Autosomal recessive nonsyndromic deafness 37 is a genetic cause of hearing loss without other health problems. People with Autosomal recessive nonsyndromic deafness 37 typically have sensorineural hearing loss that can be present at birth or start in early childhood. Hearing changes are usually lifelong, and severity can range from mild to profound. Many living with Autosomal recessive nonsyndromic deafness 37 use hearing aids, cochlear implants, and speech and language support. The condition itself is not life-threatening, and genetic counseling can help families understand inheritance and testing options.
Overview
Autosomal recessive nonsyndromic deafness 37Symptoms
Autosomal recessive nonsyndromic deafness 37 causes bilateral sensorineural hearing loss present from birth or early childhood, ranging from mild to profound, without other medical features. Families may notice poor response to sounds and delayed speech or language.
Outlook and prognosis
Most people with autosomal recessive nonsyndromic deafness 37 have stable, lifelong hearing loss that mainly affects communication rather than overall health. Early testing, hearing technology, and language support help children develop speech and learning. Adults often do well with tailored hearing aids or implants and ongoing audiology care.
Causes and risk factors
Autosomal recessive nonsyndromic deafness 37 results from mutations inherited from two carrier parents. Risk rises with family history or parental relatedness. Environmental factors like loud noise or certain medicines don’t cause it but may worsen hearing loss.
Genetic influences
Genetics are central to Autosomal recessive nonsyndromic deafness 37. It results from inheriting two nonworking copies of the same gene, typically from carrier parents. Variations in that gene affect inner-ear hair cell function, shaping age of onset, severity, and progression.
Diagnosis
Doctors suspect Autosomal recessive nonsyndromic deafness 37 when hearing tests show sensorineural loss without other features. Genetic diagnosis of Autosomal recessive nonsyndromic deafness 37 uses multigene panel testing; exam and imaging help exclude syndromic conditions and structural ear problems.
Treatment and drugs
Autosomal recessive nonsyndromic deafness 37 is managed with timely hearing support tailored to age and hearing level. Options often include digital hearing aids, bone‑anchored devices, or cochlear implants, plus speech-language therapy and family-centered communication strategies. Regular audiology follow-up helps adjust devices and monitor progress.
Symptoms
Autosomal recessive nonsyndromic deafness 37 mainly affects hearing from birth or early infancy, usually in both ears. Loved ones often notice the changes first. Parents may see early features of Autosomal recessive nonsyndromic deafness 37 such as limited responses to sound and slower speech development. This is an inner-ear (sensorineural) hearing loss without other medical findings.
Babies may not startle to sudden noises or turn toward familiar voices. Older children may miss doorbells, phone alerts, or their name being called.
Babbling may be quieter or later than peers, and first words can come later. Speech may sound unclear because hearing soft consonants is harder.
Hearing conversation can be hard, especially in background noise. People may ask for repetition or watch lips to fill in missed sounds.
TV, music, or devices may be set to a higher volume than others prefer. Sitting closer to the speaker or preferring one-on-one chats can feel easier.
How people usually first notice Autosomal recessive nonsyndromic deafness 37?
Families often notice the first signs of Autosomal recessive nonsyndromic deafness 37 when a baby doesn’t startle to loud sounds, doesn’t turn toward voices, or isn’t babbling and responding to name as expected in the first months. Newborn hearing screening—done in most hospitals—may be the earliest clue, showing a failed or “refer” result that leads to repeat testing and an audiology evaluation. For many, this is how ARNSD37 is first noticed: normal appearance and development otherwise, but consistent signs of reduced hearing that become clearer in infancy or early childhood.
Types of Autosomal recessive nonsyndromic deafness 37
Autosomal recessive nonsyndromic deafness 37 (DFNB37) is a genetic, nonsyndromic form of hearing loss, meaning hearing is affected without other body systems being involved. Variants or subtypes are generally defined by the specific gene change (mutation) within the same gene and by whether the loss is present at birth or develops early in life. Not everyone will experience every type. Clinicians often describe them in these categories:
Congenital severe-profound
Hearing loss is present from birth and is usually severe to profound in both ears. Babies may not startle to loud sounds and do not pass newborn hearing screening.
Early-childhood onset
Hearing starts near normal at birth but declines in the first years of life. Families may notice rising TV volume or delayed speech as early symptoms of Autosomal recessive nonsyndromic deafness 37.
