Dizziness, Vertigo, and Imbalance Workup
- Author: Hesham M Samy, MD, PhD; Chief Editor: Robert A Egan, MD more...
In the course of evaluating patients with vestibular and balance disorders, additional tests that are commonly considered include audiometry, vestibular tests, blood tests, computed tomography (CT), and magnetic resonance imaging (MRI). Such testing, especially vestibular testing, must be tailored to the history and physical findings in each case.
The yield of MRI in patients younger than 50 years is low (< 1%). The incidence of an acoustic tumor or other brainstem or posterior-fossa lesion also is low. Clinical judgment, careful neuro-otologic examination, and audio and vestibular studies are often helpful in rendering MRI unnecessary. Routine use of diagnostic imaging modalities in the assessment of patients with dizziness is not recommended.
It should be kept in mind that the results of audiometry and vestibular testing are not diagnostic in the medical sense. For example, unilateral vestibular loss can be due to vestibular neuronitis or a vestibular schwannoma. Equally, a unilateral hearing loss can be due to Ménière disease, idiopathic sudden hearing loss, or a vestibular schwannoma. Therefore, clinicians who perform these tests should do so in the physiologic sense and must avoid the temptation to interpret the results as indicating pathologic entities.
Physicians who are responsible for the medical interpretations of these results must have the proper training and background in neurophysiology and electrophysiology if they are to use these results effectively. They also must be aware of the limitations and variability inherent in such tests.
The most commonly performed vestibular tests are as follows:
The rotating-chair test, also referred to as sinusoidal harmonic acceleration (SHA)
Computerized dynamic posturography (CDP)
Vestibular evoked myogenic potentials
The standard ENG test battery is composed of saccadic, gaze, pursuit eye-movement, optokinetic nystagmus (OKN), head-shake nystagmus, positional nystagmus, positioning nystagmus, and bithermal caloric tests.
The saccadic test is used to evaluate voluntary fast-eye movements. The neural substrate of the saccadic system includes the frontal eye fields, the brainstem reticular formation, the oculomotor nuclei, and the cerebellum.
The test should be performed by recording each eye separately, especially if dysconjugate eye movements are suspected. A single-channel saccadic test, normally used to calibrate the equipment, should be interpreted with caution and in the light of findings from clinical examination of conjugate eye movements. Common saccadic abnormalities include dysmetria, slow saccadic velocity, and dysconjugate saccades.
The gaze test is used to evaluate the ability to generate and hold a steady gaze without drift or gaze-evoked nystagmus. The neural substrates of the gaze system are similar to those of the saccadic system. A direct-current ENG recording is used to distinguish electronic from pathologic drift. The most common abnormalities detected by the gaze test are gaze-evoked nystagmus and rebound nystagmus due to cerebellar disease.
Pursuit eye-movement test
Pursuit eye movements prevent slipping of an image on the retina while the patient is tracking moving objects. The neural substrate of the pursuit system includes the parietal cortex, the brainstem reticular formation, the cerebellum, the vestibular nuclei, and the oculomotor nuclei. Pursuit abnormalities occur with brainstem and cerebellar lesions.
Optokinetic nystagmus test
OKN is a complex central nervous system (CNS) reflex initiated by moving images on the retina. OKN supplements pursuit and vestibular eye movements to stabilize retinal images during constant-velocity head motion. The cortical origin is the parietal lobes, with vestibular nuclei, accessory optic tract, inferior olivary nucleus, cerebellum, and oculomotor nuclei participating. OKN abnormalities are seen in deep parietal-lobe lesions. OKN testing can also be used to identify subtle ocular motor abnormalities (eg, incomplete internuclear ophthalmoplegia).
Head-shake nystagmus test
Head movements produce vestibular responses with an extremely short latency (< 15 msec). Oculomotor responses are slower than this, with latencies approaching 100-200 msec. The compensation for this temporal discrepancy is the ability of the central vestibular system to maintain a memory of head motion, so that eye movements can be accurately matched to head movement.
This capability, referred to as velocity storage, is usually impaired with unilateral vestibular deficit and is tested by the head-shake test. In this test, 20 cycles of low-amplitude, high-velocity active or passive head movements are performed, followed by observation for nystagmus. This is done in both horizontal and vertical directions. Observation must be done with suppression of visual fixation by means of Frenzel goggles or an infrared video system. Head-shake nystagmus is seen with uncompensated, unilateral vestibular hypofunction.
Positional nystagmus test
Positional testing is performed by recording eye movements without visual fixation in 3 cardinal positions: supine, head right, and head left. Direction-fixed or changing positional nystagmus is usually peripheral and an objective sign of vestibular asymmetry, even if it is present in only a single head position.
