Nonsyndromic deafness

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Nonsyndromic deafness

Other names| Non-syndromic genetic deafness

Nonsyndromic deafness is hearing loss that is not associated with other signs and symptoms. In contrast, syndromic deafness involves hearing loss that occurs with abnormalities in other parts of the body. Nonsyndromic deafness constitutes 75% of all hearing loss cases, and an estimated 100 genes are thought to be linked to this condition. About 80% are linked to autosomal recessive inheritance, 15% to autosomal dominant inheritance, 1-3% through the X chromosome, and 0.5-1% are associated with mitochondrial inheritance.[1][2]

Genetic changes are related to the following types of nonsyndromic deafness:

* DFNA: nonsyndromic deafness, autosomal dominant
* DFNB: nonsyndromic deafness, autosomal recessive
* DFNX: nonsyndromic deafness, X-linked
* nonsyndromic deafness, mitochondrial

Each type is numbered in the order in which it was described. For example, DFNA1 was the first described autosomal dominant type of nonsyndromic deafness. Mitochondrial nonsyndromic deafness involves changes to the small amount of DNA found in mitochondria, the energy-producing centers within cells.[3]

Most forms of nonsyndromic deafness are associated with permanent hearing loss caused by damage to structures in the inner ear. The inner ear consists of three parts: a snail-shaped structure called the cochlea that helps process sound, nerves that send information from the cochlea to the brain, and structures involved with balance. Loss of hearing caused by changes in the inner ear is called sensorineural deafness. Hearing loss that results from changes in the middle ear is called conductive hearing loss. The middle ear contains three tiny bones that help transfer sound from the eardrum to the inner ear. Some forms of nonsyndromic deafness involve changes in both the inner ear and the middle ear; this combination is called mixed hearing loss.

The severity of hearing loss varies and can change over time. It can affect one ear (unilateral) or both ears (bilateral). Degrees of hearing loss range from mild (difficulty understanding soft speech) to profound (inability to hear even very loud noises). The loss may be stable, or it may progress as a person gets older. Particular types of nonsyndromic deafness often show distinctive patterns of hearing loss. For example, the loss may be more pronounced at high, middle, or low tones.

## Contents

* 1 Classification
* 2 Genetics
* 2.1 Genes related to nonsyndromic deafness
* 3 Diagnosis
* 4 Treatment
* 5 Epidemiology
* 6 See also
* 7 References
* 8 Further reading
* 9 External links

## Classification

Nonsyndromic deafness can occur at any age. Hearing loss that is present before a child learns to speak is classified as prelingual or congenital. Hearing loss that occurs after the development of speech is classified as postlingual.

## Genetics

Nonsyndromic deafness can have different patterns of inheritance. Between 75% and 80% of cases are inherited in an autosomal recessive pattern, which means two copies of the gene in each cell are altered. Usually, each parent of an individual with autosomal recessive deafness is a carrier of one copy of the altered gene. These carriers do not have hearing loss.

Another 20% to 25% of nonsyndromic deafness cases are autosomal dominant, which means one copy of the altered gene in each cell is sufficient to result in hearing loss. People with autosomal dominant deafness most often inherit an altered copy of the gene from a parent who has hearing loss.

Between 1% and 2% of cases show an X-linked pattern of inheritance, which means the mutated gene responsible for the condition is located on the X chromosome. Males with X-linked nonsyndromic deafness tend to develop more severe hearing loss earlier in life than females who inherit a copy of the same gene mutation. Fathers will not pass X-linked traits to their sons since they do not pass on the X chromosome to their male offspring.

Mitochondrial nonsyndromic deafness, which results from changes to the DNA in mitochondria, occurs in fewer than 1% of cases in the United States. The altered mitochondrial DNA is passed from a mother to her sons and daughters. This type of deafness is not inherited from fathers.

Late-onset progressive deafness is the most common neurological disability of the elderly. Although hearing loss of greater than 25 decibels is present in only 1% of young adults between ages 18 and 24, this increases to 10% in persons between 55 and 64 years of age and approximately 50% in octogenarians.

The relative contribution of heredity to age-related hearing impairment is not known, however, the majority of inherited late-onset deafness is autosomal dominant and non-syndromic (Van Camp et al., 1997). Over forty genes associated with autosomal dominant non-syndromic hearing loss have been localized and of these fifteen have been cloned.

