Dizziness, Vertigo, and Imbalance

Updated: Oct 27, 2022
Author: Hesham M Samy, MD, PhD; Chief Editor: Robert A Egan, MD 



Dizziness and vertigo are among the most common symptoms causing patients to visit a physician (as common as back pain and headaches). Falling can be a direct consequence of dizziness in this population, and the risk is compounded in elderly persons with other neurologic deficits and chronic medical problems.

The overall incidence of dizziness, vertigo, and imbalance is 5-10%, and it reaches 40% in patients older than 40 years. The incidence of falling is 25% in subjects older than 65 years. A report reviewing presentation to US emergency departments (EDs) from 1995 through 2004 indicated that vertigo and dizziness accounted for 2.5% of presentations.[1] The estimated number of 2011 US ED visits for dizziness or vertigo was 3.9 million.[2]

A report using data from the Swedish National study on Aging and Care (SNAC) found that in patients younger than 80 years, the prevalence of falls was 16.5% and that of dizziness was 17.8%, whereas in patients older than 80 years, the prevalence of falls was 31.7% and that of dizziness was 31.0%.[3] The younger patients tended to have more specific predictive factors, whereas the older patients tended to have more general ones.

Mild hearing loss is the most common disability worldwide. The incidence of hearing loss is 25% in people younger than 25 years, and it reaches 40% in persons older than 40 years. About 25% of the population report tinnitus.

Vertigo, dizziness, tinnitus, and hearing loss are typically associated with inner-ear diseases as opposed to central nervous system (CNS) diseases. Migraine is more prevalent (10%) than Ménière disease (< 1%). About 40% of patients with migraine have vertigo, motion sickness, and mild hearing loss. Therefore, differentiating migraine from primary inner-ear disorders is sometimes difficult.

Primary care physicians evaluate most cases of dizziness and related symptoms. Their role and that of neurologists in this setting has increased over the past decade. This article outlines the clinical approach to dizziness with emphasis on differentiating peripheral from central dizziness and on office management of the most common diseases. It also addresses indications for referral to an otolaryngologist or neuro-otologist and for specialized auditory and vestibular testing.

The patient’s history and findings on vestibular examination are critical in identifying underlying causes. Auditory, vestibular, complementary blood and radiologic tests help in narrowing the differential diagnosis and tailoring treatment. Vestibular tests should be ordered after careful history taking and examination because they do not provide the clinician with diagnostic information.

Most patients are treated medically and with vestibular rehabilitation. In addition to the appropriate medical and rehabilitative managements, safety must be emphasized and discussed with patients and their families. Occupational and physical therapists are helpful in addressing home safety and providing a structured balance-rehabilitation program.

For patient education resources, see the Brain and Nervous System Center and the Ear, Nose, and Throat Center, as well as Benign Positional Vertigo, Dizziness, Ménière Disease, and Tinnitus.


The most common causes of peripheral vertigo include BPPV, vestibular neuronitis, Ménière disease, and immune-mediated inner-ear disease. The most common cause of central dizziness is migraine, frequently referred to as vestibular migraine or migraine-associated dizziness. Other central causes include demyelination, acoustic tumors, and brainstem or cerebellar vascular lesions.

There are numerous inner ear pathologies that are the direct result of disrupted ion homeostasis. While the initial cause may be something else (eg, inflammation, ototoxicity, noise), the ultimate impact on the ear is the interference of some ion or water transport mechanism. Thus, impaired ion homeostasis is essentially the final common pathway for many inner ear diseases.[4]

In a retrospective review of 907 adults presenting to an academic ED from 2007 through 2009 with a primary complaint of dizziness, vertigo, or imbalance, 49 patients had a serious neurologic diagnosis (eg, cerebrovascular disease).[5] Benign causes of dizziness included peripheral vertigo (294 cases) and orthostatic hypotension (121 cases). Factors associated with serious diagnoses included abnormalities on focal examination, age greater than 60 years, and imbalance as the chief complaint.


The overall incidence of dizziness, vertigo, and imbalance is 5-10%, and it reaches 40% in patients older than 40 years. The incidence of falling is 25% in subjects older than 65 years. A report reviewing presentation to US emergency departments (EDs) from 1995 through 2004 indicated that vertigo and dizziness accounted for 2.5% of presentations.[1] The estimated number of 2011 US ED visits for dizziness or vertigo was 3.9 million.[2]

A report using data from the Swedish National study on Aging and Care (SNAC) found that in patients younger than 80 years, the prevalence of falls was 16.5% and that of dizziness 17.8%, whereas in patients older than 80 years, the prevalence of falls was 31.7% and that of dizziness 31%.[3] The younger patients tended to have more specific predictive factors, whereas the older patients tended to have more general ones.




Evaluation of the patient with dizziness begins with careful history taking and a complete neuro-otologic physical examination, including vestibular examination. The history is critical and should focus on the nature of the symptoms, the duration, and triggering or alleviating factors. Ask patients to describe their symptoms by using words other than “dizzy.” The rationale for using other words is that patients may use dizzy nonspecifically to describe vertigo, unsteadiness, generalized weakness, syncope, presyncope, or falling.

