The prognosis is worse when there are more areas of pain reported. Treatment may include psychotherapy (with cognitive-behavioral therapy or operant conditioning), medication (often with antidepressants but also with pain medications), and sleep therapy. According to a study performed at the Leonard M. Miller School of Medicine, antidepressants have an analgesic effect on patients suffering from pain disorder. In a randomized, placebo-controlled antidepressant treatment study, researchers found that "antidepressants decreased pain intensity in patients with psychogenic pain or somatoform pain disorder significantly more than placebo". Prescription and nonprescription pain medications do not help and can actually hurt if the patient suffers side effects or develops an addiction. Instead, antidpressants and talk therapy are recommended. CBT helps patients learn what worsens the pain, how to cope, and how to function in their life while handling the pain. Antidepressants work against the pain and worry. Unfortunately, many people do not believe the pain "is all in their head," so they refuse such treatments. Other techniques used in the management of chronic pain may also be of use; these include massage, transcutaneous electrical nerve stimulation, trigger point injections, surgical ablation, and non-interventional therapies such as meditation, yoga, and music and art therapy.

Early intervention when pain first occurs or begins to become chronic offers the best opportunity for prevention of pain disorder.

Antidepressants are "associated with improvements in pain, depression, fatigue, sleep disturbances, and health-related quality of life in people with FMS." The goal of antidepressants should be symptom reduction and if used long term, their effects should be evaluated against side effects. A small number of people benefit significantly from the SNRIs duloxetine and milnacipran and the tricyclic antidepressants (TCAs), such as amitriptyline. However, many people experience more adverse effects than benefits. While amitriptyline has been used as a first line treatment, the quality of evidence to support this use is poor.

It can take up to three months to derive benefit from the antidepressant amitriptyline and between three and six months to gain the maximal response from duloxetine, milnacipran, and pregabalin. Some medications have the potential to cause withdrawal symptoms when stopping so gradual discontinuation may be warranted particularly for antidepressants and pregabalin.

There is tentative evidence that the benefits and harms of SSRIs appear to be about similar.

The anti-convulsant drugs gabapentin and pregabalin may be used to reduce pain. Gabapentin may be of significant benefit for pain relief in about 35% of people with fibromyalgia. It is not possible to predict who will benefit, and a short trial may be recommended to test the effectiveness of this type of medication. Approximately 6/10 people who take gabapentin to treat pain related to fibromyalgia experience unpleasant side effects such as dizziness, abnormal walking, or swelling from fluid accumulation. Pregabalin demonstrates a substantial benefit in about 9% of people. Pregabalin reduced time off work by 0.2 days per week.

Treatment may involve investigation, reassurance and explanation, and possibly specialist treatment such as antidepressants or cognitive behavioral therapy.

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.

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.

Some have suggested that surgery is not an appropriate for treatment for AFP, however the frequent failure medical treatment to relieve pain has occasionally lead surgeons to attempt surgical treatments. Surgery may give a temporary remission from pain, but rarely is there a long term cure achieved via these measures. Sometimes the pain may be increased or simply migrate to an adjacent area following a surgical procedure. Descriptions of procedures such as removal of a portion of the affected branch of the trigeminal nerve, or direct injections of a caustic substance (e.g. phenol, glycerol, alcohol) into the nerve have been reported. Proponents of the so-called "Neuralgia inducing cavitational necrosis" suggest surgical exploration of the bone marrow surrounding the intra-bony course of the affected nerve to discover diseased marrow.

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.

Traditional remedies have ranged from warm baths (if the pain lasts long enough to draw a bath), warm to hot enemas, relaxation techniques, and various medications.

Yoga pose "downward facing dog" -Adho Mukha Svanasana, or modification from it seems to help to relax the muscles and ease the pain. The idea of the yoga pose is that the position will force the muscles to relax and therefore tension will relieve over time. Also relaxing one's jaw muscles will help to relax the muscles in rectal area, method used by women giving birth.

