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MASSAGE Massage Yoga Reflexology REMEDIAL, THERAPEAUTIC …Reiki is a gentle yet effective form of healing. WHAT CONDITIONS CAN IT HELP?Reiki energy is a safe, gentle, non-invasive form of REIKI hands on healing. Relief From Chronic tinnitusPresented in this book we can all make an active contribution to the healing process. Alternative Therapies For The Head Injury SurvivorAlternative and complimentary therapies for TBI that will speed the healing process and improve cognitive function and an introduction to behavior management.
INTRODUCTION: Sudden deafness is characterized by an abrupt onset, often idiopathic and tinnitus is present, and becomes the main complaint in up to 80% of patients.
OBJECTIVE: To review carefully all studies of the past 10 years on sudden deafness and tinnitus and analyze the effectiveness of oral and intratympanic steroids for tinnitus control in eight patients with sudden deafness and severe disabling tinnitus.
METHOD: An analytical prospective in which 64 patients after sudden deafness with tinnitus were monitored and 08 of these suffering with severe disabling tinnitus underwent hearing evaluation and application of the Tinnitus Handicap Inventory and Visual Analogue Scale before, during and after sudden deafness treated with oral and intratympanic steroids. Sudden sensorineural hearing loss (SSHL) was first described by De Kleyn in 1944 and defined as a hearing loss of at least 30 dB in three sequential frequencies in the standard pure-tone audiogram over 3 days or less1.
Population studies of SSHL show a wide distribution, ranging from 5 to 30 cases per 100.000 per year, with an average of 50-60 years and no sex preference.
Hypotheses are proposed to explain the pathogenesis of sudden hearing loss as the vascular, the viral, the autoimmune and the rupture of membranes one. Patients with tinnitus and SSHL are very frustrated by residual tinnitus even after accomplishment of the treatment for SSHNL.
All patients received information about the risks and expectations of therapy and signed a free informed consent form. Next, salvage therapy with intratympanic methyl-prednisolone was offered to XX patients with a diagnosis of SHL, after systemic therapy failed and no improvements were demonstrated audiometrically. All patients underwent tonal and vocal audiometry and speech recognition rate analysis done by audiologists before and after treatment. Prior to any procedure, patients were oriented as to the risks and expectations about the procedure and signed a free informed consent form. After intratympanic application of the steroid, the patient remained in the supine position and cervical rotation at 45? for 30 minutes to maximize exposure of the round window membrane to the solution. The criteria for defining successful recovery after therapy vary in the literature on intratympanic therapy.
All patients underwent Questionnaire Tinnitus Handicap Inventory (THI)5 and the Visual Analogue Scale (VAS) to assess quantitatively and qualitatively the therapeutic response in relation to tinnitus. The search strategy employed in the literature review was guided by the combination of two descriptors indexed in MeSH (Medical Subject Headings): sudden deafness and tinnitus. Most of the patients had vertigo associated with sudden deafness, being classified as mild in 75% of cases and severe in 12.5%. We performed a literature search with the following aliases: sudden hearing loss and tinnitus.
Their ages ranged from 26-73 years with a mean of 39,5 years and the ear most affected was the left ear (n = 5).
In this study, we chose to intratympanic corticosteroid associated with oral corticosteroids and showed that this association was particularly effective in relation to tinnitus, from the eight cases analyzed, seven of these showed a significant improvement verified by THI and EVA. Several factors may affect the prognosis of the PANSS (eg, hearing loss severity, symptoms duration before treatment, vertigo, type of audiogram, and the patients ages). Regarding hearing improvement, only two patients had good responses to therapeutic intervention.
Given the results, we note that in addition to the proposed intervention, especially those cases where there were no improvement or even where there were worsening of symptoms over time, there are other recommended therapies such as cognitive-behavioral and Tinnitus Retraining Therapy.
