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.

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.)

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 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.

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.

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.

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.

No known treatment for BPT currently exists. However, the condition it is self-limiting and resolves after about eighteen months.

Benign paroxysmal torticollis disappears in the early years of life with no medical intervention.

However, some cases of benign paroxysmal torticollis cases can evolve into benign paroxysmal vertigo of childhood, migrainous vertigo or typical migraines.

Several different types of magnetic resonance imaging (MRI) may be employed in diagnosis: MRI without contrast, Gd contrast enhanced T1-weighted MRI (GdT1W) or T2-weighted enhanced MRI (T2W or T2*W). Non-contrast enhanced MRI is considerably less expensive than any of the contrast enhanced MRI scans. The gold standard in diagnosis is GdT1W MRI.

The reliability of non-contrast enhanced MRI is highly dependent on the sequence of scans, and the experience of the operator.

Before the advent of MRI, electronystagmography and Computed Tomography were employed for diagnosis of acoustic neuroma.

Though outwardly similar to cluster headaches, chronic paroxysmal hemicrania is rather different, and the two headaches are not a subset of one or the other. Key differences include:

- Different gender distributions – CPH is more common in women than men, with opposite occurring with cluster headaches.

- CPH attacks occur more frequently, but are shorter.

- Individuals with CPH are far more responsive to indomethacin than individuals with cluster headaches.

- CPH attacks can be provoked by neck movement.

- In a study conducted by Sjaastad, heating a patient's body will cause the painful side of the forehead to sweat more in CPH patients, while there will be less sweating on that side for those suffering from cluster headaches.

Benign paroxysmal vertigo of childhood is an uncommon neurological disorder which presents with recurrent episodes of dizziness. The presentation is usually between the ages of 2 years and 7 years of age and is characterised by short episodes of vertigo of sudden onset when the child appears distressed and unwell. The child may cling to something or someone for support. The episode lasts only minutes and resolves suddenly and completely. It is a self-limiting condition and usually resolves after about eighteen months, although many go on to experience migrainous vertigo (or vertiginous migraine) when older.

Benign paroxysmal vertigo of childhood is a migrainous phenomenon with more than 50% of those affected having a family history of migraines affecting a first-degree relative. It has no relationship to benign paroxysmal positional vertigo which is a different condition entirely.

A ten-patient study conducted by Pareja et al. found that all patients diagnosed with CPH were responsive to indomethacin and were able to completely control their symptoms. Doses of the drug ranged from 25 mg per day to 150 mg per day with a median dose of 75 mg per 24-hour period.

Almost all cases of CPH respond positively and effectively to indometacin, but as much as 25 percent of patients discontinued use of the drug due to adverse side effects, namely complications in the gastrointestinal tract.

According to a case study by Milanlioglu et al., 100mg of lamotrigine, an antiepileptic drug, administered twice daily alleviated all painful symptoms. No side effects were noted after two months of treatment. Dosage of lamotrigine was decreased to 50mg a day after the first two months, and no symptoms or side-effects were recorded after a three-month followup.

Use of topiramate has also been found to be an effective treatment for CPH, but cluster headache medications have been found to have little effect.

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

Weber's syndrome is the only form of alternating hemiplegia that is somewhat easy to diagnose beyond the general criteria. Although Weber's syndrome is rare, a child born with the disorder typically has a port-wine stain on the face around the eye. While the port-wine stain does not necessarily mean the child has Weber's syndrome, if the port-wine stain involves the ophthalmic division of the trigeminal nerve than the likelihood of it being weber's syndrome greatly increases. If a port-wine stain around the eye is found, the patient should be screened for intracranial leptomeningeal angiomatosis. Magnetic resonance imaging (MRI)can be used to determine the presence and severity while computed cranial tomography can be used to determine the effect. MRI is the preferred diagnostic test on children presenting with port-wine stain. Other imaging techniques can be used in addition to further determine the severity of the disorder. The initial diagnosis is made based on the presence of neurologic and ophthalmic disease but the disease progresses differently in each patient so after initial diagnosis the patient should be monitored frequently in order to handle further complications resulting from the syndrome.

Bruns nystagmus is an unusual type of bilateral nystagmus most commonly occurring in patients with cerebellopontine angle tumours. It is caused by the combination of slow, large amplitude nystagmus (gaze paretic nystagmus) when looking towards the side of the lesion, and rapid, small amplitude nystagmus (vestibular nystagmus) when looking away from the side of the lesion. It occurs in 11% of patients with vestibular schwannoma, and occurs mainly in patients with larger tumours (67% of patients with tumours over 3.5 cm diameter). Bruns nystagmus is also associated with an increased incidence of balance disturbance in patients with vestibular schwannoma. It may be caused by the compression of both flocculi, the vestibular part of the cerebellum, and improvement in both the nystagmus and balance problems occur commonly after removal of the tumour.

