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1/10. Persistent bilateral hearing loss after shunt placement for hydrocephalus. Case report.

    Transient hearing decrease following loss of cerebrospinal fluid (CSF) has been reported in patients undergoing lumbar puncture, spinal anesthesia, myelography, and/or different neurosurgical interventions. The authors present the first well-documented case of a patient with persistent bilateral low-frequency sensorineural hearing loss after shunt placement for hydrocephalus and discuss the possible pathophysiological mechanisms including the role of the cochlear aqueduct. These findings challenge the opinion that hearing decreases after loss of CSF are always transient. The authors provide a suggestion for treatment.
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2/10. meningeal carcinomatosis manifested as bilateral progressive sensorineural hearing loss.

    OBJECTIVE: meningeal carcinomatosis is defined as the diffuse infiltration of the leptomeninges and subarachnoid space by malignant cells metastasizing from systemic cancer. The authors describe a rare case of meningeal carcinomatosis initially appearing as bilateral progressive sensorineural hearing loss. PATIENT: A 57-year-old man with lung cancer was referred to the authors' clinic because of progressive hearing loss, tinnitus, dizziness, and blurred vision for 1 month. RESULTS: magnetic resonance imaging revealed abnormal leptomeningeal enhancement. meningeal carcinomatosis was diagnosed by the detection of malignant cells in the cerebrospinal fluid after lumbar puncture. The patient died 1 year after diagnosis. CONCLUSIONS: meningeal carcinomatosis must be considered in the differential diagnosis in cancer patients with bilateral progressive sensorineural hearing loss. gadolinium-enhanced magnetic resonance imaging is a useful complementary diagnostic tool before lumbar puncture.
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3/10. Permanent sensorineural hearing loss following spinal anesthesia.

    A 25-year-old female developed permanent, fluctuating sensorineural hearing loss (SNHL), disabling vertigo, and tinnitus following an uneventful spinal anesthesia for cesarean section. At her first visit to the ear-nose-throat (ENT) department approximately 2 months postoperatively, pure-tone thresholds revealed profound SNHL on the right side whereas thresholds were within normal limits on the left side. The recruitment score (SISI) was 95% at 2000 Hz on the right side. Directional preponderance towards the right and the right canal paresis were evidenced by bithermal caloric testing. At follow ups the pure tone thresholds have shown some improvement, but fluctuating SNHL, disabling vertigo attacks, and tinnitus have remained. These findings imply a cochlear pathology causing endolymphatic hydrops possibly induced by lumbar puncture for spinal anesthesia.
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4/10. Enteroviruses and sudden deafness.

    A young, healthy man presented with sudden severe sensorineural hearing loss and tinnitus. The results of the workup and neuroimaging were normal, as were the auditory brain stem responses. methylprednisolone pulse therapy was associated with significant hearing improvement within 10 days. A history of a short self-limited febrile illness preceding admission (with headache, photophobia, myalgia and fatigue), a raised serum c-reactive protein level and transient leukopenia suggested an infectious cause. Lumbar puncture revealed a mononuclear pleocytosis of the cerebrospinal fluid, with negative cultures but positive polymerase chain reaction test results for enterovirus, which was later cultured from the patient's stool. The patient's wife and baby had had a similar febrile illness without hearing loss 10 days earlier, and an outbreak of enterovirus meningitis was identified in the area, which was associated with familial clustering and echovirus serotype 4 infection. The varied causes of sudden sensorineural hearing loss, which should include enterovirus, are reviewed here.
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5/10. hearing loss as a sequel of lumbar puncture.

    Only a few case reports have been published about hearing impairment following lumbar puncture, and not all were thoroughly documented by audiograms. We present nine cases of hearing loss following myelography, lumbar puncture, and spinal anesthesia. We speculate that this rare complication arises only in persons with a wholly or partially patent cochlear aqueduct, and occurs via the release of perilymphatic fluid in the cerebrospinal space. hearing loss was seen in eight of the nine patients in the lower frequencies, and in six of the nine patients on both sides. Recovery to normal hearing was noticed in six of the nine patients. Transient hearing loss may occur more often than it is generally assumed, and the symptom can remain unnoticed. Since not all of these hearing losses proved to be fully reversible, we suggest informing patients about this complication for medicolegal reasons.
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6/10. Recurrent hearing loss after myelography treated with epidural blood patch.

