In the United States each year approximately 1,000,000 individuals develop herpes zoster. Of those individuals approximately 10-18% develop postherpetic neuralgia.

Less than 10 percent of people younger than 60 develop postherpetic neuralgia after a bout of herpes zoster, while about 40 percent of people older than 60 do.

In 1995, the Food and Drug Administration (FDA) approved the Varicella vaccine to prevent chickenpox. Its effect on postherpetic neuralgia is still unknown. The vaccine—made from a weakened form of the varicella-zoster virus—may keep chickenpox from occurring in nonimmune children and adults, or at least lessen the risk of the chickenpox virus lying dormant in the body and reactivating later as shingles. If shingles could be prevented, postherpetic neuralgia could be completely avoided.

In May 2006 the Advisory Committee on Immunization Practices approved a new vaccine by Merck (Zostavax) against shingles. This vaccine is a more potent version of the chickenpox vaccine, and evidence shows that it reduces the incidence of postherpetic neuralgia. The CDC recommends use of this vaccine in all persons over 60 years old.

Psychological and social support has found to play a key role in the management of chronic illnesses and chronic pain conditions, such as trigeminal neuralgia. Chronic pain can cause constant frustration to an individual as well as to those around them. As a result, there are many advocacy groups.

Most patients have persistent headaches, although about 15% will remit, and 8% will have a relapsing-remitting type. It is not infrequent for NDPH to be an intractable headache disorder that is unresponsive to standard headache therapies.

A variety of surgeries have been performed including microvascular decompression (MVD) of the fifth, ninth, and tenth nerves; as well as partial cutting of the nervus intermedius, geniculate ganglion, chorda tympani and/or the ninth and tenth cranial nerves.

The trigeminal nerve is a mixed cranial nerve responsible for sensory data such as tactition (pressure), thermoception (temperature), and nociception (pain) originating from the face above the jawline; it is also responsible for the motor function of the muscles of mastication, the muscles involved in chewing but not facial expression.

Several theories exist to explain the possible causes of this pain syndrome. It was once believed that the nerve was compressed in the opening from the inside to the outside of the skull; but leading research indicates that it is an enlarged or lengthened blood vessel – most commonly the superior cerebellar artery – compressing or throbbing against the microvasculature of the trigeminal nerve near its connection with the pons. Such a compression can injure the nerve's protective myelin sheath and cause erratic and hyperactive functioning of the nerve. This can lead to pain attacks at the slightest stimulation of any area served by the nerve as well as hinder the nerve's ability to shut off the pain signals after the stimulation ends. This type of injury may rarely be caused by an aneurysm (an outpouching of a blood vessel); by an AVM (arteriovenous malformation); by a tumor; such as an arachnoid cyst or meningioma in the cerebellopontine angle; or by a traumatic event such as a car accident.

Short-term peripheral compression is often painless. Persistent compression results in local demyelination with no loss of axon potential continuity. Chronic nerve entrapment results in demyelination primarily, with progressive axonal degeneration subsequently. It is, "therefore widely accepted that trigeminal neuralgia is associated with demyelination of axons in the Gasserian ganglion, the dorsal root, or both." It has been suggested that this compression may be related to an aberrant branch of the superior cerebellar artery that lies on the trigeminal nerve. Further causes, besides an aneurysm, multiple sclerosis or cerebellopontine angle tumor, include: a posterior fossa tumor, any other expanding lesion or even brainstem diseases from strokes.

Trigeminal neuralgia is found in 3–4% of people with multiple sclerosis, according to data from seven studies. It has been theorized that this is due to damage to the spinal trigeminal complex. Trigeminal pain has a similar presentation in patients with and without MS.

Postherpetic neuralgia, which occurs after shingles, may cause similar symptoms if the trigeminal nerve is damaged.

When there is no [apparent] structural cause, the syndrome is called idiopathic.

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.

The pathophysiology of NDPH is poorly understood. Research points to an immune-mediated, inflammatory process. Cervical joint hypermobility and defective internal jugular venous drainage have also been suggested as causes.

In 1987, Vanast first suggested autoimmune disorder with a persistent viral trigger for CDH (now referred to as NDPH). Post-infectious origins have been approximated to make up anywhere between 30–80% of NDPH patients in different studies. Viruses that have been implicated include Epstein-Barr virus, herpes simplex virus and cytomegalovirus.

