Douglas B. Sawyer, MD, PhD

  • Chief, Division of Cardiovascular Medicine
  • Lisa M. Jacobson Professor of Medicine
  • Physician-in-Chief, Vanderbilt Heart & Vascular Institute
  • Nashville, Tennessee

It helps to determine the extent of vestibular functional deficit secondary to the trauma arrhythmia recognition test cheap trandate 100mg on line, which is important in a medicolegal context arteria esplenica cheap trandate 100 mg. Impressive haemorrhage should alert the clinician to a potential laceration of the jugular bulb or carotid artery with blood escaping through a violated tympanic membrane and/or fracture line through the temporal bone arteria vertebral buy trandate on line. The management of patients with extensive haemorrhage is based only on case reports and the optimal protocols are yet to be determined heart attack left arm buy cheap trandate 100 mg online. The role of electrical tests of facial nerve function remains debatable (see Chapter 241c heart attack 25 100mg trandate amex, Disorders of the facial nerve) heart attack 4sh buy trandate 100 mg line. Electroneuronography has its proponents, but the majority of clinicians decide on facial nerve exploration based on the onset and extent of facial nerve weakness. The perforation is initially treated conservatively with the avoidance of water or other contaminants. All of 143 tympanic membrane perforations secondary to temporal bone trauma healed spontaneously within ten weeks of the injury. The best investigation is to submit the suspicious fluid for beta-2 transferrin analysis. In a patient with an isolated otic-capsule sparing fracture of the right temporal bone, no treatment beyond observation may be indicated. Only the complications within the management capabilities of an otoneurologist will be discussed in this section. Though each of these are discussed individually, multiple complications may occur in any specific patient. Haemotympanum Haemotympanum is diagnosed by the characteristic appearance of the blue drum and is the major reason for the conductive hearing impairment found in 41 percent of patients with a temporal bone fracture. Ignelzi and Vanderark32 [***] were unable to show any advantage from the prophylactic antibiotics in patients with basilar skull fractures. The 2 percent incidence of meningitis reported in prospective controlled trials of antibiotic prophylaxis would require an extremely large study size to have sufficient power to demonstrate a difference. Audiometric investigations will confirm a Chapter 237g Ear trauma] 3497 persisting air-bone gap. Incus dislocation is the most common ossicular chain abnormality and is found singly in 80 percent of the post-traumatic conductive hearing loss ears explored. Fracture of the stapes superstructure is the next main cause of persisting conductive hearing loss. Symptoms of imbalance and hearing loss are, however, reported by patients with head injuries in the absence of a temporal bone fracture. Vertigo was reported to affect 24 percent of patients who sustained a head injury without fracture. Fifty percent of patients with a temporal bone fracture who have audiometric evidence of a hearing loss, are documented to have a sensorineural component. The data suggest that all documented sensorineural hearing losses in the presence of a temporal bone fracture persist. In the rare situation where a patient develops a bilateral profound sensorineural hearing loss secondary to labyrinthine trauma, a cochlear implant may be indicated. The gold standard of visual identification of clear fluid in the round or oval window niche is unreliable as different surgeons have different levels of sensitivity and specificity. Bed rest and vestibular sedatives alone are reported to be effective in achieving control of vertigo and resolution of hearing loss in many patients with a perilymph fistua if implemented early. In the presence of vertigo and tinnitus, early bed rest, head elevation and avoidance of straining is advised to allow spontaneous closure of a potential labyrinthine fistula. Middle ear exploration rarely confirms or treats all the symptoms of a perilymph fistula. Sixty-seven percent of patients with a traumatic facial palsy with 90 percent or greater degeneration in compound action potential on evoked electrical myography regained House-Brackmann grade 2 or better facial nerve function spontaneously. The results of patients who have been operated on are not different statistically to those who have not been operated on. Though more extensive exploration in the perigeniculate region has been advocated, the results of such surgery would appear to be no better. This is unlikely to be the case as there are series where patients with complete immediate palsies were not operated on, and 50 percent recovered HouseBrackmann grade 2 function or better. Patients who progress from an incomplete to a complete facial palsy more than 24 hours after the initial trauma should be managed likewise. Patients with immediate complete facial palsy should only be offered facial nerve exploration in centres which have the facilities and expertise to perform complete facial nerve decompression. Surgery does not appear to improve upon the natural spontaneous resolution rate of facial palsy in association with a temporal bone fracture. There are no comparative trials of the efficacy of different surgical closure approaches or techniques. The additional morbidity the patient encounters with different approaches (for example, an increased risk of epilepsy using a middle fossa approach, or donor site complications with autologous materials) can be used to inform the surgical decisionmaking process. Retrospective and prospective case series data show no benefit from prophylactic antibiotic use. However, a systematic review of five high-quality, randomized controlled trials published before 1998 found that encouraging normal activities was preferable at least in grade 1 and 2 patients. This collection of symptoms are not dissimilar to those reported by patients with post-concussion syndrome following head injury. Best clinical practice [Encouraging activity rather than rest and immobilization is recommended in patients without neurological signs following whiplash injury. Severe cases may occur as a result of sudden large pressure changes, such as slap injuries typically sustained during an assault, when water skiing, high board diving and from blast injuries. The only randomized controlled trials relating to any of the topics discussed concern the use of decongestant medications to aid Eustachian tube function. Several controlled animal experiments are referred to which examine the barotraumatic effects on both the inner and middle ears. Most evidence is of level 3 type, although large numbers of patients have been studied, often by armed forces. Much of the physics and pathophysiology behind the various clinical entities is relatively unchallenged. There is some temporal bone evidence for the various conditions described, however some of the pathophysiological explanations relating