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21.09.2015
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. Autoimmunity and inner ear disorders: An immune-complex mediated sensorineural hearing loss. Etanercept therapy for immune-mediated cochleovestibular disorders: Preliminary results in a pilot study.
Corticosteroid pharmacokinetics in the inner ear fluids: An animal study followed by clinical application. 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. Sensorineural hearing loss, moderate, bilateral, sequel of pneumococcal meningitisHistopathologic:1. A triad of vascular, viral and membrane rupture are the known theories for the causation of sudden SNHL. 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. Apical cochlear lesion, characterized by degeneration of sensory and neural tissues and a fibro-osseous response, right3. Loss of spiral ganglion cells, presumed secondary to cochlear neuritis from bacterial meningitis, bilateral.2.
Now various autoimmune disorders have also been suggested to play a role in the pathogenesis.Autoimmune inner ear disease (AIED) is a relatively new etiological mechanism of sudden or rapidly progressive hearing loss, which has been added to the previously accepted triad of viral, vascular and membrane rupture. 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. Radiation reaction of bone and fibrous tissue involving mastoid and the posterior part of the otic capsule, right4. 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). He reported 18 patients with bilateral rapidly progressive SNHL for which no cause could be identified.Scleroderma, an autoimmune disease, also known as systemic sclerosis, is characterized by sclerotic skin changes that are often accompanied by multi-system disease.
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. Cutaneous manifestations usually include sclerodactyly, mat like telengectasias and Raynaud's phenomenon.
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. Progressive fibrosis, resulting from increased deposition of collagen in the interstitium and intima of small arteries and connective tissue of involved organs is the pathologic hallmark of the disease. In the histological findings the organ of Corti was absent throughout the cochlea; the stria vascularis was atrophic throughout.
However scleroderma as the cause of sudden bilateral SNHL has not been reported much in English literature. 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. She had taken medicines outside and developed rashes and patchy bluish discoloration of skin on the arms and finger tips and distal half of feet and toes both sides. There is, however, overall hyperemia at the site of inflammation and total effective blood flow may not be altered.


On examination, right tympanic membrane was congested and bulging and left side had central perforation.
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). Pure tone audiogram [Figure 1] showed profound SNHL in the right ear and mixed hearing loss left side.
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. After 4 days, gangrenous changes were noted in middle fingers of both hands and toes (Raynaud's Disease) [Figure 2]. 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. Rheumatoid arthritis (RA) factor-qualitative and quantitative (highly elevated) and C reactive proteins were positive.
The corticosteroids, as well, have an anti-inflammatory effect on the organ of Corti and the microvasculature.
Cytoplasmic antineutrophil cytoplasmic antibodies (C-ANCA) and anti-cyclic citrullinated peptide were positive, and anti-nuclear antibody was equivocal, whereas perinuclear-ANCA was negative. Antibiotics, high doses of steroids, peripheral vasodilators, oral glycerin, and and local applications of nitroglycerine were administered. The diagnosis of the inner ear autoimmune disorder depends mainly on relatively distinct clinical course, immunological investigations and treatment response. The clinical picture usually consists of bilateral SNHL, bilateral reduced vestibular loss and symptoms of pressure with tinnitus and rarely tissue destruction of middle and external ear. There is vasculitis, ghosts of blood vessels and granulomatous substrate in the temporal bone pathology in confirmed AIED.It is characterized by proliferative vascular lesion and marked deposition of collagen in various tissues and organs.
Autoimmune disease that affects the inner ear may be either due to organ-specific disease or systemic disorder.
Probable organ-specific AIED includes tympanosclerosis, otosclerosis, otitis media with effusion, chronic suppurative otitis media with cholesteatoma and menier's disease. The clinical picture of AIED differs from other causes of severe SNHL in that it is usually rapidly progressive (over weeks to month) rather than sudden (hours to days), bilateral, asymmetric SNHL.Scleroderma is an aggressive, multistage autoimmune disorder, also known as systemic sclerosis with high mortality. It is characterized by sclerotic skin changes that are often accompanied by multi-system disease. Cutaneous manifestations include sclerodactyly, mat like telengectasias and raynauds phenomenon. The etiology and pathogenesis of scleroderma remains unknown and probably multifactorial, both cell and humoral mediated. Increased collagen production and vascular damage are potential explanations of hearing loss in scleroderma. Monteiro et al., [6] in a study of twenty six patients revealed that patients with diffuse cutaneous systemic sclerosis have a high prevalence of sensorineural hearing impairment and otological complaints.
The inner ear perilymph is capable of responding to antigen challenge and inner ear is an effective route for systemic immunization. Taleb and Linthicum [10] described the histopathological finding in the temporal bone in a case of scleroderma.No medication has been universally accepted and effective as the treatment of choice in all cases of sudden SNHL and scleroderma. High doses of steroids, vasodilators, anticoagulants, parenteral immunoglobin, methotrexate, and cyclophosphamide have been used individually or in combination.
Intravenous immunoglobin has been reported successful in a single case of hearing loss with scleroderma. Intratympanic injection of glucosteroids in the middle ear have been found to be better than oral or parenteral routes.
Concentrations of steroids in perilymph through intratympanic route have been found to be higher when compared to oral or parenteral routes. Methylprednisolone is a better option since its level in endolymph have been found to be higher than hydrocortisone and dexamethasone. Circulating antibodies, antigens, and immune complexes are removed, which may enhance the effects of immunosuppresive agents.
Stem cell has become a promising tool in the treatment of autoimmune disease by promoting tissue repair and protection from immune-attack associated damage.
It can be devastating to patients and frustrating for the otolaryngologist to diagnose and treat. The diagnosis is based on the presence of bilateral progressive or sudden asymmetrical SNHL and the response to immunosuppresive therapy. Steroids in high doses with or without cytotoxic agents have been advocated by various authors. In all cases of bilateral sudden sensorineural loss, AIED must be kept in mind as one of the cause, investigated and treated accordingly.




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