Talk:Sensory - Hearing Abnormalities

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Cite this page: Hill, M.A. (2019, October 21) Embryology Sensory - Hearing Abnormalities. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Sensory_-_Hearing_Abnormalities


http://tiny.cc/Hearing_Abnormalities

2019

Otitis media with effusion in children: Pathophysiology, diagnosis, and treatment. A review

J Otol. 2019 Jun;14(2):33-39. doi: 10.1016/j.joto.2019.01.005. Epub 2019 Jan 31.

Vanneste P1, Page C1.

Otitis media with effusion (OME) is a frequent paediatric disorder. The condition is often asymptomatic, and so can easily be missed. However, OME can lead to hearing loss that impairs the child's language and behavioural development. The diagnosis is essentially clinical, and is based on otoscopy and (in some cases) tympanometry. Nasal endoscopy is only indicated in cases of unilateral OME or when obstructive adenoid hypertrophy is suspected. Otitis media with effusion is defined as the observation of middle-ear effusion at consultations three months apart. Hearing must be evaluated (using an age-appropriate audiometry technique) before and after treatment, so as not to miss another underlying cause of deafness (e.g. perception deafness). Craniofacial dysmorphism, respiratory allergy and gastro-oesophageal reflux all favour the development of OME. Although a certain number of medications (antibiotics, corticoids, antihistamines, mucokinetic agents, and nasal decongestants) can be used to treat OME, they are not reliably effective and rarely provide long-term relief. The benchmark treatment for OME is placement of tympanostomy tubes (TTs) and (in some cases) adjunct adenoidectomy. The TTs rapidly normalize hearing and effectively prevent the development of cholesteatoma in the middle ear. In contrast, TTs do not prevent progression towards tympanic atrophy or a retraction pocket. Adenoidectomy enhances the effectiveness of TTs. In children with adenoid hypertrophy, adenoidectomy is indicated before the age of 4 but can be performed later when OME is identified by nasal endoscopy. Children must be followed up until OME has disappeared completely, so that any complications are not missed. KEYWORDS: Child; Grommet; Otitis media with effusion; Tympanostomy tube; Ventilation tube PMID: 31223299 PMCID: PMC6570640 DOI: 10.1016/j.joto.2019.01.005


2015

SOX10 mutations mimic isolated hearing loss

Clin Genet. 2015 Oct;88(4):352-9. doi: 10.1111/cge.12506. Epub 2014 Nov 6.

Pingault V1,2,3, Faubert E1, Baral V2,3, Gherbi S4, Loundon N4,5, Couloigner V4,5, Denoyelle F4,5, Noël-Pétroff N6, Ducou Le Pointe H7, Elmaleh-Bergès M8, Bondurand N2,3, Marlin S4.

Abstract

Ninety genes have been identified to date that are involved in non-syndromic hearing loss, and more than 300 different forms of syndromic hearing impairment have been described. Mutations in SOX10, one of the genes contributing to syndromic hearing loss, induce a large range of phenotypes, including several subtypes of Waardenburg syndrome and Kallmann syndrome with deafness. In addition, rare mutations have been identified in patients with isolated signs of these diseases. We used the recent characterization of temporal bone imaging aspects in patients with SOX10 mutations to identify possible patients with isolated hearing loss due to SOX10 mutation. We selected 21 patients with isolated deafness and temporal bone morphological defects for mutational screening. We identified two SOX10 mutations and found that both resulted in a non-functional protein in vitro. Re-evaluation of the two affected patients showed that both had previously undiagnosed olfactory defects. Diagnosis of anosmia or hyposmia in young children is challenging, and particularly in the absence of magnetic resonance imaging (MRI), SOX10 mutations can mimic non-syndromic hearing impairment. MRI should complete temporal bones computed tomographic scan in the management of congenital deafness as it can detect brain anomalies, cochlear nerve defects, and olfactory bulb malformation in addition to inner ear malformations.


PMID 25256313

Tmc gene therapy restores auditory function in deaf mice

Sci Transl Med. 2015 Jul 8;7(295):295ra108. doi: 10.1126/scitranslmed.aab1996.

Askew C1, Rochat C2, Pan B3, Asai Y3, Ahmed H3, Child E3, Schneider BL2, Aebischer P2, Holt JR4.

