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.

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.

TCAs include imipramine, amitriptyline, desipramine, and nortriptyline. They are generally regarded as first or second-line treatment for DPN. Of the TCAs, imipramine has been the best studied. These medications are effective at decreasing painful symptoms but suffer from multiple side effects that are dose-dependent. One notable side effect is cardiac toxicity, which can lead to fatal abnormal heart rhythms. Additional common side effects include dry mouth, difficulty sleeping, and sedation. At low dosages used for neuropathy, toxicity is rare, but if symptoms warrant higher doses, complications are more common. Among the TCAs, amitriptyline is most widely used for this condition, but desipramine and nortriptyline have fewer side effects.

Typical opioid medications, such as oxycodone, appear to be no more effective than placebo. In contrast, low-quality evidence supports a moderate benefit from the use of atypical opioids (e.g., tramadol and tapentadol), which also have SNRI properties. Opioid medications are recommended as second or third-line treatment for DPN.

Treatment is based on the underlying cause, if any. Where the likely underlying condition is known, treatment of this condition is indicated treated to reduce progression of the disease and symptoms. For cases without those conditions, there is only symptomatic treatment.

The treatment and management of radial neuropathy can be achieved via the following methods:

- Physical therapy or occupational therapy

- Surgery(depending on the specific area and extent of damage)

- Splinting

Treatment for ulnar neuropathy can entail:

NSAID (non-steroidal anti-inflammatory) medicines. there is also the option of cortisone. Another possible option is splinting, to secure elbow, a conservative procedure endorsed by some. In cases where surgery is needed, cubital tunnel release, where the ligament of the cubital tunnel is cut, thereby alleviating pressure on nerve can be performed.

Treatment for the common occurrence of ulnar neuropathy resulting from overuse, with no fractures or structural abnormalities, is treatment massage, ice, and anti-inflammatories. Specifically, deep tissue massage to the triceps, myofascial release for the upper arm connective tissue, and cross-fiber friction to the triceps tendon.

There is no current treatment, however management of hereditary neuropathy with liability to pressure palsy can be done via:

- Occupational therapist

- Ankle/foot orthosis

- Wrist splint (medicine)

- Avoid repetitive movements

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.

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.

There is currently no known pharmacological treatment to hereditary motor and sensory neuropathies. However, the majority of people with these diseases are able to walk and be self-sufficient. Some methods of relief for the disease include physical therapy, stretching, braces, and sometimes orthopedic surgery. Since foot disorders are common with neuropathy disorders precautions must be taken to strengthen these muscles and use preventative care and physical therapy to prevent injury and deformities.

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)..

Treatment is dependent upon diagnosis and the stage at which the diagnosis is secured. For toxic and nutritional optic neuropathies, the most important course is to remove the offending agent if possible and to replace the missing nutritional elements, orally, intramuscularly, or intravenously. If treatment is delayed, the injury may be irreversible. The course of treatment varies with the congenital forms of these neuropathies. There are some drug treatments that have shown modest success, such as Idebenone used to treat LOHN. Often treatment is relegated to lifestyle alterations and accommodations and supportive measures.

If a diagnosis of GCA is suspected, treatment with steroids should begin immediately. A sample (biopsy) of the temporal artery should be obtained to confirm the diagnosis and guide future management, but should not delay initiation of treatment. Treatment does not recover lost vision, but prevents further progression and second eye involvement. High dose corticosteroids may be tapered down to low doses over approximately one year.

Therapy for notalgia paresthetica is directed at controlling symptoms, as no cure exists for the condition. Available treatments include local anesthetics, topical capsaicin, topical corticosteroids, hydroxyzine, oxcarbazepine, palmitoylethanolamide and gabapentin. Paravertebral nerve block and botulinum toxin injections may also be helpful.

Some patients treated with low concentration topical capsaicin reported pain, burning, or tingling sensations with treatment, and symptoms returned within a month of ceasing treatment. Oxcarbazepine was reported to reduce the severity of symptoms in a few cases. One patient has been treated with "paravertebral nerve blocks, with bupivacaine and methylprednisolone acetate injected into the T3–T4 and T5–T6 intervertebral spaces" Hydroxyzine has also been used with considerable success in some cases as long as the pills are used daily.

High concentration topical capsaicin (8%, Qutenza) have been shown to be highly effective in treating neuropathic itch in some patients (including notalgia paresthetica) as well as in a recent proof-of-concept study, but this remains to be confirmed in randomised controlled trials.

Most recently intradermal injections of botulinum toxin type A (Botox) have been tried with some success. Even though botulinum normally wears off in three to six months, the treatment appears to be long term, and it has been theorised that botulinum type A effects lasting change in pain signaling. Unfortunately, repeated injections have been associated with diminished movement ability of the upper back and arms and its recommendation as a treatment has therefore become less popular.