Dizziness includes light-headedness, unsteadiness, motion intolerance, imbalance, floating, or a tilting sensation. It is essential to distinguish vertigo, which is a subtype of dizziness defined as an illusion of movement caused by asymmetric input to the vestibular system, from other types of dizziness. This dichotomy is helpful because true vertigo is often due to inner-ear disease, whereas other symptoms of dizziness may be due to central nervous system (CNS ), cardiovascular, or systemic diseases.

Sudden onset and vivid memory of vertiginous episodes are often due to inner-ear disease, especially if hearing loss, ear pressure, or tinnitus is also present. Gradual and ill-defined symptoms are common in CNS, cardiac, and systemic diseases.

The time course of vertigo is important:

  • Episodic vertigo that lasts for days with nausea and no other ear or CNS symptoms is usually due to vestibular neuritis, especially following viral illness

  • Episodic vertigo that lasts for seconds and is associated with head or body position changes is probably due to benign paroxysmal positional vertigo (BPPV)

  • Vertigo that lasts for hours is probably caused by Ménière disease (if associated with hydropic ear symptoms)

  • Vertigo of sudden onset that lasts for minutes can be due to migraine or brain or vascular disease, especially if cerebrovascular risk factors are present

Central vertigo secondary to brainstem or cerebellar ischemia usually lasts for 20 minutes to 24 hours and is often associated with other brainstem characteristics, including diplopia, autonomic symptoms, nausea, dysarthria, dysphagia, or focal weakness. Patients with cerebellar disease are frequently unable to ambulate during acute episodes of vertigo. Patients with peripheral vertigo can usually ambulate during episodes and are consciously aware of their environment.

A history of headaches, especially migraine headaches, can be associated with migraine-related dizziness. Previous viral illness, cold sores, or sensory changes in the cervical C2-C3 or trigeminal distributions usually indicate vestibular neuronitis or recurrent episodes of Ménière disease.

Dysdiadochokinesia and gait ataxia during episodes are more likely to be due to cerebellar diseases, especially in the elderly and in subjects with evident cardiovascular risk factors. Progressive gait difficulty, memory loss, and urinary incontinence are commonly due to normal pressure hydrocephalus (NPH). Sensory and motor symptoms and signs are usually associated with CNS diseases. The history should include a review of systems (especially head trauma and ear diseases, trauma, or surgery).

The impact of dizziness on activities of daily living at work and home should be addressed. Screening for primary or reactive anxiety and depression is important. A history of prescription medicines, over-the-counter medications, herbal medicines, and recreational drugs (including smoking and alcohol) can help to identify pharmacologically induced syndromes.

Accurate diagnosis of dizziness or unsteadiness in the elderly may be more difficult, mostly because underlying disorders may present in an atypical fashion. Although dizziness in the elderly can be attributed to weakness and fatigue at times, it may be more serious than in younger patients and should be carefully investigated.[6] In a study of of 731 elderly patients (70 yr or older) with dizziness, the 2 most common causes were found to be benign paroxysmal positional vertigo (27.6%) and hyperventilation/anxiety (15.3%).[7] In another study, benign paroxysmal positional vertigo was the most frequent diagnosis in all age groups, including those older than 70 years, being diagnosed in 53.3% of 1034 patients.[8]

To diagnose dizziness, physicians must use the essential tools of history, clinical examination, and follow-up.[6] The etiology in most of these patients mainly involves a vestibular disorder, such as BPPV, Ménière disease, or bilateral vestibular hypofunction. Appropriate management and follow-up are necessary to improve the well-being of these patients.

Physical Examination

In patients with dizziness, the general examination should emphasize assessment of vital signs, supine and standing blood-pressure measurements, and evaluation of the cardiovascular and neurologic systems. Examine the ears for visible infection or inflammation of the external or middle ear. Test hearing and discrimination by using a tuning fork and by whispering and asking the patient to repeat heard words. Examine the neck for range of motion and flexibility.

Focused neurologic examination of the cranial nerves, motor and sensory modalities, gait, and stance is important in the initial visit. Cerebellar tests, especially failure of fixation suppression (FFS) of vestibular eye movements, are important for checking the vestibulocerebellum. Failure of fixation suppression (FFS) can be tested by asking the patient to stretch his arms and look at his thumb while being passively rotated (manual rotation of examination chair). A visible nystagmus (right or left) indicates FFS that is always central in origin.

Vestibular examination

The vestibular part of the physical examination focuses on examining primarily the 2 most-used reflexes:

  • Vestibulo-ocular reflex (VOR)

  • Vestibulospinal reflex (VSR)

A robust oculocephalic reflex and intact visual acuity with active head movements (dynamic visual acuity) reflect good VOR. Absence of the oculocephalic reflex or a decrease in visual acuity with head movements reflects decreased vestibular function. Nystagmus observed under Frenzel glasses after rapid head shaking reflects asymmetric vestibular input.

Characterization of nystagmus

Nystagmus, whether spontaneous, gaze-induced, or positional, must be completely characterized to be correctly interpreted. This characterization should include provocative factors, latency, directions, effects of gaze, temporal profiles, habituation, fatigability, suppression by visual fixation, and accompanying sensation of dizziness. Failure to fully characterize nystagmus can lead to misdiagnosis.

