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.

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.

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.

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.

Radial nerve dysfunction is also known as radial neuropathy or radial mononeuropathy. It is a problem associated with the radial nerve resulting from injury consisting of acute trauma to the radial nerve. The damage has sensory consequences, as it interferes with the radial nerve's innervation of the skin of the posterior forearm, lateral three digits, and the dorsal surface of the side of the palm. The damage also has motor consequences, as it interferes with the radial nerve's innervation of the muscles associated with the extension at the elbow, wrist, and figers, as well the supination of the forearm. This type of injury can be difficult to localize, but relatively common, as many ordinary occurrences can lead to the injury and resulting mononeuropathy. One out of every ten patients suffering from radial nerve dysfunction do so because of a fractured humerus.

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.

The posterior interosseous nerve (or dorsal interosseous nerve) is a nerve in the forearm. It is the continuation of the deep branch of the radial nerve, after this has crossed the supinator muscle. It is considerably diminished in size compared to the deep branch of the radial nerve. The nerve fibers originate from cervical segments C7 and C8.

The radial nerve is one of the major nerves of the upper limb. It innervates all of the muscles in the extensor compartments of the arm. Injury to the nerve can therefore result in significant functional deficit for the individual. It is vulnerable to injury with fractures of the humeral shaft as it lies in very close proximity to the bone (it descends within the spiral groove on the posterior aspect of the humerus). Characteristic findings following injury will be as a result of radial nerve palsy (e.g. weakness of wrist/finger extension and sensory loss over the dorsum of the hand).

The vast majority of radial nerve palsies occurring as a result of humeral shaft fractures are neuropraxias (nerve conduction block as a result of traction or compression of the nerve), these nerve palsies can be expected to recover over a period of months. A minority of palsies occur as a result of more significant axonotmeses (division of the axon but preservation of the nerve sheath) or the even more severe neurotmeses (division of the entire nerve structure). As a result, it is important for individuals sustaining a Holstein–Lewis injury to be carefully followed up as if there is no evidence of return of function to the arm after approximately three months, further investigations and possibly, nerve exploration or repair may be required. The exception to this rule is if the fracture to the humerus requires fixing in the first instance. In that case, the nerve should be explored at the same time that fixation is performed.

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.

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.

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.

Anterior interosseous syndrome or Kiloh-Nevin syndrome I is a medical condition in which damage to the anterior interosseous nerve (AIN), a motor branch of the median nerve, causes pain in the forearm and a characteristic weakness of the pincer movement of the thumb and index finger.

Most cases of AIN syndrome are due to a transient neuritis, although compression of the AIN can happen. Trauma to the median nerve have also been reported as a cause of AIN syndrome.

Although there is still controversy among upper extremity surgeons, AIN syndrome is now regarded as a neuritis (inflammation of the nerve) in most cases; this is similar to Parsonage–Turner syndrome. Although the exact etiology is unknown, there is evidence that it is caused by an immune mediated response.

Studies are limited, and no randomized controlled trials have been performed regarding the treatment of AIN syndrome. While the natural history of AIN syndrome is not fully understood, studies following patients who have been treated without surgery show that symptoms can resolve starting as late as one year after onset. Other retrospective studies have shown that there is no difference in outcome in surgically versus nonsurgically treated patients. Surgical decompression is rarely indicated in AIN syndrome. Indications for considering surgery include a known space-occupying lesion that is compressing the nerve (a mass) and persistent symptoms beyond 1 year of conservative treatment.

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.

Injuries of the forearm with compression of the nerve is the most common cause: examples include

supracondylar fractures, often associated with haemorrhage into the deep musculature;

injury secondary to open reduction of a forearm fracture; or dislocation of the elbow.⁠⁠

Direct trauma from a penetrating injury such as a stab wound is a common cause for the syndrome.

Fibrous bands or arcuate (curved) ligaments may entrap the median as well as the anterior interosseous nerves, in which case a patient may experience numbness as well as pain.⁠⁠

Rheumatoid disease and gouty arthritis may be a predisposing factor in anterior interosseous nerve entrapment.

Very similar syndromes can be caused by more proximal lesions, such as brachial plexus neuritis.⁠

Anterior interosseous nerve entrapment or compression injury remains a difficult clinical diagnosis because it is mainly a motor nerve and the syndrome is often mistaken for finger ligamentous injury.⁠

Brown-Séquard syndrome is rare as the trauma would have to be something that damaged the nerve fibres on just one half of the spinal cord.

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.

Non-surgical treatment of radial tunnel syndrome includes rest, NSAID, therapy with modalities, work modification, ergonomic modification, injection if associated with lateral epicondylitis.

Patients whose conditions are more adapted to surgical intervention are those who do not respond to prolonged conservative treatment. The patient must have pain with resisted supination, positive middle finger test, positive electrodiagnostic findings, and pain relief after anesthetic injection into the radial tunnel. Based on 2002 data, surgical decompression leads to 60-70% good or excellent results.

