Sensorineural hearing loss: It is the most common type of hearing loss. This is caused by the damage to the cochlea and the auditory nerve.
Stroke: A group of brain disorders involving loss of brain functions that occur when the blood supply to any part of the brain is interrupted
Stuttering: Excessive repetition of parts of word in unintentional manner of prolongation of sounds in words, and/or struggle to “get words out.”
Streaming sound signals: Therapeutic flexibility for tinnitus sounds
Soft switching: Automatically switches from many to a single direction.
Sensorineural Hearing Loss – Hearing loss caused by damage to the sensory cells and/or nerve fibers of the inner ear. The most common type of hearing loss in adulthood. Learn more about sensorineural hearing loss.
Sign Language – Method of communication for people who are deaf in which hand movements, gestures, and facial expressions convey grammatical structure and meaning.
Sudden Hearing Loss – Loss of hearing that occurs quickly due to such causes as an explosion or a viral infection.
Speech discrimination – A test which measures the subject’s ability to distinguish words.
Speech recognition threshold (SRT) – the lowest level at which the subject can correctly repeat spondaic (two syllable) words.
Static feedback cancellation – A digital process which creates a filter in the hearing aid amplifier and is programmed into the hearing aid during the fitting. The filter cancels feedback that is occurring at that time. The filter will continue to cancel feedback that occurs in the same situation, but will not adapt to changing situations.
Sign Language – Method of communication for people who are deaf or hard of hearing in which hand movements, gestures, and facial expressions convey grammatical structure and meaning
Sound Vocalization – Ability to produce voice
Speech – Making definite vocal sounds that form words to express thoughts and ideas
Speech Disorder – Any defect or abnormality that prevents an individual from communicating by means of spoken words. Speech disorders may develop from nerve injury to the brain, muscular paralysis, structural defects, hysteria, or mental retardation.
Speech-Language Pathologist – Health professional trained to evaluate and treat people who have voice, speech, language, or swallowing disorders, including hearing impairment, that affect their ability to communicate
Stroke – Also known as a cerebro vascular accident (CVA); caused by a lack of blood to the brain, resulting in the sudden loss of speech, language, or the ability to move a body part, and, if severe enough, death
Swallowing Disorders – Any of a group of problems that interferes with the transfer of food from the mouth to the stomach
Saccule – located in the vestibule of the inner ear, this structure along with the utricle sense “straight line” head motion.
Scala media – The middle section of the cochlea, which contains endolymph. Basilar membrane is at the bottom of scala media; Reissner’s membrane is at its top.
Scala tympani – The section of the cochlea that is below basilar membrane and contains perilymph. If a cross section of one coil of the cochlea is examined, scala tympani will be on the bottom.
Scala vestibuli – The section of the cochlea that is above Reissner’s membrane and contains perilymph. If a cross section of one coil of the cochlea is examined, scala vestibuli will be on the top.
Screening (Hearing): An evaluation of the auditory system that is generally not as in-depth as a traditional hearing test and often does not include the actual assessment of an individual’s thresholds, but instead results in “pass” or “fail”.
Semicircular Canals: The three fluid-filled tubes in the vestibular portion of the inner ear that helps with equilibrium and the interpretation of the body’s position.
Sensori-Neural Hearing Loss: A decrease in an individual’s ability to hear a particular sound due to a problem in the inner ear (cochlea) or the neural system (Cranial Nerve VIII). The designation of a hearing loss as sensori-neural suggests that the sound makes it way through the outer and middle ear systems efficiently, but is not picked-up by the hair cells in the cochlea or transmitted by the hearing nerves as well as an average normal human ear’s system. Sensorineural hearing loss (SNHL)is a type of hearing loss in which the root cause lies in the vestibulocochlear nerve (Cranial nerve VIII), the inner ear, or central processing centers of the brain.
The Weber test, in which a tuning fork is touched to the midline of the forehead, localizes to the normal ear in people with this condition. The Rinne test, which tests air conduction vs. bone conduction is positive (normal), though both bone and air conduction are reduced equally.
Sensorineural hearing loss can be mild, moderate, or severe, including total deafness.
The great majority of human sensorineural hearing loss is caused by abnormalities in the hair cells of the organ of Corti in the cochlea. There are also very unusual sensorineural hearing impairments that involve the eighth cranial nerve (the vestibulocochlear nerve) or the auditory portions of the brain. In the rarest of these sorts of hearing loss, only the auditory centers of the brain are affected. In this situation, Cortical deafness, sounds may be heard at normal thresholds, but the quality of the sound perceived is so poor that speech cannot be understood.
Most sensory hearing loss is due to poor hair cell function. The hair cells may be abnormal at birth, or damaged during the lifetime of an individual. There are both external causes of damage, like noise trauma and infection, and intrinsic abnormalities, like deafness genes.
Sensory hearing loss that results from abnormalities of the central auditory system in the brain is called central hearing impairment. Since the auditory pathways cross back and forth on both sides of the brain, deafness from a central cause is unusual.
This type of hearing loss can also be caused by prolonged exposure to very loud noise, for example, being in a loud workplace without hearing protection, or having headphones set to high volumes for a long period.
