In order to diagnose radial nerve dysfunction, a doctor will conduct a physical examination. During the exam of the arm, wrist, and hand, the doctor will look for: difficulty straightening the arm at the elbow; trouble turning the arm outward; difficulty lifting the wrist; muscle loss or atrophy in the forearm; weakness of the wrist and/or fingers. In addition, tests may need to be conducted to confirm the doctors findings. These tests include: blood tests; MRI of the neck and shoulders to screen for other problems; nerve biopsy; nerve conduction tests; ultrasound of the elbow.

Radial neuropathy is not necessarily permanent. The majority of radial neuropathies due to an acute compressive event (Saturday night palsy) do recover without intervention. If the injury is demyelinating (meaning only the myelin sheath surrounding the nerve is damaged), then full recovery typically occurs within 2–4 weeks. If the injury is axonal (meaning the underlying nerve fiber itself is damaged) then full recovery may take months or years, or may never occur. EMG and nerve conduction studies are typically performed to diagnose the extent and distribution of the damage, and to help with prognosis for recovery.

Among the diagnostic procedures done to determine if the individual has ulnar neuropathy are (but may not be limited to the following):

- Nerve conduction exam/study (Nerve Conduction Velocity is a measurements made in a nerve conduction exam)

- Physical exam

- Medical history

- X ray

- CBC

- Urinalysis

- MRI

- Ultrasound

- Histology study

Electrophysiologic testing is an essential part of the evaluation of Anterior interosseous nerve syndromes. Nerve conduction studies may be normal or show pronator quadratus latency.⁠⁠

Electromyography (EMG) is generally most useful and will reveal abnormalities in the flexor pollicis longus, flexor digitorum profundus I and II and pronator quadratus muscles.⁠⁠

The role or MRI and ultrasound imaging in the diagnosis of Kiloh-Nevin syndrome is unclear.⁠

If asked to make the "OK" sign, patients will make a triangle sign instead.

This 'Pinch-Test' exposes the weakness of the Flexor pollicis longus muscle and the flexor digitorum profundus I leading to weakness of the flexion of the distal phalanges of the thumb and index finger. This results in impairment of the pincer movement and the patient will have difficulty picking up a small item, such as a coin, from a flat surface.

The distinct innervation of the hand usually enables diagnosis of an ulnar nerve impingement by symptoms alone. Ulnar nerve damage that causes paralysis to these muscles will result in a characteristic ulnar claw position of the hand at rest. Clinical tests such as the card test for Froment's sign, can be easily performed for assessment of ulnar nerve. However, a complete diagnosis should identify the source of the impingement, and radiographic imaging may be necessary to determine or rule-out an underlying cause.

Imaging studies, such as ultrasound or MRI, may reveal anatomic abnormalities or masses responsible for the impingement. Additionally, imaging may show secondary signs of nerve damage that further confirm the diagnosis of impingement. Signs of nerve damage include flattening of the nerve, swelling of the nerve proximal to site of injury, abnormal appearance of nerve, or characteristic changes to the muscles innervated by the nerve.

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.

Initial line of treatment is with anti-inflammatory drugs or cortisone injections. There have been trials with gloves which help protect the ulnar nerve from compression. The most radical treatment option is surgery to relieve tension in the volar carpal ligament which forms the roof of Guyon's canal, thereby reducing compression on the ulnar nerve.

The place of chiropractic-, physical-, occupational-, massage- and osteopathic therapy was not confirmed in scientific studies. These treatments can be both expensive as well as dangerous (causing permanent damage when performed wrongly).

It is advised to consult a physician beforehand starting any therapy, albeit an alternative approach, to avoid any permanent nerve damage.

The diagnosis may be confirmed by an EMG examination in 5 to 7 days. The evidence of denervation will be evident. If there is no nerve conduction 72 hours after the injury, then avulsion is most likely..

The most advanced diagnostic method is MR imaging of the brachial plexus using a high Tesla MRI scanner like 1.5 T or more. MR helps aid in the assessment of the injuries in specific context of site, extent and the nerve roots involved. In addition, assessment of the cervical cord and post traumatic changes in soft tissues may also be visualised.

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.

Surgical decompression can give excellent results if the clinical picture and the EMG suggest a compression neuropathy.

In brachial plexus neuritis, conservative management may be more appropriate.

Spontaneous recovery has been reported, but is said to be delayed and incomplete.

