A variety of methods may be used to diagnose axillary nerve palsy. The health practitioner may examine the shoulder for muscle atrophy of the deltoid muscle. Furthermore, a patient can also be tested for weakness when asked to raise the arm. The deltoid extension lag sign test is one way to evaluate the severity of the muscle weakness. During this test, the physician stands behind the patient and uses the patient's wrist to elevate the arm. Then, the patient is told to hold this position without the doctor's assistance. If the patient cannot hold this position on their own and an angular drop occurs, the angular lag is observed as an indicator of axillary nerve palsy. When the shoulder is at its maximum extension, only the posterior area of the deltoid muscle and the axillary nerve are working to raise the arm. Therefore, no other muscles can provide compensation, which allows the test to be an accurate measure of the axillary nerve’s dysfunction.

Additional testing includes electromyography (EMG) and nerve conduction tests. However, these should not be done right after the injury because results will be normal. These tests must be executed weeks after the initial injury and onset of symptoms. An MRI (magnetic resonance imaging) or X-Ray may also be done by a doctor.

Peripheral neuropathy may first be considered when an individual reports symptoms of numbness, tingling, and pain in feet. After ruling out a lesion in the central nervous system as a cause, diagnosis may be made on the basis of symptoms, laboratory and additional testing, clinical history, and a detailed examination.

During physical examination, specifically a neurological examination, those with generalized peripheral neuropathies most commonly have distal sensory or motor and sensory loss, although those with a pathology (problem) of the nerves may be perfectly normal; may show proximal weakness, as in some inflammatory neuropathies, such as Guillain–Barré syndrome; or may show focal sensory disturbance or weakness, such as in mononeuropathies. Classically, ankle jerk reflex is absent in peripheral neuropathy.

A physical examination will involve testing the deep ankle reflex as well as examining the feet for any ulceration. For large fiber neuropathy, an exam will usually show an abnormally decreased sensation to vibration, which is tested with a 128-Hz tuning fork, and decreased sensation of light touch when touched by a nylon monofilament.

Diagnostic tests include electromyography (EMG) and nerve conduction studies (NCSs), which assess large myelinated nerve fibers. Testing for small-fiber peripheral neuropathies often relates to the autonomic nervous system function of small thinly- and unmyelinated fibers. These tests include a sweat test and a tilt table test. Diagnosis of small fiber involvement in peripheral neuropathy may also involve a skin biopsy in which a 3 mm-thick section of skin is removed from the calf by a punch biopsy, and is used to measure the skin intraepidermal nerve fiber density (IENFD), the density of nerves in the outer layer of the skin. Reduced density of the small nerves in the epidermis supports a diagnosis of small-fiber peripheral neuropathy.

Laboratory tests include blood tests for vitamin B-12 levels, a complete blood count, measurement of thyroid stimulating hormone levels, a comprehensive metabolic panel screening for diabetes and pre-diabetes, and a serum immunofixation test, which tests for antibodies in the blood.

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.

Plexopathy symptoms often resemble spinal cord disorders. A neurosurgical consultation is usually undertaken to ensure proper diagnosis, management, and treatment. Patients with chronic symptoms will likely be advised to follow up with outpatient care from either their health care provider or specialist.

EMG test is often performed together with another test called nerve conduction study, which measures the conducting function of nerves. NCV study shows loss of nerve conduction in the distal segment (3 to 4 days after injury). According to NCV study, in axonotmesis there is an absence of distal sensory-motor responses.

Electromyography (EMG) is a medical test performed to evaluate and record the electrical activity (electromyogram) produced by skeletal muscles using an instrument called electromyograph. In axonotmesis, EMG changes (2 to 3 weeks after injury) in the denervated muscles include:

1. Fibrillation potentials (FP)

2. Positive sharp waves

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."

The first steps in the evaluation and later management of plexopathy would consist of gathering a medical history and conducting a physical examination by a healthcare clinician. Motor function defect patterns detected within either the upper or lower extremities help with diagnosis of the disorder.

X-rays of the cervical spine, chest, and shoulder are usually ordered if symptoms point to acute Brachial plexopathy. If the physical history reveals a history of diabetes, collagen vascular disease, or symptoms of infection, the physician may order a series of blood tests including a complete blood count (CBC) and a comprehensive metabolic panel (CMP).