to the described inner ear conditions are a matter of conjecture. There are numerous publications relevant to most of the topics presented in this chapter. Since the invention of scuba equipment, military, commercial and sport diving have flourished, and the clinical conditions associated with otitic barotrauma have become well recognized. Animal studies have demonstrated histological evidence of middle ear trauma after a 6100 m altitude decompression, compression cycle. Single-breath diving started many centuries ago to collect shells and find lost items. Commercial pearl diving still depends, to some extent, on these predominantly female divers. Caissons are bells that are pressurized to keep the water out, enabling workers to work for many hours at depth. Compressed air tunnelling is very similar, the air pressure maintaining the integrity of the tunnel walls until they are stabilized by concrete or other lining material. Augustus Siebe, a London-based German coppersmith, invented a surface air supplied copper diving helmet in 1819 and developed the complete waterproof suit in 1837. Deeper dives have been made possible by the incorporation into diving equipment of advanced materials, dry suits with pressure-equalization valves, thermal protection water-heated suits, various oxygen, helium, hydrogen and other gas mixtures, and by the combined use of diving bells and scuba gear. Both Alt and Vail59, 60 performed animal experiments that suggested that inner ear compression barotrauma was related to the failure of middle ear pressure equalization. Vail also hypothesized that decompression injury was caused by an effect on the inner ear by nitrogen bubbles. Pressure/volume relationships the clinical conditions resulting from various pathophysiological changes are most easily described by considering the physiological events that occur during subaqua diving with scuba apparatus. Similar events occur during flight but, because of the lower pressures involved, the resulting barotraumatic injuries are usually less pronounced. Its importance is demonstrated by the relative bubble volume decrease experienced with increased pressure (Table 237g. When diving, the largest percentage change in gas volume occurs during the first 10 metres of descent, (Table 237g. The ambient pressure doubles to two atmospheres and the corresponding gas volume is halved. In a system which has no air spaces within it, this pressure is transmitted equally throughout the structure. The total pressure of a gas mixture always equals the sum of the partial pressures each gas would exert if it alone occupied the available volume. At a constant pressure the volume of a gas dissolved in a liquid is proportional to the temperature. The amount of gas that will dissolve in a fluid, at a given temperature, is proportional to the partial pressure of that gas. Depth/m 0 Atmospheres pressure 1 Pressure/kPa 101 Volume (%) 100 Bubble (%) diameter 100 10 2 202 50 79. Head-out immersion causes a significant squeezing of blood volume from the lower limbs into the chest and into the head causing an increasing cardiac output and raised intracranial pressure and headaches respectively. As the middle ear is a bony cavity, no distension or expansion is able to take place. The vasculature within the wall of the middle ear is, however, in continuity with that of the rest of the body, and therefore the intraluminal vascular pressures reflect the ambient pressure. If a sufficient gradient exists, then oedema and even rupture of those vessels within the mucosal lining will occur. The nasopharynx is filled with inspired air from a compressed air cylinder via a regulator during breathing. This air pressure is equilibrated by the regulator in the mouthpiece to be equal with the ambient external pressure, provided the diver continues to breath normally. The middle ear pressure becomes increasingly negative compared to the ambient pressure unless equalization via the Eustachian tube takes place. This occurs by the voluntary action of the tensor and levator palati muscles opening the usually closed tube. The relatively negative pressure within the middle ear will increase with further descent resulting in a pressure differential across the tympanic membrane, which is therefore pushed inwards by the external ambient water pressure. This stretching is perceived as a sensation of external pressure and discomfort, which stimulates further attempts at equalization. If this does not prove possible, then the diver should return towards the surface to decrease the pressure gradient, thereby improving the ability to equalize. If this is not done and descent continues, then middle and inner ear barotrauma may occur. At this pressure, if no equalizing manoeuvre is performed, then mucosal congestion and oedema will occur. This is because the ambient pressure is reflected in the vasculature of the middle ear. If the pressure gradient across the tympanic membrane is large and occurs before the middle ear fills with an effusion or blood, then the tympanic membrane may rupture. If this occurs in one ear only, then a sudden influx of cold water into the middle ear may result in unequal thermal stimulation inducing a rigorous caloric vertigo. The perilymphatic space is separated from the middle ear by the oval and the round window membranes. If the diver or aviator fails to equalize his middle ears, then the pressure within the external ear canal will cause the tympanic membrane to be pushed inwards with a resultant inward force on the stapes foot plate via the ossicles. This causes a corresponding bulging of the round window membrane into the middle ear space. The pressure gradient is also increased by the ambient pressure of the spinal fluid transmitted through the aqueducts to the inner ear fluids, this pressure being relatively positive compared to the middle ear pressure. Actual inner ear perilymph pressure is really slightly higher than ambient pressure. During subsequent normal ascent, as the middle ear pressure exceeds that of the ambient pressure, passive ventilation of air through the Eustachian tube into the pharynx occurs. As a result, the usual passive ventilation, which should occur during subsequent ascent, can no longer take place. By similar mechanisms to those described during descent, the reverse effect on the oval and round windows may be seen. The tympanic membrane is pushed outwards and hence a traction force is applied to the oval window via the ossicles. The pressure gradient is increased further as the perilymphatic pressure, reflecting the ambient pressure, has decreased with ascent. It is possible, therefore for perilymphatic fistulae to occur during this phase of a dive. A sudden outflow of air down the Eustachian tube is sometimes described, immediately followed by the symptoms and signs of a perilymphatic fistula. Middle ear barotrauma (barotitis media, middle ear squeeze) Middle ear barotrauma is the most frequent pressureinduced ear condition. It is most commonly the result of pressure changes experienced during commercial flights.