In patients who suffer frequent, severe, prolonged attacks, inhaled salbutamol has been shown in some studies to reduce their duration.

The use of botulinum toxin has been proposed as analgesic, and low dose diazepam at bedtime has been suggested as preventative.

The most common approach for mild cases is simply reassurance and topical treatment with calcium-channel blocker (diltiazem, nifedipine) ointment, salbutamol inhalation and sublingual nitroglycerine.For persistent cases, local anesthetic blocks, clonidine or Botox injections can be considered. Supportive treatments directed at aggravating factors include high-fiber diet, withdrawal of drugs which have gut effects (e.g., drugs that provoke or worsen constipation including narcotics and oral calcium channel blockers; drugs that provoke or worsen diarrhea including quinidine, theophylline, and antibiotics), warm baths, rectal massage, perineal strengthening exercises, anti-cholinergic agents, non-narcotic analgesics, sedatives or muscle relaxants such as diazepam.

The opioid antagonist naloxone allowed a woman with congenital insensitivity to pain to experience it for the first time. Similar effects were observed in Na1.7 null mice treated with naloxone. As such, opioid antagonists like naloxone and naltrexone may be effective in treating the condition.

Psychotherapy, more specifically, cognitive behavioral therapy (CBT), is the most widely used form of treatment for Somatic symptom disorder. In 2016, a randomized 12-week study suggested steady and significant improvement in health anxiety measures with cognitive behavioral therapy compared to the control group.

CBT can help in some of the following ways:

- Learn to reduce stress

- Learn to cope with physical symptoms

- Learn to deal with depression and other psychological issues

- Improve quality of life

- Reduce preoccupation with symptom

Moreover, brief psychodynamic interpersonal psychotherapy (PIT) for patients with multisomatoform disorder has shown its long-term efficacy for improving the physical quality of life in patients with multiple, difficult-to-treat, medically unexplained symptoms.

Antidepressant medication has also been used to treat some of the symptoms of depression and anxiety that are common among people who have somatic symptom disorder. Medications will not cure somatic symptom disorder, but can help the treatment process when combined with CBT.

For treatment guidelines, refer to the PANDAS Physicians Network. PPN’s goal is to help medical professionals understand, diagnose and treat PANS and PANDAS. The network provides research, diagnostic, and treatment tools. PPN Guidelines for Diagnostics and Therapeutics are developed by PPN committees and advisors from the top academic medical institutions in the United States. The members have worked with, treated, and studied the patients and the disorder. PANS and PANDAS are interdisciplinary disorders, so the relevant disciplines are represented on the PPN committees and special advisory council. Some of the disciplines include: Psychiatrists, Pediatric Neurologists, Immunologists, Microbiologists, Rheumatologists, Geneticists, Otolaryngologists, etc.

A placebo-controlled trial of plasmapheresis and IVIG for PANDAS was conducted at the NIH in the late 1990’s, with children randomly assigned (by the NIH pharmacy) to receive plasmapheresis (unblinded) or IVIG/sham IVIG (double blinded). At one month evaluations, placebo infusions produced no improvements in OC or tic symptoms, while 100% of the children receiving IVIG or plasmapheresis improved. The average improvement in OC symptoms was 45% for the group receiving IVIG and nearly 65% for the children receiving plasmapheresis. The results of the trial were sufficiently robust to cause the American Society of Apheresis to include plasmapheresis as a treatment option for PANDAS, as well as for Sydenham chorea.

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).

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:

There is no specific treatment for NDPH. Often they are treated similar to migraines.

A number of medications have been used including amitriptyline, gabapentin, pregabalin, propranolol, and topiramate. There are no prospective placebo controlled trials of preventive treatment. In those with migrainous features treatment may be similar to migraines.

Opiates, or narcotics, tend to be avoided because of their side effects, including the development of medication overuse headaches and potential for dependency. NDPH is often associated with medication overuse. To avoid the development of medication overuse headaches, it is advised not to use pain relievers for more than nine days a month.

