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.

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

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.)

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.

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.

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.

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.

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.

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.

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.

Axillary nerve palsy is a neurological condition in which the axillary (also called circumflex) nerve has been damaged by shoulder dislocation. It can cause weak deltoid and sensory loss below the shoulder. Since this is a problem with just one nerve, it is a type of Peripheral neuropathy called mononeuropathy. Of all brachial plexus injuries, axillary nerve palsy represents only .3% to 6% of them.

Nerve injury is injury to nervous tissue. There is no single classification system that can describe all the many variations of nerve injury. In 1941, Seddon introduced a classification of nerve injuries based on three main types of nerve fiber injury and whether there is continuity of the nerve. Usually, however, (peripheral) nerve injury is classified in five stages, based on the extent of damage to both the nerve and the surrounding connective tissue, since supporting glial cells may be involved. Unlike in the central nervous system, neuroregeneration in the peripheral nervous system is possible. The processes that occur in peripheral regeneration can be divided into the following major events: Wallerian degeneration, axon regeneration/growth, and nerve reinnervation. The events that occur in peripheral regeneration occur with respect to the axis of the nerve injury. The proximal stump refers to the end of the injured neuron that is still attached to the neuron cell body; it is the part that regenerates. The distal stump refers to the end of the injured neuron that is still attached to the end of the axon; it is the part of the neuron that will degenerate but that remains in the area toward which the regenerating axon grows. The study of peripheral nerve injury began during the American Civil War and has greatly expanded to the point of using growth-promoting molecules.

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.

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.

Neurapraxia is most commonly observed in athletes involved in collision sports, such as American football. Athletes participating in collision sports most often suffer from cervical cord neurapraxia, also known as transient neurapraxia. Cervical cord neurapraxia is the result of a severe collision in which a blow to the crown of the athlete’s head forcefully extends or compresses the neck. Numbness, stinging, and/or weakness in the arms, legs or both, distinguish cervical cord neurapraxia. Typical episodes of transient nuerapraxia only last a few seconds and symptoms dissipate entirely. Though the severity of the injury can range, transient neurapraxia does not lead to permanent paralysis of the affected muscles. Subsequent spinal cord injury after an episode of cervical cord neurapraxia has not been observed. However, athletes who experience an episode of transient cervical neurapraxia face an approximately 50% chance of a repeat episode if they continue to participate in collision sports.

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.

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.

In cases of neurapraxia, the function of the nerves are temporarily impaired. However, the prognosis for recovery from neurapraxia is efficient and quick. Recovery begins within two to three weeks after the injury occurs, and it is complete within six to eight weeks. There are instances when function is not completely restored until four months after the instance of injury. The recovery period of neurapraxia is not an entirely ordered process, but the recovery is always complete and fast.

Most often the radiculopathy found in the patients are located in the cervical spine, most commonly affecting C6-C8 spinal nerves.

Certain injuries can also lead to radiculopathy. These injuries include lifting heavy objects improperly or suffering from a minor trauma such as a car accident. Less common causes of radiculopathy include injury caused by tumor (which can compress nerve roots locally) and diabetes (which can effectively cause ischemia or lack of blood flow to nerves).

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.

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."

Because the nerve emerges near the bottom of the brain, it is often the first nerve compressed when there is any rise in intracranial pressure. Different presentations of the condition, or associations with other conditions, can help to localize the site of the lesion along the VIth cranial nerve pathway.

The most common causes of VIth nerve palsy in adults are:

- More common: Vasculopathic (diabetes, hypertension, atherosclerosis), trauma, idiopathic.

- Less common: Increased intracranial pressure, giant cell arteritis, cavernous sinus mass (e.g. meningioma, Brain stem Glioblastoma aneurysm, metastasis), multiple sclerosis, sarcoidosis/vasculitis, postmyelography, lumbar puncture, stroke (usually not isolated), Chiari Malformation, hydrocephalus, intracranial hypertension, tuberculosis meningitis.

In children, Harley reports typical causes as traumatic, neoplastic (most commonly brainstem glioma), as well as idiopathic. Sixth nerve palsy causes the eyes to deviate inward (see: Pathophysiology of strabismus). Vallee et al. report that benign and rapidly recovering isolated VIth nerve palsy can occur in childhood, sometimes precipitated by ear, nose and throat infections.

Radiculopathy is a mechanical compression of a nerve root usually at the exit foramen or lateral recess. It may be secondary to degenerative disc disease, osteoarthritis, facet joint degeneration/hypertrophy, ligamentous hypertrophy, spondylolisthesis, or a combination of these factors. Rarer causes of radiculopathy may include radiation, diabetes mellitus, neoplastic disease, or any meningeal-based disease process. Second-stage Lyme meningitis resembles aseptic meningitis and is often associated with radiculopathies.

It is not known what percentage of people with IIH will remit spontaneously, and what percentage will develop chronic disease.

IIH does not normally affect life expectancy. The major complications from IIH arise from untreated or treatment-resistant papilledema. In various case series, the long-term risk of ones vision being significantly affected by IIH is reported to lie anywhere between 10 and 25%.