Bilateral Sensorineural Hearing Loss in the Setting of Acute Methamphetamine Overdose

Substance abuse is a rare but known cause of sensorineural hearing loss (SNHL). We report a case of acute SNHL in a 28-year-old man following an overdose of methamphetamine and incidental ingestion of fentanyl. On initial encounter, he had moderate-to-severe hearing loss in the right ear and severe-to-profound hearing loss in the left ear in addition to acute kidney injury, liver failure, and lactic acidosis. The patient was treated with a two-week course of high-dose steroids and expressed a subjective improvement in hearing. This case highlights the importance of auditory testing following a drug overdose and is one of the only documented cases of hearing loss following methamphetamine use in recent years. There is a paucity of literature regarding the mechanism causing acute SNHL secondary to methamphetamines. Proposed etiologies include neurotransmitter depletion or reduced cochlear blood flow as possible causes of ototoxicity.

Sympathetic Nervous System Regulation of Auditory Function

<b><i>Background:</i></b> The auditory system processes how we hear and understand sounds within the environment. It comprises both peripheral and central structures. Sympathetic nervous system projections are present throughout the auditory system. The function of sympathetic fibers in the cochlea has not been studied extensively due to the limited number of direct projections in the auditory system. Nevertheless, research on adrenergic and noradrenergic regulation of the cochlea and central auditory system is growing. With the rapid development of neuroscience, auditory central regulation is an extant topic of focus in research on hearing. <b><i>Summary:</i></b> As such, understanding sympathetic nervous system regulation of auditory function is a growing topic of interest. Herein, we review the distribution and putative physiological and pathological roles of sympathetic nervous system projections in hearing. <b><i>Key Messages:</i></b> In the peripheral auditory system, the sympathetic nervous system regulates cochlear blood flow, modulates cochlear efferent fibers, affects hair cells, and influences the habenula region. In central auditory pathways, norepinephrine is essential for plasticity in the auditory cortex and affects auditory cortex activity. In pathological states, the sympathetic nervous system is associated with many hearing disorders. The mechanisms and pathways of sympathetic nervous system modulation of auditory function is still valuable for us to research and discuss.

What is the prevalence of dyslipidemia in patients with idiopathic tinnitus?

Background: Dyslipidemia is a metabolic disorder that results from imbalanced and overfeeding as well as sedentary life. Elevated blood lipid levels can affect cochlear blood flow and fluidity, leading to decreased hearing and tinnitus. We aimed to determine whether there is a relationship between tinnitus and dyslipidemia by investigating the blood lipoprotein values of patients with tinnitus.Methods: The lipid profiles of the patients with idiopathic tinnitus who were selected among the patients who applied to Istanbul Haydarpaşa Numune Training and Research Hospital with the complaint of tinnitus between January 2019 and May 2020 were examined. The test results and age and gender distributions were compared with control groups without tinnitus complaints and statistical evaluation was performed.Results: Hypercholesterolemia in 42% of 6472 patients with idiopathic tinnitus, 18% low HDL, 50% high LDL, Hyperlipidemia was detected in 21%. 1942 (30%) of these patients were male; 4530 (70%) are women. The number of patients in the control group without tinnitus was 6470. Hypercholesterolemia in 49% of this group; 21% low HDL, 42% high LDL, 16% hyperlipidemia was detected. In this control group, 1950 (30%) of the patients were male and 4520 (70%) were female. Cholesterol of male and female patients with tinnutus. When the cholesterol, LDL and triglyceride values of HDL and LDL values and female and male patients in the control group were examined, a statistically significant difference was found (p <0.005). No statistically significant difference was found between HDL values of female and male patients with tinnutus and HDL values of female and male patients in the control group (P> 0.05).Conclusions: There is a statistically relationship between tinnitus and dyslipidemia. The presence of dyslipidemia is vital due to atherosclerosis caused by dyslipidemia, especially coronary artery involvement. Therefore, dyslipidemia should be treated as it causes many diseases.