There is a role for physiotherapy and this should be directed specifically towards the pattern of pain and symptoms. Soft tissue massage, stretches and exercises to directly mobilise the nerve tissue may be used.⁠

Cubital tunnel syndrome may be prevented or reduced by maintaining good posture and proper use of the elbow and arms, such as wearing an arm splint while sleeping to maintain the arm is in a straight position instead of keeping the elbow tightly bent. A recent example of this is popularization of the concept of cell phone elbow.

Because lesions to different areas of the median nerve produce similar symptoms, clinicians perform a complete motor and sensory diagnosis along the nerve course. Decreased values of nerve conduction studies are used as indicators of nerve compression and may aid in determining the localization of compression.

Palpation above the elbow joint may reveal a bony consistency. Radiography images may show an abnormal bony spur outgrowth (supracondyloid process) just proximal to the elbow joint. Attached fibrous tissue (Struthers' ligament) may compress the median nerve as it passes underneath the process. This is also known as supracondylar process syndrome. Compression at this point may also occur without the bony spur; in this case, aponeurotic tissue found at the location of where Struthers' ligament should be is responsible for the compression.

If patients mention reproduction of symptoms to the forearm during elbow flexion of 120–130 degrees with the forearm in maximal supination, then the lesion may be localized to the area underneath the lacertus fibrosus (also known as bicipital aponeurosis). This is sometimes misdiagnosed as elbow strain and medial or lateral epicondylitis.

A lesion to the upper arm area, just proximal to where motor branches of forearm flexors originate, is diagnosed if the patient is unable to make a fist. More specifically, the patient's index and middle finger cannot flex at the MCP joint, while the thumb usually is unable to oppose. This is known as hand of benediction or Pope’s blessing hand. Another test is the bottle sign—the patient is unable to close all their fingers around a cylindrical object.

Carpal tunnel syndrome (CTS) is caused by compression of the median nerve as it passes under the carpal tunnel. Nerve conduction velocity tests through the hand are used to diagnosis CTS. Physical diagnostic tests include the Phalen maneuver or Phalen test and Tinel's sign. To relieve symptoms, patients may describe a motion similar to "shaking a thermometer", another indication of CTS.

Pronator teres syndrome (also known as pronator syndrome) is compression of the median nerve between the two heads of the pronator teres muscle. The Pronator teres test is an indication of the syndrome—the patient reports pain when attempting to pronate the forearm against resistance while extending the elbow simultaneously. The physician may notice an enlarged pronator teres muscle. Tinel's sign the area around the pronator teres heads should be positive. The key to discerning this syndrome from carpal tunnel syndrome is the absence of pain while sleeping. More recent literature collectively diagnose median nerve palsy occurring from the elbow to the forearm as pronator teres syndrome.

In uncooperative patients, the skin wrinkle test offers a pain-free way to identify denervation of the fingers. After submersion in water for 5 minutes, normal fingers will become wrinkled, whereas denervated fingers will not.

In "Ape hand deformity", the thenar muscles become paralyzed due to impingement and are subsequently flattened. This hand deformity is not by itself an individual diagnosis; it is seen only after the thenar muscles have atrophied. While the adductor pollicis remains intact, the flattening of the muscles causes the thumb to become adducted and laterally rotated. The opponens pollicis causes the thumb to flex and rotate medially, leaving the thumb unable to oppose. Carpal tunnel syndrome can result in thenar muscle paralysis which can then lead to ape hand deformity if left untreated. Ape hand deformity can also be seen in the hand of benediction deformity.

The Anterior Interosseus Nerve (AIN), a branch of the median nerve, only accounts for the movement of the fingers in hand and does not have any sensory capabilities. Therefore, the AIN syndrome is purely neuropathic. AINS is considered as an extremely rare condition because it accounts for less than 1% of neuropathies in the upper limb. Patients suffering from this syndrome have impaired distal interphalangeal joint, because of which they are unable to pinch anything or make and "OK" sign with their index finger and thumb. The syndrome can either happen from pinched nerve, or even dislocation of the elbow.

