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Figure: The outer ear consists of the auricle (unlabelled), the external auditory canal, and the lateral surface of the tympanic membrane (TM). Surprisingly perhaps, hypertension, obesity and diabetes is not associated with an increased risk of hearing loss(Shargorodsky et al 2010).
Dance clubs are often very loud and may be the main source of loud noise exposure outside of occupational exposure. Musician's earplugs are available in ER-9, ER-15, and ER-25, according to ones need for noise reduction.
Although diabetes per se is not associated with an overall greater risk of hearing loss (Shargorodsky et al 2010), hearing loss starts at an early age than the normal population. Diabetics are also more prone to get external and middle ear infections, as well as more prone to develop cranial nerve palsies and stroke. As diabetes is commonly an autoimmune disorder, autoimmune inner ear disease may also contribute. In cases where a sudden drop in hearing function occurs, a medical evaluation should be performed as soon as possible.
Patients with sudden hearing loss undergo a full ear nose and throat evaluation in addition to testing such as audiogram. Most patients with sudden hearing loss recover some or all of their hearing over several weeks. Objective: The purpose of this study was to observe the effectiveness of immune modulator –Inosine Pranobex (Isoprinosine) in the treatment of sudden sensorineural hearing loss of suspected viral origin.
Setting: This study was performed in the Clinic of Otorhinolaryngology in the Medical Institute of Ministry of Interior, Sofia. Patients: The study included 28 patients with sudden hearing loss of suspected viral origin, divided randomly into two groups.
Intervention: The first group of 14 patients was treated with corticosteroids and vasodilators. Main Outcome Measures: The patients passed precise otorhinolaryngological examination, pure tone audiometry, speech audiometry, stapedial reflex testing, ABR, CT scan, hematological testing –complete blood count (CBC) and sedimentation rate, biochemistry and serologic testing for syphilis. Results: We compared the two groups before and after the treatment regarding mean hearing level at each frequency, speech reception threshold improvement, and tinnitus and balance complaints. Conclusions: Administration of a combination of corticosteroids, vasodilators and immune-modulator should be recommended for treatment of patients with sudden sensorineural hearing loss. Sudden sensorineural hearing loss is defined as 30 dB or more sensorineural hearing loss over at least three contiguous audiometric frequencies occurring within 3 days or less. The vascular courses include vasospasm, thrombosis, embolism, hemorrhage, hypercoaguability and rheologic abnormalities. The viral-vascular combination theory suggests that a viral infection initiates a hypercoagulable state secondary to the effect of viruses on the vascular system. The therapy that has been proven to be effective in the treatment of sudden sensorineural hearing loss is the etiologic based one. 28 patients of either gender (24 male and 4 female), aged between 12 and 47 years with sudden hearing loss were enrolled in the study.
Pure tone audiometry was performed weekly during the first 14 days of the treatment, 4 weeks after the onset of the disease and 2 months later. After 14 days of the treatment in the Clinic of Otorhinolaryngology and 2 weeks more at home, the results were as following in Table 2.
We compared the two groups before and after treatment regarding mean hearing level at each frequency, speech reception threshold improvement, and tinnitus and balance complaints.
It is not surprising that the cochleovestibular blood supply may be affected by circulatory disorders such as embolic phenomenon, thrombosis, vasospasm and hypercoagulable or high viscosity states resulting in sudden sensorineural hearing loss. Administration of a combination therapy of corticosteroids, vasodilators and immune-modulator should be recommended for treatment of patients with sudden sensorineural hearing loss of suspected viral origin. Persons with cochlear deficits fail OAE testing, while persons with 8th nerve deficits fail ABR testing.
The middle ear includes the medial surface of the eardrum, the ossicular chain, the eustachian tube, and the tympanic segment of the facial nerve. Postmeningitic hearing loss can be due to lesions of the cochlea, brainstem and higher auditory pathways, but usually is related to suppurative labyrinthitis (cochlear). It is a subtype of sensorineural hearing loss, and because it is due to cochlear damage, it is more specifically a cochlear problem.