Positioning nystagmus is a classic finding in patients with benign paroxysmal positional vertigo (BPPV). It is elicited by moving the patient rapidly from the sitting position to the head-right-down and head-left-down positions while observing and recording resulting nystagmus and symptoms. Hyperextension of the neck is not necessary and should be avoided. Two ENG channels are required to determine the direction of the torsional component of the nystagmus.
ENG is less sensitive than clinical observation of benign positioning nystagmus because ENG is insensitive for recording torsional BPPV components. In the authors’ opinion, ENG is not useful in evaluating patients for BPPV nystagmus.
Bithermal caloric test
Since its introduction in 1903, the caloric test has been the time-honored vestibular test in clinical neuro-otology. Although it remains the standard for evaluating unilateral vestibular deficit, it is a limited and nonphysiologic test of the vestibular system. The literature on the caloric test is extensive; therefore, only a brief description of the test and its interpretation are provided here.
Traditionally, the caloric test is performed with the patient lying with the head elevated 30°. Cold (30°C) and warm (44°C) water are used to irrigate one ear at a time. Cold irrigation is an inhibitory stimulus, and warm irrigation is excitatory. The direction of postcaloric nystagmus is determined by the quick-phase direction and is easily remembered by using the mnemonic COWS: c old o pposite, w arm s ame (ie, quick phase away from or toward the irrigated ear).
The 3 most important findings from the caloric test are unilateral weakness, bilateral weakness, and FFS of caloric-induced nystagmus. The first 2 abnormalities are due to peripheral vestibular disease; the third is due to central cerebellar disease.
Although rotational testing was introduced in 1907, almost as early as the caloric test, it lagged behind the caloric test in clinical practice for decades. However, with advances in computer technology, rotating-chair test systems were developed in the late 1970s and continue to evolve; they are now used in several vestibular testing laboratories.
The rotating-chair test (ie, SHA) is used to evaluate the integrity of the vestibulo-ocular reflex (VOR) in the low-frequency (0.1-0.32 Hz) range and, sometimes, in the high-frequency (1-4 Hz) range. The measured parameters are VOR gain, phase (latency), and symmetry. The test is most useful in determining the degree of central vestibular compensation and the residual vestibular function in cases of bilateral vestibular loss. It is not advised on a routine basis for all patients who report dizziness.
An alternative to the rotating-chair test is the active head-rotation test, which is used to evaluate VOR gain in the high-frequency range. This test is substantially less expensive and more practical than the chair test. Active head rotation involves recording head and eye position while the patient actively turns the head from side to side at progressively faster frequencies.
Computerized Dynamic Posturography
First introduced into neuro-otology in the 1970s, dynamic posturography has become an integral part of vestibular testing in many vestibular test centers. A CDP system consists of a computer-controlled platform and visual booth used to evaluate both sensory and motor components of balance. The sensory test is most clinically useful, especially in peripheral lesions, vestibular rehabilitation, and medicolegal cases. CDP is not a substitute for a careful gait examination and probably is of more value in rehabilitation than in diagnosis.
Vestibular Evoked Myogenic Potential
Vestibular evoked myogenic potential (VEMP) is an emerging diagnostic tool for identifying vestibular lesions. The VEMP test is noninvasive and causes little or no discomfort to the patient. The VEMP test is administered like the traditional auditory brain stem response [ABR] test using surface electrodes placed on sternocleidomastoid muscles to detect sound evoked potentials due to inhibitory muscle activity in response to suprathreshold tonal sounds in each ear. VEMP testing targets the vestibule and neural connections to the sternocleidomastoid muscles of the neck. The VEMP neural pathway consists of the saccule, inferior vestibular nerve, and vestibulospional tract. VEMP so far has been mainly useful in documenting abnormally low thresholds in persons with the Tullio effect, which mostly occurs in patients with fistulae or superior canal dehiscence syndrome (SCD).
Clinical Yield of Vestibular Tests
The following general observations on the clinical yield of vestibular tests may be made, based on findings from a database of 10,000 patients who underwent the 3 types of vestibular testing (ie, ENG, SHA, and CDP) between 1985 and 1995 under the direct supervision of one of the coauthors (Hamid):
First, the raw data tracings should be viewed and evaluated, particularly those acquired by using computerized systems, and clinicians should not rely on computerized analysis generated by the system software, even if the raw data are merely noise
Second, overinterpretation of oculomotor findings is common, leading to unnecessary neurologic investigations, especially MRI; in the database, the yield for abnormalities of central eye movements, saccadic dysmetria, saccadic pursuit, asymmetric optokinetic response, and gaze-evoked nystagmus was less than 5%; therefore, ENG readers are advised to cautiously interpret eye movements
Third, an ENG system prints outs only horizontal and vertical eye movements and is therefore insensitive to the pure torsional eye movements often seen with BPPV; video-based ENG (VNG) has the advantage of depicting and digitally recording pure torsional nystagmus for storing and reediting of the captured video signals
Fourth, findings on chair and dynamic posturography are infrequently abnormal, and their routine use is probably not cost-effective
Finally, most abnormalities detected by vestibular testing can be identified by means of a carefully conducted office vestibular examination
Kerber KA, Meurer WJ, West BT, Fendrick AM. Dizziness presentations in U.S. emergency departments, 1995-2004. Acad Emerg Med. 2008 Aug. 15(8):744-50. [Medline].
