Approach
The differential diagnosis of patients presenting with dizziness and vertigo can often be narrowed with a thorough history and physical exam. Imaging studies (e.g., magnetic resonance imaging [MRI] and computed tomography [CT]) are typically ordered as patients with posterior fossa neoplasms can have a variety of presentations that can mimic other vestibular disorders. Anyone presenting with unilateral inner ear type symptoms should be investigated for retrocochlear pathology. Posterior fossa tumors include vestibular schwannomas (acoustic neuroma), meningiomas, cerebellar or brainstem tumors, and epidermoid cysts.
History
Patients with labyrinthitis and vestibular neuritis typically present with severe room-spinning vertigo, associated nausea and vomiting of variable duration, disequilibrium (problems with balance), and dizziness. Spontaneous nystagmus is common. In addition, patients with labyrinthitis have unilateral hearing loss and/or tinnitus (ringing in the ear). The hearing loss is sensorineural (i.e., related to inner ear/eighth cranial nerve) rather than conductive (i.e., secondary to middle ear causes). Hearing is intact in vestibular neuritis as the cochlea is not affected. Significant hearing loss, with or without associated tinnitus, differentiates labyrinthitis from vestibular neuritis.[32] Vertigo is of gradual onset and develops over several hours; sustained vertigo may follow, which lasts from days to weeks. The vertigo in patients with labyrinthitis and vestibular neuritis may be present at rest unlike that in patients with benign paroxysmal positional vertigo. Nevertheless, it may be triggered by movements.[5] If the patient experiences more than one episode of room-spinning vertigo, a diagnosis of Meniere disease should be considered. Although vertigo may be caused by infectious conditions, there are a range of potential causes that need to be ruled out (e.g., post-traumatic vertigo, or vertigo of cerebrovascular origin).
Important questions that are critical in establishing the diagnosis include:
Can you describe your dizziness (e.g., room spinning, imbalance, floating, lightheadedness)? Dizziness is a broad term, and this question helps to determine the actual sensation experienced by the patient.
Tell me about your first episode of vertigo. How long did this episode last? This can help the clinician determine if the patient has had labyrinthitis or vestibular neuritis.
How long are your current dizzy spells? Examining the duration of the patient's dizzy spells can provide critical information for the diagnosis.
Have you ever had any prior episodes of dizziness or vertigo? Recurrent vertigo also helps to narrow down the differential diagnosis.
Do you have any other associated symptoms (i.e., hearing loss, tinnitus, or ear fullness)? Auditory symptoms concurrent with dizziness make a peripheral source of the dizziness more likely. These symptoms are common in labyrinthitis but not in vestibular neuritis.
Do changes in body position cause dizziness? A positive response to this question narrows the differential to the following: benign paroxysmal positional vertigo, orthostasis, uncompensated peripheral vestibulopathy, or bilateral vestibulopathy.
Do you have any history of headaches (e.g., migraine, muscle tension)? A positive response increases the likelihood that migraine may be the source of dizziness.
Have you started new (or changed) any drugs? There are a number of drugs that can cause dizziness.
What makes your dizziness better or worse? Movement associated dizziness helps narrow the differential diagnosis.
Have you recently had an upper respiratory tract infection? A positive response may indicate vestibular neuritis.
It is critical to evaluate for other neurologic symptoms such as dysarthria, dysphagia, facial pain or numbness, facial weakness, and extremity weakness or numbness, as these would point to a cerebrovascular accident involving the brainstem.[1][33]
Several tools, such as the Dizziness Handicap Inventory and the SF-36, can be used to assess the impact of dizziness on patients’ quality of life.[34][35]
Another approach that focuses on assessing dizziness, known as the TiTrATE (Timing, Triggers, And Targeted Exams) approach, examines the timing and potential triggers for symptoms to help diagnose the cause.[36]
Physical exam
Patients presenting in the acute setting may have significant difficulty walking. Spontaneous horizontal-rotary nystagmus (rapid involuntary movement of the eyes) with the fast phase beating toward the uninvolved ear is also frequently present.[1][4]
The patient's balance should be assessed using tandem gait and Romberg testing.[1][4] Patients will probably not be able to perform tandem gait (walking with one foot directly in front of the other foot, heel-to-toe) and may fall with Romberg testing (standing straight up with feet together and eyes closed).
