Hearing disorders in cats: Classification, pathology and diagnosis

2017 ◽  
Vol 19 (3) ◽  
pp. 276-287 ◽  
Author(s):  
George M Strain
Keyword(s):  
Hearing Loss ◽  
Hair Cells ◽  
Genetic Disorder ◽  
Companion Animals ◽  
Sensorineural Deafness ◽  
The Body ◽  
Clinical Aspects ◽  
Cochlear Hair Cells ◽  
Unilateral Deafness ◽  
Auditory Evoked Response

Practical relevance: Auditory function is a sense that is central to life for cats - being important in situational awareness of potential predators, pursuit of prey, and for communication with conspecifics, humans and other species. Deafness in cats is most frequently the result of a genetic disorder, strongly associated with white fur and blue eyes, but may also result from acquired causes such as advancing age, ototoxic drugs, infection, environmental noise and physical trauma. Deafness can be sensorineural, where there is loss of cochlear hair cells, or conductive, where sound is muffled on its way to the inner ear. Clinical challenges: Establishing whether a cat is deaf can be difficult as behavioral testing of hearing is subjective and does not reliably detect unilateral deafness. Brainstem auditory evoked response testing is an objective measure but is limited in its availability. Currently, sensorineural deafness is irreversible because no treatments are available to restore lost hair cells. Conductive hearing loss can usually be treated, although full hearing recovery following otitis media may take weeks as the body clears the middle ear of debris. Evidence base: The author draws on the published literature and his extensive research on clinical aspects and molecular genetics of deafness, principally in companion animals, to review types and forms of deafness in cats. He also discusses current diagnostic approaches and provides brief advice for managing cats with hearing loss.

Fluorocitrate Neural Dystrophy of the Guinea Pig Cochlea

1975 ◽  
Vol 33 ◽  
pp. 368-369
Author(s):  
G.J. Spector ◽  
C.D. Carr ◽  
I. Kaufman Arenberg ◽  
R.H. Maisel
Keyword(s):  
Hearing Loss ◽  
Hair Cells ◽  
Sodium Phosphate ◽  
Sensory Cells ◽  
Barium Salt ◽  
Perfusion Medium ◽  
Cochlear Hair Cells ◽  
Neural Degeneration ◽  
Sodium Phosphate Buffer ◽  
Cochlear Neurons

All studies on primary neural degeneration in the cochlea have evaluated the end stages of degeneration or the indiscriminate destruction of both sensory cells and cochlear neurons. We have developed a model which selectively simulates the dystrophic changes denoting cochlear neural degeneration while sparing the cochlear hair cells. Such a model can be used to define more precisely the mechanism of presbycusis or the hearing loss in aging man.Twenty-two pigmented guinea pigs (200-250 gm) were perfused by the perilymphatic route as live preparations using fluorocitrate in various concentrations (15-250 ug/cc) and at different incubation times (5-150 minutes). The barium salt of DL fluorocitrate, (C6H4O7F)2Ba3, was reacted with 1.0N sulfuric acid to precipitate the barium as a sulfate. The perfusion medium was prepared, just prior to use, as follows: sodium phosphate buffer 0.2M, pH 7.4 = 9cc; fluorocitrate = 15-200 mg/cc; and sucrose = 0.2M.

scholarly journals Effects of cochlear hair cell ablation on spatial learning/memory

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Z. Jason Qian ◽  
Anthony J. Ricci
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Spatial Learning ◽  
Hair Cells ◽  
Noise Exposure ◽  
Memory Errors ◽  
Cochlear Hair Cells ◽  
Cochlear Hair Cell ◽  
Cell Ablation ◽  
Spatial Learning Memory

AbstractCurrent clinical interest lies in the relationship between hearing loss and cognitive impairment. Previous work demonstrated that noise exposure, a common cause of sensorineural hearing loss (SNHL), leads to cognitive impairments in mice. However, in noise-induced models, it is difficult to distinguish the effects of noise trauma from subsequent SNHL on central processes. Here, we use cochlear hair cell ablation to isolate the effects of SNHL. Cochlear hair cells were conditionally and selectively ablated in mature, transgenic mice where the human diphtheria toxin (DT) receptor was expressed behind the hair-cell specific Pou4f3 promoter. Due to higher Pou4f3 expression in cochlear hair cells than vestibular hair cells, administration of a low dose of DT caused profound SNHL without vestibular dysfunction and had no effect on wild-type (WT) littermates. Spatial learning/memory was assayed using an automated radial 8-arm maze (RAM), where mice were trained to find food rewards over a 14-day period. The number of working memory errors (WME) and reference memory errors (RME) per training day were recorded. All animals were injected with DT during P30–60 and underwent the RAM assay during P90–120. SNHL animals committed more WME and RME than WT animals, demonstrating that isolated SNHL affected cognitive function. Duration of SNHL (60 versus 90 days post DT injection) had no effect on RAM performance. However, younger age of acquired SNHL (DT on P30 versus P60) was associated with fewer WME. This describes the previously undocumented effect of isolated SNHL on cognitive processes that do not directly rely on auditory sensory input.

