CRPS can occur at any age with the average age at diagnosis being 42. It affects both men and women; however, CRPS is three times more frequent in females than males.

CRPS affects both adults and children, and the number of reported CRPS cases among adolescents and young adults has been increasing, with a recent observational study finding an incidence of 1.16/100,000 among children in Scotland.

Good progress can be made in treating CRPS if treatment is begun early, ideally within three months of the first symptoms. If treatment is delayed, however, the disorder can quickly spread to the entire limb, and changes in bone, nerve, and muscle may become irreversible. The prognosis is not always good. Johns Hopkins Hospital reports that 77% of sufferers have spreads from the original site or flares in other parts of the body. The limb, or limbs, can experience muscle atrophy, loss of use, and functionally useless parameters that require amputation. RSD/CRPS will not "burn itself out", but if treated early, it is likely to go into remission. Once one is diagnosed with Complex Regional Pain Syndrome, the likelihood of it resurfacing after going into remission is significant. It is important to take precautions and seek immediate treatment upon any injury.

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.

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.

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.

Other causes may include:

- Anticonvulsant pharmaceutical drugs, such as topiramate, sultiame, and acetazolamide

- Anxiety and/or panic disorder

- Benzodiazepine withdrawal syndrome

- Beta alanine

- Carpal tunnel syndrome

- Cerebral amyloid angiopathy

- Chiari malformation

- Coeliac disease (celiac disease)

- Complex regional pain syndrome

- Decompression sickness

- Dehydration

- Dextromethorphan (recreational use)

- Fabry disease

- Erythromelalgia

- Fibromyalgia

- Fluoroquinolone toxicity

- Guillain–Barré syndrome (GBS)

- Heavy metals

- Herpes zoster

- Hydroxy alpha sanshool, a component of Sichuan peppers

- Hyperglycemia (high blood sugar)

- Hyperkalemia

- Hyperventilation

- Hypoglycemia (low blood sugar)

- Hypocalcemia, and in turn:

- Hypermagnesemia, a condition in which hypocalcemia itself is typically observed as a secondary symptom

- Hypomagnesemia, often as a result of long term proton-pump inhibitor use

- Hypothyroidism

- Immunodeficiency, such as chronic inflammatory demyelinating polyneuropathy (CIDP)

- Intravenous administering of strong pharmaceutical drugs acting on the central nervous system (CNS), mainly opioids, opiates, narcotics; especially in non-medical use (drug abuse)

- Ketorolac

- Lidocaine poisoning

- Lomotil

- Lupus erythematosus

- Lyme disease

- Menopause

- Mercury poisoning

- Migraines

- Multiple sclerosis

- Nitrous oxide, long-term exposure

- Obdormition

- Pyrethrum and pyrethroid (pesticide)

- Rabies

- Radiation poisoning

- Sarcoidosis

- Scorpion stings

- Spinal disc herniation or injury

- Spinal stenosis

- Stinging nettles

- Syringomyelia

- Transverse myelitis

- Vitamin B deficiency

- Vitamin B deficiency

- Withdrawal from certain selective serotonin reuptake inhibitors (or serotonin-specific reuptake inhibitors) (SSRIs), such as paroxetine or serotonin-norepinephrine reuptake inhibitors (SNRIs) such as venlafaxine

There are not a lot of studies that have investigated the prevalence of EM, so far only four have been conducted.

The mean of all the studies combined results in an EM estimation incidence of 4.7/100,000 with a mean of 1 : 3.7 of the male to female ratio, respectively.

In 1997 there was a study conducted in Norway that estimated that the annual incidence of 2/100,000, with a 1 : 2.4 male to female ratio in this study

population, respectively. In 2009 there was a population-based study of EM in the USA (Olmsted County, Minnesota), that reported that the annual incidence was 1.3/100,000, with a 1 : 5.6 male to female ratio in this study population, respectively.

The incidence in this study of primary and secondary EM was 1.1 : 0.2 per 100 000 people per year, respectively.

A study of a single centre in the south of Sweden in 2012, showed the overall annual population-based incidence was 0.36/100,000.

In New Zealand (Dunedin) a study estimated that in 2013 the incidence of EM is 15/100,000, with a 1 : 3 male to female ratio in this study

population, respectively. This last study has an estimation that is at least ten times higher than the prevalence previously reported. This study recruited individuals based on self-identification of symptoms (after self-identification, patients where invited for an assessment of an EM diagnosis), instead of participants that are identified through secondary and tertiary referrals that was conducted by the other studies.

