Presently, established empirical evidence suggests against thermography's efficacy as a reliable tool for diagnosing CRPS. Although CRPS may, in some cases, lead to measurably altered blood flow throughout an affected region, many other factors can also contribute to an altered thermographic reading, including the patient's smoking habits, use of certain skin lotions, recent physical activity, and prior history of trauma to the region. Also, not all patients diagnosed with CRPS demonstrate such "vasomotor instability" — less often, still, those in the later stages of the disease. Thus, thermography alone cannot be used as conclusive evidence for - or against - a diagnosis of CRPS and must be interpreted in light of the patient's larger medical history and prior diagnostic studies.

In order to minimise the confounding influence of external factors, patients undergoing infrared thermographic testing must conform to special restrictions regarding the use of certain vasoconstrictors (namely, nicotine and caffeine), skin lotions, physical therapy, and other diagnostic procedures in the days prior to testing. Patients may also be required to discontinue certain pain medications and sympathetic blockers. After a patient arrives at a thermographic laboratory, he or she is allowed to reach thermal equilibrium in a 16–20 °C, draft-free, steady-state room wearing a loose fitting cotton hospital gown for approximately twenty minutes. A technician then takes infrared images of both the patient's affected and unaffected limbs, as well as reference images of other parts of the patient's body, including his or her face, upper back, and lower back. After capturing a set of baseline images, some labs further require the patient to undergo cold-water autonomic-functional-stress-testing to evaluate the function of his or her autonomic nervous system's peripheral vasoconstrictor reflex. This is performed by placing a patient's unaffected limb in a cold water bath (approximately 20 °C) for five minutes while collecting images. In a normal, intact, functioning autonomic nervous system, a patient's affected extremity will become colder. Conversely, warming of an affected extremity may indicate a disruption of the body's normal thermoregulatory vasoconstrictor function, which may sometimes indicate underlying CRPS.

Scintigraphy, plain radiographs, and magnetic resonance imaging (MRI) may all be useful diagnostically. Patchy osteoporosis (post-traumatic osteoporosis), which may be due to disuse of the affected extremity, can be detected through X-ray imagery as early as two weeks after the onset of CRPS. A bone scan of the affected limb may detect these changes even sooner and can almost confirm the disease. Bone densitometry can also be used to detect changes in bone mineral density. It can also be used to monitor the results of treatment since bone densitometry parameters improve with treatment.

Erythromelalgia is a difficult condition to diagnose as there are no specific tests available. However, reduced capillary density has been observed microscopically during flaring; and reduced capillary perfusion is noted in the patient. Another test that can be done is to have the patient elevate their legs, and note the reversal (from red to pale) in skin color. Tests done at universities include quantitative sensory nerve testing, laser evoked potentials, sweat testing and epidermal sensory nerve fiber density test (which is an objective test for small fiber sensory neuropathy). Due the aforementioned factors, patients may face delays in diagnosis.

Once it has been established that it is not secondary erythromelalgia — see below — a programme of management can be put in place.

Some diseases present with symptoms similar to erythromelalgia. Complex regional pain syndrome (CRPS), for instance, presents with severe burning pain and redness except these symptoms are often unilateral (versus symmetric) and may be proximal instead of purely or primarily distal. Furthermore, attacks triggered by heat and resolved by cooling are less common with CRPS.

Erythromelalgia is sometimes caused by other disorders. A partial list of diseases known to precipitate erythromelalgia is below.

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.

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.

For secondary erythromelalgia, treatment of the underlying primary disorder is the most primary method of treatment. Although aspirin has been thought to reduce symptoms of erythromelalgia, it is rare to find evidence that this is effective. Mechanical cooling of the limbs by elevating them can help or managing the ambient environment frequently is often necessary constantly as flares occur due to sympathetic autonomic dysfunction of the capillaries. The pain that accompanies it is severe and treated separately (the pain is similar to CRPS, phantom limb or thalamic pain syndrome). Patients are strongly advised "not" to place the affected limbs in cold water to relieve symptoms when flaring occurs. It may seem a good idea, but it precipitates problems further down the line causing damage to the skin and ulceration often intractable due to the damaged skin. A possible reduction in skin damage may be accomplished by enclosing the flaring limb in a commonly available, thin, heat transparent, water impermeable, plastic food storage bag. The advice of a physician is advised depending on specific circumstances.