### Genes related to nonsyndromic deafness

Mutations in the ACTG1, CABP2, CDH23, CLDN14, COCH, COL11A2, DFNA5, ESPN, EYA4, GJB2, GJB6, KCNQ4, MYO15A, MYO6, MYO7A, OTOF, PCDH15, POU3F4, SLC26A4, STRC, TECTA, TMC1, TMIE, TMPRSS3, USH1C, and WFS1 genes cause nonsyndromic deafness, with weaker evidence currently implicating genes CCDC50, DIAPH1, DSPP, ESRRB, GJB3, GRHL2, GRXCR1, HGF, LHFPL5, LOXHD1, LRTOMT, MARVELD2, MIR96, MYH14, MYH9, MYO1A, MYO3A, OTOA, PJVK, POU4F3, PRPS1, PTPRQ, RDX, SERPINB6, SIX1, SLC17A8, TPRN, TRIOBP, SLC26A5, and WHRN.

The causes of nonsyndromic deafness can be complex. Researchers have identified more than 30 genes that, when mutated, may cause nonsyndromic deafness; however, some of these genes have not been fully characterized. Many genes related to deafness are involved in the development and function of the inner ear. Gene mutations interfere with critical steps in processing sound, resulting in hearing loss. Different mutations in the same gene can cause different types of hearing loss, and some genes are associated with both syndromic and nonsyndromic deafness. In many families, the gene(s) involved have yet to be identified.

Deafness can also result from environmental factors or a combination of genetic and environmental factors, including certain medications, peri-natal infections (infections occurring before or after birth), and exposure to loud noise over an extended period.

Types include:

