Definitions Definitions

There are many interesting terms and concepts that are related to those who are deaf-blind.  Let us look at them.

First we will look at types of deaf-blindness, then focus on Causes of deaf-blindness, finally we will look at other important terms.

Types of Deaf-Blindness

There is no "standard" definition that will conveniently group all deaf-blind persons under one category, the only similarity is that each deaf-blind person has difficult seeing and hearing.

Congenitally Deaf-Blind: people who are born with a dual sensory impairment or become deaf-blind before the age of two.

Adventitiously, or Acquired, Deaf-Blind: people who are born with sight and hearing but lose some or all of these senses later in life as a result of an illness, accident or genetics.

Functionally Deaf-Blind persons are fully deaf-blind having little or no hearing or vision.

Deaf and Visually Impaired persons are fully deaf and have some vision.

Hard of Hearing and Blind persons are fully blind, and have a hearing loss.

Hard of Hearing and Visually Impaired persons have some hearing and some vision.

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Some of the most common causes of deaf-blindness are Usher's Syndrome, Congenital Rubella Syndrome, CHARGE Association and natural aging.  Some lesser common causes of deaf-blindness are: severe head injuries & traumas, sexually transmitted diseases, such as syphlis and AIDS, drug overdosing, medical errors and self-induced injuries.

Other causes:

Various syndromes and congenital conditions affect both the eye and the ear. This can be attributed in part to the development in the embryo of the eye and ear during the same time period, during the first 12 weeks of pregnancy. There are also similarities between the two organs, such as their common origin. As a result there are many diseases and symptom complexes which affect both sense organs and result in dual sensory impairment or deafblindness. It follows that prenatal causes of deafness may be associated with visual impairment whereas with postnatal causes there will be hardly any association.

Prenatal causes of deafblindness include rubella, cytomegalovirus and toxoplasmosis. Congenital rubella syndrome consists of deafness, cataracts, glaucoma, retinopathy and heart defects. Rubella is well known but in countries with effective immunisation programmes the number of newly diagnosed children is very low. A survey of 666 people known to Sense in Britain included only 2 children with congenital rubella syndrome under the age of 5.

However there are many young people and adults with congenital rubella syndrome and their education, continuing education, quality of life and health issues remains the major concern for many readers of Deafblind Education. A later edition of Deafblind Education will include an article on the possible delayed effects or manifestations of rubella.

Cytomegalovirus or CMV is a potential prenatal cause of deafblindness. In the UK Sense's Head Office database records 7 people deafblind through CMV compared to at least 280 deafblind through rubella.

Cytomegalovirus means a large cell virus and is a commonly occurring virus. It belongs to the herpes virus group which includes chicken pox, cold sore and glandular fever viruses. Frequently the infection passes unnoticed or there may be mild flu-like symptoms. Very occasionally it is more serious and lasts longer, such as with glandular fever. Once infection has taken place the virus remains dormant or harmless within the body, usually with no ill effects. The virus can become active again at intervals. CMV is so common that by the age of 30 about half the people in Britain have already caught it and most people are likely to pick it up at some time in their lives. The virus is spread by saliva, urine and other body fluids. CMV is very difficult to avoid; it is usually caught from someone you are close to who shows no signs of being ill.

If a woman catches CMV during her pregnancy the virus may sometimes be passed on to the foetus. If this happens some babies may be damaged but perhaps only 10% of affected babies will display symptoms and in only half of these children will the disability be serious.  CMV, like the rubella virus, can cross the placenta and affect the developing foetus. It is only the first, or primary infection of a person during pregnancy which can cause problems. It is very rare that reactivation of CMV in pregnancy causes damage to the foetus.

Problems resulting from congenital cytomegalovirus vary but may include jaundice, bloodspots on the skin, enlargement of the liver or spleen, spasticity (disordered control of movement), intracranial and other calcifications (the deposition of calcium within organic tissue), mental retardation and seizures. In some cases hearing impairment may be the only sign of the CMV infection while others will have severe sight problems as well.

Estimates suggest that of 600,000 babies born in England and Wales perhaps 2,000 will have congenital Cytomegalovirus and of these about 200 have problems as a result. Most children with congenital CMV are healthy and if not tested for the virus at birth would not be suspected of having it. It is not known why some babies are affected and others are not.

Pre-natal diagnosis is not possible as at present there is no test available. There is no vaccine.