Treatments typically include rest, manipulation, strengthening of tibialis anterior, tibialis posterior, peroneus and short toe flexors, casting with a walker boot, corticosteroid and anesthetic injections, hot wax baths, wrapping, compression hose, and orthotics. Medications may include various anti-inflammatories such as Anaprox, or other medications such as Ultracet, Neurontin and Lyrica. Lidocaine patches are also a treatment that helps some patients.

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.

Currently, tendon transfers are being studied as a means of improving radial, medial, and ulnar nerve palsy.

Rapid blood transfusions, to correct anemia and raise blood pressure, may improve PION outcomes. In one report of a related disease, hypotension-induced AION, 3 out of 3 patients who received rapid transfusions reported partial recovery of vision. While rapid transfusions offer some hope, the prognosis for perioperative PION remains poor. Prevention remains the best way to reduce PION.

One retrospective report proposes that incidence of PION could be reduced in high-risk cases by altering surgical management. For example, for patients undergoing spine surgery, measures could be taken to minimize intraoperative hypotension, to accelerate the process of blood replacement, and to aggressively treat facial swelling.

There are multiple ways that tarsal tunnel can be treated and the pain can be reduced. The initial treatment, whether it be conservative or surgical, depends on the severity of the tarsal tunnel and how much pain the patient is in. There was a study done that treated patients diagnosed with tarsal tunnel syndrome with a conservative approach. Meaning that the program these patients were participated in consisted of physiotherapy exercises and orthopedic shoe inserts in addition to that program. There were fourteen patients that had supplementary tibial nerve mobilization exercises. They were instructed to sit on the edge of a table in a slumped position, have their ankle taken into dorsiflexion and ankle eversion then the knee was extended and flexed to obtain the optimal tibial nerve mobilization. Patients in both groups showed positive progress from both programs. The medial calcaneal, medial plantar and lateral plantar nerve areas all had a reduction in pain after successful nonoperative or conservative treatment. There is also the option of localized steroid or cortisone injection that may reduce the inflammation in the area, therefore relieving pain. Or just a simple reduction in the patient’s weight to reduce the pressure in the area.

Treatment of toxic and nutritional optic neuropathy is dictated by the cause of the disorder.

- Toxic optic neuropathy is treated by identification and removal of the offending agent. Depending upon the individual affected, the nature of the agent, total exposure prior to removal, and degree of vision loss at the time of diagnosis, the prognosis is variable.

- Nutritional optic neuropathy is treated with improved nutrition. A well-balanced diet with plenty of protein and green leafy vegetables, vitamin supplementation (thiamine, vitamin B, folic acid, multivitamins), and reduction of smoking and/or drinking are the mainstay of treatment. Again, prognosis is variable and dependent upon the affected individual, treatment compliance, and degree of vision loss at diagnosis.

In both toxic and nutritional neuropathy, vision generally recovers to normal over several days to weeks, though it may take months for full restoration and there is always the risk of permanent vision loss. Visual acuity usually recovers before color vision.

Once NAION happens, it was thought that there was no accepted treatment to reverse the damage. However, a recent uncontrolled retrospective large study has shown that if patients are treated with large doses of corticosteroid therapy during the early stages of NAION, in eyes with initial visual acuity of 20/70 or worse, seen within 2 weeks of onset, there was visual acuity improvement in 70% in the treated group compared to 41% in the untreated group (odds ratio of improvement: 3.39; 95% CI:1.62, 7.11; p ¼ 0.001). That study and a natural history study on NAION (Ophthalmology 2008;115: 298–305.) showed that visual acuity can improve up to 6 months and not after that. To minimize the risk of further visual loss in the fellow eye or the same eye, it is essential to reduce the risk factors. Common sense dictates trying to control the cardiovascular risk factors for many reasons, including protection from this happening to the second eye. Sudden vision loss should lead to an ophthalmological consultation. If NAION is suspected, then ideally a neuro-ophthalmologist's consultation should be obtained.

A recent Cochrane Review sought to determine the extent of safety and efficacy of optic nerve decompression surgery for NAION, compared to other treatments, or no treatment. The one study included in the review found no improvements in visual acuity among patients who underwent surgery for NAION, and adverse events (pain, double vision) experienced by participants who underwent surgery.

There is much research currently underway looking at ways to protect the nerve (neuroprotection) or even regenerate new fibers within the optic nerve. So far there is no evidence in human studies that the so-called neuroprotectors have any beneficial effect in NAION.

However, there is a new current clinical trial for the treatment of NAION in the United States with plans to include sites in India, Israel, Germany and Australia (see NORDICclinicaltrials.com and https://clinicaltrials.gov/). This trial will test the use of a synthetic siRNA that blocks caspase 2, an important enzyme in the apoptosis cycle.

In addition to such research, patents have been applied for by Pfizer, The University of Southern California, Otsuka Pharmaceutical and other individual inventors for innovations related to the treatment of anterior ischemic optic neuropathy.

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.

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.