Non-specific upper respiratory infections including rhinitis and pharyngitis are most often cited by patients. In one study, 46.5% patients recalled a specific trigger with a respiratory tract illness being the most common. In children, almost half report headache onset during an infection.

A study by Rozen and Swindan in 2007 found elevated levels of tumor necrosis factor alpha, a proinflammatory cytokine, in the cerebrospinal fluid but not the blood of patients with NDPH, chronic migraine, and post-traumatic headaches suggesting inflammation as the cause of the headaches.

NDPH as an inflammatory, post-infectious manifestation indicates a potential meningoencephalitis event in NDPH patients. Tissue specificity is a general feature of post-infectious, immune-mediated conditions, and the meninges are a type of connective tissue membrane. Inflammation of the meninges was first proposed as a possible pathophysiology for migraine in the 1960s and has recently been explored again. This hypothesis is based on meningeal mast cell activation. Reactive arthritis (ReA) is a post-infectious disease entity of synovium/joints with connective tissue membrane (synovial membrane of the joints) which provides a corollary.

NDPH has been reported in Hashimoto's encephalopathy, an immune-mediated type of encephalitis. A mean 5-year retrospective analysis of 53 patients with a history of viral meningitis and 17 patients with a history of bacterial meningitis showed an increased onset of subsequent new onset headache and increased severity of those with prior primary headaches.

A trial of the anticonvulsant drug carbamazepine is common for patients diagnosed with GN. For patients who do not tolerate or respond to carbamazepine, alternative drugs include oxcarbazepine, gabapentin, phenytoin, lamotrigine, and baclofen. In addition, tricyclics (e.g., amitriptyline) and pregabalin are useful in other types of neuropathic pain.

Both forms of facial neuralgia are relatively rare, with an incidence recently estimated between 12 and 24 new cases per hundred thousand population per year.

ATN often goes undiagnosed or misdiagnosed for extended periods, leading to a great deal of unexplained pain and anxiety. A National Patient Survey conducted by the US Trigeminal Neuralgia Association in the late 1990s indicated that the average facial neuralgia patient may see six different physicians before receiving a first definitive diagnosis. The first practitioner to see facial neuralgia patients is often a dentist who may lack deep training in facial neurology. Thus ATN may be misdiagnosed as Tempormandibular Joint Disorder.

This disorder is regarded by many medical professionals to comprise the most severe form of chronic pain known in medical practice. In some patients, pain may be unresponsive even to opioid drugs at any dose level that leaves the patient conscious. The disorder has thus acquired the unfortunate and possibly inflammatory nickname, "the suicide disease".

Symptoms of ATN may overlap with a pain disorder occurring in teeth called atypical odontalgia (literal meaning "unusual tooth pain"), with aching, burning, or stabs of pain localized to one or more teeth and adjacent jaw. The pain may seem to shift from one tooth to the next, after root canals or extractions. In desperate efforts to alleviate pain, some patients undergo multiple (but unneeded) root canals or extractions, even in the absence of suggestive X-ray evidence of dental abscess.

ATN symptoms may also be similar to those of post-herpetic neuralgia, which causes nerve inflammation when the latent herpes zoster virus of a previous case of chicken pox re-emerges in shingles. Fortunately, post-herpetic neuralgia is generally treated with medications that are also the first medications tried for ATN, which reduces the negative impact of misdiagnosis.

The subject of atypical trigeminal neuralgia is considered problematic even among experts. The term atypical TN is broad and due to the complexity of the condition, there are considerable issues with defining the condition further. Some medical practitioners no longer make a distinction between facial neuralgia (a nominal condition of inflammation) versus facial neuropathy (direct physical damage to a nerve).

Due to the variability and imprecision of their pain symptoms, ATN or atypical odontalgia patients may be misdiagnosed with atypical facial pain (AFP) or "hypochondriasis", both of which are considered problematic by many practitioners. The term "atypical facial pain" is sometimes assigned to pain which crosses the mid-line of the face or otherwise does not conform to expected boundaries of nerve distributions or characteristics of validated medical entities. As such, AFP is seen to comprise a diagnosis by reduction.

As noted in material published by the [US] National Pain Foundation: "atypical facial pain is a confusing term and should never be used to describe patients with trigeminal neuralgia or trigeminal neuropathic pain. Strictly speaking, AFP is classified as a "somatiform pain disorder"; this is a psychological diagnosis that should be confirmed by a skilled pain psychologist. Patients with the diagnosis of AFP have no identifiable underlying physical cause for the pain. The pain is usually constant, described as aching or burning, and often affects both sides of the face (this is almost never the case in patients with trigeminal neuralgia). The pain frequently involves areas of the head, face, and neck that are outside the sensory territories that are supplied by the trigeminal nerve. It is important to correctly identify patients with AFP since the treatment for this is strictly medical. Surgical procedures are not indicated for atypical facial pain."