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CHARGE Association.
By David Brown, February 1996

Identifying Characteristics
CHARGE Association is a multi-featured disorder characterised by a unique combination of diverse abnormalities. The pattern of features was first described in 1979 but the acronym ‘CHARGE’ was first used in 1981.  This is, therefore, a relatively newly-recognised condition. The acronym ‘CHARGE’ is used to describe a heterogeneous group of children who exhibit at least four of the features prefixed by the letters of the acronym and including one or other of choanal atresia and colobomata. The combination of critical features was identified as:
C       Coloboma are ocular deformities involving an absence of part of the eye, and visual impairments may or may not be present. Coloboma of the iris may reduce the child’s ability to adjust to bright light; coloboma of the retina will create a blank area in the child’s visual field. Anophthalmos or microphthalmia may also be present.
H       Heart defects include tetralogy of Fallot, patent ductus arteriosus, atrial and ventricula septal defects, and others.
A       Choanal Atresia a narrowing or a blockage of the passages between the nasal cavity and the naso-pharynx, is one of the major criteria for diagnosis. The blockage may be unilateral or bilateral, membranous or bony.
R       Retarded growth may become manifest as the child matures. The majority of children with CHARGE Association are below the third
percentile of physical growth norms.
G       Genitalia anomalies. The incomplete development or under-development of the external genitals is common in males, very rarely evidenced in females.
E       Ear anomalies can affect the external ear (lop or cup shaped, large, small or absent), middle ear (ossicular malformations, chronic serous otitis, stapedius tendon anomalies), and/or the internal ear (especially high frequency sensori-neural hearing loss). Mixed hearing loss (ie conductive loss with sensori-neural loss) is the most common form of hearing loss in CHARGE Association. Malformation or absence of the semi-circular canals is fairly common.
Evidence exists of other anomalies associated with this condition in addition to those above:
–       abnormal tongue size
–       cleft lip and/or palate
–       facial palsy
–       renal abnormalities
–       malformations of the larynx
–       atresia of the oesophagus with   tracheosophageal fistula
–       skeletal abnormalities

Historically, the medical profession considered mental retardation a characteristic feature of CHARGE Association. Recent literature suggests this may now be coming to be seen as an outcome of the other combined anomalies rather than as an integral anomaly of the Association itself.

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Toxoplasmosis is caused by a parasite called toxoplasma gondii. It forms cysts (hard-walled microscopic forms) which are passed in the faeces of its primary or main host, the cat.
In Britain, cats contaminate gardens and vegetables in their wanderings and even though they bury their faeces you can still come into contact with them, resulting in your eating the cystic form of toxoplasmosis. The infection is very likely to be contracted by children playing in sandpits, which is one reason why sandpits are supposed to be given new sand and sterilised each year.

Toxoplasmosis can affect almost all animals, including humans, but most animals carry it in their bodies. In pet-owning countries, humans can catch it from changing cat litter trays, gardening without gloves (in earth, catsÌ faeces may remain infected for 14 months), and even by eating unwashed garden vegetables. Cats alone are not the only reason for the incidence of this condition. Undercooked meat and the increasing consumption of unpasteurised goatÌs milk are two other potential causes. In France, the eating of raw or rare meat is considered a major cause of the spread of infection. Luckily the infection that can result is usually very mild. It can be a glandular-like illness or produce symptoms of a mild flu. However, in a pregnant woman the infection, although not a risk to her, can cause congenic abnormality in the unborn child in up to 40% of infections. Of these, ten per cent are likely to be seriously affected. If the disease is caught in early pregnancy it is less likely to cross the placenta to the foetus but, if it does, the effects are more serious. If the pregnant woman catches the infection later, it is more likely to cross the placenta but the effects on the foetus are less severe.

In France and Belgium the problem is considered to be so great that women are routinely screened as they are for rubella in Britain. Babies that are born with toxoplasmosis (usually when infected between the third and sixth month) may develop severe symptoms. These include hydrocephalus, calcification in the brain and chorioretinitis (damage to the retina). Epilepsy and deafness can also result. Most worrying in this regard is that eye disease may not develop until the late teens.

The Public Health Laboratory in Swansea, UK, estimated in 1988 a rate of infection of two per 1,000 pregnant women. If the French figures of 40% passing infection to their babies is the same in the United Kingdom, it could mean that about 480 babies a year are affected in the UK.

