The nerve conduction study usually provides useful information for making diagnosis. A CT scan is sometimes used to rule out some causes from the central nervous system.

Paresthesia or "persistent anesthesia" is a transient or potentially permanent condition of extended numbness after administration of local anesthesia and the injected anesthetic has terminated.

Potential causes include trauma induced to the nerve sheath during administration of the injection, hemorrhage about the sheath, type of anesthetic used, or administration of anesthetic potentially contaminated with alcohol or sterilizing solutions.

Daily oral muscle physical therapy, or the administration of antidepressants have been reported as effective therapy for occlusal dysesthesia patients. Tooth grinding, and the replacement or removal of all dental work should be avoided in patients with occlusal dysesthesia, despite the frequent requests for further surgery often made by these patients.

Antidepressants are also often prescribed for scalp dysesthesia.

Prakash et al. found that many patients suffering from burning mouth syndrome (BMS), one variant of occlusal dysesthesia, also report painful sensations in other parts of the body. Many of the patients suffering from BMS met the classification of restless leg syndrome (RLS). About half of these patients also had a family history of RLS. These results suggest that some BMS symptoms may be caused by the same pathway as RLS in some patients, indicating that dopaminergic drugs regularly used to treat RLS may be effective in treating BMS as well.

A patient suffering from dysesthesia can find it to be unbearable at times. Dysesthetic burning has been called "Dante-esque" pain. The terminology used to describe it is usually interchangeable with descriptions of Hell in classic literature. It is the "bluntest" pain of which the human body is capable, and is characterized by the absence of accurate discriminative information.

Temperature change and heat both affect the sensation and raise the level of the steady pain. This pain upgrades with tonic light touch, phasic rubbing, or rough textures to become evoked pain.

The patient often cannot endure the touch of clothing. His or her entire life becomes an exercise in avoiding evoked pain. It causes difficulty in obtaining rest because bed-clothing contacts the skin. It drives the patient to a hysterical search for relief of the pain, which ends in some degree of resignation and frequent depression. Patients indicate that it has robbed them of their identity, since their values and mental priorities are so consumed by its avoidance.

Chronic anxiety is often associated with dysesthesia. Patients suffering from this anxiety may experience numbness or tingling in the face. In one study, those patients that were examined psychologically had symptoms of anxiety, depression, obsessive-compulsive personality disorder, or somatoform disorder.

Therapy for notalgia paresthetica is directed at controlling symptoms, as no cure exists for the condition. Available treatments include local anesthetics, topical capsaicin, topical corticosteroids, hydroxyzine, oxcarbazepine, palmitoylethanolamide and gabapentin. Paravertebral nerve block and botulinum toxin injections may also be helpful.

Some patients treated with low concentration topical capsaicin reported pain, burning, or tingling sensations with treatment, and symptoms returned within a month of ceasing treatment. Oxcarbazepine was reported to reduce the severity of symptoms in a few cases. One patient has been treated with "paravertebral nerve blocks, with bupivacaine and methylprednisolone acetate injected into the T3–T4 and T5–T6 intervertebral spaces" Hydroxyzine has also been used with considerable success in some cases as long as the pills are used daily.

High concentration topical capsaicin (8%, Qutenza) have been shown to be highly effective in treating neuropathic itch in some patients (including notalgia paresthetica) as well as in a recent proof-of-concept study, but this remains to be confirmed in randomised controlled trials.

Most recently intradermal injections of botulinum toxin type A (Botox) have been tried with some success. Even though botulinum normally wears off in three to six months, the treatment appears to be long term, and it has been theorised that botulinum type A effects lasting change in pain signaling. Unfortunately, repeated injections have been associated with diminished movement ability of the upper back and arms and its recommendation as a treatment has therefore become less popular.

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

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 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.

Most patients diagnosed with cubital tunnel syndrome have advanced disease (atrophy, static numbness, weakness) that might reflect permanent nerve damage that will not recover after surgery. When diagnosed prior to atrophy, weakness or static numbness, the disease can be arrested with treatment. Mild and intermittent symptoms often resolve spontaneously.

The correlation of notalgia paraesthetica localization with corresponding degenerative changes in the spine suggest that spinal nerve impingement may be a contributing cause. According to Plete and Massey, "The posterior rami of spinal nerves arising in T2 through T6 are unique in that they pursue a right-angle course through the multifidus spinae muscle, and this particular circumstance may predispose them to harm from otherwise innocuous insults of a varied nature." Patients may have other conditions that predispose them to peripheral neuropathies (nerve damage).

The causes of this condition have not yet been completely defined. Patients are usually older persons.

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.

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.

The treatment of peripheral neuropathy varies based on the cause of the condition, and treating the underlying condition can aid in the management of neuropathy. When peripheral neuropathy results from diabetes mellitus or prediabetes, blood sugar management is key to treatment. In prediabetes in particular, strict blood sugar control can significantly alter the course of neuropathy. In peripheral neuropathy that stems from immune-mediated diseases, the underlying condition is treated with intravenous immunoglobulin or steroids. When peripheral neuropathy results from vitamin deficiencies or other disorders, those are treated as well.

The ICHD-2 lists diagnostic criteria for "persistent idiopathic facial pain" (the term that replaces AFP in this classification):

There are presently no accepted medical tests which consistently discriminate between facial pain syndromes or differentiate Atypical Facial Pain from other syndromes. However, a normal Radiograph, CT, and MRI may help to exclude other pathology such as arterio-veinous malformation, tumor, temporomandibular joint disorder, or MS.

