Iowa Head and Neck Protocols — Otology / Neurotology Section

Content created October 2026 by Celine Rabay (medical student American University of Beirut Faculty of Medicine),  Tadeas Lung MD (University of Iowa) and Alexander Claussen MD (University of Iowa)

Definitions

• Sudden Sensorineural Hearing Loss (SSNHL): Defined by the 2019 AAO-HNS Clinical Practice Guideline as acute sensorineural hearing loss of ≥30 dB across ≥3 consecutive audiometric frequencies within 72 hours, confirmed sensorineural on audiometry (air-bone gaps excluded). [AC1]

• Idiopathic SSNHL (ISSNHL): SSNHL with no identifiable etiology after thorough workup; 71–90% of cases. A diagnosis of exclusion.

• Intratympanic Steroid Therapy (ITS): Transtympanic injection of corticosteroid into the middle ear space, achieving perilymph concentrations substantially exceeding equivalent systemic doses. Delivered as salvage, primary, or combined therapy.

• Salvage ITS: ITS for incomplete recovery after primary systemic steroids; initiated at 2–6 weeks after onset per AAO-HNS guideline. The only treatment intervention carrying a Recommendation in the 2019 AAO-HNS Clinical Practice Guideline.

• Primary ITS: Intratympanic steroid therapy used as initial treatment rather than salvage therapy, particularly when systemic corticosteroids are contraindicated. Intratympanic methylprednisolone has demonstrated noninferiority to oral prednisone as primary therapy for idiopathic SSNHL. (Rauch et al., 2011)

• Combined Therapy: Concurrent or closely sequential systemic and intratympanic steroids. May be considered in poor-prognosis presentations; not yet supported by guideline-level RCT evidence.

• Round Window Membrane (RWM): Three-layered membrane separating the middle ear from the scala tympani; the primary perilymph drug entry route during ITS and the pharmacokinetic rate-limiting step.

Background

Historical Overview

SSNHL management was transformed by four landmark events. In 1980, Wilson, Byl, and Laird published the first double-blind RCT demonstrating statistically significant hearing recovery with oral corticosteroids over placebo, establishing steroid therapy as the standard of care. (Wilson et al., 1980) In the 1990s, Parnes and colleagues demonstrated that transtympanic injection could deliver corticosteroids to the round window membrane at cochlear concentrations substantially exceeding systemic dosing, establishing the pharmacokinetic rationale for ITS. (Parnes et al., 1999) The 2011 trial by Rauch et al. randomized 250 patients to oral prednisone versus intratympanic methylprednisolone as primary monotherapy and demonstrated non-inferiority of ITS, repositioning it from salvage to a first-line option. (Rauch et al., 2011) The 2019 AAO-HNS Clinical Practice Guideline upgraded salvage ITS to a Recommendation, the only treatment intervention at this level of recommendation. (Chandrasekhar et al., 2019)

Epidemiology

SSNHL affects 5–27 per 100,000 persons annually in the United States (~66,000 new cases/year), with equal sex distribution and peak incidence in the fifth to sixth decades. (Chandrasekhar et al., 2019) Approximately 98% of cases are unilateral; bilateral simultaneous SSNHL (<2%) warrants urgent evaluation for autoimmune disease, bilateral vestibular schwannoma, or neurosyphilis.

Clinical Presentation

SSNHL is a medical urgency presenting as sudden unilateral hearing loss, frequently noticed upon waking. Associated symptoms:

• Tinnitus: 41–90%; does not independently predict recovery.

• Aural fullness: 25–50%; may suggest endolymphatic hydrops or be secondary to the hearing loss.

• Vertigo / disequilibrium: 29–56%; concurrent vertigo is an independent predictor of poor recovery (see Prognostication) and be indicative of a labyrinthitis process.

Speech recognition deficits may be disproportionate to pure-tone loss. Time from onset to treatment is an independent predictor of hearing recovery.