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Age-related hearing loss happens in all individuals in varying degrees and so appropriate allowance for this and any other coexistent pathologies will need to be made heart attack 27 100 mg trandate sale. Investigations the cornerstone of investigation is a pure tone audiogram pulse pressure variation formula trandate 100mg discount, with both air and bone conduction to identify any conductive hearing loss arrhythmia practice discount trandate 100mg on line. The classical audiometric pattern is of a high-tone hearing loss with a notched appearance centred on 4 or 6 kHz blood pressure medication that doesn't cause cough discount generic trandate canada, with some recovery at 8 kHz blood pressure chart morning purchase online trandate. However pulse pressure compliance purchase cheapest trandate, the notch is often absent but significant audiometric loss at frequencies below 2 kHz is extremely uncommon. If present it should raise suspicion of some other pathological process affecting the cochlea. Some authors have suggested an analytical approach to the shape of the audiogram as an aid to predicting the likelihood of noise-induced hearing loss. Chapter 238b Noise-induced hearing loss] 3553 Tympanometry is helpful to confirm normal middle ear functioning. A conductive hearing loss is not due to noise exposure and can even provide some protection of the cochlea by virtue of the sound attenuation. In those individuals in whom a significant nonorganic component (feigned thresholds) is suspected, cortically evoked reflex audiometry may be required to provide a more objective measure of hearing thresholds. Although they may help to describe the tinnitus, there is increasing evidence that they have little role in the assessment of tinnitus severity. There is some evidence of decreased, contralateral, otoacoustic emission supression with early noise damage, although this finding is still a long way from clinical application. A value should be attached to the noiseinduced portion, and any other components, of the total hearing loss. In addition, the writer should make some effort to calculate the relative contribution to the noiseinduced hearing loss from each noise source, if there is more than one. In particular, comment should be made regarding the need (either current or predicted) for any hearing aids or rehabilitative treatment. With the changes in the civil justice system54 leading to the new Civil Procedure Rules in 1999, it is important that an expert does not comment outside his field of expertise and where there is a range of opinion on a point or subject, it is commented upon. Most commonly, one is faced with an older patient who has developed symptoms as a result of the combined effects of ageing and noise-induced hearing loss. There will be a history of excessive noise but in many cases this will not be overwhelmingly impressive or, alternatively, hearing protection may have been provided. The audiogram will show a sensorineural hearing loss, often with loss of the middle frequencies too. If not, a third idiopathic, degenerative process has to be invoked to explain the discrepancy. This may be by avoiding the excessive noise altogether or, if this is not possible, by the use of ear protection in the form of earplugs or earmuffs. Employers are under a statutory duty under the Health and Safety Act 1974 to minimize risks to employees, including those from excessive noise exposure. The 1989 Noise at Work Regulations55, 56 described two action levels for daily, personal noise exposure: a first action level at 85 dB(A) and a second at 90 dB(A). These have recently been replaced (April 6, 2006) by the Control of Noise at Work Regulations, 2005, where each action level is 5 dB lower, respectively. In summary, at the first action level, an employer must conduct a noise survey and embark on a programme of employee education and provide appropriate hearing protection. The employer is required to identify those areas where hearing protection use is required. Regular hearing tests should be offered to employees where and when a potential risk is recognized. This reduction may be by means of engineering (quieter machines) or acoustic (sound isolating) solutions. This involves the reduction of background noise (as far as possible), face-to-face conversation to maximize exposure to nonverbal communication cues and an explanation of the problem, to allow the legitimization of their hearing loss. In more severe hearing loss, directed rehabilitation programmes including psychological counselling can help the patient to understand and acknowledge their problem. This acceptance is one of the first and most crucial steps on the road to successful rehabilitation. Inclusion of, and support for, the spouse should also be provided as part of such a programme. Personal hearing protection As regards hearing protection, the choice is between earplugs, earmuffs and active noise reduction. The choice will often depend on the performance of the protector and the environment in which it will be used. They are relatively cheap and particularly efficient when other protective devices. The best earplug can perform as well as the best earmuff in terms of sound attenuation57 [****] but they are harder to fit correctly. It is well established that the real world performance of ear protectors is significantly poorer than the laboratory scores, largely as a result of inadequate or incorrect fitting. It uses electronics to provide sound inside a set of earmuffs that is 180 degrees out of phase with the ambient sound. This is a very effective form of sound attenuation, particularly for lower frequencies (o1000 Hz), but the electronics required are expensive. Its most frequent use is in military and aircraft settings where additional communication devices are required and it can be incorporated into the headset. At 85 dB(A), 5 percent of the exposed population are at risk, at 90 dB(A) that rises to 15 percent. A recent National Institute of Clinical Excellence report61 has suggested that there is significant benefit to patients in being fitted with binaural hearing aids. In those individuals with a mild high-tone hearing loss, hearing aids tend to provide little benefit. The diagnosis is clinical and requires sufficient noise exposure and the presence of a hearing loss greater than expected from age alone. Tinnitus and hyperacusis are frequent accompanying symptoms and nowadays often present without any evidence of a hearing loss or only a modest hearing loss. Treatment is essentially preventative and involves personal hearing protection (earplugs or earmuffs) or reduction of noise levels at source. Animal studies will be of assistance in building the knowledge base, as will human population studies. Advances in our understanding of hair cell regeneration may allow treatment to encourage this to take place in the noise-damaged cochlea. Hopefully, engineering and acoustic advances will make for a quieter working environment. Guidelines on the diagnosis of noise-induced hearing loss for medicolegal purposes. Alterations of basilar membrane response phase and velocity after acoustic overstimulation. Anyone involved in this field should be sensitive to the presence of and aware of the risks of high noise levels. If excessive noise levels are found then action is required, either to reduce noise levels at source or to educate and protect individuals from excess exposure. Excitotoxicity and repair of cochlear synapses after noise-trauma induced hearing loss. Noise-induced cochlear hypoxia is intensity dependent, correlates with hearing loss and precedes reduction of cochlear blood flow. Effects of intense sound exposure on the outer hair cell plasma membrane fluidity. The influence of genetic variability in oxidative stress genes on human noise susceptibility. Effects of noise and ototoxic drugs at the cellular level in the cochlea: a review. Quantitative analysis of apoptotic and necrotic outer hair cells after exposure to different levels of continuous noise. Extremely rapid induction of outer hair cell apoptosis in the chinchilla cochlea following exposure to impulse noise. Involvement of apoptosis in progression of cochlear lesion following exposure to intense noise. Contributions of mouse models to understanding of age- and mouse related hearing loss. Acceleration of age-related hearing loss by early noise exposure: evidence of a misspent youth. Combined effect of smoking and occupational exposure to noise on hearing loss in steel factory workers. The effect of low level acoustic stimulation on susceptibility to noise in blue- and browneyed young human subjects. Acrylonitrile produces transient cochlear function loss and potentiates permanent noise-induced hearing loss. Evidence of a common pathway in noise-induced hearing loss and carboplatin ototoxicity. NoiseChem: A European Commission research project on the effects of noise and industrial chemicals on hearing and balance. Combined effects of noise and styrene on hearing: comparison between active and sedentary rats. Guidelines on the diagnosis of noise-induced hearing loss for medico-legal purposes. Acoustics: Threshold of hearing by air conduction as a function of age and sex for otologically normal persons. Acoustics: Determination of occupational noise exposure and estimation of noise-induced hearing impairment. Quantification of the psychosocial disadvantages experienced by workers in a noisy industry and their nearest relatives: Perspectives for rehabilitation. The audiogram in hearing loss due to noise: A probability test to uncover other causations. Hearing loss associated with weapons noise exposure: when to investigate an asymmetrical loss. Occupational exposure to noise decreases otoacoustic emission efferent suppression. Access to justice: Final report to the Lord Chancellor on the Civil Justice System in England and Wales. The acoustic attenuation characteristics of 26 hearing protectors evaluated following the British Standard procedure. Development of a rehabilitation program for people affected with occupational hearing loss. Like William Wilde, he observed that a high rate of consanguinity resulted in an increased risk of having hearing-impaired children. The risk of consanguineous marriages was understood by showing that the indirect route of inheritance in pedigrees having first-generation common ancestors resulted in multiple affected sibships with deaf children a few generations later. In the first decades of the twentieth century, there was still some doubt as to whether simple Mendelien rules of inheritance could explain sufficiently the presence of profound childhood deafness in man. In breeds of deaf mice, the figures of the Mendelian laws could be reproduced; however, this was not the case in the offspring of human deaf couples. It took some time before it was understood that many different genes caused autosomal recessive inherited profound childhood deafness and that this was the explanation for a lower outcome of profound childhood deafness in the offspring studied. Chapter 238c Autosomal dominant nonsyndromic sensorineural hearing impairment] 3559 Autosomal dominant inherited profound childhood deafness is rare in studies of pupils at specialist schools for the hearing impaired. In cases where an autosomal dominant pattern of inheritance can be demonstrated, most of the family members involved were not severely affected and not at an early age. This low grade of expression of autosomal dominant deafness genes means that attitudes to reproductive desirability by affected and other family members over the centuries have not been significantly altered and so these autosomal dominant genes causing deafness have been transmitted into future generations over centuries. If there had been full penetrance and full expression of the gene causing profound childhood deafness, it would have prohibited the socioeconomic status that would have made it possible to have offspring. This is why autosomal dominant inherited hearing impairments are usually mild in the first decades of life. Progression of the hearing impairment can nevertheless lead to complete deafness, requiring cochlear implantation. Particularly well known are the families with low-frequency impaired audiograms, midfrequency impaired audiograms and those with progressive high frequency hearing losses. Sometimes very large families with over a hundred affected people were studied over decades. The larger the pedigree and the more affected individuals present, the better to achieve a successful gene linkage. This has led to the recognition of more than 50 nonsyndromic autosomal dominant diseases with hearing impairment as the only feature (Table 238c. There are over a 100 mutations in genes encoding connexins that are associated with deafness. These days, the name of the gene involved is frequently attached to this nomenclature making it even more precise. Pure tone threshold data are plotted in a familiar audiogram-like format covering, where possible, decade steps in age (decade audiograms). Despite this excellent auditory verbal communication, results can be achieved after cochlear implantation more than two decades after total deafness has become total.

