Tests for vertigo often attempt to elicit nystagmus and to differentiate vertigo from other causes of dizziness such as presyncope, hyperventilation syndrome, disequilibrium, or psychiatric causes of lightheadedness. Tests of vestibular system (balance) function include: electronystagmography (ENG), Dix-Hallpike maneuver, rotation tests, head-thrust test, caloric reflex test, and computerized dynamic posturography (CDP).

The HINTS test, which is a combination of three physical exam tests that may be performed by physicians at the bedside has been deemed helpful in differentiating between central and peripheral causes of vertigo. The HINTS test involves: the horizontal head impulse test, observation of nystagmus on primary gaze, and the test of skew. CT scans or MRIs are sometimes used by physicians when diagnosing vertigo.

Tests of auditory system (hearing) function include pure tone audiometry, speech audiometry, acoustic reflex, electrocochleography (ECoG), otoacoustic emissions (OAE), and the auditory brainstem response test.

A number of specific conditions can cause vertigo. In the elderly, however, the condition is often multifactorial.

A recent history of underwater diving can indicate possibility of barotrauma or decompression sickness involvement, but does not exclude all other possibilities. The dive profile (which is frequently recorded by dive computer) can be useful to assess a probability for decompression sickness, which can be confirmed by therapeutic recompression.

Definitive treatment depends on the underlying cause of vertigo. Ménière's disease patients have a variety of treatment options to consider when receiving treatment for vertigo and tinnitus including: a low-salt diet and intratympanic injections of the antibiotic gentamicin or surgical measures such as a shunt or ablation of the labyrinth in refractory cases.

Common drug treatment options for vertigo may include the following:

- Anticholinergics such as hyoscine hydrobromide (scopolamine)

- Anticonvulsants such as topiramate or valproic acid for vestibular migraines

- Antihistamines such as betahistine, dimenhydrinate, or meclizine, which may have antiemetic properties

- Beta blockers such as metoprolol for vestibular migraine

- Corticosteroids such as methylprednisolone for inflammatory conditions such as vestibular neuritis or dexamethasone as a second-line agent for Ménière's disease

All cases of decompression sickness should be treated initially with 100% oxygen until hyperbaric oxygen therapy (100% oxygen delivered in a high-pressure chamber) can be provided. Several treatments may be necessary, and treatment will generally be repeated until either all symptoms resolve, or no further improvement is apparent.

Vertigo, a distinct process sometimes confused with the broader term, dizziness, accounts for about six million clinic visits in the United States every year; between 17 and 42% of these patients are eventually diagnosed with BPPV.

Other causes of vertigo include:

- Motion sickness/motion intolerance: a disjunction between visual stimulation, vestibular stimulation, and/or proprioception

- Visual exposure to nearby moving objects (examples of optokinetic stimuli include passing cars and falling snow)

- Other diseases: (labyrinthitis, Ménière's disease, and migraine, etc.)

The condition is diagnosed by the patient's history, and by performing the Dix–Hallpike test or the roll test, or both.

The Dix–Hallpike test is a common test performed by examiners to determine whether the posterior semicircular canal is involved. It involves a reorientation of the head to align the posterior semicircular canal (at its entrance to the ampulla) with the direction of gravity. This test will reproduce vertigo and nystagmus characteristic of posterior canal BPPV.

When performing the Dix–Hallpike test, patients are lowered quickly to a supine position, with the neck extended by the clinician performing the maneuver. For some patients, this maneuver may not be indicated, and a modification may be needed that also targets the posterior semicircular canal. Such patients include those who are too anxious about eliciting the uncomfortable symptoms of vertigo, and those who may not have the range of motion necessary to comfortably be in a supine position. The modification involves the patient moving from a seated position to side-lying "without" their head extending off the examination table, such as with Dix–Hallpike. The head is rotated 45 degrees away from the side being tested, and the eyes are examined for nystagmus. A positive test is indicated by patient report of a reproduction of vertigo and clinician observation of nystagmus. Both the Dix–Hallpike and the side-lying testing position have yielded similar results, and as such the side-lying position can be used if the Dix–Hallpike cannot be performed easily.