scholarly journals Streptococcus suis infection: Clinical manifestations

2005 ◽  
Vol 58 (5-6) ◽  
pp. 236-239 ◽  
Author(s):  
Julijana Dragojlovic ◽  
Branko Milosevic ◽  
Neda Sasic ◽  
Miomir Pelemis ◽  
Milan Sasic
Keyword(s):  
Hearing Loss ◽  
Bacterial Meningitis ◽  
Clinical Symptoms ◽  
Clinical Manifestations ◽  
Sensorineural Deafness ◽  
Streptococcus Suis ◽  
The Body ◽  
Effective Prevention ◽  
Sporadic Disease ◽  
Male Patients

Introduction Streptococcus suis is a bacterium causing a disease in pigs and rarely in humans. This zoonosis is mostly found as a sporadic disease in individuals that were in contact with the affected or infected pigs: farmers, veterinarians and workers engaged in fresh pork processing. It is assumed that the bacterium enters the body through a cut abrasion in the skin. Initially, the condition resembles a flu, followed by signs of bacteriemia and sepsis. The most frequent clinical manifestation of Streptococcus suis infection is meningitis, leading to hearing loss in over 75% of patients, and subsequent arthritis, endophtalmitis, endocarditis and pneumonia. Toxic shock syndrome with hemorhagic manifestations rarely develops. Material and methods This study included five male patients aged 22 to 63 years treated in the Intensive Care Unit of the Institute of Infectious and Tropical Diseases in Belgrade, due to Streptococcus suis infection. The aim of this study was to point to the existence of this bacteria in our environment, to describe clinical manifestations of the disease and to point out the importance of its prevention. Results All patients had epidemiological evidence of being in contact with pork meat. There were no data about diseased pigs. The estimated incubation period was 4 to 8 days. All patients had meningeal signs. Clinical symptoms included shivering, fever, vomiting, headache, malaise, vertigo and tinitus. Three patients presented with alerterd level of awareness. Four patients developed very severe bilateral hearing impairemnt, whereas one endophtalmtis and one developed endocarditis. The cerebrospinal fluid (CSF) was opalescent in four patients, and only one patient presented with clear CSF. CSF examination showed typical changes characeteristic for bacterial meningitis. Streptoccocus suis was isolated in CSF in all patients, and in one patient the bacteria was isolated in blood as well. All patients underwent treatment with II and III generation cephalosporins and one with one aminoglycosides. All patients were cured, but 4 of them developed sequelae like permanent sensorineural deafness and mild ataxia. Conclusions Streptococcus suis infection is present as a zoonosis in pigs, while humans are contracted occasionally, most frequently related to occupational risk. In cases with bacterial meningitis with sepsis and hearing loss, Streptococcus suis infections must be suspected. Effective prevention requires collaboration between epidemiologists, veterinarians and human medicine physicians. .

scholarly journals Deletion of Tricellulin Causes Progressive Hearing Loss Associated with Degeneration of Cochlear Hair Cells

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Toru Kamitani ◽  
Hirofumi Sakaguchi ◽  
Atsushi Tamura ◽  
Takenori Miyashita ◽  
Yuji Yamazaki ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Hair Cells ◽  
Progressive Hearing Loss ◽  
Cochlear Hair Cells

scholarly journals Genetics of Nonsyndromic Congenital Hearing Loss

Scientifica ◽  
2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Oguz Kadir Egilmez ◽  
M. Tayyar Kalcioglu
Keyword(s):  
Hearing Loss ◽  
Inner Ear ◽  
Hair Cells ◽  
Neurotransmitter Release ◽  
Intracellular Transport ◽  
Autosomal Recessive ◽  
Treatment Options ◽  
The Body ◽  
Congenital Hearing Loss ◽  
Congenital Hearing Impairment