The consumption of two species of related fungi, "Clitocybe acromelalga" from Japan, and "Clitocybe amoenolens" from France, has led to several cases of mushroom-induced erythromelalgia which lasted from 8 days to 5 months.

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.

Phantom limb pain and phantom limb sensations are linked, but must be differentiated from one another. While phantom limb sensations are experienced by those with congenital limb deficiency, spinal cord injury, and amputation, phantom limb pain occurs almost exclusively as a result of amputation. Almost immediately following the amputation of a limb, 90-98% of patients report experiencing a phantom sensation. Nearly 75% of individuals experience the phantom as soon as anesthesia wears off, and the remaining 25% of patients experience phantoms within a few days or weeks. Of those experiencing innocuous sensations, a majority of patients also report distinct painful sensations.

Age and gender have not been shown to affect the onset or duration of phantom limb pain. Although it has not been fully explored, one investigation of lower limb amputation observed that as stump length decreased, there was a greater incidence of moderate and severe phantom pain.

Phantom pain involves the sensation of pain in a part of the body that has been removed.

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.

Electroanalgesia is a form of analgesia, or pain relief, that uses electricity to ease pain. Electrical devices can be internal or external, at the site of pain (local) or delocalized throughout the whole body. It works by interfering with the electric currents of pain signals, inhibiting them from reaching the brain and inducing a response; different from traditional analgesics, such as opiates which mimic natural endorphins and NSAIDS (non-steroidal anti-inflammatory drugs) that help relieve inflammation and stop pain at the source. Electroanalgesia has a lower addictive potential and poses less health threats to the general public, but can cause serious health problems, even death, in people with other electrical devices such as pacemakers or internal hearing aids, or with heart problems.

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.

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.

Allodynia is a clinical feature of many painful conditions, such as neuropathies, complex regional pain syndrome, postherpetic neuralgia, fibromyalgia, and migraine. Allodynia may also be caused by some populations of stem cells used to treat nerve damage including spinal cord injury. Static mechanical allodynia is a paradoxical painful hypoaesthesia, one etiology of which is lesions of A-beta fibers.

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".

MMA mostly occurs in males between the ages of 15 and 25. Onset and progression are slow. MMA is seen most frequently in Asia, particularly in Japan and India; it is much less common in North America.

Charcot–Marie–Tooth disease (CMT) is one of the hereditary motor and sensory neuropathies, a group of varied inherited disorders of the peripheral nervous system characterized by progressive loss of muscle tissue and touch sensation across various parts of the body. Currently incurable, this disease is the most commonly inherited neurological disorder, and affects approximately 1 in 2,500 people. CMT was previously classified as a subtype of muscular dystrophy.

Antibodies against voltage-gated potassium channels (VGKC), which are detectable in about 40% of patients with acquired neuromytonia, have been implicated in Morvan’s pathophysiology. Raised serum levels of antibodies to VGKCs have been reported in three patients with Morvan’s Syndrome. Binding of serum from a patient with Morvan’s Syndrome to the hippocampus in a similar pattern of antibodies to known VGKC suggest that these antibodies can also cause CNS dysfunction. Additional antibodies against neuromuscular junction channels and receptors have also been described. Experimental evidence exists that these anti-VGKC antibodies cause nerve hyperexcitability by suppression of voltage gated K+ outward currents, whereas other, yet undefined humoral factors have been implicated in anti-VGKC antibody negative neuromyotonia. It is believed that antibodies to the Shaker-type K+ channels (the Kv1 family) are the type of potassium channel most strongly associated with acquired neuromyotonia and Morvan’s Syndrome.

Whether VGKC antibodies play a pathogenic role in the encephalopathy as they do in the peripheral nervous system is as yet unclear. It has been suggested that the VGKC antibodies may cross the blood–brain barrier and act centrally, binding predominantly to thalamic and striatal neurons causing encephalopathic and autonomic features.

Sciatic nerve injury occurs between 0.5% and 2.0% of the time during total hip arthroplasty. Sciatic nerve palsy is a complication of total hip arthroplasty with an incidence of 0.2% to 2.8% of the time, or with an incidence of 1.7% to 7.6% following revision. Following the procedure, in rare cases, a screw, broken piece of trochanteric wire, fragment of methyl methacrylate bone cement, or Burch-Schneider metal cage can impinge on the nerve; this can cause sciatic nerve palsy which may resolve after the fragment is removed and the nerve freed. The nerve can be surrounded in oxidized regenerated cellulose to prevent further scarring. Sciatic nerve palsy can also result from severe spinal stenosis following the procedure, which can be addressed by spinal decompression surgery. It is unclear if inversion therapy is able to decompress the sacral vertebrae, it may only work on the lumbar aspects of the sciatic nerves.