Table 1. A table comparing sensorineural to conductive hearing loss
Sensorineural hearing loss
Conductive hearing loss
|Anatomical Site||r, cranial nerve VIII, or central processing centers||Middle ear (ossicular chain), tympanic membrane, or external ear|
|Weber Test||Sound localizes to normal ear||Sound localizes to affected ear (ear with conductive loss)|
|Rinne Test||Positive Rinne; Air conduction > Bone conduction (both air and bone conduction are decreased equally, but the difference between them is unchanged).||Negative Rinne; Bone Conduction > Air Conduction (Bone/Air Gap)|
Sensorineural hearing loss may be congenital or acquired.
- Lack of development (aplasia) of the cochlea
- Chromosomal syndromes (rare)
- Congenital cholesteatoma – squamous epithelium is normally present on either side of the tympanic membrane. Externally, within the external auditory meatus or ear canal and internally within the middle ear. Within the middle ear the simple epithelium gradually transitions into ciliated pseudostratified epithelium lining the Eustachian tube now known as the pharyngotympanic tube becoming continuous with the respiratory epitheliu in the pharynx. The squamous epithelium hyperplasia within the middle ear behaves like an invasive tumour and destroys middle ear structures if not removed.
- Delayed familial progressive
- Congenital rubella syndrome, CRS
- Suppurative labyrinthitis
- Ototoxic drugs
- Aminoglycosides (most common cause; e.g., tobramycin)
- Loop diuretics (e.g., furosemide)
- Antimetabolites (e.g., methotrexate)
- Salicylates (e.g., aspirin)
- Physical trauma – either due to a fracture of the temporal bone affecting the cochlea and middle ear, or a shearing injury affecting cranial nerve VIII.
- Noise-induced – prolonged exposure to loud noises (>90 dB) causes hearing loss which begins at 4000 Hz (high frequency). The normal hearing range is from 20 Hz to 20,000 Hz.
- Presbycusis – age-related hearing loss that occurs in the high frequency range (4000 Hz to 8000 Hz).
- Sudden hearing loss
- Idiopathic (ISSHL: idiopathic sudden sensoneurinal hearing loss), H91.2
- Vascular ischemia of the inner ear or CN 8
- Perilymph fistula, usually due to a rupture of the round or oval windows and the leakage of perilymph. The patient will most likely also experience vertigo or imbalance. A history of an event that increased intracranial pressure or caused trauma is usually present).
- Autoimmune – can be due to an IgE or IgG allergy (e.g. food)
- Autoimmune – a prompt injection of steroids into ear is necessary.
- Cerebellopontine angle tumour (junction of the pons and cerebellum) (the cerebellopontine angle is the exit site of both the facial nerve(CN7) and the vestibulocochlear nerve(CN8). Patients with these tumors often have signs and symptoms corresponding to compression of both nerves)
- Acoustic neuroma (vestibular schwannoma) – this is a schwannoma (benign neoplasm of Schwann cells)
- Meningioma – benign tumour of the pia and arachnoid maters
- Ménière’s disease – causes sensorineural hearing loss in the low frequency range (125 Hz to 1000 Hz). Ménière’s disease is characterized by sudden attacks of vertigo, lasting minutes to hours preceded by tinnitus, aural fullness, and fluctuating hearing loss.
Long term exposure to environmental noise
Populations living near airports or freeways are exposed to levels of noise typically in the 65 to 75 dbA range. If lifestyles include significant outdoor or open window conditions, these exposures over time can degrade hearing. The U.S. EPA and various states have set noise standards to protect people from these adverse health risks. The EPA has identified the level of 70 db(A) for 24 hour exposure as the level necessary to protect the public from hearing loss (EPA, 1974).
- Noise-induced hearing loss (NIHL) typically is centered at 4000 Hz.
- The louder the noise is, the shorter the safe amount of exposure is. Normally, the safe amount of exposure is reduced by a factor 2 for every additional 3 dB. For example, the safe daily exposure amount at 85 dB is 8 hours, while the safe exposure at 91 dB(A) is only 2 hours (National Institute for Occupational Safety and Health, 1998). Sometimes, a factor 2 per 5 dB is used.
- Personal audio electronics, such as iPods (iPods often reaching 115 decibels or higher), can produce powerful enough sound to cause significant NIHL, given that lesser intensities of even 70 dB can also cause hearing loss.
Hearing loss can be inherited. Both dominant and recessive genes exist which can cause mild to profound impairment. If a family has a dominant gene for deafness, it will persist across generations because it will manifest itself in the offspring even if it is inherited from only one parent. If a family had genetic hearing impairment caused by a recessive gene, it will not always be apparent, as it will have to be passed onto offspring from both parents. Dominant and recessive hearing impairment can be syndromic or nonsyndromic. Recent gene mapping has identified dozens of nonsyndromic dominant (DFNA#) and recessive (DFNB#) forms of deafness.
- The most common type of congenital hearing impairment in developed countries is DFNB1, also known as Connexin 26 deafness or GJB2-related deafness.
- The most common dominant syndromic forms of hearing impairment include Stickler syndrome and Waardenburg syndrome.
- The most common recessive syndromic forms of hearing impairment are Pendred syndrome, large vestibular aqueduct syndrome and Usher syndrome.
- MT-TL1 mutations cause hearing loss, along with diabetes and other symptoms.
Disease or illness
- Measles may result in auditory nerve damage
- Meningitis may damage the auditory nerve or the cochlea
- Autoimmune disease has only recently been recognized as a potential cause for cochlear damage. Although probably rare, it is possible for autoimmune processes to target the cochlea specifically, without symptoms affecting other organs. Wegener’s granulomatosis, an autoimmune condition, may precipitate hearing loss.
