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 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.

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.

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.

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.

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.)

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.

A variety of patient factors can lead to CTS, including heredity, size of the carpal tunnel, associated local and systematic diseases, and certain habits. Non-traumatic causes generally happen over a period of time, and are not triggered by one certain event. Many of these factors are manifestations of physiologic aging.

Examples include:

- Rheumatoid arthritis and other diseases that cause inflammation of the flexor tendons.

- With hypothyroidism, generalized myxedema causes deposition of mucopolysaccharides within both the perineurium of the median nerve, as well as the tendons passing through the carpal tunnel.

- During pregnancy women experience CTS due to hormonal changes (high progesterone levels) and water retention (which swells the synovium), which are common during pregnancy.

- Previous injuries including fractures of the wrist.

- Medical disorders that lead to fluid retention or are associated with inflammation such as: inflammatory arthritis, Colles' fracture, amyloidosis, hypothyroidism, diabetes mellitus, acromegaly, and use of corticosteroids and estrogens.

- Carpal tunnel syndrome is also associated with repetitive activities of the hand and wrist, in particular with a combination of forceful and repetitive activities

- Acromegaly causes excessive secretion of growth hormones. This causes the soft tissues and bones around the carpel tunnel to grow and compress the median nerve.

- Tumors (usually benign), such as a ganglion or a lipoma, can protrude into the carpal tunnel, reducing the amount of space. This is exceedingly rare (less than 1%).

- Obesity also increases the risk of CTS: individuals classified as obese (BMI > 29) are 2.5 times more likely than slender individuals (BMI < 20) to be diagnosed with CTS.

- "Double-crush syndrome" is a debated hypothesis that compression or irritation of nerve branches contributing to the median nerve in the neck, or anywhere above the wrist, increases sensitivity of the nerve to compression in the wrist. There is little evidence, however, that this syndrome really exists.

- Heterozygous mutations in the gene SH3TC2, associated with Charcot-Marie-Tooth, confer susceptibility to neuropathy, including the carpal tunnel syndrome.

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.

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.

Crutch paralysis is a form of paralysis which can occur when either the radial nerve or part of the brachial plexus, containing various nerves that innervate sense and motor function to the arm and hand, is under constant pressure, such as by the use of a crutch. This can lead to paralysis of the muscles innervated by the compressed nerve. Generally, crutches that are not adjusted to the correct height can cause the radial nerve to be constantly pushed against the humerus. This can cause any muscle that is innervated by the radial nerve to become partially or fully paralyzed. An example of this is wrist drop, in which the fingers, hand, or wrist is chronically in a flexed position because the radial nerve cannot innervate the extensor muscles due to paralysis. This condition, like other injuries from compressed nerves, normally improves quickly through therapy.

Mononeuropathy is a type of neuropathy that only affects a single nerve. Diagnostically, it is important to distinguish it from polyneuropathy because when a single nerve is affected, it is more likely to be due to localized trauma or infection.

The most common cause of mononeuropathy is physical compression of the nerve, known as compression neuropathy. Carpal tunnel syndrome and axillary nerve palsy are examples. Direct injury to a nerve, interruption of its blood supply resulting in (ischemia), or inflammation also may cause mononeuropathy.

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.

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.

Peripheral neuropathy may be classified according to the number and distribution of nerves affected (mononeuropathy, mononeuritis multiplex, or polyneuropathy), the type of nerve fiber predominantly affected (motor, sensory, autonomic), or the process affecting the nerves; e.g., inflammation (neuritis), compression (compression neuropathy), chemotherapy (chemotherapy-induced peripheral neuropathy).

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.

Tinel's sign is a way to detect irritated nerves. It is performed by lightly tapping (percussing) over the nerve to elicit a sensation of tingling or "pins and needles" in the distribution of the nerve. It takes its name from French neurologist Jules Tinel (1879–1952).

