There is presently no known cure for rumination. Proton pump inhibitors and other medications have been used to little or no effect.

Treatment is different for infants and the mentally handicapped than for adults and adolescents of normal intelligence. For adults and adolescents,Biofeedback and relaxation techniques, to be practice after eating or whenever regurgitation occurs, has proven to be most effective.

Among infants and the mentally handicapped, behavioral and mild aversive training has been shown to cause improvement in most cases. Aversive training involves associating the ruminating behavior with negative results, and rewarding good behavior and eating. Placing a sour or bitter taste on the tongue when the individual begins the movements or breathing patterns typical of his or her ruminating behavior is the generally accepted method for aversive training,

although some older studies advocate the use of pinching.

In patients of normal intelligence, rumination is not an intentional behavior and is habitually reversed using diaphragmatic breathing to counter the urge to regurgitate. Alongside reassurance, explanation and habit reversal, patients are shown how to breathe using their diaphragms prior to and during the normal rumination period. A similar breathing pattern can be used to prevent normal vomiting. Breathing in this method works by physically preventing the abdominal contractions required to expel stomach contents.

Supportive therapy and diaphragmatic breathing has shown to cause improvement in 56% of cases, and total cessation of symptoms in an additional 30% in one study of 54 adolescent patients who were followed up 10 months after initial treatments. Patients who successfully use the technique often notice an immediate change in health for the better. Individuals who have had bulimia or who intentionally induced vomiting in the past have a reduced chance for improvement due to the reinforced behavior. The technique is not used with infants or young children due to the complex timing and concentration required for it to be successful. Most infants grow out of the disorder within a year or with aversive training.

Treatment for pica may vary by patient and suspected cause (e.g., child, developmentally disabled, pregnant or psychogenic) and may emphasize psychosocial, environmental and family-guidance approaches, (iron deficiency) may be treatable though iron supplement through dietary changes. An initial approach often involves screening for and, if necessary, treating any mineral deficiencies or other comorbid conditions. For pica that appears to be of psychogenic cause, therapy and medication such as SSRIs have been used successfully. However, previous reports have cautioned against the use of medication until all non-psychogenic causes have been ruled out.

Looking back at the different causes of pica related to assessment, the clinician will try to develop a treatment. First, there is pica as a result of social attention. A strategy might be used of ignoring the person’s behavior or giving them the least possible attention. If their pica is a result of obtaining a favorite item, a strategy may be used where the person is able to receive the item or activity without eating inedible items. The individual’s communication skills should increase so that they can relate what they want to another person without engaging in this behavior. If pica is a way for a person to escape an activity or situation, the reason why the person wants to escape the activity should be examined and the person should be moved to a new situation. If pica is motivated by sensory feedback, an alternative method of feeling that sensation should be provided. Other non-medication techniques might include other ways for oral stimulation such as gum. Foods such as popcorn have also been found helpful. These things can be placed in a “Pica Box” that should be easily accessible to the individual when they feel like engaging in pica.

Behavior-based treatment options can be useful for developmentally disabled and mentally ill individuals with pica. Behavioral treatments for pica have been shown to reduce pica severity by 80% in people with intellectual disabilities. These may involve using positive reinforcement normal behavior. Many use aversion therapy, where the patient learns through positive reinforcement which foods are good and which ones they should not eat. Often treatment is similar to the treatment of obsessive compulsive or addictive disorders (such as exposure therapy). In some cases treatment is as simple as addressing the fact they have this disorder and why they may have it. A recent study classified nine such classes of behavioral intervention: Success with treatment is generally high and generally fades with age, but it varies depending on the cause of the disorder. Developmental causes tend to have a lower success rate.