Some therapies for tinnitus tend to focus on the impact of noise on the quality of life and humor, and include antidepressants, anticonvulsants and benzodiazepines, or attempt to mask their own noise with white noise generators. In 2005, a review of published randomized clinical trials addressing the correlation between sudden sensorineural hearing loss and tinnitus and treatment by hyperbaric oxygen therapy (HBOT).
The sudden sensorineural hearing loss (SSHL) is a considerable diagnostic challenge because it can be caused by many different diseases and there is still no definitive treatment for PANSS universally accepted. In search of a therapeutic approach, the efficacy of enoxaparin sodium associated with venous hemofiltration was studied.
In 2008, Ishida et al.15 investigated how the symptoms of ear fullness, tinnitus and otoacoustic emissions (OAE) varied over the course of recovery thresholds in pure tone audiometry in SSHL. Kleinjung et al.16, in 2009, described the case of a man of 55 years who suffered from tinnitus in the right ear as a result of a SSHL.
Hikita-Watanabe et al.17, in 2010, in an article entitled "Tinnitus as a prognostic factor of sudden deafness", rebound that in the group "buzzing rare" there was a worst prognosis to hear than in the group "buzz often". In 2012, Fioretti et al.18 described the case of a 67 years-old women with severe and disabling tinnitus in the right ear, hyperacusis and mild headache. In 2012, a research was also conducted by Ramos et al.10, in which the authors assessed the effectiveness of cochlear implants in patients with SSHL and disabling tinnitus. The tinnitus severity was assessed using the Tinnitus Handicap Inventory (THI) and the Visual Analogue Scale (VAS) before and after deployment. Given the results, it can be concluded that the reduction of tinnitus after cochlear implantation may be due to several mechanisms such as habituation, acoustic masking, direct stimulation of the cochlear nerve and reorganization of cortical areas. Michiba et al.19, in 2013, highlighted the fact that many patients are frustrated with the SSHL residual buzz, even after complete SSHL treatment. The hearing improvement rate was determined by comparing the thresholds before and 6 months after initiation of treatment. The improvement of hearing thresholds were significantly correlated with improvement in the score of tinnitus 6 months after initiation of treatment compared with before treatment. Generally, subjective feelings for the ringing residual 6 months after initiation of SSHL treatment are almost the same as 24 months after treatment.
Patients that carriers sudden deafness and severe disabling tinnitus, and underwent intratympanic and oral corticosteroids showed, in this study, significant reduction or remission of tinnitus.
Paper submitted to the ITJ-SGP (Publishing Management System) on September 4, 2013; and accepted on October 4, 2013. Sudden deafness is a disorder characterized by an abrupt sensorineural hearing loss of unknown etiology. Sudden deafness is defined by a high degree of abrupt sensorineural hearing loss without clear causes for the loss. Eighteen patients who had received MRI examinations were chosen from patients complaining of sudden deafness. Pure-tone audiometry and short-increment sensitivity index tests were conducted on all patients.
To summarize, among the 18 subjects, 3 of the 5 patients (17%) with sudden deafness showing abnormal MRI findings had SBF of the VBS, 1 (5%) had an abnormal course of the VBS, and 1 (5%) had labyrinthine enhancement. Sudden deafness refers to abrupt sensorineural hearing loss of unknown etiology, often accompanied by tinnitus and vertigo. Viral labyrinthitis causes sudden deafness owing to infections caused by such viruses as measles or mumps, and it may occur without any other general symptoms. In the past, MRI was mostly used for the diagnosis of lesions of the internal auditory canal and of the cerebellopontine angle, and particularly for acoustic neuroma in deaf patients [5].
Seltzer and Mark [4] also reported that the MRI results of all five patients experiencing sudden deafness showed Gd-DTPA enhancement of the cochlea and the vestibule. Besides viral infections, circulation disorders of the inner ear are presumed to be a major cause of sudden deafness.
Regarding the relationship between the abnormal findings on MRI and vertigo, our study found that all the cases showing abnormalities on MRI also showed canal paresis. No significant relationship was found between MRI results and the type of audiogram or degree of hearing loss. Until now, the exact cause of sudden deafness has not been clarified, but abnormal blood flow of the inner ear is known as a cause of this disorder. The Gallbladder Meridian is a yang meridian and is paired with the Liver Meridian.This Meridian's Qi (energy flow) is responsible, among other, for decision making and good judgments, as well as providing courage and initiative.


