Dr.George Thomas Kovai Hearing,Speech and Balance Centre
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Kovai Hearing Speech & Balance Centre,
7A, Artsan towers,
Ramanathapuram, ( South India )
Coimbatore - 641045
Telphone: 0422 - 4390909
Mobile:(o) 9994390909
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Hearing, Speech and balance disorders are present in a high percentage of the population. They form a large percentage when compared to other disorders. Many of these patients go undetected and are usually discovered on routine examination. When they are diagnosed at an early stage and proper intervention is carried out appropriately, their prognosis in the long term is good. Early detection and intervention programes will help in identifying many children who have these impairments. Research conducted all over the world has made it clear that early detection and invention will overcome many of the problems, these children encounter. Neural plasticity for sensory inputs is maximum during the early years of life, this implies that if active input in the form amplification for example is given during the early periods of growth the nervous system is capable of moulding, receiving and accommodating to the changes. There are certain critical periods for sensory inputs during the early stages and if the necessary input is not given during this critical period the child may lose this function permanently.
The rule of the thumb, as far as the brain is concerned is “use it or lose it”. When considering amplification for hearing impairment this has to be implemented even as early as six months for proper development of the auditory pathway and speech centres.
Hearing, speech and balance are all interrelated problems, if there is pathology in one of these systems, it might lead to problems in the other. It is therefore necessary to consider hearing speech and balance disorders as a single entity, and a detailed examination is required of all the systems.
About half of all profound childhood hearing impairment, and significant but unknown proportion of late onset or milder impairment is caused by mutations at single genetic loci. Remarkable progress has been made in the last decade in mapping and identifying the genes involved. There is no universal correct way to identify the gene underlying a genetic disease. The rule of the thumb is in testing a candidate gene for mutations. One gene is chosen from among the 1, 30, 000 or so in the human genome. If it happens to be correct gene, then people with the disease should have mutations in that gene.DNA from patients is analyzed to see if the sequence of the gene differs from the normal sequence.
One of the major influences on the psychological development of the hearing impaired child is the age at which diagnosis is made. More than 90% of hearing impaired children is born into hearing families and, unless there are other handicap that might prompt early hearing screening, many hearing impaired children are not diagnosed for anything up to three years. Such a late discovery of a hearing impairment can have a significant and far reaching impact on the child, their parents and on the relationship between them.
Children born with a hearing impairment are not aware of their handicap and will confront the tasks of development with the same enthusiasm as any other infant.The only tool they lack for the job is audition. Deafness is an invisible handicap. Sensory deprivation limits the world of experience; unfortunately deafness can cut off a person from the world of people. Out of sight really can be out of mind and limit the baby’s anticipatory reactions to the presence of his parents.
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The ear consists of three components: The external ear, middle ear, inner ear. The cochlea is the hearing mechanism inside the inner ear. It converts sound ways entering the inner ear from mechanical to electrical energy. These waves cause the movement of tiny hair cells within the cochlea. As these hair cells vibrate, they send signals to the brain, which can then be interpreted as sound. The inner ear also plays an important role in maintaining balance. The three types of hearing loss are conductive, sensorineural and mixed, conductive hearing loss occurs when the external or middle ear fails to work properly, blocking sounds from being transferred to the inner ear. Sensory hearing losses are caused by disorders in the inner ear, specifically, the cochlea this type of hearing loss may be congenital (present at birth), resulting from abnormal cochlea development or inherited conditions. Another cause of sensorineural hearing is retrocochlear hearing loss. It is related to actual problems arising in the hearing nerve or parts of the brain that process speech.

A diagnosis of profound bilateral deafness, whether at three weeks, six months, nine months or later, is a shock to parents and generates questions that reflect their feeling of deep anxiety and uncertainty about the prospects of the child. Will he or she talk? How will we talk with him or her? Must we learn sign language? and so forth. Parents know from the outset that deafness from birth imposes a severe threat to the development of language and communication and they want to do the best thing for their child.

The three major communication options are total communication, sign bilingualism and auditory oral.


Total communication: Involves the use of all methods of communication –sign, gesture, finger spelling, speech, hearing, lip movements and facial expressions. It is not intended that signs, finger spelling, and so forth, will replace speech: the use of hearing and making maximum use of residual hearing using the best possible amplification is essential in total communication. The idea is that visual communication will support audition and speech.

Sign bilingualism: This approach incorporates natural sign language and demands that it should begin as soon as the infant’s deafness has been identified the sign language developed by deaf people the world over can express their ideas and communicate with others in a manner that does not depend on hearing.
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The auditory-oral approach: This is the present day approach that is being practiced in most centres.the current auditory-oral position stakes its claim primarily on the fact that all children have residual hearing and with the aid of recent technology, hearing can be enhanced to provide sufficient auditory information to the deaf child to enable speech to be perceived and produced. The major advances in technology are digital programmable smart hearing aids that give a clear speech signal, which reduce background noise to suit the needs of an individuals hearing impairment along with cochlear implant at the earliest.Early detection and intervention of hearing impaired patients and by providing proper amplification in the form hearing aids can give desired effects. This means that sensorineural hearing impairment can be detected at birth and hearing aids fitted within the first month of detection. The importantance of amplifying the hearing of severely and profoundly deaf children during the first six months cannot be underestimated: the first months of life has been shown by scientists to be crucial to the development of the auditory processing mechanisms of the brain. If the deaf child’s auditory mechanisms can be activated during this early period, then hearing aid rejection is unlikely, thus the foundations for speech discriminations are laid in a similar manner to those of hearing children. indeed research from the US on speech perception and speech production of deaf children diagnosed and fitted with hearing aids before six months offers the remarkable but welcome finding that the appropriate spoken language reception and production can be expected in most deaf children.

The ultimate goal of all those involved in the management of the child with hearing impairment is for the child to grow up into a socially well adjusted,integrated,competent adult, with good communication skills, good employment prospects, and above all, one who is happy. In order to achieve this, the professional involved in the care of the child should aim at a number of targets, such as early identification, effective amplification (hearing aids) and language competency appropriate to the child’s maturity. With optimal educational facilities children can then access to the curriculum, and make friends and be integrated within their peer groups.

Professionals are faced with the dilemma of detecting hearing impairment early in order to ensure rapid habilitation of the child. overall: the benefits of early amplification are known to facilitate normal language acquisition. Speech and language therapy is concerned with developing interactive skills, attention-getting devices, and child-directed speech.

The aim of amplification is to compensate for the hearing impairment and thus make speech accessible. Properly fitted hearing aids which are programmed to the hearing loss of the child is a highly delicate procedure, if fitting is not done properly to give the desired benefit it will lead to rejection of the hearing aid. Ultimately for the child to be happy in his or her environment the system has to fit the child, not the child be made to fit in the with the existing system.

Although deaf children have exactly the same linguistic potential as normal hearing children, they will usually face obstacles on the way to becoming competent language users. For instance, children with normal hearing learn some of their language skills by hearing from what others speak. However for deaf children, the quantity and quality of spoken language experienced is reduced, thus making it more difficult for the child to get whatever information it needs to trigger the acquisition of the system.
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Speech and language disorders affect one’s ability to talk, listen, understand, read and write. Such disorders have different causes and may range from a few speech sound errors to repetition of sounds or words to a total loss of ability to use speech to communicate effectively. The prevalence of speech disorders in young children is 8-9%. By the first grade roughly five percent of children have noticeable speech disorders; the majority of these speech disorders have no known cause. Language disorders are also found in adults who have failed to develop normal language because of childhood autism, hearing impairment, other developmental or acquired disorders of the brain.

A speech disorders is an impairment of the articulation of speech sounds, fluency or voice.

Fluency disorders - An interruption in the flow or rhythm of speech characterized by hesitations, repetitions, or prolongations of sounds syllables, words, or phrases.

Articulation disorders - Difficulties with the way sounds are formed and strung together, usually characterized by substituting one sound for another(wabbit for rabbit),omitting a sound(han for hand), and distorting a sound (ship for sip)

Voice disorders - Characterized by inappropriate pitch (too high, too low, never changing, or interrupted by breaks); quality (harsh, hoarse, breathy, or nasal); loudness, resonance, and duration.

Form of language: Phonology is the sound system of a language and the rules that govern the sound combinations.

Morphology is the system that governs the structure of words and the constructions of word forms.

Syntax is the system that governs the order and combination of words to form sentences and relationship among the elements within a sentence.

Content of language: semantics is the system that governs the meanings of words and sentences.
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Function of language: Pragmatics is the system that combines the language components (phonology, morphology, syntax, and semantics)in functional and socially appropriate ways. Language disorders may include: impaired language development – characterized by a marked slowness or gaps in the development of language skills.

Aphasia – The loss of acquired language abilities, generally resulting from stroke or brain injury.

Language is a critical barometer of both cognitive and emotional development. Mental retardation may first become apparent with delayed speech at approximately two years.

Child abuse and neglect are correlated with delayed language. Particularly the ability to convey emotional states. Language plays a critical part in the regulation of behavior through internalized “private Speech” in which a child repeats adult prohibitions first audibly and then mentally. Language also allows children to express feelings, such as anger or frustration, without acting them out; consequently, language-delayed children show higher rates of tantrums and other externalizing behaviors.

Speech-language pathologists assist children who have communication disorders in various ways. They provide individual therapy for the child; consult with the child’s teacher about the most effective ways to facilitate the child’s communications in the class setting; and work closely with the family to develop goals and techniques for effective therapy in class and at home. The speech-language pathologist may assist vocational teachers and councilors in establishing communication goals related to the work experiences of student and suggest strategies that are effective for the important transition from school to employment and adult life.

