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.

There are few disorders on the differential diagnosis for carpal tunnel syndrome. Cervical radiculopathy can be mistaken for carpal tunnel syndrome since it can also cause abnormal or painful sensations in the hands and wrist. In contrast to carpal tunnel syndrome, the symptoms of cervical radiculopathy usually begins in the neck and travels down the affected arm and may be worsened by neck movement. Electromyography and imaging of the cervical spine can help to differentiate cervical radiculopathy from carpal tunnel syndrome if the diagnosis is unclear. Carpal tunnel syndrome is sometimes applied as a label to anyone with pain, numbness, swelling, and/or burning in the radial side of the hands and/or wrists. When pain is the primary symptom, carpal tunnel syndrome is unlikely to be the source of the symptoms. As a whole, the medical community is not currently embracing or accepting trigger point theories due to lack of scientific evidence supporting their effectiveness.

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

Although widely used, the presence of a positive Phalen test, Tinel sign, Flick sign, or upper limb nerve test alone is not sufficient for diagnosis.

- Phalen's maneuver is performed by flexing the wrist gently as far as possible, then holding this position and awaiting symptoms. A positive test is one that results in numbness in the median nerve distribution when holding the wrist in acute flexion position within 60 seconds. The quicker the numbness starts, the more advanced the condition. Phalen's sign is defined as pain and/or paresthesias in the median-innervated fingers with one minute of wrist flexion. Only this test has been shown to correlate with CTS severity when studied prospectively. The test characteristics of Phalen's maneuver have varied across studies ranging from 42–85% sensitivity and 54–98% specificity.

- Tinel's sign is a classic test to detect median nerve irritation. Tinel's sign is performed by lightly tapping the skin over the flexor retinaculum to elicit a sensation of tingling or "pins and needles" in the median nerve distribution. Tinel's sign (pain and/or paresthesias of the median-innervated fingers with percussion over the median nerve), depending on the study, has 38–100% sensitivity and 55–100% specificity for the diagnosis of CTS.

- Durkan test, "carpal compression test", or applying firm pressure to the palm over the nerve for up to 30 seconds to elicit symptoms has also been proposed.

- Hand elevation test The hand elevation test is performed by lifting both hands above the head, and if symptoms are reproduced in the median nerve distribution within 2 minutes, considered positive. The hand elevation test has higher sensitivity and specificity than Tinel's test, Phalen's test, and carpal compression test. Chi-square statistical analysis has shown the hand elevation test to be as effective, if not better than, Tinel's test, Phalen's test, and carpal compression test.

As a note, a patient with true carpal tunnel syndrome (entrapment of the median nerve within the carpal tunnel) will not have any sensory loss over the thenar eminence (bulge of muscles in the palm of hand and at the base of the thumb). This is because the palmar branch of the median nerve, which innervates that area of the palm, branches off of the median nerve and passes over the carpal tunnel. This feature of the median nerve can help separate carpal tunnel syndrome from thoracic outlet syndrome, or pronator teres syndrome.

Other conditions may also be misdiagnosed as carpal tunnel syndrome. Thus, if history and physical examination suggest CTS, patients will sometimes be tested electrodiagnostically with nerve conduction studies and electromyography. The role of confirmatory nerve conduction studies is controversial. The goal of electrodiagnostic testing is to compare the speed of conduction in the median nerve with conduction in other nerves supplying the hand. When the median nerve is compressed, as in CTS, it will conduct more slowly than normal and more slowly than other nerves. There are many electrodiagnostic tests used to make a diagnosis of CTS, but the most sensitive, specific, and reliable test is the Combined Sensory Index (also known as the Robinson index). Electrodiagnosis rests upon demonstrating impaired median nerve conduction across the carpal tunnel in context of normal conduction elsewhere. Compression results in damage to the myelin sheath and manifests as delayed latencies and slowed conduction velocities However, normal electrodiagnostic studies do not preclude the presence of carpal tunnel syndrome, as a threshold of nerve injury must be reached before study results become abnormal and cut-off values for abnormality are variable. Carpal tunnel syndrome with normal electrodiagnostic tests is very, very mild at worst.

The role of MRI or ultrasound imaging in the diagnosis of carpal tunnel syndrome is unclear. Their routine use is not recommended.

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 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.

RSIs are assessed using a number of objective clinical measures. These include effort-based tests such as grip and pinch strength, diagnostic tests such as Finkelstein's test for De Quervain's tendinitis, Phalen's Contortion, Tinel's Percussion for carpal tunnel syndrome, and nerve conduction velocity tests that show nerve compression in the wrist. Various imaging techniques can also be used to show nerve compression such as x-ray for the wrist, and MRI for the thoracic outlet and cervico-brachial areas.

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.

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.

Cubital tunnel syndrome may be prevented or reduced by maintaining good posture and proper use of the elbow and arms, such as wearing an arm splint while sleeping to maintain the arm is in a straight position instead of keeping the elbow tightly bent. A recent example of this is popularization of the concept of cell phone elbow.