- Autoinflammatory disease, such as Muckle-Wells Syndrome, can lead to hearing loss.
- Mumps (epidemic parotitis) may result in profound sensorineural hearing loss (90 dB or more), unilaterally (one ear) or bilaterally (both ears).
- Presbycusis is deafness due to loss of perception to high tones, mainly in the elderly. It is considered by some to be a degenerative process, although there has never been a proven link to aging. (See impact of environmental noise exposure above.)
- Adenoids that do not disappear by adolescence may continue to grow and may obstruct the Eustachian tube, causing conductive hearing impairment and nasal infections that can spread to the middle ear.
- AIDS and ARC patients frequently experience auditory system anomalies.
- HIV (and subsequent opportunistic infections) may directly affect the cochlea and central auditory system.
- Chlamydia may cause hearing loss in newborns to whom the disease has been passed at birth.
- Fetal alcohol syndrome is reported to cause hearing loss in up to 64% of infants born to alcoholic mothers, from the ototoxic effect on the developing fetus, plus malnutrition during pregnancy from the excess alcohol intake.
- Premature birth results in sensorineural hearing loss approximately 5% of the time.
- Syphilis is commonly transmitted from pregnant women to their fetuses, and about a third of the infected children will eventually become deaf.
- Otosclerosis is a hardening of the stapes (or stirrup) in the middle ear, and causes conductive hearing loss.
See also Ototoxicity
Some medications cause irreversible damage to the ear, and are limited in their use for this reason. The most important group is the aminoglycosides (main member gentamicin).
Various other medications may reversibly affect hearing. This includes some diuretics, sildenafil and NSAIDs, and macrolide antibiotics.
Extremely heavy hydrocodone (Vicodin) abuse is known to cause hearing impairment.
- There can be damage either to the ear itself or to the brain centers that process the aural information conveyed by the ears.
- People who sustain head injury are especially vulnerable to hearing loss or tinnitus, either temporary or permanent.
- Exposure to very loud noise (90 dB or more, such as jet engines at close range) can cause progressive hearing loss. Exposure to a single event of extremely loud noise (such as explosions) can also cause temporary or permanent hearing loss. A typical source of acoustic trauma is a too-loud music concert.
Previously, sensorineural hearing loss has been treated with hearing aids which amplify sounds at preset frequencies to overcome a sensorineural hearing loss in that range; or cochlear implants, which stimulate the cochlear nerve directly.
Some research suggests idebenone alone or combined with vitamin E may delay the onset of hearing loss or perhaps reverse it. Use of these agents for this purpose is considered experimental now.
Some audiologists and ENTs have reported if severe noise-induced hearing loss (exposures exceeding 140dB) is treated immediately (within 24 hours) with a course of steroids, it can often be almost completely reversed. This, however, is a new field without proven success.
Researchers at the University of Michigan report that a combination of high doses of vitamins A, C, and E, and Magnesium, taken one hour before noise exposure and continued as a once-daily treatment for five days, was very effective at preventing permanent noise-induced hearing loss in animals
Signal-To-Noise Ratio: The relationship between the intensity of the desired sound (signal) and other undesired sounds (noise). The louder the speech signal is presented in comparison to the background noises, the better chance a person has at understanding the speech signal.
Sign Language: The use of hand and body movements to communicate language information.
Simple harmonic motion – the vibration back and forth of an object or air molecules that results in a clean single tone, a “pure tone”. See also tutorial on acoustics review.
SNHL: Sensori-neural hearing loss.
Soma – the body of a nerve cell.
Sound Booth: A sound treated enclosure that is designed to attenuate the interference of extraneous sounds during a hearing test. Sound booths lessen but do not eliminate reverberant and ambient noises.
Sound Field Hearing Aid Testing: The analysis of the performance of a hearing aid in which a patient’s thresholds are measured, while in a sound booth with the stimuli presented through a speaker system, with and without a hearing aid inserted.
Speech Audiometry: The portion of an audiological evaluation that uses speech stimuli to measure the auditory system. Speech audiometry testing often includes the measurement of Speech Reception Thresholds (SRTs) utilizing two-syllable spondee words and the assessment of Word Recognition / Speech Discrimination scores utilizing single syllable words in a carrier phrase. Some speech audiometry tests use sentence materials instead of single word materials.
Speech Mapping: A variation of the traditional real ear analysis, during which a professional uses a special device to measure the performance of a hearing aid using speech as the input instead of a series of tones.
Speech Reading: The use of lip reading and other visual cues produced by a speaker to help with the understanding of spoken words.
Speech Reception Threshold: The use of familiar two-syllable spondee words by a hearing healthcare professional to assess the lowest intensity level at which an individual can repeat the words more than half of the time.
Spiral limbus – a part of the organ of Corti that is one point of attachment for tectorial membrane. It is composed of periosteum, the type of tissue that covers bone, and is located on top of the bony ridge called osseous spiral lamina.
Stapedius – a muscle residing in the pyramidal eminence on the posterior wall of the middle ear space whose tendon is attached to the neck of the stapes. Contraction of the stapedial muscle (e.g. in response to loud sound) increases the stiffness of the middle ear system and reduces the transmission of low-frequency sound through the middle ear.
Stapes: The smallest and last bone in the ossicular chain. It attaches to the oval window of the inner ear.
Stria vascularis – a lining of the radial wall of scala media, containing a rich network of vascularized tissue (containing networks of small veins and arteries). Endolymph is produced and nourished by stria vascularis.