Examine eye movements for evident oculomotor abnormalities, especially nystagmus. Spontaneous, gaze-evoked, post head shake, and post mastoid vibration are important to elicit, observe, and document. Differentiating peripheral from central nystagmus is key. Central nystagmus is a purely horizontal or vertical and not suppressed by visual fixation. Peripheral nystagmus is usually rotatory and most evident with removing visual fixation (eg, by using Frenzel goggles or infrared video nystagmography; see the images below). It also obeys the Alexander law; that is, the intensity of nystagmus increases with gaze in the direction of the fast phase. Post head shake and mastoid vibration nystagmus is usually a reflection of uncompensated unilateral vestibular hypofunction.

Example of Frenzel goggles used for evaluation in Example of Frenzel goggles used for evaluation in neuro-otology clinic.
Typical example of computer and headgear equipment Typical example of computer and headgear equipment used in neuro-otology clinic.

Positioning examination

The positioning examination (Dix-Hallpike test) is important for identifying BPPV commonly caused by otolith debris (canalith) floating in the semicircular canals (canalithiasis) or adhering to the cupula (cupulolithiasis). This maneuver is performed by guiding the patient rapidly from a sitting position with the head turned 45° to one side to a supine position. For torsional nystagmus, observation or video recording is more sensitive than electronystagmography (ENG). BPPV is due to posterior semicircular canal canalithiasis about 90% of the time.

Typical nystagmus related to posterior semicircular canal benign positioning and its symptoms are delayed by several seconds (latency). They peak in 20-30 seconds and then decay (paroxysmal), with complete resolution of symptoms while the patient maintains the same head position (habituation). Symptoms and reversed nystagmus may occur when the patient is brought back to a sitting position. Therefore, benign positioning nystagmus is latent, paroxysmal, geotropic, reversible, and fatigable.

The vertical component of benign positioning nystagmus is best observed by asking the patient to move the eyes away from the downward ear to determine whether the vertical component of nystagmus is due to the down posterior canal or the contralateral uppermost anterior canal (rare).

Nystagmus of the horizontal semicircular canal is less common and is usually due to canalithiasis. Typically, it is s purely horizontal, geotropic (beating toward the downward ear), and asymmetric. The direction reverses with the change in head position from one side to the other in the supine position. The intensity of nystagmus is strongest when the head is rotated to the involved side. Another, even less common form, is horizontal canal BPPV due to cupulolithiasis. Typically, nystagmus is apogeaotropic (beating away from the down ear)

Caloric testing

Caloric testing can be done as part of the bedside examination. After checking both ear canals for tympanic perforation and wax, instill 1 mL of water at 30°C. Observe the nystagmus response by using Frenzel goggles or an infrared video system. In this way, dizziness, the duration and intensity of the nystagmus, and visual fixation suppression can be evaluated.

Posture and gait assessment

The VSR can be examined with Romberg, tandem gait, and Fukuda stepping tests. These tests provide information about the patient’s postural stability when visual and proprioceptive inputs are removed. The experienced physician can observe the patient’s postural stability, limits of stability, and strategy of movement at the limits of stability. Clinical testing of postural stability is qualitative and requires both experience on the part of the examiner and cooperation on the part of the patient.

Ask the patient to run the heel repeatedly from the opposite knee down the shin to the big toe, and look for incoordination. Watch the patient walking, performing tandem gait. The normal gait is characterized by an erect posture, moderately sized steps, and the medial malleoli of the tibia tracing a straight line.

To conduct the Romberg examination, ask the patient to stand with the heels together, first with eyes open, then with eyes closed. Then, ask the patient to stand on a high-compliance surface and note any excessive postural swaying, either posteroanteriorly or to one side.

After Romberg examination, ask the patient to step in place for 30 seconds and observe poststepping position drift from midline. If positive, it reflects an uncompensated unilateral vestibular hypofunction.

Vestibular stress testing

The Hamid vestibular stress test is composed of a sensory and a motor component and is performed by using a high-compliance foam pad (HCFP). The examination is simple, easy to administer, and applicable to most patients with dizziness and disequilibrium.

In the sensory component, the patient stands on the HCFP with eyes open and arms stretched out while the examiner observes the degree of sway in the primary position and at the limits of stability. The patient then tilts the head back and moves it right and left, first with eyes open and then with eyes closed. The examiner must be prepared to catch the patient if he or she falls. Experience with this examination has shown that patients cannot stand on the HCFP with eyes closed and head tilted back unless they have an intact vestibular and balance system.

The motor component is more challenging than the sensory component and is referred to as the body-impulse test. The physician places his or her hands against the patient’s shoulders and asks the patient to push forward against the hands for a count of 10. The physician then releases his or her hands, watches the patient’s response, and catches the patient if necessary. Most patients can correct for the sudden perturbation by performing 3 corrective responses:

  • Forward bending (hip-sway strategy)

  • Stepping forward

  • Stepping back to the original position

The response pattern is repeatable and physiologic. It demonstrates the physiologic postural reaction and the switch between ankle and hip-sway strategies expected at the limits of stability.

Patients with peripheral and central dysfunction have patterns that do not include quick and corrective movements, performing a hip-sway, or taking a step. Of course, this examination is qualitative and subject to the physician’s experience and the patient’s musculoskeletal condition and ability to cooperate.