Pathophysiology

SSNHL aetiology is multifactorial. Four dominant hypotheses inform treatment rationale:

• Vascular occlusion: The labyrinthine artery is a terminal vessel without collateral circulation; vasospasm, thromboembolism, or hypercoagulability can produce cochlear infarction within minutes.

• Viral cochleitis: Direct viral invasion or immune-mediated cochlear inflammation. HSV, herpes zoster (Ramsay Hunt), CMV, and SARS-CoV-2 have the strongest evidence.

• Autoimmune inner ear disease (AIED): Estimated 1–5% of cases; typically bilateral and progressive. Provides rationale for corticosteroid therapy.

• Intracochlear membrane rupture: Reissner’s or basilar membrane disruption from barotrauma or Valsalva causes toxic endolymph-perilymph mixing.

In all mechanisms, the final common pathway is cochlear hair cell injury. Corticosteroids reduce endocochlear edema, stabilize cochlear vasculature, and modulate immune response, justifying both systemic and intratympanic routes.

Natural History and Spontaneous Recovery

Spontaneous recovery occurs in 32–65% of untreated patients (average ~47%), typically within the first 2 weeks. (Chandrasekhar et al., 2019) Recovery potential declines substantially after 2–3 months, after which persistent loss is likely permanent. Patients with severe-to-profound initial loss, vertigo, or adverse audiogram configurations have substantially lower spontaneous recovery rates and derive the greatest benefit from prompt treatment.

Diagnostic Evaluation

Audiometry

Pure-tone audiometry (air and bone conduction) and speech audiometry (WRS) are essential to confirm sensorineural loss and exclude an air-bone gap. Audiogram configuration and severity carry direct prognostic implications and must be documented precisely. Follow-up audiometry guides salvage ITS decisions.

Tuning Fork Examination

In SSNHL, Rinne is positive bilaterally and Weber lateralizes to the unaffected ear. Lateralization to the affected ear suggests a conductive component or severe contralateral loss and warrants reassessment.

MRI

MRI of the IACs/posterior fossa should be obtained to evaluate for retrocochlear pathology. Dedicated IAC MRI with gadolinium is highly sensitive; a limited noncontrast high-resolution T2-weighted study (e.g., CISS/FIESTA) is an acceptable alternative. (Chandrasekhar et al., 2019; Kim et al., 2019) ABR may be considered when MRI is contraindicated (pacemaker, cochlear implant, [AC2] severe claustrophobia).

Laboratory Testing

The AAO-HNS guideline carries a strong recommendation against routine laboratory testing. (Chandrasekhar et al., 2019) Targeted testing is appropriate only when history raises specific etiological suspicion: FTA-ABS (syphilis), ANA/anti-dsDNA/ANCA (autoimmune), hypercoagulable panel, fasting glucose/HbA1c (cardiovascular risk), Lyme serology (endemic regions). Routine CT of the temporal bones is strongly recommended against.

Differential Diagnosis

Idiopathic SSNHL is a diagnosis of exclusion. Key conditions to consider:

• Middle ear effusion, otitis media, TM perforation, cerumen impaction (conductive; excluded by otoscopy and air-bone gap)

• Vestibular schwannoma and other retrocochlear lesions (evaluated with MRI of the IACs/posterior fossa)

• Ménière’s disease / endolymphatic hydrops (fluctuating low-frequency loss, aural fullness, episodic vertigo)

• Autoimmune inner ear disease (bilateral or progressive, connective tissue disease history)

• Perilymphatic fistula (precipitated by barotrauma or Valsalva maneuver)

• Infectious: Lyme disease, neurosyphilis, viral labyrinthitis

• Labyrinthine hemorrhage (hyperintense T1 signal in the labyrinth on MRI)

• Central demyelinating disease, e.g., multiple sclerosis (bilateral SSNHL, young patient, neurological signs)

Prognostication

Four factors carry the most clinically actionable prognostic significance and should inform counseling and treatment intensity discussions.

Audiogram Configuration

• Low-frequency (upsloping): 63–88% recovery. Best prognosis. May represent endolymphatic hydrops or Ménière’s prodrome.