OMIM  | Gene  | Type

|
|

Online Mendelian Inheritance in Man (OMIM) 124900 | DIAPH1  | DFNA1
Online Mendelian Inheritance in Man (OMIM) 600101 | KCNQ4 | DFNA2A
Online Mendelian Inheritance in Man (OMIM) 612644 | GJB3  | DFNA2B
Online Mendelian Inheritance in Man (OMIM) 601544 | GJB2 | DFNA3A
Online Mendelian Inheritance in Man (OMIM) 612643 | GJB6  | DFNA3B
Online Mendelian Inheritance in Man (OMIM) 600652 | MYH14 | DFNA4
Online Mendelian Inheritance in Man (OMIM) 600994 | DFNA5  | DFNA5
Online Mendelian Inheritance in Man (OMIM) 601543 | TECTA  | DFNA8/12
Online Mendelian Inheritance in Man (OMIM) 601369 | COCH  | DFNA9
Online Mendelian Inheritance in Man (OMIM) 601316 | EYA4 | DFNA10
Online Mendelian Inheritance in Man (OMIM) 601317 | MYO7A | DFNA11, neurosensory
Online Mendelian Inheritance in Man (OMIM) 601868 | COL11A2  | DFNA13
Online Mendelian Inheritance in Man (OMIM) 602459 | POU4F3 | DFNA15
Online Mendelian Inheritance in Man (OMIM) 603622 | MYH9  | DFNA17
Online Mendelian Inheritance in Man (OMIM) 604717 | ACTG1 | DFNA20/26
Online Mendelian Inheritance in Man (OMIM) 606346 | MYO6 | DFNA22
Online Mendelian Inheritance in Man (OMIM) 605192 | SIX1 | DFNA23
Online Mendelian Inheritance in Man (OMIM) 605583 | SLC17A8  | DFNA25
Online Mendelian Inheritance in Man (OMIM) 608641 | GRHL2  | DFNA28
Online Mendelian Inheritance in Man (OMIM) 606705 | TMC1 | DFNA36
Online Mendelian Inheritance in Man (OMIM) 605594 | DSPP  | DFNA36, with dentinogenesis
Online Mendelian Inheritance in Man (OMIM) 607453 | CCDC50  | DFNA44
Online Mendelian Inheritance in Man (OMIM) 607841 | MYO1A  | DFNA48
Online Mendelian Inheritance in Man (OMIM) 613074 | MIR96  | DFNA50
Online Mendelian Inheritance in Man (OMIM) 220290 | GJB2 | DFNB1A
Online Mendelian Inheritance in Man (OMIM) 612645 | GJB6  | DFNB1B
Online Mendelian Inheritance in Man (OMIM) 600060 | MYO7A | DFNB2, neurosensory (see also Usher syndrome)
Online Mendelian Inheritance in Man (OMIM) 600316 | MYO15A  | DFNB3
Online Mendelian Inheritance in Man (OMIM) 600971 | TMIE  | DFNB6
Online Mendelian Inheritance in Man (OMIM) 600974 | TMC1 | DFNB7
Online Mendelian Inheritance in Man (OMIM) 601072 | TMPRSS3 | DFNB8, childhood onset
Online Mendelian Inheritance in Man (OMIM) 601071 | OTOF  | DFNB9
Online Mendelian Inheritance in Man (OMIM) 601386 | CDH23  | DFNB12
Online Mendelian Inheritance in Man (OMIM) 603720 | STRC | DFNB16
Online Mendelian Inheritance in Man (OMIM) 602092 | USH1C  | DFNB18
Online Mendelian Inheritance in Man (OMIM) 603629 | TECTA  | DFNB21
Online Mendelian Inheritance in Man (OMIM) 607039 | OTOA  | DFNB22
Online Mendelian Inheritance in Man (OMIM) 609533 | PCDH15  | DFNB23
Online Mendelian Inheritance in Man (OMIM) 611022 | RDX  | DFNB24
Online Mendelian Inheritance in Man (OMIM) 613285 | GRXCR1 | DFNB25
Online Mendelian Inheritance in Man (OMIM) 609823 | TRIOBP | DFNB28
Online Mendelian Inheritance in Man (OMIM) 614035 | CLDN14 | DFNB29
Online Mendelian Inheritance in Man (OMIM) 607101 | MYO3A  | DFNB30
Online Mendelian Inheritance in Man (OMIM) 607084 | WHRN  | DFNB31
Online Mendelian Inheritance in Man (OMIM) 608565 | ESRRB  | DFNB35
Online Mendelian Inheritance in Man (OMIM) 609006 | ESPN  | DFNB36
Online Mendelian Inheritance in Man (OMIM) 607821 | MYO6 | DFNB37
Online Mendelian Inheritance in Man (OMIM) 608265 | HGF | DFNB39
Online Mendelian Inheritance in Man (OMIM) 610153 | MARVELD2 | DFNB49
Online Mendelian Inheritance in Man (OMIM) 609706 | COL11A2  | DFNB53
Online Mendelian Inheritance in Man (OMIM) 610220 | PJVK  | DFNB59
Online Mendelian Inheritance in Man (OMIM) 611451 | LRTOMT  | DFNB63
Online Mendelian Inheritance in Man (OMIM) 610265 | LHFPL5  | DFNB67
Online Mendelian Inheritance in Man (OMIM) 613079 | LOXHD1 | DFNB77
Online Mendelian Inheritance in Man (OMIM) 613307 | TPRN  | DFNB79
Online Mendelian Inheritance in Man (OMIM) 613391 | PTPRQ  | DFNB84
Online Mendelian Inheritance in Man (OMIM) 613453 | SERPINB6 | DFNB91
Online Mendelian Inheritance in Man (OMIM) 614899 | CABP2  | DFNB93
Online Mendelian Inheritance in Man (OMIM) 304500 | PRPS1  | DFNX1
Online Mendelian Inheritance in Man (OMIM) 304400 | POU3F4 | DFNX2
Online Mendelian Inheritance in Man (OMIM) 580000 | MT-RNR1, COX1[4] | deafness, aminoglycoside-induced
Online Mendelian Inheritance in Man (OMIM) 500008 | (several mtDNA)  | DFN, sensorineural, mt

## Diagnosis

The diagnosis of nonsyndromic deafness involves a comprehensive assessment to determine the cause of hearing loss in an individual without associated syndromic features. Key steps in the diagnosis may include:

* Clinical evaluation: A detailed medical history will be obtained to identify factors that may contribute to hearing loss, such as exposure to loud noise, ototoxic medications, or a family history of hearing impairment. Additionally, a physical examination will be conducted to check for visible abnormalities or signs of underlying conditions.[5][6]
* Genetic testing: Genetic testing may be recommended, especially if there is a family history of hearing loss. Nonsyndromic deafness can be caused by mutations in various genes associated with auditory function. Besides, high-throughput DNA sequencing methods can be employed to screen multiple genes simultaneously.[7]
* Audiological testing: This may include different tests such as Pure-tone audiometry, Speech audiometry, Otoacoustic emissions, or Auditory brainstem response.[8]