The roll test can determine whether the horizontal semicircular canal is involved. The roll test requires the patient to be in a supine position with their head in 30° of cervical flexion. Then the examiner quickly rotates the head 90° to the left side, and checks for vertigo and nystagmus. This is followed by gently bringing the head back to the starting position. The examiner then quickly rotates the head 90° to the right side, and checks again for vertigo and nystagmus. In this roll test, the patient may experience vertigo and nystagmus on both sides, but rotating towards the affected side will trigger a more intense vertigo. Similarly, when the head is rotated towards the affected side, the nystagmus will beat towards the ground and be more intense.

As mentioned above, both the Dix–Hallpike and roll test provoke the signs and symptoms in subjects suffering from archetypal BPPV. The signs and symptoms patients with BPPV experience are typically a short-lived vertigo, and observed nystagmus. In some patients, though rarely, the vertigo can persist for years. Assessment of BPPV is best done by a medical health professional skilled in management of dizziness disorders, commonly a physiotherapist, audiologist or other physician.

The nystagmus associated with BPPV has several important characteristics which differentiate it from other types of nystagmus.

- Latency of onset: there is a 5–10 second delay prior to onset of nystagmus.

- Nystagmus lasts for 5–120 seconds.

- Positional: the nystagmus occurs only in certain positions.

- Repeated stimulation, including via Dix–Hallpike maneuvers, cause the nystagmus to fatigue or disappear temporarily.

- Rotatory/Torsional component is present, or (in the case of lateral canal involvement) the nystagmus beats in either a geotropic (towards the ground) or ageotropic (away from the ground) fashion.

- Visual fixation suppresses nystagmus due to BPPV.

Although rare, CNS disorders can sometimes present as BPPV. A practitioner should be aware that if a patient whose symptoms are consistent with BPPV, but does not show improvement or resolution after undergoing different particle repositioning maneuvers — detailed in the Treatment section below — need to have a detailed neurological assessment and imaging performed to help identify the pathological condition.

The diagnostic criteria as of 2015 define definite MD and probable MD as follows:

Definite

1. Two or more spontaneous episodes of vertigo, each lasting 20 minutes to 12 hours

2. Audiometrically documented low- to medium-frequency sensorineural hearing loss in the affected ear on at least 1 occasion before, during, or after one of the episodes of vertigo

3. Fluctuating aural symptoms (hearing, tinnitus, or fullness) in the affected ear

4. Not better accounted for by another vestibular diagnosis

Probable

1. Two or more episodes of vertigo or dizziness, each lasting 20 minutes to 24 hours

2. Fluctuating aural symptoms (hearing, tinnitus, or fullness) in the reported ear

3. Not better accounted for by another vestibular diagnosis

A common and important symptom of MD is hypersensitivity to sounds. This hypersensitivity is easily diagnosed by measuring the loudness discomfort levels (LDLs).

Symptoms of MD overlap with migraine-associated vertigo (MAV) in many ways, but when hearing loss develops in MAV is usually in both ears, and this is rare in MD, and hearing loss generally does not progress in MAV as it does in MD.

People who have had a transient ischemic attack (TIA) and stroke can present with symptoms similar to MD, and in people at risk for stroke magnetic resonance imaging (MRI) should be conducted to exclude TIA or stroke, and as TIA is often a precursor to stroke, that risk should be managed.

Other vestibular conditions that should be excluded include vestibular paroxysmia, recurrent unilateral vestibulopathy, vestibular schwannoma, or a tumor of the endolymphatic sac.

In most cases, the condition tends to be self-limiting. In 95% or greater, vestibular neuritis is a one-time experience with most people fully recovering.