Radiculopathy is a diagnosis commonly made by physicians in primary care specialities, chiropractic, orthopedics, physiatry, and neurology. The diagnosis may be suggested by symptoms of pain, numbness, and weakness in a pattern consistent with the distribution of a particular nerve root. Neck pain or back pain may also be present. Physical examination may reveal motor and sensory deficits in the distribution of a nerve root. In the case of cervical radiculopathy, Spurling's test may elicit or reproduce symptoms radiating down the arm. In the case of lumbosacral radiculopathy, a Straight leg raise maneuver may exacerbate radiculopathic symptoms. Deep tendon reflexes (also known as a Stretch reflex) may be diminished or absent in areas innervated by a particular nerve root.

For further workup, the American College of Radiology recommends that projectional radiography is the most appropriate initial study in all patients with chronic neck pain. Two additional diagnostic tests that may be of use are magnetic resonance imaging and electrodiagnostic testing. Magnetic resonance imaging (MRI) of the portion of the spine where radiculopathy is suspected may reveal evidence of degenerative change, arthritic disease, or another explanatory lesion responsible for the patient's symptoms. Electrodiagnostic testing, consisting of NCS (Nerve conduction study) and EMG (Electromyography), is also a powerful diagnostic tool that may show nerve root injury in suspected areas. On nerve conduction studies, the pattern of diminished Compound muscle action potential and normal sensory nerve action potential may be seen given that the lesion is proximal to the Posterior root ganglion. Needle EMG is the more sensitive portion of the test, and may reveal active denervation in the distribution of the involved nerve root, and neurogenic-appearing voluntary motor units in more chronic radiculopathies. Given the key role of electrodiagnostic testing in the diagnosis of acute and chronic radiculopathies, the American Association of Neuromuscular & Electrodiagnostic Medicine has issued evidence-based practice guidelines, for the diagnosis of both cervical and lumbosacral radiculopathies. The American Association of Neuromuscular & Electrodiagnostic Medicine has also participated in the Choosing Wisely Campaign and several of their recommendations relate to what tests are unnecessary for neck and back pain.

The symptoms and signs depend on which nerve is affected, where along its length the nerve is affected, and how severely the nerve is affected. Positive sensory symptoms are usually the earliest to occur, particularly tingling and neuropathic pain, followed or accompanied by reduced sensation or complete numbness. Muscle weakness is usually noticed later, and is often associated with muscle atrophy.

A compression neuropathy can usually be diagnosed confidently on the basis of the symptoms and signs alone. However, nerve conduction studies are helpful in confirming the diagnosis, quantifying the severity, and ruling out involvement of other nerves (suggesting a mononeuritis multiplex or polyneuropathy). A scan is not usually necessary, but may be helpful if a tumour or other local compressive lesion is suspected.Nerve injury, as a mononeuropathy, may cause similar symptoms to compression neuropathy. This may occasionally cause diagnostic confusion, particularly if the patient does not remember the injury and there are no obvious physical signs to suggest it.The symptoms and signs of each particular syndrome are discussed on the relevant pages, listed below.

If severe pain persists after the first 24hours it is recommended that an individual consult with a professional who can make a diagnosis and implement a treatment plan so the patient can return to everyday activities (Flegel, 2004). These are some of the tools that a professional can use to help make a full diagnosis;

Nerve conduction studies may also be used to localize nerve dysfunction ("e.g.", carpal tunnel syndrome), assess severity, and help with prognosis.

Electrodiagnosis also helps differentiate between myopathy and neuropathy.

Ultimately, the best method of imaging soft tissue is magnetic resonance imaging (MRI), though it is cost-prohibitive and carries a high false positive rate.

In terms of diagnosis of HNPP measuring nerve conduction velocity may give an indication of the presence of the disease.Other methods via which to ascertain the diagnosis of hereditary neuropathy with liability to pressure palsy are:

- Family history

- Genetic test

- Physical exam(lack of ankle reflex)

The severity of brachial plexus injury is determined by the type of nerve damage. There are several different classification systems for grading the severity of nerve and brachial plexus injuries. Most systems attempt to correlate the degree of injury with symptoms, pathology and prognosis. Seddon's classification, devised in 1943, continues to be used, and is based on three main types of nerve fiber injury, and whether there is continuity of the nerve.

1. Neurapraxia: The mildest form of nerve injury. It involves an interruption of the nerve conduction without loss of continuity of the axon. Recovery takes place without wallerian degeneration.

2. Axonotmesis: Involves axonal degeneration, with loss of the relative continuity of the axon and its covering of myelin, but preservation of the connective tissue framework of the nerve (the encapsulating tissue, the epineurium and perineurium, are preserved).

