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.

The prevalence of migraine and vertigo is 1.6 times higher in 200 dizziness clinic patients than in 200 age- and sex-matched controls from an orthopaedic clinic. Among the patients with unclassified or idiopathic vertigo, the prevalence of migraine was shown to be elevated. In another study, migraine patients reported 2.5 times more vertigo and also 2.5 more dizzy spells during headache-free periods than the controls.

MAV may occur at any age with a female:male ratio of between 1.5 and 5:1. Familial occurrence is not uncommon. In most patients, migraine headaches begin earlier in life than MAV with years of headache-free periods before MAV manifests.

In a diary study, the 1-month prevalence of MAV was 16%, frequency of MAV was higher and duration longer on days with headache, and MAV was a risk factor for co-morbid anxiety.

Brain related causes are less commonly associated with isolated vertigo and nystagmus but can still produce signs and symptoms, which mimic peripheral causes. Disequilibrium is often a prominent feature.

- Degenerative: age related decline in balance function

- Infectious: meningitis, encephalitis, epidural abscess, syphilis

- Circulatory: cerebral or cerebellar ischemia or hypoperfusion, stroke, lateral medullary syndrome (Wallenberg's syndrome)

- Autoimmune: Cogan syndrome

- Structural: Arnold-Chiari malformation, hydrocephalus

- Systemic: multiple sclerosis, Parkinson's disease

- Vitamin deficiency: Vitamin B12 deficiency

- CNS or posterior neoplasms, benign or malignant

- Neurological: Vertiginous epilepsy, abasia

- Other – There are a host of other causes of dizziness not related to the ear.

- Mal de debarquement is rare disorder of imbalance caused by being on board a ship. Patients suffering from this condition experience disequilibrium even when they get off the ship. Typically treatments for seasickness are ineffective for this syndrome.

- Motion sickness – a conflict between the input from the various systems involved in balance causes an unpleasant sensation. For this reason, looking out of the window of a moving car is much more pleasant than looking inside the vehicle.

- Migraine-associated vertigo

- Toxins, drugs, medications; it is also a known symptom of carbon monoxide poisoning.

Some people will report having an upper respiratory infection (common cold) or flu prior to the onset of the symptoms of vestibular neuronitis; others will have no viral symptoms prior to the vertigo attack.

Some cases of vestibular neuronitis are thought to be caused by an infection of the vestibular ganglion by the herpes simplex type 1 virus. However, the cause of this condition is not fully understood, and in fact many different viruses may be capable of infecting the vestibular nerve.

Acute localized ischemia of these structures also may be an important cause, especially in children, vestibular neuritis may be preceded by symptoms of a common cold. However, the causative mechanism remains uncertain.

This can also be brought on by pressure changes such as those experienced while flying or scuba diving.

Labyrinthitis, also known as vestibular neuritis, is inflammation of the inner ear. It results in vertigo and also possible hearing loss or ringing in the ears. It can occur as a single attack, a series of attacks, or a persistent condition that diminishes over three to six weeks. It may be associated with nausea and vomiting. Vestibular neuronitis may also be associated with eye nystagmus.

The cause is often not clear. It may be due to a virus, but it can also arise from bacterial infection, head injury, extreme stress, an allergy, or as a reaction to medication. 30% of affected people had a common cold prior to developing the disease. Either bacterial or viral labyrinthitis can cause permanent hearing loss in rare cases. This appears to result from an imbalance of neuronal input between the left and right inner ears.

Vestibular neuritis affects approximately 35 per million people per year. It typically occurs in those between 30 and 60 years of age. There is no significant gender difference. It derives its name from the labyrinths that house the vestibular system, which senses changes in head position.

The cause of Ménière's disease is unclear but likely involves both genetic and environmental factors. A number of theories exist including constrictions in blood vessels, viral infections, autoimmune reactions.

Causes of dizziness related to the ear are often characterized by vertigo (spinning) and nausea. Nystagmus (flickering of the eye, related to the Vestibulo-ocular reflex [VOR]) is often seen in patients with an acute peripheral cause of dizziness.

- Benign Paroxysmal Positional Vertigo (BPPV) – The most common cause of vertigo. It is typically described as a brief, intense sensation of spinning that occurs when there are changes in the position of the head with respect to gravity. An individual may experience BPPV when rolling over to the left or right, upon getting out of bed in the morning, or when looking up for an object on a high shelf. The cause of BPPV is the presence of normal but misplaced calcium crystals called otoconia, which are normally found in the utricle and saccule (the otolith organs) and are used to sense movement. If they fall from the utricle and become loose in the semicircular canals, they can distort the sense of movement and cause a mismatch between actual head movement and the information sent to the brain by the inner ear, causing a spinning sensation.