In some cases, other methods may be conducted, including imaging techniques such as CT or MRI, to examine the structures of the inner ear and identify any abnormalities in the cochlea or auditory nerve. Screening blood tests for metabolic conditions or infections that could contribute to hearing loss may also be recommended.[9][10]

## Treatment

Treatment is supportive and consists of management of- manifestations. Use of hearing aids and/or cochlear implants, suitable educational programs can be offered. Periodic surveillance is also important.[11]

## Epidemiology

About 1 in 1,000 children in the United States is born with profound deafness. By age 9, about 3 in 1,000 children have hearing loss that affects the activities of daily living. More than half of these cases are caused by genetic factors. Most cases of genetic deafness (70% to 80%) are nonsyndromic; the remaining cases are caused by specific genetic syndromes. In adults, the chance of developing hearing loss increases with age; hearing loss affects half of all people older than 80 years.

## See also

* Y-linked deafness, type 1

## References

1. ↑ Guilford, Parry; Arab, Saida Ben; Blanchard, Stéphane; Levilliers, Jacqueline; Weissenbach, Jean; Belkahia, Ali; Petit, Christine (1994). "A non–syndromic form of neurosensory, recessive deafness maps to the pericentromeric region of chromosome 13q". Nature Genetics 6 (1): 24–28. doi:10.1038/ng0194-24. ISSN 1061-4036. PMID 8136828. http://dx.doi.org/10.1038/ng0194-24.
2. ↑ Kalatzis, V (1998-09-01). "The fundamental and medical impacts of recent progress in research on hereditary hearing loss". Human Molecular Genetics 7 (10): 1589–1597. doi:10.1093/hmg/7.10.1589. ISSN 1460-2083. PMID 9735380.
3. ↑ Reference, Genetics Home. "nonsyndromic hearing loss" (in en). https://medlineplus.gov/genetics/condition/nonsyndromic-hearing-loss/.
4. ↑ Usami, S; Nishio, S; Adam, MP; Ardinger, HH; Pagon, RA; Wallace, SE; Bean, LJH; Stephens, K et al. (1993). "Nonsyndromic Hearing Loss and Deafness, Mitochondrial". University of Washington, Seattle. https://www.ncbi.nlm.nih.gov/books/NBK1422/.
5. ↑ Vona, Barbara; Doll, Julia; Hofrichter, Michaela A. H.; Haaf, Thomas (2020-08-01). "Non-syndromic hearing loss: clinical and diagnostic challenges". Medizinische Genetik 32 (2): 117–129. doi:10.1515/medgen-2020-2022. ISSN 1863-5490.
6. ↑ Funamura, Jamie L. (2017). "Evaluation and management of nonsyndromic congenital hearing loss". Current Opinion in Otolaryngology & Head and Neck Surgery 25 (5): 385–389. doi:10.1097/moo.0000000000000398. ISSN 1068-9508. PMID 28682819. http://dx.doi.org/10.1097/moo.0000000000000398.
7. ↑ Sloan-Heggen, Christina M.; Bierer, Amanda O.; Shearer, A. Eliot; Kolbe, Diana L.; Nishimura, Carla J.; Frees, Kathy L.; Ephraim, Sean S.; Shibata, Seiji B. et al. (2016-03-11). "Comprehensive genetic testing in the clinical evaluation of 1119 patients with hearing loss". Human Genetics 135 (4): 441–450. doi:10.1007/s00439-016-1648-8. ISSN 0340-6717. PMID 26969326.
8. ↑ Vona, Barbara; Doll, Julia; Hofrichter, Michaela A. H.; Haaf, Thomas (2020-08-01). "Non-syndromic hearing loss: clinical and diagnostic challenges". Medizinische Genetik 32 (2): 117–129. doi:10.1515/medgen-2020-2022. ISSN 1863-5490.
9. ↑ Sommen, Manou; van Camp, Guy; Boudewyns, An (2013). "Genetic and clinical diagnosis in non-syndromic hearing loss". Hearing, Balance and Communication 11 (3): 138–145. doi:10.3109/21695717.2013.812380. ISSN 2169-5717. http://dx.doi.org/10.3109/21695717.2013.812380.
10. ↑ Hone, S.W.; Smith, R.J.H. (2003). "Genetic screening for hearing loss". Clinical Otolaryngology and Allied Sciences 28 (4): 285–290. doi:10.1046/j.1365-2273.2003.00700.x. ISSN 0307-7772. PMID 12871240. http://dx.doi.org/10.1046/j.1365-2273.2003.00700.x.
11. ↑ Smith, Richard JH; Jones, Mary-Kayt N. (1993). "Nonsyndromic Hearing Loss and Deafness, DFNB1". GeneReviews. University of Washington, Seattle. https://www.ncbi.nlm.nih.gov/books/NBK1272/.