Treatment techniques include:

Few studies guide the treatment of individuals with OSFED. However, cognitive behavioral therapy (CBT), which focuses on the interplay between thoughts, feelings, and behaviors, has been shown to be the leading evidence-based treatment for the eating disorders of BN and BED. For OSFED, a particular cognitive behavioral treatment can be used called CBT-Enhanced (CBT-E), which was designed to treat all forms of eating disorders. This method focuses not only what is thought to be the central cognitive disturbance in eating disorders (i.e., over-evaluation of eating, shape, and weight), but also on modifying the mechanisms that sustain eating disorder psychopathology, such as perfectionism, core low self-esteem, mood intolerance, and interpersonal difficulties. CBT-E showed effectiveness in two studies (total N = 219) and well maintained over 60-week follow-up periods. CBT-E is not specific to individual types of eating disorders but is based on the concept that common mechanisms are involved in the persistence of atypical eating disorders, AN, and BN.

Treatment varies according to type and severity of eating disorder, and usually more than one treatment option is utilized. There is no well-established treatment for eating disorders, meaning that current views about treatment are based mainly on clinical experience. Family doctors play an important role in early treatment of people with eating disorders by encouraging those who are also reluctant to see a psychiatrist. Treatment can take place in a variety of different settings such as community programs, hospitals, day programs, and groups. The American Psychiatric Association (APA) recommends a team approach to treatment of eating disorders. The members of the team are usually a psychiatrist, therapist, and registered dietitian, but other clinicians may be included.

That said, some treatment methods are:

- Cognitive behavioral therapy (CBT), which postulates that an individual's feelings and behaviors are caused by their own thoughts instead of external stimuli such as other people, situations or events; the idea is to change how a person thinks and reacts to a situation even if the situation itself does not change. See Cognitive behavioral treatment of eating disorders.

- Acceptance and commitment therapy: a type of CBT

- Cognitive Remediation Therapy (CRT), a set of cognitive drills or compensatory interventions designed to enhance cognitive functioning.

- Dialectical behavior therapy

- Family therapy including "conjoint family therapy" (CFT), "separated family therapy" (SFT) and Maudsley Family Therapy.

- Behavioral therapy: focuses on gaining control and changing unwanted behaviors.

- Interpersonal psychotherapy (IPT)

- Cognitive Emotional Behaviour Therapy (CEBT)

- Music Therapy

- Recreation Therapy

- Art therapy

- Nutrition counseling and Medical nutrition therapy

- Medication: Orlistat is used in obesity treatment. Olanzapine seems to promote weight gain as well as the ability to ameliorate obsessional behaviors concerning weight gain. zinc supplements have been shown to be helpful, and cortisol is also being investigated.

- Self-help and guided self-help have been shown to be helpful in AN, BN and BED; this includes support groups and self-help groups such as Eating Disorders Anonymous and Overeaters Anonymous.

- Psychoanalysis

- Inpatient care

There are few studies on the cost-effectiveness of the various treatments. Treatment can be expensive; due to limitations in health care coverage, people hospitalized with anorexia nervosa may be discharged while still underweight, resulting in relapse and rehospitalization.

For children with anorexia, the only well-established treatment is the family treatment-behavior. For other eating disorders in children, however, there is no well-established treatments, though family treatment-behavior has been used in treating bulimia.

Rumination syndrome, or Merycism, is an under-diagnosed chronic motility disorder characterized by effortless regurgitation of most meals following consumption, due to the involuntary contraction of the muscles around the abdomen. There is no retching, nausea, heartburn, odour, or abdominal pain associated with the regurgitation, as there is with typical vomiting. The disorder has been historically documented as affecting only infants, young children, and people with cognitive disabilities (the prevalence is as high as 10% in institutionalized patients with various mental disabilities).

Today it is being diagnosed in increasing numbers of otherwise healthy adolescents and adults, though there is a lack of awareness of the condition by doctors, patients and the general public.

Rumination syndrome presents itself in a variety of ways, with especially high contrast existing between the presentation of the typical adult sufferer without a mental disability and the presentation of an infant and/or mentally impaired sufferer. Like related gastrointestinal disorders, rumination can adversely affect normal functioning and the social lives of individuals. It has been linked with depression.