Stuttering : (/ˈstʌtərɪŋ/; alalia syllabaris), also known as stammering (; alalia literalis or anarthria literalis), is a speech disorder in which the flow of speech is disrupted by involuntary repetitions and prolongations of sounds, syllables, words or phrases as well as involuntary silent pauses or blocks in which the stutterer is unable to produce sounds. The term stuttering is most commonly associated with involuntary sound repetition, but it also encompasses the abnormal hesitation or pausing before speech, referred to by stutterers as blocks, and the prolongation of certain sounds, usually vowels and semivowels. For many stutterers, repetition is the primary problem. Blocks and prolongations are learned mechanisms to mask repetition, as the fear of repetitive speaking in public is often the main cause of psychological unease. The term “stuttering”, as popularly used, covers a wide spectrum of severity: it may encompass individuals with barely perceptible impediments, for whom the disorder is largely cosmetic, as well as others with extremely severe symptoms, for whom the problem can effectively prevent most oral communication. The impact of stuttering on a person’s functioning and emotional state can be severe. This may include fears of having to enunciate specific vowels or consonants, fears of being caught stuttering in social situations, self-imposed isolation, anxiety, stress, shame, or a feeling of “loss of control” during speech. Stuttering is sometimes popularly associated with anxiety but there is actually no such correlation (though as mentioned social anxiety may actually develop in individuals as a result of their stuttering). Despite popular perceptions to the contrary, stuttering is not reflective of intelligence.
Stuttering is generally not a problem with the physical production of speech sounds or putting thoughts into words. Acute nervousness and stress can trigger stuttering in persons predisposed to it, and living with a highly stigmatized disability can result in anxiety and high allostatic stress load (i.e., chronic nervousness and stress) that reduce the amount of acute stress necessary to trigger stuttering in any given person who stutters, exacerbating the problem in the manner of a positive feedback system; the name ‘Stuttered Speech Syndrome’ has been proposed for this condition. Neither acute nor chronic stress, however, itself creates any predisposition to stuttering.
The disorder is also variable, which means that in certain situations, such as talking on the telephone, the stuttering might be more severe or less, depending on the anxiety level connected with that activity. Although the exact etiology or cause of stuttering is unknown, both genetics and neurophysiology are thought to contribute. There are many treatments and speech therapy techniques available that may help increase fluency in some stutterers to the point where an untrained ear cannot identify a problem; however, there is essentially no “cure” for the disorder at present, although many treatments are available.
Developmental stuttering is stuttering that originates when a child is learning to speak and develops as the child matures into adulthood. Other disorders with symptoms resembling stuttering are Asperger’s syndrome, cluttering, Parkinson’s speech, essential tremor, palilalia, spasmodic dysphonia, selective mutism and social anxiety.
Primary stuttering behaviors are the overt, observable signs of speech fluency breakdown, including repeating sounds, syllables, words or phrases, silent blocks and prolongation of sounds. These differ from the normal disfluencies found in all speakers in that stuttering disfluencies may last longer, occur more frequently, and are produced with more effort and strain. Stuttering disfluencies also vary in quality: normal disfluencies tend to be a repetition of words, phrases or parts of phrases, while stuttering is characterized by prolongations, blocks and part-word repetitions.
- Repetition occurs when a unit of speech, such as a sound, syllable, word, or phrase is repeated and are typical in children who are beginning to stutter. For example, “to-to-to-tomorrow”.
- Prolongations are the unnatural lengthening of continuant sounds, for example,”mmmmmmmmmilk”. Prolongations are also common in children beginning to stutter.
- Blocks are inappropriate cessation of sound and air, often associated with freezing of the movement of the tongue, lips and/or vocal folds. Blocks often develop later, and can be associated with muscle tension and effort.
The severity of a stutter is often not constant even for severe people who stutter. People who stutter commonly report dramatically increased fluency when talking in unison with another speaker, copying another’s speech, whispering, singing, and acting or when talking to pets, young children, or themselves. Other situations, such as public speaking and speaking on the telephone are often greatly feared by stutterers, and increased stuttering is reported.
Feelings and attitudes
Stuttering may have a significant negative cognitive and affective impact on the person who stutters. Joseph Sheehan, a prominent researcher in the field, has described stuttering in terms of the well-known analogy to an iceberg, with the immediately visible and audible symptoms of stuttering above the waterline and a broader set of symptoms such as negative emotions hidden below the surface. Feelings of embarrassment, shame, frustration, fear, anger, and guilt are frequent in people who stutter, and may actually increase tension and effort, leading to increased stuttering. With time, continued exposure to difficult speaking experiences may crystallize into a negative self-concept and self-image. A person who stutters may project his or her attitudes onto others, believing that they think he or she is nervous or stupid. Such negative feelings and attitudes may need to be a major focus of a treatment program.
Many people who stutter report about a high emotional cost, including jobs or promotions not received, as well as relationships broken or not pursued.
Fluency and disfluency
Linguistic tasks can invoke speech disfluency. People who stutter may “move along a continuum from fluency to dysfluency.” Tasks that trigger disfluency usually require a controlled-language processing, which involves linguistic planning. In stuttering, it is seen that many individuals have fluency when it comes to tasks that allow for automatic processing without substantial planning. For example, singing “Happy Birthday” or other relatively common, repeated linguistic discourses could be fluid in people who stutter. Tasks like this reduce semantic, syntactic, and prosodic planning, whereas spontaneous, “controlled” speech or reading aloud requires thoughts to transform into linguistic material and thereafter syntax and prosody. Some researchers hypothesize that controlled-language activated circuitry consistently does not function properly in people who stutter, whereas people who do not stutter only sometimes display disfluent speech and abnormal circuitry.
