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

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.

Otitis is a general term for inflammation or infection of the ear, in both humans and other animals.

It is subdivided into the following:

- "Otitis externa", external otitis, or "swimmer's ear" involves the outer ear and ear canal. In external otitis, the ear hurts when touched or pulled.

- "Otitis media" or middle ear infection involves the middle ear. In otitis media, the ear is infected or clogged with fluid behind the ear drum, in the normally air-filled middle-ear space. This very common childhood infection sometimes requires a surgical procedure called "myringotomy" and tube insertion.

- "Otitis interna" or labyrinthitis involves the inner ear. The inner ear includes sensory organs for balance and hearing. When the inner ear is inflamed, "vertigo" is a common symptom.

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.

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.

In the United States and other developed countries, the incidence of mastoiditis is quite low, around 0.004%, although it is higher in developing countries. The condition most commonly affects children aged from two to thirteen months, when ear infections most commonly occur. Males and females are equally affected.

With prompt treatment, it is possible to cure mastoiditis. Seeking medical care early is important. However, it is difficult for antibiotics to penetrate to the interior of the mastoid process and so it may not be easy to cure the infection; it also may recur. Mastoiditis has many possible complications, all connected to the infection spreading to surrounding structures. Hearing loss is likely, or inflammation of the labyrinth of the inner ear (labyrinthitis) may occur, producing vertigo and an ear ringing may develop along with the hearing loss, making it more difficult to communicate. The infection may also spread to the facial nerve (cranial nerve VII), causing facial-nerve palsy, producing weakness or paralysis of some muscles of facial expression, on the same side of the face. Other complications include Bezold's abscess, an abscess (a collection of pus surrounded by inflamed tissue) behind the sternocleidomastoid muscle in the neck, or a subperiosteal abscess, between the periosteum and mastoid bone (resulting in the typical appearance of a protruding ear). Serious complications result if the infection spreads to the brain. These include meningitis (inflammation of the protective membranes surrounding the brain), epidural abscess (abscess between the skull and outer membrane of the brain), dural venous thrombophlebitis (inflammation of the venous structures of the brain), or brain abscess.

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.

Medical treatment with anti-vertigo medications may be considered in acute, severe exacerbation of BPPV, but in most cases are not indicated. These primarily include drugs of the anti-histamine and anti-cholinergic class, such as meclizine and hyoscine butylbromide (scopolamine) respectively. The medical management of vestibular syndromes has become increasingly popular over the last decade, and numerous novel drug therapies (including existing drugs with new indications) have emerged for the treatment of vertigo/dizziness syndromes. These drugs vary considerably in their mechanisms of action, with many of them being receptor- or ion channel-specific. Among them are betahistine or dexamethasone/gentamicin for the treatment of Ménière's disease, carbamazepine/oxcarbazepine for the treatment of paroxysmal dysarthria and ataxia in multiple sclerosis, metoprolol/topiramate or valproic acid/tricyclic antidepressant for the treatment of vestibular migraine, and 4-aminopyridine for the treatment of episodic ataxia type 2 and both downbeat and upbeat nystagmus. These drug therapies offer symptomatic treatment, and do not affect the disease process or resolution rate. Medications may be used to suppress symptoms during the positioning maneuvers if the patient's symptoms are severe and intolerable. More dose-specific studies are required, however, in order to determine the most effective drug(s) for both acute symptom relief and long-term remission of the condition.

Post-viral cerebellar ataxia is caused by damage to or problems with the cerebellum. It is most common in children, especially those younger than age 3, and usually occurs several weeks following a viral infection. Viral infections that may cause it include the following: chickenpox, Coxsackie disease (viral infection also called hand-foot-and-mouth disease), Creutzfeldt–Jakob disease (a rare disease believed to be an infection that causes mental deterioration), Lyme disease (inflammatory bacterial disease spread by ticks), mycoplasma pneumonia (type of bacterial pneumonia), Epstein–Barr virus (a common human virus that belongs to the herpes family) and HIV.

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

People whose condition was caused by a recent viral infection should make a full recovery without treatment in a few months. Fine motor skills, such as handwriting, typically have to be practised in order to restore them to their former ability. In more serious cases, strokes, bleeding or infections may sometimes cause permanent symptoms.

Many conditions cause dizziness because multiple parts of the body are required for maintaining balance including the inner ear, eyes, muscles, skeleton, and the nervous system.

Common physiological causes of dizziness include:

- inadequate blood supply to the brain due to:

- a sudden fall in blood pressure

- heart problems or artery blockages

- loss or distortion of vision or visual cues

- disorders of the inner ear

- distortion of brain/nervous function by medications such as anticonvulsants and sedatives

- result of side effect from prescription drugs, including proton-pump inhibitor drugs (PPIs) and Coumadin (warfarin) causing dizziness/fainting

Toxic optic neuropathy refers to the ingestion of a toxin or an adverse drug reaction that results in vision loss from optic nerve damage. Patients may report either a sudden loss of vision in both eyes, in the setting of an acute intoxication, or an insidious asymmetric loss of vision from an adverse drug reaction. The most important aspect of treatment is recognition and drug withdrawal.

Among the many causes of TON, the top 10 toxins include:

- Medications

- Ethambutol, rifampin, isoniazid, streptomycin (tuberculosis treatment)

- Linezolid (taken for bacterial infections, including pneumonia)

- Chloramphenicol (taken for serious infections not helped by other antibiotics)

- Isoretinoin (taken for severe acne that fails to respond to other treatments)

- Ciclosporin (widely used immunosuppressant)

- Acute Toxins

- Methanol (component of some moonshine, and some cleaning products)

- Ethylene glycol (present in anti-freeze and hydraulic brake fluid)

Metabolic disorders may also cause this version of disease. Systemic problems such as diabetes mellitus, kidney failure, and thyroid disease can cause optic neuropathy, which is likely through buildup of toxic substances within the body. In most cases, the cause of the toxic neuropathy impairs the tissue’s vascular supply or metabolism. It remains unknown as to why certain agents are toxic to the optic nerve while others are not and why particularly the papillomacular bundle gets affected.