The term "hypochondriasis" is closely related to "somatoform pain disorder" and "conversion disorder" in the Diagnostic and Statistical Manual (DSM-IV) of the American Psychiatric Association. As of July 2011, this axis of the DSM-IV is undergoing major revision for the DSM-V, with introduction of a new designation "Complex Somatic Symptom Disorder". However, it remains to be demonstrated that any of these "disorders" can reliably be diagnosed as a medical entity with a discrete and reliable course of therapy.

It is possible that there are triggers or aggravating factors that patients need to learn to recognize to help manage their health. Bright lights, sounds, stress, and poor diet are examples of additional stimuli that can contribute to the condition. The pain can cause nausea, so beyond the obvious need to treat the pain, it is important to be sure to try to get adequate rest and nutrition.

Depression is frequently co-morbid with neuralgia and neuropathic pain of all sorts, as a result of the negative effects that pain has on one's life. Depression and chronic pain may interact, with chronic pain often predisposing patients to depression, and depression operating to sap energy, disrupt sleep and heighten sensitivity and the sense of suffering. Dealing with depression should thus be considered equally important as finding direct relief from the pain.

About 65% of persons with CH are, or have been, tobacco smokers. Stopping smoking does not lead to improvement of the condition and CH also occurs in those who have never smoked (e.g. children); it is thought unlikely that smoking is a cause. People with CH may be predisposed to certain traits, including smoking or other lifestyle habits.

Cluster headache may, but rarely, run in some families in an autosomal dominant inheritance pattern. People with a first degree relative with the condition are about 14–48 times more likely to develop it themselves, and between 1.9 and 20% of persons with CH have a positive family history. Possible genetic factors warrant further research, current evidence for genetic inheritance is limited.

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.

Primary headache syndromes have many different possible treatments. In those with chronic headaches the long term use of opioids appears to result in greater harm than benefit.

In general, children suffer from the same types of headaches as adults do, but their symptoms may be slightly different. The diagnostic approach to headache in children is similar to that of adults. However, young children may not be able to verbalize pain well. If a young child is fussy, they may have a headache.

Approximately 1% of Emergency Department visits for children are for headache. Most of these headaches are not dangerous. The most common type of headache seen in pediatric Emergency Rooms is headache caused by a cold (28.5%). Other headaches diagnosed in the Emergency Department include post-traumatic headache (20%), headache related to a problem with a ventriculoperitoneal shunt (a device put into the brain to remove excess CSF and reduce pressure in the brain) (11.5%) and migraine (8.5%). The most common serious headaches found in children include brain bleeds (subdural hematoma, epidural hematoma), brain abscesses, meningitis and ventriculoperitoneal shunt malfunction. Only 4–6.9% of kids with a headache have a serious cause.

Just as in adults, most headaches are benign, but when head pain is accompanied with other symptoms such as speech problems, muscle weakness, and loss of vision, a more serious underlying cause may exist: hydrocephalus, meningitis, encephalitis, abscess, hemorrhage, tumor, blood clots, or head trauma. In these cases, the headache evaluation may include CT scan or MRI in order to look for possible structural disorders of the central nervous system. If a child with a recurrent headache has a normal physical exam, neuroimaging is not recommended. Guidelines state children with abnormal neurologic exams, confusion, seizures and recent onset of worst headache of life, change in headache type or anything suggesting neurologic problems should receive neuroimaging.

When children complain of headaches, many parents are concerned about a brain tumor. Generally, headaches caused by brain masses are incapacitating and accompanied by vomiting. One study found characteristics associated with brain tumor in children are: headache for greater than 6 months, headache related to sleep, vomiting, confusion, no visual symptoms, no family history of migraine and abnormal neurologic exam.

Some measures can help prevent headaches in children. Drinking plenty of water throughout the day, avoiding caffeine, getting enough and regular sleep, eating balanced meals at the proper times, and reducing stress and excess of activities may prevent headaches. Treatments for children are similar to those for adults, however certain medications such as narcotics should not be given to children.

