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.

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.

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.

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

There are a number of colloquial terms used to describe radial nerve injuries, which are usually dependent on the causation factor:

- Saturday night palsy from falling asleep with one's arm hanging over the arm rest of a chair, compressing the radial nerve at the spiral groove.

- Honeymoon palsy from another individual sleeping on and compressing one's arm overnight. This can also refer to anterior interosseous nerve palsy from compression on the forearm resulting in an inability to flex the index and thumb tips. In this interpretation, it is a branch of the median nerve and not the radial nerve which is affected.

- Handcuff neuropathy from tight-fitting handcuffs compressing the superficial branch of the distal radial nerve; this is also referred to as cheiralgia paresthetica.

- Crutch palsy from poorly fitted axillary crutches.

- Squash palsy, from traction forces in a manner usually associated with the sport squash, can happen to squash players during prolonged periods between matches.

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."

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.

Treatment varies. In most cases, the best treatment is to remove the cause of compression by modifying patient behavior, in combination with medical treatment to relieve inflammation and pain. Whatever the cause, typical treatment takes several weeks to months—depending on the degree of nerve damage. Typical treatment options include:

- Active Release Technique (ART) soft tissue treatment

- Wearing looser clothing and suspenders rather than belts

- Weight loss if obesity is present

- Non-steroidal anti-inflammatory drugs (NSAIDs) to reduce inflammatory pain if pain level limits motion and prevents sleep

- Reducing physical activity in relation to pain level. Acute pain may require absolute bed rest

- Deep tissue massage to reduce tension in the gluteal muscles, most commonly the gluteus maximus. The tensor fasciae latae may also be implicated.

The lateral cutaneous nerve of the thigh can occasionally be damaged during laparoscopic hernia repair, or scarring from the operation can lead to meralgia paraesthetica.

For lower pain levels, treatment may involve having the patient:

- Seek appropriate physical therapy, such as stretching and massage, which plays a large role in the management of pain

- Learn to perform inguinal ligament stretching (from a physical therapist or from a YouTube video) which can rapidly relieve symptoms

- Use rest periods to interrupt long periods of standing, walking, cycling, or other aggravating activity

- Lose weight, and exercise to strengthen abdominal muscles

- Wear clothing that is loose at the upper front hip area

- Apply heat, ice, or electrical stimulation

- Take nonsteroidal anti-inflammatory medications for 7–10 days

- Remove hair in affected area (shave)

- Lidocaine patches (must shave area first)

- Titanium dioxide patches to interfere with the electrostatic effect of the nerves on the surface of the skin

Pain may take significant time (weeks) to stop and, in some cases, numbness persists despite treatment. In severe cases, the physician might perform a local nerve block at the inguinal ligament, using a combination of local anaesthetic (lidocaine) and corticosteroids to provide relief that may last several weeks. Pain modifier drugs for neuralgic pain (such as amitriptyline, carbamazepine or gabapentin) may be tried, but are often not as helpful in the majority of patients.

Persistent and severe cases may require surgery to decompress the nerve or, as a last resort, to resect the nerve. The latter treatment leaves permanent numbness in the area.

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.⁠

Nerve compression syndrome or compression neuropathy, also known as entrapment neuropathy, is a medical condition caused by direct pressure on a nerve. It is known colloquially as a "trapped nerve", though this may also refer to nerve root compression (by a herniated disc, for example). Its symptoms include pain, tingling, numbness and muscle weakness. The symptoms affect just one particular part of the body, depending on which nerve is affected. Nerve conduction studies help to confirm the diagnosis. In some cases, surgery may help to relieve the pressure on the nerve but this does not always relieve all the symptoms. Nerve injury by a single episode of physical trauma is in one sense a compression neuropathy but is not usually included under this heading.

There are several options of treatment when iatrogenic (i.e., caused by the surgeon) spinal accessory nerve damage is noted during surgery. For example, during a functional neck dissection that injures the spinal accessory nerve, injury prompts the surgeon to cautiously preserve branches of C2, C3, and C4 spinal nerves that provide supplemental innervation to the trapezius muscle. Alternatively, or in addition to intraoperative procedures, postoperative procedures can also help in recovering the function of a damaged spinal accessory nerve. For example, the Eden-Lange procedure, in which remaining functional shoulder muscles are surgically repositioned, may be useful for treating trapezius muscle palsy.

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

Splinting, non-steroidal anti inflammatory drugs (NSAIDs), and corticosteroid injections are regarded as conservative first-line treatments for stenosing tenosynovitis. However, NSAIDs have been found to be ineffective as a monotherapy. Early treatment of trigger thumb has been associated with better treatment outcomes. Surgical treatment of trigger thumb can be complicated by injury to the digital nerves, scarring, tenderness, or a contracture of the joint. A significantly higher rate of symptom improvement has been observed when surgical management is paired with corticosteroid injections when compared to corticosteroid injections alone.

Occupational therapy is based on relieving the symptoms and reducing the inflammation. Overall cure rate, for dutifully applied non-operative treatment, is over 95% [citation needed]. Several modalities of treatment exists, depending on the chronicity and severity of the condition.