Hyperventilation examination

If the results of vestibular examination are normal, hyperventilation for 2 minutes is helpful in identifying patients with hyperventilation syndrome. This should be done in the sitting position. Hyperventilation must be done while the physician monitors for nystagmus by using Frenzel goggles or an infrared video system. Hyperventilation can accentuate both central and peripheral vestibular dysfunction and reproduce dizziness and neurologic symptoms due to either true pathology or underlying anxiety or stress.



Diagnostic Considerations

On the basis of the patient’s history and physical findings, the examining physician should be able to formulate a differential diagnosis and determine whether the symptoms are likely to be peripheral or central (see the Table below).

Table. Features Differentiating Peripheral from Central Nystagmus (Open Table in a new window)

System or Reflex

Peripheral Lesions

Central Lesions


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, failure of fixation suppression (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

Differential Diagnoses



Approach Considerations

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.[9]

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:

  • Electro/videonystagmography (ENG)

  • 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.

Saccadic test

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.

Gaze test

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.

Dix-Hallpike test

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.

Rotating-Chair Test

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.[10] 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



Approach Considerations

Acute dizziness and vertigo is usually managed with vestibular suppressants, antiviral medication, and antiemetic medications. Steroids are useful in selected patients. Vestibular suppressants should be used for a few days at most because they delay the brain’s natural compensatory mechanism for peripheral vertigo. Vestibular rehabilitation is very useful in boosting central vestibular compensation.

Management of Peripheral Dizziness

Vestibular neuronitis

Vestibular neuronitis is the most common cause of acute vertigo, with an incidence of 170 cases per 100,000 people. It is believed to result from reactivation of herpes simplex virus infection that affects the vestibular ganglion and vestibular nerves.[11] A prodromal upper respiratory tract illness may or may not be present. Vertigo is without auditory or other central nervous system (CNS) symptoms and lasts for several days. Patients are usually ill and cannot perform home or work activities. They are commonly rated symptomatically.

A brief course of antiemetic and vestibular suppressants is usually needed in the acute phase but should be withdrawn as soon as possible to facilitate the process of central vestibular compensation.[11] Corticosteroids may improve long-term outcomes. Early vestibular rehabilitation is important.[11] Antiviral medications have not proved helpful, possibly because a large spectrum of viruses can cause vestibular neuronitis. The pharmacological treatment of choice for acute vestibular neuritis is oral steroids beginning as soon as possible with gradual tapering of the dose. One third of patients have chronic vestibular symptoms and develop benign paroxysmal positioning vertigo (BPPV).

Benign paroxysmal positioning vertigo

BPPV is the second most common cause of vertigo. The typical symptom is brief episodic vertigo upon changing head or body position. Patients may have a residual sensation of disequilibrium between episodes. BPPV is commonly either idiopathic or posttraumatic. Other causes of vertigo, such as vestibular neuronitis, Ménière disease, and delayed endolymphatic hydrops, are also associated with BPPV.

The mechanism of BPPV can involve canalithiasis (otoconia floating in the endolymph) or cupulolithiasis (otoconia adherent to cupula). The most commonly affected canal is the posterior canal (90% of cases); the horizontal canal may also be affected, but to a lesser extent.

The American Academy of Neurology has published a practice parameter for the treatment of BPPV.[12] The most effective treatment is canalith repositioning from the affected canal back to the vestibule where it is absorbed using the most common maneuvers: Epley, Semont, Lempert, and Hamid (for horizontal canal cupulolithiasis). Medications can be helpful for short-term reduction of symptoms but have not been shown to be effective in the long-term treatment of BPPV.

It is important to note that most cases of BPPV can be treated in the office once the history and examination confirm the diagnosis. Prolonged sessions of physical therapy are not necessary and not cost effective. Some of these patients may also require medications, which should be given under physician supervision, to treat severe nausea and vomiting that can result from CRP treatments.

The most common complication of the Semont or Epley maneuver is conversion of the posterior canal−horizontal canal BPPV, which is treated with the Lempert or Hamid maneuvers. A less common complication is undue cervical strain, which is especially likely with the Semont maneuver or with neck hyperextension during the Epley maneuver.

Ménière disease

Ménière disease is a disorder of the inner ear with typical symptoms of episodic vertigo, tinnitus, and hearing loss. Untreated, severe hearing loss and unilateral vestibular paresis are inevitable. Bilateral involvement occurs in about 25% of patients. The etiology is idiopathic in most cases and can also be hereditary, autoimmune, infectious, or allergic. The common pathophysiology is disordered fluid homeostasis in the inner ear, with endolymphatic hydrops representing a histologic footprint rather than an etiology.

Most patients respond to conservative therapy with salt restriction and diuretics. Corticosteroids, given orally or intratympanically, can be used to stabilize active disease and to recover speech discrimination, especially when used in early stages of the disease. Intratympanic gentamicin (chemical labyrinthectomy) is a minimally invasive procedure that has emerged as an effective method for treating the disabling vertigo of Ménière disease when hearing loss and speech discrimination have progressed to severe levels. Gentamicin is also very effective in treating Tumarkin attacks of Ménière disease.