Examination with a Weber 512-Hz tuning fork (placing the tuning fork on the forehead or maxillary teeth and asking the patient to state in which ear the sound was louder) can quickly localize the affected ear and determine whether the hearing loss is sensorineural or conductive.[37] The sound will be perceived in the affected ear when a unilateral conductive hearing loss is present or in the unaffected ear when there is a unilateral sensorineural hearing loss. The result of this test is combined with the result of the Rinne test to interpret the type of hearing loss.[37] In patients with vestibular neuritis, hearing would be normal.
Rinne testing allows the examiner to determine whether any hearing loss is secondary to middle ear (conductive hearing loss) or inner ear/eighth cranial nerve (sensorineural hearing loss) causes.[37] The base of a 512-Hz tuning fork is placed on the mastoid and the patient indicates when he or she no longer hears the sound. Once the sound is no longer audible, the tuning fork is placed in front of the ear and the patient is asked whether he or she hears the sound. If the sound is louder when the tuning fork is on the mastoid, then the patient has a conductive hearing loss. If the sound is louder with the fork in front of the ear, the hearing loss is sensorineural or normal.[37] An acute unilateral sensorineural hearing loss accompanying the vertigo may indicate labyrinthitis; hearing is not affected in vestibular neuritis.
A thorough examination of the ear with an otoscope or microscope allows diagnosis of otitis media and cholesteatoma. The presence of otorrhea (ear discharge) should alert the clinician to the presence of acute or chronic otitis media with tympanic membrane perforation. Careful inspection of the entire tympanic membrane should identify a cholesteatoma unless there is significant debris in the ear canal that obscures visualization.
How to perform an examination of the ear.
[Figure caption and citation for the preceding image starts]: An axial CT (without contrast) of the temporal bone of the left ear demonstrating direct erosion into the horizontal semicircular canal by cholesteatomaFrom the personal collection of Dr Tiffany Hwa; used with permission [Citation ends].
There should be no evidence of other neurologic deficits such as upper or lower extremity weakness, hoarseness, or facial weakness or numbness. The three-step bedside oculomotor exam Head-Impulse, Nystagmus, Test-of-Skew (HINTS) has been found to identify stroke with a high degree of sensitivity and specificity in patients with acute vestibular symptoms, and it may rule out stroke more effectively than early diffusion-weighted MRI.[38] Based on the HINTS model, one algorithm suggests that stroke should be considered in patients presenting with acute-onset dizziness if:[39]
there is a central pattern of nystagmus
there is skew deviation
there is a negative head impulse test (in patients with nystagmus)
there are any central nervous system signs on focused neurologic examination, or
the patient is unable to sit or walk unaided.
The HINTS examination, when performed by neurologists or trained physicians was found to be sufficiently accurate in ruling out a central vascular cause of vertigo in individuals presenting with acute vestibular syndrome.[40][41] However, when performed by emergency department physicians, the accuracy was found to be low in one systematic review and meta-analysis.[40]
The presence of meningeal signs should be investigated if bacterial meningitis is a consideration.
Cerebellar function should be examined by requesting the patient to perform finger to nose, heel to shin, and rapid alternating movement tests.[33]
Audiometry
An audiometric exam is useful to document the extent of hearing loss and to confirm the affected ear in patients with labyrinthitis. Hearing loss is typically of the sensorineural type. However, patients with inner ear malformations (i.e., enlarged vestibular aqueduct) may present with similar symptoms and a mixed hearing loss with a significant sensorineural component.
Vestibular testing with electronystagmography, rotary chair test, and vestibular-evoked myogenic potentials is not indicated in the acute setting. However, these tests may provide additional information on vestibular compensation and site-of-lesion testing after the patient has recovered from the acute stage of labyrinthitis.[4]
Vestibular tests
Vestibular tests such as electronystagmography, video head impulse testing, videonystagmography, rotary chair test, and vestibular-evoked myogenic potentials can provide additional information on vestibular compensation in labyrinthitis and vestibular neuritis.
