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.

Though a neuroma is a soft tissue abnormality and will not be visualized on standard radiographs, the first step in the assessment of forefoot pain is an X-ray in order to evaluate for the presence of arthritis and exclude stress fractures/reactions and focal bone lesions, which may mimic the symptoms of a neuroma. Ultrasound (sonography) accurately demonstrates thickening of the interdigital nerve within the web space of greater than 3mm, diagnostic of a Morton’s neuroma. This typically occurs at the level of the intermetatarsal ligament. Frequently, intermetatarsal bursitis coexists with the diagnosis. Other conditions that may also be visualized with ultrasound and can be clinically confused with a neuroma include synovitis/capsulitis from the adjacent metatarsophalangeal joint, stress fractures/reaction, and plantar plate disruption. MRI can similarly demonstrate the above conditions; however, in the setting where more than one abnormality coexists, ultrasound has the added advantage of determining which may be the source of the patient’s pain by applying direct pressure with the probe. Further to this, ultrasound can be used to guide treatment such as cortisone injections into the webspace, as well as alcohol ablation of the nerve.

As stated earlier, musculoskeletal disorders can cost up to $15–$20 billion in direct costs or $45–$55 billion in indirect expenses. This is about $135 million a day Tests that confirm or correct TTS require expensive treatment options like x-rays, CT-scans, MRI and surgery. 3 former options for TTS detect and locate, while the latter is a form of treatment to decompress tibial nerve pressure Since surgery is the most common form of TTS treatment, high financial burden is placed upon those diagnosed with the rare syndrome.

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.⁠

Diagnosis is based upon physical examination findings. Patients' pain history and a positive Tinel's sign are the first steps in evaluating the possibility of tarsal tunnel syndrome. X-ray can rule out fracture. MRI can assess for space occupying lesions or other causes of nerve compression. Ultrasound can assess for synovitis or ganglia. Nerve conduction studies alone are not, but they may be used to confirm the suspected clinical diagnosis. Common causes include trauma, varicose veins, neuropathy and space-occupying anomalies within the tarsal tunnel. Tarsal tunnel syndrome is also known to affect both athletes and individuals that stand a lot.

A Neurologist or a Physiatrist usually administers nerve conduction tests or supervises a trained technologist. During this test, electrodes are placed at various spots along the nerves in the legs and feet. Both sensory and motor nerves are tested at different locations. Electrical impulses are sent through the nerve and the speed and intensity at which they travel is measured. If there is compression in the tunnel, this can be confirmed and pinpointed with this test. Some doctors do not feel that this test is necessarily a reliable way to rule out TTS. Some research indicates that nerve conduction tests will be normal in at least 50% of the cases.

Given the unclear role of electrodiagnostics in the diagnosis of tarsal tunnel syndrome, efforts have been made in the medical literature to determine which nerve conduction studies are most sensitive and specific for tibial mononeuropathy at the level of the tarsal tunnel. An evidence-based practice topic put forth by the professional organization, the American Association of Neuromuscular & Electrodiagnostic Medicine has determined that Level C, Class III evidence exists for the use of tibial motor nerve conduction studies, medial and lateral plantar mixed nerve conduction studies, and medial and lateral plantar sensory nerve conduction studies. The role of needle electromyography remains less defined.

Tarsal Tunnel Syndrome (TTS) is most closely related to Carpal Tunnel Syndrome (CTS). However, the commonality to its counterpart is much less or even rare in prevalence Studies have found that patients with rheumatoid arthritis (RA) show signs of distal limb neuropathy. The posterior tibial nerve serves victim to peripheral neuropathy and often show signs of TTS amongst RA patients. Therefore, TTS is a common discovery found in the autoimmune disorder of rheumatoid arthritis

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.

Initial diagnosis often is made during routine physical examination. Such diagnosis can be confirmed by a medical professional such as a neurologist, orthopedic surgeon or neurosurgeon. A person with foot drop will have difficulty walking on his or her heels because he will be unable to lift the front of the foot (balls and toes) off the ground. Therefore, a simple test of asking the patient to dorsiflex may determine diagnosis of the problem. This is measured on a 0-5 scale that observes mobility. The lowest point, 0, will determine complete paralysis and the highest point, 5, will determine complete mobility.

