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.

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.

In terms of the diagnosis of radial neuropathy the following tests/exams can be done to ascertain the condition:

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.

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

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.

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

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.

The prognosis for complete recovery is dependent upon many factors. The most important of these is the severity and duration of compression upon the damaged nerve(s). Generally, the longer the time before intervention to remove the compression causing nerve damage, the greater the damage caused to the nerve(s).

Damage can be so severe that nerve regrowth is impossible, and the nerve damage will be permanent. In cases where the nerve has been damaged but is still capable of regrowth, recovery time is widely variable. Surgical intervention with decompression of the cauda equina can assist recovery. Delayed or severe nerve damage can mean up to several years' recovery time because nerve growth is exceptionally slow.

Review of the literature indicates that around 50-70% of patients have urinary retention (CES-R) on presentation with 30-50% having an incomplete syndrome (CES-I). The latter group, especially if the history is less than a few days, usually requires emergency MRI to confirm the diagnosis followed by prompt decompression. CES-I with its more favourable prognosis may become CES-R at a later stage.

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.

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 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.

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.

A thorough medical history and physical examination, including a neurological examination, are the first steps in making a diagnosis. This alone may be sufficient to diagnose Bell's Palsy, in the absence of other findings. Additional investigations may be pursued, including blood tests such as ESR for inflammation, and blood sugar levels for diabetes. If other specific causes, such as sarcoidosis or Lyme disease are suspected, specific tests such as angiotensin converting enzyme levels, chest x-ray or Lyme titer may be pursued. If there is a history of trauma, or a tumour is suspected, a CT scan may be used.

Examination for pain sensation, by pinprick, shows leg (lumbar nerves) analgesia with perineal (sacral nerves) escape. The maintenance of perineal sensation with absence of pain sensation over the lumbar nerve roots is typical for an extra-medullary and intra-thecal (outside the cord and within the dural sheath) process. Inability to walk, with this unusual sensory examination completes a triad of signs and usually represents spinal tuberculosis. The triad is paraplegia with lumbar loss of pain sensation and presence of perineal altered sensation.

Diagnosis is usually confirmed by an MRI scan or CT scan, depending on availability. Early surgery in acute onset of severe cases has been reported to be important.

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.

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.

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.

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.

Because there are various causes for back injuries, prevention must be comprehensive. Back injuries are predominant in manual labor so the majority low back pain prevention methods have been applied primarily toward biomechanics Prevention must come from multiple sources such as education, proper body mechanics, and physical fitness.

Facial nerve paralysis may be divided into supranuclear and infranuclear lesions.

The symptoms are usually not subtle, although asymptomatic events have been documented. Autonomic dysreflexia differs from autonomic instability, the various modest cardiac and neurological changes that accompany a spinal cord injury, including bradycardia, orthostatic hypotension, and ambient temperature intolerance. In autonomic dysreflexia, patients will experience hypertension, sweating, spasms (sometimes severe spasms) and erythema (more likely in upper extremities) and may suffer from headaches and blurred vision. Mortality is rare with AD, but morbidity such as stroke, retinal hemorrhage and pulmonary edema if left untreated can be quite severe. Older patients with very incomplete spinal cord injuries and systolic hypertension without symptoms are usually experiencing essential hypertension, not autonomic dysreflexia. Aggressive treatment of these elderly patients with rapidly acting antihypertensive medications can have disastrous results.

The cause of autonomic dysreflexia itself can be life-threatening, and must also be completely investigated and treated appropriately to prevent unnecessary morbidity and mortality.

The Consortium for Spinal Cord Medicine has developed evidence-based clinical practice guidelines for the management of autonomic dysreflexia in adults, children, and pregnant women. There is also a consumer version of this guideline.

The most-often prescribed treatments for early-stage RSIs include analgesics, myofeedback, biofeedback, physical therapy, relaxation, and ultrasound therapy. Low-grade RSIs can sometimes resolve themselves if treatments begin shortly after the onset of symptoms. However, some RSIs may require more aggressive intervention including surgery and can persist for years.

General exercise has been shown to decrease the risk of developing RSI. Doctors sometimes recommend that RSI sufferers engage in specific strengthening exercises, for example to improve sitting posture, reduce excessive kyphosis, and potentially thoracic outlet syndrome. Modifications of posture and arm use (human factors and ergonomics) are often recommended.