Treatment of people believed to have ATN or TN is usually begun with medication. The long-time first drug of choice for facial neuralgia has been carbamazepine, an anti-seizure agent. Due to the significant side-effects and hazards of this drug, others have recently come into common use as alternatives. These include oxcarbazepine, lamotrigine, and gabapentin. A positive patient response to one of these medications might be considered as supporting evidence for the diagnosis, which is otherwise made from medical history and pain presentation. There are no present medical tests to conclusively confirm TN or ATN.

If the anti-seizure drugs are found ineffective, one of the tricyclic antidepressant medications such as amitriptyline or nortriptyline, may be used. The tricyclic antidepressants are known to have dual action against both depression and neuropathic pain. Other drugs which may also be tried, either individually or in combination with an anti-seizure agent, include baclofen, pregabalin, anti-seizure drugs (to calm nerve endings), muscle relaxants, and opioid drugs such as oxycodone or an oxycodone/paracetamol combination.

For some people with ATN opioids may represent the only viable medical option which preserves quality of life and personal functioning. Although there is considerable controversy in public policy and practice in this branch of medicine, practice guidelines have long been available and published.

If drug treatment is found to be ineffective or causes disabling side effects, one of several neurosurgical procedures may be considered. The available procedures are believed to be less effective with type II (atypical) trigeminal neuralgia than with type I (typical or "classic") TN. Among present procedures, the most effective and long lasting has been found to be microvascular decompression (MVD), which seeks to relieve direct compression of the trigeminal nerve by separating and padding blood vessels in the vicinity of the emergence of this nerve from the brain stem, below the cranium.

Choice of a surgical procedure is made by the doctor and patient in consultation, based on the patient's pain presentation and health and the doctor's medical experience. Some neurosurgeons resist the application of MVD or other surgeries to atypical trigeminal neuralgia, in light of a widespread perception that ATN pain is less responsive to these procedures. However, recent papers suggest that in cases where pain initially presents as type I TN, surgery may be effective even after the pain has evolved into type II.

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.

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.

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.

The evidence for surgical therapy is poor. Surgery is normally recommended only after medication has proved ineffective, or if side effects of medication are intolerable. While there may be pain relief after surgery, there is also a considerable risk of side effects, such as facial numbness after the procedure. Microvascular decompression appears to result in the longest pain relief. Percutaneous radiofrequency thermorhizotomy may also be effective as may stereotactic radiosurgery; however the effectiveness decreases with time.

Surgical procedures can be separated into non-destructive and destructive:

Psychosocial interventions for AFP include cognitive behavioral therapy and biofeedback. A systematic review reported that there was weak evidence to support the use of these treatments to improve long-term outcomes in chronic orofacial pain, however these results were based primarily upon temporomandibular joint dysfunction and burning mouth syndrome rather than ATP and AO.

Psychosocial interventions assume 2 models of chronic facial pain, namely "inactivity" and "over activity". The former is where people with pain become conditioned to avoid physical activity as a result of exacerbating their pain. These negative thoughts and behaviors in fact prolong and intensify their symptoms. Some psychosocial interventions work on this fear-avoidance behaviour to improve functioning and thereby alleviate symptoms. The over activity model involves factors such as anxiety, depression or anger acting to increase pain by triggering autonomic, visceral and skeletal activity.

Research suggests that people with AFP are not helped greatly by health care professionals. One study reported that on average, individuals had consulted 7.5 different doctors. 91% had seen dentists, 80% physicians, 66% neurologists, 63% ear, nose and throat surgeons, 31% orthopedic and maxillofacial surgeons, 23% psychiatrists, 14% neurosurgeons and 6% ophalmologists and dermatologists. In this study, the individuals had been subjected to a wide variety of different treatments, from surgery, antidepressants, analgesics and physical therapies. None of the persons reported that surgery was beneficial, and in many cases the pain was worsened by surgery. The article sited as the source of this information was withdrawn from publication, saying the information was out of date and not meeting Cochrane methodological standards.

It has been suggested that the onset of chronic facial will likely be a life changing development for those affected.

As diagnostic criteria have been indecisive and its pathophysiology remains unclear, no permanent cure is available. Antiepileptic medications (membrane-stabilizing drugs) such as pregabalin, gabapentin, topiramate, and lamotrigine improve symptoms, but there is no effective permanent or long-term treatment for SUNCT.

However, a few short-term treatments are available and can relieve and possibly prevent some symptoms of attacks.

Lamotrigine exhibits some long-term prevention and reduction in many patients; however, titration of dose is difficult due to adverse skin reactions.

Topiramate also has preventive effects but it is accompanied by a high risk of severe side-effects for patients with a history of kidney stones, glaucoma, depression, or low body weight.