- Labyrinthitis - An inner ear infection or inflammation causing both dizziness (vertigo) and hearing loss.

- Vestibular neuronitis - an infection of the vestibular nerve, generally viral, causing vertigo

- Cochlear Neuronitis – an infection of the Cochlear nerve, generally viral, causing sudden deafness but no vertigo

- Trauma – Injury to the skull may cause either a fracture or a concussion to the organ of balance. In either case an acute head injury will often result in dizziness and a sudden loss of vestibular function.

- Surgical trauma to the lateral semicircular canal (LSC) is a rare complication which does not always result in cochlear damage. Vestibular symptoms are pronounced. Dizziness and instability usually persist for several months and sometimes for a year or more.

- Ménière's disease - an inner ear fluid balance disorder that causes lasting episodes of vertigo, fluctuating hearing loss, tinnitus (a ringing or roaring in the ears), and the sensation of fullness in the ear. The cause of Ménière's disease is unknown.

- Perilymph fistula – a leakage of inner ear fluid from the inner ear. It can occur after head injury, surgery, physical exertion or without a known cause.

- Superior canal dehiscence syndrome – a balance and hearing disorder caused by a gap in the temporal bone, leading to the dysfunction of the superior canal.

- Bilateral vestibulopathy – a condition involving loss of inner ear balance function in both ears. This may be caused by certain antibiotics, anti-cancer, and other drugs or by chemicals such as solvents, heavy metals, etc., which are ototoxic; or by diseases such as syphilis or autoimmune disease; or other causes. In addition, the function of the semicircular canal can be temporarily affected by a number of medications or combinations of medications.

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

Within the labyrinth of the inner ear lie collections of calcium crystals known as otoconia or otoliths. In patients with BPPV, the otoconia are dislodged from their usual position within the utricle, and migrate over time into one of the semicircular canals (the posterior canal is most commonly affected due to its anatomical position). When the head is reoriented relative to gravity, the gravity-dependent movement of the heavier otoconial debris (colloquially "ear rocks") within the affected semicircular canal causes abnormal (pathological) endolymph fluid displacement and a resultant sensation of vertigo. This more common condition is known as canalithiasis.

In rare cases, the crystals themselves can adhere to a semicircular canal cupula, rendering it heavier than the surrounding endolymph. Upon reorientation of the head relative to gravity, the cupula is weighted down by the dense particles, thereby inducing an immediate and sustained excitation of semicircular canal afferent nerves. This condition is termed cupulolithiasis.

There is evidence in the dental literature that malleting of an osteotome during closed sinus floor elevation, otherwise known as "osteotome sinus elevation" or "lift", transmits percussive and vibratory forces capable of detaching otoliths from their normal location and thereby leading to the symptoms of BPPV.

It can be triggered by any action which stimulates the posterior semi-circular canal, including:

- Looking up or down

- Preceding head injury

- Sudden head movement

- Rolling over in bed

- Tilting the head

BPPV may be made worse by any number of modifiers which may vary between individuals:

- Changes in barometric pressure — patients may feel increased symptoms up to two days before rain or snow

- Lack of sleep (required amounts of sleep may vary widely)

- Stress

An episode of BPPV may be triggered by dehydration, such as that caused by diarrhea. For this reason, it commonly occurs in post-operative patients who have diarrhea induced by post-operative antibiotics.

BPPV is one of the most common vestibular disorders in patients presenting with dizziness; migraine is implicated in idiopathic cases. Proposed mechanisms linking the two are genetic factors and vascular damage to the labyrinth.

Although BPPV can occur at any age, it is most often seen in people over the age of 60. Besides aging, there are no major risk factors known for developing BPPV, although previous episodes of trauma to the head, or inner ear infections known as labyrinthitis, may predispose individuals to future development of BPPV.

The disease is an inherited autosomal dominant disease, but the physiological cause of the dysfunction is still unclear. An acidophyllic mucopolysaccharide-containing substance was discovered, especially in cochleas, maculas, and crista ampullaris of patients with DFNA9 (a chromosome locus), as well as severe degeneration of vestibular and cochlear sensory axons and dendrites. It is suggested that the mucopolysaccharide deposit could cause strangulation of nerve endings.

The maculas and crista ampullaris are what allow for non-visual sensation of head movements. The crista ampullaris resides in the semicircular canals of the inner ear and detects angular acceleration, while the maculas are housed within the vestibule of the inner ear and detect linear acceleration. When affected, these organs can lead to vertigo and nausea because the body would always feel off-balance.

Benign paroxysmal positional vertigo (BPPV) is a disorder arising from a problem in the inner ear. Symptoms are repeated, brief periods of vertigo with movement, that is, of a spinning sensation upon changes in the position of the head. This can occur with turning in bed or changing position. Each episode of vertigo typically lasts less than one minute. Nausea is commonly associated. BPPV is one of the most common causes of vertigo.

