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.

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

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

The diagnosis is based on symptoms and signs alone and objective testing is expected to be normal. This syndrome may be clinically tested by flexing the patients long finger while the patient extends the wrist and fingers. Pain is a positive finding.

The chief complaint of this disease is usually pain in the dorsal aspect of the upper forearm, and any weakness described is secondary to the pain. Tenderness to palpation occurs over the area of the radial neck. Also, the disease can be diagnosed by a positive "middle finger test", where resisted middle finger extension produces pain. Radiographic evaluation of the elbow should be performed to rule out other diagnoses.

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 order to diagnose radial nerve dysfunction, a doctor will conduct a physical examination. During the exam of the arm, wrist, and hand, the doctor will look for: difficulty straightening the arm at the elbow; trouble turning the arm outward; difficulty lifting the wrist; muscle loss or atrophy in the forearm; weakness of the wrist and/or fingers. In addition, tests may need to be conducted to confirm the doctors findings. These tests include: blood tests; MRI of the neck and shoulders to screen for other problems; nerve biopsy; nerve conduction tests; ultrasound of the elbow.

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.

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

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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."

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.

Magnetic resonance imaging (MRI) can be helpful in assessing for a ligamentous injury to the medial side of the knee. Milewski et al. has found that grade I to III classification can be seen on MRI. With a high-quality image (1.5 tesla or 3 tesla magnet) and no previous knowledge of the patient’s history, musculoskeletal radiologists were able to accurately diagnose medial knee injury 87% of the time. MRI can also show associated bone bruises on the lateral side of the knee, which one study shows, happen in almost half of medial knee injuries.

Knee MRIs should be avoided for knee pain without mechanical symptoms or effusion, and upon non-successful results from a functional rehabilitation program.

Therapeutic exercises are frequently used in combination with many of the previously mentioned modalities and with great results. A variety of exercise regimens are available in patient treatment. An exercise regimen should be modified according to the abilities and weaknesses of the patient. Stabilization of the cervicothoracic region is helpful in limiting pain and preventing re-injury. Cervical and lumbar support braces typically are not indicated for radiculopathy, and may lead to weakness of support musculature. The first part of the stabilization procedure is achieving a pain free full range of motion which can be accomplished through stretching exercises. Subsequently a strengthening exercise program should be designed to restore the deconditioned cervical, shoulder girdle, and upper trunk musculature. As reliance on the neck brace diminishes, an isometric exercise regimen should be introduced. This is a preferred method of exercise during the sub-acute phase because it resists atrophy and is least likely to exacerbate the condition. Single plane resistance exercises against cervical flexion, extension, bending, and rotation are used.

A skin biopsy for the measurement of epidermal nerve fiber density is an increasingly common technique for the diagnosis of small fiber peripheral neuropathy. Physicians can biopsy the skin with a 3-mm circular punch tool and immediately fix the specimen in 2% paraformaldehyde lysine-periodate or Zamboni's fixative. Specimens are sent to a specialized laboratory for processing and analysis where the small nerve fibers are quantified by a neuropathologist to obtain a diagnostic result.

This skin punch biopsy measurement technique is called intraepidermal nerve fiber density (IENFD). The following table describes the IENFD values in males and females of a 3 mm biopsy 10-cm above the lateral malleolus (above ankle outer side of leg). Any value measured below the 0.05 Quantile IENFD values per age span, is considered a reliable positive diagnosis for Small Fiber Peripheral Neuropathy.

Anterior-posterior (AP) radiographs are useful for reliably assessing normal anatomical landmarks. Bilateral valgus stress AP images can show a difference in medial joint space gapping. It has been reported that an isolated grade III sMCL tear will show an increase in medial compartment gapping of 1.7 mm at 0° of knee flexion and 3.2 mm at 20° of knee flexion, compared to the contralateral knee. Additionally, a complete medial ligamentous disruption (sMCL, dMCL, and POL) will show increased gapping by 6.5 mm at 0° and 9.8 mm at 20° during valgus stress testing. Pellegrini-Stieda syndrome can also be seen on AP radiographs. This finding is due to calcification of the sMCL (heterotopic ossification) caused by the chronic tear of the ligament.

The diagnosis of small fiber neuropathy often requires ancillary testing. Nerve conduction studies and electromyography are commonly used to evaluate large myelinated sensory and motor nerve fibers, but are ineffective in diagnosing small fiber neuropathies.

Quantitative sensory testing (QST) assesses small fiber function by measuring temperature and vibratory sensation. Abnormal QST results can be attributed to dysfunction in the central nervous system. Furthermore, QST is limited by a patient’s subjective experience of pain sensation. Quantitative sudomotor axon reflex testing (QSART) measures sweating response at local body sites to evaluate the small nerve fibers that innervate sweat glands.