The role of surgical therapy for Ménière disease (eg, shunting the endolymphatic sac) is controversial. The literature demonstrates wide variation in the effectiveness, or lack thereof, of surgery.

Autoimmune inner-ear disease

Patients with autoimmune inner-ear disease typically present with rapidly progressive, bilateral hearing loss, with or without vertigo. Initial onset may be unilateral. However, the rapid progression, bilateral involvement, and response to steroids distinguish this disorder from Ménière disease. Autoimmune inner-ear disease can occur with or without other autoimmune disease or laboratory evidence of a systemic inflammatory disorder. Specific laboratory markers for inner-ear antigenicity have low sensitivity and thus are of little clinical utility.

Oral and intratympanic corticosteroids are effective in controlling this disease. Patients with recurrent symptoms that are steroid responsive may benefit from methotrexate or other steroid-sparing medications. These patients should be treated by a rheumatologist.

Management of Central Dizziness


Migraine is a common disorder, affecting 10% of men and 30% of women. About 25% of migraineurs have motion intolerance or sickness rather than true vertigo. The pathophysiology of migraine-associated vestibulopathy is not completely understood.[13] Vestibular symptoms usually are dissociated from headaches but sometimes can occur as an aura or as part of a headache. Patients can also have mild form of hearing loss mimicking Ménière disease.

Symptoms that qualify for a diagnosis of vestibular migraine include various types of vertigo and head motion–induced dizziness with nausea. Symptoms must be of moderate or severe intensity. Duration of acute episodes is limited to a window of between 5 minutes and 72 hours.[14] Electro/videonystagmography is typically not helpful in differentiating migraine-associated vertigo from other vestibular pathologies. However, for patients with a longstanding history of dizziness, normal findings on electro/videonystagmography are suggestive of migraine-associated dizziness.

For vestibular migraine, the theory of an ion-channel disorder is particularly interesting because different mutations of the CACNA1A gene coding for a transmembrane component of a neuronal calcium channel can provoke familial hemiplegic migraine or episodic ataxia type.[15] However, several candidate genes coding for ion-channel proteins have not been found in a population with vestibular migraine.[16]

Treatment of migraine-associated vestibulopathy is the same as that of migraine, focusing on adequate control of the frequency and intensity of symptoms using both abortive and prophylactic medications. Triggers should be minimized/eliminated, including disturbed sleep pattern, diet, and lifestyle.[13] Prophylactic and abortive medications commonly used in treating migraine should be individually tailored. In the authors’ experience, topiramate and rizatriptan benzoate are associated with long-term control of vestibular migraine.

Transient ischemic attacks

Transient ischemic attacks (TIAs) are episodes of focal neurologic symptoms involving isolated or combined brainstem symptoms such as dizziness, diplopia, or weakness. These attacks are of sudden onset and resolve within 24 hours without residual subjective symptoms or objective signs on examination. TIAs are usually due either to reduced blood flow (the hemodynamic theory; eg, cardiac dysrhythmia) or to obstructed blood flow (the embolic theory; eg, plaques from the heart).

TIAs are commonly (75% of cases) due to posterior circulation (vertebrobasilar territory). The differential diagnosis of TIAs includes migraine, partial seizures, hypoglycemia, syncope, and hyperventilation.

Cerebrovascular disease

Stroke is the third most common cause of death or disability in adults. The vertebrobasilar circulation supplies the brainstem, the cerebellum, and the inner-ear auditory and vestibular structures. Infarction of the cerebellar midline can cause acute vertigo without auditory or other neurologic features (eg, isolated vertigo).

This potentially life-threatening event must be differentiated from vestibular neuronitis. A key difference between these 2 entities is that patients experiencing cerebellar strokes are unable to ambulate without support during the acute vertigo phase. About one half of patients have other features of bulbar or long tract involvement, which make the diagnosis of stroke clear.

Evaluation of the patient with stroke is directed at identifying correctable vascular risk factors (eg, hypertension, diabetes, hyperlipidemia, and smoking) and at determining the mechanism of stroke (eg, small-vessel disease, large-vessel disease, cardioembolism, dissection, hypercoagulability, or vacuities). Secondary prophylactic therapy and rehabilitation are individualized. Both hearing loss and vertigo can occur in the setting of stroke due to central injury, peripheral injury, or both.

Multiple sclerosis

Multiple sclerosis is a disorder of recurrent, inflammatory CNS demyelination that is due to underlying autoimmune disease. The onset is usually at age 20-40 years. Episodes begin over hours to a few days and last weeks to months. Typical symptoms include the following:

  • Optic neuritis

  • Ocular motor dysfunction

  • Trigeminal neuralgia

  • Sensorimotor deficits

  • Myelopathy

  • Ataxia

  • Bladder dysfunction

Vertigo, at times mimicking vestibular neuronitis, is a presenting symptom in fewer than 10% of patients. Dizziness or vertigo occurs at some point in the course in one third of patients. Few patients present with hearing loss due to brainstem involvement.

The diagnosis of multiple sclerosis requires the presence of dissemination in time and space (ie, different neurologic symptoms at different times). A careful history, a thorough examination, and serial follow-up combined with magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) analysis help establish the diagnosis; the diagnosis should not be based on MRI abnormalities alone. Disease-modifying therapy is available, but it is only modestly effective. The search for improved treatment is ongoing.

