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.

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.

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.

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.

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.

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.

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.

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.

The mechanism of action of benign paroxysmal torticollis is not yet understood. It has been suggested that unilateral vestibular dysfunction or vascular disturbance in the brain stem may be responsible for the condition.

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.

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

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).

The pathophysiology of MAV is not completely understood; both central and peripheral defects have been observed.

In most cases, the cause of acoustic neuromas is unknown. The only statistically significant risk factor for developing an acoustic neuroma is having a rare genetic condition called neurofibromatosis type 2 (NF2). There are no confirmed environmental risk factors for acoustic neuroma. There are conflicting studies on the association between acoustic neuromas and cellular phone use and repeated exposure to loud noise. In 2011, an arm of the World Health Organization released a statement listing cell phone use as a low grade cancer risk. The Acoustic Neuroma Association recommends that cell phone users use a hands-free device.

Meningiomas are significantly more common in women than in men; they are most common in middle-aged women. Two predisposing factors associated with meningiomas for which at least some evidence exists are exposure to ionizing radiation (cancer treatment of brain tumors) and hormone replacement therapy.

Although CPH is often compared to cluster headaches, it is much less prevalent, occurring in only 1–3% of those who experience cluster headaches. CPH occurs roughly in 1 in 50,000 people, while cluster headaches are comparatively more common and are found in 1 in 1000 people.

Cluster headaches occur primarily in men, while CPH is more commonly diagnosed in women. The female to male ratio of diagnosed patients can range anywhere from 1.6:1 to 2.36:1. Symptoms may begin to appear at any age, but onset usually occurs in adulthood with a mean starting age within the thirties.

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.

Positional alcohol nystagmus (PAN) is nystagmus (visible jerkiness in eye movement) produced when the head is placed in a sideways position. PAN occurs when the specific gravity of the membrane space of the semicircular canals in the ear differs from the specific gravity of the fluid in the canals because of the presence of alcohol.

Parinaud's Syndrome results from injury, either direct or compressive, to the dorsal midbrain. Specifically, compression or ischemic damage of the mesencephalic tectum, including the superior colliculus adjacent oculomotor (origin of cranial nerve III) and Edinger-Westphal nuclei, causing dysfunction to the motor function of the eye.

Classically, it has been associated with three major groups:

1. Young patients with brain tumors in the pineal gland or midbrain: pinealoma (intracranial germinomas) are the most common lesion producing this syndrome.

2. Women in their 20s-30s with multiple sclerosis

3. Older patients following stroke of the upper brainstem

However, any other compression, ischemia or damage to this region can produce these phenomena: obstructive hydrocephalus, midbrain hemorrhage, cerebral arteriovenous malformation, trauma and brainstem toxoplasmosis infection. Neoplasms and giant aneurysms of the posterior fossa have also been associated with the midbrain syndrome.

Vertical supranuclear ophthalmoplegia has also been associated with metabolic disorders, such as Niemann-Pick disease, Wilson's disease, kernicterus, and barbiturate overdose.

The overall complication rate following surgery is around 20%; cerebrospinal fluid leak is the most common.

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.

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.

Hypnic headaches are benign primary headaches that affect the elderly, with the average age of onset being 63 ± 11 years. They are moderate, throbbing, bilateral or unilateral headaches that wake the sufferer from sleep once or multiple times a night. They typically begin a few hours after sleep begins and can last from 15–180 min. There is normally no nausea, photophobia, phonophobia or autonomic symptoms associated with the headache. They commonly occur at the same time every night possibly linking the headaches with circadian rhythm, but polysomnography has recently revealed that the onset of hypnic headaches may be associated with REM sleep.

Lithium carbonate 200–600 mg at bedtime is an effective treatment for most patients but for those that can not tolerate Lithium, Verapamil, indomethacin or methylsergilide may be tried. Two patients have also responded to flunarizine 5 mg. It has also been shown that 1–2 cups of coffee or 100–200 mg of caffeine before bed can prevent hypnic headaches.

For diagnosis of hypnic headache syndrome, headaches should occur at least 15 times per month for at least one month. Included in the differential diagnosis of a new onset nighttime headaches in the elderly is drug withdrawal, temporal arteritis, Sleep apnea, oxygen desaturated, Pheochromocytoma, intracranial causes, primary and secondary neoplasms, communicating hydrocephalus, subdural hematoma, vascular lesions, migraines, cluster headaches, chronic paroxysmal hemicrania and hypnic headache. All other causes must be ruled out before the diagnosis of hypnic headache can be made.

When a person consumes alcohol, the alcohol is carried by the bloodstream and diffused into the water compartments of the body. Normally, the specific gravity of a canal membrane is the same as the specific gravity of the surrounding fluid. Because of this, even though the Earth's gravity is a constant force of acceleration, the semicircular canals do not respond to it. Alcohol has a lighter specific gravity than water. When alcohol enters the canal membrane via capillaries, the specific gravity of the membrane is lower than that of the surrounding fluid. The alcohol does diffuse from the membrane to the fluid, but it does so very slowly. While the specific gravity of the membrane is lower than the specific gravity of the extracellular fluid, the hair cells on the membrane become responsive to the Earth's gravity. This is the condition of PAN I.

PAN I is characterized by a nystagmus to the right when the right side of the head is down. It is typically present during a rising and peak Blood Alcohol Concentration (BAC).

Acute cerebellar ataxia is the most common cause of unsteady gait in children. The condition is rare in children older than ten years of age. Most commonly acute cerebellar ataxia affects children between age 2 and 7 years.

Paroxysmal tonic upgaze (PTU) of childhood is a rare and distinctive neuro-ophthalmological syndrome characterized by episodes of sustained upward deviation of the eyes. Symptoms normally appear in babies under one year of age and are characterized by an upward stare or gaze, with the eyes rolled back, while the chin is typically held low.

Babies suffering from PTU may exhibit normal or slightly jerky side-to-side eye movement, nausea, irritability, frequent sleep, developmental and language delays, vertigo and loss of muscle tone.

The condition is generally regarded as having a benign outcome, in the sense that it improves, rather than worsens over time. The average age of recovery is at about 2.5 years.

PTU was first described in 1988. As of 2002, approximately fifty cases had been diagnosed. Because the condition is so rare, the majority of physicians have never seen it, and thus may not recognize it. Videotaping a child both in and out of the upgaze state can be vital for reaching a diagnosis.