- Modification of hand activities

- Exercise & stretching

- Local heat

- Extension splinting during sleep (custom metacarpophalangeal joint (MCP joint) blocking splint, which has reported better patient's symptomatic relief and functionality and a distal interphalangeal (DIP) joint blocking splint)

Treatment consists of injection of methylprednisolone often combined with anesthetic (lidocaine) at the site of maximal inflammation or tenderness. The infiltration of the affected site can be performed blinded or sonographically guided, and often needs to be repeated 2 or three times to achieve remission. An irreducibly locked trigger, often associated with a flexion contracture of the PIP joint, should not be treated by injections.

- Transection of the fibrous annular pulley of the sheath

For symptoms that have persisted or recurred for more than 6 months and/or have been unresponsive to conservative treatment, surgical release of the pulley may be indicated. The main surgical approaches are percutaneous release and open release. The percutaneous approach, is preferred in some centers due to its reported shorter time of recuperation of motor function, less complications, and less painful. Complication of the surgical management include, persistent trigger finger, bowstringing, digital nerve injury, and continued triggering.

Of note, diabetes seems to be a poor prognostic indicator for nonoperative treatment and may develop stiffness after surgical release.

Meralgia paresthetica or meralgia paraesthetica (or Bernhardt-Roth syndrome), is numbness or pain in the outer thigh not caused by injury to the thigh, but by injury to a nerve that extends from the spinal column to the thigh.

This chronic neurological disorder involves a single nerve—the lateral cutaneous nerve of thigh, which is also called the lateral femoral cutaneous nerve (and hence the syndrome lateral femoral cutaneous neuropathy). The term "meralgia paraesthetica" combines four Greek roots to mean "thigh pain with anomalous perception". The disorder has also been nicknamed skinny pants syndrome, in reference to a rise in teenagers wearing skin-tight pants.

According to medical professionals with the Cleveland Clinic, once an athlete suffers from an episode of cervical spinal cord, team physician or athletic trainer first stabilize the head and neck followed by a thorough neurologic inspection. If the injury is deemed severe, injured parties should be taken to a hospital for evaluation. Athletes that suffer from severe episodes of neurapraxia are urged to consult orthopaedic or spinal medical specialists. In mild cases of neurapraxia, the athlete is able to remove themselves from the field of play. However, the athlete is still advised to seek medical consultation.

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.

The posterior interosseous nerve (or dorsal interosseous nerve) is a nerve in the forearm. It is the continuation of the deep branch of the radial nerve, after this has crossed the supinator muscle. It is considerably diminished in size compared to the deep branch of the radial nerve. The nerve fibers originate from cervical segments C7 and C8.

While the exact incidence is unknown, estimates range from 33 - 57 percent of patients staying in the ICU for longer than 7 days. More exact data is difficult to obtain, since variation exists in defining the condition.

The three main risk factors for CIP and CIM are sepsis and systemic inflammatory response syndrome (SIRS), and multi-organ failure. Reported rates of CIP/CIM in people with sepsis and SIRS range from 68 to 100 percent. Additional risk factors for developing CIP/CIM include: female gender, high blood sugar (hyperglycemia), low serum albumin, and immobility. A greater severity of illness increases the risk of CIP/CIM. Such risk factors include: multi-organ dysfunction, renal failure, renal replacement therapy, duration of organ dysfunction, duration of ICU stay, low albumin, and central neurologic failure.

Certain medications are associated with CIP/CIM, such as corticosteroids, neuromuscular blocking agents, vasopressors, catecholamines, and intravenous nutrition (parenteral nutrition). Research has produced inconsistent results for the impact of hypoxia, hypotension, hyperpyrexia, and increased age on the risk of CIP/CIM. The use of aminoglycosides is "not" an independent risk for the development of CIP/CIM.

Anterior interosseous syndrome or Kiloh-Nevin syndrome I is a medical condition in which damage to the anterior interosseous nerve (AIN), a motor branch of the median nerve, causes pain in the forearm and a characteristic weakness of the pincer movement of the thumb and index finger.

Most cases of AIN syndrome are due to a transient neuritis, although compression of the AIN can happen. Trauma to the median nerve have also been reported as a cause of AIN syndrome.

Although there is still controversy among upper extremity surgeons, AIN syndrome is now regarded as a neuritis (inflammation of the nerve) in most cases; this is similar to Parsonage–Turner syndrome. Although the exact etiology is unknown, there is evidence that it is caused by an immune mediated response.

Studies are limited, and no randomized controlled trials have been performed regarding the treatment of AIN syndrome. While the natural history of AIN syndrome is not fully understood, studies following patients who have been treated without surgery show that symptoms can resolve starting as late as one year after onset. Other retrospective studies have shown that there is no difference in outcome in surgically versus nonsurgically treated patients. Surgical decompression is rarely indicated in AIN syndrome. Indications for considering surgery include a known space-occupying lesion that is compressing the nerve (a mass) and persistent symptoms beyond 1 year of conservative treatment.

This method should be used within the first 48–72 hours after the injury in order to speed up the recovery process.

