Mild bilateral sensorineural hearing loss letra,ear canal noise cancelling headphones,knocking noise in my ear - And More

Author: admin, 10.11.2015. Category: Cause Of Ringing In Ears

Are the consequences of neonatal hearing loss serious enough that we need to be concerned about them in the first place? Slide #47 shows data from an annual survey done each year by Gallaudet University showing that children with severe profound bilateral losses suffer from substantial deficits in reading comprehension. Although virtually everyone agrees that severe profound bilateral hearing loss has substantial negative consequences for all aspects of academic performance, the consequences of mild bilateral or unilateral hearing loss are less well known. The data in slide #50 come from the Greater Boston Otitis Media Study Group, where 194 children were followed prospectively for 7 years. Sensorineural Hearing Loss is a hearing loss due to impairment or degeneration of the cochlear (inner ear) resulting in an irreversible hearing loss. Bilateral Hearing Loss is a hearing loss, either sensorineural or conductive, in both ears.
Unilateral Hearing Loss is a hearing loss, either sensorineural or conductive, in one ear only. Congenital atresia of the external ears and severe tinnitus has been reported by two patients to be contralateral to the atretic ear.
Our clinical experience since 1977 with tinnitus of the severe disabling type (subjective idiopathic tinnitus [SIT]) in more than 10,000 patients leads us to consider the establishment of a clinical accuracy for the diagnosis of tinnitus as the "key" to achieving tinnitus relief with therapeutic modalities now available.
The completion of a medical audiological tinnitus patient protocol (MATPP) for SIT patients, with extensive testing of the cochleovestibular system, both peripheral and central, has been recommended to establish (1) accuracy of diagnosis of tinnitus, (2) its medical significance, and (3) a rationale for treatment based on a correlation of structure and function [4-6]. Patients with congenital atresia of the external ear and SIT completed the MATPP to establish an accurate diagnosis for the clinical type of tinnitus, to identify and treat factors influencing the clinical course of the tinnitus, and to establish a rationale for attempting tinnitus relief. The patient's tinnitus was described as a noise in "spells of increased intensity of a constant rumble in the left ear," fluctuant intensity, and increasing annoyance within 1-2 months before his neurotological consultation on November 30, 2004. We informed the patient that although no cure was available for tinnitus at this time, the goals of the consultation were to attempt to establish a clinically accurate tinnitus diagnosis and the medical significance of the tinnitus and to attempt to provide tinnitus relief by medication alone or in combination with instrumentation. We recorded the left-ear tinnitus intensity reported by the patient on a tinnitus intensity index (TII) and a tinnitus annoyance index (TAI).
Associated complaints included increased left-ear hearing loss, fluctuant left-ear blockage, and weight loss of approximately 20 pounds. Sudden-onset tinnitus in the left ear occurred while the patient was at work on May 5, 2004, in a standing position. Tinnitus originally was reported as an intermittent "highpitched ring" in the left ear at age 21-25 after exposure to loud music. The patient's significant history included congenital atresia of the right external ear, presence of allergies, presence of hearing loss following noise exposure (including to firearms), and reconstructive surgery to the external right ear at age 6-7 years, and hospitalization for kidney stones. The physical examination included evaluation of the patient's general appearance and an external inspection, both of which were found to be satisfactory. Site-of-lesion audiometry identified severe hearing loss, which was mixed and predominantly conductive, on the right. Electronystagmography (December 1, 2004) revealed no spontaneous nystagmus, positional nystagmus, or neck torsion.
A computed sinusoidal harmonic rotation test (December 1, 2004) revealed left labyrinthine asymmetry, normal saccadic eye movement, and normal OFS. QEEG (December 1, 2004) demonstrated significant electrical dysfunction in the central nervous system (CNS)(Fig. Baseline SPECT of brain findings (November 2, 2004) included bilateral parietal lobes hypoperfusion, more dominant on the right than on the left side, and bilateral mesial temporal hypoperfusion, more prominent on the right (Fig. Neuroradiology suggested findings may represent vascular deficiency as opposed to cortical atrophy.
