- causes are from damage to the hair cells or nerves that sense sound waves.
a. acoustic trauma - prolonged exposure to loud noises causes the hair cells on the cochlea to become less sensitive.
b. barotrauma (pressure trauma) or ear squeeze - usually in divers
c. head trauma - A fracture of the temporal bone can disrupt the nerves of the auditory system
d. ototoxic drugs - Certain drugs can affect hearing by damaging the nerves involved in hearing. Usually this occurs when large or toxic doses are used but may also occur with lower doses. Examples include:
i. antibiotics including aminoglycosides (gentamicin, vancomycin), erythromycins, and minocycline
ii. diuretics including furosemide and ethacrynic acid
iii. salicylates (aspirin) and nonsteroidal anti-inflammatories (NSAIDs) such as ibuprofen and naproxen
iv. antineoplastics (cancer drugs)
e. vascular diseases including sickle cell disease, diabetes, leukemia, polycythemia, and diseases in which excessive blood clotting occurs.
f. children and adults with kidney problems are more susceptible to sensorineural hearing loss.
g. Ménière's disease - A disease that affects hearing and balance and is usually associated with tinnitus. It has a gradual onset and often progresses to deafness and severe vertigo. The cause is unknown.
h. acoustic neuroma - A tumor in the auditory nerve. Usually associated with ringing in the ears.
i. infections - mumps, measles, influenza, herpes, mono, syphilis, meningitis
- not a disease, but rather a symptom, a marker for other conditions
- of the 10% of pts with some type of ear problem, 85% have tinnitus
- perception of sound in absence of an acoustic stimulus
- mb buzzing, ringing, roaring, whistling, hissing or more complex sounds
- mb intermittent, continuous, pulsatile
may be a sx of nearly all ear problems - noise exposure, head trauma, hearing problems, dizziness, loss of balance, recent dental problems, bruxism, stress, ototoxic med., smoking, caffeine
cranial N function and hearing
carotid artery bruits?, HTN? recent dental work? signs of bruxism? myofascial spasms? paraspinal and SCM muscles, TMJ
Outer ear: cerumen or foreign objects in external ear canal, external ear canal tumors, TM
perforations, and cholesteatoma
Middle ear: otosclerosis, ossicular chain discontinuity, ossicular chain fixation, and
Inner ear: cochlear hydrops, cochlear otosclerosis, perilymph fistulas, noise damage,
congenital malformations, vestibular schwannomas, presbycusis, allergic
reactions, bacterial infections, viral infections, ototoxic medications or chemical agents, meningiomas, and atrophy
Systemic: hyperlipidemia, allergies, diabetes, hypertension, hypotension, syphilis, and
cardiovascular, endocrine, and metabolic diseases
Tinnitus secondary to temporomandibular joint (TMJ) disorders, cervical injuries,
obesity, menses, stress, dietary deficiencies, and intake of stimulants such as
nicotine and caffeine have been noted by tinnitus patients.
a sudden unilateral loss of vestibular function and hearing.
acute onset of severe, often incapacitating, vertigo, frequently associated with nausea and vomiting
patient is often bedridden while the symptoms gradually subside.
vertigo eventually resolves after several days to weeks; however, unsteadiness and positional vertigo may persist for several months.
hearing loss is also present and may be the primary presenting symptom in many patients.
an URI precedes the onset of symptoms in up to 50% of cases.
usually observed in adults aged 30-60 years and is rarely observed in children.
PE:findings include spontaneous nystagmus towards the unaffected side with diminished or absent caloric responses in the affected ear.
hearing loss is usually mild to moderate and typically evident in the higher frequencies (>2000 Hz), although any degree or type of hearing loss may be present.
Unique form of viral labyrinthitis is herpes zoster oticus, (Ramsay-Hunt syndrome).
cause of this disorder is reactivation of a latent varicella-zoster virus infection occurring years after the primary infection.
initial symptoms are deep, burning, auricular pain followed a few days later by the eruption of a vesicular rash in the external auditory canal and concha. Vertigo, hearing loss, and facial weakness may follow singly or collectively.
symptoms typically improve over a few weeks; however, patients often suffer permanent hearing loss and persistent reduction of caloric responses.
defined as an abnormal sensation of motion that is elicited by certain critical provocative positions, that usually trigger nystagmus. The character and direction of the nystagmus are specific to the part of the inner ear affected and the pathophysiology.
first described by Barany in 1921. The characteristic nystagmus and vertigo associated with positioning changes were attributed at that time to the otolithic organs. In 1952, Dix and Hallpike performed the provocative positional testing named in their honor. They further defined classic nystagmus and went on to localize the pathology to the proper ear during provocation.
new variations of positional vertigo have been discovered. What was previously grouped as BPPV is now subclassified by the offending semicircular canal (SCC) (ie, posterior superior SCC vs. lateral SCC) and further divided into canalithiasis and cupulolithiasis (depending on its pathophysiology).
canalithiasis (literally, "canal rocks") is defined as the condition of particles residing in the canal portion of the SCCs (in contradistinction to the ampullary portion). These densities are considered to be free floating and mobile, causing vertigo by exerting a force. Conversely, cupulolithiasis (literally, "cupula rocks") refers to densities adhered to the cupula of the crista ampullaris. Cupulolith particles reside in the ampulla of the SCCs and are not free floating. Caffeine, red wine and carbonated beverages can aggravate.