Tumors and malformations of posterior fossa

Vestibular schwannoma (acoustic neuroma) is an uncommon lesion (incidence, 1.1 per 100,000) that typically manifests with slowly progressive unilateral hearing loss and tinnitus. Dizziness is not common, because the vestibular system can usually compensate for such gradual unilateral hypofunction. Dizziness can occur as the tumor expands in the cerebellopontine angle and effaces the brainstem and cerebellum. Arachnoid cysts can also occur in the posterior fossa and result in subtle and nonspecific dizziness and auditory symptoms.

In a cross-sectional observational study in patients with small to medium-sized vestibular schwannomas, over 50% of patients reported ongoing dizziness at a mean of 8 years after treatment. All 538 patients had sporadic vestibular schwannomas of less than 3 cm and underwent primary microsurgery, stereotactic radiosurgery, or observation. The treatment modality was not found to influence long-term dizziness handicap.[17]

Chiari malformation occurs in a few adults. It is congenital but often does not become symptomatic until age 20-40 years. Occipital headache precipitated by Valsalva maneuvers, coughing, exertion, or changing position is common. Dizziness may occur with the same precipitants.

Once suspected, the diagnosis can be confirmed by means of MRI. Surgical treatment should be considered for patients whose symptoms are more than mild.


Upright balance and posture control are not a single physiologic function; they include visual, vestibular, and proprioceptive sensory inputs. During ambulation, the CNS must instantly integrate these inputs and execute appropriate motor plans and purposeful output via an adequate musculoskeletal system. This intricate system changes with age and disease-related decline in any of these systems. For example, bilateral vestibular failure is a contributor in one fourth of elderly patients with disequilibrium. Untreated BPPV can be a risk factor for falls.

The most common fall is a simple event in which the patient has tripped but has no ominous underlying peripheral or central disorder. Hazards in the environment (eg, rugs, electrical wires, poor lighting), polypharmacy, and orthopedic factors often contribute to falls. Because of the substantial risk of injury and the resultant decline in independence or quality of life after a fall, a well-directed evaluation is indicated. Orthostatic hypotension due to aging or medications is also a common contributor. Normal pressure hydrocephalus is also a contributing factor to gait abnormalities and falling.

Vestibular Rehabilitation

Vestibular rehabilitation is an important management tool in certain vestibular disorders. It has become widely used in current clinical practice, with many reviews; most lack a critical stance while propagating its use with all vestibular disorders, sometimes using all allowed physical therapy allowances, especially for Medicare patients.

In essence, vestibular rehabilitation aims to minimize and ultimately eliminate the central vestibular asymmetry underlying persistent symptoms of imbalance and unsteadiness. It is different from traditional physical therapy of gait and balance disorders arising from biomechanical or central movement disorders such as Parkinson disease or multiple sclerosis. Vestibular rehabilitation can be performed by patients at home using tailored exercises that focus on challenging the main vestibular reflexes (VOR, VSR) and visual interaction with both reflexes.

In a study of patients who presented to the emergency department with benign paroxysmal positional vertigo, vestibular rehabilitation and medication therapy were shown to be equally efficacious. Of 26 patients, 11 received medications and 15 received vestibular rehabilitation. Two hours after treatment, there was no difference between the two groups regarding the symptoms of nausea or dizziness. Both groups reported a high level of satisfaction, and the length of stay in the ED did not differ between the two groups.[18]

Patients who have neck or other biomedical problems should have these problems addressed before starting vestibular rehabilitation. Vestibular rehabilitation is useful for most stable (nonfluctuating) peripheral vestibular disorders such as vestibular neuritis and inactive Ménière disease. It is also helpful for chronic motion intolerance from migraine and after successful treatments of BPPV.

Other forms of balance training programs such as tai chi can be also used, as long as patients can safely incorporate them with vestibular rehabilitation.[19]



Medication Summary

The goals of pharmacotherapy are to relieve vertigo, reduce morbidity, and prevent complications. Agents used for these purposes include antihistamines, benzodiazepines, phenothiazines, monoaminergic agents, and anticholinergic agents.

Antihistamines, 1st Generation

Class Summary

Antihistamines prevent the histamine response in sensory nerve endings and blood vessels and are effective in treating vertigo.

Meclizine (Antivert, Medi-Meclizine, Trav-L-Tabs)

Meclizine decreases the excitability of the inner-ear labyrinth and blocks conduction in inner-ear vestibular-cerebellar pathways. Its effects are associated with therapeutic effects in relief of nausea and vomiting. It is most effective if used as needed for 2-3 days with episodes of true vertigo.

Dimenhydrinate (Dramamine, Driminate, Triptone)

Dimenhydrinate is a 1:1 salt of 8-chlorotheophylline and diphenhydramine that is believed to be particularly useful in the treatment of vertigo. It diminishes vestibular stimulation and depresses labyrinthine function by means of its central anticholinergic activity.

Anxiolytics, Benzodiazepines

Class Summary

By binding to specific receptor sites, benzodiazepines appear to potentiate the effects of gamma-aminobutyric acid (GABA) and facilitate inhibitory GABA neurotransmission and other inhibitory transmitters. These effects may prevent vertigo and emesis.

