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.

About 22 million workers are exposed to hazardous noise, with additional millions exposed to solvents and metals that could put them at increased risk for hearing loss. Occupational hearing loss is one of the most common occupational diseases. 49% of male miners have hearing loss by the age of 50. By the age of 60, this number goes up to 70%. Construction workers also suffer an elevated risk. A screening program focused on construction workers employed at US Department of Energy facilities found 58% with significant abnormal hearing loss due to noise exposures at work. Occupational hearing loss is present in up to 33% of workers overall. Occupational exposure to noise causes 16% of adult disabling hearing loss worldwide.

The following is a list of occupations that are most susceptible to hearing loss:

- Agriculture

- Mining

- Construction

- Manufacturing

- Utilities

- Transportation

- Military

- Musicians

- Orchestra conductors

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

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

There can be damage either to the ear itself or to the central auditory pathways that process the information conveyed by the ears. People who sustain head injury are susceptible to hearing loss or tinnitus, either temporary or permanent. Contact sports like football (U.S. NFL), hockey and cricket have a notable incidence of head injuries (concussions). In one survey of retired NFL players, all of whom reported one or more concussions during their playing careers, 25% had hearing loss and 50% had tinnitus.

The facial nerve is the seventh of 12 cranial nerves. This cranial nerve controls the muscles in the face. Facial nerve palsy is more abundant in older adults than in children and is said to affect 15-40 out of 100,000 people per year. This disease comes in many forms which include congenital, infectious, traumatic, neoplastic, or idiopathic. The most common cause of this cranial nerve damage is Bell's palsy (idiopathic facial palsy) which is a paralysis of the facial nerve. Although Bell's palsy is more prominent in adults it seems to be found in those younger than 20 or older than 60 years of age. Bell's Palsy is thought to occur by an infection of the herpes virus which may cause demyelination and has been found in patients with facial nerve palsy. Symptoms include flattening of the forehead, sagging of the eyebrow, and difficulty closing the eye and the mouth on the side of the face that is affected. The inability to close the mouth causes problems in feeding and speech. It also causes lack of taste, acrimation, and sialorrhea.

The use of steroids can help in the treatment of Bell's Palsy. If in the early stages, steroids can increase the likelihood of a full recovery. This treatment is used mainly in adults. The use of steroids in children has not been proven to work because they seem to recover completely with or without them. Children also tend to have better recovery rates than older adults. Recovery rate also depends on the cause of the facial nerve palsy (e.g. infections, perinatal injury, congenital dysplastic). If the palsy is more severe patients should seek steroids or surgical procedures. Facial nerve palsy may be the indication of a severe condition and when diagnosed a full clinical history and examination are recommended.

Although rare, facial nerve palsy has also been found in patients with HIV seroconversion. Symptoms found include headaches (bitemporal or occipital), the inability to close the eyes or mouth, and may cause the reduction of taste. Few cases of bilateral facial nerve palsy have been reported and is said to only effect 1 in every 5 million per year.

Other causes may include:

- Diabetes mellitus

- Facial nerve paralysis, sometimes bilateral, is a common manifestation of sarcoidosis of the nervous system, neurosarcoidosis.

- Bilateral facial nerve paralysis may occur in Guillain–Barré syndrome, an autoimmune condition of the peripheral nervous system.

- Moebius syndrome is a bilateral facial paralysis resulting from the underdevelopment of the VII cranial nerve (facial nerve), which is present at birth. The VI cranial nerve, which controls lateral eye movement, is also affected, so people with Moebius syndrome cannot form facial expression or move their eyes from side to side. Moebius syndrome is extremely rare, and its cause or causes are not known.

Gradually developing NIHL refers to permanent cochlear damage from repeated exposure to loud sounds over a period of time. Unlike acoustic trauma, this form of NIHL does not occur from a single exposure to a high-intensity sound pressure level. Gradually developing NIHL can be caused by multiple exposures to excessive noise in the workplace or any source of repetitive, frequent exposures to sounds of excessive volume, such as home and vehicle stereos, concerts, nightclubs, and personal media players.

Central facial palsy can be caused by a lacunar infarct affecting fibers in the internal capsule going to the nucleus. The facial nucleus itself can be affected by infarcts of the pontine arteries.

Prolonged exposure to loud sound or noise levels can lead to tinnitus. Ear plugs or other measures can help with prevention.

