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.

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

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.

There is strong evidence to show that chronic orofacial pain (including AFP) is associated with psychological factors. Sometimes stressful life events appear to precede the onset of AFP, such as bereavement or illness in a family member. Hypochondriasis, especially cancerophobia, is also often cited as being involved. Most people with AFP are "normal" people who have been under extreme stress, however other persons with AFP have neuroses or personality disorders, and a small minority have psychoses. Some have been separated from their parents as children.

Depression, anxiety and altered behavior are strongly correlated with AFP. It is argued whether this is a sole or contributing cause of AFP, or the emotional consequences of suffering with chronic, unrelieved pain. It has been suggested that over 50% of people with AFP have concomitant depression or hypochondria. Furthermore, about 80% of persons with psychogenic facial pain report other chronic pain conditions such as listed in the table.

ATN is usually attributed to inflammation or demyelination, with increased sensitivity of the trigeminal nerve. These effects are believed to be caused by infection, demyelinating diseases, or compression of the trigeminal nerve (by an impinging vein or artery, a tumor, or arteriovenous malformation) and are often confused with dental problems. An interesting aspect is that this form affects both men and women equally and can occur at any age, unlike typical trigeminal neuralgia, which is seen most commonly in women. Though TN and ATN most often present in the fifth decade, cases have been documented as early as infancy.

Atypical trigeminal neuralgia (ATN), or type 2 trigeminal neuralgia, is a form of trigeminal neuralgia, a disorder of the fifth cranial nerve. This form of nerve pain is difficult to diagnose, as it is rare and the symptoms overlap with several other disorders. The symptoms can occur in addition to having migraine headache, or can be mistaken for migraine alone, or dental problems such as temporomandibular joint disorder or musculoskeletal issues. ATN can have a wide range of symptoms and the pain can fluctuate in intensity from mild aching to a crushing or burning sensation, and also to the extreme pain experienced with the more common trigeminal neuralgia.

Notalgia paraesthetica (NP) or notalgia paresthetica (also known as "Hereditary localized pruritus", "Posterior pigmented pruritic patch", and "Subscapular pruritus") is a chronic sensory neuropathy. Notalgia paraesthetica is a common localized itch, affecting mainly the area between the shoulder blades (especially the T2–T6 dermatomes) but occasionally with a more widespread distribution, involving the shoulders, back, and upper chest. The characteristic symptom is pruritus (itch or sensation that makes a person want to scratch) on the back, usually on the left hand side below the shoulder blade (mid to upper back). It is occasionally accompanied by pain, paresthesia (pins and needles), or hyperesthesia (unusual or pathologically increased sensitivity of the skin to sensory stimuli, such as pain, heat, cold, or touch), which results in a well circumscribed hyperpigmentation of a skin patch in the affected area.

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.

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.

Neuralgia-inducing cavitational osteonecrosis (NICO) is a controversial term, and it is questioned to exist by many. Osteonecrosis of the jaws refers to the death of bone marrow in the maxilla or the mandible due to inadequate blood supply. It is not necessarily a painful condition, typically there will be no pain at all unless bone necrotic bone becomes exposed to the mouth or through the facial skin, and even then this continues to be painless in some cases. When pain does occur, it is variable in severity, and may be neuralgiform or neuropathic in nature. The term NICO is used to describe pain caused by ischemic osteonecrosis of the jaws, where degenerative extracellular cystic spaces (cavitations inside the bone) are said to develop as a result of ischemia and infarctions in the bone marrow, possibly in relation to other factors such as a hereditary predisposition for thrombus formation within blood vessels, chronic low-grade dental infections and the use of vasoconstrictors in local anesthetics during dental procedures. This proposed phenomenon has been postulated to be the cause of pain in some patients with AFP or trigeminal neuralgia, but this is controversial. NICO is said to be significantly more common in females, and the lesions may or may not be visible on radiographs. When they are visible, the appearance is very variable. About 60% of the lesions appear as a "hot spot" on an technetium 99 bone scan. Proponents of NICO recommend decortication (surgical removal of a section of the cortical plate, originally described as a treatment for osteomyelitis of the jaws) and curettage of the necrotic bone from the cavitation, and in some reported cases, this has relieved the chronic pain. However, NICO appears to show a tendency to recur and develop elsewhere in the jaws. The American Association of Endodontists Research and Scientific Affairs Committee published a position statement on NICO in 1996, stating:

""Most affected sites with a postoperative NICO diagnosis have been in edentulous areas [where the teeth have been lost]. However, some patients with long, frustrating histories of pain associated with endodontically treated teeth have been presented the treatment option of tooth extraction followed by periapical curettage in an attempt to alleviate pain. The American Association of Endodontists cannot condone this practice when NICO is suspected. Because of the lack of clear etiological data, a NICO diagnosis should be considered only as a last resort when all possible local odontogenic causes for facial pain have been eliminated. If a NICO lesion is suspected in relation to an endodontically treated tooth, if possible, periradicular surgery and curettage should be attempted, not extraction. In addition, the practice of recommending the extraction of endodontically treated teeth for the prevention of NICO, or any other disease, is unethical and should be reported immediately to the appropriate state board of dentistry.""