Recovery from acute labyrinthine inflammation generally takes from one to six weeks, but it is not uncommon for residual symptoms (dysequilibrium and/or dizziness) to last for a couple of months.

Recovery from a temporary damaged inner ear typically follows two phases:

1. An acute period, which may include severe vertigo and vomiting

2. approximately two weeks of sub-acute symptoms and rapid recovery

The treatment for vestibular neuronitis depends on the cause. However, symptoms of vertigo can be treated in the same way as other vestibular dysfunctions with vestibular rehabilitation.

From 3% to 11% of diagnosed dizziness in neuro-otological clinics are due to Meniere's. The annual incidence rate is estimated to be about 15/100,000 and the prevalence rate is about 218/100,000, and around 15% of people with Meniere's disease are older than 65. In around 9% of cases a relative also had MD, signalling that there may be a genetic predisposition in some cases.

The odds of MD are greater for people of white ethnicity, with severe obesity, and women. Several conditions are often comorbid with MD, including arthritis, psoriasis, gastroesophageal reflux disease, irritable bowel syndrome, and migraine.

Tests of vestibular system (balance) function include electronystagmography (ENG), Videonystagmograph (VNG), rotation tests, Computerized Dynamic Posturography (CDP), and Caloric reflex test.

Tests of auditory system (hearing) function include pure-tone audiometry, speech audiometry, acoustic-reflex, electrocochleography (ECoG), otoacoustic emissions (OAE), and auditory brainstem response test (ABR; also known as BER, BSER, or BAER).

Other diagnostic tests include magnetic resonance imaging (MRI) and computerized axial tomography (CAT, or CT).

The presence of dehiscence can be detected by a high definition (0.6 mm or less) coronal CT scan of the temporal bone, currently the most reliable way to distinguish between superior canal dehiscence syndrome (SCDS) and other conditions of the inner ear involving similar symptoms such as Ménière's disease and perilymphatic fistula. Other diagnostic tools include the vestibular evoked myogenic potential or VEMP test, videonystagmography (VNG), electrocochleography (ECOG) and the rotational chair test. An accurate diagnosis is of great significance as unnecessary exploratory middle ear surgery may thus be avoided. Several of the symptoms typical to SCDS (e.g. vertigo and Tullio) may also be present singly or as part of Ménière's disease, sometimes causing the one illness to be confused with the other. There are reported cases of patients being affected by both Ménière's disease and SCDS concurrently.

As SCDS is a very rare and still a relatively unknown condition, obtaining an accurate diagnosis of this distressing (and even disabling) disease may take some time as many health care professionals are not yet aware of its existence.

When diagnosing, PLF should be differentiated from Ménière's disease. Tympanostomy has been reported to be a way to diagnose and cure PLF.

Once diagnosed, the gap in the temporal bone can be repaired by surgical resurfacing of the affected bone or plugging of the superior semicircular canal. These techniques are performed by accessing the site of the dehiscence either via a middle fossa craniotomy or via a canal drilled through the transmastoid bone behind the affected ear. Bone cement has been the material most often used, in spite of its tendency to slippage and resorption, and a consequent high failure rate; recently, soft tissue grafts have been substituted.

No specific treatment may be available, but withdrawal of the ototoxic drug may be warranted when the consequences of doing so are less severe than those of the ototoxicity.

Ototoxic monitoring during exposure is recommended by the American Academy of Audiology to allow for proper detection and possible prevention or rehabilitation of the hearing loss through a cochlear implant or hearing aid. Monitoring can be completed through performing otoacoustic emissions testing or high frequency audiometry. Successful monitoring includes a baseline test before, or soon after, exposure to the ototoxin. Follow-up testing is completed in increments after the first exposure, throughout the cessation of treatment. Shifts in hearing status are monitored and relayed to the prescribing physician to make treatment decisions.