## Further reading

* Pandya, Arti (21 April 2011). Nonsyndromic Hearing Loss and Deafness, Mitochondrial. University of Washington, Seattle. NBK1422. https://www.ncbi.nlm.nih.gov/books/NBK1422/. In Adam, M. P.; Mirzaa, G. M.; Pagon, R. A.; Wallace, S. E.; Bean LJH; Gripp, K. W.; Amemiya, A. (1993). GeneReviews. Seattle WA: University of Washington, Seattle. https://www.ncbi.nlm.nih.gov/books/NBK1116/.
* Smith, Richard JH; Sheffield, Abraham M; Camp, Guy Van (19 April 2012). "Nonsyndromic Hearing Loss and Deafness, DFNA3 – RETIRED CHAPTER, FOR HISTORICAL REFERENCE ONLY". Nonsyndromic Hearing Loss and Deafness, DFNA3. University of Washington, Seattle. NBK1536. https://www.ncbi.nlm.nih.gov/books/NBK1536/. In GeneReviews
* Smith, Richard JH; Camp, Guy Van (2 January 2014). "GJB2-Related Autosomal Recessive Nonsyndromic Hearing Loss". Nonsyndromic Hearing Loss and Deafness, DFNB1. University of Washington, Seattle. NBK1272. https://www.ncbi.nlm.nih.gov/books/NBK1272/. In GeneReviews
* Huijun Yuan; Xue Z Liu (4 August 2011). "DFNX1 Nonsyndromic Hearing Loss and Deafness – RETIRED CHAPTER, FOR HISTORICAL REFERENCE ONLY". DFNX1 Nonsyndromic Hearing Loss and Deafness. University of Washington, Seattle. NBK57098. https://www.ncbi.nlm.nih.gov/books/NBK57098/. In GeneReviews
* Smith, Richard JH; Gurrola, II, Jose G; Kelley, Philip M (14 June 2011). "OTOF-Related Deafness". OTOF-Related Deafness. University of Washington, Seattle. NBK1251. https://www.ncbi.nlm.nih.gov/books/NBK1251/. In GeneReviews

## External links

Classification|

* ICD-10: H90.5

|

External resources|

* Orphanet: 87884

Template:Hearing and balance Template:Cytoskeletal defects

* v
* t
* e

Genetic disorders relating to deficiencies of transcription factor or coregulators

(1) Basic domains|

| 1.2|

* Feingold syndrome
* Saethre–Chotzen syndrome

|

1.3|

* Tietz syndrome

(2) Zinc finger
DNA-binding domains|

| 2.1|

* (Intracellular receptor): Thyroid hormone resistance
* Androgen insensitivity syndrome
* PAIS
* MAIS
* CAIS
* Kennedy's disease
* PHA1AD pseudohypoaldosteronism
* Estrogen insensitivity syndrome
* X-linked adrenal hypoplasia congenita
* MODY 1
* Familial partial lipodystrophy 3
* SF1 XY gonadal dysgenesis

|

2.2|

* Barakat syndrome
* Tricho–rhino–phalangeal syndrome

2.3|

* Greig cephalopolysyndactyly syndrome/Pallister–Hall syndrome
* Denys–Drash syndrome
* Duane-radial ray syndrome
* MODY 7
* MRX 89
* Townes–Brocks syndrome
* Acrocallosal syndrome
* Myotonic dystrophy 2

