular disease or autoimmune reaction. We present the case of a 19-year-old woman with Type 1 diabetes mellitus who experienced sudden hearing loss on her right side. She had no complications related to diabetes. After being referred to the hospital she was diagnosed with sudden sensorineural right-sided hearing loss accompanied by high frequency tinnitus. After administration of vasoactive drugs, there was partial improvement after 7 days, followed by gradual improvement over the next 4 weeks to 5 months. The tinnitus did not disappear completely. We conclude that hearing organ disturbances can be present in Type 1 diabetes and represent an early complication.
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8/26. pathology and pathophysiology of idiopathic sudden sensorineural hearing loss.

    BACKGROUND: The cause and pathogenesis of idiopathic sudden sensorineural hearing loss remain unknown. Proposed theories include vascular occlusion, membrane breaks, and viral cochleitis. AIMS: To describe the temporal bone histopathology in 17 ears (aged 45-94 yr) with idiopathic sudden sensorineural hearing loss in our temporal bone collection and to discuss the implications of the histopathologic findings with respect to the pathophysiology of idiopathic sudden sensorineural hearing loss. methods: Standard light microscopy using hematoxylin and eosin-stained sections was used to assess the otologic abnormalities. RESULTS: Hearing had recovered in two ears and no histologic correlates were found for the hearing loss in both ears. In the remaining 15 ears, the predominant abnormalities were as follows: 1) loss of hair cells and supporting cells of the organ of corti (with or without atrophy of the tectorial membrane, stria vascularis, spiral limbus, and cochlear neurons) (13 ears); 2) loss of the tectorial membrane, supporting cells, and stria vascularis (1 ear); and 3) loss of cochlear neurons only (1 ear). Evidence of a possible vascular cause for the idiopathic sudden sensorineural hearing loss was observed in only one ear. No membrane breaks were observed in any ear. Only 1 of the 17 temporal bones was acquired acutely during idiopathic sudden sensorineural hearing loss, and this ear did not demonstrate any leukocytic invasion, hypervascularity, or hemorrhage within the labyrinth, as might be expected with a viral cochleitis. DISCUSSION: The temporal bone findings do not support the concept of membrane breaks, perilymphatic fistulae, or vascular occlusion as common causes for idiopathic sudden sensorineural hearing loss. The finding in our one case acquired acutely during idiopathic sudden sensorineural hearing loss as well as other clinical and experimental observations do not strongly support the theory of viral cochleitis. CONCLUSION: We put forth the hypothesis that idiopathic sudden sensorineural hearing loss may be the result of pathologic activation of cellular stress pathways involving nuclear factor-kappaB within the cochlea.
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9/26. conversion disorder in a child presenting as sudden sensorineural hearing loss.

    Pseudohypoacacusis is a form of conversion disorder in which a hearing loss is found in the absence of organic disease. A case of an 11-year-old boy with auditory conversion disorder after mild head trauma is reported. The child presented with unilateral hearing loss, with no accompanying vestibular symptoms and no history of otologic disease. Auditory testing revealed severe right-sided sensorineural hearing loss, however, CT scan was normal. There was a family history of conversion disorder and the child was undergoing an emotionally stressful period. It was decided to treat the child conservatively with close monitoring and a repeat audiogram 2 weeks later. One week after presentation, the child's hearing suddenly returned to normal after a second very minor head injury. It is important to consider pseudohypoacusis or conversion disorder even in cases such as trauma, when the clinical history supports a diagnosis of hearing loss.
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10/26. Abnormal vestibular evoked myogenic potentials in the presence of normal caloric responses.

    OBJECTIVE: Combined use of vestibular evoked myogenic potential (VEMP) and caloric response testing has enabled us to examine the function of the inferior and superior vestibular nerves separately. Although results of VEMP testing and caloric response testing have been reported for many diseases, a clinical entity showing abnormal VEMP responses but normal caloric test responses has rarely been reported. The aim of the study was to investigate clinical features of diseases showing abnormal VEMP responses with normal caloric test responses. STUDY DESIGN: Retrospective. SETTING: University hospital. patients: Eight hundred eleven patients with balance problems who had undergone both caloric response and VEMP testing were included in the study. MAIN OUTCOME MEASURES: The amplitudes and latencies of the first positive-negative peak of the VEMP (p13-n23) were measured. RESULTS: Forty of the 811 patients (5%) were found to have abnormal VEMP responses with normal caloric test responses. Clinical diagnoses of these patients were Meniere's disease (n = 12), acoustic neuroma (n = 8), sudden deafness with vertigo (n = 6), and other diseases (n = 6). Eight patients could not be diagnosed as having a disease already recognized. Clinical manifestations of these eight patients were rotatory vertigo in six patients and non-rotatory dizziness in two. None of these patients showed abnormalities other than VEMP responses on neurologic or neurotologic examinations. CONCLUSION: Apart from Meniere's disease, acoustic neuroma, and sudden deafness with vertigo, which are already known as diseases with abnormal VEMP responses but normal caloric test responses, some patients might be diagnosed as having a disease that involves only the inferior vestibular nerve region.
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