It is difficult to distinguish between nerve damage and structural damage due to similarity of the symptoms. Diagnosis of ototoxicity typically results from ruling out all other possible sources of hearing loss and is often the catchall explanation for the symptoms. Treatment options vary depending on the patient and the diagnosis. Some patients experience only temporary symptoms that do not require drastic treatment while others can be treated with medication. Physical therapy may prove useful for regaining balance and walking abilities. Cochlear implants are sometimes an option to restore hearing. Such treatments are typically taken to comfort the patient, not to cure the disease or damage caused by ototoxicity. There is no cure or restoration capability if the damage becomes permanent, although cochlear nerve terminal regeneration has been observed in chickens, which suggests that there may be a way to accomplish this in humans.

The difficulty of making the right vestibular diagnosis is reflected in the fact that in some populations, more than one third of the patients with a vestibular disease consult more than one physician – in some cases up to more than fifteen.

Diagnosis of a balance disorder is complicated because there are many kinds of balance disorders and because other medical conditions—including ear infections, blood pressure changes, and some vision problems—and some medications may contribute to a balance disorder. A person experiencing dizziness should see a physiotherapist or physician for an evaluation. A physician can assess for a medical disorder, such as a stroke or infection, if indicated. A physiotherapist can assess balance or a dizziness disorder and provide specific treatment.

The primary physician may request the opinion of an otolaryngologist to help evaluate a balance problem. An otolaryngologist is a physician/surgeon who specializes in diseases and disorders of the ear, nose, throat, head, and neck, sometimes with expertise in balance disorders. He or she will usually obtain a detailed medical history and perform a physical examination to start to sort out possible causes of the balance disorder. The physician may require tests and make additional referrals to assess the cause and extent of the disruption of balance. The kinds of tests needed will vary based on the patient's symptoms and health status. Because there are so many variables, not all patients will require every test.

In aviation and underwater diving, alternobaric vertigo is dizziness resulting from unequal pressures being exerted between the ears due to one Eustachian tube being less patent than the other.

Patients are advised to treat with bed rest and avoiding activities that increase intracranial pressure (i.e. weightlifting, valsalva, scuba diving, flying in airplanes) with the hopes of the membrane healing on their own. Appropriate Physical therapy / vestibular rehabilitation techniques can be helpful in managing symptoms of movement sensitivity.

This might have occurred due to barotrauma of descent, and/or the effects of nasal decongestants. It is due to unequal increase in middle ear pressures on ascent, is usually mild, and most often cleared by further ascent. When the pressures in both ears reach ambient levels, the stimulus for the dizziness stops. Although most often mild, the vertigo can persist until the diver reaches the surface continuing the unequal pressures, which can damage the inner ear or ear drum.

Alternobaric vertigo is most pronounced when the diver is in the vertical position; the spinning is towards the ear with the higher pressure and tends to develop when the pressures differ by 60 cm of water or more. Ear clearing may be a remedy. A similar vertigo can also occur as a result of unequal heating stimulation of one inner ear labyrinth over the other due to diving in a prone position in cold water - the undermost ear being stimulated.

MAV is not recognized as a distinct diagnostic entity. Lembert and Neuhauser propose criteria for definite and probable migraine-associated vertigo.

A diagnosis of "definite migraine-associated vertigo" includes a case history of:

- episodic vestibular symptoms of at least moderate severity;

- current or previous history of migraine according to the 2004 "International Classification of Headache Disorders";

- one of the following migrainous symptoms during two or more attacks of vertigo: migrainous headache, photophobia, phonophobia, visual or other auras; and

- other causes ruled out by appropriate investigations.

A diagnosis of "probable migraine-associated vertigo" includes a case history of episodic vestibular symptoms of at least moderate severity and one of the following:

- current or previous history of migraine according to the 2004 "International Classification of Headache Disorders";

- migrainous symptoms during vestibular symptoms;

- migraine precipitants of vertigo in more than 50% of attacks, such as food triggers, sleep irregularities, or hormonal change;

- response to migraine medications in more than 50% of attacks; and

- other causes ruled out by appropriate investigations.