Congenital hearing impairment affects nearly 1 in every 1000 live births and is the most frequent birth defect in developed societies. Hereditary types of hearing loss account for more than 50% of all congenital sensorineural hearing loss cases and are caused by genetic mutations. HL can be either nonsyndromic, which is restricted to the inner ear, or syndromic, a part of multiple anomalies affecting the body. Nonsyndromic HL can be categorised by mode of inheritance, such as autosomal dominant (called DFNA), autosomal recessive (DFNB), mitochondrial, and X-linked (DFN). To date, 125 deafness loci have been reported in the literature: 58 DFNA loci, 63 DFNB loci, and 4 X-linked loci. Mutations in genes that control the adhesion of hair cells, intracellular transport, neurotransmitter release, ionic hemeostasis, and cytoskeleton of hair cells can lead to malfunctions of the cochlea and inner ear. In recent years, with the increase in studies about genes involved in congenital hearing loss, genetic counselling and treatment options have emerged and increased in availability. This paper presents an overview of the currently known genes associated with nonsyndromic congenital hearing loss and mutations in the inner ear.

scholarly journals Disruption of Hars2 in Cochlear Hair Cells Causes Progressive Mitochondrial Dysfunction and Hearing Loss in Mice

2021 ◽  
Vol 15 ◽  
Author(s):  
Pengcheng Xu ◽  
Longhao Wang ◽  
Hu Peng ◽  
Huihui Liu ◽  
Hongchao Liu ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Hair Cell ◽  
Mitochondrial Dysfunction ◽  
Hair Cells ◽  
Cell Loss ◽  
Outer Hair Cells ◽  
Hair Cell Loss ◽  
Progressive Hearing Loss ◽  
Cochlear Hair Cells ◽  
Inner Hair Cells

Mutations in a number of genes encoding mitochondrial aminoacyl-tRNA synthetases lead to non-syndromic and/or syndromic sensorineural hearing loss in humans, while their cellular and physiological pathology in cochlea has rarely been investigated in vivo. In this study, we showed that histidyl-tRNA synthetase HARS2, whose deficiency is associated with Perrault syndrome 2 (PRLTS2), is robustly expressed in postnatal mouse cochlea including the outer and inner hair cells. Targeted knockout of Hars2 in mouse hair cells resulted in delayed onset (P30), rapidly progressive hearing loss similar to the PRLTS2 hearing phenotype. Significant hair cell loss was observed starting from P45 following elevated reactive oxygen species (ROS) level and activated mitochondrial apoptotic pathway. Despite of normal ribbon synapse formation, whole-cell patch clamp of the inner hair cells revealed reduced calcium influx and compromised sustained synaptic exocytosis prior to the hair cell loss at P30, consistent with the decreased supra-threshold wave I amplitudes of the auditory brainstem response. Starting from P14, increasing proportion of morphologically abnormal mitochondria was observed by transmission electron microscope, exhibiting swelling, deformation, loss of cristae and emergence of large intrinsic vacuoles that are associated with mitochondrial dysfunction. Though the mitochondrial abnormalities are more prominent in inner hair cells, it is the outer hair cells suffering more severe cell loss. Taken together, our results suggest that conditional knockout of Hars2 in mouse cochlear hair cells leads to accumulating mitochondrial dysfunction and ROS stress, triggers progressive hearing loss highlighted by hair cell synaptopathy and apoptosis, and is differentially perceived by inner and outer hair cells.

scholarly journals Peripheral Vestibular Dysfunction Is a Common Occurrence in Children With Non-syndromic and Syndromic Genetic Hearing Loss

2021 ◽  
Vol 12 ◽  
Author(s):  
Alicia Wang ◽  
A. Eliot Shearer ◽  
Guang Wei Zhou ◽  
Margaret Kenna ◽  
Dennis Poe ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Hair Cells ◽  
Cochlear Implantation ◽  
Vestibular Evoked Myogenic Potentials ◽  
Common Finding ◽  
Vestibular Loss ◽  
Cochlear Hair Cells ◽  
Vestibular Hair Cells ◽  
Vestibular Testing