Stable moderate
Hearing loss stays relatively steady over time at a mild-to-moderate level. People may hear low-pitched sounds better than high-pitched ones and benefit from hearing aids.
Progressive course
Hearing decreases gradually from mild or moderate to more severe levels across childhood or adolescence. Regular hearing tests guide timely adjustments in hearing aids or consideration of cochlear implants.
Genotype-linked variability
Different pathogenic changes within the same DFNB37 gene can relate to earlier onset or faster progression. Researchers describe these categories to better understand patterns of the condition.
What genetics can tell you about symptoms
People with autosomal recessive nonsyndromic deafness 37 often have congenital, bilateral sensorineural hearing loss because both copies of a hearing gene carry changes that disrupt inner ear hair cell function. Specific variants can cause mild to profound loss and may affect certain sound frequencies.
Causes and risk factors
Autosomal recessive nonsyndromic deafness 37 happens when both copies of the MYO6 gene have damaging changes.
These changes are usually inherited from two carrier parents, and new changes are rare.
Doctors distinguish between risk factors you can change and those you can’t.
Non‑modifiable risk factors for autosomal recessive nonsyndromic deafness 37 include a family history, two carrier parents, and parents who are closely related, such as cousins.
Modifiable factors do not cause it, but loud noise and some antibiotics or chemotherapy drugs can add extra hearing loss over time.
Environmental and biological risk factors
Autosomal recessive nonsyndromic deafness 37 usually starts very early in life and is present from birth. Doctors often group risks into internal (biological) and external (environmental). For this specific condition, environmental risk factors for autosomal recessive nonsyndromic deafness 37 have not been shown to play a clear role in whether it occurs. The points below clarify what is and isn’t linked to it.
Older maternal or paternal age has not been shown to raise the chance of this condition. Most research has not found a consistent link for this specific form.
Infections like cytomegalovirus (CMV) or rubella can cause other types of hearing loss. They have not been tied to autosomal recessive nonsyndromic deafness 37.
Certain medicines in pregnancy, including some antibiotics that can harm the ear, may cause hearing problems. They are not known to cause this specific nonsyndromic form.
Lack of oxygen at birth or a long intensive care stay can be linked with hearing loss in general. These events are not linked to a higher likelihood of autosomal recessive nonsyndromic deafness 37.
Genetic risk factors
Most cases trace back to changes in the MYO6 gene, which helps inner-ear hair cells do their job. Autosomal recessive nonsyndromic deafness 37 usually appears when someone inherits two altered copies—one from each parent. Some risk factors are inherited through our genes. When discussing the genetic causes of Autosomal recessive nonsyndromic deafness 37, MYO6 is the key gene doctors look for.
MYO6 gene changes: Harmful changes in the MYO6 gene disrupt how inner-ear hair cells move and sense sound. In Autosomal recessive nonsyndromic deafness 37, both copies of MYO6 are altered. This is the primary known genetic cause.
Recessive inheritance pattern: A child is affected only when they inherit one changed copy of the gene from each parent. When both parents are carriers, each pregnancy has a 25% chance of Autosomal recessive nonsyndromic deafness 37.
Silent carrier status: Carriers usually hear normally and may not know they carry a MYO6 change. Risk rises if a carrier has children with another carrier. Carrier testing can identify this.
Family history clues: Having a sibling or close relative with confirmed MYO6-related hearing loss suggests a higher chance of carrier status. This can increase the likelihood of the condition in future children.
Parental relatedness: When partners are biologically related (for example, cousins), they are more likely to share the same rare gene change. This raises the chance their child will inherit two MYO6 changes and develop Autosomal recessive nonsyndromic deafness 37.
Founder variants: In some communities, an ancestral MYO6 change is more common, leading to higher carrier rates. Two partners from the same group may face increased risk for an affected child.
Variant type matters: Some MYO6 changes completely block the gene’s work, while others act more like a dimmer switch. This can influence whether hearing loss is present at birth or develops early in childhood.
Dominant vs recessive: Other MYO6 changes can cause a different, dominant form of inherited hearing loss in a family. This differs from Autosomal recessive nonsyndromic deafness 37 and affects how risk shows up across generations.
Genetic testing insight: Sequencing the MYO6 gene or using a multigene hearing-loss panel can confirm the diagnosis and identify carriers. In some cases, genetic testing can give a clearer picture of your personal risk.