Speech-Language Pathology: is the study of human communication disorders. This includes disorders of speech and language, which have a congenital or acquired origin.

Speech: is a motor act where sounds are modified in meaningful combinations by the lips, tongue, teeth, palate, vocal cords, and lungs for communication.

Language: is a system of arbitrary symbols intended to represent concepts and ideas. It is rule-governed and shared by a given community. Normally, we use oral (Verbal), gestural (non-verbal) and written language to communicate.
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Communication: is the exchange of information through a two-way interaction requiring participation of a sender and a receiver. If the sender does not speak clearly or intelligibly, his/her message may not be received in the correct form. In the same way if the receiver has difficulty in understanding language, or has a sensory impairment such as hearing loss he or she may not be able to decode the message.

The normal speech language skills can be broken down due to various congenital or acquired reasons. Some of the common conditions affecting the normal process of speech and language skills are listed below.

Mental Retardation: Mental retardation is a term used when a person has certain limitations in mental functioning and in skills such as communicating, taking care of him or herself, and social skills. These limitations will result in delayed development of all basic skills. There fore children with mental retardation are found to take longer time to speak, walk, and take care of their personal needs such as dressing or eating. They may require a special schooling and professional help.

Autism spectrum disorders: Autism spectrum disorders (ASDs) are a group of pervasive developmental disorders characterized by significant impairments in social interaction, communication and the presence of unusual behaviors and interests. The onset of the disorder is before three years of age. Severity can vary from mild to moderate. Unusual behavioral patterns, deficient communication skills and lack of social interaction are the triad features typical of Autism.

Celebral Palsy:Cerebral palsy refers to a group of disorders that affect the motor skills of a person. The ability to move and maintain balance and posture is affected. People with cerebral palsy have damage to the motor areas of the brain. There is abnormality in the muscle tone leading to lack of motor control. It is due to a nonprogressive brain abnormality.

Specific language Impairment(SLI): SLI is a developmental language disorder in the absence of frank neurological, sensori-motor, non-verbal cognitive or social emotional deficits (Watkins, 1994). Children with SLI lag behind their peers in language production and language comprehension, resulting in learning and reading disabilities in school. Specific language impairment can present in the form of either receptive language impairment or expressive language impairment or both.
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Articulation Disorders: "Articulation" is the production of speech sounds. Incorrect production of speech sounds (Misarticulation) could be due to various organic etiologies such as cleft palate, cleft lip, tongue-tie or other dysfunctions related to oral cavity structures. Misarticulations could also be due to functional reasons. Misarticulations due to a language processing difficulty are referred as phonological disorder. Adults and children can have articulation problems. An appropriate speech therapy can help one to outgrow this problem.

Aphasia: "Aphasia" is the most common cause of language impairment in adults caused by damage to the areas of the brain responsible for language function. Damage to the brain can be caused by stroke, tumor or head injury. Different aspects of language can be affected to varying degrees depending on the location and severity of the damage. Damage to Broca's area, a region in the frontal lobe of the left hemisphere, results in expressive aphasia (Broca's aphasia). This causes impairment in the ability to produce language. Damage to Wernicke's area, a region in the left temporal lobe, results in receptive aphasia, or Wernicke's aphasia. This impairs one's ability to understand language. Things are not usually so clear-cut in reality. Individual differences in brain function and differences in location and spread of damage mean that impairment is unique to the individual.

Stuttering: Stuttering refers to dysfluency in speech. Dysfluencies that are more characteristic of stuttering include sound, syllable or whole word repetition, prolongations (unnatural stretching out of sounds), and blocks (sound gets stuck and can't come out). Severity of stuttering can vary from mild to severe depending on the frequency of occurrence of blocks. An effective speech therapy can help the people suffering from stuttering to lead a better quality of life.

Voice: Voice disorder is suspected when ones voice is too loud or too soft or is too high or low pitched. Voice disorders are divided into 2 categories: organic voice disorders and functional voice disorders. Organic voice disorders stem form disease or pathology. They require medical intervention. Organic voice disorders include cancer, vocal fold paralysis, endocrine changes, granuloma, heamangioma, papilloma and laryngeal web. Functional voice disorders result from abuse or misuse of the voice. Misuse of the voice includes talking too much or too loudly, yelling, or using an unnatural pitch (faking a deep or high voice). Abuse occurs with nonverbal vocal behavior such as excessive throat clearing, laughing, crying, coughing and smoking. Misuse and abuse can cause physiological changes to the vocal folds, creating vocal nodules, polyps, contact ulcers and edema. These conditions can often be managed by voice therapy.
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Apraxia: Apraxia is a motor disorder in which volitional or voluntary movement is impaired without muscle weakness. The ability to select and sequence movements is impaired. Apraxia can be developmental or acquired. Developmental apraxia is seen in children but no definite lesion sites in the brain are attributed. Acquired apraxia can result from stroke, head injury, brain tumors, toxins, or infections. Treatment approaches vary depending on the severity of the disorder.

Dysarthria: Dysarthria is a speech disorder that is due to a weakness or in coordination of the speech muscles. Speech is slow, weak, imprecise or uncoordinated. Cerebral palsy is the most common childhood dysarthria. In adults, dysarthria is can be caused by stroke, degenerative disease (Parkinson's, Huntington's, amyotrophic lateral sclerosis, multiple sclerosis, myasthenia gravis), infections (meningitis), brain tumors, and toxins (drug or alcohol abuse, lead poisoning, carbon monoxide, etc.).

Language development chart listed below gives a short summary of major language developmental milestones expected at each age intervals.

Age of the child in months Language development
0-6
  • Vocalization with intonation
  • Responds to his name
  • Responds to friendly and angry tones
6-12
  • Uses one or more words with meaning (spoken in context)
  • Understands simple instructions.
  • Uses gestures to attain needs
12-18
  • Has vocabulary of approximately 5-20 words
  • Produces jargon utterances with emotional content
  • Is able to follow simple commands
18-24
  • Can name a number of objects in the surroundings
  • Is able to use at least two prepositions.
  • Combines words into a short sentence.
  • Vocabulary of approximately 150-300 words.
  • Can use two pronouns correctly: I, me, and you.
  • Responds to such commands as "show me your eyes (nose, mouth, hair)"
24-36
  • Use pronouns I, you, me correctly.
  • Is using some plurals and past tenses.
  • Knows at least three prepositions, usually in, on, under
  • Knows chief parts of body
  • Handles three word sentences easily
  • Has in the neighborhood of 900-1000 words
  • Verbs begin to predominate
  • Relates his experiences so that they can be followed with reason
  • Able to reason out such questions as "what must you do when you are sleepy, hungry, cool, or thirsty?"

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The ability of man to walk upright on two legs and keep equilibrium is dependent on the integrity of a complex system consisting of the three major ‘receptor organs’. The impulses from the vestibular part of the inner ear, the eyes and somatosensory stimuli form skin, muscles, tendons and joints are so harmoniously balanced that, under normal conditions, they are integrated subconsciously.

The first sensory organ to be formed is the inner ear,which by midterm is fully differentiated.in fact all the sensory systems are structurally fully developed at birth and it is just a matter of learning and adaptation that completes the maturation.at birth the newborn infant experiences a new world, where there is sudden exposure to new kinds of movements and positions.

The task of keeping good balance is performed by three different systems.
    - The vestibular system (organ of balance situated in the inner ear)
    - The visual system (organ of sight – eyes)
    - The somatosensory / proprioceptive system (skin and joints of the bones)

A balance disorders is a disturbance that causes an individual to feel unsteady,giddy,or have a sensation of movement, spinning or floating.An organ in our inner ear,the labyrinth is an important part of our vestibular system, to maintain the body’s position.These systems, along with the brain and the nervous system can be the source of the balance problems.

The balance system works with the visual and skeletal systems (the muscles and joints and their sensors) to maintain orientation or balance.For example, visual signals are sent to the brain about the body’s position in relation to its surroundings.These signals are processed by the brain,and compared to information from the vestibular and the skeletal systems.An example of interaction between the visual and vestibular systems is called vestibular-ocular reflex.nystagmus(an involuntary rhythmic eye movement)that occur when a person is spun around and then suddenly stops is an example of a vestibularocular reflex.

When balance is impaired ,an individual has difficulty in maintaining orientation,for example,an individual may experience the “room Spinning” and may not be able to walk without straggering,or may not even be able to arise.Some of the symptoms a person with a balance disorders may experience are:

  1. A sensation of dizziness or vertigo (spinning).
  2. Falling or a feeling of falling.
  3. Light-headedness or felling woozy.
  4. Visual blurring.
  5. Disorientation.
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Some individuals may also experience nausea and vomiting,diarrhoea,faintness,changes in heart rate and blood pressure,fear,anxiety, or panic.Some react to the symptoms of fatigue, depression and decreased concentration.The symptoms may appear and disappear over short time periods or may last for a longer period of time.

