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.

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.

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.

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.

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.

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.

Geniculate ganglionitis or geniculate neuralgia (GN), also called nervus intermedius neuralgia, Ramsay Hunt syndrome, or Hunt's neuralgia, is a rare disorder characterized by severe paroxysmal neuralgic pain deep in the ear, that may spread to the ear canal, outer ear, mastoid or eye regions. GN may also occur in combination with trigeminal or glossopharyngeal neuralgia.

The pain of GN is sharp, shooting or burning and can last for hours. Painful attacks can be triggered by cold, noise, swallowing or touch, but triggers are usually unique to the sufferer. Other related symptoms that may be experienced include increased salivation, bitter taste, tinnitus and vertigo.

GN is rare, and only limited data is available regarding the incidence, prevalence, and risk factors associated with this condition. Middle-aged adults, however, seem to be predominantly affected, women more than men.

GN may be caused by compression of somatic sensory branch of cranial nerve VII which goes through the nervus intermedius. In sufferers of GN, signals sent along these nerves are altered and interpreted by the geniculate ganglion (a structure in the brain) as GN pain. GN may also develop following herpes zoster oticus (Ramsay Hunt syndrome), where cold sores occur on the ear drum or ear. This may also be associated with facial paresis (weakness), tinnitus, vertigo and deafness. Disorders of lacrimation, salivation and/or taste sometimes accompany the pain. There is a common association with herpes zoster.

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.

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 affects about 0.1% of the general population at some point in their life. Males are affected about four times more often than females. The condition usually starts between the ages of 20 and 50 years, although it can occur at any age. About one in five of adults reports the onset of cluster headache between 10 and 19 years.

Trigeminal autonomic cephalgia (TAC) is the name for a type of primary headache that occurs with pain on one side of the head in the trigeminal nerve area and symptoms in autonomic systems on the same side, such as eye watering and redness or drooping eyelids. TACs include

- Cluster headache

- Paroxysmal hemicrania (chronic or episodic)

- Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT)

- Short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms (SUNA)

- Long-lasting autonomic symptoms with hemicrania (LASH)

TACs can be differentiated by the length and frequency of recurrence of the headaches.

Treatment for TACs varies depending on the exact type, but can include medication such as Indomethacin (in the case of chronic paroxysmal hemicrania) or acute and prophylactic therapy (in the case of cluster headache).

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.

Short-lasting unilateral neuralgiform headache with conjunctival injection and tearing (SUNCT syndrome), is a rare headache disorder that belongs to the group of headaches called trigeminal autonomic cephalalgia (TACs). Symptoms include excruciating burning, stabbing, or electrical headaches mainly near the eye and typically these sensations are only on one side of the body. The headache attacks are typically accompanied by cranial autonomic signs that are unique to SUNCT. Each attack can last from five seconds to six minutes and may occur up to 200 times daily.

TACs are caused by activation of the autonomic nervous system of the trigeminal nerve in the face.

As of 2015 about 50 cases have been described in the medical literature. Onset of the symptoms usually come later in life, at an average age of about 50. Although the majority of patients are men over the age of 50, it is not uncommon to find SUNCT present among other age groups, including children and infants.

Approximately 64–77% of people have a headache at some point in their lives. During each year, on average, 46–53% of people have headaches. Most of these headaches are not dangerous. Only approximately 1–5% of people who seek emergency treatment for headaches have a serious underlying cause.

More than 90% of headaches are primary headaches. Most of these primary headaches are tension headaches. Most people with tension headaches have "episodic" tension headaches that come and go. Only 3.3% of adults have chronic tension headaches, with headaches for more than 15 days in a month.

Approximately 12–18% of people in the world have migraines. More women than men experience migraines. In Europe and North America, 5–9% of men experience migraines, while 12–25% of women experience migraines.

Cluster headaches are very rare. They affect only 1–3 per thousand people in the world. Cluster headaches affect approximately three times as many men as women.