Little comprehensive data regarding rumination syndrome in otherwise healthy individuals exists because most sufferers are private about their illness and are often misdiagnosed due to the number of symptoms and the clinical similarities between rumination syndrome and other disorders of the stomach and esophagus, such as gastroparesis and bulimia nervosa. These symptoms include the acid-induced erosion of the esophagus and enamel, halitosis, malnutrition, severe weight loss and an unquenchable appetite. Individuals may begin regurgitating within a minute following ingestion, and the full cycle of ingestion and regurgitation can mimic the binging and purging of bulimia.

Diagnosis of rumination syndrome is non-invasive and based on a history of the individual. Treatment is promising, with upwards of 85% of individuals responding positively to treatment, including infants and the mentally handicapped.

Prevention aims to promote a healthy development before the occurrence of eating disorders. It also intends early identification of an eating disorder before it is too late to treat. Children as young as ages 5–7 are aware of the cultural messages regarding body image and dieting. Prevention comes in bringing these issues to the light. The following topics can be discussed with young children (as well as teens and young adults).

- Emotional Bites: a simple way to discuss emotional eating is to ask children about why they might eat besides being hungry. Talk about more effective ways to cope with emotions, emphasizing the value of sharing feelings with a trusted adult.

- Say No to Teasing: another concept is to emphasize that it is wrong to say hurtful things about other people's body sizes.

- Body Talk: emphasize the importance of listening to one's body. That is, eating when you are hungry (not starving) and stopping when you are satisfied (not stuffed). Children intuitively grasp these concepts.

- Fitness Comes in All Sizes: educate children about the genetics of body size and the normal changes occurring in the body. Discuss their fears and hopes about growing bigger. Focus on fitness and a balanced diet.

Internet and modern technologies provide new opportunities for prevention. On-line programs have the potential to increase the use of prevention programs. The development and practice of prevention programs via on-line sources make it possible to reach a wide range of people at minimal cost. Such an approach can also make prevention programs to be sustainable.

One form of treatment is Cognitive behavioral therapy which promotes desensitization methods.

A number of pharmaceuticals may be used in an attempt to bring the polydipsia under control, including:

- Atypical antipsychotics, such as clozapine, olanzapine and risperidone

- Demeclocycline, a tetracycline antibiotic, which is effective due to the side effect of inducing nephrogenic diabetes insipidus. Demeclocycline is used for cases of psychogenic polydipsia, including those with nocturnal enuresis (bed-wetting). Its mechanism of action involves direct inhibition of vasopressin at the DCTs, thus reducing urine concentration.

There are a number of emerging pharmaceutical treatments for psychogenic polydipsia, although these need further investigation:

- ACE Inhibitors, such as enalapril

- Clonidine, an alpha-2 adrenergic agonist

- Irbesartan, an angiotensin II receptor antagonist

- Propranolol, a sympatholytic beta blocker

- Vasopressin receptor antagonists, such as conivaptan

- Acetazolamide, a carbonic anhydrase inhibitor

Lithium was previously used for treatment of PPD as a direct competitive ADH agonist, but is now generally avoided due to its toxic effects on the thyroid and kidneys.

It is important to note that the majority of psychotropic drugs (and a good many of other classes) can cause dry mouth as a side effect, but this is not to be confused with true polydipsia in which a dangerous drop in serum sodium will be seen.

Treatment requires a firm and transparent diagnosis based on positive features which both health professionals and patients can feel confident about. It is essential that the health professional confirms that this is a common problem which is genuine, not imagined and not a diagnosis of exclusion.

Confidence in the diagnosis does not improve symptoms, but appears to improve the efficacy of treatments such as physiotherapy which require altering established abnormal patterns of movement.

A multi-disciplinary approach to treating functional neurological disorder is recommended.