Lifestyle risk factors
Autosomal recessive nonsyndromic deafness 37 is a genetic condition; lifestyle habits do not cause it, but they can influence how hearing changes over time and how well symptoms are managed. Focusing on lifestyle risk factors for Autosomal recessive nonsyndromic deafness 37 can help protect any residual hearing and improve day‑to‑day communication. The elements below connect specific habits to real effects on hearing, devices, and quality of life.
Regular exposure to loud music, tools, or venues can accelerate loss of any residual hearing in people with Autosomal recessive nonsyndromic deafness 37. Safe‑listening habits (lower volumes, shorter durations, hearing protection) help preserve hearing and reduce tinnitus.
High volumes directly into the ear canal add mechanical and metabolic stress to the cochlea. Keeping volumes under 60% and taking listening breaks can reduce further damage and listening fatigue.
Tobacco and nicotine reduce inner‑ear blood flow and increase oxidative stress, which may worsen any remaining hearing in this condition. Quitting or avoiding secondhand smoke supports cochlear health and device benefit.
Excess alcohol can impair central auditory processing and balance, complicating communication and mobility for those with deafness 37. Limiting intake may reduce dizziness and improve hearing device performance in daily life.
Risk prevention
Because this is a genetic hearing condition, you can’t fully prevent it, but you can lower risks for future children and protect hearing health across the family. Some prevention is universal, others are tailored to people with specific risks. If you notice early symptoms of autosomal recessive nonsyndromic deafness 37, prompt testing helps families plan support. Work with audiology and genetics teams to choose steps that fit your situation.
A simple blood or saliva test can show if you and your partner carry the gene linked to autosomal recessive nonsyndromic deafness 37. Genetic counseling explains results and next steps.
Options like IVF with embryo testing (PGT-M) or targeted prenatal testing can reduce the chance of having a child with this condition. A genetics specialist can explain benefits, limits, and timing.
Make sure every baby has a hospital or early outpatient hearing screen, and follow up quickly if it’s not passed. Early confirmation of autosomal recessive nonsyndromic deafness 37 allows timely support and education.
When a gene change is found in one child, testing close relatives can identify other carriers. This helps relatives plan pregnancies and watch for early symptoms.
Transmission
Autosomal recessive nonsyndromic deafness 37 is not contagious—it doesn’t spread through contact, coughing, or bodily fluids. It is passed down in an autosomal recessive pattern, which means a child needs two changed copies of the same gene, one from each parent, to have the condition. Parents are usually hearing and carry one changed copy each; when two carriers have a child, there is a 25% (1 in 4) chance the child will have Autosomal recessive nonsyndromic deafness 37, a 50% (1 in 2) chance the child will be a carrier, and a 25% chance the child will inherit neither change. These chances are the same in every pregnancy and for all sexes. New gene changes can occur, but the genetic transmission of Autosomal recessive nonsyndromic deafness 37 most often involves two carrier parents, with risk higher in families where the parents are related.
When to test your genes
Test your genes if hearing loss runs in your family, especially with early-onset or childhood cases, or if a relative has confirmed DFNB37 variants. Consider testing during family planning, pregnancy, or before newborn screening to clarify risks and guide early interventions. If you already have unexplained sensorineural hearing loss, genetic testing can confirm cause and personalize care.
Diagnosis
Autosomal recessive nonsyndromic deafness 37 is typically identified when hearing problems show up early and no other health features stand out. Getting a diagnosis is often a turning point toward answers and support. In practice, the genetic diagnosis of Autosomal recessive nonsyndromic deafness 37 brings together hearing tests, review of family history, and genetic testing to confirm the cause. Doctors aim to confirm sensorineural hearing loss, rule out other explanations, and pinpoint the underlying genetic changes.
Hospitals use quick, painless screenings soon after birth to flag possible hearing loss. A failed screen doesn’t confirm a condition but signals the need for full testing.
Detailed hearing tests measure how soft sounds need to be before they’re heard and how clearly speech is understood. Results help map the type and degree of sensorineural hearing loss.
Tiny sounds made by the inner ear are measured to see if the cochlea is working as expected. If emissions are absent, auditory brainstem response testing often follows to confirm hearing levels.
Electrodes on the skin track how the hearing nerve and brainstem respond to clicks or tones. This helps estimate hearing thresholds in babies and confirms sensorineural hearing loss.