An MRI of the brain with gadolinium (May 10, 2004) showed none of the following: acute infarct or intracranial mass lesion, cerebellopontine angle mass or abnormal enhancement within the IAC or inner ears bilaterally, or otomastoiditis.
MRI and MRA scans (December 16, 2004) demonstrated a small area of flow gap or narrowing in the proximal portion of the straight sinus. Tinnitus was diagnosed to be predominantly of a central type in the left ear but to be subclinical in the right ear and to have a bilateral cochlear component. Additional diagnoses included an anxiety syndrome and bilateral heterochromia of the irises. Arteriovenous (AV) fistula, dural fistula, bilateral SEH, autoimmune inner-ear disease, hereditary sensorineural hearing loss, anterior internal cerebral artery (AICA) syndrome (left-sided), and cerebrovascular disease all were recommended to be ruled out. The initial ear, nose, and throat (ENT) consultation took place 2 days later (May 8, 2004).
The patient made an emergency room visit (May 9, 2004) for evaluation of recurrent and increased intensity of the rumble and with concern about left-ear hearing. Neurotological consultation and follow-up visits (November 30, 2004-December 7, 2004) clinically established the following diagnoses: tinnitus of a predominantly central type in the left ear, with a left cochlear component, and subclinical in the right ear. Neurotological recommendations (December 4, 2004) for attempting tinnitus control included general rules pertaining to diet, such as elimination of stimulants and caffeine, and use of ear protection from noise, and specific recommendations of a combined therapy via medication and instrumentation, differentiating between sensory and affect components. For the sensory component, we recommended medication initially, followed by introduction of instrumentation. For treatment of the affect component, we recommended follow-up with neuropsychiatry and psychology for the anxiety syndrome complaint and for fear. Close observation was advised to include clinical consideration of gradual, progressive cerebrovascular disease.
Neurological followup evaluation (December 9, 2004) reported the tinnitus to be associated with "pressure pulsations" in the left head area. Neurological follow-up on January 14, 2005, reported persistent pulsation tinnitus on the left side of the patient's head.
A neurotological follow-up visit on January 25, 2005, reflected attempts of tinnitus relief from December 7, 2004, to January 25, 2005, as initially recommended and which, by cooperation between the neurologist and the patient, were completed. The patient reported overall improvement-"water sound in back of head" gone since December 14, 2004-and described the quality of tinnitus frequency as "midrange electric motor" and "80-90% gone." Location of the tinnitus-left ear and back of the head on the right side-was significant. During telephone communication with the neurology physician (February 4, 2005), the patient reported that he was "doing OK," although concern about steroid dependence persisted in order to maintain tinnitus relief. In a telephone communication with the neurotology physician (February 15, 2005), the patient reported tinnitus relief was being maintained.
At a follow-up visit with neurotology (March 8, 2005), the patient reported tinnitus relief of 15-20% and increasing periods of "ignoring the complaint," with associated reduction in anxiety. During telephone communications with the neurotologist (March 15, 2005-April 12, 2005), the patient reported continued increasing periods and degrees of tinnitus relief.
In telephone communication between the neurotologist and the patient (September 13, 2005), the patient reported tinnitus relief in excess of 90%, absence of any spells, occasional ear blockage prior to or accompanying the tinnitus, no imbalance, and occasional hyperacusis with tinnitus. During further telephone communication with the neurotologist (December 20, 2005), the patient reported tinnitus "rumble" relief in excess of 90%.
