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.

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.

BPI has shown to occur in 44% to 70% of traumatic injuries, such as motorcycle accidents, sporting activities, or workplace accidents. With 22% being motorcycle injuries and about 4.2% having plexus damage. People that have accidents with riding motorcycles and snowmobiles, have higher risks of getting BPI.

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.

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.)

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.

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.

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

Among the causes of ulnar neuropathy are the following-

Much more commonly, ulnar neuropathy is caused by overuse of the triceps muscle and repetitive stress combined with poor ergonomics. Overused and hypertonic triceps muscle causes inflammation in the tendon and adhesions with the connective tissue surrounding that tendon and muscle. These in turn impinge on or trap the ulnar nerve. Ulnar neuropathy resulting from repetitive stress is amenable to massage and can usually be fully reversed without cortisone or surgery.

Center for Occupational and Environmental Neurology , Baltimore, MD has this to say:

“Repetitive Strain Injuries (RSI) refers to many different diagnoses of the neck/shoulder, arm, and wrist/hand area usually associated with work-related ergonomic stressors. Other terms used for Repetitive Strain Injuries are overuse syndrome, musculoskeletal disorders, and cumulative trauma disorders. Some of the more common conditions under these headings include:

Cubital Tunnel Syndrome-compression of the ulnar nerve in the cubital tunnel at the elbow.”

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.

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.

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.

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.

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.

This is the least severe form of nerve injury, with complete recovery. In this case, the axon remains intact, but there is myelin damage causing an interruption in conduction of the impulse down the nerve fiber. Most commonly, this involves compression of the nerve or disruption to the blood supply (ischemia). There is a temporary loss of function which is reversible within hours to months of the injury (the average is 6–9 weeks). Wallerian degeneration does not occur, so recovery does not involve actual regeneration. There is frequently greater involvement of motor than sensory function with autonomic function being retained. In electrodiagnostic testing with nerve conduction studies, there is a normal compound motor action potential amplitude distal to the lesion at day 10, and this indicates a diagnosis of mild neuropraxia instead of axonotmesis or neurotmesis.

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.

Reactivation of herpes zoster virus, as well as being associated with Bell's palsy, may also be a direct cause of facial nerve palsy. Reactivation of latent virus within the dorsal root ganglion of the facial nerve is associated with vesicles affecting the ear canal, and termed Ramsay Hunt syndrome type II. In addition to facial paralysis, symptoms may include ear pain and vesicles, sensorineural hearing loss, and vertigo. Management includes Antiviral drugs and oral steroids.

Otitis media is an infection in the middle ear, which can spread to the facial nerve and inflame it, causing compression of the nerve in its canal. Antibiotics are used to control the otitis media, and other options include a wide myringotomy (an incision in the tympanic membrane) or decompression if the patient does not improve.

Chronic otitis media usually presents in an ear with chronic discharge (otorrhea), or hearing loss, with or without ear pain (otalgia). Once suspected, there should be immediate surgical exploration to determine if a cholesteatoma has formed as this must be removed if present. Inflammation from the middle ear can spread to the canalis facialis of the temporal bone - through this canal travels the facial nerve together with the steatoacoustisus nerve. In the case of inflammation the nerve is exposed to edema and subsequent high pressure, resulting in a periferic type palsy.

Lyme disease, caused by chronic "Borrelia burgdorferi" infection, is a common cause of facial nerve paralysis in areas.

In many cases recovery happens spontaneously and no treatment is needed. This spontaneous recovery can occur because distance between the injury location and the deltoid muscle is small. Spontaneous recovery may take as long as 12 months.

In order to combat pain and inflammation of nerves, medication may be prescribed.

Surgery is an option, but it has mixed results within the literature and is usually avoided because only about half of people who undergo surgery see any positive results from it. Some suggest that surgical exploration should be considered if no recovery occurs after 3 to 6 months. Some surgical options include nerve grafting, neurolysis, or nerve reconstruction. Surgery results are typically better for younger patients (under 25) and for nerve grafts less than six centimeters.

For some, recovery does not occur and surgery is not possible. In these cases, most patients’ surrounding muscles can compensate, allowing them to gain a satisfactory range of motion back. Physical therapy or Occupational therapy will help retrain and gain muscle tone back.

CES is often concurrent with congenital or degenerative diseases and represents a high cost of care to those admitted to the hospital for surgery. Hospital stays generally last 4 to 5 days, and cost an average of $100,000 to $150,000, unless the patient lives in a country where healthcare is free at the point of delivery.

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.

The radial nerve, like any other in the nervous system, is vulnerable to damage. This damage can originate when the nerve fibers experience pressure, stretching, or cutting. All of the aforementioned issues can prevent an action potential from continuing down the nerve, which would interrupt signal transduction to and from the brain. As a result of the interrupted signal, the patient may experience loss of feeling or motor control.

There are many ways to acquire radial nerve palsy.

The term "Saturday Night Palsy" refers to an injury to the radial nerve in the spiral groove of the humerus caused while sleeping in a position that would under normal circumstances cause discomfort. It can occur when a person falls asleep while heavily medicated and/or under the influence of alcohol with the underside of the arm compressed by a bar edge, bench, chair back, or like object. Sleeping with the head resting on the arm can also cause radial nerve palsy.

Breaking the humerus and deep puncture wounds can also cause the condition.

Posterior interosseus palsy is distinguished from radial nerve palsy by the preservation of elbow extension.

Symptoms vary depending on the severity and location of the trauma; however, common symptoms include wrist drop (the inability to extend the wrist upward when the hand is palm down); numbness of the back of the hand and wrist, specifically over the first web space which is innervated by the radial nerve; and inability to voluntarily straighten the fingers or extend the thumb, which is performed by muscles of the extensor group, all of which are primarily innervated by the radial nerve. Loss of wrist extension is due to paralysis of the posterior compartment of forearm muscles; although the elbow extensors are also innervated by the radial nerve, their innervation is usually spared because the compression occurs below, distal, to the level of the axillary nerve, which innervates the long head of the triceps, and the upper branches of the radial nerve that innervate the remainder of the Triceps.

Various etiologies of CES include fractures, abscesses, hematomas, and any compression of the relevant nerve roots. Injuries to the thoracolumbar spine will not necessarily result in a clinical diagnosis of CES, but in all such cases it is necessary to consider. Few epidemiological studies of CES have been done in the United States, owing to difficulties such as amassing sufficient cases as well as defining the affected population, therefore this is an area deserving of additional scrutiny.

Traumatic spinal cord injuries occur in approximately 40 people per million annually in the United States, resulting from traumas due to motor vehicle accidents, sporting injuries, falls, and other factors. An estimated 10 to 25% of vertebral fractures will result in injury to the spinal cord. Thorough physical examinations are required, as 5 to 15% of trauma patients have fractures that initially go undiagnosed.

The most frequent injuries of the thoracolumbar region are to the conus medullaris and the cauda equina, particularly between T12 and L2. Of these two syndromes, CES is the more common. CES mainly affects middle-aged individuals, particularly those in their forties and fifties, and presents more often in men. It is not a typical diagnosis, developing in only 4 to 7 out of every 10,000 to 100,000 patients, and is more likely to occur proximally. Disc herniation is reportedly the most common cause of CES, and it is thought that 1 to 2% of all surgical disc herniation cases result in CES.

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.

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.