Children who have headaches will not necessarily have headaches as adults. In one study of 100 children with headache, eight years later 44% of those with tension headache and 28% of those with migraines were headache free. In another study of people with chronic daily headache, 75% did not have chronic daily headaches two years later, and 88% did not have chronic daily headaches eight years later.

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.""

The rash and pain usually subside within three to five weeks, but about one in five people develop a painful condition called postherpetic neuralgia, which is often difficult to manage. In some people, shingles can reactivate presenting as "zoster sine herpete": pain radiating along the path of a single spinal nerve (a "dermatomal distribution"), but without an accompanying rash. This condition may involve complications that affect several levels of the nervous system and cause many cranial neuropathies, polyneuritis, myelitis, or aseptic meningitis. Other serious effects that may occur in some cases include partial facial paralysis (usually temporary), ear damage, or encephalitis. During pregnancy, first infections with VZV, causing chickenpox, may lead to infection of the fetus and complications in the newborn, but chronic infection or reactivation in shingles are not associated with fetal infection.

There is a slightly increased risk of developing cancer after a shingles infection. However, the mechanism is unclear and mortality from cancer did not appear to increase as a direct result of the presence of the virus. Instead, the increased risk may result from the immune suppression that allows the reactivation of the virus.

Although shingles typically resolves within 3–5 weeks, certain complications may arise:

- Secondary bacterial infection

- Motor involvement, including weakness especially in "motor herpes zoster"

- Eye involvement: trigeminal nerve involvement (as seen in herpes ophthalmicus) should be treated early and aggressively as it may lead to blindness. Involvement of the tip of the nose in the zoster rash is a strong predictor of herpes ophthalmicus.

- Postherpetic neuralgia, a condition of chronic pain following shingles

Varicella zoster virus (VZV) has a high level of infectivity and has a worldwide prevalence. Shingles is a re-activation of latent VZV infection: zoster can only occur in someone who has previously had chickenpox (varicella).

Shingles has no relationship to season and does not occur in epidemics. There is, however, a strong relationship with increasing age. The incidence rate of shingles ranges from 1.2 to 3.4 per 1,000 person‐years among younger healthy individuals, increasing to 3.9–11.8 per 1,000 person‐years among those older than 65 years, and incidence rates worldwide are similar.

This relationship with age has been demonstrated in many countries, and is attributed to the fact that cellular immunity declines as people grow older.

Another important risk factor is immunosuppression. Other risk factors include psychological stress. According to a study in North Carolina, "black subjects were significantly less likely to develop zoster than were white subjects." It is unclear whether the risk is different by gender. Other potential risk factors include mechanical trauma and exposure to immunotoxins.

There is no strong evidence for a genetic link or a link to family history. A 2008 study showed that people with close relatives who had had shingles were twice as likely to develop it themselves, but a 2010 study found no such link.

Adults with latent VZV infection who are exposed intermittently to children with chickenpox receive an immune boost. This periodic boost to the immune system helps to prevent shingles in older adults. When routine chickenpox vaccination was introduced in the United States, there was concern that, because older adults would no longer receive this natural periodic boost, there would be an increase in the incidence of shingles.

Multiple studies and surveillance data, at least when viewed superficially, demonstrate no consistent trends in incidence in the U.S. since the chickenpox vaccination program began in 1995. However, upon closer inspection, the two studies that showed no increase in shingles incidence were conducted among populations where varicella vaccination was not as yet widespread in the community. A later study by Patel "et al." concluded that since the introduction of the chickenpox vaccine, hospitalization costs for complications of shingles increased by more than $700 million annually for those over age 60. Another study by Yih "et al". reported that as varicella vaccine coverage in children increased, the incidence of varicella decreased, and the occurrence of shingles among adults increased by 90%. The results of a further study by Yawn "et al". showed a 28% increase in shingles incidence from 1996 to 2001. It is likely that incidence rate will change in the future, due to the aging of the population, changes in therapy for malignant and autoimmune diseases, and changes in chickenpox vaccination rates; a wide adoption of zoster vaccination could dramatically reduce the incidence rate.

In one study, it was estimated that 26% of those who contract shingles eventually present complications. Postherpetic neuralgia arises in approximately 20% of people with shingles. A study of 1994 California data found hospitalization rates of 2.1 per 100,000 person-years, rising to 9.3 per 100,000 person-years for ages 60 and up. An earlier Connecticut study found a higher hospitalization rate; the difference may be due to the prevalence of HIV in the earlier study, or to the introduction of antivirals in California before 1994.