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Dehiscence or thinning of bone overlying the superior semicircular canal in a temporal bone study blood pressure 6080 order 100 mg trandate free shipping. Endolymphatic sac tumours: histopathologic confirmation blood pressure variations cheap 100 mg trandate with visa, clinical characterization pulse pressure factors effective trandate 100 mg, and implication in von Hippel-Lindau disease prehypertension ne demek cheap trandate 100mg with visa. Hearing preservation surgery for small endolymphatic sac tumours in patients with von HippelLindau syndrome blood pressure medication with a b purchase cheapest trandate and trandate. The pathology hypertension code for icd 9 buy generic trandate pills, symptomatology and diagnosis of certain common disorders of the vestibular system. Incidence and growth pattern of vestibular schwannomas in a Danish county, 1977-98. A novel moesin, ezrin-, radixin-like gene is a candidate for the neurofibromatosis 2 tumour supressor. The value of enhanced magnetic resonance imaging in the evaluation of endocochlear disease. Viral infections of the inner ear: clinical, virologic, and pathologic studies in humans and animals. Herpes zoster auris associated with facial nerve palsy and auditory nerve symptoms. The saccus endolymphaticus and an operation for draining the same for the relief of vertigo. Membranous hydrops in the inner ear of the guinea pig after obliteration of the endolymphatic duct. The relationship of postural sway in standing to the incidence of falls in geriatric subjects. Sensory and neural degeneration with aging, as seen in microdissections of the human inner ear. Clinical and pathological observations on a case of leukaemia with deafness and vertigo. Distribution pattern of blood in the inner ear following spontaneous subarachnoid 96. Positional alcohol nystagmus in patients with unilateral and bilateral labyrinthine destructions. This is not surprising since approximately one-quarter of people experience dizziness at some time in their life and in 80 percent of cases this is severe enough to see a doctor. Reciprocally, some clinical histories are so typical that the absence of corroborative findings on a single visit to the clinic should not make the clinician rule out a diagnosis. The symptoms that patients with balance or vestibular disorders may report are vertigo, dizziness, nausea, motion intolerance, unsteadiness and oscillopsia. It is of vital importance, in all balance symptoms, to identify triggers provoking the symptoms, such as position, movements or visual or acoustic triggers. It is equally important to determine if the symptom is acute, episodic or chronic, and whether it occurs alone or in association with other symptoms. Vertigo and dizziness Vertigo, when defined as an illusion of either oneself or the environment rotating, is a reliable symptom. It indicates involvement of the angular motion sensing system, that is, the semicircular canals and their central projections. However, such involvement can occur from the labyrinth up to the vestibular cortex so that the site of the lesion will have to be presumed by additional symptoms (Table 240b. Acute vertigo is terrifying and disabling and its duration can be a good guide to diagnosis. Illusions that one is moving linearly, such as falling vertically downwards or linear vertigo, can arise from disorders of the otolith system but it is extremely difficult to confirm selective otolith lesions and thus the clinical value of linear vertigo as a symptom is less well established. Dizziness or giddiness are common terms employed by vestibular patients to describe their problems. One should encourage the patient to describe what they mean by dizziness and/ or to compare it to situations that they may have experienced. Body language is also important as many patients wave a hand round-and-round when describing their dizziness; this is often rotational vertigo. When the dizziness is nonrotational it is less certain that the problem lies in the vestibular system. Descriptions such as rocking or swimming sensations, lightheadedness, walking on cotton wool, feeling detached, can also be vestibular. Such evidence may be difficult to find on vestibular testing, such as a significant caloric canal paresis, or a preceding history of rotational vertigo. There are numerous nonprimarily vestibular causes of dizziness and lightheadedness, including anaemias, drug toxicity and psychological dizziness to name just a few (Table 240b. If there is an objective, visible balance problem this is more likely to be a neurological gait disorder, with patients just perceiving their own objective dysequilibrium. If these patients trip over or are pushed over in a crowd they can stumble or fall. The lesion may lie anywhere in the somatosensory motor chain (peripheral nerves, spinal cord, cerebellum or cerebrum) and the clinician should enquire about symptoms represented at these various levels in the neuraxis, such as weakness, numbness, incoordination, tremor, sphincters, memory and other cortical functions. Enquiries as to the presence of falls as a result of poor postural balance should be actively made, particularly in the elderly patient. The patient is bedridden and terrified of even going to the toilet; any movement brings more vertigo, nausea and vomiting. A patient with vestibular neuritis may have strong rotational vertigo and nausea for three days, followed by dizziness for three weeks and by lightheadedness for three months. In these latter stages, however, patients tend to avoid head movements or looking at moving visual scenes. Why in some patients the last three months become three or thirty years of lightheadedness, dizziness and motion intolerance is not completely understood. A complex interrelation between lack of effective vestibular compensation, idiosyncratic perceptual style and anxiety may be at play. Paroxysmal oscillopsia can be spontaneous, as in paroxysmal nystagmus and ocular oscillations of central origin, vestibular paroxysmia or, more commonly, voluntary nystagmus. Some patients with idiopathic bilateral loss of vestibular function present with paroxysmal oscillopsia. In vestibular neuritis, patients can report a recent upper respiratory tract infection. Herpes zoster oticus, or Ramsay Hunt syndrome can have a peripheral facial palsy and show herpetic vesicles in the outer ear canal. The presence of risk factors such as smoking, hypertension, obesity or diabetes can suggest a vascular aetiology. In all these conditions the vertigo is usually severe and prolonged, inevitably leading to autonomic symptoms, such as nausea, vomiting, pallor, sweating and malaise. It must be borne in