Stuttering is typically a developmental disorder beginning in early childhood and continuing into adulthood in at least 20% of affected children. The mean onset of stuttering is 30 months. Although there is variability, early stuttering behaviours usually consist of word or syllable repetitions, and secondary behaviours such as tension, avoidance or escape behaviours are absent. Most young children are unaware of the interruptions in their speech. With early stutterers, disfluency may be episodic, and periods of stuttering are followed by periods of relative fluency.
Though the rate of early recovery is very high, with time a young stutterer may transition from easy, relaxed repetition to more tense and effortful stuttering, including blocks and prolongations. Some propose that parental reaction may affect the development of chronic stutter. Recommendations to slow down, take a breath, say it again, etc. may increase the child’s anxiety and fear, leading to more difficulties with speaking and, in the “cycle of stuttering” to ever yet more fear, anxiety and expectation of stuttering. With time secondary stuttering including escape behaviours such as eye blinking, lip movements, etc. may be used, as well as fear and avoidance of sounds, words, people, or speaking situations. Eventually, many become fully aware of their disorder and begin to identify themselves as “stutterers.” With this may come deeper frustration, embarrassment and shame. Other, rarer, patterns of stuttering development have been described, including sudden onset with the child being unable to speak, despite attempts to do so. The child usually is unable to utter the first sound of a sentence, and shows high levels of awareness and frustration. Another variety also begins suddenly with frequent word and phrase repetition, and does not develop secondary stuttering behaviours. Another way stuttering comes about is through child development. Many toddlers and preschool age children stutter as they are learning to talk, and although many parents worry about it, most of these children will outgrow the stuttering and will have normal speech as they get older. Since most of these children don’t stutter as adults, this normal stage of speech development is usually referred to as pseudostuttering or as a normal dysfluency. As children learn to talk, they may repeat certain sounds, stumble on or mispronounce words, hesitate between words, substitute sounds for each other, and be unable to express some sounds. Children with a normal dysfluency usually have brief repetitions of certain sounds, syllables or short words; however, the stuttering usually comes and goes and is most noticeable when a child is excited, stressed or overly tired. Stuttering is also believed to be caused by neurophysiocology. Neurogenic stuttering is a type of fluency disorder in which a person has difficulty in producing speech in a normal, smooth fashion. Individuals with fluency disorders may have speech that sounds fragmented or halting, with frequent interruptions and difficulty producing words without effort or struggle. Neurogenic stuttering typically appears following some sort of injury or disease to the central nervous system. Injuries to the brain and spinal cord, including cortex, subcortex, cerebellar, and even the neural pathway regions.
In rare cases, stuttering may be acquired in adulthood as the result of a neurological event such as a head injury, tumour, stroke or drug use. The stuttering has different characteristics from its developmental equivalent: it tends to be limited to part-word or sound repetitions, and is associated with a relative lack of anxiety and secondary stuttering behaviors. Techniques such as altered auditory feedback (see below), which may promote fluency in stutterers with the developmental condition, are not effective with the acquired type.
Psychogenic stuttering may also arise after a traumatic experience such as a grief, the breakup of a relationship or as the psychological reaction to physical trauma. Its symptoms tend to be homogeneous: the stuttering is of sudden onset and associated with a significant event, it is constant and uninfluenced by different speaking situations, and there is little awareness or concern shown by the speaker.
Causes of developmental stuttering
No single, exclusive cause of developmental stuttering is known. A variety of hypotheses and theories suggests multiple factors contributing to stuttering. Among these is the strong evidence that stuttering has a genetic basis. Children who have first-degree relatives who stutter are three times as likely to develop a stutter. However, twin and adoption studies suggest that genetic factors interact with environmental factors for stuttering to occur, and many stutterers have no family history of the disorder. There is evidence that stuttering is more common in children who also have concomitant speech, language, learning or motor difficulties. Robert West, a pioneer of genetic studies in stuttering, has suggested that the presence of stuttering is connected to the fact that articulated speech is the last major acquisition in human evolution.
Another view is that a stutter is a complex tic.
In a 2010 article, three genes were found to correlate with stuttering: GNPTAB, GNPTG, and NAGPA. Researchers estimated that alterations in these three genes were present in 9% of stutterers with a family history.
In some stutterers, congenital factors may play a role. These may include physical trauma at or around birth, as well as cerebral palsy and mental retardation. In other stutterers, there could be added impact due to stressful situations such as the birth of a sibling, moving, or a sudden growth in linguistic ability.
There is clear empirical evidence for structural and functional differences in the brains of stutterers. Research is complicated somewhat by the possibility that such differences could be the consequences of stuttering rather than a cause, but recent research on older children confirm structural differences thereby giving strength to the argument that at least some of the differences are not a consequence of stuttering.
Auditory processing deficits have also been proposed as a cause of stuttering. Stuttering is less prevalent in deaf and hard-of-hearing individuals, and stuttering may be improved when auditory feedback is altered, such as masking, delayed auditory feedback (DAF), or frequency altered feedback. There is some evidence that the functional organization of the auditory cortex may be different in stutterers.