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 most MS-associated optic neuritis, visual function spontaneously improves over 2–3 months, and there is evidence that corticosteroid treatment does not affect the long term outcome. However, for optic neuritis that is not MS-associated (or atypical optic neuritis) the evidence is less clear and therefore the threshold for treatment with intravenous corticosteroids is lower. Intravenous corticosteroids also reduce the risk of developing MS in the following two years in patients with MRI lesions; but this effect disappears by the third year of follow up.

Paradoxically, oral administration of corticosteroids in this situation may lead to more recurrent attacks than in non-treated patients (though oral steroids are generally prescribed after the intravenous course, to wean the patient off the medication). This effect of corticosteroids seems to be limited to optic neuritis and has not been observed in other diseases treated with corticosteroids.

A Cochrane Systematic Review studied the effect of corticosteroids for treating people with acute optic neuritis. Specific corticosteroids studied included intravenous and oral methylprednisone, and oral prednisone. The authors conclude that current evidence does not show a benefit of either intravenous or oral corticosteroids for rate of recovery of vision (in terms of visual acuity, contrast sensitivity, or visual fields)..

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.

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.⁠

Optic neuritis typically affects young adults ranging from 18–45 years of age, with a mean age of 30–35 years. There is a strong female predominance. The annual incidence is approximately 5/100,000, with a prevalence estimated to be 115/100,000.

AON is a rare disease and the natural history of the disease process is not well defined. Unlike typical optic neuritis, there is no association with multiple sclerosis, but the visual prognosis for AON is worse than typical optic neuritis. Thus AON patients have different treatment, and often receive chronic immunosuppression. No formal recommendation can be made regarding the best therapeutic approach. However, the available evidence to date supports treatment with corticosteroids and other immunosuppressive agents.

Early diagnosis and prompt treatment with systemic corticosteroids may restore some visual function but the patient may remain steroid dependent; vision often worsens when corticosteroids are tapered. As such, long-term steroid-sparing immunosuppressive agents may be required to limit the side-effects of steroids and minimize the risk of worsening vision.

The diagnosis is based on symptoms and signs alone and objective testing is expected to be normal. This syndrome may be clinically tested by flexing the patients long finger while the patient extends the wrist and fingers. Pain is a positive finding.

The chief complaint of this disease is usually pain in the dorsal aspect of the upper forearm, and any weakness described is secondary to the pain. Tenderness to palpation occurs over the area of the radial neck. Also, the disease can be diagnosed by a positive "middle finger test", where resisted middle finger extension produces pain. Radiographic evaluation of the elbow should be performed to rule out other diagnoses.

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.

Signals from the sciatic nerve and it branches can be blocked, in order to interrupted transmission of pain signal from the innervation area, by performing a regional nerve blockade called a sciatic nerve block.

The treatment of peripheral neuropathy varies based on the cause of the condition, and treating the underlying condition can aid in the management of neuropathy. When peripheral neuropathy results from diabetes mellitus or prediabetes, blood sugar management is key to treatment. In prediabetes in particular, strict blood sugar control can significantly alter the course of neuropathy. In peripheral neuropathy that stems from immune-mediated diseases, the underlying condition is treated with intravenous immunoglobulin or steroids. When peripheral neuropathy results from vitamin deficiencies or other disorders, those are treated as well.

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 severe pain of HNA can be controlled with an anti-inflammatory drug such as prednisone, although it is unknown whether these anti-inflammatory drugs actually slow or stop the nerve degeneration process.

Nerve regeneration after an episode is normal, and in less severe cases a full recovery of the nerves and muscles can be expected. However, in a severe case permanent nerve damage may occur.

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.

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.

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.

EMG &NCV can help to treatment with the diagnosis of the location and severity of the lesion.

The Mayo Clinic proposed a revised set of criteria for diagnosis of Devic's disease in 2006. Those new guidelines require two absolute criteria plus at least two of three supportive criteria. In 2015 a new review was published by an international panel refining the previous clinical case definition but leaving the main criteria unmodified:

Absolute criteria:

1. Optic neuritis

2. Acute myelitis

Supportive criteria:

1. Brain MRI not meeting criteria for MS at disease onset

2. Spinal cord MRI with continuous T2-weighted signal abnormality extending over three or more vertebral segments, indicating a relatively large lesion in the spinal cord

3. NMO-IgG seropositive status (The NMO-IgG test checks the existence of antibodies against the aquaporin 4 antigen.)