mind that any vertigo is more tolerable when the head is kept still. Only provocation, not exacerbation, of vertigo by movements or positions of the head should be labelled as positional vertigo. Intense vertigo can be so overwhelming that some patients may not volunteer other symptoms (Table 240b. The presence of triggers becomes critically important for diagnosis in the patient with recurrent vertigo or dizziness. Incorrectly, clinicians often jump to the conclusion that dizziness related to neck movements (inevitably associated with head movements! In some patients with migraineassociated vertigo, food or sleep deprivation or certain foods (chocolate, cheese, red wine) may be triggers. Orthostatic hypotension induces lightheadedness or dizziness on standing up suddenly or after being standing up for a long time, particularly in the heat or motionless. Exercise, alcohol or stress can trigger an attack in patients with episodic ataxias or channelopathies, which usually includes vertigo (Tables 240b. Patients with presyncopal dizziness can report sensations of feeling hot or cold, clammy and sweaty, greying out of vision and bilateral tinnitus. The presence of migrainous symptoms, such as visual aura, throbbing headaches, nausea, photo-phono phobia, must be enquired;15 migraineous vertigo can precede, overlap, follow or occur independently of a migraine headache. Since vertigo and dizziness are so prevalent in the community, this small proportion of patients makes up enough absolute numbers to fill up specialized clinics. There is no simple explanation as to why some patients do not fully recover from a single attack or episodic vertigo. The actual vestibular loss is unlikely to be the reason since patients with vestibular schwannomas rarely suffer from any troublesome dizziness. Failure of the compensatory mechanisms is also often invoked and this may be due to a variety of factors. Finally, the otologist should bear in mind the possibility that the sense of unsteadiness reported by the patient may be due to a general medical disorder or to neurological or psychogenic gait disorders (Table 240b. The latter, particularly in the form of an overcautious gait, can be triggered in the elderly by a fall or an episode of vertigo so full investigation is warranted. A standard neuro-otological assessment should include auroscopy, eye movement, positional manoeuvres and posture and gait examination. Auroscopy is covered in Chapter 235, Clinical examination of the ears and hearing. The oculomotor examination should include: search for spontaneous and gaze-evoked nystagmus; convergence; smooth pursuit; saccades; vestibulo-ocular reflexes; positional manoeuvres. If there is an infantile squint, the ocular examination is more difficult to interpret. Since spontaneous nystagmus often enhances by convergence, it is convenient to examine convergence at the same time, by slowly moving an object in and out along the visual axis. Absence of convergence occurs in midbrain lesions but one must remember that reduced/ absent convergence is extremely common in normal people above the age of 60 years of age. While in primary gaze, one should undertake a cover test, particularly in patients with difficult to interpret eye signs. The cover test is usually part of the examination to assess diplopia and ocular alignment, but what we suggest here is a simplified version of the test, looking for the presence of latent nystagmus. The value of discovering latent nystagmus, which is essentially asymptomatic, lies in the fact that this condition is often associated with congenital squints, nystagmus, square wave jerks, abnormal pursuit or optokinetic nystagmus. When examining nystagmus as well as other eye movements, patients have to be clearly instructed to look at a predetermined object and the eyes should be well illuminated. The presence of spontaneous nystagmus in primary gaze immediately raises the question, is this caused by a central or peripheral lesion If the patient is in the middle of an acute vertigo attack, with severe unsteadiness and nausea, it can be peripheral or central, but if the patient comes as a routine ambulatory patient and does not look acutely ill, the nystagmus is more likely to be of central origin. The nystagmus is essentially horizontal, with a minor torsional (rotatory) component. Note that at one week after labyrinthectomy the nystagmus in the light was negligible but increased notably in the dark. At one month follow-up vestibular compensation had effectively reduced the nystagmus in the dark. Also note the rectilinear slow phase velocity of the nystagmus, in agreement with its peripheral origin. For instance, downbeat nystagmus in primary gaze, which is always of central origin, often does not enhance on looking down but on looking sideways. A subacute peripheral vestibular lesion can have a gaze-evoked nystagmus, that is, a second degree nystagmus as discussed above. Instead, the term gaze paretic implies that the patient has difficulty in holding gaze in an eccentric position in the orbit. A useful classification for the severity of the nystagmus, based on this observation, has stood the test of time. The presence of a clinically observable torsional component in the spontaneous right beating nystagmus indicated that the lesion was central rather than peripheral. The vestibular nystagmus beats, as expected in any destructive vestibular lesion, in the opposite direction of the tumour. Gaze paretic nystagmus can be present in all directions of gaze in the same patient, typically in symmetrical processes such as cerebellar degenerations. In order for the clinician to reach these conclusions confidently, the examination has to be technically correct. Since pursuit movements are visually guided, rule number one is that the patient should be able to see the target correctly. In patients either too young, too old or with attentional problems, a substantial, solid target such as a key, a toy, a mobile phone or a credit card can increase performance. Make sure that in elderly subjects, with presbiopia and age-related convergence insufficiency, the object is presented at a comfortable viewing distance. Sometimes, the examination must be conducted with the patient wearing his own glasses. Rule number two is that the target has to be moved at a slow speed, taking four to five seconds to travel from right to left and vice versa. When pursuit is broken, say, to the right, the lesion is likely to be in the ipsilateral (right) cerebellum or parietal lobe. Investigation of pursuit eye movements is a vital component of the neuro-otological examination. Typically, large vestibular schwannomas compressing the brainstem produce this nystagmus combination.