The pathophysiology of SUNCT is incompletely understood. Recent studies suggest the existence of a relationship between the hypothalamus and the condition.

Functional MRI and deep brain stimulation of a large patient pool showed activation of the posterior hypothalamus during attacks of primary SUNCT, on both sides and contralaterally (on the opposite side). Functional MRI studies suggest brain stem activation during attacks as well. Activation of the trigeminocervical complex and other related structures results from innervation from branches of trigeminal and upper cervical nerves.

There exists a direct connection between trigeminal nucleus caudalis, which is located in the brain stem, and the posterior hypothalamus. Therefore, it is possible that stimulation of the peripheral trigeminal nerve activates the hypothalamus and the hypothalamus in turn communicates with the trigeminal nucleus caudalis via neurotransmitters such as orexin.

Elevated levels of prolactin, secretion of which is regulated by the hypothalamus, seem to be associated with SUNCT attacks. Some patients with a pituitary tumor only experience attacks at night. These patients only exhibit higher levels of prolactin at night, even where hormone levels, including prolactin, were normal throughout the day.

SUNCT is considered a primary headache (or condition), but can also occur as a secondary symptom of other conditions. However, a patient can only be diagnosed with SUNCT as a primary condition.

A pituitary tumor causes SUNCT as a secondary headache. Some patients with a pituitary tumor complain of short-lasting heachaches. Upon removal of the tumor, the symptoms of SUNCT may disappear permanently.

Although it occurs very rarely, paranasal sinusitis can also cause secondary SUNCT. The symptoms of SUNCT in such cases can be removed permanently with endoscopic sinus surgery.

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.

To relieve pain, some doctors suggest pressing the tongue against the roof of the mouth to warm the area, tilting the head back for 20 seconds, or drinking something warmer than whatever caused the headache. Some people report relief from breathing in through the mouth and out through the nose, thus passing warm air through the nasal passages.

Trigeminal trophic syndrome (Trigeminal trophic lesion) is a rare disease caused by the interruption of peripheral or central sensory pathways of the trigeminal nerve. A slowly enlarging, uninflammed ulcer can occur in the area that has suffered the trigeminal nerve damage; including but not limited to the cheek beside the ala nasi. These sores affect the skin supplied by the sensory component of the trigeminal nerve. Similar lesions may also occur in the corners of the eyes, inside the ear canal, on the scalp or inside the mouth.

It has been stated that the ulceration is due to the constant "picking" of the patient. While this does occur it should not be limited to this alone. The lack of feeling or pain allows the patient to continue itching or picking the area. Even though there is no feeling, there is constant neuropathic pain.

Sixty cases were reported from 1982 to 2002.

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 International Headache Society's International Classification of Headache Disorders classifies hemicrania continua as a primary headache disorder.

Hemicrania continua (HC) is a persistent unilateral headache that responds to indomethacin. It is usually unremitting, but rare cases of remission have been documented. Hemicrania continua is considered a primary headache disorder, meaning that it is not caused by another condition.

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.

Another theory into the cause of cold-stimulus headaches is explained by increased blood flow to the brain through the anterior cerebral artery, which supplies oxygenated blood to most medial portions of the frontal lobes and superior medial parietal lobes. This increase in blood volume and resulting increase in size in this artery is thought to bring on the pain associated with a cold-stimulus headache.

When the anterior cerebral artery constricts, reining in the response to this increased blood volume, the pain disappears. The dilation, then quick constriction, of this blood vessel may be a type of self-defense for the brain.

This inflow of blood cannot be cleared as quickly as it is coming in during the cold-stimulus headache, so the blood flow could raise the pressure inside the skull and induce pain that way. As the intracranial pressure and temperature in the brain rise the blood vessel contracts, and the pressure in the brain is reduced before reaching dangerous levels.

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.

Postencephalitic trophic ulcer is an ulceration of the nose similar to trigeminal trophic lesions, and has been reported following epidemic encephalitis and herpes zoster of the trigeminal nerve.