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.

Other causes may include:

- Diabetes mellitus

- Facial nerve paralysis, sometimes bilateral, is a common manifestation of sarcoidosis of the nervous system, neurosarcoidosis.

- Bilateral facial nerve paralysis may occur in Guillain–Barré syndrome, an autoimmune condition of the peripheral nervous system.

- Moebius syndrome is a bilateral facial paralysis resulting from the underdevelopment of the VII cranial nerve (facial nerve), which is present at birth. The VI cranial nerve, which controls lateral eye movement, is also affected, so people with Moebius syndrome cannot form facial expression or move their eyes from side to side. Moebius syndrome is extremely rare, and its cause or causes are not known.

The mechanism of radial neuropathy is such that it can cause focal demyelination and axonal problems/degeneration (which is nerve fiber reaction to insult, and therefore axon death occurs). These would be caused via laceration or compression of the nerve in question.

Central facial palsy can be caused by a lacunar infarct affecting fibers in the internal capsule going to the nucleus. The facial nucleus itself can be affected by infarcts of the pontine arteries.

The incidence of hemifacial spasm is approximately 0.8 per 100,000 persons. Hemifacial spasm is more prevalent among females over 40 years of age. The estimated prevalence for women is 14.5 per 100,000 and 7.4 per 100,000 in men. Prevalence for hemifacial spasm increase with age, reaching 39.7 per 100,000 for those aged 70 years and older. One study divided 214 hemifacial patients based on the cause of the disease. The patients who had a compression in the facial nerve at the end of the brain stem as the primary hemifacial spasm and patients who had peripheral facial palsy or nerve lesion due to tumors, demyelination, trauma, or infection as secondary hemifacial spasm. The study found that 77% of hemifacial spasm is due to primary hemifacial spasm and 23% is due to secondary hemifacial spasm. The study also found both sets of patients to share similar age at onset, male to female ratios, and similar affected side. Another study with 2050 patients presented with hemifacial spasm between 1986 and 2009, only 9 cases were caused by a cerebellopontine angle syndrome, an incidence of 0.44%.

The facial nerve is the seventh of 12 cranial nerves. This cranial nerve controls the muscles in the face. Facial nerve palsy is more abundant in older adults than in children and is said to affect 15-40 out of 100,000 people per year. This disease comes in many forms which include congenital, infectious, traumatic, neoplastic, or idiopathic. The most common cause of this cranial nerve damage is Bell's palsy (idiopathic facial palsy) which is a paralysis of the facial nerve. Although Bell's palsy is more prominent in adults it seems to be found in those younger than 20 or older than 60 years of age. Bell's Palsy is thought to occur by an infection of the herpes virus which may cause demyelination and has been found in patients with facial nerve palsy. Symptoms include flattening of the forehead, sagging of the eyebrow, and difficulty closing the eye and the mouth on the side of the face that is affected. The inability to close the mouth causes problems in feeding and speech. It also causes lack of taste, acrimation, and sialorrhea.

The use of steroids can help in the treatment of Bell's Palsy. If in the early stages, steroids can increase the likelihood of a full recovery. This treatment is used mainly in adults. The use of steroids in children has not been proven to work because they seem to recover completely with or without them. Children also tend to have better recovery rates than older adults. Recovery rate also depends on the cause of the facial nerve palsy (e.g. infections, perinatal injury, congenital dysplastic). If the palsy is more severe patients should seek steroids or surgical procedures. Facial nerve palsy may be the indication of a severe condition and when diagnosed a full clinical history and examination are recommended.

Although rare, facial nerve palsy has also been found in patients with HIV seroconversion. Symptoms found include headaches (bitemporal or occipital), the inability to close the eyes or mouth, and may cause the reduction of taste. Few cases of bilateral facial nerve palsy have been reported and is said to only effect 1 in every 5 million per year.

The exact incidence of Frey syndrome is unknown. The disorder most often occurs as a complication of the surgical removal of a parotid gland (parotidectomy). The percentage of individuals who develop Frey syndrome after a parotidectomy is controversial and reported estimates range from 30-50 percent. In follow-up examinations, approximately 15 percent of affected individuals rated their symptoms as severe. Frey syndrome affects males and females in equal numbers.