She still has a lot of healing to do before she’ll be able to eat solid food again and live completely free of Tinnitus and pain.
It gives you a deep sensation of Ear candling can help with ear aches and soothe tinnitus. August 2006 Relieve tinnitus with especially developed therapies, including Shiatsu, Reiki, classical massage and deep-tissue massage.
Eight patients treated with intratympanic and oral corticosteroids were selected, just two patients showed improvement over the hearing but seven of them showed big improvement in their tinnitus, which was demonstrated by an improvement in the values of the degrees of severity of tinnitus.
In most cases, there is a unilateral hearing loss, with bilateral involvement reported en less than 5%1.
However, the current trend is to consider the sudden deafness as a disease of multifactorial etiology2. In idiopathic cases, the oral corticosteroids are widely used, although the supporting evidence is weak. However, there are few theories trying to explain its mechanism, one of than associates this symptom with a maladaptive attempts of a cortical reorganization process due to peripheral deafferentation4. The majority ask doctors about the prognosis of residual tinnitus at the final day of medical treatment for SSNHL. From June 2011 to July 2013, 64 patients with a diagnosis of sudden sensorineural hearing loss were seen at the otorhinolaryngology outpatient and emergency unit of our Center, Eight was suffering from severe disabling tinnitus. A detailed clinical history was taken, followed by an otoneurological examination, and an initial audiological assessment by tonal and vocal audiometry, impedance testing, speech recognition rate (SRR), laboratory tests, and an image exam (magnetic resonance imaging with contrast of the inner auditory canal). Eight patients suffering from severe disabling tinnitus agreed to undergo rescue therapy and signed the free informed consent form to be included in this study. All patients with fluctuating hearing loss or suspected Meniere's disease were also excluded from this study. A second injection was done if there was any possibility that the first injection was not adequate. A 20 dB improvement at 0.5, 1 and 2KHz, or a 20% improvement in discrimination was enough to consider the intervention as successful.
In the Visual Analogue Scale (VAS) score ranges from 1 to 10, where 10 represents the highest degree of tinnitus severity. However, corticosteroids seem to have universal acceptance and are the ones with proven effectiveness. Such treatments aim to improve inner ear oxygenation and include vasodilators, plasma expanders, steroids and anticoagulants11. In the EVA, it is observed that 100% of patients had a score greater than or equal to 7 and a significant reduction in scores of patients 1, 2, 3, 4, 7 and 8, in order to reduce at least two points on score and the same was observed in the degree of severity in THI (Table 1). Patient 2, despite their age, presents a clinical STD (sexually transmitted disease) that could prevent or reduce the effectiveness of the proposed treatment.
The administration of hyperbaric oxygen is based on the argument that both the hearing loss and the tinnitus may result from a hypoxic event in the cochlea, and that hyperbaric oxygen therapy may be able to reverse the oxygen deficit. Eight patients were followed with improvement in SSHL auditory thresholds (Group A) and eight patients with poor hearing improvement (Group B), to elucidate the behavior of these symptoms in your ongoing recovery. Several therapeutic efforts including intravenous steroids and graft in the round window showed no positive responses.
All subjects had SSHL, although the group "short" had a better prognosis than the group "longer duration" when restricted to SSHL accompanied by tinnitus. Ten patients with sudden hearing loss and severe-profound unilateral tinnitus associates were implanted with a mean age of 42.7 years deployment. It was conducted a prospective study that analyzed gender, laterality and age of patients, along with changes in the level of hearing and tinnitus, after scoring early SSHL to determine the prognostic factors of residual tinnitus after the last day of treatment for SSHL.