There are other tests that may help determine the underlying etiology for this diagnosis. Such tests may include MRI, MRN, or EMG to assess the surrounding areas of damaged nerves and the damaged nerves themselves, respectively. The nerve that communicates to the muscles that lift the foot is the peroneal nerve. This nerve innervates the anterior muscles of the leg that are used during dorsi flexion of the ankle. The muscles that are used in plantar flexion are innervated by the tibial nerve and often develop tightness in the presence of foot drop. The muscles that keep the ankle from supination (as from an ankle sprain) are also innervated by the peroneal nerve, and it is not uncommon to find weakness in this area as well. Paraesthesia in the lower leg, particularly on the top of the foot and ankle, also can accompany foot drop, although it is not in all instances.

A common yoga kneeling exercise, the Varjrasana has, under the name "yoga foot drop," been linked to foot drop.

Although the origin of the disease is unknown, there is speculation that it is an aggressive healing response to small tears in the plantar fascia, almost as if the fascia over-repairs itself following an injury. There is also some evidence that it might be genetic.

In the early stages, when the nodule is single and/or smaller, it is recommended to avoid direct pressure to the nodule(s). Soft inner soles on footwear and padding may be helpful.

MRI and sonogram (diagnostic ultrasound) are effective in showing the extent of the lesion, but cannot reveal the tissue composition. Even then, recognition of the imaging characteristics of plantar fibromatoses can help in the clinical diagnosis.

Surgery of Ledderhose's disease is difficult because tendons, nerves, and muscles are located very closely to each other. Additionally, feet have to carry heavy load, and surgery might have unpleasant side effects. If surgery is performed, the biopsy is predominantly cellular and frequently misdiagnosed as fibrosarcoma. Since the diseased area (lesion) is not encapsulated, clinical margins are difficult to define. As such, portions of the diseased tissue may be left in the foot after surgery. Inadequate excision is the leading cause of recurrence.

Radiotherapy has been shown to reduce the size of the nodules and reduce the pain associated with them. It is approximately 80% effective, with minimal side-effects.

Post-surgical radiation treatment may decrease recurrence. There has also been variable success in preventing recurrence by administering gadolinium. Skin grafts have been shown to control recurrence of the disease.

In few cases shock waves also have been reported to at least reduce pain and enable walking again. Currently in the process of FDA approval is the injection of collagenase. Recently successful treatment of Ledderhose with cryosurgery (also called cryotherapy) has been reported.

Cortisone injections, such as Triamcinolone, and clobetasol ointments have been shown to stall the progression of the disease temporarily, although the results are subjective and large-scale studies far from complete. Injections of superoxide dismutase have proven to be unsuccessful in curing the disease while radiotherapy has been used successfully on Ledderhose nodules.

One way to prevent this injury from occurring is to be informed and educated about the risks involved in hurting your wrist and hand. If patients do suffer from median nerve palsy, occupational therapy or wearing a splint can help reduce the pain and further damage. Wearing a dynamic splint, which pulls the thumb into opposition, will help prevent an excess in deformity. This splint can also assist in function and help the fingers flex towards the thumb. Stretching and the use of C-splints can also assist in prevention of further damage and deformity. These two methods can help in the degree of movement the thumb can have. While it is impossible to prevent trauma to your arms and wrist, patients can reduce the amount of compression by maintaining proper form during repetitive activities. Furthermore, strengthening and increasing flexibility reduces the risk of nerve compression.

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.

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.

Orthotics and corticosteroid injections are widely used conservative treatments for Morton’s neuroma. In addition to traditional orthotic arch supports, a small foam or fabric pad may be positioned under the space between the two affected metatarsals, immediately behind the bone ends. This pad helps to splay the metatarsal bones and create more space for the nerve so as to relieve pressure and irritation. It may however also elicit mild uncomfortable sensations of its own, such as the feeling of having an awkward object under one's foot. Corticosteroid injections can relieve inflammation in some patients and help to end the symptoms. For some patients, however, the inflammation and pain recur after some weeks or months, and corticosteroids can only be used a limited number of times because they cause progressive degeneration of ligamentous and tendinous tissues.

