The majority of patients present in their mid-30s to late 40s. This is likely due to a combination of the slow growth of the bone and the decreased participation in activities associated with surfer's ear past the 30's. However surfer's ear is possible at any age and is directly proportional to the amount of time spent in cold, wet, windy weather without adequate protection.

The normal ear canal is approximately 7mm in diameter and has a volume of approximately 0.8 ml (approximately one-sixth of a teaspoon). As the condition progresses the diameter narrows and can even close completely if untreated, although sufferers generally seek help once the passage has constricted to 0.5-2mm due to the noticeable hearing impairment. While not necessarily harmful in and of itself, constriction of the ear canal from these growths can trap debris, leading to painful and difficult to treat infections.

These can be both congenital or develop over time with the thinning of the otic capsule by the persistent pulsations of the intracranial pressures against the bones of the skull. Finally, disease conditions—for example cholesteatoma—can result in a labyrinthine fistula. Traumatic events, with excessive pressure changes to the inner ear such as in scuba diving, head trauma, or an extremely loud noise can lead to rupture and leakage.

PLF is a cause of dizziness, imbalance, and hearing loss—any or all of these symptoms can exist. Vertigo (an illusion of motion) is not common in this disorder. The most common cause of this fistula is head or ear trauma. Rapid increases of intracranial pressure can also result in a PLF. Rarely, these fistulas can be congenital, leading to progressive hearing loss and vertigo in childhood. It has also been a complication of a stapedectomy.

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.

Myringosclerosis seems to be more common than tympanosclerosis. Most research has not been conducted upon the general, healthy population, but rather those with otitis media or patients who have had tympanostomy tubes in prior procedures. Of the children studied who had 'glue ear', and who were treated with tympanostomy tubing, 23-40% of cases had tympanosclerosis. One study suggested that people with atherosclerosis were more likely to have tympanosclerosis than otherwise healthy individuals.

The widespread use of wetsuits has allowed people to surf in much colder waters, which has increased the incidence and severity of surfer's ear for people who do not properly protect their ears.

- Avoid activity during extremely cold or windy conditions.

- Keep the ear canal as warm and dry as possible.

- Ear plugs

- Wetsuit hood

- Swim cap

- Diving helmet

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.

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.

In most cases, tympanosclerosis does not cause any recognisable hearing loss up to ten years after the initial disease onset. Sclerotic changes seem to stabilise, but not resolve or dissolve, after 3 years.

More commonly, keratin accumulates in a pouch of tympanic membrane which extends into the middle ear space. This abnormal folding or 'retraction' of the tympanic membrane arises in one of the following ways:

- "Wittmaack's theory" : Invagination of tympanic membrane from the attic or part of pars tensa in the form of retraction pockets lead to the formation of cholesteatoma.

- "Ruedi's theory" : The basal cells of germinal layer of skin proliferate under the influence of infection and lay down keratinising squamous epithelium.

- "Habermann's theory": The epithelium from the meatus or outer drum surface grows into the middle ear through a pre-existing perforation and form cholesteatoma.

Cholesteatoma may also arise as a result of metaplasia of the middle ear mucosa or implantation following trauma.

In one study, the number of new cases of cholesteatoma in Iowa was estimated in 1975–6 to be just under one new case per 10,000 citizens per year. Cholesteatoma affects all age groups, from infants through to the elderly. The peak incidence occurs in the second decade.

The aging process has three distinct components: physiologic degeneration, extrinsic damage (nosocusis), and intrinsic damage (sociocusis). These factors are superimposed on a genetic substrate, and may be overshadowed by general age-related susceptibility to diseases and disorders.

Hearing loss is only weakly correlated with age. In preindustrial and non-industrial societies, persons retain their hearing into old age. In the Framingham cohort study, only 10% of the variability of hearing with age could be explained by age-related physiologic deterioration. Within family groups, heredity factors were dominant; across family groups, other, presumably sociocusis and nosocusis factors were dominant.

- Heredity: factors like early aging of the cochlea and susceptibility of the cochlea for drug insults are genetically determined.

- Oxidative stress

- General inflammatory conditions

Nosocusis factors are those that can cause hearing loss, which are not noise-based and separate from pure presbycusis. They may include:

- Ototoxic drugs: Ingestion of ototoxic drugs like aspirin may hasten the process of presbycusis.

- vascular degeneration

- Atherosclerosis: May diminish vascularity of the cochlea, thereby reducing its oxygen supply.

- Dietary habits: Increased intake of saturated fat may accelerate atherosclerotic changes in old age.

- Smoking: Is postulated to accentuate atherosclerotic changes in blood vessels aggravating presbycusis.

- Diabetes: May cause vasculitis and endothelial proliferation in the blood vessels of the cochlea, thereby reducing its blood supply.

- Hypertension: causes potent vascular changes, like reduction in blood supply to the cochlea, thereby aggravating presbycusis.