Stages of Autosomal recessive nonsyndromic deafness 37
Autosomal recessive nonsyndromic deafness 37 does not have defined progression stages. This condition usually appears as congenital or early-childhood sensorineural hearing loss that may stay fairly stable or slowly change over time, and hearing is described by degree on audiology tests rather than by stages. Many families first learn of it through newborn hearing screening or when early symptoms of Autosomal recessive nonsyndromic deafness 37—like not startling to loud sounds or delayed babbling—raise questions. Different tests may be suggested to help confirm the diagnosis, including age-appropriate hearing tests (like otoacoustic emissions and auditory brainstem response), with genetic testing sometimes used to identify the underlying cause and guide counseling.
Outlook and prognosis
Many people ask, “What does this mean for my future?”, especially after a diagnosis of Autosomal recessive nonsyndromic deafness 37 (DFNB37). For most people, this condition affects hearing but not overall health or life span. Hearing loss is usually present from birth or early childhood and tends to be stable or slowly progressive rather than rapidly worsening. Early symptoms of Autosomal recessive nonsyndromic deafness 37 often show up as missed responses to soft sounds, delayed speech, or needing the TV louder than peers. Doctors call this the prognosis—a medical word for likely outcomes.
The outlook is not the same for everyone, but most people with DFNB37 do well with timely hearing supports. Hearing aids, remote microphones, communication strategies, and—when appropriate—cochlear implants can open access to language, school, and work. With ongoing care, many people maintain strong communication, healthy social connections, and independent lives. Mortality is not increased by DFNB37 itself, and other organs are typically unaffected.
Looking at the long-term picture can be helpful. Regular hearing checks catch small changes early so technology and strategies can be adjusted. Genetic testing can sometimes provide more insight into prognosis, including whether the hearing loss is likely to remain stable or slowly change over time. Talk with your doctor about what your personal outlook might look like, including options for education supports, speech and language therapy, and workplace accommodations as needs evolve.
Long-term effects
People with this condition primarily experience lifelong hearing challenges that affect communication at home, school, and work. Long-term effects vary widely, ranging from stable hearing levels to gradual changes over the years. Parents may wonder about early symptoms of Autosomal recessive nonsyndromic deafness 37; in practice, it shows up as early, isolated hearing loss without effects on other organs.
Hearing loss is typically sensorineural and affects both ears. In Autosomal recessive nonsyndromic deafness 37, it often begins early in life and persists.
Hearing can remain stable for some or slowly decline for others. Doctors often describe these as long-term effects or chronic outcomes.
If hearing loss is present before speech develops, spoken language may emerge later or differ from peers. Early access to communication makes a long-term difference.
Communication barriers can affect participation in classrooms and meetings, especially in noisy settings. Many living with Autosomal recessive nonsyndromic deafness 37 do well academically with accessible communication.
How is it to live with Autosomal recessive nonsyndromic deafness 37?
Living with autosomal recessive nonsyndromic deafness 37 often means growing up with stable, congenital hearing loss while otherwise feeling healthy, learning, and developing typically. Daily life can involve using hearing aids or cochlear implants, captions, sign language, and thoughtful communication strategies at home, school, and work; many find that early support and consistent access to language make a big difference in confidence and connection. Families, partners, and friends may adjust how they communicate—facing each other when speaking, reducing background noise, or learning signs—which can deepen relationships and reduce stress for everyone. With accessible environments and community support, many build rich social lives and thrive academically and professionally.
Treatment and drugs
Treatment for autosomal recessive nonsyndromic deafness 37 focuses on improving hearing and communication rather than changing the underlying gene change. Options often include digital hearing aids, which amplify sound, and for those with more severe hearing loss, cochlear implants that directly stimulate the hearing nerve; early symptoms of autosomal recessive nonsyndromic deafness 37 may prompt earlier fitting, which can support speech and language development. Beyond devices, speech and language therapy, auditory training, and family-centered communication strategies (including sign language, if preferred) help with day-to-day understanding at home, school, and work. Doctors sometimes recommend a combination of lifestyle changes and drugs, though medicines play a limited role here and are mainly used for related issues like ear infections or to protect remaining hearing when possible. Supportive care can make a real difference in how you feel day to day, and regular follow-up with an audiologist and ear, nose, and throat specialist helps fine-tune devices and plan for changing hearing needs over time.