Treatment options can include:

- Physiotherapy and occupational therapy

- Medication such as sleeping tablets, painkillers, anti-epileptic medications and anti-depressants (for patients suffering with depresssion co-morbid or for pain relief)

Physiotherapy with someone who understands functional disorders may be the initial treatment of choice for patients with motor symptoms such as weakness, gait (walking) disorder and movement disorders. Nielsen et al. have reviewed the medical literature on physiotherapy for functional motor disorders up to 2012 and concluded that the available studies, although limited, mainly report positive results. Since then several studies have shown positive outcomes. In one study, up to 65% of patients were very much or much improved after five days of intensive physiotherapy even though 55% of patients were thought to have poor prognosis. In a randomised controlled trial of physiotherapy there was significant improvement in mobility which was sustained on one year follow up. In multidisciplinary settings 69% of patients markedly improved even with short rehabilitation programmes. Benefit from treatment continued even when patients were contacted up 25months after treatment.

For patients with severe and chronic FND a combination of physiotherapy, occupational therapy and cognitive behavioural therapy may be the best combination with positive studies being published in patients who have had symptoms for up to three years before treatment.

Cognitive behavioural therapy (CBT) alone may be beneficial in treating patients with dissociative (non-epileptic) seizures. A randomised controlled trial of patients who undertook 12 sessions of CBT which taught patients how to interrupt warning signs before seizure onset, challenged unhelpful thoughts and helped patients start activities they had been avoiding found a reduction in the seizure frequency with positive outcomes sustained at six month follow up. A large multicentre trial of CBT for dissociative (non-epileptic) seizures started in 2015 in the UK.

For many patients with FND, accessing treatment can be difficult. Availability of expertise is limited and they may feel that they are being dismissed or told 'it's all in your head' especially if psychological input is part of the treatment plan. Some medical professionals are uncomfortable explaining and treating patients with functional symptoms. Changes in the diagnostic criteria, increasing evidence, literature about how to make the diagnosis and how to explain it and changes in medical training is slowly changing this

After a diagnosis of functional neurological disorder has been made, it is important that the neurologist explains the illness fully to the patient to ensure the patient understands the diagnosis.

Some, but not all patients with FND may experience low moods or anxiety due to their condition. However, they will often not seek treatment due being worried that a doctor will blame their symptoms on their anxiety or depression.

It is recommended that the treatment of functional neurological disorder should be balanced and involve a whole-person approach. This means that it should include professionals from multiple departments, including neurologists, general practitioners (or primary health care providers), physiotherapists, occupational therapists. At the same time, ruling out secondary gain, malingering, conversion disorder and other factors, including the time and financial resources involved in assessing and treating patients who demand hospital resources but would be better served in psychological settings, must all be balanced.

Behavioural treatments may involve the use of a token economy to provide positive reinforcement to desirable behaviour. Furthermore, cognitive therapy techniques can be used to address the thought patterns that lead to compulsive drinking behaviour. Success has been seen in trials of this technique, with emphasis on the development of coping techniques (e.g. taking small sips of water, having ice cubes instead of drinks) in addition to challenging delusions leading to excessive drinking.

Psychogenic polydipsia often leads to institutionalisation of mentally ill patients, since it is difficult to manage in the community. Most studies of behavioural treatments occur in institutional settings and require close monitoring of the patient and a large degree of time commitment from staff.

CGD is relatively unresponsive to antidepressants or interpersonal psychotherapy; however, recent studies support the use of CG-targeted psychotherapy (similar to PTSD-targeted psychotherapy). Other methods of psycho-pharmacological treatment are under investigation.

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.

There is considerable research into the causes, diagnosis and treatments for FGIDs. Diet, microbiome, genetics, neuromuscular function and immunological response all interact. Heightened mast cell activation has been proposed to be a common factor among FGIDs, contributing to visceral hypersensitivity as well as epithelial, neuromuscular, and motility dysfunction.

There is no evidence-based criteria for treating SPS, and there have been no large controlled trials of treatments for the condition. The rarity of the disease complicates efforts to establish guidelines.