Intravenous lidocaine can abolish symptoms during its administration, or reduce frequency and duration of attacks. However, administration of intravenous lidocaine requires careful monitoring of ECG and blood pressure.

Methylprednisolone therapy shows some promise in short-term prevention of attacks, even though its mechanism of action is yet to be discovered.

The calcium channel blocker verapamil is reported to be useful in alleviating symptoms (lower frequency and duration of attacks), even though some patients experience worsened symptoms.

Various medications that are often used in other headache syndromes such as nonsteroidal anti-inflammatory drugs, acetaminophen, tricyclic antidepressants, calcium channel antagonists do not relieve the symptoms of SUNCT.

There have been attempts to alter oxygen supply during attacks to alleviate the symptoms since some of the headaches are caused by decreased oxygen supply; however, elevated blood oxygen level did not affect the symptoms.

Researchers now focus on the administration of various combination of medications and therapies to treat symptoms of SUNCT.

Lithium, methysergide, and topiramate are recommended alternative treatments, although there is little evidence supporting the use of topiramate or methysergide. This is also true for tianeptine, melatonin and ergotamine. Valproate, sumatriptan and oxygen are not recommended as preventative measures. Botulinum toxin injections have shown limited success. Evidence for baclofen, botulinum toxin, and capsaicin is unclear.

The other primarily recommended treatment of acute attacks is subcutaneous or intranasal sumatriptan. Sumatriptan and zolmitriptan have both been shown to improve symptoms during an attack with sumatriptan being superior. Because of the vasoconstrictive side-effect of triptans, they may be contraindicated in people with ischemic heart disease.

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.

Hemicrania continua generally responds only to indomethacin 25–300 mg daily, which must be continued long term. Unfortunately, gastrointestinal side effects are a common problem with indomethacin, which may require additional acid-suppression therapy to control.

In patients who are unable to tolerate indomethacin, the use of celecoxib 400–800 mg per day (Celebrex) and rofecoxib 50 mg per day (Vioxx - no longer available) have both been shown to be effective and are likely to be associated with fewer GI side effects. There have also been reports of two patients who were successfully managed with topiramate 100–200 mg per day (Topamax) although side effects with this treatment can also prove problematic.

Greater Occipital Nerve [GON] block comprising 40 mg Depomedrone and 10mls of 1% Lignocaine injected into the affected nerve is effective, up to a period of approximately three months. Changing the 'cocktail' to include [for example] 10mls of .5% Marcaine and changing to 2% Lignocaine, whilst in theory should increase the longevity, renders the injection completely ineffective. See 4.2 Posology and method of administration [flocculation]

Occipital nerve stimulation may be highly effective when other treatments fail to relieve the intractable pain.

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.

An April 2013 Cochrane Collaboration meta-analysis of 6 randomized controlled trials (RCTs) investigating oral antiviral medications given within 72 hours after the onset of herpes zoster rash in immunocompetent people for preventing postherpetic neuralgia (PHN) found no significant difference between placebo and acyclovir. Combining four RCTs, 44.1% of the acyclovir treatment group developed herpetic neuralgia whereas 53.3% of the placebo group developed herpetic neuralgia. Heterogeneity between the four RCTs was moderate: Chi =3.36, df = 2 (P=0.19); I = 40%.

Additionally, there was no significant difference in preventing the incidence of PHN found in the one RCT included in the meta-analysis that compared placebo to PO famciclovir treatment within 72 hours of HZ rash onset. Studies using valaciclovir treatment were not included in the meta-analysis.

PHN was defined as pain at the site of the dermatomic rash at 120 days after the onset of rash, and incidence was evaluated at 1, 4, and 6 months after rash onset.

There was a slight reduction in the incidence of pain at 4 weeks after the onset of rash in the aciclovir group (153 study participants with pain out of 347 study participants in the aciclovir group) versus the placebo group (184 study participants with pain out of 345 study participants in the placebo group). Patients who are prescribed PO antiviral agents after the onset of rash should be informed that their chances of developing PHN are no different than those not taking PO antiviral agents.

A randomized controlled trial found that amitriptyline 25 mg per night for 90 days starting within two days of onset of rash can reduce the incidence of postherpetic neuralgia from 35% to 16% (number needed to treat is 6).

Migraine can be somewhat improved by lifestyle changes, but most people require medicines to control their symptoms. Medications are either to prevent getting migraines, or to reduce symptoms once a migraine starts.

Preventive medications are generally recommended when people have more than four attacks of migraine per month, headaches last longer than 12 hours or the headaches are very disabling. Possible therapies include beta blockers, antidepressants, anticonvulsants and NSAIDs. The type of preventive medicine is usually chosen based on the other symptoms the person has. For example, if the person also has depression, an antidepressant is a good choice.