Abstract

Genetic hearing loss accounts for up to 50% of prelingual deafness worldwide, yet there are no biologic treatments currently available. To investigate gene therapy as a potential biologic strategy for restoration of auditory function in patients with genetic hearing loss, we tested a gene augmentation approach in mouse models of genetic deafness. We focused on DFNB7/11 and DFNA36, which are autosomal recessive and dominant deafnesses, respectively, caused by mutations in transmembrane channel-like 1 (TMC1). Mice that carry targeted deletion of Tmc1 or a dominant Tmc1 point mutation, known as Beethoven, are good models for human DFNB7/11 and DFNA36. We screened several adeno-associated viral (AAV) serotypes and promoters and identified AAV2/1 and the chicken β-actin (Cba) promoter as an efficient combination for driving the expression of exogenous Tmc1 in inner hair cells in vivo. Exogenous Tmc1 or its closely related ortholog, Tmc2, were capable of restoring sensory transduction, auditory brainstem responses, and acoustic startle reflexes in otherwise deaf mice, suggesting that gene augmentation with Tmc1 or Tmc2 is well suited for further development as a strategy for restoration of auditory function in deaf patients who carry TMC1 mutations. Copyright © 2015, American Association for the Advancement of Science.

PMID 26157030

Congenital stapes malformation: Rare conductive hearing loss in a patient with Waardenburg syndrome

Laryngoscope. 2015 Jul 7. doi: 10.1002/lary.25443. [Epub ahead of print]

Melzer JM1, Eliason M1, Conley GS1.

Abstract

Waardenburg syndrome is a known autosomal dominant cause of congenital hearing loss. It is characterized by a distinctive phenotypic appearance and often involves sensorineural hearing loss. Temporal bone abnormalities and inner ear dysmorphisms have been described in association with the disease. However, middle ear abnormalities as causes of conductive hearing loss are not typically seen in Waardenburg syndrome. We discuss a case of an 8-year-old female who meets diagnostic criteria for Waardenburg syndrome type 3 and who presented with a bilateral conductive hearing loss associated with congenital stapes fixation. We discuss management strategy in this previously unreported phenotype. LEVEL OF EVIDENCE: NA Laryngoscope, 2015. © 2015 The American Laryngological, Rhinological and Otological Society, Inc.

PMID 26152551

2014

Analysis of incidence and genetic predisposition of pre auricular sinus

Int J Pediatr Otorhinolaryngol. 2014 Dec;78(12):2255-7. doi: 10.1016/j.ijporl.2014.10.027. Epub 2014 Oct 25.

An SY1, Choi HG2, Lee JS3, Kim JH3, Yoo SW3, Park B3.

Abstract

OBJECTIVES: To evaluate the incidence of preauricular sinus, the association between preauricular sinus of a parent and their children, and the odds of hearing impairments in patients with preauricular sinus. METHODS: A cross-sectional study was performed using data from the Korea National Health and Nutrition Examination Survey. We evaluated data from 23,533 subjects who were interviewed between 2010 and 2012. RESULTS: The incidence of unilateral preauricular sinus was 1.3% and that of bilateral preauricular sinus was 0.3%. Female gender was statistically associated with preauricular sinus (adjusted odd ratio, AOR=1.401). There was no statistical difference between right- and left-sided preauricular sinus. There was an association between parents and their children for bilateral preauricular sinus (AOR of father's bilateral preauricular sinus=35.711; AOR of mother's bilateral preauricular sinus=7.683), but there was no association found for unilateral preauricular sinus. There was no link found between hearing impairment and preauricular sinus. CONCLUSION: This large population-based study provides reliable information about the incidence of preauricular sinus, the association between preauricular sinus in parents and their children, and the lack of an association with hearing impairment; these results can help clinicians in the management of their patients. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved. KEYWORDS: Auricle; Ear; Etiology; Fistula; Prevalence; Sinus

PMID 25465450


2010

Ringing ears: the neuroscience of tinnitus

J Neurosci. 2010 Nov 10;30(45):14972-9.

Roberts LE, Eggermont JJ, Caspary DM, Shore SE, Melcher JR, Kaltenbach JA.

Department of Psychology, Neuroscience, and Behaviour, McMaster University, Hamilton, Ontario L8S 4K1, Canada. roberts@mcmaster.ca

Abstract

Tinnitus is a phantom sound (ringing of the ears) that affects quality of life for millions around the world and is associated in most cases with hearing impairment. This symposium will consider evidence that deafferentation of tonotopically organized central auditory structures leads to increased neuron spontaneous firing rates and neural synchrony in the hearing loss region. This region covers the frequency spectrum of tinnitus sounds, which are optimally suppressed following exposure to band-limited noise covering the same frequencies. Cross-modal compensations in subcortical structures may contribute to tinnitus and its modulation by jaw-clenching and eye movements. Yet many older individuals with impaired hearing do not have tinnitus, possibly because age-related changes in inhibitory circuits are better preserved. A brain network involving limbic and other nonauditory regions is active in tinnitus and may be driven when spectrotemporal information conveyed by the damaged ear does not match that predicted by central auditory processing.