• Mid-frequency (U-shaped): 36–71% recovery. Intermediate prognosis.

• Flat loss: 40–56% recovery. Associated with elevated neutrophil-to-lymphocyte ratio (NLR[AC3] ) and lower HDL, suggesting a metabolic-inflammatory phenotype. (Cadoni et al., 2025)

• High-frequency (downsloping): 19–38% recovery. Poor prognosis; reflects preferential basal cochlear injury.

• Profound flat loss (>90 dB): <15–20% recovery. Confirmed as the strongest independent predictor of poor outcome (OR = 4.68) in a 2025 meta-analysis of 2,632 patients. (Chen et al., 2025)

Initial Hearing Severity

Patients with initial PTA ≥70 dB have substantially lower complete recovery rates. (Chen et al., 2025) This threshold frequently guides decisions regarding combined versus systemic-only therapy.

Presence of Vertigo

True vertigo at presentation is the second strongest independent predictor of poor outcome (OR = 1.95), confirmed in a 2025 meta-analysis of severe-to-profound SSNHL. (Chen et al., 2025) These patients warrant guarded prognosis counseling and discussion of more intensive treatment.

Time to Treatment

Earlier treatment is consistently associated with better outcomes. (Kennedy et al., 2025) Initial corticosteroid therapy may be offered within 2 weeks of onset.  (Chandrasekhar et al., 2019) The AAO-HNS guideline recommends salvage ITS at 2–6 weeks for incomplete responders. (Chandrasekhar et al., 2019)

Recovery Classification Systems

• Siegel Criteria: Complete recovery = final hearing better than 25 dB; Partial recovery = more than 15 dB gain and final hearing 25–45 dB; Slight improvement = more than 15 dB gain and final hearing poorer than 45 dB; No improvement = less than 15 dB gain and final hearing poorer than 75 dB. Most widely used in the ITS literature. (Siegel, 1975)

• AAO-HNS 2019 Criteria: Complete recovery = return to within 10 dB of the unaffected ear and word recognition score within 5–10% of the unaffected ear; Partial recovery = ≥10 dB improvement in PTA without complete recovery; No recovery = <10 dB improvement. The lower partial recovery threshold (10 vs. 15 dB) may yield higher reported partial recovery rates for the same dataset. (Chandrasekhar et al., 2019)

Prognostic Summary

Key prognostic factors and their relative impact on hearing recovery:

Practical Treatment Algorithm

Pathway 1: PTA <70 dB, No Systemic Steroid Contraindications

• Step 1. Confirm sensorineural loss by audiometry; exclude conductive component.

• Step 2. Initiate oral prednisone 1 mg/kg/day (max 60 mg/day) as soon as possible and within 2 weeks of symptom onset, for 7–14 days followed by a taper.  (Chandrasekhar et al., 2019)

• Step 3. Obtain MRI of the IACs/posterior fossa to evaluate for retrocochlear pathology. (Chandrasekhar et al., 2019)

• Step 4. Follow-up audiometry at 2–4 weeks.

• Step 5.  Incomplete recovery at 2–6 weeks from onset: offer salvage ITS (dexamethasone 24 mg/mL compounded or 10 mg/mL stock solution, or methylprednisolone 40 mg/mL or 30 mg/mL); inject 0.4–0.8 mL into the middle ear space, with up to 4 injections over a 2-week period.  (Chandrasekhar et al., 2019)

Pathway 2: Severe-to-Profound SSNHL (PTA ≥70 dB) or Multiple Poor Prognostic Features

• Step 1. Confirm diagnosis; exclude conductive component.

• Step 2. Initiate oral prednisone 1 mg/kg/day (max 60 mg/day) as soon as possible and within 2 weeks of symptom onset, for 7–14 days followed by a taper. (Chandrasekhar et al., 2019)

• Step 3. Discuss combined therapy: early ITS concurrent with or immediately following systemic steroids may be considered, supported by retrospective meta-analytic data. (Alqahtani et al., 2025) Counsel patient that combined therapy is not guideline-endorsed standard of care.