AFP and AO can be difficult to diagnose, and are often misdiagnosed with resultant inappropriate attempts of treatment, e.g. root canal therapy which may at best have only a temporary benefit, or at worst lead to an increase in the pain. Excluding an organic cause for the pain is the most important part of the diagnosis. Odontogenic pain should especially be ruled out, since this accounts for over 95% of cases of orofacial pain.

There is considerable symptom overlap between atypical facial pain and temporomandibular joint dysfunction.

The diagnosis of facial pain generally is often multidisciplinary.

Of people that have a sympathectomy, it is impossible to predict who will end up with a more severe version of this disorder, as there is no link to gender, age or weight. There is no test or screening process that would enable doctors to predict who is more susceptible.

Compartment syndrome is a clinical diagnosis made by a physician. It can be tested for by gauging the pressure within the muscle compartments. If the pressure is sufficiently high, a fasciotomy will be required to relieve the pressure. Various recommendations of the intracompartmental pressure are used with some sources quoting >30 mmHg as an indication for fasciotomy while others suggest a <30 mmHg difference between intracompartmental pressure and diastolic blood pressure. This latter measure may be more sensible in the light of recent advances in permissive hypotension, which allow patients to be kept hypotensive in resuscitation. It is now relatively easy to measure compartment and subcutaneous pressures using the pressure transducer modules (with a simple intravenous catheter and needle) that are attached to most modern anaesthetic machines.

Most commonly compartment syndrome is diagnosed through a diagnosis of its underlying cause and not the condition itself. According to Blackman one of the tools to diagnose compartment syndrome is X-ray to show a tibia/fibula fracture, which when combined with numbness of the extremities is enough to confirm the presence of compartment syndrome.

Obdormition (; from Latin "obdormire" "to fall asleep") is a medical term describing numbness in a limb, often caused by constant pressure on nerves or lack of movement. This is colloquially referred to as the limb "going to sleep," and usually followed by paresthesia, colloquially called "pins and needles".

Compensatory hyperhidrosis is a form of neuropathy. It is encountered in patients with myelopathy, thoracic disease, cerebrovascular disease, nerve trauma or after surgeries. The exact mechanism of the phenomenon is poorly understood. It is attributed to the perception in the hypothalamus (brain) that the body temperature is too high. The sweating is induced to reduce body heat.

Excessive sweating due to nervousness, anger, previous trauma or fear is called hyperhidrosis.

Compensatory hyperhidrosis is the most common side effect of endoscopic thoracic sympathectomy, a surgery to treat severe focal hyperhidrosis, often affecting just one part of the body. It may also be called "rebound" or "reflex hyperhidrosis". In a small number of individuals, compensatory hyperhidrosis following sympathectomy is disruptive, because afflicted individuals may have to change sweat-soaked clothing two or three times a day.

According to Dr Hooshmand, sympathectomy permanently damages the temperature regulatory system. The permanent destruction of thermoregulatory function of the sympathetic nervous system causes latent complications, e.g., RSD in contralateral extremity.

Following surgery for axillary (armpit), palmar (palm) hyperhidrosis (see focal hyperhidrosis) and blushing, the body may sweat excessively at untreated areas, most commonly the lower back and trunk, but can be spread over the total body surface below the level of the cut. The upper part of the body, above the sympathetic chain transection, the body becomes anhidriotic, where the patient is unable to sweat or cool down, which further compromises the body's thermoregulation and can lead to elevated core temperature, overheating and hyperthermia. Below the level of the sympathetic chain interruption, body temperature is significantly lower, creating a stark contrast that can be observed on thermal images. The difference in temperatures between the sympathetically under- and overactive regions can be as high as 10 Celsius.

Diagnosis is made based on clinical signs and symptoms and a starch iodine test, called the Minor Iodine-Starch test. The affected area of the face is painted with iodine which is allowed to dry, then dry corn starch is applied to the face. The starch turns blue on exposure to iodine in the presence of sweat.

If these symptoms are observed/experienced it is important to contact a physician specializing in sports medicine (MD/DO), a doctor of podiatric medicine (DPM), or other qualified health care professional immediately so as to get the appropriate advice/treatment before serious damage occurs.

The 5 Ps of Anterior Compartment Syndrome:

1. Pain

2. Pallor

3. Paresthesia

4. Pulselessness

5. Paralysis (If not treated)

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.

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.

Acute compartment syndrome is a medical emergency requiring immediate surgical treatment, known as a fasciotomy, to allow the pressure to return to normal. Although only one compartment is affected, fasciotomy is done to release all compartments. For instance, if only the deep posterior compartment of a leg is affected, the treatment would be fasciotomy (with medial and lateral incisions) to release all compartments of the leg in question, namely the anterior, lateral, superficial posterior and deep posterior.

An acute compartment syndrome has some distinct features such as swelling of the compartment due to inflammation and venous occlusion. Decompression of the nerve traversing the compartment might alleviate the symptoms (Rorabeck, 1984). Until definitive fasciotomy can be performed, the extremity should be placed at the level of the heart. Hypotension should also be avoided, as this decreases perfusion pressure to the compartment. Supplemental oxygen also optimizes tissue and neural oxygenation.

A compartment syndrome is an increased pressure within a muscular compartment that compromises the circulation to the muscles.