PMID 21068300


http://www.youtube.com/watch?v=0HIfqyHbKgY


Inner Ear

File:Earlabyrinthsm.jpg[images/senses/earlabyrinth.jpg Inner ear labyrinth]

common cavity, severe cochlear hypoplasia

References

Mylanus EA, Rotteveel LJ, Leeuw RL. Congenital malformation of the inner ear and pediatric cochlear implantation. Otol Neurotol. 2004 May;25(3):308-17.

(See also [#Cochlear_Implant Cochlear Implant])

Blaser S, Propst EJ, Martin D, Feigenbaum A, James AL, Shannon P, Papsin BC. Inner ear dysplasia is common in children with Down syndrome (trisomy 21). Laryngoscope. 2006 Dec;116(12):2113-9.

Search PubMed: inner ear anomalies

Middle Ear

Middle ear abnormalities (ossicular anomalies) are rare and can be part of first arch syndrome.

Middle ear abnormalities include:

  • familial expansile osteolysis
  • malleus/incus fixation
  • absence of the long process of the incus
  • congenital fixation of stapes (stapes anchored to oval window)
  • failure of annular ligament development
  • cholesteatoma

Familial Expansile Osteolysis (FEO)

A rare congenital (autosomal dominant, 18q21.1-q22) disorder similar to Paget’s disease of bone. Osteolytic lesions occur in all bones (mainly long bones) causing medullar expansions and lead eventually to middle ear and jaw abnormalities.

Malleus/Incus Fixation

Congenital Fixation of Stapes

In this condition the stapes is anchored to oval window often by growth of bone around teh stapes (otosclerosis). Surgicallly treated by stapedectomy, where the bone and stapes is removed and replaced by a prosthesis.

Cholesteatoma

Squamous epithelium that has been trapped within the skull base during development (congenital) and also occurs in an acquired form. The presence of this abnormality leads to erosion of the bones (temporal bone, middle ear, or mastoid) in which the epithelium is embedded.

References

Daneshi A, Shafeghati Y, Karimi-Nejad MH, Khosravi A, Farhang F. Hereditary bilateral conductive hearing loss caused by total loss of ossicles: a report of familial expansile osteolysis. Otol Neurotol. 2005 Mar;26(2):237-40.

Seidman MD, Babu S. A new approach for malleus/incus fixation: no prosthesis necessary. Otol Neurotol. 2004 Sep;25(5):669-73.

Wehrs RE. Congenital absence of the long process of the incus. Laryngoscope. 1999 Feb;109(2 Pt 1):192-7.

Search PubMed: Middle ear ossicular anomalies | familial expansile osteolysis | cholesteatoma |


Congenital Deafness

The two main forms of congenital deafness are:

Conductive - disease of outer and middle ear

Sensorineural - cochlear or central auditory pathway

Outer ear Malformation

rare meatal atresia, canal narrow or not formed, part of first arch syndrome

Congenital malformations Statistics

Congenital sensorineural hereditary or acquired (see [#References recent reviews])

Hereditary

  • recessive- severe
  • dominant- mild
  • can be associated with abnormal pigmentation
  • hair and irises

Acquired

  • rubella (German measles)
  • maternal infection during 2nd month of pregnancy
  • vaccination of young girls
  • streptomycin
  • antibiotic
  • thalidomide

Conductive Hearing Loss

  • produced by otitis media with effusion, is widespread in young children.
  • temporary blockage of outer or middle ear
  • See also: [#Conductive recent Ref] | [senseslink.htm#Hearing%20Links Senses WWW Link]

Conductive Hearing Loss

Moore DR, Hine JE, Jiang ZD, Matsuda H, Parsons CH, King AJ. Conductive hearing loss produces a reversible binaural hearing impairment. J Neurosci. 1999 Oct 1;19(19):8704-11. (J Neuroscience Link)

The authors of the above paper tested ferrets by long-term plugging of ear canal and found:

  1. Repeated testing during the 22 months after unplugging revealed a gradual return to normal levels of unmasking.
  2. Results show that a unilateral conductive hearing loss, in either infancy or adulthood, impairs binaural hearing both during and after the hearing loss.
  3. Show scant evidence for adaptation to the plug and demonstrate a recovery from the impairment that occurs over a period of several months after restoration of normal peripheral function.