Sclerosing alcohol injections are an increasingly available treatment alternative if the above management approaches fail. Dilute alcohol (4%) is injected directly into the area of the neuroma, causing toxicity to the fibrous nerve tissue. Frequently, treatment must be performed 2–4 times, with 1–3 weeks between interventions. A 60–80% success rate has been achieved in clinical studies, equal to or exceeding the success rate for surgical neurectomy with fewer risks and less significant recovery. If done with more concentrated alcohol under ultrasound guidance, the success rate is considerably higher and fewer repeat procedures are needed.

Radio Frequency Ablation is also used in the treatment of Morton's Neuroma The outcomes appear to be equally or more reliable than alcohol injections especially if the procedure is done under ultrasound guidance.

If such interventions fail, patients are commonly offered surgery known as neurectomy, which involves removing the affected piece of nerve tissue. Postoperative scar tissue formation (known as stump neuroma) can occur in approximately 20%-30% of cases, causing a return of neuroma symptoms. Neurectomy can be performed using one of two general methods. Making the incision from the dorsal side (the top of the foot) is the more common method but requires cutting the deep transverse metatarsal ligament that connects the 3rd and 4th metatarsals in order to access the nerve beneath it. This results in exaggerated postoperative splaying of the 3rd and 4th digits (toes) due to the loss of the supporting ligamentous structure. This has aesthetic concerns for some patients and possible though unquantified long-term implications for foot structure and health. Alternatively, making the incision from the ventral side (the sole of the foot) allows more direct access to the affected nerve without cutting other structures. However, this approach requires a greater post-operative recovery time where the patient must avoid weight bearing on the affected foot because the ventral aspect of the foot is more highly enervated and impacted by pressure when standing. It also has an increased risk that scar tissue will form in a location that causes ongoing pain.

Cryogenic neuroablation is a lesser known alternative to neurectomy surgery. Cryogenic neuroablation (also known as cryo injection therapy, cryoneurolysis, cryosurgery or cryoablation) is a term that is used to describe the destruction of axons to prevent them from carrying painful impulses. This is accomplished by making a small incision (~3 mm) and inserting a cryoneedle that applies extremely low temperatures of between −50 °C to −70 °C to the nerve/neuroma. This results in degeneration of the intracellular elements, axons, and myelin sheath (which houses the neuroma) with wallerian degeneration. The epineurium and perineurium remain intact, thus preventing the formation of stump neuroma. The preservation of these structures differentiates cryogenic neuroablation from surgical excision and neurolytic agents such as alcohol. An initial study showed that cryo neuroablation is initially equal in effectiveness to surgery but does not have the risk of stump neuroma formation.

Recently, an increasing number of procedures are being performed at specialist centers which offer a range of procedures to treat Morton's neuroma under ultrasound guidance. Recent studies have shown excellent results for the treatment of Morton's neuroma with ultrasound guided sclerosing alcohol injections, ultrasound guided radiofrequency ablation, and ultrasound guided cryo-ablation.

Treatment is directed at the pathology causing the paralysis. If it is because of trauma such as a gunshot or knife wound, there may be other life-threatening conditions such as bleeding or major organ damage which should be dealt with on an emergent basis. If the syndrome is caused by a spinal fracture, this should be identified and treated appropriately. Although steroids may be used to decrease cord swelling and inflammation, the usual therapy for spinal cord injury is expectant.

The first line of treatment is often to treat the patients pain with neuropathic drugs such as tricyclic antidepressants, serotonin reuptake inhibitors, and anticonvulsants. The second lines of drugs to treat pain are non-steroidal anti-inflammatories, tramadol, and opioids. Other techniques used to facilitate healing of the nerve and pain are either static or dynamic splinting that can both help protect the injured part as well as improve function. Sometimes surgery is an option, although the prognosis is still very poor of regaining function of the affected nerve. The goal of surgery is to join healthy nerve to unhealthy nerve. The most common surgical techniques include external neurolysis, end-to-end repair, nerve grafting, and nerve transfer from somewhere else in the body.