The etiology of the symptom of tinnitus, as described at the time of and following completion of neurotological consultation (November 30, 2004-December 7, 2004), is considered to have a chiefly vascular basis, reflecting insufficiency of the anterior and posterior intracerebral circulation, and to be a predominantly "soft" sign of gradual, progressive cerebrovascular disease. The clinical history of the original tinnitus, described as an intermittent high-pitched ring in the left ear, is traced to age 21-25 and occurred after exposure to loud music (TII: best = 0 [95%] and 7 [3 days in duration after noise exposure]). Within the limits of examination at this time, we hypothesized that the clinical course of the tinnitus as described is a reflection of a gradual alteration in the hemodynamics of the intracerebral circulation, highlighted at this time by SPECT of brain of hypoperfusion in regions of interest supplied by the right MCA. We considered a presumptive left SEH to be clinically related to alteration in homeostatic mechanisms between the fluid compartments of the brain and inner ear, with the resultant accompanying imbalance and reported left-ear hearing loss (May 5, 2004). Acknowledged was the clinical history of a sudden onset of the tinnitus and the clinical history of tinnitus described as an increase in left-ear ringing 3-4 years ago. We recommended SPECT of brain in an attempt to improve the accuracy of the tinnitus diagnosis, to monitor the efficacy of modalities of therapy attempting tinnitus relief, and to provide a basis for neuroprotective drug therapy.
In an attempt to establish a specific vascular etiology, to exclude AV dural fistula, AV malformations, and cisternal and venous sinus anomalies, we recommended MRI, MRA, and MRV, which were reported to be essentially normal. In summary, we considered the tinnitus complaint in the left ear (as described on November 30, 2004) and its clinical course predominantly to be a "soft" sign of CNS dysfunction, on a vascular basis, superimposed on a preexisting sensorineural hearing loss.
Is the reported SPECT of brain finding of hypoperfusion of the MCA in patients with a congenital atresia of the external ear an anomaly or a coincidence of occurrence [10-12]?
We consider to be clinically significant the objective demonstration of hypoperfusion in brain areas of distribution of the MCA on the side of the congenital atretic ear in two patients. Over the long term, the inclusion of nuclear medicine imaging of brain and follow-up in cases of congenital atretic ear wherein this finding was demonstrated will determine the significance of the clinical course of cerebrovascular disease and cochleovestibular complaints in atretic and nonatretic ears. Is brain plasticity altered in the patient with a congenital atretic ear for tinnitus therapies hypothesized to occur at brain cortex [13-20]?
Electrical and air conduction UHF thresholds of hearing (10-20 kHz) in the two cases of congenital atresia of the external ear (in both the ipsilateral and contralateral ears) were greater than expected for the age of the patient.
Is the identification of a UHF sensorineural hearing loss greater than expected for the age of a patient, particularly a tinnitus patient with a congenital atresia of the external ear, a sign of predisposition to the effects of noise exposure and gradually increasing sensorineural hearing loss? Is the finding of hypoperfusion in brain areas of distribution of the MCA in congenital atresia of the external ear a predisposition or a factor (or both) in the development of SEH [27-31]? We considered the SEH and tinnitus in the contralateral ear to be a sign of the effect or presence of a vascular anomaly or an alteration in the intracerebral circulatory pattern on the side of the brain contralateral and secondary to the hypoperfusion in brain areas of the MCA in the atretic ear. The diagnosis of a delayed SEH in patients with tinnitus of the severe disabling type has been reported to be frequent and to influence the clinical course of tinnitus [27]. Clinically, the tinnitus described as a ringing in the ear contralateral to the atresia is considered a soft sign of inner-ear dysfunction.
What pathology in this tinnitus patient is reflected in the action of the drugs selected for attempting tinnitus relief (i.e., specifically steroids)? In addition to therapy directed at factors identified as influencing the clinical course of the tinnitus, therapy directed to the GABA-A receptor is hypothesized to increase inhibition at the brain cortex and provide neuroprotection, with resultant increased tinnitus relief and reduction or elimination of the steroid.
What is the incidence of an autoimmune etiology in patients with sensorineural hearing loss? The clinical history of the tinnitus in association with an alteration in hearing in the nonatretic ear introduces the consideration of autoimmune inner-ear disease.
What is the incidence of occurrence of objective and subjective tinnitus in the tinnitus population and, in particular, in the tinnitus patient with an atretic ear?
In the patient in this report, the objective tinnitus was the rumble auscultated with the stethoscope at the left lateral neck overlying the external ear and left postauricular fold. Is the congenital atretic external ear part of a syndrome that includes the MCA and a loss in the UHFs (10-20 kHz)?


SPECT of brain has demonstrated hypoperfusion in brain areas of distribution of the MCA on the side of an atretic ear.
A neuroprotective drug therapy strategy targeting the GABA-A receptor (RTT-GABA), for treatment of a severe, disabling, predominantly central-type tinnitus, with a clinical diagnosis of brain cortical ischemia based on brain SPECT, resulted in significant longterm tinnitus relief.
The incidence of hypoperfusion in brain areas of distribution of the MCA on the side of the atretic ear in patients with congenital atresia of the external ear remains to be established. The authors gratefully express their appreciation to the Martha Entenmann Tinnitus Research Center, Inc., for support of this educational and research effort.
Fortunately, there is a wealth of data on this question, and only three very brief examples will be given related to children with severe profound bilateral losses, children with mild bilateral and unilateral losses, and children with fluctuating conductive losses (slide #46).
There are, however, a number of studies demonstrating that even mild or unilateral sensorineural hearing loss has substantial negative consequences. Although virtually all newborn hearing screening programs focus only on identifying children with permanent congenital hearing loss, some children with fluctuating conductive losses are often identified.
Each time the child visited his or her primary- care physician, data were collected about episodes of otitis media (there were an average of 7 visits per year during the birth to 3-year-old period).
Sensorineural hearing loss can be caused by aging, noise exposure, birth defects, medication and viral or bacterial infections.
This can be caused by impacted cerumen (wax), punctured eardrum, birth defects or otosclerosis. The use of the nuclear medicine imaging technique of single-photon emission computed tomography (SPECT) of brain has demonstrated hypoperfusion in brain areas supplied by the middle cerebral artery on the side of the atretic ear. Multifactorial elements influence the clinical course of SIT and attempts for establishing tinnitus relief [1-3]. We present these findings to support previous recommendations of extensive cochleovestibular and brain function testing to be completed in SIT patients. As far as we can determine, these findings, highlighted by brain SPECT, have not previously been reported in patients with congenital atresia of the external ear.
Also demonstrated were memory interference and increased tinnitus intensity reported with increasing left-ear blockage.
The TII at that time was reported as best (0; 95%) and worst (7) for 3 days after noise exposure. Ocular examination revealed symmetrical eyelids, clear conjunctivae, heterochromic irises, and equally reactive pupils without sign of spontaneous labyrinthine irritation. SPECT of brain: bilateral parietal lobes hypoperfusion, more dominant on the right than on the left side, and bilateral mesial temporal hypoperfusion, more prominent on the right.
Sinusitis was seen bilaterally, although it was more pronounced in the maxillary than the ethmoid sinus. A partial obstruction in this area was suspected, although artifact may have accounted for this finding. Hearing loss was mixed moderate-severe and predominantly of the conductive type in the right ear and of a mild sensorineural type in the left, with a bilateral cochlear component and involvement of the central auditory pathways bilaterally (see Fig. An objective tinnitus and presumptive secondary endolymphatic hydrops (SEH) was diagnosed in the left ear. SPECT of brain (December 2, 2004) reported hypoperfusion in regions of interest in brain consistent with distribution of the right MCA (see Fig. The diagnoses included atypical left-ear tinnitus, congenital right-ear deafness, structural anatomy of the seventh and eighth nerve complexes to be normal right as reported on the MRI obtained on May 10, 2004. Instrumentation recommendations were deferred pending tinnitus relief results and would include (if necessary) a trial tinnitus masker and UHF acoustic stimulation and external electrical stimulation and tinnitus retraining therapy. Follow-up with an internist was recommended to maintain stable blood pressure and to complete a metabolic battery with appropriate treatment as necessary. We further advised that the patient consider Klonopin use if no medical contraindication existed.
Progression complaints of hearing loss, tinnitus, vertigo, and ear blockage, alone and or in combination, were to be clinically considered a "soft" sign of gradual, progressive CNS disease. We hypothesized this original tinnitus to have been clinically predominantly a cochlear type before May 2004 and considered it to have become since age 21-25 years subclinical in the left ear.