Primary erythromelalgia management is symptomatic, i.e. treating painful symptoms only. Specific management tactics include avoidance of attack triggers such as: heat, change in temperature, exercise or over exertion, alcohol and spicy foods. This list is by no means comprehensive as there are many triggers to set off a 'flaring' episode that are inexplicable. Whilst a cool environment is helpful in keeping the symptoms in control, the use of cold water baths is strongly discouraged. In pursuit of added relief sufferers can inadvertently cause tissue damage or death, i.e. necrosis. See comments at the end of the preceding paragraph regarding possible effectiveness of plastic food storage bags to avoid/reduce negative effects of submersion in cold water baths.

One clinical study has demonstrated the efficacy of IV lidocaine or oral mexilitine, though it should be noted that differences between the primary and secondary forms were not studied. Another trial has shown promise for misoprostol, while other have shown that gabapentin, venlafaxine and oral magnesium may also be effective, but no further testing was carried out as newer research superseded this combination.

Strong anecdotal evidence from EM patients shows that a combination of drugs such as duloxetine and pregabalin is an effective way of reducing the stabbing pains and burning sensation symptoms of erythromelalgia in conjunction with the appropriate analgesia. In some cases, antihistamines may give some relief. Most people with erythromelalgia never go into remission and the symptoms are ever present at some level, whilst others get worse, or the EM is eventually a symptom of another disease such as systemic scleroderma.

Some suffering with EM are prescribed ketamine topical creams as a way of managing pain on a long term basis. Feedback from some EM patients has led to reduction in usage as they believe it is only effective for short periods.

Living with erythromelalgia can result in a deterioration in quality of life resulting in the inability to function in a work place, lack of mobility, depression, and is socially alienating; much greater education of medical practitioners is needed. As with many rare diseases, many people with EM end up taking years to get a diagnosis and to receive appropriate treatment.

Research into the genetic mutations continues but there is a paucity of clinical studies focusing on living with erythromelalgia. There is much urgency within pharmaceutical companies to provide a solution to those who suffer with pain such as that with erythromelalgia.

Pharmacological techniques are often continued in conjunction with other treatment options. Doses of pain medications needed often drop substantially when combined with other techniques, but rarely are discontinued completely. Tricyclic antidepressants, such as amitriptyline, and sodium channel blockers, mainly carbamazepine, are often used to relieve chronic pain, and recently have been used in an attempt to reduce phantom pains. Pain relief may also be achieved through use of opioids, ketamine, calcitonin, and lidocaine.

Deep brain stimulation is a surgical technique used to alleviate patients from phantom limb pain. Prior to surgery, patients undergo functional brain imaging techniques such as PET scans and functional MRI to determine an appropriate trajectory of where pain is originating. Surgery is then carried out under local anesthetic, because patient feedback during the operation is needed. In the study conducted by Bittar et al., a radiofrequency electrode with four contact points was placed on the brain. Once the electrode was in place, the contact locations were altered slightly according to where the patient felt the greatest relief from pain. Once the location of maximal relief was determined, the electrode was implanted and secured to the skull. After the primary surgery, a secondary surgery under general anesthesia was conducted. A subcutaneous pulse generator was implanted into a pectoral pocket below the clavicle to stimulate the electrode. It was found that all three patients studied had gained satisfactory pain relief from the deep brain stimulation. Pain had not been completely eliminated, but the intensity had been reduced by over 50% and the burning component had completely vanished.

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.

Electroanalgesia poses serious health problems in those patients who need other electrical equipment in their bodies, such as pacemakers and hearing aids, because the electrical signals of the multiple devices can interfere with each other and fail. People with heart problems, such as irregular heartbeat, are also at risk because the devices can throw off the normal electrical signal of the heart.

Despite its wasting and at times long-lasting effects, most cases resolve themselves and recovery is usually good in 18–24 months, depending on how old the person in question is. For instance, a six-year-old could have brachial neuritis for only around 6 months, but a person in their early fifties could have it for over 3 years.