    Transient hearing impairment is a known sequel after various procedures that result in loss of cerebrospinal fluid, such as lumbar puncture, spinal anesthesia and myelography. But persistent or recurrent hearing loss after dural puncture is a rare entity. We present a case with recurrent low-frequency sensorineural hearing loss after myelography. The patient was treated successfully by means of an epidural blood patch, although the conservative treatment was ineffective.
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7/10. Therapeutic acupuncture for sensori-neural deafness.

    This article presents a case report of a 29 year-old Nigerian male with sensori-neural deafness since the age of 7 years managed by therapeutic acupuncture according to the classical Chinese technique. The patient was examined by radiological pictures in addition to biochemical and physical examinations. No medications were administered during the course of therapy. The study indicates that the impressive result obtained is due to the ability of therapeutic acupuncture to improve speech discrimination and hearing ability in our patient with sensori-neural deafness.
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8/10. Cogan's syndrome manifesting as sudden bilateral deafness: diagnosis and management.

    Cogan's syndrome is an uncommon entity of nonsyphilitic interstitial keratitis with vestibulo-auditory disturbances. Although it is unusual, Cogan's syndrome should be considered in the differential diagnosis of patients with sudden hearing loss, even when they lack ophthalmologic symptoms. Systemic manifestations are not uncommon and, along with serologic and hematologic abnormalities, may help in making the diagnosis, which requires a high index of suspicion. Treatment with steroids has largely been based on symptoms. We suggest using the c-reactive protein level as a monitor of subclinical disease activity; it is therefore beneficial in the adjustment of steroid therapy. We have described the case of a 41-year-old woman who sought treatment for an upper respiratory infection syndrome and severe vertigo. Evaluation included hematologic and serologic studies, lumbar puncture, and CT and MRI scans. Abnormal findings consisted of an elevated white blood cell count and an ESR of 112 mm/hr. Six days later, profound, bilateral sensorineural hearing loss developed suddenly. Intensive corticosteroid and vasodilator therapies were instituted, but there was no improvement in hearing levels. Ten days later eye pain and redness developed, and ophthalmologic evaluation revealed an interstitial keratitis consistent with Cogan's syndrome. Steroid eye drops and oral prednisone therapy promptly relieved the eye symptoms. Steroid tapering was associated with diffuse joint pain and swelling consistent with a systemic vasculitis. After rheumatologic consultation, steroid dosage was titrated to the CRP level and ESR, and vasculitic symptoms resolved. Hearing levels did not improve, and the patient had cochlear implantation. Thirteen cases of bilateral sudden deafness due to Cogan's syndrome have been reported previously. This is the first case in which there were no immediate eye symptoms.
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9/10. Repetitive hearing loss following dural puncture treated with autologous epidural blood patch.

    A case of repetitive hearing loss following an otherwise uncomplicated diagnostic dural puncture is presented. The patient developed severe postdural puncture headache (PDPH) and three episodes of pronounced vestibulocochlear disturbances within five weeks after only one dural puncture. On all three occasions the headache and the associated symptoms were treated with an autologous epidural blood patch (AEBP) resulting in the immediate disappearance of all the subjective complaints of postdural puncture headache and the normalization of an audiological test within minutes.
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10/10. Bilateral disc edema in retinitis pigmentosa.

    retinitis pigmentosa (RP), one of the most common forms of hereditary retinal degeneration, is characterized by night blindness and constricted visual fields. In addition to bone spicule pigmentation, other ocular findings may include posterior subcapsular cataracts, cystoid macular edema, and hyaline bodies or drusen of the optic nerve. Rarely, optic nerve head (ONH) edema has been reported to be associated with RP. A 44-year-old white male with RP and neurosensory hearing loss (Usher's syndrome type II) presented to our clinic for routine examination. A dilated fundus examination revealed bone spicule pigmentation, vessel attenuation, several flame hemorrhages on or adjacent to the nerves, and ONH edema in the right eye. B-scan ultrasonography revealed drusen of the right ONH but not of the left. Late stage fluorescein angiography showed hyperfluorescence and dye leakage from both optic discs which was more pronounced in the right eye than the left. Computed tomography (CT) of the head and orbits and cerebrospinal fluid (CSF) examination by lumbar puncture were normal. The differential diagnosis of bilateral ONH edema in this case included ONH drusen or papilledema secondary to increased intracranial pressure. This patient was found to have RP with asymmetric, bilateral ONH edema of unknown cause. One theory regarding the cause of the ONH edema is disc vessel leakage secondary to an inflammatory reaction caused by rapid photoreceptor and retinal pigment epithelium (RPE) degeneration.
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