There is evidence of differences in linguistic processing between stutterers and non-stutterers. Brain scans of adult stutterers have found increased activation of the right hemisphere, which is associated with emotions, than in the left hemisphere, which is associated with speech. In addition reduced activation in the left auditory cortex has been observed.
The capacities and demands model has been proposed to account for the heterogeneity of the disorder. In this approach, speech performance varies depending on the capacity that the individual has for producing fluent speech, and the demands placed upon the person by the speaking situation. Capacity for fluent speech, which may be affected by a predisposition to the disorder, auditory processing or motor speech deficits, and cognitive or affective issues. Demands may be increased by internal factors such as lack of confidence or self esteem or inadequate language skills or external factors such as peer pressure, time pressure, stressful speaking situations, insistence on perfect speech, and the like. In stuttering, the severity of the disorder is seen as likely to increase when demands placed on the person’s speech and language system is exceeded by their capacity to deal with these pressures.
Neuroimaging of developmental stuttering in adults
Several neuroimaging studies have emerged in order to identify areas associated with stuttering. Brain imaging studies have primarily been focused on adults. In general, during stuttering, cerebral activities change dramatically in comparison to silent rest or fluent speech between stutterers and non-stutterers.
Studies utilizing positron-emission tomography (PET) have found during tasks that invoke disfluent speech, stutterers show hypoactivity in cortical areas associated with language processing, such as Broca’s area, but hyperactivity in areas associated with motor function. One such study that evaluated the stutter period found that there was over activation in the cerebrum and cerebellum, and relative deactivation of the left hemisphere auditory areas and frontal temporal regions.
In non-stuttering, normal speech, PET scans show that both hemispheres are active but that the left hemisphere may be more active. By contrast, stutterers yield more activity on the right hemisphere, suggesting that it might be interfering with left-hemisphere speech production. Another comparison of scans anterior forebrain regions are disproportionately active in stuttering subjects, while post-rolandic regions are relatively inactive.
Functional magnetic resonance imaging (fMRI) has found abnormal activation in the right frontal operculum (RFO), which is an area associated with time-estimation tasks, occasionally incorporated in complex speech.
Researchers have explored temporal cortical activations by utilizing magnetoencephalography (MEG). In single-word-recognition tasks, non-stutterers showed cortical activation first in occipital areas, then in left inferior-frontal regions such as Broca’s area, and finally, in motor and premotor cortices. The stutterers also first had cortical activation in the occipital areas, but, interestingly, the left inferior-frontal regions were activated only after the motor and premotor cortices were activated.
It is important to note that the neurological abnormalities found in adults does not conclude if childhood stuttering caused these abnormalities or if the abnormalities cause stuttering. Future research should address a longitudinal case study to track the development of brain structure in relation to stuttering.
Physiopathology of developmental stuttering
Much evidence from neuroimaging techniques has supported the theory that the right-hemisphere of stutterers interferes of left-hemisphere speech production. Additionally, stutterers seem to activate motor programs before the articulatory or linguistic processing is initiated.
Overactivity and underactivity
During speech production, stutterers show overactivity in the anterior insula, cerebellum and bilateral midbrain. They show underactivity in the ventral premotor, Rolandic opercular and sensorimotor cortex bilaterally and Heschl’s gyrus in the left hemisphere. Additionally, speech production in stutterers yields underactivity in cortical motor and premotor areas.
Though neuroimaging studies have not yet found specific cortical correlates, there is much evidence that there are differences in the brain physiology of adults who stutter in comparison to those who do not.
Asymmetry has been found between the left and right planum temporale in comparing stutterers and non-stutterers. These studies have also found that there are anatomical differences in the Rolandic operculum and arcuate fasciculus.
Recent studies have found that adults who stutter have elevated levels of the neurotransmitter dopamine, and have thus found dopamine antagonists that reduce stuttering (see anti-stuttering medication below). Overactivity of the midbrain has been found at the level of the substantia nigra extended to the red nucleus and subthalamic nucleus, which all contribute to the production of dopamine.
Main article: Stuttering therapy
Fluency shaping therapy
Fluency shaping therapy, also known as “speak more fluently”, “prolonged speech” or “connected speech”, trains stutterers to speak fluently by controlling their breathing, phonation, and articulation (lips, jaw, and tongue). It is based on operant conditioning techniques.
Stutterers are trained to reduce their speaking rate by stretching vowels and consonants, and using other fluency techniques such as continuous airflow and soft speech contacts. The result is very slow, monotonic, but fluent speech, used only in the speech clinic. After the stutterer masters these fluency skills, the speaking rate and intonation are increased gradually. This more normal-sounding, fluent speech is then transferred to daily life outside the speech clinic, though lack of speech naturalness at the end of treatment remains a frequent criticism. Fluency shaping approaches are often taught in intensive group therapy programs, which may take two to three weeks to complete, but more recently the Camperdown program, using a much shorter schedule, has been shown to be effective.
Stuttering modification therapy
The goal of stuttering modification therapy is not to eliminate stuttering but to modify it so that stuttering is easier and less effortful. The rationale is that since fear and anxiety causes increased stuttering, using easier stuttering and with less fear and avoidance, stuttering will decrease. The most widely known approach was published by Charles Van Riper in 1973 and is also known as block modification therapy.