We further conjectured a resultant ischemia at brain cortex with noisy spells at the brain cortex owing to left cortical activation and a cochlear tone (as previously outlined), reflecting activation of a subclinical left-ear tinnitus, due to possible interference in AICA blood flow to the left cochlea. Alteration in aeration of the middle ears secondary to Eustachian tube dysfunction or SEH (or both) identified in the left ear may result in fluctuation in hearing or progressive sensorineural hearing loss (or both). The hearing in the left ear has been stable clinically and confirmed by audiometric testing since November 30, 2004, and when the patient was last seen (September 13, 2005). When seen in initial neurotological consultation (November 30, 2004), the ear blockage had been predominantly located in the left ear and clinically related to left inner-ear SEH. The report of interference in memory 3 months before November 30, 2004, was considered significant.
The report of SPECT perfusion asymmetries in the brain was the basis for recommending a neuroprotective receptor-targeted therapy directed at the GABA-A receptor, in an attempt to treat a presumptive ischemia of the affected cortical areas. We considered the medical significance of the tinnitus symptom to be gradual, progressive cerebrovascular disease. What is the incidence of the hypoperfusion in brain areas of distribution of the MCA in patients with a congenital atresia of the external ear?
Follow-up nuclear medicine imaging studies in the atretic ear population with and without tinnitus will determine its incidence of occurrence. Nuclear medicine positron emission tomography imaging of brain before and after UHF stimulation revealed a correlation of metabolism of brain at the cortex, with residual neuronal function in the 10- to 20-kHz range of hearing [25].
Additional considerations to explain differences in UHF thresholds include exposure to loud noise and a hereditary sensorineural hearing loss.
Follow-up studies by hearing conservation programs in general and specifically for the population of tinnitus patients with a congenital atresia of the external ear will provide answers to this question. It is considered to be a reflection of the SEH: the result of failure to reestablish "normal" homeostatic mechanisms controlling the hemodynamics of the intracerebral vascular and spinal fluid systems in response to hypoperfusion in the areas of distribution of the right MCA. Within the limits of examination and supported by blood testing, we did not identify any evidence of autoimmune inner-ear disease.
Correlation of the findings of the neurotological workup with extensive testing of the cochleovestibular system (both central and peripheral and objective testing of CNS metabolic and electrophysiological responses) provided for accuracy of the tinnitus diagnosis and a rationale for achieving significant tinnitus relief. The medical significance of an objective and subjective tinnitus of the severe disabling type, as demonstrated with SPECT of brain, may be a soft sign of gradual, progressive cerebrovascular disease.
We suggest that the findings of hypoperfusion in brain areas of distribution of the MCA on the side of the atretic ear and hearing UHF thresholds in the ear contralateral to the atresia are part of a syndrome in patients with congenital atresia of the external ear. That gap continues to widen over time, with the average deaf child or youth never exceeding a grade equivalent of 3 years, in spite of the fact that most of them are enrolled in educational programs specifically designed for deaf students. Slide #48 summarizes information about five different students in which a sample of children with unilateral hearing loss were compared to similar children with normal hearing, and measures were taken about their performance in math, language, and social functioning. The reason for presenting this information is to emphasize the point that even mild fluctuating hearing losses have an important negative effect on developmental outcomes.
Data were also collected periodically on a wide variety of measures related to intellectual ability, cognitive functioning, and language competency by trained diagnosticians who were uninformed about the purposes of the study. There is no cure for this type of hearing ,loss; however, most patients with sensorineural hearing loss can be helped with hearing aids.
Surgery or medication can be an appropriate therapy for conductive hearing loss in some cases. Ultrahigh-frequency audiometry (UHFA) has revealed a bilateral loss of hearing greater than expected for the age of affected patients.
The clinical course of two cases of congenital atresia of the external ear and tinnitus supports this clinical experience. In addition, the patient experienced an occasional perception of "water rushing" 4-5 days after a reduction in the rumble intensity and a "ring" in the left ear. The patient reported an increased frequency of occurrence within the last 3-4 years and an increased intensity (average TII, 3) after left-ear rumble. A review of symptoms revealed anxiety, memory interference of 3 months' duration, and kidney stone.