A Holstein–Lewis fracture is a fracture of the distal third of the humerus resulting in entrapment of the radial nerve.

The international debate regarding the relationship between CTS and repetitive motion in work is ongoing. The Occupational Safety and Health Administration (OSHA) has adopted rules and regulations regarding cumulative trauma disorders. Occupational risk factors of repetitive tasks, force, posture, and vibration have been cited.

The relationship between work and CTS is controversial; in many locations, workers diagnosed with carpal tunnel syndrome are entitled to time off and compensation.

Some speculate that carpal tunnel syndrome is provoked by repetitive movement and manipulating activities and that the exposure can be cumulative. It has also been stated that symptoms are commonly exacerbated by forceful and repetitive use of the hand and wrists in industrial occupations, but it is unclear as to whether this refers to pain (which may not be due to carpal tunnel syndrome) or the more typical numbness symptoms.

A review of available scientific data by the National Institute for Occupational Safety and Health (NIOSH) indicated that job tasks that involve highly repetitive manual acts or specific wrist postures were associated with incidents of CTS, but causation was not established, and the distinction from work-related arm pains that are not carpal tunnel syndrome was not clear. It has been proposed that repetitive use of the arm can affect the biomechanics of the upper limb or cause damage to tissues. It has also been proposed that postural and spinal assessment along with ergonomic assessments should be included in the overall determination of the condition. Addressing these factors has been found to improve comfort in some studies. A 2010 survey by NIOSH showed that 2/3 of the 5 million carpal tunnel cases in the US that year were related to work. Women have more work-related carpal tunnel syndrome than men.

Speculation that CTS is work-related is based on claims such as CTS being found mostly in the working adult population, though evidence is lacking for this. For instance, in one recent representative series of a consecutive experience, most patients were older and not working. Based on the claimed increased incidence in the workplace, arm use is implicated, but the weight of evidence suggests that this is an inherent, genetic, slowly but inevitably progressive idiopathic peripheral mononeuropathy.

One way to prevent this injury from occurring is to be informed and educated about the risks involved in hurting your wrist and hand. If patients do suffer from median nerve palsy, occupational therapy or wearing a splint can help reduce the pain and further damage. Wearing a dynamic splint, which pulls the thumb into opposition, will help prevent an excess in deformity. This splint can also assist in function and help the fingers flex towards the thumb. Stretching and the use of C-splints can also assist in prevention of further damage and deformity. These two methods can help in the degree of movement the thumb can have. While it is impossible to prevent trauma to your arms and wrist, patients can reduce the amount of compression by maintaining proper form during repetitive activities. Furthermore, strengthening and increasing flexibility reduces the risk of nerve compression.

Several risk factors of CMC OA of the thumb are known. Each of these risk factors does not cause CMC OA by itself, but acts as a predisposing factor influencing the process of OA in some way. Risk factors include: female gender, suffering from obesity, repetitive heavy manual labor, familial predisposition and hormonal changes, such as menopause.

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

Ape hand deformity, also known as simian hand, is a deformity in humans who cannot move the thumb away from the rest of the hand. It is an inability to abduct the thumb. Abduction of the thumb refers to the specific capacity to orient the thumb perpendicularly to the ventral (palmar) surface of the hand. Opposition refers specifically the ability to "swing" the first metacarpal such that the tip of the thumb may touch the distal end of the 5th phalanx and if we put the hand on the table as the palm upward the thumb can not point to the sky. The Ape Hand Deformity is caused by damage to the distal median nerve (also called a Median Claw lesion), and subsequent loss of opponens pollicis muscle function. The name "ape hand deformity" is misleading, as apes have opposable thumbs.

It can occur with an injury of the median nerve either at the elbow or the wrist, impairing the thenar muscles and opponens pollicis muscle.

Ape hand deformity is one aspect of median nerve palsy, which is usually caused by deep injuries to the arm, forearm and wrist area.

Ape hand caused by median and ulnar nerve lesions

Brown-Séquard syndrome may be caused by a spinal cord tumour, trauma [such as a gunshot wound or puncture wound to the cervical (neck) or thoracic spine (back)], ischemia (obstruction of a blood vessel), or infectious or inflammatory diseases such as tuberculosis, or multiple sclerosis. In its pure form, it is rarely seen. The most common cause is penetrating trauma such as a gunshot wound or stab wound to the spinal cord. Decompression sickness may also be a cause of Brown-Séquard syndrome.

The presentation can be progressive and incomplete. It can advance from a typical Brown-Séquard syndrome to complete paralysis. It is not always permanent and progression or resolution depends on the severity of the original spinal cord injury and the underlying pathology that caused it in the first place.

The most common finding is oculomotor nerve dysfunction leading to ophthalmoplegia. This is often accompanied by ophthalmic nerve dysfunction, leading to hypoesthesia of the upper face. The optic nerve may eventually be involved, with resulting visual impairment.