Infections(viral or bacterial),head injury,disorders of blood circulation affecting the inner ear or brain,certain medications, and ageing may change our balance system and result in a balance problem.Individuals who have illnesses,brain disorders,or injuries of the visual or skeletal systems,such as eyes muscles imbalance and arthritis,may also experience balance difficulties.A conflict of signals to the brain about the sensation of movement can cause motion sickness (for instance,when an individual tries to read while riding in a car).Some symptoms of motion sickness are dizziness,sweating,nausea,vomiting,and generalized discomfort.Balance disorders can be due to problems in any of the four areas:

  1. Peripheral vestibular disorders, a disturbance in the labyrinth.
  2. Central vestibular disorder, a problem in the brain or its connecting nerves.
  3. Systematic disorders, a problem of the body other than the head and brain.
  4. Vascular disorders or blood flow problems.
Balance training programmers for those suffering from a vestibular deficiency whether it is acute or chronic are instituted.Findings in recent year have stressed the fact that vestibular rehabilitation is necessary. The central nervous system seems to have a large capacity of central compensation,adaptation and plasticity but it needs ‘clever’ exercises.

It is important,in vestibular rehabilitation, to stimulate the vestibular, visual and somatosensory systems and their interaction.The vestibular system performs best at rather high frequencies and velocities, whereas the visual systems displays a maximum capacity at lower velocity.The best rehabilitation for children is playing and sport activities. when experiencing an acute vestibular loss it is necessary to start activities as soon as possible,these can be physical activities,depending on age,include table tennis and bicycling,if the child is fond of swimming,use goggles so that the child can use vision.Make sure that activities following a vestibular loss are carried out in sufficient light,at least in the beginning.

Hearing,speech and balance disorders are commonly encountered in children with disabilities,it is mandatory that they be identified at the earliest and appropriate treatment and management of these cases instituted.Early intervention will help in preventing impairment disability and handicap,the prognosis and out come measures following early diagnoses and intervention willl go a long way in the well being of the individual concerned and help him lead a normal life similar to his peers.
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Three forms of peripheral vestibular disorders, each with its typical symptoms and clinical signs, can be differentiated;

- Bilateral peripheral loss of vestibular function (bilateral vestibulopathy). The main symptoms are oscillopsia during head movements (failure of the vestibule-ocular reflex) and instability of gait and posture. The latter two symptoms increase in darkness and on uneven ground (due to reduced or absent visual or somatosensory information).

- Acute/subacute unilateral failure of vestibular function (labyrinth and / or vestibular nerve), which causes a vestibular tonus imbalance. Main symptoms are rotatory vertigo (for a few days or weeks), nausea, oscillopsia and a tendency to fall in a certain direction.

- Inadequate paroxysmal stimulation of the peripheral vestibular system of the labyrinth (e.g., during benign paroxysmal positioning vertigo) or of the vestibular nerve (e.g., during vestibular paroxysmia due to ectopic discharges). The main symptoms are attacks of rotatory or postural vertigo.

PATIENT HISTORY:
The main symptoms of an attack of Meniere’s disease include rotatory vertigo with spontaneous nystagmus and a tendency to fall in a certain direction, nausea and vomiting, and “ear symptoms” such as tinnitus, reduced hearing and a feeling of fullness in one ear. Single attacks usually last several hours and mostly have no antecedent signs or recognizable precipitating factors. They occur both in daytime and at night. One-third of patients, however, report that increased tinnitus and hearing loss, as well as a subjective feeling of fullness of the ear, precede the vertigo attack (aura). Monosymptomatic attacks that are purely cochlear or vestibular can occur, particularly at the beginning of Meniere’s disease. During the course of the disease most patients develop a persistent hypoacusis of the affected ear.

Clinical Syndrome and Cource: Meniere’s disease is typically a combination of abruptly occurring attacks with vestibular and / or cochlear symptoms, fluctuating, slowly progressive hearing reduction, and in the course of time tinnitus. During the attack there is first a unilateral short vestibular excitation, then a temporary vestibular deficit with the follow clinical findings:
  • During the initial vestibular excitation: ipsiversive rotatory vertigo and ipsiversive nystagmus,
  • During the vestibular deficit: contraversive rotatory vertigo and contraversive nystagmus,
  • In addition there are cochlear symptoms in the form of tinnitus, reduced hearing of the affected ear, as well as pressure and a feeling of fullness in the ear, and
  • Deviation of gait and a tendency to fall.
The diagnosis of monosymptomatic forms is frequently difficult to determine of indeterminate (see below).The American Academy of Ophthalmology and Otolaryngology, Head and Neck Surgery formulated the following diagnostic criteria in 1995:

Certain Meniere’s disease:
  • Histopathological confirmation of endolymphatic hydrops.
  • Symptoms as in “definite Meniere’s disease” criteria Definite Meniere’s disease.
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Definite Meniere’s disease:
  • Two or more attacks of vertigo, each lasting more than 20 min.
  • Audiometrically documented hearing loss in at least one examination.
  • Tinnitus or aural fullness in the affected ear.
  • Other causes excluded Probable Meniere’s disease.

Probable Meniere’s disease:

  • Episodic vertigo episode.
  • Audiometrically documented hearing loss in at least one examination.
  • Tinnitus or aural fullness in the affected ear.
  • Other causes excluded .
Possible Meniere’s disease:

  • Episodic vertigo but without documented hearing loss.
  • Sensorineural hearing loss, fluctuating or fixed, with disequilibrium, but without definite episodes of vertigo.
  • Other causes excluded.
It seems to us that these recommendations require improvement in at least two respects: as regards the certainty of the diagnosis of Meniere’s disease and its distinction from other differential diagnoses, since there are several overlaps, e.g., with basilar / vestibular migraine, perilymph fistula and vestibular paroxysmia.

The onset of Meniere’s disease is usually between the fourth and sixth decades; it seldom occurs in childhood or after the eighth decade. Men are affected somewhat more often than women (Sade and Yaniv 1984; Stahle et al. 1978). The disease begins in one ear with very irregular attacks, which at first generally increase in frequency and then decrease in frequency in the course of several years. The patients are initially free of complaints in the attack-free interval, but then develop increasing deficits such as unilateral peripheral vestibular hypo function, unilateral tinnitus and hearing disorder (usually low frequencies). The extent of fluctuation of these deficits is unusual when compared with other inner-ear illnesses.

While the onset of the disease is unilateral, the other ear can also become affected in time. The longer one follows a patient with Meniere’s disease, the more often one sees bilateral illnesses (Morrison 1986). In an early stage (up to 2years’ duration), about 15% of the cases are bilateral; 30-60% of these become bilateral after one to two decades. In the meantime it has become generally acknowledged that the course of Meniere’s disease is on the whole relatively benign, having a remission rate (of the episodes but not of chronic hearing loss) of about 80% within 5-10 years (Friberg et al. 1984). The spontaneous remission of these attacks probably occurs when there is a permanent fistula of the membrane separating endolymph and perilymph, for this would allow the continual, asymptomatic drainage of excess endolymph.
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Aetiology, Pathophysiology and Therapeutic Principles:

Meniere’s disease develops from endolymphatic labyrinthine hydrops with periodical rupturing of the membrane separating the endolymph space from the perilymph space. This triggers attacks that generally last several hours. The overflow of the potassium-rich endolymph into the perilymph space (here ionic ratios are similar to those in the extracellular space) leads to a potassium- induced depolarization of the vestibulocochlear nerve, which causes an initially temporary excitation and finally a block of conduction, as the fast sodium canal can no longer switch into an active state due to the stronger depolarization. The cause of hydrops is an impaired resorption in the endolymphatic sac mainly due to perisaccular fibrosis or an obliteration of the endolymphatic duct, which interrupts the longitudinal endolymph flow.

Endolymphatic hydrops can also occur without symptoms and has either an inflammatory (labyrinthits) traumatic (perilymph fistula), auto immunological or idiopathic aetiology (Schuknecht and Gulya 1983). The attacks generally last several hours, during which the vertigo changes from an acute rotatory vertigo into a postural vertigo, which later turns into a gait instability. In rare cases the first phase of the acute attacks can also be characterized by a brief, severe rotatory vertigo or a sudden drop attacks due to the hydrops and shifting of the otoliths (Tumarkin’s otolithic crises, see below).

Despite various indications that an inflammatory origin or an auto immunological process is involved, so far prospective studies on immune-inhibiting medications are lacking. Reviews of the literature covering a large number of therapy studies have agreed that positive effects on the frequency of attacks have been confirmed for only betahistine and diuretics (Claes and van de Heyning 1997; James and Thorp 2001). For this reason the H1 agonist and H3 antagonist betahistine is currently recommended as the prophylactic therapy of first choice. It improves the microcirculation by acting on the precapillary sphincters of the stria vascularis and at the same time exercises a regulating influence by means of the H3 receptors on the vestibular nuclei (Van Cauwenberge and de Moor 1997; Yabe et al. 1993). This possibly leads to reduced production and increased resorption of the endolymph. A placebo-controlled double-blind study has shown that it has a significant influence on the natural course of the disease, especially on the vestibular symptoms (Meyer 1985). The production of endolymph can also be reduced by the method suggested by Schuknecht, i.e., “switching off the inner ear” by the instillation and diffusion of ototoxic antibiotics (e.g., gentamycin), which may also lead to destruction of the hair cells. In the meantime this method has been so refined that it is possible to selectively affect the secretory epithelium while largely sparing the vestibular and cochlear sensory cells.