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Common sense would seem to tell us that almost all of the hearing impaired would benefit from at least Chapter 239e Accessory devices] 3667 considering accessory devices in addition to a personal hearing aid and indeed selection of a particular personal hearing aid that may have features pulse pressure is calculated by trandate 100mg cheap, such as an inductive coupler or direct audio input pulse pressure variation normal values buy genuine trandate online, may be determined by the need for accessory devices heart attack grill menu trandate 100mg with mastercard. Surprisingly prehypertension diabetes cheap trandate 100mg free shipping, the effectiveness in terms of disability and handicap reduction achievable by using accessory aids has only recently been addressed and the identification of particular groups likely to benefit blood pressure chart health canada generic trandate 100 mg without prescription, and in what circumstances hypertension vs high blood pressure purchase cheap trandate line, has been poorly researched with most available literature limited to simple descriptions of the devices available. Accessory devices to date have often been the products of small electronic and engineering companies and often seem to be targeted at the severely and profoundly hearing impaired. Technical specifications abound, but real-life performance is often lacking and there is still a great need for the individual to try out these devices at home to see if they are suitable. Recently, with the maturation of digital technology, more sophisticated equipment is becoming available which offers the prospect of a significant improvement, but we are only just beginning to understand why only a minority of the hearing impaired make full use of what has been available for some time. We will not go into great technical detail, this is available from more detailed texts and the manufacturers, but we will hopefully address the issues from a more patient/client perspective. We will then review the few scientific studies available and the evidence base for the role and effectiveness of accessory devices. Aids to communication Perhaps the fundamental difficulty of the hearing impaired using a personal hearing aid is hearing in noise. Normally this means the separation of the signal of interest, usually speech, from a noisy or reverberant environment. For normal people, a speech-to-noise (S/N) ratio of 16 dB or better is required for clear understanding of speech. Plomp and Mimpen5 have estimated that for every 5 dB of hearing impairment a 1 dB increase in S/N ratio is required to maintain comprehension. Moving the microphone closer to the sound source and/ or away from the noise would clearly be a great help. The first resembles a body-worn personal hearing aid with lightweight headphones with the microphone either in the unit or linked by a wire to the main unit. This type of system is simple, easy to operate and inexpensive and it is surprising that they are not more widely used. They seem to have found most favour in homes for the elderly and in hospital wards. The first are aids to communication whether purely auditory, using speech directly or some other meaningful input, such as text. The second are alerting or warning devices, which enable the listener to respond to important signals, such as doorbells and alarm clocks. Telephones are a category worthy of separate consideration because of their importance in our lives and where both communication and alerting are factors to be considered. Within these broad categories there are personal devices, as well as those used in public areas, such as churches, theatres, etc. Radio systems were first used in classrooms and this is still where they are most used but their application is becoming more widespread. Most modern systems allow an input from the surrounding class, which can be mixed to provide the desired balance. In a more open conference situation, a microphone can be placed in the centre of the table, but here the advantage of the microphone being placed very close to the speaker is reduced. The disadvantages of these versatile systems is that they are fairly complex and expensive and have to be set up carefully to achieve best performance. Systems using a loop are available for use within buildings or for linking directly to a telephone. In a typical room installation, a remote microphone is linked to an amplifier, which feeds its output to a wire, looped round a room. The field can be brought closer by the user wearing a loop around his/her neck or sitting on an adapted cushion. The technology is simple and cheap, but there are a number of disadvantages: the signal strength varies in the field and is greatest nearest to the loop wire. The position of the telecoil within the hearing aid is also a factor and, unlike a direct coupling, acoustic feedback can be a problem, particularly with high-powered aids. These can also be linked to lights to provide a visual alert or a vibrotactile stimulus. Universal devices are available, equipped with a microphone, which can be sited close to the normal alerting device and set to go off at a particular sound level input. More dedicated devices can be wired to the house lights or linked into the house wiring system which can carry a signal to any part of the house via a mains socket. Last, but not least, a dog is often a highly effective alerting device and many are now trained to respond to auditory signals, much like the familiar guide dog for the blind. Telephones Talking on the telephone is a particular problem for the hearing impaired, especially the more severely and profoundly affected, as there are no visual clues. Video telephones are becoming a reality and these devices should be a great help to the hearing impaired, although they are appearing as mobile cell phones and seem more aimed at the lifestyle market than the hearing impaired. There are particular problems for the hearing impaired using mobile digital phones and this has been the topic of quite a few articles. This also takes in unwanted background noise and although useful for the normal hearing user can make listening more difficult for the hearing-impaired user. A very simple tactic for the hearing-impaired user is to cover the mouthpiece when listening or push the mute button if one is fitted. Many hearing aid users attempt to use their ordinary hearing aids with an unadapted telephone. Simply turning the earpiece away from the aid can help or there are very simple acoustic telepads available which can help this problem. Amplified handsets are available often with a gain control and these can be either portable or fixed. Gains of about 20 dB are typically possible and these can allow the hearing-impaired user to use them without their personal aid. In general, telephones are becoming more hearing impaired friendly and the manufacturers and telephone companies are able to advise and supply appropriate equipment. For the more profoundly impaired and those with very poor speech discrimination, there may be residual difficulties despite providing an enhanced audio signal and systems using text may be needed. There may also be situations where even the more moderately impaired may want to get a very clear message and using text is helpful. Systems are available to convert speech into text, but to date these have usually been via a fast stenotypist and are not fully automatic. Warning and alerting devices Devices in this area were originally aimed at the more profoundly impaired, but their use has become more widespread. Here we are considering an alerting stimulus, which is a much simpler proposition than the complex sounds of speech. Ordinary daily living requires us to respond to a wide variety of signals and warnings, which may include telephones ringing, alarm clocks, doorbells, fire alarms, etc. Doorbell alerting systems are often simply a louder bell or the repositioning of a standard device and the same is Chapter 239e Accessory devices] 3669 Text telephones are available aimed at the profoundly impaired. This type of system