ED Approach to Dizziness
AVS-acute vestibular syndrome
Treatment Article (Walker MF Treatment of Vestibular Neuritis)
quick phase nystagmus towards the intact ear)
treat with steroid taper similar to Bell’s palsy
(Stroke 2009;40:XX Kattah JC)
horizontal head impulse test is a measure of the (VOR) vestibulo-ocular reflex
abnormal leans towards AVS, but does not rule-out central
AVS should be associated with horizontal nystagmus that beats predominantly in one direction and increases in intensity when the patient looks in the direction of the fast phase. vertical nystagmus = central cause
Test of Skew
vertical ocular misalignment
Ocular tilt reaction=skew deviation, head tilt, and ocular counterroll
test with alt cover
tell pt to look straight ahead
cover eyes alternately
will see skewed eye move
long tract signs-
(Acad Emerg Med 2009;16:970)
BPPV-short lived less than a minute
article claims suppressants do not work
APV-may be more prevalent in the ED population, continuous dizziness lasting days to weeks. Even when a single spell, lasts hours.
should get steroids and suppressants (H1, Anticholinergics, Promethazines, Benzos)
The physical examination should focus on the systems that are involved in postural control and dizziness. Because the only objective sign of vertigo is nystagmus, examination of the eyes is extremely important in evaluating the dizzy patient. The general physical examination is often unrewarding in the dizzy patient. Possible etiologic clues include pressure asymmetry; orthostatic blood pressure change; cardiac irregularities; ear, nose, and throat abnormalities; head or neck bruit; abnormal range of neck motion; congenital abnormalities; or the stigmata of other illness that may cause dizziness.
The primary utility of the general neurologic evaluation is in looking for other indications or clinical signs that imply brain stem or other central nervous system sources for the patient’s complaints. Signs of abnormal central nervous system origin are most often found in examination of the cranial nerves. Mental status examination may give evidence of psychiatric or cognitive difficulties, which may affect the quality of the subjective data obtained from the patient. The Romberg has traditionally been considered a test of proprioceptive function. If this is negative, performing the sharpened Romberg may reveal subtle balance deficiencies undetectable with the ordinary Romberg test, especially in patients with acoustic tumors. A sharpened Romberg test is performed by having the patient place the heel of one foot to the toe of the other, with arms folded and eyes closed. Normal individuals should be able to stand in this position for longer than 30 seconds without significant sway.
Observation of the patient’s gait during the examination may reveal signs of unsteadiness, staggering, or a broad-based stance during walking. Additionally, one may get a sense of how well the patient is able to function.
The eyes should be carefully observed, preferably in a subdued light, for the presence of nystagmus. Vestibular nystagmus typically consists of a horizontal-rotatory, jerky motion with a slow and a fast component. Nystagmus that is equally rapid in both directions is not vestibular in origin. True vestibular nystagmus should also be suppressed by fixation of the gaze, convergence of the eyes, or gazing in the direction of the slow phase. Vertical nystagmus is never seen in vestibular disorders, whereas nystagmus in which the eyes wander or oscillate is often ocular in nature and may be related to a congenital disorder.
Ménière’s syndrome presents with a symptom constellation of aural fullness, fluctuating sensorineural hearing loss, tinnitus, and vertigo. The attack of vertigo reaches a maximal intensity within minutes of its onset then slowly subsides over the next several hours. The patient is usually left with a sense of unsteadiness and dizziness after the acute episode. In most cases, the patient is able to localize the symptom to the involved ear because of the associated hearing-related symptoms. In the early stages, the sensorineural hearing loss is in the low frequencies and is completely reversible, but in later stages a residual hearing loss remains and may involve both the middle and the high frequencies. The episodes may occur at irregular intervals for years, with periods of remission unpredictably intermixed. Eventually the syndrome reaches a burned-out phase, resulting in significant permanent hearing loss but a cessation of the vertigo.
Ménière’s syndrome is, by definition, idiopathic. Multiple causes have been suspected, including allergy, an autoimmune disorder, viral infection, and hormonal effects.8 The pathologic correlate is an excessive accumulation of endolymph, resulting in hydrops. As the volume of the endolymph increases, the membranous labyrinth expands and ruptures, resulting in hearing loss and vertigo.19
The treatment is largely aimed at preventing osmotic shifts in the endolymph. Medications, including vasodilator therapy and diuretics, are helpful for many patients.28 Patients are empirically placed on a low-sodium diet and asked to restrict caffeine and smoking. Specific treatment of any underlying allergies with immunotherapy or dietary avoidance of offending food allergens is also recommended. In a minority of cases, medical treatment is insufficient to control the episodes of vertigo, necessitating a surgical procedure. An endolymphatic mastoid shunt may be placed in the endolymphatic sac to decompress excess endolymph, or a selective sectioning of the vestibular nerve may be performed. In cases in which vertigo is disabling and there is no longer any useful hearing, a labyrinthectomy, with destruction of the neural elements, results in an effective control of vertigo.
The most prominent symptoms of tumors in the brain stem are hearing loss and tinnitus, rather than vertigo. Acoustic neuromas are benign schwannomas of the vestibular nerve sheath and are the most common cerebellopontine angle tumor. The vertigo associated with acoustic neuromas is usually mild or may even be absent: The slow growth rate of the tumor allows for central compensation. An acute attack of vertigo may be precipitated by a sudden swelling or hemorrhage of the tumor with brain stem compression. Other than eighth nerve dysfunction, the earliest neurologic sign in these patients is the loss of the corneal reflex.34 The diagnostic test of choice when the history or audiometric or other findings suggest this diagnosis would be a magnetic resonance imaging scan with gadolinium enhancement. The treatment is surgical removal of the tumor.
from small cerebellar hemorrhage adjacent to the vermis
looks just like BPPV except may have direction changing nystagmus
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Signs of Vestibular Neuritis
- Spontaneous, unidirectional, horizontal nystagmus is the most important physical finding.
- Fast phase oscillations beat toward the healthy ear.
- Nystagmus may be positional and apparent only when gazing toward the healthy ear, or during Hallpike maneuvers.
- Patients may suppress their nystagmus by visual fixation.
- Patient tends to fall toward his or her affected side when attempting ambulation or during Romberg tests.
- Affected side has either unilaterally impaired or no response to caloric stimulation.
- Vestibular neuronitis is unlikely if any of the following findings are present. The following symptoms should be absent:
- Multidirectional, nonfatiguing nystagmus suggesting vertigo of central origin
- Hearing loss
- Other cranial nerve deficits
- Truncal ataxia (suggests cerebellar disease or another CNS process)
- Inflamed tympanic membrane
- Mastoid tenderness
- High fever
- Nuchal rigidity
Isolated dizziness was associated with only 0.7% (9 of 1297) rate of stroke/tia. Imbalance with dizziness as referent was more likely to be stroke (Stroke 2006;37:2484)
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