Bruns nystagmus is named for Ludwig Bruns (1858 – 1915).

There is no diagnostic test for alternating hemiplegia, which makes it very difficult to diagnose. Also, because alternating hemiplegia is extremely rare, it is frequently missed and the patient is often misdiagnosed. Proper diagnosis, however, is critical for early treatment of the disorder. There are many criteria that can help in the proper general diagnosis of alternating hemiplegia.

The eye findings of Parinaud's Syndrome generally improve slowly over months, especially with resolution of the causative factor; continued resolution after the first 3–6 months of onset is uncommon. However, rapid resolution after normalization of intracranial pressure following placement of a ventriculoperitoneal shunt has been reported.

Treatment is primarily directed towards etiology of the dorsal midbrain syndrome. A thorough workup, including neuroimaging is essential to rule out anatomic lesions or other causes of this syndrome. Visually significant upgaze palsy can be relieved with bilateral inferior rectus recessions. Retraction nystagmus and convergence movement are usually improved with this procedure as well.

Acute Cerebellar ataxia is a diagnosis of exclusion. Urgent CT scan is necessary to rule out cerebellar tumor or hemorrhage as cause of the ataxia; however in acute cerebellar ataxia, the CT will be normal. CSF studies are normal earlier in the course of disease. Later on CSF shows moderate elevation of proteins.

Supportive treatment is the only intervention for acute cerebellar ataxia of childhood. Symptoms may last as long as 2 or 3 months.

Alexanders law refers to spontaneous nystagmus that occurs after an acute unilateral vestibular loss. It was first described in 1912 and has three elements to explain how the vestibulo-ocular reflex responds to an acute vestibular insult. The first element says that spontaneous nystagmus after an acute vestibular impairment has the fast phase directed toward the healthy ear. The direction of the nystagmus, by convention, is named for the fast phase, so the spontaneous nystagmus is directed toward the healthy ear. The second element says nystagmus is greatest when gaze is directed toward the healthy ear, is attentuated at central gaze and may be absent when gaze is directed toward the impaired ear. The third element says that spontaneous nystagmus with central gaze is augmented when vision is denied. This became apparent with the implementation of electrographic testing.

Alexander's law states that in individuals with nystagmus, the amplitude of the nystagmus increases when the eye moves in the direction of the fast phase (saccade).

It is manifested during spontaneous nystagmus in a patient with a vestibular lesion. The nystagmus becomes more intense when the patient looks in the quick-phase than in the slow-phase direction.

The law was named after Gustav Alexander who described it in 1912.

Patients who develop PSH after traumatic injury have longer hospitalization and longer durations in intensive care in cases where ICU treatment is necessary. Patients often are more vulnerable to infections and spend longer times on ventilators, which can lead to an increased risk of various lung diseases. PSH does not affect mortality rate, but it increases the amount of time it takes a patient to recover from injury, compared to patients with similar injuries who do not develop PSH episodes. It often takes patients who develop PSH longer to reach similar levels of the brain activity seen in patients who do not develop PSH, although PSH patients do eventually reach these same levels.

As of 1993 only approximately 30 people with AHC had been described in scientific literature. Due to the rarity and complexity of AHC, it is not unusual for the initial diagnosis to be incorrect, or for diagnosis to be delayed for several months after the initial symptoms become apparent. The average age of diagnosis is just over 36 months. Diagnosis of AHC is not only difficult because of its rarity, but because there is no diagnostic test, making this a diagnosis of exclusion. There are several generally accepted criteria which define this disorder, however other conditions with a similar presentation, such as HSV encephalitis, must first be ruled out. Due to these diagnostic difficulties, it is possible that the commonness of the disease is underestimated.

The following descriptions are commonly used in the diagnosis of AHC. The initial four criteria for classifying AHC were that it begins before 18 months of age, includes attacks of both hemiplegia on either side of the body, as well as other autonomic problems such as involuntary eye movement (episodic monocular nystagmus), improper eye alignment, choreoathetosis, and sustained muscle contractions (dystonia). Finally, patients suffer from intellectual disabilities, delayed development, and other neurological abnormalities. These diagnostic criteria were updated in 1993 to include the fact that all of these symptoms dissipate immediately upon sleeping. Diagnostic criteria were also expanded to include episodes of bilateral hemiplegia which shifted from one side of the body to the other.

Recent criteria have been proposed for screening for AHC early, in order to improve the diagnostic timeline. These screening criteria include focal or unilateral paroxysmal dystonia in the first 6 months of life, as well as the possibility of flaccid hemiplegia either with or separate from these symptoms. Paroxysmal ocular movements should also be considered, and these should include both binocular and monocular symptoms which show in the first 3 months of life.