Non-drug treatment
Living with autosomal recessive nonsyndromic deafness 37 often centers on clear communication at home, school, and work. Many benefit from a mix of hearing technology, therapy, and language access chosen to match hearing levels and family goals. Non-drug treatments often lay the foundation for skill-building, social connection, and independence. Early, family-centered support tends to improve outcomes across speech, language, and learning.
Modern digital devices amplify the sounds you want while reducing background noise. They can be fitted in infancy and adjusted as hearing needs change.
For severe to profound hearing loss, these devices bypass damaged inner-ear cells and directly stimulate the hearing nerve. Candidacy is based on hearing tests, speech outcomes, and family goals.
This coaching-based approach helps children use hearing technology to develop listening and spoken language. Families learn day-to-day strategies to build skills during play and routines.
A complete visual language offers full, natural communication from day one. It can be used alone or alongside hearing devices to support learning and social connection.
Your genes may have an impact on how drugs work for you
For many people with autosomal recessive nonsyndromic deafness 37, genes that change inner-ear ion flow can also affect how certain meds—like aminoglycoside antibiotics or loop diuretics—impact hearing. Pharmacogenetic testing may guide safer choices or dosing when treatment is needed.
Pharmacological treatments
There are currently no medicines that reverse or restore the genetic hearing loss in Autosomal recessive nonsyndromic deafness 37. Medicines, when used, play a supporting role—for example, treating ear infections or protecting the ears during other necessary treatments. Doctors also try to avoid drugs known to harm the inner ear. Not everyone responds to the same medication in the same way.
There are no medications proven to improve hearing in Autosomal recessive nonsyndromic deafness 37. Drug therapy does not change early symptoms of autosomal recessive nonsyndromic deafness 37. Ask your doctor why a specific drug was recommended for you.
Aminoglycoside antibiotics such as gentamicin and streptomycin can damage inner-ear cells and are avoided when alternatives exist. Loop diuretics like furosemide and chemotherapy drugs such as cisplatin and carboplatin also carry hearing-risk, so doctors use them only when necessary. Your care team will weigh benefits and risks carefully.
If a bacterial ear infection develops, antibiotics such as amoxicillin or amoxicillin–clavulanate may be prescribed to protect overall ear health. Treating infection won’t change baseline sensorineural hearing, but it can prevent extra damage and reduce pain. Never stop or change a prescription without checking with your healthcare provider.
For those receiving a cochlear implant, short-course antibiotics like cefazolin and pain relievers such as acetaminophen or ibuprofen are commonly used. These medicines help prevent infection and manage pain but do not treat the genetic cause of hearing loss. Dosing may be increased or lowered gradually to match comfort and healing.
Genetic influences
This form of hearing loss is usually caused by changes in a gene that helps the inner ear’s sound‑sensing cells do their job, often MYO6. It follows an autosomal recessive pattern: a child needs two nonworking copies—one from each parent—to develop this condition, while parents typically have normal hearing and carry one changed copy. A “carrier” means you hold the gene change but may not show symptoms. Because the gene is important for hair cell movement in the cochlea, early symptoms of Autosomal recessive nonsyndromic deafness 37 often appear at birth or in the first months of life, with severe to profound hearing loss in both ears. Still, the exact age of onset and how quickly hearing changes can differ between families. Genetic testing that looks at MYO6 and other hearing‑loss genes can confirm the cause, clarify recurrence risks for relatives, and guide options such as early hearing support and future family planning.
Is Autosomal recessive nonsyndromic deafness 37 genetic?
Genetics are central to Autosomal recessive nonsyndromic deafness 37. It results from inheriting two nonworking copies of the same gene, typically from carrier parents. Variations in that gene affect inner-ear hair cell function, shaping age of onset, severity, and progression.