Several medicines have ototoxic effects, and can have a cumulative effect that can increase the damage done by noise. If ototoxic medications must be administered, close attention by the physician to prescription details, such as dose and dosage interval, can reduce the damage done.

Some conditions that are associated with hyperacusis include:

- Acoustic shock

- Adverse drug reaction

- Anxiety

- Autism spectrum

- Lyme disease

- Migraine

- Ménière's disease

- Endolymphatic hydrops

- Multiple Sclerosis

- Noise-induced hearing loss

- Posttraumatic stress disorder

- Severe head trauma

- Superior canal dehiscence syndrome (SCDS)

- Systemic lupus erythematosus (SLE)

- Tay–Sachs disease

- Williams syndrome

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

The most common cause of hyperacusis is overexposure to excessively high decibel (sound pressure) levels.

Some come down with hyperacusis suddenly as a result of taking ear sensitizing drugs, Lyme disease, Ménière's disease, head injury, or surgery. Others are born with sound sensitivity, develop superior canal dehiscence syndrome, have had a history of ear infections, or come from a family that has had hearing problems.

Some psychoactive drugs such as LSD, methaqualone, or phencyclidine ("angel-dust") can cause hyperacusis. An antibiotic, ciprofloxacin has also been seen to be a cause, known as "ciprofloxacin-related hyperacusis".

Degrees of vision loss vary dramatically, although the ICD-9 released in 1979 categorized them into three tiers: normal vision, low vision, and blindness. Two significant causes of vision loss due to sensory failures include media opacity and optic nerve diseases, although hypoxia and retinal disease can also lead to blindness. Most causes of vision loss can cause varying degrees of damage, from total blindness to a negligible effect. Media opacity occurs in the presence of opacities in the eye tissues or fluid, distorting and/or blocking the image prior to contact with the photoreceptor cells. Vision loss often results despite correctly functioning retinal receptors. Optic nerve diseases such as optic neuritis or retrobulbar neuritis lead to dysfunction in the afferent nerve pathway once the signal has been correctly transmitted from retinal photoreceptors.

Partial or total vision loss may affect every single area of a person's life. Though loss of eyesight may occur naturally as we age, trauma to the eye or exposure to hazardous conditions may also cause this serious condition. Workers in virtually any field may be at risk of sustaining eye injuries through trauma or exposure. A traumatic eye injury occurs when the eye itself sustains some form of trauma, whether a penetrating injury such as a laceration or a non-penetrating injury such as an impact. Because the eye is a delicate and complex organ, even a slight injury may have a temporary or permanent effect on eyesight.

The cause of acoustic neuromas is usually unknown; however there is a growing body of evidence that sporadic defects in tumor suppressor genes may give rise to these tumors in some individuals. In particular, loss or mutation of a tumor suppressor gene on the long arm of chromosome 22 is strongly associated with vestibular schwannomas. Other studies have hinted at exposure to loud noise on a consistent basis. One study has shown a relationship between acoustic neuromas and prior exposure to head and neck radiation, and a concomitant history of having had a parathyroid adenoma (tumor found in proximity to the thyroid gland controlling calcium metabolism). There are even controversies on hand held cellular phones. Whether or not the radiofrequency radiation has anything to do with acoustic neuroma formation, remains to be seen. To date, no environmental factor (such as cell phones or diet) has been scientifically proven to cause these tumors. The Acoustic Neuroma Association (ANA) does recommend that frequent cellular phone users use a hands free device to enable separation of the device from the head.

Although there is an inheritable condition called Neurofibromatosis Type 2 (NF2) which can lead to acoustic neuroma formation in some people, most acoustic neuromas occur spontaneously without any evidence of family history (95%). NF2 occurs with a frequency of 1 in 30,000 to 1 in 50,000 births. The hallmark of this disorder is bilateral acoustic neuromas (an acoustic neuroma on both sides) usually developing in late childhood or early adulthood, frequently associated with other brain and spinal chord tumors.

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.

Vestibular schwannoma is a rare condition: incident rate in the U.S. in 2010 was 11/1,000,000 persons, mean age 53. Occurrence was equally distributed versus age, gender and laterality. In patients with unilateral hearing loss, only about 1 in 1000 has acoustic neuroma.

People with diabetes mellitus are at higher risk for any kind of peripheral neuropathy, including ulnar nerve entrapments.