Besides avoiding any further attacks of Meniere’s disease and treating acute attacks, another important principle of treatment is to promote central compensation of the peripheral vestibular deficits by means of physical therapy.
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Pragmatic Theraphy:

  • Treatment of Attacks . The acute attacks are itself limited. Vertigo and nausea can be reduced by antivertiginous drugs used in other acute disorders of labyrinthine function, e.g. dimenhydrinate 100 mg as suppository or benzodiazepine.
  • Prophylactic Therapy . The goal of prophylactic treatment is to reduce the endolymphatic hydrops. Therefore in cases of repeating attacks of rotatory vertigo, possibly with fluctuating loss of inner-ear hearing, tinnitus or pressure in the ear, the following treatment is indicated;
  • Betahistine,3x2 tablets/day containing 20-24 mg for 6-12 months; dose can be tapered depending on course (the patient should keep a vertigo diary, in order to document the effects of therapy).
  • If improvement is insufficient, hydrochlorothiazide plus triamterene (a half to one tablet in the mornings) can be administered in addition to betahistine.
Otolaryngologists recommend administration of steroids or a salt-free diet; however, no studies have yet proven their efficacy. In rare cases of frequent Meniere’s attacks (with or without inner-ear hearing loss) that are refractory to drug treatment:
  • Intratympanic instillations of ototoxic antibiotics are indicated (e.g., 1-2ml gentamycin at concentrations of 20-40 mg/ml) at interims of 2 or, better, more weeks.

    Instillations used to be done on a daily basis until Magnusson at al. (1991) observed that the onset ofototoxic effects was delayed. Nowadays only single instillations are recommended at interims of several weeks. However, there is still no consensus on the dose and the duration of the interims (Blakely 2000).

    Endolymphatic sac operations used to be performed everywhere and were considered at first to be a type of shunt operation. However, it was realized that they had only a placebo effect (Thomson et al.1981); nowadays they are no longer performed. Currently less than 1-3% of patients are considered for operative measures.
  • Treatment of Vestibular Drop Attacks. (Tumarkin’s Otolithic Crisis):

  • Recurrent vestibular drop attacks (Tumarkin’s otolithic crisis) pose an extreme impairment to patients in their everyday life. Moreover, they are dangerous because of the high rate of injuries. Depending on clinical judgement as to the severity of the disorder, intratympanic gentamycin treatment can be administered with success (Odkvist and Bergenius 1988). The prerequisite for such treatment is that the causative ear can be definitely identified.

  • Ineffective Treatment
    Endolymphatic sac operations are nowadays no longer performed. The efficacy of a large number of conservative treatment programmes (e.g., circulation-promoting measures with vasodilators, low-molecular weight dextrans, hydroxyethyl starches) has not been proven.
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The first attacks of Meniere’s disease must be differentiated from an acute unilateral vestibular deficit, e.g., in connection with vestibular neuritis. Here the duration of the attacks is helpful: whereas in Meniere’s disease they generally last several hours and at most one day, in vestibular neuritis they last several days. The accompanying symptoms are also helpful for the diagnosis, for example, “ear symptoms” in Meniere’s disease and inflamed eye signs and hearing disturbances in Cogan’s syndrome of hearing disorders and possibly central signs of infarctions of the AICA /labyrinthine artery. Central disorders of the ocular motor system or central vestibular function also occur after lacunar infarctions of MS plaques in the area of the entry zone of the VIIIth cranial nerve (“fascicular lesion”). Since a caloric hypo reactivity occurs in all of the above-named diseases, this cannot be used in the differential diagnosis.

Rare, sudden recurrent falls, so-called vestibular drop attacks (Tumarkin’s otolithic crisis), which occur in the early or late stages of Meniere’s disease without definite triggers, antecedent signs or disturbances of consciousness, are difficult to differentiate from drop attacks caused by vertebrobasilar ischaemia (Baloh et al.1990). Such attacks apparently result from fluctuations in endolymphatic pressure caused by unilateral exacerbation of the otoliths and inadequate vestibulospinal postural reaction.

Another important differential diagnosis is basilar/ vestibular migraine, which can manifest not only in the form of short attacks, but also as attacks lasting several hours. Signs that the attacks is a vestibular migraine are: (1) central ocular motor disorders during the attack-free interval, (2) the absence of progressive hearing loss despite many attacks, (3) the association with other neurological symptoms such as numbness of the face (basilar migraine), (4) head and neck pain, and (5) response to prophylactic treatment with beta-blockers. There is increasing indication in the recent literature of a link between Meniere’s disease and vestibular migraine (Radtke et al. 2002). Vestibular paroxysmia, which is caused by neurovascular compression, is also characterized by recurrent attacks with vertigo and/or occasionally other ear symptoms. These attacks, contrary to Meniere’s disease, typically last only seconds.

References

American Academy of Ophthalmology and Otolaryngology (1995) Committee on Hearing and Equilibrium guidelines for diagnosis and evaluation of therapy in Meniere’s disease. Otolaryngol Head Neck Surg 113:181-185 .

Baloh RW, Jacobson K, Winter T (1990) Drop attacks with Meniere’s syndrome. Ann Neurol 28:384-387 .
Blakly BW (2000) Update on intratympanic gentamicin for Meniere’s disease. Laryngoscope 110:236-240 .

Claes J, van de Heyning PH (1997) Medical treatment of Meniere’s disease: a review of literature. Acta Otolaryngol (Stockh ) Suppl 526:37-42 .

Friberg U, Stahle J, Svedberg A (1984) The natural course of Meniere’s disease. Acta Otolaryngol (Stockh) Suppl 406:72-77 .

James A, Thorp M (2001) Meniere’s disease. Clinical Evidence 5:348-355 .

Magnusson M, Padoan S, Karlberg M, Johansson R (1991) Delayed onset of ototoxic effect of gentamicin in treatment of Meniere’s disease. Acta Otolaryngol (Stockh) Suppl 481:610-612 .

Meyer ED (1985) Zur Behandlung des Morbus Meniere mit Betahistinmesilat (Aequamen)- Doppel-blindstudie gegen Placebo (cross over). Laryng Rhinol Otol 64:269-272.

Morrison AW (1986) Predictive test for Meniere’s disease. Am J Otol 7:5-10 .

Odkvist LM, Bergenius J (1988) Drop attacks in Minere’s disease. Acta Otolaryngol (Stockh) Suppl 455:82-85 .

Radtke A, Lempert T Gresty MA et al (2002) Migraine and Meniere’s disease: is there a link? Neurology 59:1700-1704 .

Sade J Yaniv E (1984) Meniere’s disease in infants. Acta Otolaryngol (Stockh ) 97:33-37 .

Schuknecht HF, Gulya AJ (1983) Endolymphatic hydrops: an overview and classification. Ann Otol 92 (Suppl.106): 1-20 .

Stahle J, Stahle C, Arenberg IK (1978) Incidence of Meniere’s disease. Arch Otolaryngol 104:99-102.

Thomson J, Bretlau M, Tos M, Johnson J (1981) Placebo effect in surgery of Meniere’s disease. Arch Otolaryngol 107:271-277 .

Van Cauwenberge PB, De Moor SEG (1997) Physiopathology of H3- receptors and pharmacology of betahistine. Acta Otolayaryngol Stockh) 526:43-46 .

Yabe T, de Waele C, Serafin M etal (1993) Medial vestibular nucleus in guinea-pig: histaminergic receptors. Exp Brain Res 93:249-258 .
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Case Study
A 25-year-old woman who worked as a registered nurse presented with the chief complaint of acute vertigo that began 3 days before evaluation. The patient’s vertigo was associated with nausea and vomiting for several hours. Following this episode, the patient had disequilibrium, gait instability, and a complaint of poor vision for 2 days. She had no associated complaints of hearing loss or tinnitus and no fullness or stuffiness in the ears. There were no complaints of changes in strength or sensation. The patient had experienced a flu-like illness that had begun approximately 2 weeks before that onset of the vertigo. At the time of evaluation, she noticed imbalance in the dark and spatial disorientation, especially after large head movements. She had no significant past medical history, and family history was noncontributory.

Based on the patient’s history, what is the most likely diagnosis?
This patient’s history is consistent with an acute vestibular syndrome characterized by vertigo, nausea, vomiting, blurred vision, and disequilibrium. The absence of auditory symptoms and the prior flu-like illness suggest the possibility of vestibular neuritis. Other, less likely conditions includes endolymphatic hydrops and a demyelinating disorder. The absence of other otologic symptoms argues against endolymphatic hydrops. The absence of nonvestibular neurologic symptoms and the absence of previous neurologic deficits make a demyelinating lesion very unlikely. A demyelinating lesion would have to be located precisely at the root entry zone of the eighth nerve to present in this way.

Physical Examination
Neurological examination revealed a left-beating horizontal-torsional nystagmus on leftward gaze with the upper poles of the eyes beating to the left. The remainder of the cranial nerve examination was normal. Strength, sensation, and coordination were normal. The patient had a negative Romberg’s test. Gait was wide-based, and the patient could not tandem walk. The otologic examination was normal. The neurotologic examination was abnormal. Behind infrared glasses, the patient’s nystagmus increased in intensity; if was now observed in the primary position, and both the frequency and amplitude of the nystagmus were higher. The head thrust test was abnormal, with refixation saccades noted following head rotation from left to right. The patient was unable to stand on a compliant foam surface with her eyes closed without losing her balance. Past-pointing was present with arm deviation to the right. On the stepping, test, the patient rotated almost 180 degrees to the right.

What is the pathophysiology of the patient’s symptoms and signs?
The patient is suffering from an acute vestibular syndrome almost certainly caused by an acute, profound imbalance between the afferent activity from the left and right labyrinths. Because a large difference in neural activity normally occurs only during large head movements, the central nervous interprets an acute loss of vestibular activity on one side as the head rotating briskly toward the intact ear. Patients thus experience vertigo. Vegetative symptoms of nausea, vomiting, and diaphoresis result from activity in the pathways from the vestibular system to the autonomic nervous system.