• Step 4. Obtain MRI of the IACs/posterior fossa to evaluate for retrocochlear pathology. (Chandrasekhar et al., 2019)

• Step 5. If HBOT available and patient within 2 weeks of onset: discuss as adjunct per AAO-HNS Option designation. (Chandrasekhar et al., 2019; Sun et al., 2025)

• Step 6. Follow-up audiometry at 2–4 weeks; offer salvage ITS at 2–6 weeks if combined therapy not already initiated.

• Step 7. Persistent profound hearing loss despite treatment: initiate hearing rehabilitation and consider cochlear implant evaluation as appropriate.

Pathway 3: Systemic Steroid Contraindications

• Step 1. Primary ITS: dexamethasone 24 mg/mL (compounded), or 10 mg/mL stock solution if compounded concentration is unavailable, or methylprednisolone 40 mg/mL or 30 mg/mL; inject 0.4–0.8 mL into the middle ear space, with up to 4 injections over 2 weeks. (Chandrasekhar et al., 2019)

• Step 2. Obtain MRI of the IACs/posterior fossa to evaluate for retrocochlear pathology. (Chandrasekhar et al., 2019)

• Step 3. Follow-up audiometry at ITS course completion and at 4–6 weeks.

Pathway 4: Incomplete Recovery After Primary Systemic Steroids (Salvage)

• Step 1. Define incomplete recovery: failure to achieve complete recovery by AAO-HNS criteria (return to within 10 dB of the unaffected ear and word recognition score within 5–10% of the unaffected ear) at 2–6 weeks after onset.

• Step 2. Offer salvage ITS 2–6 weeks after symptom onset: dexamethasone 24 mg/mL (compounded), or 10 mg/mL stock solution if compounded concentration is unavailable, or methylprednisolone 40 mg/mL or 30 mg/mL; inject 0.4–0.8 mL, with up to 4 injections over 2 weeks. (Chandrasekhar et al., 2019)

• Step 3. Counsel regarding variable response to salvage ITS; earlier treatment initiation is associated with greater PTA recovery. (Kennedy et al., 2025)

• Step 4. If HBOT accessible and patient within 1 month of onset: combined HBOT +  steroid therapy may be offered (Chandrasekhar et al., 2019) 

• Step 5. Persistent profound hearing loss despite treatment: initiate hearing rehabilitation and cochlear implant evaluation as appropriate.

Current Management Options

• A. Systemic Corticosteroids as Primary Therapy

  Guideline Designation: Option (Grade C) — 2019 AAO-HNS Clinical Practice Guideline. (Chandrasekhar et al., 2019)

  Regimen: Prednisone 1 mg/kg/day (usual maximum 60 mg/day), administered at full dose for 7–14 days followed by a taper over a similar time period. Equivalent regimens are methylprednisolone 48 mg/day or dexamethasone 10 mg/day. (Chandrasekhar et al., 2019)

  Efficacy: Wilson et al. established statistically significant hearing recovery over placebo. (Wilson et al., 1980) The 2011 trial by Rauch et al. demonstrated mean PTA improvement of approximately 30.7 dB with oral prednisone versus 28.7 dB with intratympanic methylprednisolone, meeting the criterion for noninferiority. (Rauch et al., 2011)

  Advantages: Widely available; no procedural skill required; appropriate when ITS access is unavailable.

  Disadvantages: Systemic side effects (hyperglycemia, mood disturbance, insomnia, GI irritation). Contraindicated in uncontrolled diabetes, severe hypertension, active peptic ulcer, recent surgery, psychiatric vulnerability, or immunosuppression. Achieves substantially lower cochlear concentrations than ITS.

• B. Intratympanic Steroids as Salvage Therapy

  Guideline Designation: Recommendation (Grade B) — 2019 AAO-HNS CPG. The only treatment intervention at this level of recommendation. (Chandrasekhar et al., 2019)

  Indications: Incomplete recovery at 2–6 weeks after onset following a course of systemic steroids.

  Cochlear Drug Delivery: ITS bypasses the blood-labyrinth barrier; drug diffuses passively across the RWM into the scala tympani perilymph, achieving cochlear concentrations substantially exceeding systemic doses. (Parnes et al., 1999) RWM permeability is the pharmacokinetic rate-limiting step; fibrosis, adipose deposition, false membranes, or prior middle ear disease impair drug entry. Perilymph concentrations follow a basal-to-apical gradient, highest at the round window.

  Technique:

1. Position the patient with the affected ear up and maintain the head in the otologic position for 15–30 minutes after injection. (Chandrasekhar et al., 2019)

2. Topical anesthesia: topical phenol may be used. (Rauch et al., 2011)

3. Using a narrow-gauge spinal needle, inject 0.4–0.8 mL of steroid solution into the middle ear space. (Chandrasekhar et al., 2019)

4. Optional posteroinferior “borehole” perforation as a pressure-relief vent.

5. Patient instructed not to swallow or yawn to prevent Eustachian tube drainage. Administer up to 4 injections over a 2-week period. (Chandrasekhar et al., 2019)

Procedural Pearls:

• Inadequate middle ear fill is the most common pitfall. Ensure adequate filling of the middle ear space; recommended injection volume is 0.4–0.8 mL. (Chandrasekhar et al., 2019)

• Warn patients before the first injection of transient vertigo (minutes, benign) and muffled hearing (20–30 min, resolves as the Eustachian tube drains).

• TM perforations heal spontaneously in >95% of cases; persistent perforation (<5%) requires monitoring and may need tympanoplasty.
  
   

Drug Selection:

• Dexamethasone: 24 mg/mL compounded solution, or 10 mg/mL stock solution if the compounded concentration is unavailable. Intratympanic administration achieves high cochlear-fluid concentrations, although methylprednisolone demonstrates a more favorable inner-ear pharmacokinetic profile. (Parnes et al., 1999; Chandrasekhar et al., 2019)

• Methylprednisolone: 40 mg/mL or 30 mg/mL may be used for intratympanic therapy. Intratympanic administration achieves high cochlear-fluid concentrations, with methylprednisolone demonstrating a favorable inner-ear pharmacokinetic profile. (Parnes et al., 1999; Chandrasekhar et al., 2019)

  Efficacy: In a retrospective cohort, 41% of patients receiving IT steroids achieved partial or complete hearing recovery; earlier treatment initiation was associated with greater PTA recovery. (Kennedy et al., 2025)

  Advantages: Avoids systemic corticosteroid exposure; outpatient administration; repeat dosing possible; recommended as salvage therapy for incomplete recovery 2–6 weeks after symptom onset. (Chandrasekhar et al., 2019)

  Disadvantages / Complications: Transient pain or dizziness, infection, persistent tympanic membrane perforation, and vasovagal or syncopal reactions may occur but are infrequent. (Chandrasekhar et al., 2019)

• C. Intratympanic Steroids as Primary Monotherapy

  Evidence Basis: Noninferiority established in the randomized trial by Rauch et al. (Rauch et al., 2011)

  Indications: Contraindications to systemic corticosteroids: uncontrolled diabetes mellitus, active peptic ulcer disease, severe psychiatric conditions, recent major surgery, severe hypertension, active immunosuppression, or patient preference after informed discussion.

  Schedule: Dexamethasone 24 mg/mL (compounded), or 10 mg/mL stock solution if the compounded concentration is unavailable, or methylprednisolone 40 mg/mL or 30 mg/mL; inject 0.4–0.8 mL into the middle ear space, with up to 4 injections over a 2-week period. Initial corticosteroid therapy should be offered within 2 weeks of symptom onset. (Chandrasekhar et al., 2019)

  Evidence: 250 patients with unilateral SSNHL presenting within 14 days of onset and PTA ≥50 dB were randomized to oral prednisone or intratympanic methylprednisolone. Oral prednisone 60 mg/day for 14 days followed by a 5-day taper resulted in a mean PTA improvement of 30.7 dB, compared with 28.7 dB following four 1-mL injections of methylprednisolone 40 mg/mL over 2 weeks. Intratympanic therapy met the prespecified criterion for noninferiority. (Rauch et al., 2011)

