Sensorineural hearing loss va disability 40,ringing in ears worse at night club,tinnitus behandlung heidelberg hotels,harmonic sound therapy tinnitus 2014 - Easy Way

Enlarged vestibular aqueduct (EVA), the most common radiological finding in children with sensorineural hearing loss, is associated with variable auditory and vestibular symptoms.
Twenty patients diagnosed with sensorineural hearing loss and EVA were included in the study group and 20 healthy individuals matched for age and sex were included in the control group. Both groups were subjected to the following: complete history taking, general and neurological examination, full ENT examination, pure tone audiometry, tymanometry, high-resolution computed tomography, vestibular evoked myogenic potentials (VEMP), caloric test, and computerized dynamic posturography. The VEMP amplitude of wave p13–n23 was higher in ears with EVA and it correlated positively with its size.
Some patients showed abnormalities in the caloric test, which indicates a peripheral vestibular lesion. Audiovestibular manifestations in a radiologically confirmed enlarged vestibular aqueduct in congenital nonsyndromic sensorineural hearing loss in Egypt. In 1978, Valvassori and Clemis 1 were the first to use imaging and to find an association between enlargement of the vestibular aqueduct and sensorineural hearing loss (SNHL).
Enlarged vestibular aqueduct in congenital non-syndromic sensorineural hearing loss in Egypt.
The large vestibular aqueduct syndrome and sensorineural hearing loss in the pediatric population. Characteristics of vestibular evoked myogenic potentials in children with enlarged vestibular aqueduct.
Large vestibular aqueduct syndrome: audiological, radiological, clinical, and genetic features.
The large vestibular aqueduct: a new definition based on audiologic and computed tomography correlation.
Coronal computed tomography of the normal vestibular aqueduct in children and young adults. The large vestibular aqueduct syndrome in children: a review of 12 cases and the description of a new clinical entity. Diagnostic yield of high-resolution computed tomography for pediatric sensorineural hearing loss.
Clinical investigation and mechanism of air-bone gaps in large vestibular aqueduct syndrome.
Clinical and diagnostic characterization of canal dehiscence syndrome: a great otologic mimicker. Superior semicircular canal dehiscence presenting as conductive hearing loss without vertigo.
Vestibular-evoked myogenic potentials in the diagnosis of superior canal dehiscence syndrome. The caloric test showed an absent response in four patients, unilateral weakness in six patients, and normal results in 10 patients. There was no statistically significant difference in the results of computerized dynamic posturography.

The characteristics of hearing affection have been studied extensively in patients with EVA, but not much information exists on vestibular affection in these patients.Al Attia et al. 5 reported an 18-year-old Egyptian man with Pendred syndrome.The aim of this study was to detect vestibular findings in patients with EVA. The study was carried out on two groups: the study group included 20 children with nonsyndromic SNHL and diagnosed with EVA by high-resolution computed tomography (HRCT).
Single-component, single-frequency tympanometry with a probe tone of 226 Hz was performed to exclude middle ear abnormalities. A noncontrast computerized tomography (CT) scan of the petrous temporal bone in axial and coronal planes was performed in all patients included in the study.
The radiological dimensions of the VA were measured at both the operculum and the midpoint on the right and the left side. They were instructed to turn and hold their heads as far as possible toward the side contralateral to the stimulated ear. The active electrode was placed over the middle portion of the ipsilateral sternocleidomastoid muscle. The reference and the ground electrodes were placed over the upper sternum and on the midline forehead, respectively. Auditory stimuli consisted of clicks presented to the ear ipsilateral to the contracted sternocleidomastoid muscle.
Electromyograph responses from each side were amplified, bandpass filtered (20 Hz–2 kHz), and averaged using a Neuropack evoked potential recorder. Thereafter, the mean peak latency (in ms) and peak-to-peak amplitude (in mV) of each peak (p13 and n23) were measured.
The sensory organization test (SOT) procedure requires patients to stand on a pressure-sensitive, dynamic tilted force plate facing a sway-referenced visual surround, instructed and strapped into a safety harness to prevent injury in the event of a loss of balance. HRCT did not indicate any associated congenital anomalies.The range of the dimensions of the vestibular aqueduct at the midpoint and the operculum in ears with EVA, unaffected ears, and the control group is presented in [Table 2]. There was a statistically significant difference between the ears with EVA and the control group in the mean of the VEMP amplitude, which was larger in ears with EVA. There was no correlation between the size of the VA and the latency of p13–n23, degree of hearing loss, caloric test results, and the results of computerized dynamic posturography. The aim of this study was to determine vestibular findings in patients with EVA.In this study, we investigated 20 patients diagnosed with SNHL and EVA. Our study was in favor with the study group that comprised 16 patients (32 ears) suffering from nonsyndromic SNHL since childhood. The study group was divided according to the VA size into three groups: groups A, B, and C.
Group A included six ears (four patients) with EVA, group B included 11 ears (seven patients) with borderline EVA, and group C included 15 ears (nine patients) with a normal VA size 4.
Similarly, there were no statistically significant differences between the three groups in laterality, degree of hearing loss, and audiometric configuration.