Most adults recover spontaneously from toxoplasmosis without any treatment at all, although it is possible to treat the condition using sulpha drugs. Eye treatment of toxoplasma infections is more complicated, and pregnant women must be given a different drug since the usual one is too toxic. No treatment manages to eradicate all cysts. This means that an infection which may appear to have been cured can be reactived later.

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Goldenhar Syndrome was named in 1952, when Dr Goldenhar wrote about a number of facial problems that tend to occur together. Goldenhar is quite variable with some common abnormalities.

A variety of terms have been used to describe this extremely variable disorder. According to medical literature, when malformations primarily involve the jaw, mouth, and ears and, in most cases, affect one side of the body (unilateral), the disorder is often referred to as Hemifacial Microsomia. If abnormalities of the vertebrae and the eyes are also present, the disorder is often called Goldenhar Syndrome. Within medical literature, the term Oculo-Auriculo-Vertebral (OAV) Spectrum is often used synonymously with Goldenhar Syndrome and Hemifacial Microsomia. However, due to the complexity and varying severity and expression of OAV Spectrum, some researchers suggest that Hemifacial Microsomia and Goldenhar Syndrome actually represent different aspects or levels of severity of OAV Spectrum. Goldenhar Syndrome is also considered a variant of Cranofacial Microsomia which is the second most common facial birth defect after cleft lip and palate.

Occurrence & Inheritance Patterns
Goldenhar is prevalent in males (70%) and affected individuals may have asymmetrical small ears and mouth with hypoplasia of the jaw, mouth and eyes (with epibular dermoids). In addition abnormalities often involve the skeletal, cardiac, central nervous and renal systems. Hearing loss varies from near normal to severe; vision defect, including diplopia of
various degrees. Moderate learning disabilities may occur in about 10% of cases.

There is very little evidence to explain why Goldenhar Syndrome occurs. In most cases it appears to occur randomly, with no apparent cause; nothing similar has ever happened in the family before, and there is little chance of it happening again. However, in some cases, positive family histories have been present that have suggested autosomal dominant or recessive inheritance. In addition, some researchers suggest that the disorder may be caused by the interaction of many genes, possibly in combination with environmental factors – multifactorial inheritance.

There are cases of identical twins in which only one has the syndrome, even though they received the same genetic blueprint; whilst other researchers describe examples of siblings having Goldenhar Syndrome. There are a few families with an affected person having a 50% chance of passing on the syndrome. Family history may include cleft lip or palate, unusually shaped ears, asymmetry of face, small chin, skeletal problems, eye abnormalities, internal problems or speech and dental problems.

What is known is that a baby’s face forms during the 8th-12th week of pregnancy, by several different types of tissue growing together, meeting at the same time and place to form facial features. The tissues that will become the face and jaw start out separate from the upper part of the face. In Goldenhar Syndrome, something goes wrong with this meeting. Sometimes the tissue does not seal leaving the mouth and upper jaw longer on one side; sometimes there is extra skin where tissue has sealed near the ear, or skin covers the ear opening; and sometimes the chin and jaw lines do not properly develop.

Children with Goldenhar Syndrome usually look forward to a long life and normal intelligence.

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Rubella is a childhood disease. It is caused by a virus which may be transmitted from person to person in the air as droplets through coughing and sneezing or close contact. A person with rubella is infectious for about two weeks, or occasionally a little longer, starting from five to seven days before the rash appears. However, an affected person may not know that they have rubella and feel perfectly well and may not even develop a rash. If someone has been in contact with an infectious person it takes two to three weeks before they develop the infection too. A person infected with rubella may feel generally unwell for a couple of days, perhaps have swollen glands, a slight temperature, or a sore throat, and may get a rash which starts around the face and can spread down the body and the limbs. Some people, particularly women, may experience pain or discomfort in their joints. Other people may be infectious but show no signs or symptoms of having rubella at all.

Pregnancy and Rubella
Infection with Rubella is particularly dangerous for pregnant women as it affects the growing foetus. Although a woman who contracts rubella in pregnancy does not always pass it on to her baby, the earlier in her pregnancy she has the infection, the more likely transmission is, and as a result identifiable damage. Contact up to the 18th week of pregnancy is particularly serious. The virus is passed in the maternal blood stream to the placenta and from there to the foetus. If transmission does occur, then it will happen just before or around the time that the woman gets the rubella rash. Occasionally, rubella infection in pregnancy can result in miscarriage or stillbirth.

Babies born with congenital rubella have the virus circulating in their bodies for much longer than adults or children with the acquired infection. This means that a congenitally affected baby can remain infectious for six months to a year, or occasionally even longer.