GABA agonists, usually diazepam but sometimes other benzodiazepines, are the primary treatment for SPS. Drugs that increase GABA activity alleviate muscle stiffness caused by a lack of GABAergic tone. They increase pathways that are dependent upon GABA and have muscle relaxant and anticonvulsant effects, often providing symptom relief. Because the condition worsens over time, patients generally require increased dosages, leading to more side effects. For this reason, gradual increase in dosage of benzodiazepines is indicated. Baclofen, a GABA agonist, is generally used when individuals taking high doses of benzodiazepines have high side effects. In some cases it has shown improvements in electrophysiological and muscle stiffness when administered intravenously. Intrathecal baclofen administration may not have long-term benefits though, and there are potential serious side effects.

Treatments that target the autoimmune response are also used. Intravenous immunoglobin is the best second-line treatment for SPS. It often decreases stiffness and improves quality of life and startle reflex. It is generally safe, but there are possible serious side effects and it is expensive. The European Federation of Neurological Societies suggests it be used when disabled patients do not respond well to diazepam and baclofen. Steroids, rituximab, and plasma exchange have been used to suppress the immune system in SPS patients, but the efficacy of these treatments is unclear. Botulinum toxin has been used to treat SPS, but it does not appear to have long-term benefits and has potential serious side effects. In paraneoplastic cases, tumors must be managed for the condition to be contained. Opiates are sometimes used to treat severe pain, but in some cases they exacerbate symptoms.

Behavioral treatment can be effective in some cases. Sedative hypnotics may also help relieve the symptoms. Additionally, education about normal patterns of the sleep-wake cycle may alleviate anxiety in some patients. For patients with severe depression resulting from the fear of having insomnia, electroconvulsive therapy appears to be a safe and effective treatment.

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

Some of the differential or comorbid medical diagnoses may include:

- achalasia – There have been cases where achalasia, a disorder of the esophagus which affects peristalsis, has been misdiagnosed as AN. It has been reported in cases where there is sub-clinical manifestation of anorexia nervosa and also in cases where the full diagnostic criteria AN have been met.

- acute pandysautonomia is one form of an autonomic neuropathy, which is a collection of various syndromes and diseases which affect the autonomic neurons of the autonomic nervous system (ANS). Autonomic neuropathies may be the result of an inherited condition or they may be acquired due to various premorbid conditions such as diabetes and alcoholism, bacterial infection such as Lyme disease or a viral illness. Some of the symptoms of ANS which may be associated with an ED include nausea, dysphagia, constipation, pain in the salivary glands, early saiety. It also affects peristalsis in the stomach. Acute pandysautonomia may cause emotional instability and has been misdiagnosed as various psychiatric disorders including hysterical neurosis and anorexia nervosa.

- Lupus: various neuropsychiatric symptoms are associated with systemic lupus erythematosus (SLE), including depression. Anorexia and weight loss also may occur with SLE and while rare it may be misdiagnosed as AN.

- Lyme disease is known as the "great imitator", as it may present as a variety of psychiatric or neurologic disorders including anorexia nervosa. "A 12 year old boy with confirmed Lyme arthritis treated with oral antibiotics subsequently became depressed and anorectic. After being admitted to a psychiatric hospital with the diagnosis of anorexia nervosa, he was noted to have positive serologic tests for Borrelia burgdorferi. Treatment with a 14 day course of intravenous antibiotics led to a resolution of his depression and anorexia; this improvement was sustained on 3 year follow-up." Serologic testing can be helpful but should not be the sole basis for diagnosis. The Centers for Disease Control (CDC) issued a cautionary statement (MMWR 54;125) regarding the use of several commercial tests. Clinical diagnostic criteria have been issued by the CDC (CDC, MMWR 1997; 46: 531-535).

- Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) is a rare genetic disorder characterized by gastrointestinal dysmotility, severe cachexia progressive external ophthalmoplegia, post-prandial emesis (vomiting after eating), peripheral neuropathy, and diffuse leukoencephalopathy. Onset is prior to age 20 in 60% of cases. ""Miss A" was a 21-year-old Indian woman diagnosed as having treatment-resistant anorexia nervosa." It was subsequently proven to be MNGIE

- superior mesenteric artery syndrome (SMA syndrome) "is a gastrointestinal disorder characterized by the compression of the third or transverse portion of the duodenum against the aorta by the superior mesenteric artery resulting in chronic partial, incomplete, acute or intermittent duodenal obstruction". It may occur as a complication of AN or as a differential diagnosis. There have been reported cases of a tentative diagnosis of AN, where upon treatment for SMA syndrome the patient is asymptomatic.

- Addison's disease is a disorder of the adrenal cortex which results in decreased hormonal production. Addison's disease, even in subclinical form, may mimic many of the symptoms of anorexia nervosa.

- Brain tumors: There are multiple cases were the neuropsychiatric symptoms of a brain tumor were attributed to AN, resulting in misdiagnosis. The tumors in these cases were noted in various regions of the brain including the medulla oblongata, hypothalamus, pituitary gland, pineal gland and the obex.

- Simmond's disease (organic hypopituitarism) – "A 20-year-old Japanese man with a hypothalamic tumor which caused hypopituitarism and diabetes insipidus was mistakenly diagnosed as anorexia nervosa because of anorexia, weight loss, denial of being ill, changes in personality, and abnormal behavior resembling the clinical characteristics of anorexia nervosa"

- Brain calcification either dystrophic calcification or metastatic calcification can present with neuropsychiatric symptoms including those associated with AN and comorbid disorders such as obsessive compulsive disorder.

- cysts that occur in the central nervous system such as dermoid cysts and arachnoid cysts can cause neuropsychiatric symptoms including psychosis.

- Celiac disease is an inflammatory disorder triggered by peptides from wheat and similar grains which cause an immune reaction in the small intestine. "information on the role of the gastrointestinal system in causing or mimicking eating disorders is scarce."(Leffler DA "et al.")

- Gall bladder disease which may be caused by inflammation, infection, gallstones, obstruction of the gallbladder or torsion of the gall bladder – Many of the symptoms of gall bladder disease may mimic anorexia nervosa (AN). Laura Daly, a woman from Missouri, suffered from an inherited disorder in which the gall bladder was not properly attached; the resultant complications led to multiple erroneous diagnoses of AN. Upon performance of a CCK test, standard imaging techniques are done with the patient lying prone, in this instance it was done with the patient in an upright position. The gall bladder was shown to be in an abnormal position having flipped over the liver. The gallbladder was removed and the patient has since recovered. The treatment was performed by William P. Smedley in Pennsylvania.

- colonic tuberculosis misdiagnosed as anorexia nervosa in a physician at the hospital where she worked – "This patient, who had severe wasting, was misdiagnosed as having anorexia nervosa despite the presence of other symptoms suggestive of an organic disease, namely, fever and diarrhea"(Madani, A 2002).

- Crohn's disease: "We report three cases of young 18 to 25 year-old girls, initially treated for anorexia nervosa in a psychiatric department. Diagnosis of Crohn's disease was made within 5 to 13 years."(Blanchet C, Luton JP. 2002)"This disease should be diagnostically excluded before accepting anorexia nervosa as final diagnosis". (Wellmann W "et al.")

- hypothyroidism, hyperthyroidism, hypoparathyroidism and hyperparathyroidism may mimic some of the symptoms of, can occur concurrently with, be masked by or exacerbate an eating disorder and/or various comorbid disorders such as anxiety and depression.

- Insulinomas are (pancreatic tumors) that cause an overproduction of insulin, causing hypoglycemia. Various neurological deficits have been ascribed to this condition including misdiagnosis as an eating disorder.

- Multiple sclerosis (encephalomyelitis disseminata) is a progressive autoimmune disorder in which the protective covering (myelin sheath) of nerve cells is damaged as a result of inflammation and resultant attack by the bodies own immune system. In its initial presentation, MS has been misdiagnosed as an eating disorder.