Because lesions to different areas of the median nerve produce similar symptoms, clinicians perform a complete motor and sensory diagnosis along the nerve course. Decreased values of nerve conduction studies are used as indicators of nerve compression and may aid in determining the localization of compression.

Palpation above the elbow joint may reveal a bony consistency. Radiography images may show an abnormal bony spur outgrowth (supracondyloid process) just proximal to the elbow joint. Attached fibrous tissue (Struthers' ligament) may compress the median nerve as it passes underneath the process. This is also known as supracondylar process syndrome. Compression at this point may also occur without the bony spur; in this case, aponeurotic tissue found at the location of where Struthers' ligament should be is responsible for the compression.

If patients mention reproduction of symptoms to the forearm during elbow flexion of 120–130 degrees with the forearm in maximal supination, then the lesion may be localized to the area underneath the lacertus fibrosus (also known as bicipital aponeurosis). This is sometimes misdiagnosed as elbow strain and medial or lateral epicondylitis.

A lesion to the upper arm area, just proximal to where motor branches of forearm flexors originate, is diagnosed if the patient is unable to make a fist. More specifically, the patient's index and middle finger cannot flex at the MCP joint, while the thumb usually is unable to oppose. This is known as hand of benediction or Pope’s blessing hand. Another test is the bottle sign—the patient is unable to close all their fingers around a cylindrical object.

Carpal tunnel syndrome (CTS) is caused by compression of the median nerve as it passes under the carpal tunnel. Nerve conduction velocity tests through the hand are used to diagnosis CTS. Physical diagnostic tests include the Phalen maneuver or Phalen test and Tinel's sign. To relieve symptoms, patients may describe a motion similar to "shaking a thermometer", another indication of CTS.

Pronator teres syndrome (also known as pronator syndrome) is compression of the median nerve between the two heads of the pronator teres muscle. The Pronator teres test is an indication of the syndrome—the patient reports pain when attempting to pronate the forearm against resistance while extending the elbow simultaneously. The physician may notice an enlarged pronator teres muscle. Tinel's sign the area around the pronator teres heads should be positive. The key to discerning this syndrome from carpal tunnel syndrome is the absence of pain while sleeping. More recent literature collectively diagnose median nerve palsy occurring from the elbow to the forearm as pronator teres syndrome.

In uncooperative patients, the skin wrinkle test offers a pain-free way to identify denervation of the fingers. After submersion in water for 5 minutes, normal fingers will become wrinkled, whereas denervated fingers will not.

In "Ape hand deformity", the thenar muscles become paralyzed due to impingement and are subsequently flattened. This hand deformity is not by itself an individual diagnosis; it is seen only after the thenar muscles have atrophied. While the adductor pollicis remains intact, the flattening of the muscles causes the thumb to become adducted and laterally rotated. The opponens pollicis causes the thumb to flex and rotate medially, leaving the thumb unable to oppose. Carpal tunnel syndrome can result in thenar muscle paralysis which can then lead to ape hand deformity if left untreated. Ape hand deformity can also be seen in the hand of benediction deformity.

The Anterior Interosseus Nerve (AIN), a branch of the median nerve, only accounts for the movement of the fingers in hand and does not have any sensory capabilities. Therefore, the AIN syndrome is purely neuropathic. AINS is considered as an extremely rare condition because it accounts for less than 1% of neuropathies in the upper limb. Patients suffering from this syndrome have impaired distal interphalangeal joint, because of which they are unable to pinch anything or make and "OK" sign with their index finger and thumb. The syndrome can either happen from pinched nerve, or even dislocation of the elbow.

The symptoms and signs depend on which nerve is affected, where along its length the nerve is affected, and how severely the nerve is affected. Positive sensory symptoms are usually the earliest to occur, particularly tingling and neuropathic pain, followed or accompanied by reduced sensation or complete numbness. Muscle weakness is usually noticed later, and is often associated with muscle atrophy.