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.

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.

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.

If severe pain persists after the first 24hours it is recommended that an individual consult with a professional who can make a diagnosis and implement a treatment plan so the patient can return to everyday activities (Flegel, 2004). These are some of the tools that a professional can use to help make a full diagnosis;

Nerve conduction studies may also be used to localize nerve dysfunction ("e.g.", carpal tunnel syndrome), assess severity, and help with prognosis.

Electrodiagnosis also helps differentiate between myopathy and neuropathy.

Ultimately, the best method of imaging soft tissue is magnetic resonance imaging (MRI), though it is cost-prohibitive and carries a high false positive rate.

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.

Diagnosis is largely based on patient description and relevant details about recent surgeries, hip injuries, or repetitive activities that could irritate the nerve. Examination checks for sensory differences between the affected leg and the other leg. Accurate diagnosis may require an abdominal and pelvic examination to exclude problems in those areas.

Electromyographic (EMG) nerve-conduction studies may be required. X-rays may be needed to exclude bone abnormalities that might put pressure on the nerve; likewise CT or MRI scans to exclude soft tissue causes such as a tumor.

PNE can be caused by pregnancy, scarring due to surgery, accidents and surgical mishaps. Anatomic abnormalities can result in PNE due to the pudendal nerve being fused to different parts of the anatomy, or trapped between the sacrotuberous and sacrospinalis ligaments. Heavy and prolonged bicycling, especially if an inappropriately shaped or incorrectly positioned bicycle seat is used, may eventually thicken the sacrotuberous and/or sacrospinous ligaments and trap the nerve between them, resulting in PNE.

Similar to a tinel sign digital palpitation of the ischial spine may produce pain. In contrast, patients may report temporary relief with a diagnostic pudendal nerve block (see Injections), typically infiltrated near the ischial spine.

Electromyography can be used to measure motor latency along the pudendal nerve. A greater than normal conduction delay can indicate entrapment of the nerve.

Imaging studies using MR neurography may be useful. In patients with unilateral pudendal entrapment in the Alcock's canal, it is typical to see asymmetric swelling and hyperintensity affecting the pudendal neurovascular bundle.

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.

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.⁠

The most-often prescribed treatments for early-stage RSIs include analgesics, myofeedback, biofeedback, physical therapy, relaxation, and ultrasound therapy. Low-grade RSIs can sometimes resolve themselves if treatments begin shortly after the onset of symptoms. However, some RSIs may require more aggressive intervention including surgery and can persist for years.

General exercise has been shown to decrease the risk of developing RSI. Doctors sometimes recommend that RSI sufferers engage in specific strengthening exercises, for example to improve sitting posture, reduce excessive kyphosis, and potentially thoracic outlet syndrome. Modifications of posture and arm use (human factors and ergonomics) are often recommended.

Initial line of treatment is with anti-inflammatory drugs or cortisone injections. There have been trials with gloves which help protect the ulnar nerve from compression. The most radical treatment option is surgery to relieve tension in the volar carpal ligament which forms the roof of Guyon's canal, thereby reducing compression on the ulnar nerve.

The place of chiropractic-, physical-, occupational-, massage- and osteopathic therapy was not confirmed in scientific studies. These treatments can be both expensive as well as dangerous (causing permanent damage when performed wrongly).

It is advised to consult a physician beforehand starting any therapy, albeit an alternative approach, to avoid any permanent nerve damage.

The severity of brachial plexus injury is determined by the type of nerve damage. There are several different classification systems for grading the severity of nerve and brachial plexus injuries. Most systems attempt to correlate the degree of injury with symptoms, pathology and prognosis. Seddon's classification, devised in 1943, continues to be used, and is based on three main types of nerve fiber injury, and whether there is continuity of the nerve.

1. Neurapraxia: The mildest form of nerve injury. It involves an interruption of the nerve conduction without loss of continuity of the axon. Recovery takes place without wallerian degeneration.

2. Axonotmesis: Involves axonal degeneration, with loss of the relative continuity of the axon and its covering of myelin, but preservation of the connective tissue framework of the nerve (the encapsulating tissue, the epineurium and perineurium, are preserved).

3. Neurotmesis: The most severe form of nerve injury, in which the nerve is completely disrupted by contusion, traction or laceration. Not only the axon, but the encapsulating connective tissue lose their continuity. The most extreme degree of neurotmesis is transsection, although most neurotmetic injuries do not produce gross loss of continuity of the nerve but rather, internal disruption of the nerve architecture sufficient to involve perineurium and endoneurium as well as axons and their covering. It requires surgery, with unpredictable recovery.

A more recent and commonly used system described by the late Sir Sydney Sunderland, divides nerve injuries into five degrees: first degree or neurapraxia, following on from Seddon, in which the insulation around the nerve called myelin is damaged but the nerve itself is spared, and second through fifth degree, which denotes increasing severity of injury. With fifth degree injuries, the nerve is completely divided.

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.