The tinnitus was assessed subjectively by a questionnaire before, 6 and 24 months after initiation of treatment. The scores of tinnitus in all three items were significantly better 6 months after initiation of treatment comparing with the last treatment. Especially younger patients with hearing improvement achieve an improvement of tinnitus in the period between 6 and 24 months after initiation of treatment. Specialist in Otology and Neurotology by Harvard Medical School, Boston, MA, USA, PhD in Medical Sciences from the University of Brasilia, Professor at Health Sciences School - University of Brasilia - Brasilia - DF - Brazil.
To determine whether establishing the pathogenesis of this disease is possible, this study analyzed the magnetic resonance imaging (MRI) of early stages of sudden deafness in combination with the clinical results of treatments.
Many theories seek to explain the etiology of sudden deafness; however, its exact causes are not specified. If it is not cured at an early stage, deafness can be permanent; thus, an early and accurate diagnosis is essential.
They were hospitalized at Pusan National University Hospital from November 2000 to May 2001. The vestibular function test consisted of air-caloric tests, and the results were measured with electronystagmography. Figure 1 shows the Gd-DTPA-enhanced T1-weighted coronal image of patient 9, who had vertigo and sudden deafness in the left ear; the image reveals increased gadolinium enhancement in the left labyrinth. Gd-DTPA TI-weighted coronal image in left ear of subject with sudden deafness with vertigo. The patient having an abnormal course of the VBS and the patient having labyrinthine enhancement also showed vertigo and canal paresis. Schuknecht and Donovan [2] reported that the pathological findings of the temporal bones of patients having idiopathic sudden deafness showed an atrophy of the striae vascularis, the tectorial membrane, and the organ of Corti; these pathological findings are similar to those of a viral cochlear inflammation.
The inner ear artery, which supplies blood to the inner ear, is provided through the anterior inferior cerebellar artery, the basal artery, and the posteroinferior cerebellar artery with the rostral vertebral artery [6].
The response to treatment tended to be slow in patients with abnormal MRI findings, as compared with patients in whom MRI findings were normal.
In many cases, the etiology remains unknown and constitutes a major challenge, even after complete otologic evaluation, and these cases are classified as idiopathic sudden deafness3. Intratympanic dexamethasone has been trialled in patients with sudden sensorineural hearing loss, because it provides a high concentration of steroids in the labyrinth in animal models1, although its evidence are conflicting. This study was approved by the institutional review board of the Medical School and the University Hospital in which it was carried out.
Below are the details of inclusion criteria, the audiometric assessment, application technique, analysis of The Tinnitus Handicap Inventory and Analogue Visual Scale for Tinnitus and outcome of recovery of Hearing Loss and Tinnitus.
The speech recognition rate (SRR) was based on the percentage of correct answers for monosyllables. EMLA cream was placed in the outer ear canal and the tympanic membrane and left for 30 to 45 minutes, after which it was removed. Failure of oral prednisolone therapy was absence of improvement, as just described, after 14 days of treatment. In relation to the mean-tone, obtained as a result of the following classifications: mild (25%), moderate (25%), severe (25%) and deep (25%).
Sudden hearing loss can occur mainly in the age group 43-53 years7, with equal gender distribution. Already Patient 4 also showed no change in auditory thresholds, showed a significant change in their tinnitus. Significant increase of 25% was found in the hearing threshold of patients undergoing this type of therapy, but in relation to tinnitus, the study was not conclusive13. Seven patients (70%) treated with enoxaparin sodium and venous hemofiltration (group A) had reduced subjective tinnitus and four patients (40%) showed a complete hearing recovery after the first procedure.
Given the failure of the rapies performed, it was suggested the cochlear implant that, according to the authors, is a routine procedure for patients with profound bilateral sensorineural hearing loss, and succeeded, some reports showed a suppression of tinnitus as a side effect after implantation.
This indicates that the tinnitus by itself cannot be a problem sign in the prognosis of hearing, but may be an essential sound for the early recovery of the damaged auditory system. Shortly after the standard fitting procedure, the patient reported a reduction of tinnitus, hyperacusis, and the headache disappeared completely in the follow-up of 3, 6 and 12 months. Seven patients experienced an improvement inTHI in different degrees and in only one patient there was no change.