Medical and surgical treatments have been recommended to treat organic dysphonias. An effective treatment for spasmodic dysphonia (hoarseness resulting from periodic breaks in phonation due to hyperadduction of the vocal folds) is botulinum toxin injection. The toxin acts by blocking acetylcholine release at the thyro-arytenoid muscle. Although the use of botlinum toxin injections is considered relatively safe, patients' responses to treatment differ in the initial stages; some have reported experiencing swallowing problems and breathy voice quality as a side-effect to the injections. Breathiness may last for a longer period of time for males than females.

Surgeries involve myoectomies of the laryngeal muscles to reduce voice breaks, and laryngoplasties, in which laryngeal cartilage is altered to reduce tension.

Other specified feeding or eating disorder or OSFED is the "DSM-5" category that replaces the category formerly called Eating Disorder Not Otherwise Specified (EDNOS) in "DSM-IV", and that captures feeding disorders and eating disorders of clinical severity that do not meet diagnostic criteria for anorexia nervosa (AN), bulimia nervosa (BN), binge eating disorder (BED), avoidant/restrictive food intake disorder (ARFID), pica, or rumination disorder. OSFED includes five examples: atypical AN, BN (of low frequency and/or limited duration), BED (of low frequency and/or limited duration), purging disorder, and night eating syndrome (NES).

The condition may worsen as a result of persistent attempts to treat the symptoms through conventional methods of dealing with insomnia. The prescription of hypnotics or stimulants may lead to drug dependency as a complication.

Nonetheless, chronic SSM may increase risk for depression, anxiety, and substance abuse. It has also been noted that patients with this condition may sometimes opt to take medications over other treatments "for the wrong reasons (e.g. because of euphoriant properties)."

In individuals with autism, schizophrenia, and certain physical disorders (such as Kleine-Levin syndrome), nonnutritive substances may be eaten. In such instances, pica should not be noted as an additional diagnosis.

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.

Botulinum toxin (Botox) is often used to improve some symptoms of spasmodic dysphonia. Whilst the level of evidence for its use is limited, it remains a popular choice for many patients due to the predictability and low chance of long term side effects. It results in periods of some improvement. The duration of benefit averages 10–12 weeks before the patient returns to baseline. Repeat injection is required to sustain good vocal production.

Indirect therapies take into account external factors that may influence vocal production. This incorporates maintenance of vocal hygiene practices, as well as the prevention of harmful vocal behaviours. Vocal hygiene includes adequate hydration of the vocal folds, monitoring the amount of voice use and rest, avoidance of vocal abuse (e.g., shouting, clearing of the throat), and taking into consideration lifestyle choices that may affect vocal health (e.g., smoking, sleeping habits). Vocal warm-ups and cool-downs may be employed to improve muscle tension and decrease risk of injury before strenuous vocal activities. It should be taken into account that vocal hygiene practices alone are minimally effective in treating dysphonia, and thus should be paired with other therapies.

To minimise the risk of this condition developing from its most common cause, overly rapid reversal of hyponatremia, the hyponatremia should be corrected at a rate not exceeding 10 mmol/L/24 h or 0.5 mEq/L/h; or 18 m/Eq/L/48hrs; thus avoiding demyelination. No large clinical trials have been performed to examine the efficacy of therapeutic re-lowering of serum sodium, or other interventions sometimes advocated such as steroids or plasma exchange.

Alcoholic patients should receive vitamin supplementation and a formal evaluation of their nutritional status.

Once osmotic demyelination has begun, there is no cure or specific treatment. Care is mainly supportive. Alcoholics are usually given vitamins to correct for other deficiencies. The favourable factors contributing to the good outcome in CPM without hyponatremia were: concurrent treatment of all electrolyte disturbances, early Intensive Care Unit involvement at the advent of respiratory complications, early introduction of feeding including thiamine supplements with close monitoring of the electrolyte changes and input.

Research has led to improved outcomes. Animal studies suggest that inositol reduces the severity of osmotic demyelination syndrome if given before attempting to correct chronic hyponatraemia. Further study is required before using inositol in humans for this purpose.