Pharmacogenetics—how genetics influence drug effects
For people with Autosomal recessive nonsyndromic deafness 37, care centers on hearing devices and communication support, and genetics can also shape medication choices for Autosomal recessive nonsyndromic deafness 37. Genetic testing can sometimes identify how your body responds to medicines that affect hearing, including certain antibiotics. In particular, some inherited changes in mitochondrial DNA can make aminoglycoside antibiotics trigger sudden, permanent hearing loss even at usual doses, so clinicians often avoid them or use close monitoring and alternatives when possible. There is also ongoing research into genetic markers tied to a higher risk of hearing damage from chemotherapy such as cisplatin; while not routine yet, teams caring for cancer will plan extra hearing checks and protection strategies. Differences in drug‑processing genes may influence how well pain relievers like codeine or tramadol work after ear procedures; depending on whether you process these drugs quickly or slowly, doctors may choose different options. Knowing the specific gene causing the hearing loss can help set expectations for hearing aids or cochlear implant benefit, which guides timing and planning of treatment. If antibiotics, chemotherapy, or surgery are being considered, let your care team know about the hearing history so they can tailor medicines and discuss whether drug–gene testing could lower the risk of further damage.
Interactions with other conditions
Day-to-day, it can feel like one health issue amplifies the other, especially when ear health is involved. In Autosomal recessive nonsyndromic deafness 37, the hearing loss itself is not tied to other organ problems, but separate conditions can still influence how well someone hears. Doctors call it a “comorbidity” when two conditions occur together. Chronic ear infections, significant noise exposure, or medicines that can harm the inner ear (such as certain antibiotics or chemotherapy drugs) may further reduce hearing or make symptoms like tinnitus more noticeable. Migraine, diabetes, and thyroid disorders aren’t caused by this condition, but when present, they can complicate care and may affect how stable hearing feels over time. Mental health concerns like stress, anxiety, or low mood can also interact with communication challenges, so coordinated support—from audiology, primary care, and mental health—often helps keep the overall impact of Autosomal recessive nonsyndromic deafness 37 in check.
How genes can cause diseases
Humans have more than 20,000 genes, each carrying out one or a few specific functions in the body. One gene instructs the body to digest lactose from milk, another tells the body how to build strong bones and another prevents the body's cells from beginning to multiply uncontrollably and developing into cancer. As all of these genes combined are the building instructions for our body, a defect in one of these genes can have severe health consequences.
Through decades of genetic research, we know the genetic code of any healthy/functional human gene. We have also identified that in certain positions on a gene, some individuals may have a different genetic letter from the one you have. We call these hotspots "Genetic Variations" or "Variants" in short. In many cases, studies have been able to show that having the genetic letter "G" in the position makes you healthy, but having the letter "A" in the same position disrupts the gene function and causes a disease. Genopedia allows you to view these variants in genes and summarizes all that we know from scientific research, which genetic letters (Genotype) have good or bad consequences on your health or on your traits.
History
Families and communities once noticed patterns: two hearing parents might welcome several children who were hard of hearing from birth, while relatives in the next street heard normally. Story by story, people with Autosomal recessive nonsyndromic deafness 37 grew up learning to communicate in their homes and schools, long before the condition had a name or a genetic explanation.
First described in the medical literature as a form of congenital, isolated hearing loss that did not come with other health differences, it stood apart from conditions where hearing loss is part of a broader syndrome. Early reports focused on what could be observed—stable, usually severe to profound hearing loss present from infancy—without tools to explain why it appeared in some families and not others.
From early theories to modern research, the story of Autosomal recessive nonsyndromic deafness 37 moved from careful family histories to laboratory insights. In the late 20th and early 21st centuries, advances in genetics linked certain recurring family patterns to specific genes that help inner‑ear cells sense sound. Researchers learned that “autosomal recessive” meant a child was affected when both parents carried one silent, nonworking copy of the same gene, even though the parents heard normally.
Over time, descriptions became more precise. Clinicians separated this condition from other nonsyndromic forms by mapping where the gene sits and how changes in it affect the tiny structures of the inner ear. As genetic testing became more available, what once looked like one broad group of childhood hearing loss resolved into several distinct types, including Autosomal recessive nonsyndromic deafness 37, each with its own genetic cause but similar day‑to‑day challenges.
In recent decades, awareness has grown alongside better newborn hearing screening and earlier referrals to audiology and speech‑language services. This shift let many families learn the cause sooner and choose hearing supports—like hearing aids, cochlear implants, or sign language—earlier in life. Historical differences highlight why a clear name and genetic explanation matter: they guide expectations, family planning, and connections to community resources.
Not every early description was complete, yet together they built the foundation of today’s knowledge. Today, the history of Autosomal recessive nonsyndromic deafness 37 reflects a wider change in medicine: moving from describing what is seen and heard in the clinic to understanding the underlying biology, so care can be offered earlier and with greater confidence.