Anesthesia dolorosa or anaesthesia dolorosa or deafferentation pain is pain felt in an area (usually of the face) which is completely numb to touch. The pain is described as constant, burning, aching or severe. It can be a side effect of surgery involving any part of the trigeminal system, and occurs after 1–4% of peripheral surgery for trigeminal neuralgia. No effective medical therapy has yet been found. Several surgical techniques have been tried, with modest or mixed results. The value of surgical interventions is difficult to assess because published studies involve small numbers of mixed patient types and little long term follow-up.

- Gasserian ganglion stimulation is stimulation of the gasserian ganglion with electric pulses from a small generator implanted beneath the skin. There are mixed reports, including some reports of marked, some of moderate and some of no improvement. Further studies of more patients with longer follow-up are required to determine the efficacy of this treatment.

- Deep brain stimulation was found in one review to produce good results in forty-five percent of 106 cases. Though relief may not be permanent, several years of relief may be achieved with this technique.

- Mesencephalotomy is the damaging of the junction of the trigeminal tract and the periaqueductal gray in the brain, and has produced pain relief in a group of patients with cancer pain; but when applied to six anesthesia dolorosa patients, no pain relief was achieved, and the unpleasant sensation was in fact increased.

- Dorsal root entry zone lesioning, damaging the point where sensory nerve fibers meet spinal cord fibers, produced favorable results in some patients and poor results in others, with incidence of ataxia at 40%. Patient numbers were small, follow-up was short and existing evidence does not indicate long term efficacy.

- One surgeon treated thirty-five patients using trigeminal nucleotomy, damaging the nucleus caudalis, and reported 66% "abolition of allodynia and a marked reduction in or (less frequently) complete abolition of deep background pain."

Otitis media is a particularly common cause of otalgia in early childhood, often occurring secondary to other infectious illnesses, such as colds, coughs, or conjunctivitis.

Treatments are generally directed toward stopping the inflammation and suppressing the immune system. Typically, corticosteroids such as prednisone are used. Additionally, other immune suppression drugs, such as cyclophosphamide and others, are considered. In case of an infection, antimicrobial agents including cephalexin may be prescribed. Affected organs (such as the heart or lungs) may require specific medical treatment intended to improve their function during the active phase of the disease.

Ear pain can be caused by disease in the external or middle ear(because of infection), or inner ear, but the three are indistinguishable in terms of the pain experienced.

External ear pain may be:

- Mechanical: trauma, foreign bodies such as hairs, insects or cotton buds.

- Infective (otitis externa): "Staphylococcus", "Pseudomonas", "Candida", herpes zoster, or viral Myringitis. (See Otitis externa)

Middle ear pain may be:

- Mechanical: barotrauma (often iatrogenic), Eustachian tube obstruction leading to acute otitis media.

- Inflammatory / infective: acute otitis media, mastoiditis.

People whose condition was caused by a recent viral infection should make a full recovery without treatment in a few months. Fine motor skills, such as handwriting, typically have to be practised in order to restore them to their former ability. In more serious cases, strokes, bleeding or infections may sometimes cause permanent symptoms.

Granulomatous meningoencephalitis (GME) is an inflammatory disease of the central nervous system (CNS) of dogs and, rarely, cats. It is a form of meningoencephalitis. GME is likely second only to encephalitis caused by "canine distemper virus" as the most common cause of inflammatory disease of the canine CNS. The disease is more common in female toy dogs of young and middle age. It has a rapid onset. The lesions of GME exist mainly in the white matter of the cerebrum, brainstem, cerebellum, and spinal cord. The cause is only known to be noninfectious and is considered at this time to be idiopathic. Because lesions resemble those seen in allergic meningoencephalitis, GME is thought to have an immune-mediated cause, but it is also thought that the disease may be based on an abnormal response to an infectious agent. One study searched for viral DNA from "canine herpesvirus", "canine adenovirus", and "canine parvovirus" in brain tissue from dogs with GME, necrotizing meningoencephalitis, and necrotizing leukoencephalitis (see below for the latter two conditions), but failed to find any.

Arachnoiditis is a chronic disorder with no known cure, and prognosis may be hard to determine because of an unclear correlation between the beginning of the disease and the appearance of symptoms. For many, arachnoiditis is a disabling disease that causes chronic pain and neurological deficits, and may also lead to other spinal cord conditions, such as syringomyelia.