For example, in carpal tunnel syndrome where the median nerve is compressed at the wrist, Tinel's sign is often "positive" causing tingling in the thumb, index, middle finger and the radial half of the fourth digit. Tinel's sign is sometimes referred to as "distal tingling on percussion" or DTP. This distal sign of regeneration can be expected during different stage of somatosensory recovery.

Although most frequently associated with carpal tunnel syndrome, Tinel's sign is a generalized term, and can also be positive in tarsal tunnel syndrome, or in ulnar nerve impingement at the wrist (Guyon's canal syndrome), where it affects the other (ulnar) half of the fourth digit and the fifth digit.

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.

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 theory is that the radial nerve becomes irritated and/or inflamed from friction caused by compression by muscles in the forearm.

Some speculate that Radial Tunnel Syndrome is a type of repetitive strain injury (RSI), but there is no detectable pathophysiology and even the existence of this disorder is questioned.

The term "radial tunnel syndrome" is used for compression of the posterior interosseous nerve, a division of the radial nerve, at the lateral intermuscular septum of arm, while "supinator syndrome" is used for compression at the arcade of Frohse.

The "radial tunnel" is the region from the humeroradial joint past the proximal origin of the supinator muscle. Some scientists believe the radial tunnel extends as far as the distal border of the supinator. The radial nerve is commonly compressed within a 5 cm region near the elbow, but it can be compressed anywhere along the forearm if the syndrome is caused by injury (e.g. a fracture that puts pressure on the radial nerve). The radial nerve provides sensation to the skin of posterior arm, posterior and lateral forearm and wrist, and the joints of the elbow, wrist and hand. The nerve also provides sensory branches that travel to the periosteum of the lateral epicondyle, the anterior radiohumeral joint, and the annular ligament. It provides motor function through innervation to most extensor muscles of the posterior arm and forearm. Therefore, it is extremely important in upper body extremity movement and can cause significant pain to patients presenting with radial tunnel syndrome. Unlike carpal tunnel syndrome, radial tunnel syndrome does not present tingling or numbness, since the posterior interosseous nerve mainly affects motor function.

This problem is often caused by: bone tumors, injury (specifically fractures of the forearm), noncancerous fatty tumors (lipomas), and inflammation of surrounding tissue.

Globally diabetic neuropathy affects approximately 132 million people as of 2010 (1.9% of the population).

Diabetes is the leading known cause of neuropathy in developed countries, and neuropathy is the most common complication and greatest source of morbidity and mortality in diabetes. It is estimated that neuropathy affects 25% of people with diabetes. Diabetic neuropathy is implicated in 50–75% of nontraumatic amputations.

The main risk factor for diabetic neuropathy is hyperglycemia. In the DCCT (Diabetes Control and Complications Trial, 1995) study, the annual incidence of neuropathy was 2% per year but dropped to 0.56% with intensive treatment of Type 1 diabetics. The progression of neuropathy is dependent on the degree of glycemic control in both Type 1 and Type 2 diabetes. Duration of diabetes, age, cigarette smoking, hypertension, height, and hyperlipidemia are also risk factors for diabetic neuropathy.

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

The mechanisms of diabetic neuropathy are poorly understood. At present, treatment alleviates pain and can control some associated symptoms, but the process is generally progressive.

As a complication, there is an increased risk of injury to the feet because of loss of sensation (see diabetic foot). Small infections can progress to ulceration and this may require amputation.

The posterior interosseous nerve may be entrapped at the arcade of Frohse, which is part of the supinator muscle. Posterior interosseous neuropathy is purely a motor syndrome resulting in finger drop and radial wrist deviation on extension.

Malformations of the upper extremities can occur In the third to seventh embryonic week. In some cases the TPT is hereditary. In these cases, there is a mutation on chromosome 7q36. If the TPT is hereditary, it is mostly inherited as an autosomal dominant trait, non-opposable and bilateral. The sporadic cases are mostly opposable and unilateral.