During otoscopic examination, the external leftear canal was found to be satisfactory, whereas signs of reconstructive external right-ear surgery and right external canal atresia were seen. Among the tuning-fork evaluations, the Weber test showed right lateralization, whereas the Rinne test was positive on the left and negative on the right. Rightsided gaze testing showed a right-beating nystagmus with ocular fixation suppression (OFS), downward gaze testing resulted in vertical up-beating nystagmus with OFS, and left-sided gaze testing revealed dysrhythmia with no OFS. We considered magnetic resonance imaging (MRI) or magnetic resonance angiography (MRA) for further evaluation. A Diamox stress test could differentiate between the two but was deferred due to allergy to sulfa. An audiometric test (May 8, 2004) reported no response in the right ear but left-ear hearing within normal limits for language and speech and a mild sensorineural hearing loss at 4 kHz.
Intramuscular Decadron (10 mg) and continued Medrol Dosepak and Ativan (1 mg) for anxiety were recommended. Hearing loss in the right ear was predominantly mixed and involved a cochlear component, whereas there was a predominantly cochlear-type hearing loss in the left ear within normal limits for language and speech (see Fig.
A neuroprotective drug protocol was recommended of a receptor-targeted therapy, gabapentin (100-mg tablet in one dose to be titrated based on the TII), and clonazepam (Klonopin, 25 mg at bedtime), if not medically contraindicated, the dose to be titrated based on the TAI. Any deterioration in the patient's condition was to be assessed by an internist, a neurologist, or an ENT specialist, and should include audiometry in an attempt to maintain hearing. Neuroradiological follow-up including CT scan of the temporal bones confirmed right external-ear canal atresia, a dilated right IAC, and a normal left temporal bone.
The complaint of ear blockage was reduced in the left ear, and no vertigo or balance complaint remained. The rumble sound was objectively auscultated over the left external ear (November 30, 2004). We further hypothesized that a cerebrovascular factor, gradual in onset, "triggered" the subclinical left-ear tinnitus to manifest itself as spells of noise at the brain cortex, located in the head, and as a "tone" in the left-ear cochlea. Alteration in underlying homeostatic mechanisms maintaining normal function of the fluid compartments of the blood-brain and bloodlabyrinth barriers are hypothesized to have contributed to the left-ear SEH.


The UHFA findings of a loss of hearing greater than expected for the age of the patient may be a reflection not only of noise exposure in the past but, more significantly, together with the heterochromia of the irises, of a hereditary sensorineural hearing loss. To be considered at this time was a left-ear AICA syndrome associated with gradual, progressive cerebrovascular disease.
Recommendations included replacing the antiseizure medication topiramate (Topamax) with gabapentin (Neurontin) in combination with clonazepam (Klonopin). We advised the patient to enter into this decision-making process if the tinnitus complaint persisted and the significance of the tinnitus complaint outweighed the incidence of potential complications of angiography. Accurate tinnitus diagnosis by inclusion of peripheral and central tests of cochleovestibular function or dysfunction combined with tests of brain function (SPECT, QEEG) provided a rationale for tinnitus treatment that resulted in significant tinnitus relief, maintenance of hearing, and control of balance. Specifically, brain plasticity at the cortex was most effective with UHF acoustic stimulation when the integrity of the brain at the cortex was intact and the residual neuronal function in the 10- to 14-kHz range of hearing did not exceed audiometric thresholds (30-40 dB). For the future, routine hearing testing, including establishment of UHF audiometric thresholds in all patients with congenital atresia of the external ear, will provide an answer to the question of whether this observation is special for patients with congenital atresia of the external ear and will assist in the determination of its medical significance for hearing conservation in general.