44 patients with SSHL were followed, all treated with systemic steroids administration for 2 weeks and oral ingestion of vasoactive drugs and B12 vitamin for 6 months. Among the comparison between 6 and 24 months after initiation of treatment, there was no significant change. Oral vs intratympanic corticosteroid therapy for idiopathic sudden sensorineural hearing loss: a randomized trial.


Intratympanic dexamethasone injections as a treatment for severe, disabling tinnitus: does it work? Cochlear implant in patients with sudden unilateral sensorineural hearing loss and associated tinnitus.
Hyperbaric oxygen therapy for idiopathic sudden sensorineural hearing loss and tinnitus: a systematic review of randomized controlled trials. Sodium enoxaparin and venovenous hemofiltration in treating sudden sensorineural hearing loss and tinnitus. Otoacoustic emissions, ear fullness and tinnitus in the recovery course of sudden deafness. Curing tinnitus with a Cochlear Implant in a patient with unilateral sudden deafness: a case report.
The MRI findings of 18 patients with sudden deafness included three cases of slow blood flow of the vertebrobasilar system, one case of abnormal course of the vertebrobasilar system, and one case of labyrinthine enhancement. Recently, magnetic resonance imaging (MRI) has become an important method for evaluation of ear diseases.
Various suspected causes of sudden deafness include circulation disorder of the inner ear, viral infection, rupture of the cochlear membrane, syphilis, and allergy. The 4-mm-thick axial and coronal MRI tests produced TI-weighted images, Gd-enhanced T1-weighted images, proton density images, and T2-weighted images.
Figure 2 shows the proton density axial image of patient 2, who had vertigo and sudden deafness in the right ear; this image displays increased signals in the basal artery, due to the SBF of the basal artery.
In addition, the patients showing abnormal MRI findings did not respond well to treatment as compared to those with normal MRI findings (Table 2).
Generally, labyrinthitis caused by viral infection, blood circulation disorders, or rupture of the inner ear membrane are believed to cause sudden deafness [1]. The inflammation in the inner ear membrane can be found by conducting an antibody (Ab) test for viruses in the blood of affected patients. In many cases, the decrease in the blood supply to the inner ear artery is caused by a decrease in the blood supply to the VBS or by vascular obstruction of the inner ear artery itself [7,8]. However, the number of cases examined in this study was small; therefore, no statistical significance is claimed.
Therefore, we concluded that MRI is indispensable for examining patients with sudden deafness, especially those patients with accompanying vertigo. Labyrinthine enhancement on gadolinium enhanced MRI in sudden deafness and vertigo:Correlation with audiologic and electronystagmographic studies. Contrast enhancement of labyrinth on MR scans in patients with sudden hearing loss and vertigo:Evidence of labyrinthine disease.
Sudden sensorineural hearing loss associated with slow blood flow of the vertebrobasilar system. A great habit to take on, is having a green smoothie (leafy greens + other veggies - juiced or blended) a day! Only 2 patients had improvement of hearing (from severe to normal, mild to normal), keeping unchanged all other results and no worsening (Table 2 and Figure 2). Patient 8, 73 years, has hypertension and diabetes, as well as probable hearing loss due to presbycusis before the episode of sudden deafness. In group B, eight patients (80%) treated with conventional therapy showed a reduction of subjective tinnitus and hearing score also improved in eight patients (80%) - the hearing remained unchanged in two patients (20%). All patients in both groups had ear fullness and tinnitus in association with the onset of the SSHL. One year after the onset of symptoms on the right side, the cochlear implant was performed, and resulted in a complete suppression of tinnitus after activating the implant. It was concluded that, according to the survey of tinnitus, the time factor is the most reliable item for subjective tinnitus.
MRI showed many abnormal findings in the temporal bone of sudden-deafness patients who also complained of vertigo.