Neonatal Hearing Screening

State Wide Infant Screening Hearing Program (SWISH) A newborn hearing testing program using an automated auditory response technology. Program was introduced in NSW Australia in 2002 across 17 area health service coordinators.

Automated Auditory Brainstem Response (AABR) - uses a stimulus which is delivered through earphones and detected by scalp electrodes. The test takes between 8 to 20 minutes and has a sensitivity 96-99%.

Puig T, Municio A, Meda C. Universal neonatal hearing screening versus selective screening as part of the management of childhood deafness. Cochrane Database Syst Rev. 2005 Apr 18;(2):CD003731.

(More? [../Child/neonatalscreening.htm#Hearing Child Notes - Neonatal Hearing Screening | ][../Child/neonatalscreening.htm Child Notes - Neonatal Screening])

Links: NSW Statewide Infant Screening - Hearing Program What is SWISH? | American Speech-Language-Hearing Association - Audiological Assessment of Children Birth to 5 Years of Age: 2004 (PDF Format)

Otitis Media

Otitis media (ear infection or "glue ear") is not an abnormality, but a very common developmental problem associated with fluid in the middle ear and can ooccur with or without accompanied signs and symptoms of ear infection. Prolonged or repeated occurance can lead to developmental delay in learning, speech and even damage to the middle ear structures.

Otitis media woth effusion (OME) is defined as middle ear effusion without signs or symptoms of an acute infection.

A recent [#CochraneOME Cochrane study] has shown that between the ages of one and three years it has a prevalence of 10% to 30% and a cumulative incidence of 80% at the age of four years.

Lous J, Burton MJ, Felding JU, Ovesen T, Rovers MM, Williamson I. Grommets (ventilation tubes) for hearing loss associated with otitis media with effusion in children. Cochrane Database Syst Rev. 2005 Jan 25;(1):CD001801.

Links: NIH National Institute on Deafness and Other Communication Disorders - Otitis Media | American Academy of Family Physicians - Otitis Media | Medline Plus - Otitis Media |

Cochlear Implant

Moller AR. Physiological basis for cochlear and auditory brainstem implants. Adv Otorhinolaryngol. 2006;64:206-23.

Kral A, Tillein J. Brain plasticity under cochlear implant stimulation. Adv Otorhinolaryngol. 2006;64:89-108.

Geers AE. Factors influencing spoken language outcomes in children following early cochlear implantation. Adv Otorhinolaryngol. 2006;64:50-65.

Das S, Buchman CA. Bilateral cochlear implantation: current concepts. Curr Opin Otolaryngol Head Neck Surg. 2005 Oct;13(5):290-3.

Search PubMed: Cochlear Implant

Human Genes

There are chromosomal abnormalities, such as trisomy 21 (Down Syndrome) that are commonly associated with hearing disorders associated with outer, middle and inner ear defects.

The following table lists only a few of the growing number of known genes associated with hearing loss.


Symbol Description Position
DFN1 deafness, X-linked 1, progressive Xq22
DFN2 deafness, X-linked 2, perceptive, congenital Xq22
DFN4 deafness, X-linked 4, congenital sensorineural Xp21.2
DFNB9 deafness, autosomal recessive 9 2p23-p22
DIAPH1 diaphanous (Drosophila, homolog) 1 5q31
GJB2 gap junction protein, beta 2, 26kD (connexin 26) 13q11-q12
MYO7A myosin VIIA (Usher syndrome 1B (autosomal recessive, severe)) 11q13.5
POU4F3 POU domain, class 4, transcription factor 3 5q31

 