Saber Tehrani AS, Coughlan D, Hsieh YH, Mantokoudis G, Korley FK, Kerber KA, et al. Rising annual costs of dizziness presentations to U.S. emergency departments. Acad Emerg Med. 2013 Jul. 20 (7):689-96. [Medline].
Olsson Möller U, Midlöv P, Kristensson J, Ekdahl C, Berglund J, Jakobsson U. Prevalence and predictors of falls and dizziness in people younger and older than 80 years of age-A longitudinal cohort study. Arch Gerontol Geriatr. 2012 Sep 18. [Medline].
Navi BB, Kamel H, Shah MP, Grossman AW, Wong C, Poisson SN, et al. Rate and predictors of serious neurologic causes of dizziness in the emergency department. Mayo Clin Proc. 2012 Nov. 87(11):1080-8. [Medline].
Katsarkas A. Dizziness in aging: the clinical experience. Geriatrics. 2008 Nov. 63(11):18-20. [Medline].
van Leeuwen RB, Bruintjes TD. Dizziness in the elderly: diagnosing its causes in a multidisciplinary dizziness unit. Ear Nose Throat J. 2014 Apr-May. 93(4-5):162, 164, 166-7. [Medline].
Lüscher M, Theilgaard S, Edholm B. Prevalence and characteristics of diagnostic groups amongst 1034 patients seen in ENT practices for dizziness. J Laryngol Otol. 2014 Feb. 128(2):128-33. [Medline].
Fakhran S, Alhilali L, Branstetter BF 4th. Yield of CT Angiography and Contrast-Enhanced MR Imaging in Patients with Dizziness. AJNR Am J Neuroradiol. 2012 Oct 25. [Medline].
Murofushi T, Shimizu K, Takegoshi H, Cheng PW. Diagnostic value of prolonged latencies in the vestibular evoked myogenic potential. Arch Otolaryngol Head Neck Surg. 2001 Sep. 127(9):1069-72. [Medline].
Walker MF. Treatment of vestibular neuritis. Curr Treat Options Neurol. 2009 Jan. 11(1):41-5. [Medline].
Fife TD, Iverson DJ, Lempert T, Furman JM, Baloh RW, Tusa RJ, et al. Practice parameter: therapies for benign paroxysmal positional vertigo (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology. 2008 May 27. 70(22):2067-74. [Medline].
Honaker J, Samy RN. Migraine-associated vestibulopathy. Curr Opin Otolaryngol Head Neck Surg. 2008 Oct. 16(5):412-5. [Medline].
Lempert T, Olesen J, Furman J, et al. Vestibular migraine: diagnostic criteria. J Vestib Res. 2012. 22(4):167-72. [Medline].
Jen J, Kim GW, Baloh RW. Clinical spectrum of episodic ataxia type 2. Neurology. 2004 Jan 13. 62(1):17-22. [Medline].
von Brevern M, Ta N, Shankar A, et al. Migrainous vertigo: mutation analysis of the candidate genes CACNA1A, ATP1A2, SCN1A, and CACNB4. Headache. 2006 Jul-Aug. 46(7):1136-41. [Medline].
Carlson ML, Tveiten OV, Driscoll CL, Neff BA, Shepard NT, Eggers SD, et al. Long-term Dizziness Handicap in Patients with Vestibular Schwannoma: A Multicenter Cross-sectional Study. Otolaryngol Head Neck Surg. 2014 Oct 1. [Medline].
Sacco RR, Burmeister DB, Rupp VA, Greenberg MR. Management of benign paroxysmal positional vertigo: a randomized controlled trial. J Emerg Med. 2014 Apr. 46(4):575-81. [Medline].
Hamid MA, Samy HM. Vestibular and Balance Rehabilitation. Hamid M, Sismanis A, Eds. Medical Otology & Neurotology. New York, NY: Thieme; 2006.
|System or Reflex||Peripheral Lesions||Central Lesions|
|Oculomotor||Spontaneous nystagmus with eyes closed||Saccades (velocity, accuracy), internuclear ophthalmoplegia, saccadic pursuit, gaze-evoked nystagmus|
|Vestibulo-ocular reflex (VOR)||Nystagmus without fixation, nystagmus after head shaking, eye-head mismatch, unilateral and bilateral vestibular loss||Hyperactive VOR, FFS, positional nystagmus, bilateral vestibular loss|
|Vestibulospinal reflex (VSR)||Cautious gait; normal spontaneous movement; normal, spontaneous, and correct movement||Wide-based gait, minimal spontaneous movement|