What is ISSNHL?
Idiopathic Sudden Sensorineural Hearing Loss (ISSNHL) is a rapid-onset hearing impairment that occurs in the inner ear or the vestibulocochlear nerve. It is characterized by a loss of at least 30 decibels in three contiguous frequencies, developing over a period of 72 hours or less, with no identifiable cause.
Common Sources of
ISSNHL
Include:
Key characteristics of ISSNHL include:
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Sudden onset of hearing loss, often noticed upon waking
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Unilateral hearing loss in about 95% of cases
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Potential accompanying symptoms such as tinnitus and vertigo
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Absence of other neurological symptoms
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No identifiable cause despite thorough investigation
Audiometric features of ISSNHL:
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Low-frequency (upsloping) hearing loss
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Mid-frequency (U-shaped) hearing loss
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High-frequency (downsloping) hearing loss
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Flat hearing loss affecting all frequencies
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Total or near-total hearing loss
Factors potentially associated with ISSNHL:
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Viral infections (e.g., herpes simplex, cytomegalovirus)
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Vascular occlusion
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Autoimmune inner ear disease
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Ototoxic medications
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Acoustic neuroma (in rare cases)
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Stress and sudden changes in atmospheric pressure
Prompt recognition and treatment of ISSNHL is crucial, as delays in intervention can significantly reduce the chances of hearing recovery.
How HBOT Helps with
ISSNHL
Hyperbaric Oxygen Therapy (HBOT) has emerged as a valuable adjunctive treatment for ISSNHL. Here’s how HBOT specifically addresses the challenges of this condition:
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Enhanced Oxygenation of the Inner Ear: HBOT dramatically increases oxygen levels in the perilymph and endolymph of the inner ear, supporting the function of hair cells and neurons in the oxygen-starved cochlea.
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Reduction of Cochlear Edema: The hyperbaric environment helps reduce edema in the cochlea, which can alleviate pressure on hair cells and improve their function.
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Stimulation of Cochlear Blood Flow: HBOT promotes vasodilation and neoangiogenesis in the cochlea, improving microcirculation and potentially reversing ischemia-related damage.
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Modulation of Inflammatory Response: HBOT can help regulate the inflammatory process in the inner ear, potentially mitigating autoimmune-related damage in some cases of ISSNHL.
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Enhancement of Stem Cell Mobilization: HBOT has been shown to mobilize stem cells from the bone marrow, which may contribute to repair processes in the damaged cochlea.
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Synergy with Corticosteroid Treatment: When used in combination with standard corticosteroid therapy, HBOT can enhance the overall effectiveness of treatment for ISSNHL.
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Potential Antiviral Effects: In cases where ISSNHL may be related to viral infection, HBOT’s potential antiviral properties could be beneficial.
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Reduction of Oxidative Stress: While providing high levels of oxygen, HBOT also stimulates antioxidant defenses, potentially protecting cochlear structures from oxidative damage.
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Improvement in Tinnitus: Many patients with ISSNHL also experience tinnitus, and HBOT has shown potential in reducing the severity of tinnitus symptoms.
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Enhancement of Neural Plasticity: HBOT may promote neural plasticity in the auditory system, potentially aiding in the reorganization and recovery of auditory function.
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Mitigation of Reperfusion Injury: In cases where ISSNHL is related to vascular events, HBOT can help mitigate reperfusion injury when blood flow is restored to the cochlea.
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Extended Treatment Window: While early intervention is crucial, HBOT has shown potential benefits even when initiated beyond the typical treatment window for ISSNHL, offering hope for patients with delayed diagnosis.
HBOT treatment for ISSNHL typically involves daily sessions at 2.0 to 2.5 atmospheres absolute (ATA) for 90-120 minutes. The number of treatments can vary but often ranges from 10 to 20 sessions, depending on the patient’s response and the time elapsed since the onset of hearing loss.
What Happens in Our Bodies During HBOT for
ISSNHL
During HBOT treatment for Idiopathic Sudden Sensorineural Hearing Loss, several physiological processes occur that specifically address the unique challenges of this condition:
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Hyperoxia Induction in Cochlear Fluids: Blood oxygen levels increase dramatically, with oxygen dissolved directly in the plasma. This leads to significantly increased oxygen levels in the perilymph and endolymph of the inner ear, supporting the metabolic needs of hair cells and neurons.