Heat: Applying heat to the injured area can cause blood flow and swelling to increase.

Alcohol: Alcohol can inhibit your ability to feel if your injury is becoming more aggravated, as well as increase blood flow and swelling.

Re-injury: Avoid any activities that could aggravate the injury and cause further damage.

Massage: Massaging an injured area can promote blood flow and swelling, and ultimately do more damage if done too early.

Anesthesia dolorosa or anaesthesia dolorosa or deafferentation pain is pain felt in an area (usually of the face) which is completely numb to touch. The pain is described as constant, burning, aching or severe. It can be a side effect of surgery involving any part of the trigeminal system, and occurs after 1–4% of peripheral surgery for trigeminal neuralgia. No effective medical therapy has yet been found. Several surgical techniques have been tried, with modest or mixed results. The value of surgical interventions is difficult to assess because published studies involve small numbers of mixed patient types and little long term follow-up.

- Gasserian ganglion stimulation is stimulation of the gasserian ganglion with electric pulses from a small generator implanted beneath the skin. There are mixed reports, including some reports of marked, some of moderate and some of no improvement. Further studies of more patients with longer follow-up are required to determine the efficacy of this treatment.

- Deep brain stimulation was found in one review to produce good results in forty-five percent of 106 cases. Though relief may not be permanent, several years of relief may be achieved with this technique.

- Mesencephalotomy is the damaging of the junction of the trigeminal tract and the periaqueductal gray in the brain, and has produced pain relief in a group of patients with cancer pain; but when applied to six anesthesia dolorosa patients, no pain relief was achieved, and the unpleasant sensation was in fact increased.

- Dorsal root entry zone lesioning, damaging the point where sensory nerve fibers meet spinal cord fibers, produced favorable results in some patients and poor results in others, with incidence of ataxia at 40%. Patient numbers were small, follow-up was short and existing evidence does not indicate long term efficacy.

- One surgeon treated thirty-five patients using trigeminal nucleotomy, damaging the nucleus caudalis, and reported 66% "abolition of allodynia and a marked reduction in or (less frequently) complete abolition of deep background pain."

Injury to the spinal accessory nerve can cause an accessory nerve disorder or spinal accessory nerve palsy, which results in diminished or absent function of the sternocleidomastoid muscle and upper portion of the trapezius muscle.

Foot drop is a gait abnormality in which the dropping of the forefoot happens due to weakness, irritation or damage to the common fibular nerve including the sciatic nerve, or paralysis of the muscles in the anterior portion of the lower leg. It is usually a symptom of a greater problem, not a disease in itself. Foot drop is characterized by inability or impaired ability to raise the toes or raise the foot from the ankle (dorsiflexion). Foot drop may be temporary or permanent, depending on the extent of muscle weakness or paralysis and it can occur in one or both feet. In walking, the raised leg is slightly bent at the knee to prevent the foot from dragging along the ground.

Foot drop can be caused by nerve damage alone or by muscle or spinal cord trauma, abnormal anatomy, toxins, or disease. Toxins include organophosphate compounds which have been used as pesticides and as chemical agents in warfare. The poison can lead to further damage to the body such as a neurodegenerative disorder called organophosphorus induced delayed polyneuropathy. This disorder causes loss of function of the motor and sensory neural pathways. In this case, foot drop could be the result of paralysis due to neurological dysfunction. Diseases that can cause foot drop include trauma to the posterolateral neck of fibula, stroke, amyotrophic lateral sclerosis, muscular dystrophy, poliomyelitis, Charcot Marie Tooth disease, multiple sclerosis, cerebral palsy, hereditary spastic paraplegia, Guillain–Barré syndrome, and Friedreich's ataxia. It may also occur as a result of hip replacement surgery or knee ligament reconstruction surgery.

Stenosing tenosynovitis is most commonly caused by overuse from chronic repetitive activities using the hand or the involved finger. Examples include work activities (e.g., computer use, materials handling) or recreational activities (e.g., knitting, golf, racket sports). Carpenters who use hammers suffer from this as well as those who continuously grip wood or other materials when cutting them due to having to use your hands as a clamp to hold things in place.

Primary stenosing tenosynovitis can be idiopathic, occurring in middle age women more frequently than in men, but can present also in infancy.

Secondary stenosing tenosynovitis can be caused by disease or entities that cause connective tissue disorders including the following:

- Rheumatoid arthritis and psoriatic arthritis—therefore the clinician must assess the hands for rheumatologic deformities.

- Gout

- Diabetes mellitus

- Amyloidosis

- Systemic lupus erythematosus

Others causes may include the following:

- Direct trauma to the site

- During the postpartum period

- Congenital

CIP/CIM can lead to difficulty weaning a person from a mechanical ventilator, and is associated with increased length of stay in the ICU and increased mortality (death). It can lead to impaired rehabilitation. Since CIP/CIM can lead to decreased mobility (movement), it increases the risk of pneumonia, deep vein thrombosis, and pulmonary embolism.

Critically ill people that are in a coma can become completely paralyzed from CIP/CIM. Improvement usually occurs in weeks to months, as the innervation to the muscles are restored. About half of patients recover fully.