  Patient Counseling: Primary ITS is noninferior to oral prednisone in appropriately selected patients and minimizes systemic corticosteroid exposure. Treatment typically requires up to 4 intratympanic injections over approximately 2 weeks. (Rauch et al., 2011; Chandrasekhar et al., 2019)

  Advantages: Avoids systemic corticosteroid exposure; noninferior to oral prednisone as primary therapy in the randomized trial by Rauch et al.; achieves high local cochlear drug concentrations; office-based procedure. (Rauch et al., 2011; Parnes et al., 1999)

  Limitations: Requires repeated office-based procedures and a trained otolaryngologist; optimal drug, concentration, and treatment schedule remain heterogeneous across studies.

  D. Combined Systemic and Intratympanic Steroids

  Guideline Designation: No guideline recommendation. Evidence derives from retrospective cohorts and meta-analyses only; no prospective RCT has directly evaluated this approach.

  Rationale: Systemic and intratympanic routes achieve cochlear loading via distinct pharmacokinetic pathways (spiral modiolar artery vs. round window diffusion), hypothetically saturating both cochlear compartments simultaneously.

  Patient Selection: May be considered in: initial PTA ≥70 dB, high-frequency or profound audiogram, concurrent vertigo, age >40, treatment delay >2 weeks, or multiple poor prognostic factors. Patients must be explicitly counseled that combined therapy is not guideline-endorsed standard of care.

  Evidence: A 2025 meta-analysis found combined therapy associated with significantly greater mean PTA improvement than systemic steroids alone in patients with initial PTA ≥70 dB. (Alqahtani et al., 2025) These findings are hypothesis-generating; retrospective designs limit causal inference. Prospective RCT evidence is needed.

• E. Hyperbaric Oxygen Therapy (HBOT)

  Guideline Designation: Option (Grade C) — 2019 AAO-HNS CPG. HBOT combined with steroid therapy may be offered as initial therapy within 2 weeks of onset or as salvage therapy within 1 month of onset. (Chandrasekhar et al., 2019)

  Regimen: 100% O₂ at 2.0–2.5 ATA for approximately 90 minutes per session, generally for 10–20 sessions. (Rhee et al., 2018)

  Efficacy: A 2025 review found HBOT combined with steroids superior to steroids alone, particularly for low-frequency thresholds. (Sun et al., 2025) Evidence is strongest for severe-to-profound loss presenting within 2 weeks.

  Limitations: Limited facility availability; requirement for multiple treatment sessions may limit accessibility and insurance coverage; claustrophobia; contraindications include untreated pneumothorax.

  F. Therapies Not Recommended

  Guideline Designation: Strong Recommendation Against — 2019 AAO-HNS Clinical Practice Guideline. (Chandrasekhar et al., 2019)

• Antivirals (acyclovir, valacyclovir): No demonstrated benefit in idiopathic SSNHL. Acceptable only for confirmed herpetic infection (Ramsay Hunt syndrome).

• Thrombolytics: No RCT benefit; bleeding risk.

• Vasodilators / vasoactive substances (carbogen, pentoxifylline, low-molecular-weight dextran): No demonstrated benefit.

• Routine CT temporal bones: No diagnostic benefit in typical SSNHL; radiation exposure without indication.

References

Alqahtani, S. Y., Altwairqi, R. G., Abuduruk, S. H., Aloufi, B. A., Almalki, Z. A., Mujahed, R. A., & Althobaiti, T. S. (2025). Systematic review and meta-analysis of intratympanic steroid injection in sudden sensory neural hearing loss as initial, combined, or salvage treatment compared to systemic steroids alone. Journal of Otology, 20(1), 44–50. https://doi.org/10.26599/JOTO.2025.9540008