There was no correlation between the VA midpoint and operculum and different variables (age and average pure tone thresholds). Arjmand and Webber 13–15 found that the hearing threshold level in patients with EVA ranged from none to profound, with 65% of ears having mild or moderate hearing impairment. The mechanism of hearing loss is a breach in homeostasis of inner ear electrolytes and the transmission of cerebrospinal fluid pressure fluctuations through the patent VA 16.The patients in our study were evaluated by axial and coronal HRCT. The place at which the VA is measured is also variable, from midway between the common crus and external aperture to the external pore 20,21.
Other authors have defined the EVA by comparing it with the posterior semicircular canals 22 or the diameter of the facial nerve 23,24.In this study, EVA was bilateral in 14 (70%) patients and unilateral in six (30%) patients.
In different studies, the incidence of bilateral EVA has ranged from 55 to 94% 2, 3, 13, 25. 4, who reported bilateral SNHL of variable degrees ranging from slight SNHL to total hearing loss.
Seven patients had borderline EVA, four of them had bilateral borderline EVA, and the remaining three patients had unilateral borderline EVA.
Nine patients had vestibular aqueduct dimensions that were within normal, six of them had bilateral normal VA, and the other three had unilateral normal VA.In the current study, six (30%) patients had vestibular symptoms in the form of vertigo and nausea in four (20%) patients and imbalance in two (10%) patients. 28 found that one patient complained of positional vertigo and in one patient, vertigo increased on coughing and sneezing.
Vestibular complaints such as vertigo and imbalance may be caused by an underdeveloped vestibular 12,28.In our patients, VEMP findings were larger VEMP amplitude in ears with EVA (34 ears) when compared with either the control group (40 ears) or unaffected ears (six ears) [Table 6].
29 found VEMP abnormalities in patients with EVA, indicating possible saccular dysfunction. 33 30 found that nine (53%) of 17 patients with EVA had unilateral or bilateral weakness on electronystagmography testing.The mechanism of vestibular abnormalities is believed to be because of the degeneration of vestibular hair cells as a result of osmotic changes or injury caused by chemical imbalance 34. 12 postulated that vestibular dysfunction in all patients with EVA may be because of vestibular end-organ pathology.On comparing the computerized dynamic posturography of SOT parameters between the study group and the control group, there was no statistically significant difference between the two groups. Unfortunately, these results obtained could not be compared with others because of the scarcity of researches at this point 35.In this study, there was a significant positive correlation between the size of EVA and VEMP amplitude, but there was no correlation between the size of EVA and the degree of SNHL, VEMP latencies, caloric test results, and computerized dynamic posturography. 23 have reported a significant correlation between VA size and severity of hearing impairment in patients with EVA and cochlear dysplasia.
Several other reports have failed to show a relationship between VA size and the degree of SNHL [12],[36].
VEMP, caloric test, and computerized dynamic posturography testing were effective for the evaluation of patients with EVA.

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