BPPV can result from a head injury or simply occur among those who are older. A specific cause is often not found. The underlying mechanism involves a small calcified otolith moving around loose in the inner ear. It is a type of balance disorder along with labyrinthitis and Ménière's disease. Diagnosis is typically made when the Dix–Hallpike test results in nystagmus (a specific movement pattern of the eyes) and other possible causes have been ruled out. In typical cases medical imaging is not needed.

BPPV is often treated with a number of simple movements such as the Epley maneuver or Brandt–Daroff exercises. Medications may be used to help with nausea. There is tentative evidence that betahistine may help with the vertigo but its use is not generally needed. BPPV is not a serious condition. Typically it resolves in one to two weeks. It however may recur in some people.

The first medical description of the condition occurred in 1921 by Robert Barany. About 2.4% of people are affected at some point in time. Among those who live until their 80s, 10% have been affected. BPPV affects females twice as often as males. Onset is typically in the person's 50s to 70s.

Benign paroxysmal positional vertigo - Migraine is commonly associated with BPPV, the most common vestibular disorder in patients presenting with dizziness. The two may be linked by genetic factors or by vascular damage to the labyrinth.

Ménière's disease - There is an increased prevalence of migraine in patients with Ménière's disease and migraine leads to a greater susceptibility of developing Ménière’s disease. But they can be distinguished. Ménière's disease may go on for days or even years, while migraines typically do not last longer than 24 hours.

Motion sickness is more prevalent in patients with migraine.

Psychiatric syndromes Dizziness and spinning vertigo are the second most common symptom of panic attacks, and they can also present as a symptom of major depression. Migraine is a risk factor for developing major depression and panic disorder and vice versa.

A stroke (either ischemic or hemorrhagic) involving the posterior fossa is a cause of central vertigo. Risk factors for a stroke as a cause of vertigo include increasing age and known vascular risk factors. Presentation may more often involve headache or neck pain, additionally, those who have had multiple episodes of dizziness in the months leading up to presentation are suggestive of stroke with prodromal TIAs. The HINTS exam as well as imaging studies of the brain (CT, CT angiogram, and/or MRI) are helpful in diagnosis of posterior fossa stroke.

Vestibulocochlear dysfunction progressive familial, known also as familial progressive vestibulocochlear dysfunction is an autosomal dominant disease that results in sensorineural hearing loss and vestibular areflexia. Patients report feelings of vague dissiness, blurred vision, dysequilibrium in the dark, and progressive hearing impairment.

Vertigo is recorded as a symptom of decompression sickness in 5.3% of cases by the US Navy as reported by Powell, 2008 It including isobaric decompression sickness.

Decompression sickness can also be caused at a constant ambient pressure when switching between gas mixtures containing different proportions of inert gas. This is known as isobaric counterdiffusion, and presents a problem for very deep dives. For example, after using a very helium-rich trimix at the deepest part of the dive, a diver will switch to mixtures containing progressively less helium and more oxygen and nitrogen during the ascent. Nitrogen diffuses into tissues 2.65 times slower than helium, but is about 4.5 times more soluble. Switching between gas mixtures that have very different fractions of nitrogen and helium can result in "fast" tissues (those tissues that have a good blood supply) actually increasing their total inert gas loading. This is often found to provoke inner ear decompression sickness, as the ear seems particularly sensitive to this effect.

Those at the overall highest risk for lateral medullary syndrome are men at an average age of 55.06. Having a history of hypertension, diabetes and smoking all increase the risk of large artery atherosclerosis. Large artery atherosclerosis is thought to be the greatest risk factor for lateral medullary syndrome due to the deposits of cholesterol, fatty substances, cellular waste products, calcium and fibrin. Otherwise known as plaque build up in the arteries.

Autoimmune inner ear disease (AIED) was first defined by Dr. Brian McCabe in a landmark paper describing an autoimmune loss of hearing. The disease results in progressive sensorineural hearing loss (SNHL) that acts bilaterally and asymmetrically, and sometimes affects an individual's vestibular system. AIED is used to describe any disorder in which the inner ear is damaged as a result of an autoimmune response. Some examples of autoimmune disorders that have presented with AIED are Cogan's syndrome, relapsing polychondritis, systemic lupus erythematosus, granulomatosis with polyangiitis, polyarteritis nodosa, Sjogren's syndrome, and Lyme disease.

Research has come to the consensus that AIED is the result of antibodies or other immune cells that cause damage to structures of the inner ear such as the cochlea and vestibular system. Of note, AIED is the only known SNHL that responds to medical treatment, but withholding treatment for longer than three months may result in permanent hearing loss and the need for cochlear implant installation.