NDPH, like other primary headaches, has been linked to comorbid psychiatric conditions, mainly mood and anxiety and panic disorders. The spectrum of anxiety disorders, particularly panic disorder, should be considered in NDPH patients presenting with psychiatric symptoms. Simultaneous treatment of both disorders may lead to good outcomes.

Medications within the tetracycline family, mexiletine, corticosteroids and nerve blocks are being studied. Occipital nerve block have been reported to be helpful for some people. 23/71 people had undergone a nerve block for their severe headache. The NDPH-ICHD group responded to the nerve block much more often (88.9%) than the NDPH with migraine features (42.9% responded to nerve block).

To date, cognitive behavioral therapy (CBT) is the best established treatment for a variety of somatoform disorders including somatization disorder. CBT aims to help patients realize their ailments are not catastrophic and to enable them to gradually return to activities they previously engaged in, without fear of "worsening their symptoms". Consultation and collaboration with the primary care physician also demonstrated some effectiveness. The use of antidepressants is preliminary but does not yet show conclusive evidence. Electroconvulsive shock therapy (ECT) has been used in treating somatization disorder among the elderly; however, the results were still debatable with some concerns around the side effects of using ECT. Overall, psychologists recommend addressing a common difficulty in patients with somatization disorder in the reading of their own emotions. This may be a central feature of treatment; as well as developing a close collaboration between the GP, the patient and the mental health practitioner.

Acupuncture is sometimes used for TMD. There is limited evidence that acupuncture is an effective symptomatic treatment for TMD. A short term reduction in muscular pain of muscular origin can usually be observed after acupuncture in TMD, and this is more than is seen with placebo. There are no reported adverse events of acupuncture when used for TMD, and some suggest that acupuncture is best employed as an adjuvent to other treatments in TMD. However, some suggest that acupuncture may be no more effective than sham acupuncture, that many of the studies investigating acupuncture and TMD suffer from significant risk of bias, and that the long term efficacy of acupuncture for TMD is unknown.

High-voltage pulsed galvanic stimulation (HGVS) has been shown to be of prophylactic benefit, to reduce the incidence of attacks. The patient is usually placed in the left lateral decubitus position and a sterile probe is inserted into the anus. The negative electrode is used and the stimulator is set with a pulse frequency of 80 to 120 cycles per second. The voltage (intensity) is started at 0, progressively raised to a threshold of patient discomfort, and then is decreased to a level that the patient finds comfortable. As the patient's tolerance increases, the voltage can be gradually increased to 250 to 350 Volts. Each treatment session usually lasts between 15 and 60 minutes. Several studies have reported short-term success rates that ranged from 65 to 91%.

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.

All destructive procedures will cause facial numbness, post relief, as well as pain relief.

- Percutaneous techniques which all involve a needle or catheter entering the face up to the origin where the nerve splits into three divisions and then damaging this area, purposely, to produce numbness but also stop pain signals. These techniques are proven effective especially in those where other interventions have failed or in those who are medically unfit for surgery such as the elderly.

- Balloon compression - inflation of a balloon at this point causing damage and stopping pain signals.

- Glycerol injection- deposition of a corrosive liquid called glycerol at this point causes damage to the nerve to hinder pain signals.

- Radiofrequency thermocoagulation rhizotomy - application of a heated needle to damage the nerve at this point.

- Stereotactic radiosurgery is a form of radiation therapy that focuses high-power energy on a small area of the body

For secondary erythromelalgia, treatment of the underlying primary disorder is the most primary method of treatment. Although aspirin has been thought to reduce symptoms of erythromelalgia, it is rare to find evidence that this is effective. Mechanical cooling of the limbs by elevating them can help or managing the ambient environment frequently is often necessary constantly as flares occur due to sympathetic autonomic dysfunction of the capillaries. The pain that accompanies it is severe and treated separately (the pain is similar to CRPS, phantom limb or thalamic pain syndrome). Patients are strongly advised "not" to place the affected limbs in cold water to relieve symptoms when flaring occurs. It may seem a good idea, but it precipitates problems further down the line causing damage to the skin and ulceration often intractable due to the damaged skin. A possible reduction in skin damage may be accomplished by enclosing the flaring limb in a commonly available, thin, heat transparent, water impermeable, plastic food storage bag. The advice of a physician is advised depending on specific circumstances.

Primary erythromelalgia management is symptomatic, i.e. treating painful symptoms only. Specific management tactics include avoidance of attack triggers such as: heat, change in temperature, exercise or over exertion, alcohol and spicy foods. This list is by no means comprehensive as there are many triggers to set off a 'flaring' episode that are inexplicable. Whilst a cool environment is helpful in keeping the symptoms in control, the use of cold water baths is strongly discouraged. In pursuit of added relief sufferers can inadvertently cause tissue damage or death, i.e. necrosis. See comments at the end of the preceding paragraph regarding possible effectiveness of plastic food storage bags to avoid/reduce negative effects of submersion in cold water baths.

One clinical study has demonstrated the efficacy of IV lidocaine or oral mexilitine, though it should be noted that differences between the primary and secondary forms were not studied. Another trial has shown promise for misoprostol, while other have shown that gabapentin, venlafaxine and oral magnesium may also be effective, but no further testing was carried out as newer research superseded this combination.

Strong anecdotal evidence from EM patients shows that a combination of drugs such as duloxetine and pregabalin is an effective way of reducing the stabbing pains and burning sensation symptoms of erythromelalgia in conjunction with the appropriate analgesia. In some cases, antihistamines may give some relief. Most people with erythromelalgia never go into remission and the symptoms are ever present at some level, whilst others get worse, or the EM is eventually a symptom of another disease such as systemic scleroderma.

Some suffering with EM are prescribed ketamine topical creams as a way of managing pain on a long term basis. Feedback from some EM patients has led to reduction in usage as they believe it is only effective for short periods.

Living with erythromelalgia can result in a deterioration in quality of life resulting in the inability to function in a work place, lack of mobility, depression, and is socially alienating; much greater education of medical practitioners is needed. As with many rare diseases, many people with EM end up taking years to get a diagnosis and to receive appropriate treatment.

Research into the genetic mutations continues but there is a paucity of clinical studies focusing on living with erythromelalgia. There is much urgency within pharmaceutical companies to provide a solution to those who suffer with pain such as that with erythromelalgia.

A number of medications can be used to treat this disorder. Alpha blockers and/or antibiotics appear to be the most effective with NSAIDs such as ibuprofen providing lesser benefit.

- Treatment with antibiotics is controversial. Some have found benefits in symptoms while others have questioned the utility of a trial of antibiotics. Antibiotics are known to have anti-inflammatory properties and this has been suggested as an explanation for their partial efficacy in treating CPPS. Antibiotics such as fluoroquinolones, tetracyclines, and macrolides have direct anti-inflammatory properties in the absence of infection, blocking inflammatory chemical signals (cytokines) such as interleukin-1 (IL-1), interleukin-8 and tumor necrosis factor (TNF), which coincidentally are the same cytokines found to be elevated in the semen and EPS of men with chronic prostatitis.

- The effectiveness of alpha blockers (tamsulosin, alfuzosin) is questionable in men with CPPS. A 2006 meta-analysis found that they are moderately beneficial when the duration of therapy was at least 3 months.

- An estrogen reabsorption inhibitor such as mepartricin improves voiding, reduces urological pain and improves quality of life in patients with chronic non-bacterial prostatitis.

- Therapies that have not been properly evaluated in clinical trials although there is supportive anecdotal evidence include gabapentin, benzodiazepines, and amitriptyline.

Treatment is similar to treatment for benign fasciculation syndrome.

Carbamazepine therapy has been found to provide moderate reductions in symptoms.