Electronic fluency device
Main article: Electronic fluency device
Altered auditory feedback, so that stutterers hear their voice differently, have been used for over 50 years in the treatment of stuttering. Altered auditory feedback effect can be produced by speaking in chorus with another person, by blocking out the stutterer’s voice while talking (masking), by delaying the stutterer’s voice slightly (delayed auditory feedback) and/or by altering the frequency of the feedback (frequency altered feedback). Studies of these techniques have had mixed results, with some stutterers showing substantial reductions in stuttering, while others improved only slightly or not at all. In a 2006 review of the efficacy of stuttering treatments, none of the studies on altered auditory feedback met the criteria for experimental quality, such as the presence of control groups.
The effectiveness of pharmacological agents, such as benzodiazepines, anti-convulsants, anti-depressants, antipsychotic and antihypertensive medications, and dopamine antagonists in the treatment of stuttering has been evaluated in studies involving both adults and children. A comprehensive review of pharmacological treatments of stuttering in 2006 concluded that few of the drug trials were methodologically sound. Of those that were, only one, not unflawed study, showed a reduction in the frequency of stuttering to less than 5% of words spoken. In addition, potentially serious side effects of pharmacological treatments were noted, such as weight gain and the potential for blood pressure increases. There is one new drug studied especially for stuttering named pagoclone, which was found to be well-tolerated “with only minor side-effects of headache and fatigue reported in a minority of those treated”.
Support groups and the self-help movement
With existing behavioral, prosthetic, and pharmaceutical treatments providing limited relief from the overt symptoms of stuttering, support groups and the self-help movement continues to gain popularity and support by professionals and people who stutter. One of the basic tenets behind the self-help movement is that since a cure does not exist, quality of living can be improved by not thinking about the stammer for prolonged periods. Psychoanalysis has claimed success in the treament of stuttering, such as the therapy used on King George in “The King’s Speech.” Mere acceptance of this so called “disorder”, displays a complete lack of self-confidence and a “give-up” attitude. Support groups further focus on the fact that stuttering is not a physical impediment but a psychological one.
Several treatment initiatives advocate diaphragmatic breathing (or costal breathing) as a means by which stuttering can be controlled. Performing vocal artists, who have strengthened their diaphragm, tend to stutter when speaking but not when singing because singing involves voluntary diaphragm usage while speaking involves involuntary diaphragm usage primarily.
Among preschoolers, the prognosis for recovery is good. Based on research, about 65% of preschoolers who stutter recover spontaneously in the first two years of stuttering, and about 74% recover by their early teens. In particular, girls seem to recover well. For others, early intervention is effective in helping the child achieve normal fluency.
Once stuttering has become established, and the child has developed secondary behaviors, the prognosis is more guarded, and only 18% of children who stutter after five years recover spontaneously. However, with treatment young children may be left with little evidence of stuttering.
The stuttering mindset is more deeply ingrained in adult stutterers. With adult stutterers, there is no known cure, though they may make partial recovery or even complete recovery with intervention. Stutterers often learn to stutter less severely and be less affected emotionally, though others may make no progress with therapy.
The lifetime prevalence, or the proportion of individuals expected to stutter at one time in their lives, is about 5%, and overall males are affected two to five times more often than females. Most stuttering begins in early childhood, and studies suggest that 2.5% of children under the age of 5 stutter. The sex ratio appears to widen as children grow: among preschoolers, boys who stutter outnumber girls who stutter about two to one, or less. but widens to three to one at first grade and five to one at fifth grade, due to higher recovery rates in girls. Due to high (approximately 65–75%) rates of early recovery, the overall prevalence of stuttering is generally considered to be approximately 1%.
Cross-cultural studies of the stuttering prevalence were very active in early and middle of the 20th century, particularly under the influence of the works of Wendell Johnson, who claimed that the onset of stuttering was connected to the cultural expectations and the pressure put on young children by anxious parents. Johnson claimed there were cultures where stuttering, and even the word “stutterer”, were absent (for example, among some tribes of American Indians). Later studies found that this claim was not supported by the facts, so the influence of cultural factors in stuttering research declined. It is generally accepted by contemporary scholars that stuttering is present in every culture and in every race, although the attitude towards the actual prevalence differs. Some believe stuttering occurs in all cultures and races at similar rates, about 1% of general population (and is about 5% among young children) all around the world. A US-based study indicated that there were no racial or ethnic differences in the incidence of stuttering in preschool children. At the same time, there are cross-cultural studies indicating that the difference between cultures may exist. For example, summarizing prevalence studies, E. Cooper and C. Cooper conclude: “On the basis of the data currently available, it appears the prevalence of fluency disorders varies among the cultures of the world, with some indications that the prevalence of fluency disorders labeled as stuttering is higher among black populations than white or Asian populations” (Cooper & Cooper, 1993:197).
Different regions of the world are researched very unevenly. The largest number of studies had been conducted in European countries and in North America, where the experts agree on the mean estimate to be about 1% of the general population (Bloodtein, 1995. A Handbook on Stuttering). African populations, particularly from West Africa, might have the highest stuttering prevalence in the world—reaching in some populations 5%, 6% and even over 9%. Many regions of the world are not researched sufficiently, and for some major regions there are no prevalence studies at all (for example, in China). Some claim the reason for this might be a lower incidence in general population in China.
Lewis Carroll, the well-known author of Alice’s Adventures in Wonderland, was afflicted with a stammer, as were his siblings.
