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.

The severe pain of HNA can be controlled with an anti-inflammatory drug such as prednisone, although it is unknown whether these anti-inflammatory drugs actually slow or stop the nerve degeneration process.

Nerve regeneration after an episode is normal, and in less severe cases a full recovery of the nerves and muscles can be expected. However, in a severe case permanent nerve damage may occur.

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.

The site and type of brachial plexus injury determine the prognosis. Avulsion and rupture injuries require timely surgical intervention for any chance of recovery. For milder injuries involving buildup of scar tissue and for neurapraxia, the potential for improvement varies, but there is a fair prognosis for spontaneous recovery, with a 90–100% return of function.

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.

A nerve may be compressed by prolonged or repeated external force, such as sitting with one's arm over the back of a chair (radial nerve), frequently resting one's elbows on a table (ulnar nerve), or an ill-fitting cast or brace on the leg (peroneal nerve). Part of the patient's body can cause the compression and the term "entrapment neuropathy" is used particularly in this situation. The offending structure may be a well-defined lesion such as a tumour (for example a lipoma, neurofibroma or metastasis), a ganglion cyst or a haematoma. Alternatively, there may be expansion of the tissues around a nerve in a space where there is little room for this to occur, as is often the case in carpal tunnel syndrome. This may be due to weight gain or peripheral oedema (especially in pregnancy), or to a specific condition such as acromegaly, hypothyroidism or scleroderma and psoriasis.

Some conditions cause nerves to be particularly susceptible to compression. These include diabetes, in which the blood supply to the nerves is already compromised, rendering the nerve more sensitive to minor degrees of compression. The genetic condition HNPP is a much rarer cause.

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.

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.

Fourth cranial nerve palsy also known as Trochlear nerve palsy, is a condition affecting Cranial Nerve 4 (IV), the Trochlear Nerve, which is one of the Cranial Cranial Nerves that causes weakness or paralysis to the Superior Oblique Muscle that it innervates. This condition often causes vertical or near vertical double vision as the weakened muscle prevents the eyes from moving in the same direction together.

Because the fourth cranial nerve is the thinnest and has the longest intracranial course of the cranial nerves, it is particularly vulnerable to traumatic injury.

To compensate for the double-vision resulting from the weakness of the superior oblique, patients characteristically tilt their head down and to the side opposite the affected muscle.

When present at birth, it is known as congenital fourth nerve palsy.

Anatomically, damage to the axillary nerve or suppression of it causes the palsy. This suppression, referred to as entrapment, causes the nerve pathway to become smaller and impulses cannot move through the nerve as easily. Furthermore, if trauma causes damage to the myelin sheath, or injures the nerve another way, this will also reduce the ability of nerve impulse flow.

Usually, an outside force is acting to suppress the nerve, or cause nerve damage. Most commonly, shoulder dislocation or fractions in the shoulder can cause the palsy. Contact sports such as football and hockey can cause the injury Other cases have been caused by repeated crutch pressure or injuries accidentally caused by health professionals (iatrogenesis). Furthermore, following an anterior shoulder operation; damage to the axillary nerve is possible and has been documented by various surgeons, thus causing axillary nerve palsy. Other possible causes include: deep infection, pressure from a cast or splint, fracture of the humerus, or nerve disorders in which the nerves become inflamed.

There are rare causes of axillary nerve palsy that do occur. For instance, axillary nerve palsy can occur after there is blunt trauma in the shoulder area without any sort of dislocation or fracture. Examples of this blunt trauma may include: being hit by heavy an object, falling on shoulder, a strong blow while participating in boxing, or motor vehicle accidents. Another rare cause of axillary nerve palsy can occur after utilizing a side birthing position. When the patient lies on their side for a strenuous amount of time, they can develop axillary nerve palsy. This rare complication of labor can occur due to the prolonged pressure on the axillary nerve while in a side-birth position. Some patients who are diagnosed with nodular fasciitis may develop axillary nerve palsy if the location of the rapid growth is near the axilla. In the case of Nodular Fasciitis, a fibrous band or the growth of a schwannoma can both press against the nerve, causing axillary nerve palsy.

An injury to the axillary nerve normally occurs from a direct impact of some sort to the outer arm, though it can result from injuring a shoulder via dislocation or compression of the nerve. The axillary nerve comes from the posterior cord of the brachial plexus at the coracoid process and provides the motor function to the deltoid and teres minor muscles. An EMG can be useful in determining if there is an injury to the axillary nerve. The largest numbers of axillary nerve palsies arise due to stretch injuries which are caused by blunt trauma or iatrogenesis. Axillary nerve palsy is characterized by the lack of shoulder abduction greater than 30 degrees with or without the loss of sense in the low two thirds of the shoulder. Normally the patients that have axillary nerve palsy are involved in blunt trauma and have a number of shoulder injuries. Surgery is not always required to solve the problem (information from: Midha, Rajiv, Zager, Eric. Surgery of Peripheral Nerves: A Case-Based Approach. Thieme Medical Publishers, Inc. 2008.)

People who suffer from neurotmesis often face a poor prognosis. They will more than likely never regain full functionality of the affected nerve, but surgical techniques do give people a better chance at regaining some function. Current research is focused on new ways to regenerate nerves and advance surgical techniques.