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.

Known causes include physical trauma, acoustic neuroma, measles, labyrinthitis, microtia, meningitis, Ménière's disease, Waardenburg syndrome, mumps (epidemic parotitis), and mastoiditis.

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.

A 1998 study of schoolchildren found that per thousand, 6-12 had some form of unilateral hearing loss and 0-5 had moderate to profound unilateral hearing loss. It was estimated that in 1998 some 391,000 school-aged children in the United States had unilateral hearing loss.

TAA is an old term for a constellation of elements that can lead to a mitochondrial optic neuropathy. The classic patient is a man with a history of heavy alcohol and tobacco consumption. Respectively, this combines nutritional mitochondrial impairment, from vitamin deficiencies (folate and B-12) classically seen in alcoholics, with tobacco-derived products, such as cyanide and ROS. It has been suggested that the additive effect of the cyanide toxicity, ROS, and deficiencies of thiamine, riboflavin, pyridoxine, and b12 result in TAA.

The second most common cause of SJS and TEN is infection, particularly in children. This includes upper respiratory infections, otitis media, pharyngitis, and Epstein-Barr virus, Mycoplasma pneumoniae and cytomegalovirus infections. The routine use of medicines such as antibiotics, antipyretics and analgesics to manage infections can make it difficult to identify if cases were caused by the infection or medicines taken.

Viral diseases reported to cause SJS include: herpes simplex virus (debated), AIDS, coxsackievirus, influenza, hepatitis, and mumps.

In pediatric cases, Epstein-Barr virus and enteroviruses have been associated with SJS.

Recent upper respiratory tract infections have been reported by more than half of patients with SJS.

Bacterial infections linked to SJS include group A beta-hemolytic streptococci, diphtheria, brucellosis, lymphogranuloma venereum, mycobacteria, "Mycoplasma pneumoniae", rickettsial infections, tularemia, and typhoid.

Fungal infections with coccidioidomycosis, dermatophytosis, and histoplasmosis are also considered possible causes. Malaria and trichomoniasis, protozoal infections, have also been reported as causes.

Although SJS can be caused by viral infections and malignancies, the main cause is medications. A leading cause appears to be the use of antibiotics, particularly sulfa drugs. Between 100 and 200 different drugs may be associated with SJS. No reliable test exists to establish a link between a particular drug and SJS for an individual case. Determining what drug is the cause is based on the time interval between first use of the drug and the beginning of the skin reaction. Drugs discontinued more than 1 month prior to onset of mucocutaneous physical findings are highly unlikely to cause SJS and TEN. SJS and TEN most often begin between 4 and 28 days after culprit drug administration. A published algorithm (ALDEN) to assess drug causality gives structured assistance in identifying the responsible medication.

SJS may be caused by adverse effects of the drugs vancomycin, allopurinol, valproate, levofloxacin, diclofenac, etravirine, isotretinoin, fluconazole, valdecoxib, sitagliptin, oseltamivir, penicillins, barbiturates, sulfonamides, phenytoin, azithromycin, oxcarbazepine, zonisamide, modafinil, lamotrigine, nevirapine, pyrimethamine, ibuprofen, ethosuximide, carbamazepine, bupropion, telaprevir, and nystatin.

Medications that have traditionally been known to lead to SJS, erythema multiforme, and toxic epidermal necrolysis include sulfonamide antibiotics, penicillin antibiotics, cefixime (antibiotic), barbiturates (sedatives), lamotrigine, phenytoin (e.g., Dilantin) (anticonvulsants) and trimethoprim. Combining lamotrigine with sodium valproate increases the risk of SJS.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are a rare cause of SJS in adults; the risk is higher for older patients, women, and those initiating treatment. Typically, the symptoms of drug-induced SJS arise within a week of starting the medication. Similar to NSAIDs, paracetamol (acetaminophen) has also caused rare cases of SJS. People with systemic lupus erythematosus or HIV infections are more susceptible to drug-induced SJS.

There are several causes of toxic optic neuropathy. Among these are: ingestion of methanol (wood alcohol), ethylene glycol (automotive antifreeze), disulfiram (used to treat chronic alcoholism), halogenated hydroquinolones (amebicidal medications), ethambutol and isoniazid (tuberculosis treatment), and antibiotics such as linezolid and chloramphenicol. Tobacco is also a major cause of toxic optic neuropathy.

The predominant cause of nutritional optic neuropathy is thought to be deficiency of B-complex vitamins, particularly thiamine (vitamin B), cyanocobalamin (vitamin B) and recently copper Deficiency of pyridoxine (vitamin B), niacin (vitamin B), riboflavin (vitamin B), and/or folic acid also seems to play a role. Those individuals who abuse alcohol and tobacco are at greater risk because they tend to be malnourished. Those with pernicious anemia are also at risk due to an impaired ability to absorb vitamin B from the intestinal tract.

The illness is generally self-limiting. Management on the whole is preventative, by limiting exposure to mouldy environments with ventilation, or by wearing respiratory protection such as facemasks.

Some cases may be viral in origin, perhaps preceded by an upper respiratory tract infection. Viral causes include Coxsackie virus, mumps and adenoviruses. Some cases develop postpartum .