Mitochondrial Damage and Necroptosis in Aging Cochlea

Age-related hearing loss (ARHL) is an irreversible, progressive neurodegenerative disorder and is presently untreatable. Previous studies using animal models have suggested mitochondrial damage and programmed cell death to be involved with ARHL. Thus, we further investigated the pathophysiologic role of mitochondria and necroptosis in aged C57BL/6J male mice. Aged mice (20 months old) exhibited a significant loss of hearing, number of hair cells, neuronal fibers, and synaptic ribbons compared to young mice. Ultrastructural analysis of aged cochleae revealed damaged mitochondria with absent or disorganized cristae. Aged mice also showed significant decrease in cochlear blood flow, and exhibited increase in gene expression of proinflammatory cytokines (IL-1β, IL-6, and TNF-α), receptor-interacting serine/threonine-protein kinase 1 and 3 (RIPK1 and RIPK3) and the pseudokinase mixed-lineage kinase domain-like (MLKL). Immunofluorescence (IF) assays of cytochrome C oxidase I (COX1) confirmed mitochondrial dysfunction in aged cochleae, which correlated with the degree of mitochondrial morphological damage. IF assays also revealed localization and increased expression of RIPK3 in sensorineural tissues that underwent significant necroptosis (inner and outer hair cells and stria vascularis). Together, our data shows that the aging cochlea exhibits damaged mitochondria, enhanced synthesis of proinflammatory cytokines, and provides new evidence of necroptosis in the aging cochlea in in vivo.

Acoustic Trauma Modulates Cochlear Blood Flow and Vasoactive Factors in a Rodent Model of Noise-Induced Hearing Loss

Noise exposure affects the organ of Corti and the lateral wall of the cochlea, including the stria vascularis and spiral ligament. Although the inner ear vasculature and spiral ligament fibrocytes in the lateral wall consist of a significant proportion of cells in the cochlea, relatively little is known regarding their functional significance. In this study, 6-week-old male C57BL/6 mice were exposed to noise trauma to induce transient hearing threshold shift (TTS) or permanent hearing threshold shift (PTS). Compared to mice with TTS, mice with PTS exhibited lower cochlear blood flow and lower vessel diameter in the stria vascularis, accompanied by reduced expression levels of genes involved in vasodilation and increased expression levels of genes related to vasoconstriction. Ultrastructural analyses by transmission electron microscopy revealed that the stria vascularis and spiral ligament fibrocytes were more damaged by PTS than by TTS. Moreover, mice with PTS expressed significantly higher levels of proinflammatory cytokines in the cochlea (e.g., IL-1β, IL-6, and TNF-α). Overall, our findings suggest that cochlear microcirculation and lateral wall pathologies are differentially modulated by the severity of acoustic trauma and are associated with changes in vasoactive factors and inflammatory responses in the cochlea.

Purinergic Signaling and Cochlear Injury-Targeting the Immune System?

Hearing impairment is the most common sensory deficit, affecting more than 400 million people worldwide. Sensorineural hearing losses currently lack any specific or efficient pharmacotherapy largely due to the insufficient knowledge of the pathomechanism. Purinergic signaling plays a substantial role in cochlear (patho)physiology. P2 (ionotropic P2X and the metabotropic P2Y) as well as adenosine receptors expressed on cochlear sensory and non-sensory cells are involved mostly in protective mechanisms of the cochlea. They are implicated in the sensitivity adjustment of the receptor cells by a K+ shunt and can attenuate the cochlear amplification by modifying cochlear micromechanics. Cochlear blood flow is also regulated by purines. Here, we propose to comprehend this field with the purine-immune interactions in the cochlea. The role of harmful immune mechanisms in sensorineural hearing losses has been emerging in the horizon of cochlear pathologies. In addition to decreasing hearing sensitivity and increasing cochlear blood supply, influencing the immune system can be the additional avenue for pharmacological targeting of purinergic signaling in the cochlea. Elucidating this complexity of purinergic effects on cochlear functions is necessary and it can result in development of new therapeutic approaches in hearing disabilities, especially in the noise-induced ones.