The incidence of hemifacial spasm is approximately 0.8 per 100,000 persons. Hemifacial spasm is more prevalent among females over 40 years of age. The estimated prevalence for women is 14.5 per 100,000 and 7.4 per 100,000 in men. Prevalence for hemifacial spasm increase with age, reaching 39.7 per 100,000 for those aged 70 years and older. One study divided 214 hemifacial patients based on the cause of the disease. The patients who had a compression in the facial nerve at the end of the brain stem as the primary hemifacial spasm and patients who had peripheral facial palsy or nerve lesion due to tumors, demyelination, trauma, or infection as secondary hemifacial spasm. The study found that 77% of hemifacial spasm is due to primary hemifacial spasm and 23% is due to secondary hemifacial spasm. The study also found both sets of patients to share similar age at onset, male to female ratios, and similar affected side. Another study with 2050 patients presented with hemifacial spasm between 1986 and 2009, only 9 cases were caused by a cerebellopontine angle syndrome, an incidence of 0.44%.

In terms of prognosis radial neuropathy is not necessarily permanent, though sometimes there could be partial loss of movement/sensation.Complications may be possible deformity of the hand in some individuals.

If the injury is axonal (the underlying nerve fiber itself is damaged) then full recovery may take months or years ( or could be permanent). EMG and nerve conduction studies are typically performed to diagnose the extent and distribution of the damage, and to help with prognosis for recovery.

In terms of the prognosis of ulnar neuropathy early decompression of the nerve sees a return to normal ability (function). which should be immediate.Severe cubital tunnel syndrome tends to have a faster recovery process in individuals below the age of 70, as opposed to those above such an age. Finally, revisional surgery for cubital tunnel syndrome does not result well for those individuals over 50 years of age.

The prognosis is usually good in terms of recovery. Rate of recovery depends on the distance from the site of injury, and axonal regeneration can go up to 1 inch per month. Complete recovery can take anywhere from 6 months to a year

Trauma is the most frequent cause of peripheral nerve lesions. There are two classifications of trauma which include civilian trauma and military trauma. Civilian trauma is most commonly caused by motor vehicle accidents but also by lacerations caused by glass, knives, fans, saw blades or fractures and occasionally sports injuries. Of the civilian injuries, stretch injuries are the most common types and are considered to be a closed injury, where the tissue is unexposed. Stretch injures are commonly the result of dislocation, such as a shoulder dislocation that stretches nerves. Opposite of civilian trauma, there is military trauma which most commonly results in open injuries from blasts often by bombs or improvised explosive devices. Other mechanisms of injury are less common but include ischemia, thermal, electric shock, radiation, adverse reactions to certain chemotherapy medications, percussion and vibration.

External pressure reduces flow in the vessels supplying the nerve with blood (the vasa nervorum). This causes local ischaemia, which has an immediate effect on the ability of the nerve axons to transmit action potentials. As the compression becomes more severe over time, focal demyelination occurs, followed by axonal damage and finally scarring.

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.

Most patients diagnosed with cubital tunnel syndrome have advanced disease (atrophy, static numbness, weakness) that might reflect permanent nerve damage that will not recover after surgery. When diagnosed prior to atrophy, weakness or static numbness, the disease can be arrested with treatment. Mild and intermittent symptoms often resolve spontaneously.

Axonotmesis is an injury to the peripheral nerve of one of the extremities of the body. The axons and their myelin sheath are damaged in this kind of injury, but the endoneurium, perineurium and epineurium remain intact. Motor and sensory functions distal to the point of injury are completely lost over time leading to Wallerian Degeneration due to ischemia, or loss of blood supply. Axonotmesis is usually the result of a more severe crush or contusion than neurapraxia.

Axonotmesis mainly follows a stretch injury. These stretch injuries can either dislocate joins or fracture a limb, due to which peripheral nerves are severed. If the sharp pain from the exposed axon of the nerve is not observed, one can identify a nerve injury from abnormal sensations in their limb. A doctor may ask for a Nerve Conduction Velocity (NCV) test to completely diagnose the issue. If diagnosed as nerve injury, Electromyography performed after 3 to 4 weeks shows signs of denervations and fibrillations, or irregular connections and contractions of muscles.

The mechanism of radial neuropathy is such that it can cause focal demyelination and axonal problems/degeneration (which is nerve fiber reaction to insult, and therefore axon death occurs). These would be caused via laceration or compression of the nerve in question.

HNA is an episodic disorder; it is characterized by episodes generally lasting 1–6 weeks. During an episode, the nerves of the brachial plexus are targeted by the body as antigens, and the body's immune system begins to degenerate the nerves of the brachial plexus. The exact order or location of the nerve degeneration cannot be predicted before an episode. Other areas of the nervous system that have been affected are the phrenic nerves and the recurrent laryngeal. As the nerves lose function, the muscles associated with those nerves begin to atrophy. In brachial plexus degeneration, atrophy may occur in the deltoid muscles. In phrenic nerve degeneration, the diaphragm may be affected. In this case, breathing can be impaired due to a lack of muscle control of the diaphragm. If the recurrent larangyl nerve is targeted, the pharynx will begin to atrophy and voice function may be lost.

As illustrated by the risk factors above, perioperative hypoxia is a multifactorial problem. Amidst these risk factors it may be difficult to pinpoint the optic nerve’s threshold for cell death, and the exact contribution of each factor.

Low blood pressure and anemia are cited as perioperative complications in nearly all reports of PION, which suggests a causal relationship. However, while low blood pressure and anemia are relatively common in the perioperative setting, PION is exceedingly rare. Spine and cardiac bypass surgeries have the highest estimated incidences of PION, 0.028% and 0.018% respectively, and this is still extremely low. This evidence suggests that optic nerve injury in PION patients is caused by more than just anemia and low blood pressure.

Evidence suggests that the multifactorial origin of perioperative PION involves the risks discussed above and perhaps other unknown factors. Current review articles of PION propose that vascular autoregulatory dysfunction and anatomic variation are under-investigated subjects that may contribute to patient-specific susceptibility.

Brachial plexus injury is found in both children and adults, but there is a difference between children and adults with BPI.