Possible outcomes of rubella infection in pregnancy
Damage is not inevitable following maternal rubella infection, or even foetal infection, but it is more likely the earlier the infection occurs. After the first four months of pregnancy it is rare. Damage or disability not related to rubella is always possible, even if it is unlikely.

Effects of Rubella
Rubella may damage the eye, resulting in cataract (opaqueness of the lens). This is one of the typical signs of congenital rubella. One eye may escape harm or both may be affected. Sometimes microphthalmos (abnormally small eye or eyes) is present as well, though it is uncommon. Pigmentory retinopathy (speckled colouring of the retina) is very common in children with congenital rubella, but does not affect the sight.  Hearing loss which may be conductive or sensorineural, is one of the commonest results of congenital rubella and may often appear as the only defect. The Organ of Corti is the part of the inner ear which links the ear and the brain, and is often the part that is damaged by
rubella. Hearing loss may be mild or severe, present in one or both ears and can also deteriorate over time.  Heart abnormalities are sometimes seen in babies with congenitalrubella and may include failure of the duct between the pulmonary artery and aorta to close (patent ductus arteriosus); opening(s) in the dividing wall between left and right ventricles (ventricular septal defect), or other heart defects.

Many babies with congenital rubella do not grow properly in the womb. Why this happens is not altogether understood. It may be because the infected placenta is not able to function to full capacity and thus affects nutritional supply to the foetus. It could be that the rubella virus may be directly responsible for slowing down the foetal rate of growth.

The rubella virus may also cause neurological problems which may be mild to severe, although this does not always occur. Learning disabilities, mental retardation and seizure disorders can occur but may not do so.

It is important to be aware that congenital rubella can affect people in different ways. Evidence suggests that people with congenital rubella may develop some problems later in life, including hearing and vision deterioration and endocrinological dysfunction. People with congenital rubella should have access to regular health check-ups, including vision and hearing assessments throughout their life.

According to WHO there is an estimated 300,000 babies affected by rubella every year(1). Congenital rubella is preventable with the rubella vaccine, available as a single vaccine or the combined measles, mumps and rubella (MMR) vaccine. Mass vaccination programmes are in action in many countries around the world.

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Alstrom Syndrome (AS) was first described by Carl Henry Alstrom of Sweden in 1959 in a paper he co-authored with B. Hallgren, I.B. Nilsson and H. Asander1 . Alstràm Syndrome is a hereditary and very rare, life threatening disorder which begins to take effect during early childhood. At present there are 104 children and adults world-wide known to have this condition which can be quite variable and have an age-related progression.

Alstrom Syndrome is autosomal recessive and even though it has been mapped to chromosome 2p13, the gene responsible for the disorder has not been identified. Prenatal tests are not available for Alstrom Syndrome but diagnosis is made when particular features of the syndrome are observed.  In clinical medicine, diagnosis is made when four out of five principal features of AS are present. These are degeneration of the retina (retinopathy) at an early age i.e. under 1 year, which is usually first noticed as involuntary eye movements (nystagmus) and/or light sensitivity (photophobia). In addition, infantile obesity, cardiomyopathy (infantile or adolescent), mild to moderate sensorineual hearing loss may also be observed in early childhood, and type 2 diabetes mellitus or high levels of insulin in the blood (hyperinsulinemia) usually begin in adolescence.

Presentation of features
Alstrom Syndrome tends to progress in a particular order with one of the first signs being either infantile dilated cardiomyopathy and/or nystagmus and photophobia.  Both can occur as early as 1-3 weeks of age. Obesity is usually seen beginning in the first year or two of life. Hyperinsulinemia/insulin resistance has been documented in children as young as 2 years old, but there is not a lot of information about this yet. Sensorineural hearing loss occurs at approximately 4 -6 years of age. Diabetes may develop, usually after adolescence. There may be kidney and liver problems too.

Pattern of inheritance
Alstrom Syndrome is autosomal recessive which means that for a child to have the condition they must inherit one mutated gene from their mother and one from their father.

As the diagram shows, for each pregnancy there is a probability of 25% that parents who are carriers of the mutated gene will have a child with Alstrom Syndrome. There is also a probability of 25% of having an unaffected child who will not be a carrier and a probability of 50% that they will have unaffected children who are carriers of the gene. Boys and girls have an equal chance of inheriting the gene responsible for Alstrom Syndrome.