Although AIED has been studied extensively over the past 25 years, no clear mechanism of pathogenesis has emerged. A recent paper performed a literature review of all relevant articles dating back to 1980, and proposed a mechanism of pathogenesis which includes an inflammatory response and immune cell attack on inner ear structures. This response leads to an over-activation of other immune cells such as T helper cells, resulting in vascular changes and cochlear harm. AIED appears to be a consequence of damaged sensorineural hearing due to electrochemical disturbances, microthrombosis, and immune cell deposition. Additionally, self-reactive antibodies and T-cells contribute to the aforementioned damage. Research has suggested a valuable next step in uncovering AIED pathogenesis is inquiry into the role of interleukin-1β (IL-1β).

Bilateral Vestibulopathy results as the culmination of damage done to both inner ears. Bilateral Vestibulopathy causes problems in vision, hearing and motor coordination.

The condition is thought to be under-reported in the medical literature. A study of 27 cases conducted by Timothy C Hain in 1999 noted all but one patient to be female. The average age in this series was 49 years. This apparent gender disparity, however, may be due in part to the fact that the questionnaire which formed the basis of the study was circulated in a publication with a predominantly female reader base.

Subsequent studies have produced conflicting results with regard to the gender distribution of MdDS. The trends in Hain's report have recently been supported by the MdDS Balance Disorder Foundation, in a study of over 100 individuals diagnosed with MdDS. The female:male ratio was approximately 9:1; the average age of onset was 43–45 years. However, another recent study found that 44% of subjects who had experienced MdDS for 2 years or more were male, suggesting a more even distribution.

It has been shown to occur in excursions of as little as 30 minutes though it has been unclear how long it takes for symptoms to occur. The most commonly reported inciting event was a prolonged ocean cruise (~45%); however, shorter boating excursions (~22%), aircraft travel (~15%), and automobile travel (~8%) have all been described.

Mal de Débarquement syndrome has been noted as far back to the times of Erasmus Darwin in 1796, and Irwin J A (1881) "The pathology of seasickness".

Cases of MdDS have been reported in children as young as eight and in both genders. Men may have a more difficult time obtaining a diagnosis due to the disparity of women reported. When sailors and soldiers returned from World War II, the syndrome was reported at a higher rate in males.

AIED is generally caused by either antibodies or immune cells that cause damage to the inner ear. There are several theories that propose a cause of AIED:

- Bystander damage – Physical damage to the inner ear may lead to cytokine release that signals for an immune response. This may be a component of the "attack/remission cycle" of Meniere's disease.

- Cross-reactions – Accidental damage of the inner ear by antibodies or T-cells that recognize an inner ear antigen that is similar to a bacterial or viral antigen

- Genetic factors – Predisposition to developing an autoimmune disorder based on genes inherited

- Intolerance – The immune system may not be aware of all the antigens present in the inner ear until physical damage releases some of these antigens. As a result, the immune system treats these unfamiliar antigens as foreign and mounts an immune response.

Currently, the cross-reactions theory appears to be the favored mechanism of AIED pathogenesis.

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.

Superior canal dehiscence syndrome (SCDS) is a set of hearing and balance symptoms, related to a rare medical condition of the inner ear, known as "superior canal dehiscence". The symptoms are caused by a thinning or complete absence of the part of the temporal bone overlying the superior semicircular canal of the vestibular system. There is evidence that this rare defect, or susceptibility, is congenital. There are also numerous cases of symptoms arising after physical trauma to the head. It was first described in 1998 by Lloyd B. Minor of Johns Hopkins University in Baltimore.

According to current research, in approximately 2.5% of the general population the bones of the head develop to only 60–70% of their normal thickness in the months following birth. This genetic predisposition may explain why the section of temporal bone separating the superior semicircular canal from the cranial cavity, normally 0.8 mm thick, shows a thickness of only 0.5 mm, making it more fragile and susceptible to damage through physical head trauma or from slow erosion. An explanation for this erosion of the bone has not yet been found.

It is estimated that up to 16.5% of elementary school aged children present elevated SOR behaviors in the tactile or auditory modalities. However, this figure might represent an underestimation of Sensory Over Responsivity prevalence, since this study did not include children with developmental disorders or those delivered preterm, who are more likely to present it.

This figure is, nonetheless, larger than what previous studies with smaller samples had shown: an estimate of 5–13% of elementary school aged children.

Incidence for the remaining subtypes is currently unknown.

The cause of benign paroxysmal torticollis in infants is thought to be migrainous. More than 50% of infants have a family history of migraine in first degree relatives. The cause is likely to be genetic.