However, a recent study found that diabetes, atherosclerosis and hypertension had no correlation to presbycusis, suggesting that these are nosocusis (acquired hearing loss) factors, not intrinsic factors.

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

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.

Aural atresia is the underdevelopment of the middle ear and canal and usually occurs in conjunction with microtia. Atresia occurs because patients with microtia may not have an external opening to the ear canal, though. However, the cochlea and other inner ear structures are usually present. The grade of microtia usually correlates to the degree of development of the middle ear.

Microtia is usually isolated, but may occur in conjunction with hemifacial microsomia, Goldenhar Syndrome or Treacher-Collins Syndrome. It is also occasionally associated with kidney abnormalities (rarely life-threatening), and jaw problems, and more rarely, heart defects and vertebral deformities.

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.

Otosclerosis or otospongiosis is an abnormal growth of bone near the middle ear. It can result in hearing loss. The term otosclerosis is something of a misnomer. Much of the clinical course is characterised by lucent rather than sclerotic bony changes, hence it is also known as otospongiosis.

Some over-the-counter as well as prescription drugs and certain industrial chemicals are ototoxic. Exposure to

these can result in temporary or permanent hearing loss.

Some medications cause irreversible damage to the ear, and are limited in their use for this reason. The most important group is the aminoglycosides (main member gentamicin). A rare mitochondrial mutation, m.1555A>G, can increase an individual's susceptibility to the ototoxic effect of aminoglycosides. Long term hydrocodone (Vicodin) abuse is known to cause rapidly progressing sensorineural hearing loss, usually without vestibular symptoms. Methotrexate, a chemotherapy agent, is also known to cause hearing loss. In most cases hearing loss does not recover when the drug is stopped. Paradoxically, methotrexate is also used in the treatment of autoimmune-induced inflammatory hearing loss.

Various other medications may reversibly degrade hearing. This includes loop diuretics, sildenafil (Viagra), high or sustained dosing of NSAIDs (aspirin, ibuprofen, naproxen, and various prescription drugs: celecoxib, etc.), quinine, and macrolide antibiotics (erythromycin, etc.).

Prolonged or repeated environmental or work-related exposure to ototoxic chemicals can also result in sensorineural hearing loss. Some of these chemicals are:

- butyl nitrite - chemical used recreationally known as 'poppers'

- carbon disulfide - a solvent used as a building block in many organic reactions

- styrene, an industrial chemical precursor of polystyrene, a plastic

- carbon monoxide, a poisonous gas resulting from incomplete combustion

- heavy metals: tin, lead, manganese, mercury

- hexane, an industrial solvent and one of the significant constituents of gasoline

- ethylbenzene, an industrial solvent used in the production of styrene

- toluene and xylene, highly poisonous petrochemical solvents. Toluene is a component of high-octane gasolne; xylene is used in the production of polyester fibers and resins.

- trichloroethylene, an industrial degreasing solvent

- Organophosphate pesticides

There is no treatment to correct an enlarged vestibular aqueduct. Any hearing loss will need management with amplification and support in education and at work. If the hearing loss becomes severe to profound cochlear implants can be of significant value. Vestibular disturbance is usually short-lived and associated with head trauma but significant vestibular hypofunction may require rehabilitation.

People with enlarged vestibular aqueducts are advised to avoid head trauma where possible. This usually means avoiding contact sports such as boxing and rugby, but also horse riding, trampolining and other sports where head injury may occur. Some have symptoms when flying and should limit these activities if affected.

It may be that a genetic tendency to develop otosclerosis is inherited by some people. Then a trigger, such as a viral infection (like measles), actually causes the condition to develop.

These are much more common in premature babies, particularly those under 1500 g at birth. Premature birth can be associated with problems that result in sensorineural hearing loss such as anoxia or hypoxia(poor oxygen levels), jaundice, intracranial haemorrhages, meningitis. Fetal alcohol syndrome is reported to cause hearing loss in up to 64% of infants born to alcoholic mothers, from the ototoxic effect on the developing fetus, plus malnutrition during pregnancy from the excess alcohol intake.

Anotia ("no ear") describes a rare congenital deformity that involves the complete absence of the pinna, the outer projected portion of the ear, and narrowing or absence of the ear canal. This contrasts with microtia, in which a small part of the pinna is present. Anotia and microtia may occur unilaterally (only one ear affected) or bilaterally (both ears affected). This deformity results in conductive hearing loss, deafness.

While there is no cure, most people with tinnitus get used to it over time; for a minority, it remains a significant problem.

Microtia is a congenital deformity where the pinna (external ear) is underdeveloped. A completely undeveloped pinna is referred to as anotia. Because microtia and anotia have the same origin, it can be referred to as microtia-anotia. Microtia can be unilateral (one side only) or bilateral (affecting both sides). Microtia occurs in 1 out of about 8,000–10,000 births. In unilateral microtia, the right ear is most commonly affected. It may occur as a complication of taking Accutane (isotretinoin) during pregnancy.