To determine whether establishing the pathogenesis of sudden deafness is possible, we analyzed MRI scans of early stages of sudden deafness in combination with the clinical results of treatments. However, no theory has yet been established for the causes of this disease, so making a definite diagnosis is very difficult. All patients were managed with same treatment protocol, which consists of high-dose steroid, low-molecular-weight dextran, and carbogen (95% O2 + 5% CO2) therapy. Figure 3 depicts the proton density axial image of patient 6, who had vertigo and sudden deafness in the left ear; this image shows increased signals in the left vertebrobasilar artery, due to the SBF.
These researchers further reported that when the enhancement was confined to certain segments of the cochlea, deafness existed at the frequency of the region predicted by the enhancement. Although the exact mechanism and significance of SBF in sudden deafness are unknown, a temporary decrease in blood flow occurred at the onset of sudden deafness [11].
In particular, 5 of the 11 (45%) patients with sudden deafness and accompanying vertigo showed abnormalities on MRI, and 3 of the 11 patients (27%) showed SBF.
In CW Cummings, JM Fredrickson, LA Harker (eds), Otolaryngology Head and Neck Surgery, 3rd ed.
The procedure is well tolerated and relatively easy to perform as outpatient procedure performed under local anesthesia (topical), general anesthesia can be avoided, most patients understand the concept of intratympanic therapy and easily accepts the proposed therapy.
Regarding the THI scores, it ranged from 58 to 96, prior to initiation of therapy, 8-82 and 30 days after.
Such comorbidities could not justify the improvement in hearing thresholds after the proposed therapy.
None of the patients experienced side effects from this treatment, and the authors concluded that this option can be beneficial as adjuvant therapy for hearing improvement in patients with PANSS, but cost factors are the main obstacles to the use of this therapy14.
However, these symptoms improved only in Group A, showing a significant relationship between recovery of hearing thresholds and improvement of aural fullness.
Clinical improvement was also reflected by a decrease in the scores of questionnaires THI and VAS. The hearing recovery was determined by comparing the hearing levels before and after treatment and tinnitus was subjectively evaluated by using a questionnaire. As compared with normal cases, the cases showing abnormal findings on MRI did not respond well to treatment. To discover the exact causes of sudden deafness, the authors examined the relationships between patients' symptoms and the results of acoustic and vestibular function tests by analyzing abnormal findings on MRI, in particular the slow blood flow (SBF) of the vertebrobasilar system (VBS) and labyrinthine enhancement on MRI augmented by gadolinium (Gd-DTPA).
Figure 4 shows the proton density axial image of patient 5, who had vertigo and sudden deafness in the right ear; the image exhibits an abnormal course of the right vertebrobasilar artery.
Therefore, gadolinium enhancement of the labyrinth is characteristic of labyrinthine diseases [3,4,6]. Additionally, they reported that viral labyrinthitis was diagnosed in nine patients and leutic labyrinthitis was diagnosed in two.
However, it should be emphasized again that in relation to complaints of tinnitus, it has undergone a significant change, in which catastrophic change of the degree to mild (Table 1). Given this, the authors suggested the use of cochlear implants as a possible therapy for tinnitus persisted after sudden deafness. We concluded that MRI is indispensable for examining patients with sudden deafness, especially those who have accompanying vertigo.
We obtained an average difference of 38.6 points among patients who reported an improvement in tinnitus before and after the course of oral steroids and intratympanic. In group A, the OAE responses appeared simultaneously with the improvement in hearing levels in five patients (63%). Referring to EVA, there was a change from 7 to 10 points before therapy and from 1 to 8 points after it, in relation to intensity.
It was concluded that patients with hearing improvement PANSS (Group A) tend to have OAE responses and sensations of fullness in the ear and tinnitus improved almost simultaneously with the hearing improvement. In relation to the nuisance, there was a change from 7 to 10 points before and 0-08 points after therapy. The authors concluded that patients with poor hearing improvement tend to have absent OAE and ear fullness and tinnitus persisted. The latter group also reported that the SBF of the VBS demonstrated high-signal proton density images [12-14].



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