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)..

A range of medications that act on the central nervous system has been found to be useful in managing neuropathic pain. Commonly used treatments include tricyclic antidepressants (such as nortriptyline or amitriptyline), the serotonin-norepinephrine reuptake inhibitor (SNRI) medication duloxetine, and antiepileptic therapies such as gabapentin, pregabalin, or sodium valproate. Few studies have examined whether nonsteroidal anti-inflammatory drugs are effective in treating peripheral neuropathy.

Symptomatic relief for the pain of peripheral neuropathy may be obtained by application of topical capsaicin. Capsaicin is the factor that causes heat in chili peppers. The evidence suggesting that capsaicin applied to the skin reduces pain for peripheral neuropathy is of moderate to low quality and should be interpreted carefully before using this treatment option. Local anesthesia often is used to counteract the initial discomfort of the capsaicin. Some current research in animal models has shown that depleting neurotrophin-3 may oppose the demyelination present in some peripheral neuropathies by increasing myelin formation.

High-quality evidence supports the use of cannabis for neuropathic pain.

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.

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.

Mild cases are usually treated by the administration of analgesia and muscle relaxers. Reduced and limited physical activity with repeated follow-ups with the health care provider are required for one diagnosed with plexopathy. Individuals with prolonged, chronic symptoms will require additional testing and treatment. With brachial plexopathy, surgical decompression may be warranted if the pathophysiology of the disease is causing pressure on the affected nerves. In some cases of brachial plexopathy, no treatment is required and recovery happens on its own. Treatment for lumbosacral plexopathy that is not caused by trauma, but instead from diabetic plexopathy, is directed at controlling the person's blood sugar level. By preventing the deterioration of the nerve fibers from hyperglycemia, patients may recover significant muscle strength. For radiation-induced plexopathies, treatment options are limited to pain/symptom mananagement and provision of assistive devices.

Schwann cells provide the nerve with protection through the production of Nerve Growth Factors, and because these cells are intact this kind of nerve injury can be cured and normal feeling and sensations can be restored. Surgery can be done in order to help the nerve heal. The surgery will help with nerve regeneration, providing guidance to the nerve sprouts on where to attach on the proximal side of the injury. Damaged nerve axons can reattach themselves after surgery. Treatment of axonotmesis also consists of:

- Physical therapy or Occupational Therapy. Physical or Occupational therapy aims include:

- Pain relief

- Maintain range of motion

- Reducing muscular atrophy

- Patient education

- Use of assistive devices (Orthotic needs)

While pain symptoms may be effectively controlled using medications such as NSAID, amitriptyline, or vitamin B6 supplementation, effective treatment generally requires resolving the underlying cause.

Mild to moderate symptoms, such as pain or paresthesia, are treated conservatively with non-surgical approaches. Physiotherapy treatments can prove effective at treating cubital tunnel syndrome symptoms and can include:

- Joint mobilizations

- Neural flossing/gliding

- Strengthening/stretching exercises

- Activity modification

It is important to identify positions and activities that aggravate symptoms and to find ways to avoid them. For example, if the person experiences symptoms when holding a telephone up to the head, then the use of a telephone headset will provide immediate symptomatic relief and reduce the likelihood of further damage and inflammation to the nerve. For cubital tunnel syndrome, it is recommended to avoid repetitive elbow flexion and also avoiding prolonged elbow flexion during sleep, as this position puts stress of the ulnar nerve.

Surgery is recommended for those who are not improved with conservative therapy or those with serious or progressive symptoms. The surgical approaches vary, and may depend on the location or cause of impingement. Cubital and ulnar tunnel release can be performed wide awake with no general anaesthesia, no regional anaesthesia, no sedation and no tourniquet, and are usually done by Plastic Surgeons

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.

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.⁠

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.

Physiotherapy

To increase strength of muscle

To improve muscle functions

Electrical modalities =Electric stimulation.etc.

Occupational Therapy

Positioning, ROM, Sensory, Splinting

The prognosis is usually good in terms of recovery. Rate of recovery depends on the distance from the site of injury, and axonal regeneration can go up to 1 inch per month. Complete recovery can take anywhere from 6 months to a year

Attacks are treated with short courses of high dosage intravenous corticosteroids such as methylprednisolone IV.

Plasmapheresis can be an effective treatment when attacks progress or do not respond to corticosteroid treatment. Clinical trials for these treatments contain very small numbers, and most are uncontrolled, though some report high success percentage.

There are many treatments to facilitate the process of recovery in people who have brachial plexus injuries. Improvements occur slowly and the rehabilitation process can take up to many years. Many factors should be considered when estimating recovery time, such as initial diagnosis of the injury, severity of the injury, and type of treatments used. Some forms of treatment include nerve grafts, medication, surgical decompression, nerve transfer, physical therapy, and occupational therapy.