2.5|

* Autoimmune polyendocrine syndrome type 1

(3) Helix-turn-helix domains|

| 3.1|

* ARX
* Ohtahara syndrome
* Lissencephaly X2
* MNX1
* Currarino syndrome
* HOXD13
* SPD1 synpolydactyly
* PDX1
* MODY 4
* LMX1B
* Nail–patella syndrome
* MSX1
* Tooth and nail syndrome
* OFC5
* PITX2
* Axenfeld syndrome 1
* POU4F3
* DFNA15
* POU3F4
* DFNX2
* ZEB1
* Posterior polymorphous corneal dystrophy
* Fuchs' dystrophy 3
* ZEB2
* Mowat–Wilson syndrome

|

3.2|

* PAX2
* Papillorenal syndrome
* PAX3
* Waardenburg syndrome 1&3
* PAX4
* MODY 9
* PAX6
* Gillespie syndrome
* Coloboma of optic nerve
* PAX8
* Congenital hypothyroidism 2
* PAX9
* STHAG3

3.3|

* FOXC1
* Axenfeld syndrome 3
* Iridogoniodysgenesis, dominant type
* FOXC2
* Lymphedema–distichiasis syndrome
* FOXE1
* Bamforth–Lazarus syndrome
* FOXE3
* Anterior segment mesenchymal dysgenesis
* FOXF1
* ACD/MPV
* FOXI1
* Enlarged vestibular aqueduct
* FOXL2
* Premature ovarian failure 3
* FOXP3
* IPEX

3.5|

* IRF6
* Van der Woude syndrome
* Popliteal pterygium syndrome

(4) β-Scaffold factors
with minor groove contacts|

| 4.2|

* Hyperimmunoglobulin E syndrome

|

4.3|

* Holt–Oram syndrome
* Li–Fraumeni syndrome
* Ulnar–mammary syndrome

4.7|

* Campomelic dysplasia
* MODY 3
* MODY 5
* SF1
* SRY XY gonadal dysgenesis
* Premature ovarian failure 7
* SOX10
* Waardenburg syndrome 4c
* Yemenite deaf-blind hypopigmentation syndrome

4.11|

* Cleidocranial dysostosis

(0) Other transcription factors|

| 0.6|

* Kabuki syndrome

|

Ungrouped|

* TCF4
* Pitt–Hopkins syndrome
* ZFP57
* TNDM1
* TP63
* Rapp–Hodgkin syndrome/Hay–Wells syndrome/Ectrodactyly–ectodermal dysplasia–cleft syndrome 3/Limb–mammary syndrome/OFC8

Transcription coregulators|

| Coactivator:|

* CREBBP
* Rubinstein–Taybi syndrome

|

Corepressor:|

* HR (Atrichia with papular lesions)

Template:Scleroprotein disease

* v
* t
* e

Genetic disorder, membrane: Solute carrier disorders

1-10|

* SLC1A3
* Episodic ataxia 6
* SLC2A1
* De Vivo disease
* SLC2A5
* Fructose malabsorption
* SLC2A10
* Arterial tortuosity syndrome
* SLC3A1
* Cystinuria
* SLC4A1
* Hereditary spherocytosis 4/Hereditary elliptocytosis 4
* SLC4A11
* Congenital endothelial dystrophy type 2
* Fuchs' dystrophy 4
* SLC5A1
* Glucose-galactose malabsorption
* SLC5A2
* Renal glycosuria
* SLC5A5
* Thyroid dyshormonogenesis type 1
* SLC6A19
* Hartnup disease
* SLC7A7
* Lysinuric protein intolerance
* SLC7A9
* Cystinuria

11-20|

* SLC11A1
* Crohn's disease
* SLC12A3
* Gitelman syndrome
* SLC16A1
* HHF7
* SLC16A2
* Allan–Herndon–Dudley syndrome
* SLC17A5
* Salla disease
* SLC17A8
* DFNA25

21-40|

* SLC26A2
* Multiple epiphyseal dysplasia 4
* Achondrogenesis type 1B
* Recessive multiple epiphyseal dysplasia
* Atelosteogenesis, type II
* Diastrophic dysplasia
* SLC26A4
* Pendred syndrome
* SLC35C1
* CDOG 2C
* SLC39A4
* Acrodermatitis enteropathica
* SLC40A1
* African iron overload

see also solute carrier family

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