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".

Frey's syndrome often results as a side effect of surgeries of or near the parotid gland or due to injury to the auriculotemporal nerve, which passes through the parotid gland in the early part of its course. The Auriculotemporal branch of the Trigeminal nerve carries parasympathetic fibers to the sweat glands of the scalp and the parotid salivary gland. As a result of severance and inappropriate regeneration, the parasympathetic nerve fibers may switch course, resulting in "gustatory Sweating" or sweating in the anticipation of eating, instead of the normal salivatory response.

It is often seen with patients who have undergone endoscopic thoracic sympathectomy, a surgical procedure wherein part of the sympathetic trunk is cut or clamped to treat sweating of the hands or blushing. The subsequent regeneration or nerve sprouting leads to abnormal sweating and salivating. It can also include discharge from the nose when smelling certain food.

Rarely, Frey's syndrome can result from causes other than surgery, including accidental trauma, local infections, sympathetic dysfunction and pathologic lesions within the parotid gland.

An example of such, rare trauma or localized infection; can be seen in situations where a hair follicle has become ingrown and is causing trauma or localized infection near or over one of the branches of the auriculotemporal nerve.

Microvascular decompression appears to be the most popular surgical treatment at present. Microvascular decompression relieves pressure on the facial nerve, which is the cause of most hemifacial spasm cases. Excellent to good results are reported in 80% or more cases with a 10% recurrence rate. In the present series approximately 10% had previously failed surgery. Serious complications can follow microsurgical decompressive operations, even when performed by experienced surgeons. These include cerebellar haematoma or swelling, brain stem infarction (blood vessel of the brain stem blocked), cerebral infarction (ischemic stroke resulting from a disturbance in the blood vessels supplying blood to the brain), subdural haematoma and intracerebral infarction (blockage of blood flow to the brain). Death or permanent disability (hearing loss) can occur in 2% of patients of hemifacial spasm.

Neuritis () is inflammation of a nerve or the general inflammation of the peripheral nervous system. Symptoms depend on the nerves involved but may include pain, paresthesia (pins-and-needles), paresis (weakness), hypoesthesia (numbness), anesthesia, paralysis, wasting, and disappearance of the reflexes.

Cranial nerve disease is an impaired functioning of one of the twelve cranial nerves. Although it could theoretically be considered a mononeuropathy, it is not considered as such under MeSH.

It is possible for a disorder of more than one cranial nerve to occur at the same time, if a trauma occurs at a location where many cranial nerves run together, such as the jugular fossa. A brainstem lesion could also cause impaired functioning of multiple cranial nerves, but this condition would likely also be accompanied by distal motor impairment.

A neurological examination can test the functioning of individual cranial nerves, and detect specific impairments.

A compartment space is anatomically determined by an unyielding fascial (and osseous) enclosure of the muscles. The anterior compartment syndrome of the lower leg (often referred to simply as anterior compartment syndrome), can affect any and all four muscles of that compartment: tibialis anterior, extensor hallucis longus, extensor digitorum longus, and peroneus tertius.

This term is often mistakenly used to describe various related/proximal conditions, including Anterior Shin Splints. It is important to distinguish between the two, as shin splints rarely causes serious health problems, while Anterior Compartment Syndrome can lead to irreversible damage.

The true compartment syndrome arises due to increased pressure within the unyielding anterior compartment of the leg. The pressure obstructs venous outflow, which causes further swelling and increased pressure. The resultant ischemia leads to necrosis (death of tissue) of the muscles and nerves. The process can begin with swelling of the tibialis anterior, extensor hallucis longus, extensor digitorum longus, and/or the peroneus tertius muscles in response to strong eccentric contractions sufficient to produce postexercise soreness.

Ramsay Hunt syndrome type 2 refers to shingles of the geniculate ganglion. After initial infection, varicella zoster virus lies dormant in nerve cells in the body, where it is kept in check by the immune system. Given the opportunity, for example during an illness that suppresses the immune system, the virus travels to the end of the nerve cell, where it causes the symptoms described above.

The affected ganglion is responsible for the movements of facial muscles, the touch sensation of a part of ear and ear canal, the taste function of the frontal two-thirds of the tongue, and the moisturization of the eyes and the mouth. The syndrome specifically refers to the combination of this entity with weakness of the muscles activated by the facial nerve. In isolation, the latter is called Bell's Palsy.

However, as with shingles, the lack of lesions does not definitely exclude the existence of a herpes infection. Even before the eruption of vesicles, varicella zoster virus can be detected from the skin of the ear.

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)