Percutaneous electrical nerve stimulation, or PENS, is used mainly in the treatment of intractable pain associated with chronic low back pain syndrome, cancer, and other disorders. It is a technique involving insertion of an ultra-fine acupuncture needle which probes into the soft tissues or muscles to electrically stimulate nerve fibers in the sclerotomal, myotomal, or dermatomal distribution corresponding to the patient's pain symptoms. PENS is related to both electroacupuncture and transcutaneous electrical nerve stimulation.

Secondary Raynaud's is managed primarily by treating the underlying cause and as primary Raynaud's, avoiding triggers, such as cold, emotional and environmental stress, vibrations and repetitive motions, and avoiding smoking (including passive smoking) and sympathomimetic drugs.

CMT can be diagnosed through symptoms, through measurement of the speed of nerve impulses (nerve conduction studies), through biopsy of the nerve, and through DNA testing. DNA testing can give a definitive diagnosis, but not all the genetic markers for CMT are known. CMT is first noticed when someone develops lower leg weakness, such as foot drop; or foot deformities, including hammertoes and high arches. But signs alone do not lead to diagnosis. Patients must be referred to a physician specialising in neurology or rehabilitation medicine. To see signs of muscle weakness, the neurologist asks patients to walk on their heels or to move part of their leg against an opposing force. To identify sensory loss, the neurologist tests for deep tendon reflexes, such as the knee jerk, which are reduced or absent in CMT. The doctor also asks about family history, because CMT is hereditary. The lack of family history does not rule out CMT, but helps rule out other causes of neuropathy, such as diabetes or exposure to certain chemicals or drugs.

In 2010, CMT was one of the first diseases where the genetic cause of a particular patient's disease was precisely determined by sequencing the whole genome of an affected individual. This was done by the scientists employed by the Charcot Marie Tooth Association (CMTA) Two mutations were identified in a gene, SH3TC2, known to cause CMT. Researchers then compared the affected patient's genome to the genomes of the patient's mother, father, and seven siblings with and without the disease. The mother and father each had one normal and one mutant copy of this gene, and had mild or no symptoms. The offspring that inherited two mutant genes presented fully with the disease.

The severity of symptoms vary widely even for the same type of CMT. There have been cases of monozygotic twins with varying levels of disease severity, showing that identical genotypes are associated with different levels of severity (see penetrance). Some patients are able to live a normal life and are almost or entirely asymptomatic. A 2007 review stated that "Life expectancy is not known to be altered in the majority of cases".

It is important to distinguish Raynaud's "disease" (primary Raynaud's) from "phenomenon" (secondary Raynaud's). Looking for signs of arthritis or vasculitis as well as a number of laboratory tests may separate them. If suspected to be secondary to systemic sclerosis, one tool which may help aid in the prediction of systemic sclerosis is thermography.

A careful medical history will often reveal whether the condition is primary or secondary. Once this has been established, an examination is largely to identify or exclude possible secondary causes.

- Digital artery pressure: pressures are measured in the arteries of the fingers before and after the hands have been cooled. A decrease of at least 15 mmHg is diagnostic (positive).

- Doppler ultrasound: to assess blood flow.

- Full blood count: this may reveal a normocytic anaemia suggesting the anaemia of chronic disease or renal failure.

- Blood test for urea and electrolytes: this may reveal renal impairment.

- Thyroid function tests: this may reveal hypothyroidism.

- An autoantibody screen, tests for rheumatoid factor, Erythrocyte sedimentation rate, and C-reactive protein, which may reveal specific causative illnesses or a generalised inflammatory process.

- Nail fold vasculature: this can be examined under the microscope.

To aid in the diagnosis of Raynaud's phenomenon, multiple sets of diagnostic criteria have been proposed. Table 1 below provides a summary of these various diagnostic criteria.

Recently, International Consensus Criteria were developed for the diagnosis of primary Raynaud's phenomenon by a panel of multiple experts in the fields of rheumatology and dermatology.