Diazepam (Valium, Diastat)

Diazepam is effective in treating vertigo, acute episodes in particular. It depresses all levels of the central nervous system (CNS), including the limbic system and the reticular formation, possibly by increasing the activity of GABA. Individualize the dosage, and cautiously increase it so as to avoid adverse effects. Discontinue as quickly as possible to maximize the cerebellar vestibular compensation process.

Phenothiazine Derivatives

Class Summary

Phenothiazines are effective in treating emesis, possibly because of their effects in the dopaminergic mesolimbic system.

Promethazine (Phenergan, Phenadoz, Promethegan)

Promethazine is an antidopaminergic drug that is effective in the treatment of emesis. It blocks postsynaptic mesolimbic dopaminergic receptors in the brain and reduces stimuli to the brainstem reticular system. Glycopyrrolate is safer and has fewer adverse effects. Promethazine is well tolerated by elderly patients and does not have the potential for causing extrapyramidal syndrome.

Prochlorperazine (Compro)

Prochlorperazine is an antidopaminergic drug that blocks postsynaptic mesolimbic dopamine receptors. It has anticholinergic activity and can depress the reticular activating system (this effect may be responsible for relief of nausea and vomiting).

Alpha/Beta Adrenergic Agonists

Class Summary

Monoaminergic agents may be used to treat vertigo; their effect may involve modulation of the sympathetic system.


Ephedrine stimulates release of epinephrine stores, producing alpha- and beta-adrenergic receptors.

Anticholinergic Agents

Class Summary

Anticholinergic agents are thought to work centrally by suppressing conduction in the vestibular-cerebellar pathways.

Glycopyrrolate (Robinul, Cuvposa)

Glycopyrrolate blocks the action of acetylcholine at parasympathetic sites.

Scopolamine (Transderm Scop)

Scopolamine blocks the action of acetylcholine at parasympathetic sites in smooth muscle, secretory glands, and the CNS. It antagonizes the actions of histamine and serotonin. Transdermal application may be the most effective for motion sickness. Use of scopolamine in the treatment of vestibular neuronitis is limited by the drug's slow onset of action. Severe adverse effects preclude its use in elderly. Glycopyrrolate is more effective and has fewer adverse effects, especially in elderly patients.


Questions & Answers


What is the role of the vestibular exam in the evaluation of dizziness, vertigo, and imbalance?

Which patient group is at highest risk for falls due to dizziness and vertigo?

What is the overall incidence of dizziness, vertigo, and imbalance in the US?

What is the global prevalence of dizziness, vertigo, and imbalance?

What is the most common disability associated with dizziness, vertigo, and imbalance?

Which type of disorders are vertigo and dizziness most often associated with?

Which specialists should be consulted in the management of dizziness, vertigo, and imbalance?

What are the treatment options for dizziness, vertigo, and imbalance?

What patient education resources are available for dizziness, vertigo, and imbalance?

What are the common causes of peripheral vertigo and central dizziness?

What are the inner ear pathologies associated with dizziness, vertigo, and imbalance?

What is the association between neurologic disorders and dizziness, vertigo, and imbalance?

What is the incidence of dizziness, vertigo, and imbalance in the US?

What is the global prevalence of dizziness, vertigo, and imbalance?


What is included in the evaluation of dizziness, vertigo, and imbalance?

How are dizziness and vertigo characterized?

How is vertigo differentiated from other types of dizziness?

How does the time course of vertigo help identify its etiology?

What are the signs and symptoms of central vertigo?

How does medical history help differentiate migraine-related dizziness from vestibular neuronitis or Ménière disease?

Which sensory and motor symptoms suggest a specific etiology for dizziness and imbalance?

What history finding suggests pharmacologically-induced dizziness?

Which etiologies of dizziness, vertigo, and imbalance is most common in the elderly?

How is the etiology of dizziness, vertigo, and imbalance diagnosed?

What should be included in the physical exam of dizziness, vertigo, and imbalance?

What are the 2 most-used reflexes examined in patients with dizziness, vertigo, and imbalance?

What is included in the vestibular exam of dizziness, vertigo, and imbalance?

How is nystagmus characterized in patients with dizziness, vertigo, and imbalance?

Which ocular findings are used to differentiate peripheral from central nystagmus in the evaluation of dizziness, vertigo, and imbalance?

What is the role of positioning exam (Dix-Hallpike test) in the evaluation of dizziness, vertigo, and imbalance?

What does a positioning exam reveal about dizziness, vertigo, and imbalance?

How is a vertical component of benign positioning nystagmus assessed in patients with dizziness, vertigo, and imbalance?

Which physical findings suggests horizontal nystagmus in patients with dizziness, vertigo, and imbalance?

How is caloric testing performed in the evaluation of dizziness, vertigo, and imbalance?

What is the role of vestibulospinal reflex (VSR) exam in the evaluation of dizziness, vertigo, and imbalance?

How is the Romberg exam conducted in the evaluation of dizziness, vertigo, and imbalance?

What is the Hamid vestibular stress test for dizziness, vertigo, and imbalance?