3. Neurotmesis: The most severe form of nerve injury, in which the nerve is completely disrupted by contusion, traction or laceration. Not only the axon, but the encapsulating connective tissue lose their continuity. The most extreme degree of neurotmesis is transsection, although most neurotmetic injuries do not produce gross loss of continuity of the nerve but rather, internal disruption of the nerve architecture sufficient to involve perineurium and endoneurium as well as axons and their covering. It requires surgery, with unpredictable recovery.

A more recent and commonly used system described by the late Sir Sydney Sunderland, divides nerve injuries into five degrees: first degree or neurapraxia, following on from Seddon, in which the insulation around the nerve called myelin is damaged but the nerve itself is spared, and second through fifth degree, which denotes increasing severity of injury. With fifth degree injuries, the nerve is completely divided.

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.

With Seddon's classification of nerve injuries, it is often tough to identify whether a particular nerve injury is neurotmesis, or axonotmesis, which has damage to the nerve fibres but preservation of the nerve trunk. Due to the damage involved in both of these conditions they will both show paralysis of muscles that are supplied by nerves below the site of the lesion, and will have sensory deficits in accordance with the individual nerves that are damaged. The only way to know for sure if a nerve injury is in fact neurotmesis is to allow for the normal progression of nerve regeneration to take place (nerves regenerate at a rate of approximately 2–4 mm/day proximal to the lesion), and if, after that time, there is still profound muscle paralysis and degeneration in these areas, then it is likely to have been a neurotmesis injury.

Neurotmesis is diagnosed through clinical evaluation of symptoms, physical evaluation, and other diagnostic studies. Patients often undergo a series of muscle strength tests, sensory exam which includes feeling the sensation of light touch, pinprick, vibration, and others. Other tests involved with diagnosis of nerve injury are electromyography (EMG) and nerve conduction studies (NCS). These help to distinguish upper from lower motor neuron disorder as well as diagnose primary muscle disease.

RSIs are assessed using a number of objective clinical measures. These include effort-based tests such as grip and pinch strength, diagnostic tests such as Finkelstein's test for De Quervain's tendinitis, Phalen's Contortion, Tinel's Percussion for carpal tunnel syndrome, and nerve conduction velocity tests that show nerve compression in the wrist. Various imaging techniques can also be used to show nerve compression such as x-ray for the wrist, and MRI for the thoracic outlet and cervico-brachial areas.

When an underlying medical condition is causing the neuropathy, treatment should first be directed at this condition. For example, if weight gain is the underlying cause, then a weight loss program is the most appropriate treatment. Compression neuropathy occurring in pregnancy often resolves after delivery, so no specific treatment is usually required. Some compression neuropathies are amenable to surgery: carpal tunnel syndrome and cubital tunnel syndrome are two common examples. Whether or not it is appropriate to offer surgery in any particular case depends on the severity of the symptoms, the risks of the proposed operation, and the prognosis if untreated. After surgery, the symptoms may resolve completely, but if the compression was sufficiently severe or prolonged then the nerve may not recover fully and some symptoms may persist. Drug treatment may be useful for an underlying condition (including peripheral oedema), or for ameliorating neuropathic pain.

Ulnar tunnel syndrome may be characterized by the location or zone within the Guyon's canal at which the ulnar nerve is compressed. The nerve divides into a superficial sensory branch and a deeper motor branch in this area. Thus, Guyon's canal can be separated into three zones based on which portion of the ulnar nerve are involved. The resulting syndrome results in either muscle weakness or impaired sensation in the ulnar distribution.

Zone 2 type syndromes are most common, while Zone 3 are least common.

Treatment is directed at the pathology causing the paralysis. If it is because of trauma such as a gunshot or knife wound, there may be other life-threatening conditions such as bleeding or major organ damage which should be dealt with on an emergent basis. If the syndrome is caused by a spinal fracture, this should be identified and treated appropriately. Although steroids may be used to decrease cord swelling and inflammation, the usual therapy for spinal cord injury is expectant.

While conservative approaches for rehabilitation are ideal, some patients will not improve and surgery is still an option. Patients with large cervical disk bulges may be recommended for surgery, however most often conservative management will help the herniation regress naturally. Procedures such as foraminotomy, laminotomy, or discectomy may be considered by neurosurgeons and orthopedic surgeons.

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.