Treatment for brachial plexus injuries includes orthosis/splinting, occupational or physical therapy and, in some cases, surgery. Some brachial plexus injuries may heal without treatment. Many infants improve or recover within 6 months, but those that do not have a very poor outlook and will need further surgery to try to compensate for the nerve deficits. The ability to bend the elbow (biceps function) by the third month of life is considered an indicator of probable recovery, with additional upward movement of the wrist, as well as straightening of thumb and fingers an even stronger indicator of excellent spontaneous improvement. Gentle range of motion exercises performed by parents, accompanied by repeated examinations by a physician, may be all that is necessary for patients with strong indicators of recovery.

The exercises mentioned above can be done to help rehabilitate from mild cases of the injury. However, in more serious brachial plexus injuries surgical interventions can be used. Function can be restored by nerve repairs, nerve replacements, and surgery to remove tumors causing the injury. Another crucial factor to note is that psychological problems can hinder the rehabilitation process due to a lack of motivation from the patient. On top of promoting a lifetime process of physical healing, it is important to not overlook the psychological well-being of a patient. This is due to the possibility of depression or complications with head injuries.

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.

Currently, there is no cure for Devic's disease, but symptoms can be treated. Some patients recover, but many are left with impairment of vision and limbs, which can be severe.

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 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.

Proper management of diabetes mellitus can prevent proximal diabetic neuropathy from ever occurring.

The incidence of proximal diabetic neuropathy incidence is thought to be correlated to blood glucose control in diabetics, and is likely reversible with better control.

Medication helps reduce the pain involved in proximal diabetic neuropathy. Most patients take oral medication that is prescribed by a doctor. Common types of medication used to treat diabetic amyotrophy include anticonvulsives (e.g. gabapentin, pregabalin) as well as opioid medications, although the latter category is not optimally indicated for neuropathic pain.

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.

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."

Non-surgical methods of treatment are usually attempted first, leaving surgery as a last resort. Pain medications are often prescribed as the first attempt to alleviate the acute pain and allow the patient to begin exercising and stretching. There are a variety of other non-surgical methods used in attempts to relieve the condition after it has occurred, often in combination with pain killers. They are either considered indicated, contraindicated, relatively contraindicated, or inconclusive based on the safety profile of their risk-benefit ratio and on whether they may or may not help:

In the majority of cases, spinal disc herniation doesn't require surgery, and a study on sciatica, which can be caused by spinal disc herniation, found that "after 12 weeks, 73% of people showed reasonable to major improvement without surgery." The study, however, did not determine the number of individuals in the group that had sciatica caused by disc herniation.

- Initial treatment usually consists of non-steroidal anti-inflammatory pain medication (NSAIDs), but the long-term use of NSAIDs for people with persistent back pain is complicated by their possible cardiovascular and gastrointestinal toxicity.

- Epidural corticosteroid injections provide a slight and questionable short-term improvement in those with sciatica but are of no long term benefit. Complications occur in 0 to 17% of cases when performed on the neck and most are minor. In 2014, the US Food and Drug Administration (FDA) suggested that the "injection of corticosteroids into the epidural space of the spine may result in rare but serious adverse events, including loss of vision, stroke, paralysis, and death." and that "The effectiveness and safety of epidural administration of corticosteroids have not been established, and FDA has not approved corticosteroids for this use.".

Depending on the severity of the lesion, physicians may recommend either conservative treatment or surgery. The first step is simply to rest and modify daily activities that aggravate the symptoms. Patients may be prescribed anti-inflammatory drugs, Physical or Occupational therapy, splints for the elbow and wrists, and corticosteroid injections as well. This is the most common treatment for CTS. Especially involving compression at the wrist, such as in CTS, it is possible to recover without treatment. Physical therapy can help build muscle strength and braces or splints help recover. In pronator teres syndrome, specifically, immobilization of the elbow and mobility exercise within a pain-free range are initially prescribed. However, if the patient is not relieved of symptoms after a usual 2 to 3 month refractory period, then decompression surgery may be required. Surgery involves excising the tissue or removing parts of the bone compressing the nerve.

Many tendon transfers have been shown to restore opposition to the thumb and provide thumb and finger flexion. In order to have optimal results the individual needs to follow the following principles of tendon transfer: normal tissue equilibrium, movable joints, and a scar-free bed. If these requirements are met then certain factors need to be considered such as matching up the lost muscle mass, fiber length, and cross-sectional area and then pick out muscle-tendon units of similar size, strength, and potential excursion.

For patients with low median nerve palsy, it has been shown that the flexor digitorum superficialis of the long and ring fingers or the wrist extensors best approximate the force and motion that is required to restore full thumb opposition and strength. This type of transfer is the preferred method for median nerve palsy when both strength and motion are required. In situations when only thumb mobility is desired, the extensor indicis proprius is an ideal transfer.

For high median nerve palsy, the brachioradialis or the extensor carpi radialis longus transfer is more appropriate to restore lost thumb flexion and side-to-side transfer of the flexor digitorum profundus of the index finger are generally sufficient. To restore independent flexion of the index finger could be performed by using the pronator teres or extensor carpi radialis ulnaris tendon muscle units. All of the mentioned transfers are generally quite successful because they combine a proper direction of action, pulley location, and tendon insertion.