It is considered clinically significant that the diagnosis of a secondary (delayed) endolymphatic hydrops was identified in two cases of congenital atresia of the external ear, in the tinnitus ear contralateral to the side of the atresia. We recommend conducting a complete evaluation of the cochleovestibular system, both peripheral and central, including nuclear medicine imaging (SPECT of brain, UHFA, and QEEG), in an MATPP for SIT patients to improve the accuracy of the tinnitus diagnosis, to provide a rationale for treatment, and to monitor the clinical course of the tinnitus complaint. As far as we know, the finding of hypoperfusion in brain areas of distribution of the MCA on the side of the atretic ear has not been previously reported. GABA-A-benzodiazepine- chloride receptor-targeted therapy for tinnitus control: Preliminary report. As shown in slide #49, children with unilateral hearing loss lagged substantially behind their peers regardless of the measure used, whether math, language, or social functioning. Results at 7 years of age for two groups of children are reported here: those with less than 30 days of otitis media over the 3-year period compared to those with 130 or more days of otitis media over the same period.
Quantitative electroencephalography (QEEG) has shown a significant central nervous system electrical dysfunction correlated with the SPECT of brain findings.
A sensation of "vertigo" of approximately 24-hour duration described as a "drunk feeling" followed the rumble sensation. Clinically, an ischemia was presumed to be present based on our past SPECT of brain experiences with tinnitus patients of the severe disabling type [10]. Physical examination was consistent with the diagnosis of chronic vasomotor rhinosinusitis, chronic catarrhal otitis media, and Eustachian tube dysfunction on the left. The patient reported an improvement, which included elimination of the vertigo and left-ear blockage and a reduction in the tinnitus intensity.
Initial neurological recommendations included continuation of the steroids in a tapered dosage and a trial of Topamax and verapamil if the tinnitus complaint persisted or recurred.
The patient reported no associated complaint of hearing loss, vertigo, ear blockage, nausea, headache, drowsiness, or blurring of vision. Our advice was to follow the neurological recommendation of Mobic, 7.5 mg bid, to assist in prednisone reduction, which was reported by the patient to be effective. The clinical history of spells of this tinnitus, which are influenced by steroids, is considered to be mainly cortical in location.
We considered both auditory percepts to be a clinical reflection of altered hemodynamics in cerebrovascular circulation.
Normal Eustachian tube function control has been maintained with decongestant nasal steroid spray.
We recommended neurological consultation follow-up to establish the neurological significance of these complaints and correlation with SPECT results, MRI reports, and central cochleovestibular test findings. The MRA results (December 16, 2004) showed a small area of flow gap or narrowing in the proximal portion of the straight sinus, leading to suspicion of a partial obstruction or artifact in this area. Clinically, such tinnitus patients reported tinnitus relief as most effective and demonstrated hypometabolism at the cortex. The diagnosis of SEH was supported by the subjective complaint of ear blockage in the tinnitus ear and its reduction with diuretic therapy. A maintenance dose of Klonopin and a gradually increasing dosage of the antiseizure drug gabapentin replaced the Topamax. Presented at the Thirty-First Congress of the Neurootological and Equilibriometric Society, Bad Kissingen, Germany, March 24-27, 2004.
Proceedings of the Fifth International Symposium on Meniere's Disease and Inner Ear Homeostasis Disorders. Even though the sample sizes are quite small in each of the studies, matching was generally done quite well and the results are very consistent. After statistically adjusting the results for a variety of demographic and socio-economic status variables, children with fewer episodes of otitis media did substantially better than their peers on all measures. The annoyance included interference in communication, concentration, performance, and participation in social activities.
A screening test revealed mixed moderate-severe right-sided hearing loss and mild left sensorineural hearing loss. Cranial nerve examination showed the eighth cranial nerve on both sides to be abnormal and the remaining nerves normal. The GABA-A receptor, with its inhibitory activity in brain function, exerts a neuroprotective action [8,11].
MRI of the IACs and brain (May 10, 2004) demonstrated no cerebellopontine or IAC angle tumor and no mass, otomastoiditis, acute infarct, or intracranial mass lesion.