References

Recent Reviews Abnormal Development

  • Zim SA. Microtia reconstruction: an update. Curr Opin Otolaryngol Head Neck Surg. 2003 Aug;11(4):275-81.
  •  Webster WS. [See Related Articles ] Teratogen update: congenital rubella. Teratology. 1998 Jul;58(1):13-23. Review.
  • Yates JA, et al. [See Related Articles] Isolated congenital internal auditory canal atresia with normal facial nerve function. Int J Pediatr Otorhinolaryngol. 1997 Jul 18;41(1):1-8. Review.
  • Lambert PR, et al. [See Related Articles] Congenital malformations of the external auditory canal. Otolaryngol Clin North Am. 1996 Oct;29(5):741-60. Review. PMID: 8893214; UI: 97048378.
  • Lin AE, et al.  [See Related Articles] Further delineation of the branchio-oculo-facial syndrome. Am J Med Genet. 1995 Mar 13;56(1):42-59. Review. MID: 7747785; UI: 95266633.
  • Strasnick B, et al  [See Related Articles] Teratogenic hearing loss. J Am Acad Audiol. 1995 Jan;6(1):28-38. Review. PMID: 7696676; UI: 95210704.
  • Kossowska E, et al. [See Related Articles] Prenatal and neonatal prophylaxis in otorhinolaryngology. Int J Pediatr Otorhinolaryngol. 1980 Jun;2(2):85-98. Review. PMID: 6765128; UI: 84160924.
  • Gottlieb G. [See Related Articles] Conceptions of prenatal development: behavioral embryology. Psychol Rev. 1976 May;83(3):215-34. Review. No abstract available.PMID: 188059; UI: 77079452.
  • Holme RH, Steel KP Genes involved in deafness. Curr Opin Genet Dev 1999 Jun;9(3):309-314
    • "Remarkable progress has been made over the past few years in the field of hereditary deafness. To date, mutations in at least 35 genes are known to cause hearing loss. We are now beginning to understand the function of many of these genes, which affect diverse aspects of ear development and function."

Articles

Rowe TM, Rizzi M, Hirose K, Peters GA, Sen GC. A role of the double-stranded RNA-binding protein PACT in mouse ear development and hearing. Proc Natl Acad Sci U S A. 2006 Mar 29; [Epub ahead of print]

List of references from a 1999 search [../Refer/senses/ear_rev.htm Ear Development Reviews] | [../Refer/senses/select.htm Selected Research Articles and Reviews]

WWW Links

Australian Newborn hearing screening program (about 1 in 500 babies are born with a hearing loss Factsheet)

Western Australian pamphlet PDF: Your Newborn Baby Hearing Test

Medline Plus Ear Disorders

New Zealand National Screening Unit - Newborn Hearing Screening

First 100 cochlear implant search Aug 2010

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2: Kaplan DM, Puterman M. Pediatric cochlear implants in prelingual deafness: medium and long-term outcomes. Isr Med Assoc J. 2010 Feb;12(2):107-9. PubMed PMID: 20550036.


3: Migirov L, Borisovsky G, Carmel E, Wolf M, Kronenberg J. Integration of cochlear-implanted children into the general Israeli community. Isr Med Assoc J. 2010 Feb;12(2):97-9. PubMed PMID: 20550033.


4: Social Security Administration. Revised medical criteria for evaluating hearing loss. Final rules. Fed Regist. 2010 Jun 2;75(105):30693-704. PubMed PMID: 20518150.


5: Tan JH, Yeh BI, Seet CS. Deafness due to haemorrhagic labyrinthitis and a review of relapses in Streptococcus suis meningitis. Singapore Med J. 2010 Feb;51(2):e30-3. Review. PubMed PMID: 20358139.


6: Aronoff JM, Yoon YS, Freed DJ, Vermiglio AJ, Pal I, Soli SD. The use of interaural time and level difference cues by bilateral cochlear implant users. J Acoust Soc Am. 2010 Mar;127(3):EL87-92. PubMed PMID: 20329812; PubMed Central PMCID: PMC2833183.


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220: Middlebrooks JC. Auditory cortex phase locking to amplitude-modulated cochlear implant pulse trains. J Neurophysiol. 2008 Jul;100(1):76-91. Epub 2008 Mar 26. PubMed PMID: 18367697; PubMed Central PMCID: PMC2493473.


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234: Lee KH, Warchol ME. Promotion of neurite outgrowth and axon guidance in spiral ganglion cells by netrin-1. Arch Otolaryngol Head Neck Surg. 2008 Feb;134(2):146-51. PubMed PMID: 18283156.


235: Figueras B, Edwards L, Langdon D. Executive function and language in deaf children. J Deaf Stud Deaf Educ. 2008 Summer;13(3):362-77. Epub 2008 Feb 4. PubMed PMID: 18252699.


236: Xu L, Pfingst BE. Spectral and temporal cues for speech recognition: implications for auditory prostheses. Hear Res. 2008 Aug;242(1-2):132-40. Epub 2007 Dec 28. PubMed PMID: 18249077; PubMed Central PMCID: PMC2610393.


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309: Ho T, Vrabec JT, Burton AW. Hydrocodone use and sensorineural hearing loss. Pain Physician. 2007 May;10(3):467-72. PubMed PMID: 17525781.


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335: Middlebrooks JC, Snyder RL. Auditory prosthesis with a penetrating nerve array. J Assoc Res Otolaryngol. 2007 Jun;8(2):258-79. Epub 2007 Jan 30. PubMed PMID: 17265124; PubMed Central PMCID: PMC2538356.


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