What is the significance of the patient’s nystagmus being horizontal-torsional?
The patient’s nystagmus is caused by the imbalance in afferent activity from the left and right labyrinths and is probably a result of imbalance semicircular canal activity rather than imbalance of otolith activity. Because of the orientation of the three semicircular canal pairs, the afferent activity from the intact ear, if unopposed by activity in the affected ear, combines to produce a slow component of nystagmus whose direction has specific characteristics. The unopposed left (lesioned) ear, horizontal semicircular canal activity drives the eyes horizontally towards the right, and the combined activity of the two left vertical semicircular canals, that is, the left superior and left posterior semicircular canals causes a slow torsional movement of the eyes, with the upper poles moving towards the right. No vertical component is produce because the left superior semicircular canals tends to drive the eyes up, while the left posterior semicircular canal tends to drive the eyes down, thereby canceling the vertical influences. Thus, the predominantly horizontal-torsional nystagmus suggests a net effect of three unopposed semicircular canals of the patient’s left ear combining to produce a nystagmus whose slow component has a horizontal direction toward the lesioned ear and whose quick component (for which the nystagmus direction is named) beats horizontally toward the intact ear.
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Why did the patient’s nystagmus increase during gaze toward the right and decrease during gaze toward the left?

The alterations in the patient’s nystagmus as a function of eye position in the orbit are typical of most types of nystagmus wherein the intensity of the nystagmus, including its frequency and amplitude, increase when a patient looks in the direction of the quick component. This phenomenon, whereby the magnitude of the nystagmus changes as a function of eye position, is known has Alexander’s law and is illustrated. The physiologic basis for Alexander’s law may relate to an alteration in the neural integrator leading to a combined effect of a vestibular nystagmus and a gaze-evoked nystagmus. For example, when a patient with a right-beating nystagmus looks to the right, both the gaze-evoked nystagmus and the vestibular imbalance causes leftward eye movement, thereby increasing the magnitude of the nystagmus. However, on left gaze, the vestibular imbalance and the gaze-evoked nystagmus oppose on another, thereby decreasing the intensity of the nystagmus.

Vestibular nystagmus, which is unidirectional, is sometimes graded in severity based upon its presence in different horizontal gaze positions. Specifically, Alexander’s system,1 which was originally apply to patient’s observed during visual fixation, includes first-degree, second-degree, and third-degree vestibular nystagmus. In third-degree nystagmus, the nystagmus is unidirectional and can be observed regardless of horizontal gaze position, but the intensity of the nystagmus is maximal with gaze in the direction of the quick component of nystagmus and is minimal, but still observable, when horizontal gaze is directed away from the quick component. In second-degree nystagmus, the nystagmus is observed only when the patient gazes straight ahead or in the direction of the quick component. In first-degree nystagmus, the nystagmus can be observed only with gaze in the directional of the quick component. This patient had a first-degree vestibular nystagmus since left-beating nystagmus was observed only with leftward gaze.

Why is the patient’s nystagmus increased in magnitude when she is wearing infrared glasses?
Vestibular nystagmus, whether physiologic, can be significantly inhibited by visual fixation when vision and visual fixation and visual tracking mechanisms are intact. Infrared or Frenzel glasses allow the patient’s eyes to be observed while they significantly reduce visual fixation. An increase in a patient’s nystagmus on wearing infrared or Frenzel glasses supports the idea that patient’s nystagmus originates from a vestibular imbalance, usually peripheral. Illustrates the influence of loss of visual fixation on the various grades of severity of vestibular nystagmus. Note that in its mildest from, a vestibular nystagmus may be absent with lateral gaze to the right or the left, depending on the direction of the nystagmus. In clinical parlance, a horizontal-torsinal nystagmus that increases in magnitude with loss of visual fixation is called vestibular nystagmus.

Laboratory Testing

Videonystagmography: Ocular motor testing was normal. Testing confirmed the presence of a left-beating spontaneous vestibular nystagmus that increased with loss of visual fixation. Caloric testing revealed absent responses in the right ear, including absent responses to ice-water irrigation:

  • Audiometric testing was normal.
  • An MRI scan of the brain was normal.
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How do results of laboratory testing influence the diagnostic considerations for this case?
The most significant finding on vestibular laboratory testing is the reduced vestibular response in the right ear on caloric testing. Although a unilateral caloric weakness was suspected from the clinical evaluation, laboratory testing provides objective evidence of a severe loss of sensitivity in the right labyrinth, confirming the clinical suspicion.

The normal audiometric test suggests that the patient is suffering from a pure vestibular syndrome such as vestibular neuritis as opposed to a more generalized labyrinthitis, which is commonly associated with a high-frequency hearing loss, or from endolymphatic hydrops, which is often associated with a low-tone sensorineural hearing loss.

Diagnosis / Differential Diagnosis

As noted, this patient is almost certainly suffering from vestibular neuritis (2,3,4). Other names for this condition include vestibular neurolabyrinthitis, vestibular labyrinthitis, vestibular neuronitis, and acute vestibulopathy of uncertain etiology. These terms are used interchangeably. It should be realized that a peripheral vestibular lesion could actually be affecting the hair cells, the eight nerve afferents, or the eighth nerve root entry zone. From the vestibular signs and symptoms alone, a distinction cannot be made among these three localizations. Postmortem temporal bone histopathology suggests that Scarpa’s ganglion is affected primarily (5). Illustrates atrophy of the vestibular nerve thought to be the result of a viral vestibular neuritis. Vestibular neuritis appears to have a predilection for the superior division of the vestibular nerve (6,7). Other entities that should be considered include labyrinthine infarction. It would be rare for a mass lesion such as an acoustic neuroma to present solely with an acute vestibular syndrome without hearing loss, tinnitus, or other neurological signs or symptoms.The patient was given a diagnosis of vestibular neuritis.

Treatment / Management: A short (10- to 14-day) course of corticosteroids, for example prednisone, 1 mg/kg per day, decreases the duration of vestibular symptoms and may also reduce the chance of future recurrent episodes of acute vertigo.(8). Corticosteroids also have been shown experimentally to speed vestibular compensation. Antiviral agents such as acyclovir may be considered since viral reactivation is thought to be involved in the pathogenesis of the condition; however, there are no data to conclusively support its use in this setting (9). This patient was treated with a 2 week course of corticosteroids. Vestibular suppressants and antinausea agents were also prescribed on an as-needed basis for symptomatic relief..

Follow– Up
The patient was seen in follow-up 1 month after the initial presentation. At that time, she was very much improved and experienced symptoms only during rapid head movement, which caused transitory dizziness and lightheadedness, and during walking in dimly lit or dark environments. The patient also noted some difficulty with driving, especially immediately after rapid head movements just before changing lanes.

Physical examination at the 1-month follow-up visit revealed no nystagmus with visual fixation. However, infrared glasses, a low-amplitude, left-beating horizontal-torsional. The patient’s gait had a normal base, but three was some difficulty during tandem walking. The patient was able to stand on a complaint foam pad even with her eyes closed with minimal difficulty. Her rotation on the stepping test improves, rotating only 45 degrees right, and past-pointing was absent.
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The patient was referred for a course of vestibular rehabilitation (10).

By what process did this patient’s symptoms and signs almost completely resolve? Despite the fact that the patient’s vestibular loss in the right ear almost certainly persists, vestibular compensation, a process that involved rebalancing of the activity in central vestibular structures, has occurred. Through this mechanism, vestibule-ocular, vestibulospinal, perceptual and autonomic symptoms and signs improve substantially, although some symptoms (as noted above in this patient) are likely to persist. Vestibular compensation occurs automatically in individuals with a normal central nervous system, normal vision proprioception, and adequate physical activity. This patient’s recovery is typical even for individual who have suffer complete unilateral peripheral vestibular loss. The causes of vestibular compensation is thought to involve brain-stem and cerebellar structures, so that resting activity in the left and right vestibular nuclei becomes more or less balanced despite unilaterally reduced or absent vestibular nerve activity.

Summary
A 25-years old woman presented with the acute onset of a vestibular syndrome indicative of an acute unilateral peripheral vestibular loss. The patient’s history suggested a viral/postviral affliction of the vestibular labyrinth or nerve. Examination revealed horizontal-torsional spontaneous vestibular nystagmus, poor tandem walking, and an inability to stand on a compliant foam surface with the eyes closed. Laboratory testing revealed a right reduced vestibular response. The patient was treated with a 2-week course of corticosteroids. Vestibular suppressant agents and anti nausea agents were used only on an as-needed basis. Through the process of vestibular compensation, the patient’s symptoms decreased dramatically. At the 1 month follow-up evaluation, nystagmus was present only while the patient was wearing infrared glasses, and she could tandem walk and stand on a compliant surface.