In 1997 researchers at the Jackson Laboratory in Bar Harbor, Maine, USA located the gene for Alstrom syndrome on chromosome 2. Genetic researchis being conducted world-wide to identify the mutation responsible for such devastating effects on multiple organ systems. Research is also taking place in Canada, United States of America, France, Italy and the United Kingdom.

Children with Alstrom Syndrome can and do lead full and productive lives. Even though there is no cure for Alstrom Syndrome treatment/therapy is possible to alleviate some of the symptoms
experienced by those that have the condition. For instance, diabetes mellitus may be controlled with medication combined with diet and exercise, and the use of hearing aids can help children and adults cope with hearing loss.

World-wide distribution of Alstrom Syndrome
As stated earlier there are 104 known children and adults with Alstrom Syndrome who live in 16 different countries around the world. Most of these are in developed countries such as Canada, the United States of America and the United Kingdom, the latter having the largest group of diagnosed AS children and adults.

The distribution of Alstrom Syndrome affected individuals mostly seen in developed countries highlights the concern that there are probably many more AS cases in developing countries going undiagnosed, and this may be attributable to lack of information about the syndrome.  Undiagnosed children could be missing out on vital medical treatment and educational approaches appropriate to their needs.

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One of the earliest steps towards identification of Stickler syndrome began in 1960 when Dr Gunnar B. Stickler examined a twelve year old boy at the Mayo Foundation in Richmond, Minnesota, United States of America. The boy had bony enlargement of several joints and was extremely short sighted. The boyÌs mother was blind and as Dr Stickler was to discover, other members of the family had similar symptoms too. He also noted that Dr Charles Mayo had attended to an ancestor of this family back in 1887.

With the assistance of colleagues, Dr Stickler studied the family’s health in an attempt to define their medical condition. As a result of this study the results were published in June 1965. Dr Stickler also tentatively named the medical condition ProgressiveArthro-ophthalmopathy, now more commonly referred to as Stickler Syndrome.

Stickler Syndrome
This condition is an autosomal dominant condition and is progressive. It can affect both sexes and is normally passed on from parent to child. It affects the bodyÌs collagen (connective tissue) which is the most plentiful protein in the body - about one third of the body’s protein is made up of collagen. Collagen forms a major part of connective tissue, which can be described as the supportive tissue of the organs of the body. Some connective tissue acts like a glue or binding, in other areas it acts like scaffolding, and can also allow for the elastic stretching and tightening, especially in the muscles. Collagen is also an important part of cartilage which covers the bone ends of the joints. In the eye it is found in the sclera, cornea and vitreous humour.

Several genes which control and direct collagen synthesis (the building up of complex substances by the joining and interaction of simpler materials) may cause Stickler syndrome. Clinical manifestations of the various types of Stickler syndrome are very similar and very few clinicians could ever tell the difference but genetic testing is a method now used to more accurately distinguish between the types. However, in 1999 the National Institutes of Health, USA found a new mutation that has not had the gene located so a negative genetic test for Stickler syndrome is still not a definitive answer.

Symptoms of Stickler syndrome
There may be slightly different manifestations between the various types of Stickler syndrome, and symptoms and severity of this condition can vary from person to person, even within a family. An individual may develop any number of problems from a variety of defects associated with this syndrome.

This variety includes eye problems such as short-sightedness (myopia), high risk of retinal detachments (which may affect both eyes), cataracts and glaucoma. Hearing loss is possible and may be conductive, sensorineural or both. Sensorineural hearing loss in Stickler syndrome is less common than conductive loss, but may still affect up to 40% of individuals. Hearing loss in childhood may also be caused by a cleft palate.

Skeletal problems are usually evident with stiff joints and over-flexible joints. Early joint disease may develop, leading to osteoarthritis in the 3rd and 4th decade of life. Curvature of the spine (scoliosis) may also be evident too. Facial and oral problems include a flat face with a small nose and little or no nasal bridge but facial appearance tends to improve with age.  A cleft palate is sometimes seen in babies and may affect their feeding as well as having an impact upon their speech later  in life but can be corrected with surgery where necessary.

Micrognathia, where the lower jaw is smaller than the upper resulting in poor contact between the chewing surfaces of the upper and lower teeth, may also be seen. Other problems may also be evident and identifiable through medical investigation such as x-ray.