Sciatic nerve injury may also occur from improperly performed injections into the buttock, and may result in sensory loss.

In one case, a patient was diagnosed with both Morvan's syndrome and pulmonary hyalinizing granulomas (PHG). PHG are rare fibrosing lesions of the lung, which have central whorled deposits of lamellar collagen. How these two diseases relate to one another is still unclear.

Thymoma, prostate adenoma, and in situ carcinoma of the sigmoid colon have also been found in patients with Morvan’s Syndrome.

The sciatic nerve (; also called "ischiadic nerve", "ischiatic nerve", "butt nerve") is a large nerve in humans and other animals. It begins in the lower back and runs through the buttock and down the lower limb. It is the longest and widest single nerve in the human body, going from the top of the leg to the foot on the posterior aspect. The sciatic nerve provides the connection to the nervous system for nearly the whole of the skin of the leg, the muscles of the back of the thigh, and those of the leg and foot. It is derived from spinal nerves L4 to S3. It contains fibers from both the anterior and posterior divisions of the lumbosacral plexus.

There are many causes of TOS. The most frequent cause is trauma, either sudden (as in a clavicle fracture caused by a car accident), or repetitive (as in a legal secretary who works with his/her hands, wrists, and arms at a fast paced desk station with non-ergonomic posture for many years). TOS is also found in certain occupations involving lots of lifting of the arms and repetitive use of the wrists and arms.

One cause of arterial compression is trauma, and a recent case involving fracture of the clavicle has been reported.

The two groups of people most likely to develop TOS are those suffering from neck injuries due to traffic accidents and those who use computers in non-ergonomic postures for extended periods of time. TOS is frequently a repetitive stress injury (RSI) caused by certain types of work environments. Other groups which may develop TOS are athletes who frequently raise their arms above the head (such as swimmers, volleyball players, dancers, badminton players, baseball pitchers, and weightlifters), rock climbers, electricians who work long hours with their hands above their heads, and some musicians.

Raynaud's phenomenon, or "Secondary Raynaud's", occurs "secondary to" a wide variety of other conditions.

Secondary Raynaud's has a number of associations:

- Connective tissue disorders:

- scleroderma

- systemic lupus erythematosus

- rheumatoid arthritis

- Sjögren's syndrome

- dermatomyositis

- polymyositis

- mixed connective tissue disease

- cold agglutinin disease

- Ehlers-Danlos syndrome

- Eating disorders:

- anorexia nervosa

- Obstructive disorders:

- atherosclerosis

- Buerger's disease

- Takayasu's arteritis

- subclavian aneurysms

- thoracic outlet syndrome

- Drugs:

- beta-blockers

- cytotoxic drugs – particularly chemotherapeutics and most especially bleomycin

- ciclosporin

- bromocriptine

- ergotamine

- sulfasalazine

- anthrax vaccines whose primary ingredient is the Anthrax Protective Antigen

- stimulant medications, such as those used to treat ADHD (amphetamine and methylphenidate)

- OTC pseudoephedrine medications (Chlor-Trimeton, Sudafed, others)

- Occupation:

- jobs involving vibration, particularly drilling and prolonged use of a String trimmer (weed whacker), suffer from vibration white finger

- exposure to vinyl chloride, mercury

- exposure to the cold (e.g., by working as a frozen food packer)

- Others:

- physical trauma, such as that sustained in auto accidents or other traumatic events

- Lyme disease

- hypothyroidism

- cryoglobulinemia

- malignancy

- chronic fatigue syndrome

- reflex sympathetic dystrophy

- carpal tunnel syndrome

- magnesium deficiency

- multiple sclerosis

- erythromelalgia (clinically presenting as the opposite of Raynaud's, with hot and warm extremities) often co-exists in patients with Raynaud's)

Raynaud's can "herald" these diseases by periods of more than twenty years in some cases, making it effectively their first presenting symptom. This may be the case in the CREST syndrome, of which Raynaud's is a part.

Patients with Secondary Raynaud's can also have symptoms related to their underlying diseases. Raynaud's phenomenon is the initial symptom that presents for 70% of patients with scleroderma, a skin and joint disease.

When Raynaud's phenomenon is limited to one hand or one foot, it is referred to as Unilateral Raynaud's. This is an uncommon form, and it is always secondary to local or regional vascular disease. It commonly progresses within several years to affect other limbs as the vascular disease progresses.