Hearing loss (HL) is the most common sensory deficit in humans and is frequently accompanied by peripheral vestibular loss (PVL). While often overlooked, PVL is an important sensory dysfunction that may impair development of motor milestones in children and can have a significant negative impact on quality of life. In addition, many animal and in vitro models of deafness use vestibular hair cells as a proxy to study cochlear hair cells. The extent of vestibular end organ dysfunction associated with genetic pediatric hearing loss is not well-understood. We studied children with a known genetic cause of hearing loss who underwent routine preoperative vestibular testing prior to cochlear implantation between June 2014 and July 2020. Vestibular testing included videonystagmography, rotary chair, video head impulse testing, and/or vestibular evoked myogenic potentials. Etiology of HL was determined through history, physical examination, imaging, laboratory testing, and/or genetic testing. Forty-four children (21 female/23 male) met inclusion criteria; 24 had genetic non-syndromic and 20 had genetic syndromic forms of HL. Mean age at the time of testing was 2.8 ± 3.8 years (range 7 months−17 years). The most common cause of non-syndromic HL was due to mutations in GJB2 (n = 13) followed by MYO15A (3), MYO6 (2), POU3F4 (2), TMPRSS3 (1), CDH23 (1), TMC1 (1), and ESRRB (1). The most common forms of syndromic HL were Usher syndrome (4) and Waardenburg (4), followed by SCID/reticular dysgenesis (3), CHARGE (2), CAPOS (1), Coffin-Siris (1), Jervell and Lange-Nielsen (1), Noonan (1), peroxisome biogenesis disorder (1), Perrault (1), and Trisomy 21 (1). Overall, 23 patients (52%) had PVL. A larger proportion of children with syndromic forms of HL had PVL (12/20, 60%) compared with children with genetic non-syndromic HL (11/24, 46%), though without statistical significant (p = 0.3). The occurrence of PVL varied by affected gene. In conclusion, PVL is a common finding in children with syndromic and non-syndromic genetic HL undergoing vestibular evaluation prior to cochlear implantation. Improved understanding of the molecular physiology of vestibular hair cell dysfunction is important for clinical care as well as research involving vestibular hair cells in model organisms and in vitro models.

scholarly journals Hearing Loss in Neurological Disorders

2021 ◽  
Vol 9 ◽  
Author(s):  
Siyu Li ◽  
Cheng Cheng ◽  
Ling Lu ◽  
Xiaofeng Ma ◽  
Xiaoli Zhang ◽  
...  
Keyword(s):  
Hearing Loss ◽  
Hair Cells ◽  
Neurological Disorders ◽  
Molecular Mechanisms ◽  
Relevant Literature ◽  
Autism Spectrum ◽  
Supporting Cells ◽  
Cochlear Hair Cells ◽  
Wide Range ◽  
Histological Characteristics

Sensorineural hearing loss (SNHL) affects approximately 466 million people worldwide, which is projected to reach 900 million by 2050. Its histological characteristics are lesions in cochlear hair cells, supporting cells, and auditory nerve endings. Neurological disorders cover a wide range of diseases affecting the nervous system, including Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), autism spectrum disorder (ASD), etc. Many studies have revealed that neurological disorders manifest with hearing loss, in addition to typical nervous symptoms. The prevalence, manifestations, and neuropathological mechanisms underlying vary among different diseases. In this review, we discuss the relevant literature, from clinical trials to research mice models, to provide an overview of auditory dysfunctions in the most common neurological disorders, particularly those associated with hearing loss, and to explain their underlying pathological and molecular mechanisms.

scholarly journals Correlation between Carotid–Cochlear and Sensorineural Hearing Loss: A Cross-Sectional Study

2018 ◽  
Vol 01 (02) ◽  
pp. 089-093
Author(s):  
Raghul Sekar ◽  
Arun Alexander ◽  
Nagarajan Krishnan
Keyword(s):  
Hearing Loss ◽  
Carotid Artery ◽  
Sensorineural Hearing Loss ◽  
Hair Cells ◽  
Fluid Pressure ◽  
Sensorineural Deafness ◽  
Normal Subjects ◽  
Sensorineural Hearing ◽  
P Value ◽  
Strong Negative Correlation

Abstract Background Sensorineural hearing loss is a condition with several etiologies and varies with the age of the individual. Carotid–cochlear interval is the minimum distance between basal turn of cochlea and the genu of petrous part of internal carotid artery. It is believed that constant pulsations from carotid can cause fluid pressure changes within the cochlea leading to damage to hair cells causing hearing loss. Objective To study the correlation between carotid–cochlear interval and degree of hearing loss at different frequencies in patients with sensorineural deafness and compare this interval with normal subjects. Methods Seventy cases with sensorineural hearing loss between 18 and 60 years undergoing HRCT temporal bone were grouped together and 70 cases with normal hearing undergoing CT nose and paranasal sinuses were grouped together. Carotid–cochlear interval measured in both the groups was correlated with the degree and frequency of hearing loss and compared with normal subjects. Results The mean carotid–cochlear interval in sensorineural hearing loss and in normal subjects was found to be 1.30 + 0.68 (SD) mm and 1.83 + 0.74 (SD) mm, respectively with p < 0.001. The coefficient of correlation between carotid–cochlear interval and pure tone average in patients with sensorineural deafness was r = −0.740 with p-value < 0.001. Conclusion Carotid–cochlear interval is significantly low in patients with sensorineural hearing loss and bears a strong negative correlation with the degree of hearing loss at mid- and high-frequency ranges. Thus we hypothesize that pulsations from carotid artery cause damage to hair cells in the organ of Corti producing audiological symptoms such as hearing loss.

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