The air conduction UHFA identified thresholds of sensorineural hearing loss greater than expected for the age of the patient (Fig. We also recommended discussion with a neurologist of an angiogram to rule out AV malformation or dural fistula if the tinnitus complaint persisted or progressed. The subjective tinnitus described as an occasional ringing is thought to be mostly cochlear in location. The complaint of ear blockage will be recurrent in this patient, and accurate diagnosis will determine the selection of treatment. Also recommended was that complaints of progressing or deteriorating hearing loss, tinnitus, vertigo, and ear blockage, alone or in combination, be followed up by repeat ENT and neurological consultation in an attempt to maintain hearing and to maximize attempts at tinnitus relief. We hypothesized that the original left-ear bruit was an objective tinnitus found on auscultation, reflecting predominance of the left vascular drainage. The etiology of the SEH (delayed) in both cases of congenital atresia of the external ear is considered to be cerebrovascular.
The difference averaged about one-half standard deviation, which is equivalent to more than a year's worth of development in reading or math achievement. Completion of the medical audiological tinnitus patient protocol, including SPECT of brain, UHFA, and QEEG, accurately established the clinical tinnitus diagnosis of predominantly a central-type tinnitus, a clinical hypothesis that the medical significance of the tinnitus is a "soft" sign of cerebrovascular disease, and provided a rationale for treatment directed to a presumed ischemia of brain based on a receptor-targeted therapy targeted to the GABA-A receptor, resulting in significant tinnitus relief. Steroid therapy and a low-sodium diet received prior to November 30, 2004, resulted in a reduction of spells of the rumble. The findings of SPECT of brain in areas of distribution of the MCA were the basis for recommending various tests. Factors that are identified in the clinical history and can influence (and have influenced) the clinical course of the ringing tinnitus included fluctuation in bilateral aeration of the middle ears, SEH identified in the left ear, noise exposure, and stress. We considered this vascular hypothesis to be supported by the central cochleovestibular test findings (auditory brainstem response, QEEG), the SPECT of brain report (December 2, 2004), and the clinical response of the patient to treatment with steroids and antiseizure medication. Close attention by patient and ENT specialists will improve the ability to maintain hearing and balance.
In addition, the alteration in the hemodynamics of the cere-brovascular circulation has been hypothesized also to involve the AICA, a long-term effect that may include SEH. The introduction of Mobic-a nonsteroidal antiinflammatory agent, on a neurologist's recommendation-in combination with gabapentin and Klonopin, was accompanied by elimination of the steroid and an increase in and maintenance of long-term tinnitus relief.
The goal of the patient for this consultation was to obtain information about the tinnitus complaint, to obtain tinnitus relief, to identify the medical significance of the tinnitus, to maintain hearing in the left ear in view of right hearing loss associated with congenital atresia in the right external ear, and a concern for the need for long-term prednisone therapy. On nasal assessment, mild right septal deviation and mild right-to-left hypertrophy of the turbinates were seen. UHF electrical-acoustic testing revealed sensorineural hearing loss greater than expected for the age of the patient (Fig. Computed tomography (CT) scan of temporal bones (January 7, 2005) revealed right external canal atresia but no CT abnormality of the right bony labyrinth.
A follow-up neurological visit (July 9, 2004) reported the trial of verapamil for 2-3 days to be associated with an increased tinnitus intensity and was stopped by the patient. The neurotological workup and particularly the SPECT of brain identified significant bilateral perfusion asymmetries, greater on the right than on the left (see Fig. The extensive medical evaluation, to the limits of examina tion, has excluded coagulopathy and autoimmune disease. Paradoxically, the "dependence" on the steroid for tinnitus relief may have been a sign of a steroid toxicity related to increasing stress before and during the initial course of the tinnitus. As far as we can determine, these findings, highlighted by the brain SPECT, have not previously been reported in patients with congenital atresia of the external ear.
A dilated right internal auditory canal (IAC) showed no enhancing mass, but the right demonstrated abnormal pinna with calcifications. 4), highlighted by the perfusion asymmetry in regions of interest in brain areas of distribution of the right MCA. The affect component is complex and reflective of the frustration of patients with the complaint of tinnitus and fear of loss of hearing in the left nonatretic ear. Control of the foregoing factors highlighted by control of blood pressure is considered to provide an increased prognosis to maintain hearing and balance and tinnitus relief. Auscultation of the left ear side overlying the external auditory meatus and in the postauricular fold discovered a bruit (November 30, 2004).



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