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.

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.

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.

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.

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

The first steps in the evaluation and later management of plexopathy would consist of gathering a medical history and conducting a physical examination by a healthcare clinician. Motor function defect patterns detected within either the upper or lower extremities help with diagnosis of the disorder.

X-rays of the cervical spine, chest, and shoulder are usually ordered if symptoms point to acute Brachial plexopathy. If the physical history reveals a history of diabetes, collagen vascular disease, or symptoms of infection, the physician may order a series of blood tests including a complete blood count (CBC) and a comprehensive metabolic panel (CMP).

Plexopathy symptoms often resemble spinal cord disorders. A neurosurgical consultation is usually undertaken to ensure proper diagnosis, management, and treatment. Patients with chronic symptoms will likely be advised to follow up with outpatient care from either their health care provider or specialist.

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.

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.

EMG test is often performed together with another test called nerve conduction study, which measures the conducting function of nerves. NCV study shows loss of nerve conduction in the distal segment (3 to 4 days after injury). According to NCV study, in axonotmesis there is an absence of distal sensory-motor responses.

Electromyography (EMG) is a medical test performed to evaluate and record the electrical activity (electromyogram) produced by skeletal muscles using an instrument called electromyograph. In axonotmesis, EMG changes (2 to 3 weeks after injury) in the denervated muscles include:

1. Fibrillation potentials (FP)

2. Positive sharp waves

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.

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.

In terms of diagnosis of HNPP measuring nerve conduction velocity may give an indication of the presence of the disease.Other methods via which to ascertain the diagnosis of hereditary neuropathy with liability to pressure palsy are:

- Family history

- Genetic test

- Physical exam(lack of ankle reflex)

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.

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.

Initial screening for CIP/CIM may be performed using an objective scoring system for muscle strength. The Medical Research Council (MRC) score is one such tool, and sometimes used to help identify CIP/CIM patients in research studies. The MRC score involves assessing strength in 3 muscle groups in the right and left sides of both the upper and lower extremities. Each muscle tested is given a score of 0-5, giving a total possible score of 60. An MRC score less than 48 is suggestive of CIP/CIM. However, the tool requires that patients be awake and cooperative, which is often not the case. Also, the screening tool is non-specific, because it does not identify the cause a person's muscle weakness.

Once weakness is detected, the evaluation of muscle strength should be repeated several times. If the weakness persists, then a muscle biopsy, a nerve conduction study (electrophysiological studies), or both should be performed.

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.

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.

Peripheral neuropathy may first be considered when an individual reports symptoms of numbness, tingling, and pain in feet. After ruling out a lesion in the central nervous system as a cause, diagnosis may be made on the basis of symptoms, laboratory and additional testing, clinical history, and a detailed examination.

During physical examination, specifically a neurological examination, those with generalized peripheral neuropathies most commonly have distal sensory or motor and sensory loss, although those with a pathology (problem) of the nerves may be perfectly normal; may show proximal weakness, as in some inflammatory neuropathies, such as Guillain–Barré syndrome; or may show focal sensory disturbance or weakness, such as in mononeuropathies. Classically, ankle jerk reflex is absent in peripheral neuropathy.

A physical examination will involve testing the deep ankle reflex as well as examining the feet for any ulceration. For large fiber neuropathy, an exam will usually show an abnormally decreased sensation to vibration, which is tested with a 128-Hz tuning fork, and decreased sensation of light touch when touched by a nylon monofilament.

Diagnostic tests include electromyography (EMG) and nerve conduction studies (NCSs), which assess large myelinated nerve fibers. Testing for small-fiber peripheral neuropathies often relates to the autonomic nervous system function of small thinly- and unmyelinated fibers. These tests include a sweat test and a tilt table test. Diagnosis of small fiber involvement in peripheral neuropathy may also involve a skin biopsy in which a 3 mm-thick section of skin is removed from the calf by a punch biopsy, and is used to measure the skin intraepidermal nerve fiber density (IENFD), the density of nerves in the outer layer of the skin. Reduced density of the small nerves in the epidermis supports a diagnosis of small-fiber peripheral neuropathy.

Laboratory tests include blood tests for vitamin B-12 levels, a complete blood count, measurement of thyroid stimulating hormone levels, a comprehensive metabolic panel screening for diabetes and pre-diabetes, and a serum immunofixation test, which tests for antibodies in the blood.

The serum creatine phosphokinase (CPK) can be mildly elevated. While the CPK is often a good marker for damage to muscle tissue, it is not a helpful marker in CIP/CIM, because CIP/CIM is a gradual process and does not usually involve significant muscle cell death (necrosis). Also, even if necrosis is present, it may be brief and is therefore easily missed. If a lumbar puncture (spinal tap) is performed, the protein level in the cerebral spinal fluid would be normal.

Adson's sign and the costoclavicular maneuver lack specificity and sensitivity and should comprise only a small part of the mandatory comprehensive history and physical examination undertaken with a patient suspected of having TOS. There is currently no single clinical sign that makes the diagnosis of TOS with any degree of certainty.

Additional maneuvers that may be abnormal in TOS include Wright's Test, which involves hyperabducting the arms over the head with some extension and evaluating for loss of radial pulses or signs of blanching of the skin in the hands indicating a decrease in blood flow with the maneuver. The "compression test" is also used, exerting pressure between the clavicle and medial humeral head causes radiation of pain and/or numbness into the affected arm.

Doppler arteriography, with probes at the fingertips and arms, tests the force and "smoothness" of the blood flow through the radial arteries, with and without having the patient perform various arm maneuvers (which causes compression of the subclavian artery at the thoracic outlet). The movements can elicit symptoms of pain and numbness and produce graphs with diminished arterial blood flow to the fingertips, providing strong evidence of impingement of the subclavian artery at the thoracic outlet. Doppler arteriography does not utilize probes at the fingertips and arms, and in this case is likely being confused with plethysmography, which is a different method that utilizes ultrasound without direct visualization of the affected vessels. It should also be noted that Doppler ultrasound (not really 'arteriography') would not be used at the radial artery in order to make the diagnosis of TOS. Finally, even if a Doppler study of the appropriate artery were to be positive, it would not diagnose neurogenic TOS, by far the most common subtype of TOS. There is plenty of evidence in the medical literature to show that arterial compression does not equate to brachial plexus compression, although they may occur together, in varying degrees. Additionally, arterial compression by itself does not make the diagnosis of arterial TOS (the rarest form of TOS). Lesser degrees of arterial compression have been shown in normal individuals in various arm positions and are thought to be of little significance without the other criteria for arterial TOS.

In many cases recovery happens spontaneously and no treatment is needed. This spontaneous recovery can occur because distance between the injury location and the deltoid muscle is small. Spontaneous recovery may take as long as 12 months.

In order to combat pain and inflammation of nerves, medication may be prescribed.

Surgery is an option, but it has mixed results within the literature and is usually avoided because only about half of people who undergo surgery see any positive results from it. Some suggest that surgical exploration should be considered if no recovery occurs after 3 to 6 months. Some surgical options include nerve grafting, neurolysis, or nerve reconstruction. Surgery results are typically better for younger patients (under 25) and for nerve grafts less than six centimeters.

For some, recovery does not occur and surgery is not possible. In these cases, most patients’ surrounding muscles can compensate, allowing them to gain a satisfactory range of motion back. Physical therapy or Occupational therapy will help retrain and gain muscle tone back.

EMG &NCV can help to treatment with the diagnosis of the location and severity of the lesion.

In terms of the differential diagnosis for polyneuropathy one must look at the following: