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Terms in this set (38)

True vertigo tests:
a. caloric testing (cold water in ear)
​cold water into external canal produces tonic eye deviation to side of cold water and horizontal nystagmus to opposite side
​1-10 ml of ice water, with pt supine, head 30 degrees elevation. Record degree and duration of nystagmus from each ear with 5-minute break between.
Test + for vest. dysfunction is asymmetry > 20% with affected ear producing less severe or less prolonged nystagmus; with nystagmus, pt has transient vertigo identical to usual dizziness
​b. Nylen-Bárány maneuver:
​- patient sits at the end of the examining table and is laid back quickly, while the head is supported and the neck is carefully hyperextended. The head is first turned toward one shoulder; then, the maneuver is repeated with the head turned toward the other shoulder; look for nystagmus (there may be a 10-20 sec. latency period)
c. Dix-Hallpike maneuver - to identify BPPV commonly caused by otolith debris (canalith) floating in the semicircular canals (canalithiasis) or adhering to the cupula (cupulolithiasis). BPPV is due to posterior semicircular canal canalithiasis approximately 90% of the time.
- is performed by rapidly moving the patient from a sitting position to the supine position with the head turned 45° to the right. After waiting approximately 20-30 seconds, the patient is returned to the sitting position. If no nystagmus is observed, the procedure is then repeated on the left side.

Non-vertigo tests:​
d. lightheadheadness
orthostatic hypotension- BP drop of 15-20 mm Hg
​cardiovascular reflexes
​carotid sinus massage
valsalva
e. disequilibrium
​cerebellar and proprioception
​walking and turning
​forward & backward walking
​drifts toward side of lesion ​

f. miscellaneous
hyperventilation for 2 minutes by the clock
​ sitting, breathe quickly and deeply, while observing for nystagmus
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%

Physical:
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.

Etiology​
​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:
migraine headache​hypothyroidism
labyrinthitis​multiple sclerosis
otitis media​ischemic stroke
subarachnoid hemorrhage​ ​salicylate toxicity
transient ischemic attack​vestibular 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]

Prognosis:
​​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.

Risk factors
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.
Complications:
- 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