Because of the unusual-sounding speech that is produced and the behaviors and attitudes that accompany a stutter, it has long been a subject of scientific interest and speculation as well as discrimination and ridicule. Stutterers can be traced back centuries to the likes of Demosthenes, who tried to control his disfluency by speaking with pebbles in his mouth. The Talmud interprets Bible passages to indicate Moses was also a stutterer, and that placing a burning coal in his mouth had caused him to be “slow and hesitant of speech” (Exodus 4, v.10)
Galen’s humoral theories were influential in Europe in the Middle Ages for centuries afterward. In this theory, stuttering was attributed to imbalances of the four bodily humors: yellow bile, blood, black bile, and phlegm. Hieronymus Mercurialis, writing in the sixteenth century, proposed methods to redress the imbalance including changes in diet, reduced lovemaking (in men only), and purging. Believing that fear aggravated stuttering, he suggested techniques to overcome this. Humoral manipulation continued to be a dominant treatment for stuttering until the eighteenth century. Partly due to a perceived lack of intelligence because of his stutter, the man who became the Roman Emperor Claudius was initially shunned from the public eye and excluded from public office.
In and around eighteenth and nineteenth century Europe, surgical interventions for stuttering were recommended, including cutting the tongue with scissors, removing a triangular wedge from the posterior tongue, and cutting nerves, or neck and lip muscles. Others recommended shortening the uvula or removing the tonsils. All were abandoned due to the high danger of bleeding to death and their failure to stop stuttering. Less drastically, Jean Marc Gaspard Itard placed a small forked golden plate under the tongue in order to support “weak” muscles.
Notker Balbulus, from a medieval manuscript.
Italian pathologist Giovanni Morgagni attributed stuttering to deviations in the hyoid bone, a conclusion he came to via autopsy. Blessed Notker of St. Gall (ca. 840–912), called Balbulus (“The Stutterer”) and described by his biographer as being “delicate of body but not of mind, stuttering of tongue but not of intellect, pushing boldly forward in things Divine,” was invoked against stammering.
Famous Englishmen who stammered were King George VI and Prime Minister Winston Churchill, who led the UK through World War II.
George VI went through years of speech therapy, most successfully under Australian speech therapist Lionel Logue, for his stammer. This is dealt with in the Academy Award-winning film The King’s Speech (2010) in which Colin Firth plays George VI. The film is based on an original screenplay by David Seidler who also used to stutter as a child until age 16.
Churchill claimed, perhaps not directly discussing himself, that “[s]ometimes a slight and not unpleasing stammer or impediment has been of some assistance in securing the attention of the audience…” However, those who knew Churchill and commented on his stutter believed that it was or had been a significant problem for him. His secretary Phyllis Moir in her 1941 book ‘I was Winston Churchill’s Private Secretary’ commented that ‘Winston Churchill was born and grew up with a stutter’. Moir writes also about one incident ‘It’s s s simply s s splendid” he stuttered, as he always did when excited.’ Louis J. Alber, who helped to arrange a lecture tour of the United States wrote in Volume 55 of The American Mercury (1942) ‘Churchill struggled to express his feelings but his stutter caught him in the throat and his face turned purple’ and ‘Born with a stutter and a lisp, both caused in large measure by a defect in his palate, Churchill was at first seriously hampered in his public speaking. It is characteristic of the man’s perseverance that, despite his staggering handicap, he made himself one of the greatest orators of our time.’
For centuries “cures” such as consistently drinking water from a snail shell for the rest of one’s life, “hitting a stutterer in the face when the weather is cloudy”, strengthening the tongue as a muscle, and various herbal remedies were used. Similarly, in the past people have subscribed to theories about the causes of stuttering which today are considered odd. Proposed causes of stuttering have included tickling an infant too much, eating improperly during breastfeeding, allowing an infant to look in the mirror, cutting a child’s hair before the child spoke his or her first words, having too small a tongue, or the “work of the devil.”
Notable personalities who have stuttered include actress Marilyn Monroe, U. S. Vice President Joe Biden, Scatman John, British politicians Jack Straw and Ed Balls, actors James Earl Jones and Sam Neill, authors John Updike and Margaret Drabble, journalist John Stossel, singer Carly Simon, sportscaster Bill Walton, and singer Mel Tillis.
Jazz and Euro Dance musician Scatman John wrote the song “Scatman (Ski Ba Bop Ba Dop Bop)” to help children who stutter overcome adversity. Born John Paul Larkin, Scatman spoke with a stutter himself and won the American Speech-Language-Hearing Association’s Annie Glenn Award for outstanding service to the stuttering community.
Fiction character Albert Arkwright from British sitcom Open All Hour, stammered and much of the series’ humour revolved around this. Recurring character Reginald Barclay from the Star Trek television franchise and the Emperor Claudius from the I, Claudius series by Robert Graves and acted by Derek Jacobi are portrayed as suffering from and overcoming their stuttering.
Cartoon character Porky Pig has a notable stutter. This arose because his original voice artist, Joe Dougherty, had an authentic stammer. However, Dougherty’s stutter caused recording sessions to take longer than otherwise necessary, and so Warner Bros. replaced him with Mel Blanc, who provided Porky’s voice for the rest of his life. Porky’s stutter is probably most pronounced when he says “Th-th-th-that’s all, folks!” Also a stutterer is the cartoon character Keswick from TUFF Puppy.
Superior olivary complex – a nucleus in the auditory central nervous system, located just after cochlear nucleus and prior to lateral lemniscus.
Swimplugs: Material used to keep water out of the ear canal. They can be custom or non-custom made and are often used to prevent infections that can result from water getting into the ear canal or middle ear cavity.
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