Abortive therapies for migraines may be oral, if the migraine is mild to moderate, or may require stronger medicine given intravenously or intramuscularly. Mild to moderate headaches should first be treated with acetaminophen (paracetamol) or NSAIDs, like ibuprofen. If accompanied by nausea or vomiting, an antiemitic such as metoclopramide (Reglan) can be given orally or rectally. Moderate to severe attacks should be treated first with an oral triptan, a medication which mimics serotonin (an agonist) and causes mild vasoconstriction. If accompanied by nausea and vomiting, parenteral (through a needle in the skin) triptans and antiemetics can be given.

Several complementary and alternative strategies can help with migraines. The American Academy of Neurology guidelines for migraine treatment in 2000 stated relaxation training, electromyographic feedback and cognitive behavioral therapy may be considered for migraine treatment, along with medications.

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.

Hemicrania was mentioned in 1881 in The Therapeutic Gazette Vol. 2, by G.S.Davis, and the incident has been cited in King's American Dispensatory (1898 and later editions) in the description of the strong analgesic Jamaican Dogwood, a relatively low dose of which reportedly produced convulsions and prolonged respiratory depression over six hours in an elderly woman with this condition.

In newer times, Hemicrania continua was described in 1981; at that time around 130 cases were described in the literature. However, rising awareness of the condition has led to increasingly frequent diagnosis in headache clinics, and it seems that it is not as rare as these figures would imply. The condition occurs more often in women than men and tends to present first in adulthood, although it has also been reported in children as young as 5 years old.

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.

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."

Medication is the main method of managing pain in TMD, mostly because there is little if any evidence of the effectiveness of surgical or dental interventions. Many drugs have been used to treat TMD pain, such as analgesics (pain killers), benzodiazepines (e.g. clonazepam, prazepam, diazepam), anticonvulsants (e.g. gabapentin), muscle relaxants (e.g. cyclobenzaprine), and others. Analgesics that have been studied in TMD include non-steroidal anti-inflammatory drugs (e.g. piroxicam, diclofenac, naproxen) and cyclo-oxygenase-2 inhibitors (e.g. celecoxib). Topical methyl salicylate and topical capsaicin have also been used. Other drugs that have been described for use in TMD include glucosamine hydrochloride/chondroitin sulphate and propranolol. Despite many randomized control trials being conducted on these commonly used medications for TMD a systematic review carried out in 2010 concluded that there was insufficient evidence to support or not to support the use of these drugs in TMD. Low-doses of anti-muscarinic tricyclic antidepressants such as amitriptyline, or nortriptyline have also been described. In a subset of people with TMD who are not helped by either noninvasive and invasive treatments, long term use of opiate analgesics has been suggested, although these drugs carry a risk of drug dependence and other side effects. Examples include morphine, fentanyl, oxycodone, tramadol, hydrocodone, and methadone.

Botulinum toxin solution ("Botox") is sometimes used to treat TMD. Injection of botox into the lateral pterygoid muscle has been investigated in multiple randomized control trials, and there is evidence that it is of benefit in TMD. It is theorized that spasm of lateral pterygoid causes anterior disc displacement. Botulinum toxin causes temporary muscular paralysis by inhibiting acetylcholine release at the neuromuscular junction. The effects usually last for a period of months before they wear off. Complications include the creation of a "fixed" expression due to diffusion of the solution and subsequent involvement of the muscles of facial expression, which lasts until the effects of the botox wear off. Injections of local anesthetic, sometimes combined with steroids, into the muscles (e.g. the temoralis muscle or its tendon) are also sometimes used. Local anesthetics may provide temporary pain relief, and steroids inhibit pro-inflammatory cytokines. Steroids and other medications are sometimes injected directly into the joint (See Intra-articular injections).

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).

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.

The phenomenon is common enough to have been the subject of research published in the "British Medical Journal" and "Scientific American". A study conducted by Maya Kaczorowski demonstrated a higher incidence of sphenopalatine ganglioneuralgia in subjects consuming the ice cream sample in less than 30 seconds vs. those who consumed slowly, with no time limit (27.3% and 12.5% respectively). However, Kaczorowski was ultimately not able to draw a clear connection between the speed of consumption and incidence of sphenopalatine ganglioneuralgia.

According to research by Nigel Bird, Anne MacGregor, and Marcia I. Wilkinson published in the journal "Headache", in their study "17% of the migraine patients and 46% of the students developed headache following palatal application or a swallow of ice cream."

It has been suggested that the natural history of TMD is benign and self-limiting, with symptoms slowly improving and resolving over time. The prognosis is therefore good. However, the persistent pain symptoms, psychological discomfort, physical disability and functional limitations may detriment quality of life. It has been suggested that TMD does not cause permanent damage and does not progress to arthritis in later life, however degenerative disorders of the TMJ such as osteoarthritis are included within the spectrum of TMDs in some classifications.