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Reduction of Cochlear Edema: HBOT causes vasoconstriction in normal tissues, which helps reduce edema in the cochlea. This can alleviate pressure on delicate inner ear structures and improve their function.
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Enhancement of Cochlear Blood Flow: The alternating hyperoxic and relative hypoxic states during and after HBOT stimulate the release of angiogenic factors, promoting the formation of new blood vessels in the cochlea and improving microcirculation.
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Modulation of Inner Ear Inflammation: HBOT affects the production and activity of various inflammatory mediators, potentially dampening harmful inflammatory responses in the inner ear.
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Stimulation of Antioxidant Defenses: While HBOT increases oxygen levels, it also upregulates antioxidant defenses, helping to protect sensitive cochlear structures from oxidative stress.
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Mobilization of Stem Cells: The hyperbaric environment activates and mobilizes stem cells from the bone marrow, which may migrate to the damaged cochlea and contribute to tissue repair.
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Enhancement of Mitochondrial Function: Increased oxygen availability supports improved mitochondrial function in cochlear cells, potentially aiding in cellular repair and survival.
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Modulation of Neurotransmitter Activity: HBOT may influence the activity of neurotransmitters in the auditory system, potentially affecting signal transmission and perception.
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Reduction of Cochlear Ischemia: By improving oxygen delivery and promoting microcirculation, HBOT helps alleviate ischemic conditions in the cochlea that may contribute to ISSNHL.
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Stimulation of Neuroplasticity: The hyperoxic environment may promote neuroplasticity in the auditory cortex, potentially aiding in the reorganization of auditory processing in response to sudden hearing loss.
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Enhancement of Cellular Energy Production: Increased oxygen availability supports ATP production in cochlear cells, providing energy for cellular repair processes.
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Modulation of Gene Expression: HBOT has been shown to influence gene expression, potentially activating genes involved in cellular repair and protection in the context of ISSNHL.

Protocol
HBOT treatment for ISSNHL typically involves pressurizing the chamber to 2.0-2.5 atmospheres absolute (ATA) for about 90-120 minutes. Treatments are usually administered daily, with the total number of sessions ranging from 10 to 20 or more, depending on the patient’s response and the time elapsed since the onset of hearing loss.
It’s important to note that the physiological responses to HBOT in ISSNHL can continue for some time after each treatment session. The cumulative effect of multiple treatments leads to sustained improvements in cochlear oxygenation, reduction of edema, and enhancement of cellular function, potentially improving the chances of hearing recovery.
References
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Cianci, P., Sato, R., & Slade, J. B. (2013). Adjunctive hyperbaric oxygen therapy in the treatment of thermal burns. Undersea & Hyperbaric Medicine, 40(1), 89-108.
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Thom, S. R. (2011). Hyperbaric oxygen: its mechanisms and efficacy. Plastic and Reconstructive Surgery, 127(Suppl 1), 131S-141S.
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Bhutani, S., & Vishwanath, G. (2012). Hyperbaric oxygen and wound healing. Indian Journal of Plastic Surgery, 45(2), 316-324.
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Villanueva, E., Bennett, M. H., Wasiak, J., & Lehm, J. P. (2004). Hyperbaric oxygen therapy for thermal burns. Cochrane Database of Systematic Reviews, (3).
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Zamboni, W. A., Browder, L. K., & Martinez, J. (2003). Hyperbaric oxygen and wound healing. Clinics in Plastic Surgery, 30(1), 67-75.
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Slade, J. B., Hattori, T., Ray, C. S., Baumgartner, T. J., & Hemba, E. (2001). Statewide experience with adjunctive hyperbaric oxygen therapy for thermal burns. Undersea & Hyperbaric Medicine, 28(Suppl), 62.
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Mathieu, D., Marroni, A., & Kot, J. (2017). Tenth European Consensus Conference on Hyperbaric Medicine: recommendations for accepted and non-accepted clinical indications and practice of hyperbaric oxygen treatment. Diving and Hyperbaric Medicine, 47(1), 24-32.
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Roeckl-Wiedmann, I., Bennett, M., & Kranke, P. (2005). Systematic review of hyperbaric oxygen in the management of chronic wounds. British Journal of Surgery, 92(1), 24-32.