Points To Remember
  • An acute unilateral vestibular syndrome is characterized by vertigo, nausea, vomiting, blurred vision, and disequilibrium. These symptoms and signs result from an imbalance between the afferent activity from the left and right labyrinths. The central nervous system interprets this imbalance as a brisk continuous head rotation toward the intact ear.
  • Vegetative symptoms of nausea, vomiting, and diaphoresis caused by activity in the pathways from the vestibular system to the autonomic nervous system.
  • The direction of acute vestibular nystagmus is typically horizontal-torsional. This direction of nystagmus results primarily from the unopposed horizontal semicircular canal afferent activity from the intact side that produces a horizontal direction of nystagmus. The afferent activity from the two intact vertical semicircular canals sum with one another such that torsionaly the upper pole of the eye drifts (torts or rolls) toward the lesioned ear. The vertical eye movement drives of the two vertical semicircular canals cancel one another. The net effect of the three unopposed semicircular canals of the intact ear thus combines to produce a predominantly horizontal-torsional nystagmus whose slow component is toward the lesioned ear and whose quick component (for which the nystagmus direction is named) beats toward the intact ear. (Zee 1985; Curthoys 2000).
  • Alexander’s law, wherein the intensity of nystagmus (including its frequency and amplitude) increases when a patient looks in the direction of the quick component, is typical of most types of nystagmus. The physiologic basis for Alexander’s law may be related to changes in the neural integrator leading to gaze-evoked nystagmus.
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  • Visual fixation inhibits vestibular nystagmus when vision and visual fixation / visual tracking mechanisms are intact. Infrared or Frenzel glasses allow the patient’s eyes to be observed while visual fixation is significantly reduced. Thus, an increase in a patient’s nystagmus when wearing infrared or Frenzel glasses supports the idea that the patient’s nystagmus originates from a vestibular imbalance. In clinical parlance, a horizontal-torsional nystagmus that increases in magnitude with loss of visual fixation is called vestibular nystagmus.
  • Vestibular compensation rebalances the neural activity in central vestibular structures. This process causes a reduction of the symptoms and signs of an acute vestibular syndrome. Through compensation, vestibule-ocular, vestibulospinal, perceptual, and autonomic symptoms and signs of the acute vestibular syndrome largely resolve. Vestibular compensation occurs automatically in individuals with a normal central nervous system, normal vision and proprioception, and adequate physical activity. The process of vestibular compensation is thought to involve brainstem and cerebellar structures, so that resting activity in the left and right vestibular nuclei becomes more or less balanced despite unilaterally reduced or absent vestibular nerve activity. Vestibular neuritis is the diagnostic designation given to an acute vestibular syndrome, without obvious cause, that occurs without auditory or neurological signs or symptoms. The underlying pathogenesis is thought to involve viral activation within the vestibular nerve. Other conditions that can cause an acute vestibular syndrome include endolymphatic hydrops, a demyelinating disorder, and infarction involving the labyrinth or brainstem / cerebellum.
  • Treatment of vestibular neuritis with a short (10- to 14-day) course of corticosteroids may decrease the duration of vestibular symptoms and may improve long-term recovery.
References
Leigh RJ, Zee DS: Neurology of Eye Movements, ed 3. New York: Oxford University Press, 1999.

Dix MR, Hallpike CS: The pathology, symptomotology and diagnosis of certain common disorders of the vestibular system. Proc R Soc Med 45:341-354, 1952.

Coats AC: Vestibular neuronitis. Acta laryngol (suppl) 251:5-28, 1969.

Schuknecht HF, Kitamura K: Vestibular neuritis. Ann Otol Rhinol Laryngol (suppl) 78(90):1-19; 1981.

Baloh RW, Lopez I, Ishiyama A, Wackym PA, Honrubia V: Vestibular neuritis: Clinical pathologic correlation. Otolaryngol Head Neck Surg 114:586-592, 1996.

Fetter M, Dichgan J: Vestibular neuritis spares the inferior division of the vestibular nerve. Brain 119:755-763, 1996.

Gacek RR, Gacek MR: Vestibular neuronitis. Am J Otol 20:553-554, 1999.

Ariyasu L, Byl FM, Sprague MS, Adour KK: The beneficial effect of methylprednisolone in acute vestibular vertigo. Arch Otolaryngol Head Neck Surg 116:700-703, 1990.

Flohr H, Luneburg U: Effects of ACTH on vestibular compensation. Brain Res 248:169-173, 1982.

Strupp M, Arbusow V, Maag KP, Gall C, Brandt T, Vestibular exercises improve central vestibulospinal compensation after vestibular neuritis. Neurology 51(3):838-844, 1998.
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Patient History.
The main symptoms of benign paroxysmal positioning vertigo (BPPV) include brief, sometimes severe attacks of rotatory vertigo with and without nausea, which are caused by rapid changes in head position relative to gravity. Typical triggers include lying down or sitting up in bed, turning around in bed, and also bending over to tie shoelaces, or extending the head in order to look up or do something above the head. If BPPV is elicited while the patient is upright, he is in danger of falling. Attacks of vertigo frequently occur in the morning and are most pronounced during the first change in position after sleep; repeated changes in position cause a transient lessening of the symptoms. The complaints are so typical that diagnosis can often be made solely on the basis of the patient history; occasionally even the affected ear can be identified (“rotatory vertigo only occurs when I lie on my right side”).

Clinical Features and Course.
Benign paroxysmal positioning vertigo is the most common cause of vertigo, not only in the elderly. It is so frequent that about one-third of all over 70-years old have experienced BPPV at least once. This condition is characterized by brief attacks of rotatory vertigo and simultaneous positioning rotatory-linear nystagmus toward the undermost ear. It can be accompanied by nausea. BPPV is elicited by extending the head or positioning the head or body toward the affected ear. Rotatory vertigo and nystagmus occur after such positioning with short latency of seconds in the form of a crescendo/ decrescendo course of maximally 30-60 seconds. The beating direction of the nystagmus depends on the direction of gaze; it is primarily rotating when gaze is to the undermost ear and mostly vertical (to the forehead) during gaze to the uppermost ear. The nystagmus corresponds to an (ampullofugal) excitation of the posterior canal of the undermost ear.

Benign paroxysmal positioning vertigo can appear at any time from childhood to senility, but the idiopathic form is typically a disease of old age, peaking in the sixth to seventh decades. More than 90% of all cases are classified as degenerative or idiopathic (women: men = 2:1), whereas the symptomatic cases (women: men = 1:1) are most frequently caused by head injury (17%) or vestibular neuritis (15%). BPPV also occurs strikingly often in cases of extensive bed rest in connection with other illnesses or after operations. About 10% of the spontaneous cases and 20% of the trauma cases show a bilateral, generally asymmetrically pronounced BPPV.

It is called benign because it generally resolves spontaneously within weeks to months; in some cases, however, it can last for years. We found that the history of the disorder until diagnosis lasted more than 4 weeks in 50% of our patients and more than 6 months in 10%. If not treated, BPPV persisted in about 30% of our patients; another 20-30% had relapses within month’s years (recurrence risk of 15% per year).

Pathophysiology and Therapeutic Principles:
According to the histologically based cupulolithiasis model of Sehuknecht (1969), heavy, anorganic particles (otoconia) of specific weight, which become detached as a result of trauma or spontaneous degeneration from the utricular otoliths of the cupula, settle in the underlying ampulla of the posterior canal. Whereas the cupula normally has the same specific weight as the endolymph, it is heavier with these particles, i.e., the canal is transformed from a sensor of rotatory acceleration into a transducer of linear acceleration. This hypothesis was generally accepted for many years, despite its inability to explain many of the typical criteria of nystagmus in causes of positioning vertigo.

In contrast, the canalolithiasis hypothesis, discussed by Parnes and McClure (1991) and Epley (1992) and proven by Brandt and Steddin (1993), can explain all symptoms of positioning nystagmus. According to this hypothesis, the particles float freely within the endolymph of the canal instead of being firmly attached to the cupula, and the “heavy conglomerate”, which almost fills the canal, is assumed to be the cause of the positioning vertigo. The movement of the conglomerate causes either an ampullofugal or an ampullopetal deflection of the endolymph depending on the direction of the sedimentation. A valid model of the pathomechanism of BPPV must be able to predict the direction, latency, duration and fatigability of the typical nystagmus, as well as changes in these parameters due to other head manoeuvres.
  • Latency. Rotatory vertigo and nystagmus develop as soon as the particles in the canal precipitate due to gravity. This causes a deflection of the cupula, which exceeds the stimulus threshold of the sensory epithelium after 1-5 seconds.
  • Duration. The particles move to and precipitate at the lowest point within the canal after the change in position. Depending on their size and composition, this requires about 10 seconds.
  • Course of Attacks. After the positioning, the particles precipitate away from the canal wall and are accelerated by the forces of gravity. The particles are accelerated from standstill, reach a maximal speed during their fall, and return to standstill at the lowest point in the canal. This explains the temporal crescendo-decrescendo-like course of the attacks; the cupula time constant increases the duration of the nystagmus and vertigo.
  • Direction of Nystagmus. The ampullofugal stimulation of the posterior canal causes eye movements around the axis of ocular rotation, which is perpendicular to the canal plane, by means of the vestibulo-ocular reflex (VOR). To the physician this will appear to be a combination of linear (toward the forehead and the undermost ear) and rotatory eye movements.
  • Reversal of Nystagmus. If the direction of the positioning movement is reversed when sitting up, the particles move in the opposite direction. Now the cupula is deflected in the opposite (ampullopetal) direction. This results in reversal of both the rotatory vertigo and the direction of nystagmus due to inhibition of the vestibular hair cells.
  • Fatigability. The loose particles form a plug or clump, which falls apart more and more during changes in the head position. Small particles cannot cause suction or pressure on the cupula independently of each other, as does a single clump, whose volume almost fills the canal. If the patient holds his head still for several hours (e.g., during sleep), the particles, which had fallen apart before, coalesce into a clump in the lowest place within the canal and again induce vertigo when the head position is changed.
  • Liberatory Manoeuvre. The efficacy of positioning (liberatory) manoeuvres of the head can only be explained by canalolithiasis, i.e., the clot moves freely within the canal. As a result of these manoeuvres, the plug is washed out of the canal and then cannot cause any positioning vertigo (Brandt and Steddin 1993; Brandt et al. 1994). Proceeding from the explanations of cupulolithiasis or canalolithiasis, Brandt and Daroff (1980) were the first to devise an effective exercise programme, which, by means of the simple physical measure of head positioning, loosens the heavy degenerative otolithic material and distributes it into other areas of the labyrinth, where it comes to rest and no longer impairs canal function. Originally the exercises were based on the concept of cupulolithiasis. Nowadays, in accordance with the modification of Semont et al. (1988), we recommend that the patient’s position be changed from the inducing position by a tilt of 180degree to the opposite side. In 1992, Epley proposed another liberatory manoeuvre that involved turning the patient from a supine position into a head hanging position. All these manoeuvres are effective (Hilton and Pinder 2002; Radke et al. 2004) and can be explained by the mechanism of canalolithiasis (Brandt et al. 1994). Only in very rare cases that are refractory to these manoeuvres should surgery, i.e., the obliteration of the canal, be considered (Parnes and McClure 1991).
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Physical Liberatory Manoeuvres
When correctly performed, all three physical liberatory manoeuvres (Semont or Epley liberatory manoeuvres, Brandt-Daroff exercises; are successful in almost all patients (Herdman et al. 1993). We recommend Semont’s liberatory manoeuvre depicted in as the therapy of first choice. The three positioning steps are performed quickly with the aid of a therapist as the patient lies on the examination couch and then by the patient himself at home. It is important that the head of the sitting patient is turned by 45 degree to the healthy ear, in order to put the responsible posterior canal into a position parallel to the plane of movement during the positioning. Relief is thus achieved in about 90% of cases within one week.