We have encountered several patients in our practice with transient hearing loss after going to a loud club. These ear plugs require a visit to a clinic to get an impression made, so that they are specific for the ear being fitted. The effects of type I diabetes mellitus on the cochlear structure and vasculature in human temporal bones.


A long-term study on hearing status in patients with nasopharyngeal carcinoma after radiotherapy. Unsuccessful cochlear implantation in two patients with superficial siderosis of the central nervous system. Further studies such as MRI or CT may be ordered in certain cases, as there is a small chance that the hearing loss may be due to a tumor. There are some patients who will not recover well without treatment, and since treatment rendered late is often ineffective, early treatment is offered to most patients.
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The second group of 14 patients was treated with corticosteroids, vasodilators and immune modulator - Isoprinosine. The patients with vertigo passed observation for nystagmus, static and kinetic tests, posturography and electronystagmography (ENG). 4 patients recovered totally, 19 patients improved their hearing with 20 dB and 5 patients showed no improvement. The phylogenetically newer portion of the inner ear, which includes the cochlea and saccule, is relatively more susceptible to various agents than the pars superior. Experimental studies have shown that the ganglion cells are the most sensitive to ischemia, while the pathologic data indicates that the organ of Corti, stria vascularis and tectorial membrane are the predominant structures affected in cases of sudden sensineural hearing loss (7). One of the mechanism by which hearing loss develops is through changes in cellular immunity. We used a combination of medicines, according to the viral-vascular etiologic theory (8-10). 8 patients noted their hearing loss upon first awakening in the morning, 2 patients – after stress situation, 18 patients had in their history a viral upper respiratory infection as 2 patients were in contact with varicella – infected persons, 1 woman was with rubeolla and 15 patients had in their history symptoms of influenza. Ophthalmologic, neurological and rheumatologic consultations were carried out to rule out systemic vasculitic diseases. The vascular etiologic theory is favored because of the sudden nature of the onset of hearing loss. This type of treatment result in earlier hearing recovery and less extensive cochlear destruction compared to steroids and vasodilators.
Therapy of idiopathic sudden sensorineural hearing loss: antiviral treatment of experimental herpes simplex virus infection of the inner ear. Oral steroid treatment of sudden sensorineural hearing loss: a ten-year retrospective analysis. Treatment of idiopathic sudden sensorineural hearing loss with antiviral therapy: a prospective, randomized, double blind clinical trial. Recovery of hearing: results of delayed medical treatment in patients with idiopathic sudden hearing loss. The inner ear includes the auditory-vestibular nerve, the cochlea and the vestibular system (semicircular canals).
The piccolo generates sound levels up to 112db…roughly equivalent to a jackhammer at 30 feet.
Pathological studies suggest that it is due to microangiopathic involvement of inner ear blood vessels and subsequent stria vascularis atrophy and hair cell loss (Fukushima et al, 2004). It is unclear what causes this condition but a viral or inflammatory process in the inner ear may be a possibility.
The findings in animal models of hearing loss of vascular origin are of extensive cochlear fibrosis and ossification. The otorhinolaryngologic examination included otoscopy, anterior rhinoscopy and pharyngoscopy. The treatment of sensorineural hearing loss often proves to be frustrating to the clinician as, in the majority of cases, the etiology is unknown and the underlying disease process is irreversible. The underlying pathophysiology can be explained by the occurrence of sudden anoxic injury to the cochlea. The recovery is significantly related, as well, to onset of hearing loss and audiogram type. For patients whose hearing does recover completely, a hearing aid is the most effective treatment. Sudden hearing loss may be idiopathic but also significant differential diagnoses must be considered.