Signs & Sxs: onset is typically sudden, many wake up with the condition, noticing the vertigo while trying to sit up suddenly. Usually triggered by the sudden action of moving from the erect position to the supine position while angling the head 45° toward the side of the affected ear. Symptoms start very violently and usually dissipate within 20 or 30 seconds
thereafter, propensity for positional vertigo may extend for days to weeks, occasionally for months or years. In many, the symptoms periodically resolve and then recur.
severity covers a wide spectrum. In patients with extreme cases, the slightest head movement may be associated with nausea and vomiting.
usually do not feel dizzy all the time. Severe dizziness occurs as attacks triggered by head movements. At rest between episodes, patients usually have few or no symptoms. However, some patients complain of a continual sensation of a "foggy or cloudy" sensorium.
Etiology: A few factors predispose patients to BPPV. These include inactivity, acute alcoholism, major surgery, and central nervous system (CNS) disease.
idiopathic pathology - 39%trauma - 21%
ear diseases - 29%otitis media - 9%
vestibular neuritis - 7%Ménière's disease - 7%
otosclerosis - 4%sudden sensorineural hearing loss - 2%
CNS disease - 11%vertebral basilar insufficiency - 9%
acoustic neuroma - 2%cervical vertigo - 2%
generally unremarkable. All findings except those from the Dix-Hallpike maneuver may be normal.
Dix-Hallpike maneuver is the standard clinical test for BPPV.
finding of classic rotatory nystagmus with latency and limited duration is considered pathognomonic. A negative test result only suggests that active canalithiasis is not present at that moment.
disorder in which there is an increase in volume and pressure of the endolymph of the inner ear.
typically presents with waxing and waning hearing loss and tinnitus associated with vertigo. Patients may report an abnormal sensation of pressure or fullness in the ears.
multiple episodes may occur over a span of years, with remissions in between each acute episode.
Up to 50% of patients with Ménière's syndrome have a positive family history
exact cause of Ménière's is unknown. The current theory is that it is the response of the inner ear to injury.
Age: typically occurs in early- to mid-adulthood; men and women are affected equally
Signs & Sxs: prodrome of a fullness or blocked sensation in one ear
tinnitus followed by a decrease in hearing
vertigo is experienced concurrently with or follows shortly after the hearing symptoms; typically lasts minutes to hours but may last as long as several days.
nausea, vomiting, diarrhea, pallor, and sweating common with an acute attack.
Course: following an acute episode, hearing may return to normal. After multiple episodes, hearing usually is decreased.
headache and gait unsteadiness may persist for several days
recurrences are the rule; however, frequency of recurrences are unpredictable.
rarely, patients may experience such severe vertigo that they will collapse to the ground. These Ménière-related drop attacks are known as Tumarkin crises. Bilateral Ménière's disease occurs in as many as one third of these patients.
PE: complete neurological examination is necessary to R/O other conditions, esp. cranial nerve examination
vestibular maneuvers (Nylen-Bárány, Dix Hallpike) may be helpful in diagnosing this syndrome. Interpretation of either of the following maneuvers is identical.
Differential dx includes:
otitis mediaischemic stroke
subarachnoid hemorrhage salicylate toxicity
transient ischemic attackvestibular neuronitis
Diagnosis: 3 criteria necessary
1. isolated attacks of whirling, vertigo usu with n/v lasting for several hours
2. tinnitus - multipitched, multisounds, roaring, whistling
severe, unilateral, continuous, constant, fluctuating
3. sensory hearing loss (progressive) [10-15% are bilateral]
alternating attacks and remissions are normal
balance problems tend to resolve with time, while hearing tends to worsen.
most symptoms can be managed with treatment including a low-salt, low sugar diet and avoidance of chocolate, coffee and alcohol
approximately 5-10% of patients require surgery for incapacitating vertigo.
Etio: 2nd most common dz of childhood (URI # 1); ~ 20 million annual physician visits
more than one third of children experience 6 or more episodes of AOM by age 7 years. 1st infx often within 1 month of solid food introduction
anatomic and immunologic factors in the presence of acute infection are the main causes of acute otitis media.
Pneumococcus species, Haemophilus influenzae, and Moraxella species are most commonly involved in otitis media.
less common causes are other bacteria, Mycoplasma species, and viruses.
sterile effusions occur in approximately 20% of cases studied.
daycare leads to an increased incidence of Uri's.
bottle-feeding increases the incidence compared with breastfeeding.
smoking in the household clearly increases the incidence
family history of middle ear disease increases the incidence.
AOM in the first year of life is a risk factor for recurrent acute otitis media.
Signs & Sxs: throbbing (or often NO) pain, fever, decreased hearing, n/v, moodiness,
dizziness, discharge if ruptures
PE:bulging, red TM, possible fluid line (yellow-gray if pus)
if perforation occurs in a marginal location, esp. pars flaccida, check regularly for cholesteatoma formation.
- serous OME is the most common complication.
may cause mild discomfort in some patients; however, if it is bilateral, hearing loss with resultant speech delay may occur in infants.
- mastoiditis used to be a common complication, but now with antibiotics it is rare.
- perforation of the tympanic membrane is a frequent, but usually not serious
chronic inflammation of middle ear that persists at least 6 weeks with signs of infection (fever, otalgia, irritability)
Etio:i) acute OM resulting in perforation - central perforation à conductive hearing loss
ii) trauma to ear, head
iii) ET blockage - inflammation, adenoids
Signs & Sxs: hearing loss, chronic d/c, painless, recurrent OM, frequent sore throats,
runny nose, colds
PE:hole in the TM, usu. normal color