The positioning nystagmus toward the uppermost ear indicates that the plug has left the canal, i.e., the therapy was successful. Conversely, positioning nystagmus toward the undermost healthy ear indicates that the liberatory manoeuvre failed and must be repeated.

Epley’s alternative liberatory manoeure requires that the patient’s head and trunk be rotated after being tilted backward into a slightly head-hanging position. This manoeuvre is as effective as Semont’s. If, however, the plug is not dislodged during the outpatient visit, the patient can be quickly instructed how to proceed on his own at home. Series of these exercises should be performed five to tem times per day, preferable three times during the early morning and three times at noon. The manoeuvres seem to be most effective them, since the clot, which develops during rest, can be more easily removed from the canal then single otoconia. As a rule almost all patients are free of complaints after several days or sometimes a few weeks (Hilton and Pinder 2002; Levat et al. 2003). Despite successful liberatory manoeuvres, many patients complain of transient postural vertigo and dizziness afterwards. This can be explained by the partial repositioning of the otoconia toward the otolith organs (i.e., most likely an otolithic vertigo). Patients should be informed in advance about this side-effect of the manoeuvres, which goes away within a few days.

Following effective physical liberation, approximately 50% of patient will experience a recurrence of attacks; most often patients have positioning vertigo in the morning of the day after the manoeuvres. About 20% of such attacks occur in the first two weeks. The estimated recurrence rate per year is 15% and the recurrence rate of BPPV 40 months after treatment is about 50%. This high recurrence rate emphasizes the need for patient counseling. The recurrences are most likely due to reentry of the debris into the posterior canal from the utricular cavity. They should be treated with the same manoeuvre that induced resolution of the initial episode.
  • Surgery. Selective neurectomy (Gacek 1978) is difficult, and there is a risk of a permanent hearing loss. Neurectomy has now been replaced by plugging of the posterior canal (Parnes and McClure 1991; Pace-Balzan and Rutka 1991). It is evidently a safer and more effective measure than sectioning of the nerve; however, in our opinion it is used too often in some centres, i.e., before the possibilities of the simple, effective physical therapy have been exhausted.
  • Ineffective Measures. Because of the pathomechanism of BPPV, drug treatment with antivertignious substances is neither possible, nor are drugs sufficiently effective against the symptoms in the long term. The exception is sensitive patients who have severe nausea after a single manoeuvre. In this case the administration of for example, dimenhydrinate (100 mg) half an hour before performing the liberatory manoeuvres can make therapy easier.
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Benign paroxysmal positioning vertigo of the horizontal canal (McClure 1985; Baloh et al. 1993) is less frequent than posterior BPPV but is still diagnosed too seldom. Its cardinal features differ from those of posterior BPPV:
  • It can be induced by turning the head along the longitudinal axis of the supine body (either to the right or to the left). This results in an ampullopetal deflection of the cupula (with more severe vertigo and nystagmus) when the head is turned to the side of the affected ear.
  • The beating direction of nystagmus corresponds to the stimulation or inhibition canal, i.e., it beats linear and horizontal to the undermost ear.
  • Repeated positioning manoeuvres cause hardly any fatigue of the positioning nystagmus.
  • The duration of the attacks and the nystagmus is longer because of the so-called central storage mechanism of velocity for the horizontal canal. Positioning nystagmus frequently shows a reversal of direction during the arracks; this corresponds to post rotatory nystagmus (so-called PI and PII).
The typical case of horizontal BPPV can also only be explained by canalolithiasis (Strupp et al. 1995), although it has occasionally been observed that the mechanism switches from canalolithiasis to cupulolithiasis (Steddin and Brandt 1996). In the rare form of horizontal BPPV due to cupulolithiasis (characterized by nystagmus beating horizontally to the uppermost ear,), the “zero point” of positional nystagmus (beyond which direction changes) can be determined by turning the patient’s head 10-20degree around the longitudinal axis while in the supine position; this possible because the cupula of the ipsilateral horizontal canal is then parallel to the gravity vector (Bisdorff and Debatisse 2001). In this way one can also determine which side is affected by horizontal BPPV.

There is strong evidence that persistent horizontal BPPV occurs when there is a certain narrowness of the canal and the congealed clump cannot leave the canal, which narrows toward its in an ampullofugal direction, because of its size. Otherwise it could be assumed that the particles would independently and inevitably leave the canal with every accidental rotation around the longitudinal axis of the body (e.g., in bed). The striking feature of horizontal BPPV, i.e., it does not fatigue, agrees with this assumption, as does the general experience that horizontal BPPV is more difficult to treat than posterior BPPV.

Serial and alternating positioning according to the method of Brandt and Daroff (1980) are more likely to lead to success (Herdman et al. 1993), as the repeated bilateral head positioning evidently cause the disintegration of the conglomerate and wash out the particles from the canal. Lempert and Tiel-Wilck (1996) have also reported success with simple 270 degree rotations toward the unaffected ear around the longitudinal axis while the patient is supine. Bed rest with positioning of the head to the side of the unaffected ear (for 12 hours) is evidently more effective (Vannucchi et al. 1997). We recommend a combination of both methods.
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The diagnosis of BPPV can in most cases be made on the basis of a typical patient history (brief rotatory vertigo when turning over or sitting up/ lying down in bed) and the clinical findings. Especially in cases of therapy-refractory rotatory vertigo (despite correct positioning exercises), the following syndromes should be considered along with unilateral BPPV in the differential diagnosis.
  • Central positional nystagmus (infrequent, see below).
  • Bilateral BPPV, particularly post-traumatic (ca. 10%).
  • BPPV of the horizontal canal (too rarely diagnosed, see above).
  • Vestibular paroxysmia.
  • Central infratentorial lesions that mimic BPPV.
Central Positional Vertigo / Nystagmus:
Central positional nystagmus and central positional vertigo are caused by infratentorial lesions, which involve connections between the vestibular nuclei in the medulla oblongata and cerebellar structures close to the midline (vermis). It is important to distinguish between peripheral and central vestibular disorders, as the latter require further laboratory diagnostics. Four characteristic forms of central positional vertigo/nystagmus can be distinguished, although the symptoms overlap and combinations occur:
  • Central downbeat nystagmus, typically in head-hanging position (with or without accompanying vertigo).
  • Central positional nystagmus (without vertigo).
  • Central paroxysmal positional / positioning vertigo with nystagmus.
  • “central positioning vomiting”.
These central vestibular disorders occur much more seldom than the typical BPPV. However, it can be difficult to distinguish peripheral and central function disorders in the individual patient (Bertholon et al. 2002). The following clinical rules are important for diagnosing a central positional vertigo / nystagmus (Buttner et al. 1999):
  • Persisting positional nystagmus (slow-phase velocity >5° /s) without associated vertigo.
  • Positioning-induced vomiting after single head movements without any substantial vertigo or nystagmus.
  • Positional / positioning vertigo with nystagmus of purely torsional or vertical character (downbeat or upbeat directions); a purely horizontal direction of nystagmus is typical for hBPPV.
  • Positional / positioning nystagmus that does not correspond to the plane of the semicircular canal stimulated by the head positioning (e.g., torsional nystagmus after stimulation of the horizontal canal). In practice this seems to be the most important feature by which a central positional nystagmus can be identified.

According to earlier rules, positional nystagmus beating toward the uppermost ear or lasting longer than 1 minute indicated a central pathology; this is no longer considered a reliable differentiating feature, as both occur with the cupulolithiasis variant of BPPV.