Cadoni G, Rizzuti A, Sollazzo M, Picciotti PM, Galli J. Audiogram Shape: Does It Have a Significant Prognostic Role in Idiopathic Sudden Sensorineural Hearing Loss Outcome? Journal of Personalized Medicine. 2025; 15(8):379. https://doi.org/10.3390/jpm15080379

Chandrasekhar, S. S., Tsai Do, B. S., Schwartz, S. R., Bontempo, L. J., Faucett, E. A., Finestone, S. A., Hollingsworth, D. B., Kelley, D. M., Kmucha, S. T., Moonis, G., Poling, G. L., Roberts, J. K., Stachler, R. J., Zeitler, D. M., Corrigan, M. D., Nnacheta, L. C., & Satterfield, L. (2019). Clinical Practice Guideline: Sudden Hearing Loss (Update). Otolaryngol Head Neck Surg, 161(1_suppl), S1–s45. https://doi.org/10.1177/0194599819859885

Chen, L., Qiu, J., Zhang, Q., Xi, Z., Wu, Q., Xu, M., Zhang, Q., Jin, Y., Yang, J., Duan, M., Zhang, Q., & Zhang, Z. (2025). Analysis of the Reasons for Poor Prognosis in Severe to Profound Sudden Sensorineural Hearing Loss: A Systematic Review and Meta-Analysis. Diagnostics (Basel), 15(21). https://doi.org/10.3390/diagnostics15212770

Kennedy, D. J., Williams, E., Wolf, L., Golden, J., Lana, A., Wiefels, M., Pyle, M., Yunis, V., & Hoffer, M. (2025). Intratympanic steroid administration and predictors of recovery in sudden sensorineural hearing loss. PLoS One, 20(10), e0332809. https://doi.org/10.1371/journal.pone.0332809

Kim, D. H., Lee, S., & Hwang, S. H. (2019). Non-contrast Magnetic Resonance Imaging for Diagnosis and Monitoring of Vestibular Schwannomas: A Systematic Review and Meta-analysis. Otol Neurotol, 40(9), 1126–1133. https://doi.org/10.1097/mao.0000000000002416

Parnes, L. S., Sun, A. H., & Freeman, D. J. (1999). Corticosteroid pharmacokinetics in the inner ear fluids: an animal study followed by clinical application. Laryngoscope, 109(7 Pt 2), 1–17. https://doi.org/10.1097/00005537-199907001-00001

Rauch, S. D., Halpin, C. F., Antonelli, P. J., Babu, S., Carey, J. P., Gantz, B. J., Goebel, J. A., Hammerschlag, P. E., Harris, J. P., Isaacson, B., Lee, D., Linstrom, C. J., Parnes, L. S., Shi, H., Slattery, W. H., Telian, S. A., Vrabec, J. T., & Reda, D. J. (2011). Oral vs intratympanic corticosteroid therapy for idiopathic sudden sensorineural hearing loss: a randomized trial. Jama, 305(20), 2071–2079. https://doi.org/10.1001/jama.2011.679

Rhee, T. M., Hwang, D., Lee, J. S., Park, J., & Lee, J. M. (2018). Addition of Hyperbaric Oxygen Therapy vs Medical Therapy Alone for Idiopathic Sudden Sensorineural Hearing Loss: A Systematic Review and Meta-analysis. JAMA Otolaryngol Head Neck Surg, 144(12), 1153–1161. https://doi.org/10.1001/jamaoto.2018.2133

Siegel, L. G. (1975). The treatment of idiopathic sudden sensorineural hearing loss. Otolaryngol Clin North Am, 8(2), 467–473.

Sun, Y., Wang, S., Fu, H., Ge, X., & Pan, S. (2025). Hyperbaric oxygen therapy for sudden sensorineural hearing loss (Review). Mol Med Rep, 32(5). https://doi.org/10.3892/mmr.2025.13672

Wilson, W. R., Byl, F. M., & Laird, N. (1980). The efficacy of steroids in the treatment of idiopathic sudden hearing loss. A double-blind clinical study. Arch Otolaryngol, 106(12), 772–776. https://doi.org/10.1001/archotol.1980.00790360050013