Medications offered can include the immunosuppressant prednisone, intravenous gamma globulin (IVIG), anticonvulsants such as gabapentin or Gabitril and antiviral medication, depending on the underlying cause..

In addition to treatment of the underlying disorder, palliative care can include the use of topical numbing creams, such as lidocaine or prilocaine. Care must be taken to apply only the necessary amount, as excess can contribute to the condition. Otherwise, these products offer extremely effective, but short-lasting, relief from the condition.

Paresthesia caused by stroke may receive some temporary benefit from high doses of Baclofen multiple times a day. HIV patients who self-medicate with cannabis report that it reduces their symptoms.

Paresthesia caused by shingles is treated with appropriate antiviral medication.

The differential focuses on distinguishing it from similar entities such as quadrilateral space syndrome, which involves the teres minor and variably the deltoid, and suprascapular nerve impingement at the spinoglenoid notch, which predominantly involves the infraspinatus.

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."

Breathing difficulties can occur, resulting from neuromyotonic activity of the laryngeal muscles. Laryngeal spasm possibly resulting from neuromyotonia has been described previously, and this highlights that, in patients with unexplained laryngospasm, neuromytonia should be added to the list of differential diagnoses.

Studies have shown subtly decreased metabolism on positron emission tomography (PET) and single photon emission computed tomography (SPECT) in the left inferior frontal and left temporal lobes. and or basal ganglia hypermetabolism. Ancillary laboratory tests including MRI and brain biopsy have confirmed temporal lobe involvement. Cranial MRI shows increased signal in the hippocampus.

Cerebral spinal fluid (CSF) shows normal protein, glucose, white blood cell, and IgG index but there are weak oligoclonal bands, absent in the blood. Marked changes in circadian serum levels of neurohormones and increased levels of peripheral neurotransmitters were also observed. The absence of morphological alterations of the brain pathology, the suggestion of diffusion of IgG into the thalamus and striatum, more marked than in the cortex (consistent with effects on the thalamolimbic system) the oligoclonal bands in the CSF and the amelioration after PE all strongly support an antibody-mediated basis for the condition. Raised CSF IgG concentrations and oligoclonal bands have been reported in patients with psychosis. Anti-acetylcholine receptors (anti-AChR) antibodies have also been detected in patients with thymoma, but without clinical manifestations of myasthenia gravis. There have also been reports of non-paraneoplastic limbic encephalitis associated with raised serum VGKC suggesting that these antibodies may give rise to a spectrum of neurological disease presenting with symptoms arising peripherally, centrally, or both. Yet, in two cases, oligoclonal bands were absent in the CSF and serum, and CSF immunoglobulin profiles were unremarkable.

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.

Allodynia (Ancient Greek "" "állos" "other" and "" "odúnē" "pain") refers to central pain sensitization (increased response of neurons) following normally non-painful, often repetitive, stimulation. Allodynia can lead to the triggering of a pain response from stimuli which do not normally provoke pain. Temperature or physical stimuli can provoke allodynia, which may feel like a burning sensation, and it often occurs after injury to a site. Allodynia is different from hyperalgesia, an extreme, exaggerated reaction to a stimulus which is normally painful.

It has been proposed that a vertebral subluxation can negatively affect general health by altering the neurological communication between the brain, spinal cord and peripheral nervous system. Although individuals may not always be symptomatic, straight chiropractors believe that the presence of vertebral subluxation is in itself justification for correction via spinal adjustment.

Chiropractic treatment of vertebral subluxation focuses on delivering a chiropractic adjustment which is a high velocity low amplitude (HVLA) thrust to the dysfunctional spinal segments to help correct the chiropractic subluxation complex. Spinal adjustment is the primary procedure used by chiropractors in the adjustment. Adjustment/manipulation has been shown to help with low back pain, neck pain and tension type headaches, but further studies are inconclusive on the use of spinal manipulation outside the treatment of neuromusculoskeletal disorders.

Signals from the sciatic nerve and it branches can be blocked, in order to interrupted transmission of pain signal from the innervation area, by performing a regional nerve blockade called a sciatic nerve block.

CMC OA is diagnosed based on clinical findings and radiologic imaging.