What are the limitations of vestibular stress tests in the evaluation of dizziness, vertigo, and imbalance?

What is the role of hyperventilation testing in the evaluation of dizziness, vertigo, and imbalance?


What is the basis for forming a differential diagnosis for dizziness, vertigo, and imbalance?

What are the differential diagnoses for Dizziness, Vertigo, and Imbalance?


Which tests are performed in the diagnosis of dizziness, vertigo, and imbalance?

What is the role of MRI in the diagnosis for dizziness, vertigo, and imbalance?

What is the role of audiometry and vestibular testing in the diagnosis of dizziness, vertigo, and imbalance?

What type of training is necessary to interpret vestibular test results for dizziness, vertigo, and imbalance?

What are the most commonly performed vestibular tests for the diagnosis of dizziness, vertigo, and imbalance?

What is the included in the standard electro/videonystagmography (ENG) test battery for the diagnosis of dizziness, vertigo, and imbalance?

What is the role of the saccadic test in the diagnosis of dizziness, vertigo, and imbalance?

How is the saccadic test performed in the evaluation of dizziness, vertigo, and imbalance?

What is the role of the gaze test in the diagnosis of dizziness, vertigo, and imbalance?

What is the role of the pursuit eye-movement test in the diagnosis of dizziness, vertigo, and imbalance?

What is the role of the optokinetic nystagmus (OKN) test in the diagnosis of dizziness, vertigo, and imbalance?

What is the role of the head-shake nystagmus test in the diagnosis of dizziness, vertigo, and imbalance?

What is the role of the positional nystagmus test in the diagnosis of dizziness, vertigo, and imbalance?

What is the role of the Dix-Hallpike test in the diagnosis of dizziness, vertigo, and imbalance?

What is the role of the bithermal caloric test in the diagnosis of dizziness, vertigo, and imbalance?

What are the most important findings of the bithermal caloric test for the diagnosis of dizziness, vertigo, and imbalance?

When were rotating-chair test systems developed for the diagnosis of dizziness, vertigo, and imbalance?

What is the role of the rotating-chair test in the diagnosis of dizziness, vertigo, and imbalance?

What is an alternative to the rotating-chair test for the diagnosis of dizziness, vertigo, and imbalance?

What is the role of computerized dynamic posturography in the diagnosis of dizziness, vertigo, and imbalance?

What is the role of vestibular evoked myogenic potential (VEMP) in the diagnosis of dizziness, vertigo, and imbalance?

What are the limitations of vestibular tests for the diagnosis of dizziness, vertigo, and imbalance?


What are the treatments options for acute dizziness and vertigo?

What is vestibular neuronitis-related acute vertigo?

What is Ménière disease?

What are the treatments options for vestibular neuronitis-related acute vertigo?

What is benign paroxysmal positioning vertigo (BPPV)?

What is the mechanism causing benign paroxysmal positioning vertigo (BPPV)?

What are the treatment options for benign paroxysmal positioning vertigo (BPPV)?

What are conservative therapies for Ménière disease?

What is the role of surgical therapy in the treatment of Ménière disease?

How is autoimmune inner-ear disease differentiated from Ménière disease?

What are the treatment options for autoimmune inner-ear disease?

What is migraine headache-caused dizziness?

How frequently is dizziness or vertigo a symptom of multiple sclerosis?

How is vestibular migraine diagnosed?

What is the pathogenesis of vestibular migraine?

What are the treatment options for vestibular migraine dizziness?

What are transient ischemic attacks (TIAs)?

How does a stroke cause vertigo?

What is a stroke differentiated from vestibular neuronitis?

What is the focus of evaluation of stroke?

How is multiple sclerosis diagnosed?

What is vestibular schwannoma (acoustic neuroma)?

What are the prevalence of dizziness in vestibular schwannoma (acoustic neuroma)?

What are some clinical manifestations of vestibular schwannoma (acoustic neuroma)?

How is vestibular schwannoma (acoustic neuroma) diagnosed?

What is the role of CNS in disequilibrium?

What is the cause of most falls in the elderly?

What is the role of vestibular rehabilitation in the management of dizziness, vertigo, and imbalance?

What are the goals of vestibular rehabilitation for dizziness, vertigo, and imbalance?

What is the efficacy of vestibular rehabilitation for dizziness, vertigo, and imbalance?

In which groups of patients in vestibular rehabilitation most beneficial for dizziness, vertigo, and imbalance?

What is the role of tai chi in the vestibular rehabilitation of dizziness, vertigo, and imbalance?


What are the goals of drug treatment for dizziness, vertigo, and imbalance?

Which medications in the drug class Anticholinergic Agents are used in the treatment of Dizziness, Vertigo, and Imbalance?

Which medications in the drug class Alpha/Beta Adrenergic Agonists are used in the treatment of Dizziness, Vertigo, and Imbalance?

Which medications in the drug class Phenothiazine Derivatives are used in the treatment of Dizziness, Vertigo, and Imbalance?

Which medications in the drug class Anxiolytics, Benzodiazepines are used in the treatment of Dizziness, Vertigo, and Imbalance?

Which medications in the drug class Antihistamines, 1st Generation are used in the treatment of Dizziness, Vertigo, and Imbalance?