can be enhanced by using a communication assistant in a relay station that can quickly type the spoken word for the user. When considering provision on a population basis, as has been done for personal hearing aids, then clearly hard evidence on what works is vital. There have been many good general review articles on what is available,12, 13, 14 and on likely candidacy,15 but the general literature unfortunately goes little beyond technical specifications. There are a few studies in the disability and handicap domains on the performance of systems with real people and epidemiological reports on possession of devices. The current problem with the wide adaptation of this technology is the capacity and speed of the phone lines with many current systems using several parallel lines to transmit visual information of sufficiently high quality. Broadband technology should help in this area and would allow the use of sign language, such that the prelingually deaf may at long last have access to the telephone. There are text systems being developed which can work in real time with modern fast personal computers, such that speech can be rapidly and accurately converted into text, although to date these have been marketed as a personal secretary substitute rather than an aid for the hearing impaired. This is already starting to open up many exciting possibilities, not just in signal processing but also in communication. New technology, such as Bluetooth, may change the way that digital devices can communicate with each other. Bluetooth is named after a Norwegian king who was able to get various tribes talking to each other. A Bluetooth-enabled hearing aid using a short-range networking system should be able to link with telephones or distant microphones without the need for other equipment. This is slowly starting to happen with the mobile phone companies at the forefront of new developments. Beecher10 has described a system using Bluetooth with a wristband acting as a control centre. Currently, Bluetooth technology is still rather bulky and the need for battery power is such that currently it would be difficult to fit a system that would both transmit and receive into a small hearing aid, but this will almost certainly improve. Generally speaking, reports from affluent and technologically advanced countries, such as the United States, and socially advanced countries like Scandinavia show the highest rates of possession. There is supporting evidence from other sources that cost, access to information and the ability to try out equipment are important factors in accessory aid possession. Other factors, which have been shown to be important, are embarrassment and stigma. It is worth looking at what has actually been shown to help in real-life situations. Self-report has tended to be the main research tool, but performance tests have also been used. Clearly, the effectiveness of alerting devices should be easy to assess by self-report and certainly simple alerting systems, such as light systems, dogs and properly situated bells, have been shown to be effective and helpful, although the difficulty in using a purely auditory signal in the profoundly impaired has been demonstrated. Recent studies have shown that difficulty at work for the hearing-impaired causes considerable stress and optimal performance, which may involve using accessory devices, could be critical in this situation. Individuals will make a personal judgement on how much a hearing impairment affects them and how far they will go to deal with their disability and considering accessory aids is probably currently considered as going quite far. This is a complex area and there has been much work in this field in recent years, a detailed discussion of which is beyond the scope of this article, but certain points emerge such as the importance of significant others. Accessory devices have come under the auspices of the Social Services Department who often are not fully aware of how the patient is managed in the Audiology Department. The provision of accessory aids has been perhaps artificially separated from other aspects or rehabilitation. It is, of course, not only a matter of providing systems such as radio aids; the difficulty in setting up currently available systems optimally together with maintenance and troubleshooting should not be underestimated. The problem is that many devices are complex and have amplification characteristics such as available gain and maximum power output similar to personal hearing aids and a consideration of the frequency response of the device in relation to the pattern of the individuals hearing loss may be important. Involvement of a hearing professional is clearly desirable in selection and fitting Chapter 239e Accessory devices] 3671 of all but the simplest device so that benefit can be maximized. Clearly the patient must have the ability to try out a particular device and be involved in the selection process. Significant others should also be involved, especially when they may be involved in setting up and using the device in question. There have been a number of different strategies suggested for content and timing of device selection. Certain common themes can be noted, however, and the list given under Best clinical practice below is simply a suggestion of how accessory aids could be provided in a conventional audiology practice. Remote microphones linked to a personal aid offer an excellent method of improving signal-to-noise ratios. The severely and profoundly impaired have difficulty with purely auditory devices. That being said it is clear that relatively cheap, low technology devices and simple home modifications are effective, but to date individuals have made surprisingly little use of what would seem to be helpful. Perhaps the poor uptake of devices such as radio aids linked to remote microphones is the greatest disappointment. This would clearly be a solution to the signal-to-noise ratio problem of which so many of the hearing impaired bitterly complain and the development of convenient technology in this area is keenly awaited. At the centre is, of course, the hearing-impaired individual with a particular lifestyle, together with significant others, and we are just beginning to really understand how an individual lives with his/her disability. There is evidence that the deaf and hard of hearing are becoming more aware of what is possible and available and will demand the best rehabilitation which will include the most effective accessory aids both for personal and public applications. Actual and predicted wordrecognition performance of elderly hearing-impaired listeners. Using talking lights illumination-based communication networks to enhance word comprehension by people who are deaf or hard of hearing. Candidacy and management of assistive listening devices: Special needs of the elderly. Provision of hearing aid services: A comparison between the Nordic countries and the United Kingdom. Acquisition of hearing aids and assistive listening devices among the pediatric hearing-impaired population. Clinical characterization of severely and profoundly hearing impaired adults attending an audiology clinic. Factors associated with assistive technology discontinuance among individuals with disabilities. Telephone performance of persons with hearing handicap in relation to speech reception threshold. Comparison of conventional amplification and assistive listening devices in elderly persons. Group rehabilitation of middle aged males with noise-induced hearing loss and their spouses: Evaluation of short and long term effects. Outcomes of hearing aid fitting for older people with hearing impairment and their significant others. By the age of 65, one-third of the population has suffered symptoms of imbalance and in the community, one in five of the adult population have suffered such symptoms, with 30 percent of these suffering symptoms for more than five years. Thus conditions affecting the vestibular system are important both numerically, and also in terms of social and economic morbidity.

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