Note that, in both of the above criteria, headache is not required to make the diagnosis of migraine-associated vertigo.

They add that, in patients with a clear-cut history, no vestibular tests are required. Other historical criteria which are helpful in making the diagnosis of migraine-associated vertigo are vertiginous symptoms throughout the patient’s entire life, a long history of motion intolerance, sensitivity to environmental stimuli, illusions of motion of the environment, and vertigo that awakens the patient.

Treatment of migraine-associated vertigo is the same as the treatment for migraine in general.

Endolymphatic hydrops is a disorder of the inner ear. It consists of an excessive build-up of the endolymph fluid, which fills the hearing and balance structures of the inner ear. Endolymph fluid, which is partly regulated by the endolymph sac, flows through the inner ear and is critical to the function of all sensory cells in the inner ear. In addition to water, endolymph fluid contains salts such as sodium, potassium, chloride and other electrolytes. If the inner ear is damaged by disease or injury, the volume and composition of the endolymph fluid can change, causing the symptoms of endolymphatic hydrops.

The symptoms of endolymphatic hydrops include the feeling of pressure or fullness in the ears, hearing loss, tinnitus (ringing in the ears) and balance problems. Individuals who have Meniere’s disease have a degree of endolymphatic hydrops that is strong enough to trigger the symptoms of this disease, but individuals with endolymphatic hydrops do not always progress to Meniere’s disease.

About 20–30% of the population report to have experienced dizziness at some point in the previous year.

Treatment differs depending on the cause. Each cause has a different treatment, and may involve either medical treatment, surgery, or therapy. If serious damage has already been done, then the focus of treatment is upon avoidance of vestibular suppressants and ototoxins. It is recommended that you tell your physicians to avoid drugs that end in mycin ( Azithromycin, Erythromycin ) because of possible reactions which could lead to setbacks. Vestibular rehabilitation is important. Your physician will try to keep the administering of drugs to a minimum.

Your physician will make on your history, physical examination or vestibular tests in a rotary chair. There are several different causes of Bilateral Vestibulopathy, including Gentamicin toxicity, but the rotary chair test will determine the effects on both ears. Tests for syphilis, an antibody test for autoimmune inner ear disease or audiograms may be important in determining if you have bilateral vestibulopathy.

Ototoxic effects are also seen with quinine, pesticides, solvents, asphyxiants and heavy metals such as mercury and lead. When combining multiple ototoxins, the risk of hearing loss becomes greater.

Ototoxic chemicals in the environment (from contaminated air or water) or in the workplace interact with mechanical stresses on the hair cells of the cochlea in different ways. For organic solvents such as toluene, styrene or xylene, the combined exposure with noise increases the risk of hearing loss in a synergistic manner. Carbon monoxide, has been shown to increase the severity of the hearing loss from noise. Given the potential for enhanced risk of hearing loss, exposures and contact with products such as paint thinners, degreasers, white spirits, exhaust, should be kept to a minimum. Noise exposures should be kept below 85 decibels, and the chemical exposures should be below the recommended exposure limits given by regulatory agencies.

Drug exposures mixed with noise potentially lead to increased risk of ototoxic hearing loss. Noise exposure combined with the chemotherapeutic cisplatin puts individuals at increased risk of ototoxic hearing loss. Noise at 85 dB SPL or above added to the amount of hair cell death in the high frequency region of the cochlea In chinchillas. The American Academy of Audiology includes in their position statement that exposure to noise at the same time as aminoglycosides may exacerbate ototoxicity. The American Academy of Audiology recommends people being treated with ototoxic chemotherapeutics avoid excessive noise levels during treatment and for several months following cessation of treatment. Opiates in combination with excessive noise levels may also have an additive affect on ototoxic hearing loss.

Previous noise exposure has not been found to potentiate ototoxic hearing loss.