Pattern of inheritance
As an autosomal dominant condition, Stickler syndrome affects males and females (see diagram below). For each pregnancy there is a 50% chance of a child being born with Stickler syndrome, as only one mutated gene from either parent is required to pass on the condition. Boys and girls have an equal chance of inheriting the mutated gene from either of their parents, but it is also possible for a child to be born with the mutated gene even though neither parent themselves are affected.

Prognosis and management of Stickler syndrome
People with Stickler syndrome generally have a good quality of life.  Early diagnosis of the condition means aspects of the condition can be managed and symptoms of the condition alleviated where possible. Regular eye tests may identify possible development of retinal detachment, cataract or glaucoma that may be treated with eye drops or
surgery where necessary.

Acute or chronic otitis media (fluid behind the eardrums) can lead to one form of conductive hearing loss and is often referred to as glue ear. Minor surgery may help to drain the fluid whilst hearing aids may be a safe and effective alternative to surgery.

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Usher Syndrome?

Usher Syndrome is the name given to a group of conditions in which hearing loss is combined with Retinitis Pigmentosa.  The name comes from the person who noticed the correlation between the two conditions, Dr Charles H. Usher. Usher Syndrome affects between 3 and 6 percent of the Deaf community.  Currently, there are 3 types of Usher Syndrome.

Type I
   Born profoundly deaf.
   Has balance problems.
   Nightblind in early childhood.
Type II
   Born hard of hearing.
   Has no balance problems.
   Blind spots by teens. Legally blind in early adulthood
Type III
   Born with good hearing or mild hearing loss.
   Has some balance problems.
   Nightblind in childhood, blindspots by early adulthood, legally blind by middle age

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Other Important Information

Vision:  Types and Degrees of Loss

Visual Acuity:  a measure of the eye's ability to distinguish object detail and shape; it measures the smallest identifiable object that can be seen at a specified distance (e.g., 20/100 means that the eye sees at 20 feet what a typical eye sees at 100 feet.)

Normal Vision:  is considered to be 20/20.

Normal Range of Vision:  is considered to be between 20/20 and 20/70.

Legally Blind:  20/200 or less visual acuity in the better eye with maximum correction, or presence of a field defect to the extent that the visual field is 20 degrees or less.

Functionally Blind:  if, based on visual and learning assessments, it is determined that a student would best benefit from tactile media as a primary tool in reading and writing (Tarver, P.; Blaha, R., 1996).

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Hearing Loss: Types & Degrees of Loss

There are three TYPES of hearing loss:  conductive, sensorineural and central.  A student could experience one, two or all three types of hearing loss.

Conductive:  occurs when a barrier to sound is present in the outer or middle ear.  This type of hearing loss is often treatable medically.

Sensorineural:  some sounds may be heard while others are not; usually there is no medical treatment for this type of hearing loss.

Central:  damage to the brain precludes processing of auditory stimuli.

Another condition, known as tinnitus, is a ringing or buzz in the ear, which  interferes with hearing and is a symptom of other disorders (e.g., cardiovascular, thyroid, head injury).  Tobacco, caffeine and salt can also contribute to tinnitus.

The DEGREE of hearing loss is ascertained by determining at what level of loudness (measured in decibels) a student begins to hear a certain pitch (frequency).  With normal hearing a student can detect all speech sounds even at a soft conversation level (10 to 15 decibels on an audiogram).

Minimal Loss:  difficulty hearing soft sounds; rapid conversation and noisy environments often result in lost information;  loss between 16 to 25 decibels on an audiogram.

Mild Loss:  difficulty understanding normal speech; requires use of a hearing aid or FM system in some situations; loss between 26 to 40 decibels.

Moderate Loss:  difficulty understanding loud speech; hearing aids and/or FM systems frequently needed;  can hear discussion from 3 to 5 feet away if environment is controlled;  loss between 41 to 55 decibels.

Severe Loss:  can understand amplified speech only; hearing aids and FM systems needed for all communication; loss between 56 and 80 decibels.

Profound Loss:  difficulty understanding amplified speech;  students rely on vision rather than hearing to process information; loss of 81 decibels or more

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An interpreter is a bicultural, bilingual professional who interprets (works between languages) while being sensitive to the environmental factors which impede or foster the message and conducts him/herself in a professional, ethical manner.


 An intervenor is trained to provide sensory information compensating for vision and hearing loss, to facilitate learning and interaction with the physical environment and society.  Intervening can include interpreting, transliterating, guiding, and providing personal care.  However, intervenors may not be formally trained interpreters.

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