Laboratory tests
Patients with labyrinthitis secondary to bacterial meningitis should have appropriate cerebrospinal fluid cultures performed. Additional serologic testing for syphilis and HIV may be warranted if the presentation is atypical or if the patient has additional risk factors.[42] If the serologic tests are negative, autoimmune conditions (e.g., Cogan syndrome or Behcet disease) may be considered in patients with variable duration and fluctuating inner ear symptoms.[43] It should be recognized that viral testing may not yield positive results at the time of illness and that there is no role for empiric antiviral therapy in the treatment of labyrinthitis and vestibular neuritis in the absence of other indications. For patients who have severe nausea and vomiting, a basic metabolic panel should be evaluated to select the appropriate crystalloid and electrolyte replacement. Check capillary blood glucose in all patients with suspected stroke and arrange urgent neuroimaging.[44]
Imaging
Imaging can help to further assess the differential diagnoses for a patient presenting with hearing loss with or without vertigo.
If a stroke is suspected, brain imaging (nonenhanced CT or MRI) should be ordered (at most within 1 hour of arrival at hospital).[45] Most acute strokes would not be picked up by CT, but a normal CT scan does not rule out a stroke - particularly in the first few hours. There might be a delay on MRI, but a normal diffusion-weighted MRI scan is very unlikely if the patient has had a stroke.[46] If a temporal bone fracture is suspected based on the patient’s history, a CT scan of the head can delineate the extent of the fracture.[47]
Most patients presenting with isolated symptoms suggestive of labyrinthitis may present without further contributory history of presenting illness to guide diagnostics. Thus, once stabilized clinically in the acute setting and rule-out of time-sensitive diagnoses like stroke, further work-up may be warranted to assess or rule out potential contributors to their symptoms. Contrast-enhanced MRI or CT scans of the head can reveal inner ear malformations and temporal bone neoplasms. A CT scan may also be useful in patients with suspected superior semicircular canal dehiscence (SSCD), and also to assess the extent of disease in cases of a superimposed infection with cholesteatoma, given the right clinical picture to suggest these conditions, with the caveat that acute prolonged vertigo would be atypical in SSCD and would typically present in this manner only with a concurrent superimposed infection in cholesteatoma.[48][49]
Any patient with an asymmetric hearing loss should undergo a retrocochlear evaluation with gadolinium-enhanced MRI to investigate other causes of hearing loss. For example, over 10% of patients with vestibular schwannomas (acoustic neuromas) present with sudden hearing loss. Labyrinthine enhancement on gadolinium-enhanced MRI in the setting of meningitis is a significant predictor of hearing loss.[50]
Do not order routine CT of the head for the initial evaluation of a patient with sudden sensorineural hearing loss alone (with the exception of patients with focal neurologic findings, a history of trauma, or chronic ear disease, who may require a CT scan).[51][52] CT provides no additional useful information that would change the patient management, yet it is expensive and exposes the patient to radiation.[52] In patients with persistent vertigo, a head CT with or without contrast may be appropriate.[49] CT head is not thought to be useful in patients with peripheral vertigo.[49]
Diagnostic Criteria
The Bárány Society have defined a set of criteria that needs to be fulfilled to diagnose vestibular neuritis:[1]
Acute or subacute onset of sustained spinning or nonspinning vertigo (i.e., an acute vestibular syndrome) of moderate to severe intensity with symptoms lasting for at least 24 hours.
Spontaneous peripheral vestibular nystagmus, that is, a nystagmus with a trajectory appropriate to the semicircular canal afferents involved, generally horizontal-torsional, direction-fixed, and enhanced by removal of visual fixation.
Unambiguous evidence of reduced vestibulo-ocular reflex function on the side opposite the direction of the fast phase of the spontaneous nystagmus.
No evidence of acute central neurologic symptoms or acute audiologic symptoms such as hearing loss or tinnitus or other otologic symptoms such as otalgia.
No acute central neurologic signs, namely no central ocular motor or central vestibular signs, in particular, no skew deviation, no gaze-evoked nystagmus, and no acute audiologic signs.
Not better accounted for by another disease or disorder.
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