Additional evidence of that type of etiology is indicated by the fact that patients had substantial hearing improvement with mono steroid treatment. Otorhinolaryngologists make efforts to treat the sudden sensorineural hearing loss according to the established etiologic courses as viral, vascular or viral-vascular combination (11-15). Effects of anoxia result in changes in the cochlea microphonics with loss of the action potential.


So the combination of immune-mediator (Isoprinosine), corticosteroid (Methylprednisolon) and vasodilator (Cavinton) proved to be effective in treatment of sudden sensorineural hearing loss. Treatment aimed at the possible etiologic agent might be beneficial only in the very early phase of the hearing loss. The audiometric patterns from the pure tone audiometry were variable with mild to profound hearing losses. Support for a viral theory is the antecedent history of a viral upper respiratory infection and epidemic of viral diseases, such as parainfluenza, mumps, varicella, rubeola, and adenovirus infections. Despite restoration of the cochlea blood flow, loss of endocochlear potentials may be irreversible after 30 minutes (4).
The patients, included in our study, did not have in their history any of these well-established courses or mentioned upper diseases. The entire examined group had tinnitus, which preceded the hearing loss by several hours with usually a roaring quality. Patients treated by the same course of corticosteroids and vasodilators and in addition immune-modulator – Isoprinosine – 3g per day (3x2 tabl.) for a period of 5 days. Histological analyses of temporal bones from patients who suffered from sudden sensorineural hearing loss displayed atrophy of the organ of Corti, stria vascularis and tectorial membrane.
Hearing recovery in profound losses tends to occur in the low tones, which correlates with involvement at the apex of the cochlea rather than the basal end. Etiology of the sudden sensorineural hearing loss includes as well viral, vascular and viral-vascular combination. The arterial supply to the cochlea is such that the basal turn is fed first by the main cochlear artery with the cochlear apex fed last. Patients in our study reported antecedent history of upper respiratory infection within a month or less of onset of the hearing loss.
Haemaglutination and slaging of blood may occur when virus particles attach to erythrocytes. The findings in animal models of hearing loss of vascular origin prove extensive cochlear fibrosis and ossification.
The viruses of mumps, measles, herpes simplex, herpes zoster, adenoviruses and influenza deserve particular attention in view of their clearly demonstrated etiologic role in sudden sensineural hearing loss. In the histological findings the organ of Corti was absent throughout the cochlea; the stria vascularis was atrophic throughout. The spiral ganglion cells were considerably decreased in the basal turn and somewhat decreased in the apical turn. Patients with measurable speech discrimination scores on presentation uniformly improved with treatment, even if their pure tone-average was profound. The cutaneus lesions associated with herpes zoster infections make this form of viral neurinitis and ganglionitis relatively easy to diagnose clinically and to relate etiologically the sudden sensorineural loss to the virus (6). Presence of vertigo is associated with more severe losses and represents a greater insult to the labyrinth and those patients recover worse.
The patients with vertigo passed observation for nystagmus, static and kinetic tests, posturography and ENG. The vascular endothelium is invaded and inclusion bodies may be seen in the endothelial cells in viral diseases. Application of combination of steroid, vasodilator and immunostimulater significantly improves the recovery outcomes in cases of sudden sensorineural hearing loss. There is, however, overall hyperemia at the site of inflammation and total effective blood flow may not be altered.
Infiltration of lymphocytes, plasma cells, macrophages and polymorphonuclear leukocytes occurs.
Necrosis of neuroepithelium may occur and is indicated by hyperchromatism, fragmentation and lysis of nuclei (5).
The most common route of access of viral particles to the inner ear is a viremia in the early phase of viral illness in which virions are deposited within the membranous cochlea. Isoprinosine was used to support the mechanism of immune answer to the foreign agent – the virions and to reduce the damage of the cochlea structures. Medications like Acyclovir may be unhelpful when the cause is a virus that is not in the herpes family, that’s why Isoprinosine is favored. The corticosteroids, as well, have an anti-inflammatory effect on the organ of Corti and the microvasculature.



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