Cubital tunnel syndrome is more common in people who spend long periods of time with their elbows bent, such as when holding a telephone to the head. Flexing the elbow while the arm is pressed against a hard surface, such as leaning against the edge of a table, is a significant risk factor. The use of vibrating tools at work or other causes of repetitive activities increase the risk, including throwing a baseball.

Damage to or deformity of the elbow joint increases the risk of cubital tunnel syndrome. Additionally, people who have other nerve entrapments elsewhere in the arm and shoulder are at higher risk for ulnar nerve entrapment. There is some evidence that soft tissue compression of the nerve pathway in the shoulder by a bra strap over many years can cause symptoms of ulnar neuropathy, especially in very large-breasted women.

Many types of sense loss occur due to a dysfunctional sensation process, whether it be ineffective receptors, nerve damage, or cerebral impairment. Unlike agnosia, these impairments are due to damages prior to the perception process.

Sciatic nerve injury occurs between 0.5% and 2.0% of the time during total hip arthroplasty. Sciatic nerve palsy is a complication of total hip arthroplasty with an incidence of 0.2% to 2.8% of the time, or with an incidence of 1.7% to 7.6% following revision. Following the procedure, in rare cases, a screw, broken piece of trochanteric wire, fragment of methyl methacrylate bone cement, or Burch-Schneider metal cage can impinge on the nerve; this can cause sciatic nerve palsy which may resolve after the fragment is removed and the nerve freed. The nerve can be surrounded in oxidized regenerated cellulose to prevent further scarring. Sciatic nerve palsy can also result from severe spinal stenosis following the procedure, which can be addressed by spinal decompression surgery. It is unclear if inversion therapy is able to decompress the sacral vertebrae, it may only work on the lumbar aspects of the sciatic nerves.

Sciatic nerve injury may also occur from improperly performed injections into the buttock, and may result in sensory loss.

Cranial nerve disease is an impaired functioning of one of the twelve cranial nerves. Although it could theoretically be considered a mononeuropathy, it is not considered as such under MeSH.

It is possible for a disorder of more than one cranial nerve to occur at the same time, if a trauma occurs at a location where many cranial nerves run together, such as the jugular fossa. A brainstem lesion could also cause impaired functioning of multiple cranial nerves, but this condition would likely also be accompanied by distal motor impairment.

A neurological examination can test the functioning of individual cranial nerves, and detect specific impairments.

Cervical radiculopathy is less prevalent in the United States than lumbar radiculopathy with an occurrence rate of 83 cases per 100,000. According to the AHRQ’s 2010 National Statistics for cervical radiculopathy the most affected age group is between 45 and 64 years with 51.03% of incidents. Females are affected more frequently than males and account for 53.69% of cases. Private insurance was the payer in 41.69% of the incidents followed by Medicare with 38.81%. In 71.61% of cases the patients’ income was considered not low for their zipcode. Additionally over 50% of patients lived in large metropolitans (inner city or suburb). The South is the most severely affected region in the US with 39.27% of cases. According to a study performed in Minnesota, the most common manifestation of this set of conditions is the C7 monoradiculopathy, followed by C6.

Perioperative PION patients have a higher prevalence of cardiovascular risk factors than in the general population. Documented cardiovascular risks in people affected by perioperative PION include high blood pressure, diabetes mellitus, high levels of cholesterol in the blood, tobacco use, abnormal heart rhythms, stroke, and obesity. Men are also noted to be at higher risk, which is in accordance with the trend, as men are at higher risk of cardiovascular disease. These cardiovascular risks all interfere with adequate blood flow, and also may suggest a contributory role of defective vascular autoregulation.

Bernese periacetabular osteotomy resulted in major nerve deficits in the sciatic or femoral nerves in 2.1% of 1760 patients, of whom approximately half experienced complete recovery within a mean of 5.5 months.

Sciatic nerve exploration can be done by endoscopy in a minimally invasive procedure to assess lesions of the nerve. Endoscopic treatment for sciatic nerve entrapment has been investigated in deep gluteal syndrome; "Patients were treated with sciatic nerve decompression by resection of fibrovascular scar bands, piriformis tendon release, obturator internus, or quadratus femoris or by hamstring tendon scarring."

The disease can be considered to be hereditary, but its penetrance and the degree of expression is so highly variable that it may be difficult to detect an inheritance pattern. Most of the implicated genes are transmitted in an autosomal dominant fashion. One genome-wide analysis associates otosclerosis with variation in RELN gene.

Loci include: