Patients with CFS benefit from a well-balanced diet and eating regularly (eating little and often), including slow-release starchy foods in meals and snacks. Although elimination diets are not generally recommended, many people experience relief of CFS symptoms with these diets, including gastrointestinal complaints. To avoid the risk of malnutrition, they should be supervised by a dietitian.

Antidepressants are mostly ineffective in treating CFS. Antiviral and immunological therapies have provided some benefit, but are limited by their side effects.

Steroid replacement therapy is not effective.

There is some preliminary evidence that the immunomodulatory medication rintatolimod improves exercise capacity, as well as cognitive function and quality of life, based on two trials. The US FDA has repeatedly denied commercial approval, citing numerous deficiencies in both trials, and concluding that the available evidence is insufficient to demonstrate its safety or efficacy in CFS.

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.

Sudden cessation of high-dose corticosteroids, opioids, barbiturates, benzodiazepines, caffeine or alcohol can induce myalgia in many respects.

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

The report of Da Costa shows that patients recovered from the more severe symptoms when removed from the strenuous activity or sustained lifestyle that caused them. A reclined position and forced bed rest was the most beneficial.

Other treatments evident from the previous studies were improving physique and posture, appropriate levels of exercise where possible, wearing loose clothing about the waist, and avoiding postural changes such as stooping, or lying on the left or right side, or the back in some cases, which relieved some of the palpitations and chest pains, and standing up slowly can prevent the faintness associated with postural or orthostatic hypotension in some cases.

Pharmacological intervention came in the form of digitalis, or "fox glove", which acts as a sodium-potassium ATPase inhibitor, increasing stroke volume and decreasing heart rate.

There is no known cure for CVS, but there are medications that can be used for treatment, intervention, and prevention. There is a growing body of publications on both individual cases and the experiences of the CVS cohort. Treatment is usually on an individual basis, based on trial and error.

The most common therapeutic strategies for those already in an attack are maintenance of salt balance by appropriate intravenous fluids and, in some cases, sedation. Having vomited for a long period prior to attending a hospital, patients are typically severely dehydrated. For a number of patients, potent anti-emetic drugs such as ondansetron (Zofran) or granisetron (Kytril), and dronabinol (Marinol) may be helpful in either preventing an attack, aborting an attack, or reducing the severity of an attack. Lifestyle changes may be recommended, such as extended rest and reduction of stress. Because the symptoms of CVS are similar (or perhaps identical) to those of the disease well-identified as "abdominal migraine", treatment of CVS with a regimen of anti-migraine drugs, such as topiramate and amitriptyline, is showing promise in preventing recurrent attacks.

Treatment is similar to treatment for benign fasciculation syndrome.

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

For more severe disease, oral corticosteroids may be necessary to reduce the inflammatory response. When large amounts of steroids are required or if the disease is severe and is not responding to steroid therapy, other immunosuppressive medications often are recommended. These immunosuppressive drugs include methotrexate, cyclophosphamide, cyclosporine or azathioprine. In some cases, combinations of these medicines are prescribed. Occasionally, if the disease has damaged blood vessels, cochlear implantation may

need to be done to correct the problem.

Cinnarizine is mainly used to treat nausea and vomiting associated with motion sickness, vertigo, Ménière's disease, or Cogan's syndrome. Studies have shown it to produce significant improvement in hearing loss in some patients.

Most patients experience an improvement of their symptoms, but for some, OI can be gravely disabling and can be progressive in nature, particularly if it is caused by an underlying condition which is deteriorating. The ways in which symptoms present themselves vary greatly from patient to patient; as a result, individualized treatment plans are necessary.

OI is treated both pharmacologically and non-pharmacologically. Treatment does not cure OI; rather, it controls symptoms.

Physicians who specialize in treating OI agree that the single most important treatment is drinking more than two liters (eight cups) of fluids each day. A steady, large supply of water or other fluids reduces most, and for some patients all, of the major symptoms of this condition. Typically, patients fare best when they drink a glass of water no less frequently than every two hours during the day, instead of drinking a large quantity of water at a single point in the day.

For most severe cases and some milder cases, a combination of medications are used. Individual responses to different medications vary widely, and a drug which dramatically improves one patient's symptoms may make another patient's symptoms much worse. Medications focus on three main issues:

Medications that increase blood volume:

- Fludrocortisone (Florinef)

- Erythropoietin

- Hormonal contraception

Medications that inhibit acetylcholinesterase:

- Pyridostigmine

Medications that improve vasoconstriction:

- Stimulants: (e.g., Ritalin or Dexedrine)

- Midodrine (ProAmatine)

- Ephedrine and pseudoephedrine (Sudafed)

- Theophylline (low-dose)

- Selective serotonin reuptake inhibitors (SSRI's - Prozac, Zoloft, and Paxil)

Behavioral changes that patients with OI can make are:

- Avoiding triggers such as prolonged sitting, quiet standing, warm environments, or vasodilating medications

- Using postural maneuvers and pressure garments

- Treating co-existing medical conditions

- Increasing fluid and salt intake

- Physical therapy and exercise unless contraindicated by an underlying condition such as chronic fatigue syndrome where traditional exercise can worsen the condition

Many drugs taken to relieve typical symptoms of motion sickness (including nausea, dizziness, etc.) contain compounds that may exacerbate drowsiness. Antihistamines are commonly used to treat motion sickness; however, side effects include drowsiness and impaired cognitive abilities. Anticholinergics such as scopolamine have also proved effective against motion sickness, but may induce drowsiness. These treatments may be combined with stimulants to counteract typical motion-induced nausea and dizziness while also preventing sedation.

However, many stimulants possess addictive properties, which result in a high potential for substance abuse. Some stimulants also tend to interfere with normal sleep patterns. Modafinil has been studied as a possible treatment for the sopite syndrome that does not appear to have the same side effects of normal stimulants. Modafanil appears to be effective when taken in combination with anticholinergics such as scopolamine, but studies of Modafanil-only treatments for motion sickness remain inconclusive.

Pharmacological methods of treatment include fludrocortisone, midodrine, somatostatin, erythropoietin, and other vasopressor agents. However, often a patient with pure autonomic failure can mitigate his or her symptoms with far less costly means. Compressing the legs and lower body, through crossing the legs, squatting, or the use of compression stockings can help. Also, ingesting more water than usual can increase blood pressure and relieve some symptoms.

No specific cure is known. Treatment is largely supportive. Nonsteroidal anti-inflammatory drugs (NSAIDs) are indicated for tender lymph nodes and fever, and corticosteroids are useful in severe extranodal or generalized disease.

Symptomatic measures aimed at relieving the distressing local and systemic complaints have been described as the main line of management of KFD. Analgesics, antipyretics, NSAIDs, and corticosteroids have been used. If the clinical course is more severe, with multiple flares of bulky enlarged cervical lymph nodes and fever, then a low-dose corticosteroid treatment has been suggested.

Amphetamine is a stimulant that has been found to improve both physical and cognitive performance. Amphetamine blocks the reuptake of dopamine and norepinephrine, which delays the onset of fatigue by increasing the amount of dopamine, despite the concurrent increase in norepinephrine, in the central nervous system. Amphetamine is a widely used substance among collegiate athletes for its performance enhancing qualities, as it can improve muscle strength, reaction time, acceleration, anaerobic exercise performance, power output at fixed levels of perceived exertion, and endurance.

Methylphenidate has also been shown to increase exercise performance in time to fatigue and time trial studies.

Caffeine is the most widely consumed stimulant in North America. In small doses, caffeine can improve endurance. Recently, it has also been shown to delay the onset of fatigue in exercise. The most probable mechanism for the delay of fatigue is through the obstruction of adenosine receptors in the central nervous system. Adenosine is a neurotransmitter that decreases arousal and increases sleepiness. By preventing adenosine from acting, caffeine removes a factor that promotes rest and delays fatigue.

There is no standard method of treating or managing POIS. Patients need to be thoroughly examined in an attempt to find the causes of their POIS symptoms, which are often difficult to determine, and which vary across patients. Once a cause is hypothesized, an appropriate treatment can be attempted. At times, more than one treatment is attempted, until one that works is found.

Affected individuals typically avoid sexual activity, especially ejaculation, or schedule it for times when they can rest and recover for several days afterwards. In case post-coital tristesse (PCT) is suspected, patients could be treated with selective serotonin reuptake inhibitors.

Another patient, in whom POIS was suspected to be caused by cytokine release, was successfully treated with nonsteroidal anti-inflammatory drugs (NSAIDs) just prior to and for a day or two after ejaculation. The patient took diclofenac 75 mg 1 to 2 hours prior to sexual activity with orgasm, and continued twice daily for 24 to 48 hours.

One POIS patient with erectile dysfunction and premature ejaculation had much lower severity of symptoms on those occasions when he was able to maintain penile erection long enough to achieve vaginal penetration and ejaculate inside his partner. The patient took tadalafil to treat his erectile dysfunction and premature ejaculation. This increased the number of occasions on which he was able to ejaculate inside his partner, and decreased the number of occasions on which he experienced POIS symptoms. This patient is thought to have Dhat syndrome rather than true POIS.

In one patient, the POIS symptoms were so severe, that he decided to undergo castration in order to relieve them. The POIS symptoms were cured by the castration.

Two patients, in whom POIS was suspected to be caused by auto-immune reaction to their own semen, were successfully treated by allergen immunotherapy with their own autologous semen. They were given multiple subcutaneous injections of their own semen for three years. Treatment with autologous semen "might take 3 to 5 years before any clinically relevant symptom reduction would become manifest".

Treatments are not always successful, especially when the cause of POIS in a particular patient has not been determined. In one patient, all of whose routine laboratory tests were normal, the following were attempted, all without success: ibuprofen, 400 mg on demand; tramadol 50 mg one hour pre-coitally; and escitalopram 10 mg daily at bedtime for 3 months.

In various studies, about one half of the patients who seek medical treatment for symptoms of MCS meet the criteria for depressive and anxiety disorders. Because many people eliminate whole categories of food in an effort to reduce symptoms, a complete review of the patient's diet may be needed to avoid nutritional deficiencies.

Chronic fatigue syndrome a.k.a. Myalgic Encephalomyelitis, Channelopathy, Ehlers Danlos Syndrome, Stickler Syndrome, Hypokalemia, Hypotonia (Low Muscle Tone), Exercise intolerance, Mastocytosis, Peripheral neuropathy, Eosinophilia myalgia syndrome, Barcoo Fever, Herpes, Hemochromatosis a.k.a. Iron Overload Disorder, Delayed onset muscle soreness, AIDS, HIV, Tumor-induced osteomalacia, Hypovitaminosis D, infarction

Anumonye reported treatment success with lorazepam; others found benefit with antidepressants and relaxation exercises.

Functional somatic syndrome is a term used to refer to physical symptoms that are poorly explained. It encompass disorders such as chronic fatigue syndrome, fibromyalgia, chronic widespread pain, temporomandibular disorder, irritable bowel syndrome, lower back pain, tension headache, atypical face pain, non-cardiac chest pain, insomnia, palpitation, dyspepsia, and dizziness. General overlap exists between this term, somatization, and somatoform.

There is little hard evidence of death as a result of the condition. However, in severe cases the fluid loss can lead to potentially life-threatening electrolyte imbalances. The patient can also become malnourished if the attacks last too long without adequate replenishment of nutrients. With adequate medical interventions, most patients can be properly supported during an episode.

The treatment for post-polio syndrome is generally palliative and consists of rest, analgesia (pain relief) and utilisation of mechanisms to make life easier such as powered wheelchairs. There are no reversive therapies. Fatigue is usually the most disabling symptom; energy conservation can significantly reduce fatigue episodes. Such conservation can be achieved with lifestyle changes, reducing workload and daytime sleeping. Weight loss is also recommended if patients are obese. In some cases, the use of lower limb orthotics can reduce energy usage.

Medications for fatigue, such as amantadine and pyridostigmine, have not been found to be effective in the management of PPS. Muscle strength and endurance training are more important in managing the symptoms of PPS than the ability to perform long aerobic activity. Management should focus on treatments such as hydrotherapy and developing other routines that encourage strength but do not affect fatigue levels. The recent trend is towards use of intravenous immunoglobulin (IVIG) which has yielded promising, albeit modest results, but there is insufficient evidence to recommend it as a treatment.

PPS increases the stress on the musculoskeletal system due to increasing muscular atrophy. A recent study showed that in a review of 539 PPS patients, 80 percent reported pain in muscles and joints and 87 percent had fatigue. Joint instability can cause significant pain in individuals with PPS and should be adequately treated with painkillers. Supervised activity programs and decreasing mechanical stress with braces and adaptive equipment are recommended.

Because PPS can fatigue facial muscles, as well as cause dysphagia (difficulty swallowing), dysarthria (difficulty speaking) or aphonia (inability to produce speech), persons with PPS may become malnourished due to difficulty eating. Compensatory routines can help relieve these symptoms such as eating smaller portions at a time and sitting down whilst eating. PPS with respiratory involvement requires special management such as breathing exercises, chest percussion with a stethoscope on regular occasions for observation of the disease and management of secretions. Failure to properly assess PPS with respiratory involvement can increase the risk of missing aspiration pneumonia (an infection of the lower respiratory tract) in an individual. Severe cases may require permanent ventilation or tracheostomy. Sleep apnoea may also occur. Other management strategies that may lead to improvement include smoking cessation, treatment of other respiratory diseases and vaccination against respiratory infections such as influenza.

POTS treatment involves using multiple methods in combination to counteract cardiovascular dysfunction, address symptoms, and simultaneously address any associated disorders. For most patients, water intake should be increased, especially after waking, in order to expand blood volume (reducing hypovolemia). 8–10 cups of water daily are recommended. Increasing salt intake, by adding salt to food, taking salt tablets, or drinking sports drinks and other electrolyte solutions is an effective way to raise blood pressure by helping the body retain water. Different physicians recommend different amounts of sodium to their patients. Salt intake is not appropriate for people with high blood pressure. Combining these techniques with gradual physical training enhances their effect. In some cases, when increasing oral fluids and salt intake is not enough, intravenous saline or the drug desmopressin is used to help increase fluid retention.

Large meals worsen symptoms for some people. These people may benefit from eating small meals frequently throughout the day instead. Alcohol and food high in carbohydrates can also exacerbate symptoms of orthostatic hypotension. Excessive consumption of caffeine beverages should be avoided, because they can promote urine production (leading to fluid loss) and consequently hypovolemia. Exposure to extreme heat may also aggravate symptoms.

Prolonged physical inactivity can worsen the symptoms of POTS. Techniques that increase a person's capacity for exercise, such as endurance training or graded exercise therapy, can relieve symptoms for some patients. Aerobic exercise performed for 20 minutes a day, three times a week, is sometimes recommended for patients who can tolerate it. Exercise may have the immediate effect of worsening tachycardia, especially after a meal or on a hot day. In these cases, it may be easier to exercise in a semi-reclined position, such as riding a recumbent bicycle, rowing or swimming.

When changing to an upright posture, finishing a meal or concluding exercise, a sustained hand grip can briefly raise the blood pressure, possibly reducing symptoms. Compression garments can also be of benefit by constricting blood pressures with external body pressure.

The primary treatment for children is the removal of enlarged tonsils and adenoids via a tonsillectomy and adenoidectomy. Orthodontic treatment is frequently recommended and CPAP may also be necessary for children with UARS.