A compression neuropathy can usually be diagnosed confidently on the basis of the symptoms and signs alone. However, nerve conduction studies are helpful in confirming the diagnosis, quantifying the severity, and ruling out involvement of other nerves (suggesting a mononeuritis multiplex or polyneuropathy). A scan is not usually necessary, but may be helpful if a tumour or other local compressive lesion is suspected.Nerve injury, as a mononeuropathy, may cause similar symptoms to compression neuropathy. This may occasionally cause diagnostic confusion, particularly if the patient does not remember the injury and there are no obvious physical signs to suggest it.The symptoms and signs of each particular syndrome are discussed on the relevant pages, listed below.

Diagnostic methods vary, and are based on specific possible etiologies; however, an X-ray computed tomography scan of the face (or magnetic resonance imaging, or both) may be helpful.

Diagnosis of Harlequin syndrome is made when the individual has consistent signs and symptoms of the condition, therefore, it is made by clinical observation. In addition, a neurologist or primary care physician may require an MRI test to rule out similar disorders such as Horner's syndrome, Adie's syndrome, and Ross' syndrome. In an MRI, a radiologist may observe areas near brain or spinal cord for lesions, or any damage to the nerve endings. It is also important that the clinician rules out traumatic causes by performing autonomic function tests. Such tests includes the following: tilt table test, orthostatic blood pressure measurement, head-up test, valsalva maneuver, thermoregulatory sweat test, tendon reflex test, and electrocardiography (ECG). CT scan of the heart and lungs may also be performed to rule out a structural underlying lesion. The medical history of the individual should be carefully noted.

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.

Curb as a visible blemish is an easy diagnosis, as swelling in the distal lateral hock region is, by definition, curb. However, ultrasound is an essential tool in the diagnosis and in establishing a treatment plan. Diagnostic anesthesia (local or nerve blocks) can be helpful, but is not perfectly specific in this area.

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."

Several different types of magnetic resonance imaging (MRI) may be employed in diagnosis: MRI without contrast, Gd contrast enhanced T1-weighted MRI (GdT1W) or T2-weighted enhanced MRI (T2W or T2*W). Non-contrast enhanced MRI is considerably less expensive than any of the contrast enhanced MRI scans. The gold standard in diagnosis is GdT1W MRI.

The reliability of non-contrast enhanced MRI is highly dependent on the sequence of scans, and the experience of the operator.

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.

Electrical stimulation can promote nerve regeneration. The frequency of stimulation is an important factor in the success of both quality and quantity of axon regeneration as well as growth of the surrounding myelin and blood vessels that support the axon. Histological analysis and measurement of regeneration showed that low frequency stimulation had a more successful outcome than high frequency stimulation on regeneration of damaged sciatic nerves.

Surgery can be done in case a nerve has become cut or otherwise divided. Recovery of a nerve after surgical repair depends mainly on the age of the patient. Young children can recover close-to-normal nerve function. In contrast, a patient over 60 years old with a cut nerve in the hand would expect to recover only protective sensation, that is, the ability to distinguish hot/cold or sharp/dull. Many other factors also affect nerve recovery. The use of autologous nerve grafting procedures that involve redirection of regenerative donor nerve fibers into the graft conduit has been successful in restoring target muscle function. Localized delivery of soluble neurotrophic factors may help promote the rate of axon regeneration observed within these graft conduits.

An expanding area of nerve regeneration research deals with the development of scaffolding and bio-conduits. Scaffolding developed from biomaterial would be useful in nerve regeneration if they successfully exhibit essentially the same role as the endoneurial tubes and Schwann cell do in guiding regrowing axons.

The site and type of brachial plexus injury determine the prognosis. Avulsion and rupture injuries require timely surgical intervention for any chance of recovery. For milder injuries involving buildup of scar tissue and for neurapraxia, the potential for improvement varies, but there is a fair prognosis for spontaneous recovery, with a 90–100% return of function.