Evidence Supporting the Hypothesis That Inflammation-Induced Vasospasm Is Involved in the Pathogenesis of Acquired Sensorineural Hearing Loss.

Michael Eisenhut

doi:10.1155/2019/4367240

Abstract

Sensorineural hearing loss is mainly acquired and affects an estimated 1.3 billion humans worldwide. It is related to aging, noise, infection, ototoxic drugs, and genetic defects. It is essential to identify reversible and preventable causes to be able to reduce the burden of this disease. Inflammation is involved in most causes and leads to tissue injury through vasospasm-associated ischemia. Vasospasm is reversible. This review summarized evidence linking inflammation-induced vasospasm to several forms of acquired sensorineural hearing loss. The link between vasospasm and sensorineural hearing loss is directly evident in subarachnoid haemorrhage, which involves the release of vasoconstriction-inducing cytokines like interleukin-1, endothelin-1, and tumour necrosis factor. These proinflammatory cytokines can also be released in response to infection, autoimmune disease, and acute or chronically increased inflammation in the ageing organism as in presbyacusis or in noise-induced cochlear injury. Evidence of vasospasm and hearing loss has also been discovered in bacterial meningitis and brain injury. Resolution of inflammation-induced vasospasm has been associated with improvement of hearing in autoimmune diseases involving overproduction of interleukin-1 from inflammasomes. There is mainly indirect evidence for vasospasm-associated sensorineural hearing loss in most forms of systemic or injury- or infection-induced local vascular inflammation. This opens up avenues in prevention and treatment of vascular and systemic inflammation as well as vasospasm itself as a way to prevent and treat most forms of acquired sensorineural hearing loss. Future research needs to investigate interventions antagonising vasospasm and vasospasm-inducing proinflammatory cytokines and their production in randomised controlled trials of prevention and treatment of acquired sensorineural hearing loss. Prime candidates for interventions are hereby inflammasome inhibitors and vasospasm-reducing drugs like nitric oxide donors, rho-kinase inhibitors, and magnesium which have the potential to reduce sensorineural hearing loss in meningitis, exposure to noise, brain injury, arteriosclerosis, and advanced age-related and autoimmune disease-related inflammation.

Highlights

Vasospasm is a consistent feature of all forms of cerebral inflammation including forms caused by infections like bacterial meningitis, cerebral malaria, and sterile vascular inflammation as detectable in diabetic ketoacidosis and brain injury [1, 2]
A pooled analysis of 226 cases of sudden sensorineural hearing loss (SNHL) in children from two centres in China demonstrated 85% of children had unilateral hearing loss, of which the largest proportion was profound (51%). e hearing loss was reversible to a variable extent in 48.6% [3, 4], and there was no dominance of a side
Inflammation is a normal adaptive response aimed at restoring tissue functionality and homeostasis after infection and tissue injury, and suppressing it could have unintended negative consequences

Summary

Introduction

Vasospasm is a consistent feature of all forms of cerebral inflammation including forms caused by infections like bacterial meningitis, cerebral malaria, and sterile vascular inflammation as detectable in diabetic ketoacidosis and brain injury [1, 2]. In “vasospasm-related” sensorineural hearing loss (SNHL), which is caused by ischemia, the pattern should be a sudden loss of hearing across several frequencies, which in most cases would start or be exclusively unilateral because a synchronicity of vasospasm occurring at exactly the same time in both ears is unlikely unless caused by a factor which acts on both labyrinthine arteries like an ototoxic. Infection, autoimmune-, or arteriosclerosis-related transient vascular stenosis is likely due to an asymmetrical exposure of the supply artery to cytokines causing vasospasm. E hearing loss should be sensorineural but reversible in a percentage of patients indicating that not hair cell loss but temporary hair cell dysfunction secondary to temporary ischemia as found in a transient vasospasm is responsible in some cases. I have attempted to summarize the evidence for a link between inflammation-induced vasospasm and acquired SNHL as well as approaches to prevention and treatment

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