References
Baloh RW, Jacobson K, Honrubia V (1993) Horizontal semicircular canal variant of benign positional vertigo. Neurology 43:2542-2549
Bertholon P, Bronstein AM, Davies RA et al (2002) Positional down beating nystagmus in 50 patients: cerebellar disorders and possible anterior semicircular canalithiasis. J Neurol Neurosurg Psychiatry 72:366-372
Bisdorff AR, Debatisse D (2001) Localizing signs in positional vertigo due to lateral canal cupulolithiasis. Neurology 57:1085-1088
Brandt T, Daroff RB (1980) Physical therapy for benign paroxysmal positional vertigo. Arch Otolaryngol 106:484-485
Brandt T, Steddin S, Daroff RB (1994) Therapy for benign paroxysmal positioning vertigo, revisited. Neurology 44:796-800
Brandt T, Steddin S (1993) Current view of the mechanism of benign paroxysmal positioning vertigo: cupulolithiasis? J Vestib Res 3:373-382
Buttner U, Brandt T, Helmchen C (1999) Diagnostic criteria for central versus peripheral positioning nystagmus and vertigo. Acta Otolaryngol (Stockh) 119:1-5
Epley JM (1978) The canalith repositioning procedure: for treatment of benign paroxysmal positioning vertigo. Otolaryngol Head Neck Surg 10:299-304
Gacek RR (1978) Hurther observations on posterior ampullary nerve transaction for positional vertigo. Ann Otol Rhinol Laryngol 87:300-306
Herdman SJ, Tusa RJ, Zee DS et al (1993) Single treatment approaches to benign paroxysmal vertigo. Arch Otolaryngol Head Neck Surg 119:450-454
Hilton M, Pinder D (2002) The Epley manoeuvre for benign paroxysmal positional vertigo—a systematic review. Clin Otolaryngol 27:440-445
Lempert T, Tiel-Wilck K (1996) A positional maneuver for treatment of horizontal-canal benign positional vertigo. Laryngoscope 106:476-478
Levat E, van Melle G, Monnier P, Maire R (2003) Efficacy of the Semont maneuver in benign paroxysmal positional vertigo. Arch Otolaryngol Head Neck Surg 129:629-633
McClure JA (1985) Horizontal canal BPV. J Otolaryngol 14:30-35 Pace-Balzan A, Rutka JA (1991) Posterior semicircular canal occlusion in normal hearing ear. Otolaryngol Head Neck Surg 104:52-57
Radtke A, von Brevern M, Tiel-Wilck K et al (2004) Self-treatment of benign paroxymal positional vertigo—Semont maneuver vs Epley procedure. Neurology 63:150-152
Schuknecht HF (1969) Cupulolithiasis. Arch Otolaryngol 90:765-778
Semont A, Freyss G, Vitte E (1988) Curing the BPPV with a liberatory manoeuvre. Adv Otorhinolaryngol 42:290-293
Steddin S, Brandt T (1996) Horizontal canal benign paroxysmal positioning vertigo (h-BPPV): transition of canalolithiasis to cupulolithiasis. Ann Neurol 40:918-922
Strupp M, Brandt T, Steddin S (1995) Horizontal canal benign paroxysmal positioning vertigo: reversible ipsilateral caloric hypoexcitability caused by canalolithiasis? Neurology 45:2072-2076
Vanucchi P, Giannoni B, Pagnini P (1997) Treatment of horizontal semicircular canal benign paroxysmal positional vertigo. J Vestib Res 7:1-6

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Vertigo or dizziness is a common manifestation of the malfunction of the vestibular system. Labyrinth, which is an apparatus in the inner ear (acoustic nerve), transmits movement information to the vestibular nerve and the brainstem and cerebellum. Lack of coordination in any one or all of these has to be determined to get to the cause of vertigo. Caloric stimulation is a test which uses differences in temperature to diagnose ear nerve damage as a cause of dizziness or vertigo.

Caloric stimulation is performed to evaluate the acoustic nerve, which provides both hearing and helps with maintaining the balance. This test may be recommended in cases of suspected vertigo both physiological and psychological, suspected toxicity induced hearing loss, anemia’s and to determine the extent of nerve damage in a comatose person.

Brown- Sequard was the first to describe the effects of introducing cold water into the ear canal in the mid- 19th century. The clinical application and implications were first demonstrated by Barany in 1960. He used ice water stimulus and postulated that caloric stimulation of the auditory canal induced the formation of convection currents within the semicircular canals of the vestibular labyrinth. Fitzgerald-Hallpike finally standardized the technique in 1942 and came to be called after their name.

Caloric testing is a part of the spectrum of ENG testing determining the degree to which the vestibular system is responsive as well as the symmetric balance between the two ears. ENG further determines whether or not dizziness may be due to inner ear disease. There are four main parts to the ENG. The calibration test, which evaluates rapid eye movement, the tracking test, which evaluates movement of the eyes as they follow a visual target, the positional test, which measures dizziness associated with positions of the head and the caloric test, which measures responses to warm and cold water circulated through a small, soft tube in the ear canal. It has got several variants namely:
  • Monothermal test-a single large bolus of ice water is given rather than two irrigations with hot and cold.
  • Air caloric-air is used instead of water.
  • Bilateral irrigation-both sides are irrigated simultaneously.
  • Balloon test-a water filled balloon is used instead of water.
  • Ice water caloric-used to confirm complete loss.
The caloric test procedure is performed with eyes opened in darkness or in a dimly illuminated room with the patient looking at a Ganzfeld or nonpatterned background. Concentration is induced such that a certain level of mental alertness is maintained. EOG calibrations are typically checked after each or every other stimulus. An otoscopic examination is carried out before the caloric testing to rule out any major pathological conditions. Cool water (30°C) and warm water (44°C) are administered for 60 to 90 seconds to each ear in asset order. This stimuli result in a heating effect in the temporal bone that lasts for 10 to 20 minutes. Although nystagmus effect does get in a much shorter time (2-3 minutes) because of the effects of adaptation the prolonged heating effect of single temperature irrigation requires that at least 10 minutes be allowed between successive irrigations.

Biphasic caloric irrigation can reduce patient nausea and shorten the wait between stimuli to about 2 minutes by use of irrigation with water at 43.5°C for 45 seconds, 30.5°C for 65seconds, and 43.5°C for 23 seconds. Eye movements are recorded for a period of several seconds before onset of an irrigation, during the irrigation, and until the nystagmus has ended. Standard computer algorithms exist for distinguishing fast from slow components of nystagmus and for determining the velocity of each slow component. A plot of slow component velocity is then formed, and the maximum slow component is determined on the basis of three to five slow components with highest velocity. Date are interpreted in terms of unilateral weakness (UW) and directional preponderance (DP), according to formulae described by Jongkees and others:

UW= 100% ? ((R30° +R44° ) – (L30° +L44° )) (R30° +R44° +L30° +L44°)

DP= 100 X ((R30° +L44° ) – (R44° +L30° )) / (R30° +L44° +R44°+L30°)

A UW of greater than 20% and DP of greater than 25% are usually considered significant aberrations. UW is a sign of decreased responsiveness of the horizontal semicircular canal or the ampullary nerve that provides its innervations. DP is commonly seen in patients with spontaneous nystagmus.

The equipment needed for performance of the caloric test is minimal. Syringes, preferably of 30- or 50- mL in plastic is ideal for irrigation. The syringe is attached to a short length of soft plastic tubing. At least 100 mL of ice cold bactriostatic saline is kept ready. Plastic emesis basin to collect water that drains from the ear canal, otoscope, several sizes of ear speculums, and equipment for removal of cerumen, towels and a thermometer also form a part of the instrumentation..

Hence the basic test is simple and not too expensive. The results are consistent and reliable. As early as the 1970’s caloric testing was performed to detect central vertigo and found rather accurate. Comparison of test result for both people clinically diagnosed as having vertigo and without vertigo clearly showed the difference in result.

A more recent and modified version of the caloric test was performed and nystagmus noted for abnormal results in vertigo patients. It was found that caloric deficit was higher in vertigo patients.

Eye movements are usually recorded with either EOG or a video method. From the peak slow-phase velocity of nystagmus four numbers are obtained:
  1. Cold right
  2. Cold left
  3. Warm right
  4. Warm left.
These four numbers are used to compute three additional numbers:
  • Total response – sum of all responses. Should be 20 or >.
  • Directional preponderance – right- beating – left-beating/ total. It should be 35% or less.
  • Unilateral paresis –right-left/ total. This is called “Jongkee’s formula” (described above) and should be 25% or less.
These studies are in cognizance with the fact that caloric testing is a simple, less expensive and reliable test for preliminary confirmation of vertigo. Thus caloric testing is a non linear combination of convection induced stimulation of the canal, a direct effect of temperature on the nerve, transduction responses in the mechanics of the cupula, adaptation responses in the nerve and brainstem, and other central processing effects, mainly including velocity storage.

References Sakata E, Otsu K. Simple method of differential diagnosis of peripheral and central vertigo-development of diagnostic method and studies of 178 cases, No To Shinkei. 1976 Feb; 28 (2): 187-96.

Goebel JA, Paige GD. Dynamic posturography and caloric test results in patients with and without vertigo. Otolaryngol Head Neck Surg. 1989 Jun; 100 (6): 553-8.

Goebel JA, Garcia P, Prevalence of post headshake nystagmus in patients with caloric deficits and vertigo. Otolaryngol Head Neck Surg. 1992 Feb; 106 (2): 121-7.

Heide, G et al. J Neurol Neurosurg Psychiatry 1999; 66: 787-790 .
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