There are no medications currently approved for the treatment of obesity in children. The American Academy of Pediatrics recommends medications for obesity be discourage. Orlistat and sibutramine may be helpful in managing moderate obesity in adolescence. Metformin is minimally useful. A Cochrane review in 2016 concluded that medications might reduce BMI and bodyweight to a small extent in obese children and adolescents. This conclusion was based only on low quality evidence.

Obesity in children is treated with dietary changes and physical activity. Dieting and missing meals should; however, be discourage. The benefit of tracking BMI and providing counselling around weight is minimal.

Polyphagia usually occurs early in the course of diabetic ketoacidosis. However, once insulin deficiency becomes more severe and ketoacidosis develops, appetite is suppressed.

There are numerous ways in which individuals can reduce emotional distress without engaging in emotional eating. The most salient choice is to minimize maladaptive coping strategies and to maximize adaptive strategies. A study conducted by Corstorphine et al. in 2007 investigated the relationship between distress tolerance and disordered eating. These researchers specifically focused on how different coping strategies impact distress tolerance and disordered eating. They found that individuals who engage in disordered eating often employ emotional avoidance strategies. If an individual is faced with strong negative emotions, they may choose to avoid the situation by distracting themselves through overeating. Discouraging emotional avoidance is thus an important facet to emotional eating treatment. The most obvious way to limit emotional avoidance is to confront the issue through techniques like problem solving. Corstorphine et al. showed that individuals who engaged in problem solving strategies enhance one's ability to tolerate emotional distress. Since emotional distress is correlated to emotional eating, the ability to better manage one's negative affect should allow an individual to cope with a situation without resorting to overeating.

One way to combat emotional eating is to employ mindfulness techniques. For example, approaching cravings with a nonjudgmental inquisitiveness can help differentiate between hunger and emotionally-driven cravings. An individual may ask his or herself if the craving developed rapidly, as emotional eating tends to be triggered spontaneously. An individual may also take the time to note his or her bodily sensations, such as hunger pangs, and coinciding emotions, like guilt or shame, in order to make conscious decisions to avoid emotional eating.

Emotional eating disorder predisposes individuals to more serious eating disorders and physiological complications. Therefore, combatting disordered eating before such progression takes place has become the focus of many clinical psychologists.

The word "polyphagia" () uses combining forms of "" + "", from the Greek words πολύς (polys), "very much" or "many", and φαγῶ (phago), "eating" or "devouring".

NES is sometimes comorbid with excess weight; as many as 28% of individuals seeking gastric bypass surgery were found to suffer from NES in one study. However, not all individuals with NES are overweight. Night eating has been associated with diabetic complications. Many people with NES also experience depressed mood and anxiety disorders.

Night eating syndrome (NES) is an eating disorder, characterized by a delayed circadian pattern of food intake. Although there is some degree of comorbidity with binge eating disorder, it differs from binge eating in that the amount of food consumed in the evening/night is not necessarily objectively large nor is a loss of control over food intake required. It was originally described by Dr. Albert Stunkard in 1955 and is currently included in the other specified feeding or eating disorder category of the DSM-5. Research diagnostic criteria have been proposed and include evening hyperphagia (consumption of 25% or more of the total daily calories after the evening meal) and/or nocturnal awakening and ingestion of food two or more times per week. The person must have awareness of the night eating to differentiate it from the parasomnia sleep-related eating disorder (SRED). Three of five associated symptoms must also be present: lack of appetite in the morning, urges to eat in the evening/at night, belief that one must eat in order to fall back to sleep at night, depressed mood, and/or difficulty sleeping.

NES affects both men and women, between 1 and 2% of the general population, and approximately 10% of obese individuals. The age of onset is typically in early adulthood (spanning from late teenage years to late twenties) and is often long-lasting, with children rarely reporting NES. People with NES have been shown to have higher scores for depression and low self-esteem, and it has been demonstrated that nocturnal levels of the hormones melatonin and leptin are decreased. The relationship between NES and the parasomnia SRED is in need of further clarification. There is debate as to whether these should be viewed as separate diseases, or part of a continuum. Consuming foods containing serotonin has been suggested to aid in the treatment of NES, but other research indicates that diet by itself cannot appreciably raise serotonin levels in the brain. A few foods (for example, bananas) contain serotonin, but they do not affect brain serotonin levels, and various foods contain tryptophan, but the extent to which they affect brain serotonin levels must be further explored scientifically before conclusions can be drawn, and "the idea, common in popular culture, that a high-protein food such as turkey will raise brain tryptophan and serotonin is, unfortunately, false."

Several drug therapies have been used on patients with KLS, but none of them have been subject to randomized controlled trials. A 2016 Cochrane Review concluded that "No evidence indicates that pharmacological treatment for Kleine-Levin syndrome is effective and safe".

In several cases, stimulants, including modafinil, have been reported to have a limited effect on patients, often alleviating sleepiness. They can cause behavioral problems, but they may pose fewer issues if used in older patients with mild symptoms. In some case reports, lithium has been reported to decrease the length of episodes and the severity of their symptoms and to increase the time between episodes. It has been reported to be effective in about 25 to 60 percent of cases. Its use carries the risk of side effects in the thyroid or kidneys. Anti-psychotics and benzodiazepines can help alleviate psychotic and anxiety related symptoms, respectively. Carbamazepine has been reported to be less effective than lithium but more effective than some drugs in its class. Electroconvulsive therapy is not effective and worsens symptoms.

KLS patients generally do not need to be admitted to hospitals. It is recommended that caregivers reassure them and encourage them to maintain sleep hygiene. It may also be necessary for patients to be prevented from putting themselves in dangerous situations, such as driving.

Emotional eating may qualify as avoidant coping and/or emotion-focused coping. As coping methods that fall under these broad categories focus on temporary reprieve rather than practical resolution of stressors, they can initiate a vicious cycle of maladaptive behavior reinforced by fleeting relief from stress. Additionally, in the presence of high insulin levels characteristic of the recovery phase of the stress-response, glucocorticoids trigger the creation of an enzyme that stores away the nutrients circulating in the bloodstream after an episode of emotional eating as visceral fat, or fat located in the abdominal area. Therefore, those who struggle with emotional eating are at greater risk for abdominal obesity, which is in turn linked to a greater risk for metabolic and cardiovascular disease.

Lithium is the only drug that appears to have a preventive effect. In two studies of more than 100 patients, lithium helped prevent recurrence of symptoms in 20% to 40% of cases. The recommended blood level of lithium for KLS patients is 0.8-1.2 mEq/ml. It is not known if other mood stabilizers have an effect on the condition. Anti-depressants do not prevent recurrence.

The most common treatment for reducing bipolar II disorder symptoms is medication, usually in the form of mood stabilizers. However, treatment with mood stabilizers may produce a flat affect in the patient, which is dose-dependent. Concurrent use of SSRI antidepressants may help some with bipolar II disorder, though these medications should be used with caution because it is believed that they may cause a hypomanic switch.

The pharmaceutical management of bipolar II disorder is not generally supported by strong evidence, with limited randomised controlled trials (RCTs) published in the literature. Some medications used are:

- Lithium - There is strong evidence that lithium is effective in treating both the depressive and hypomanic symptoms in bipolar II. In addition, its action as a mood stabilizer can be used to decrease the risk of hypomanic switch in patients treated with antidepressants.

- Anticonvulsants - there is evidence that lamotrigine decreases the risk of relapse in rapid cycling bipolar II. It appears to be more effective in bipolar II than bipolar I, suggesting that lamotrigine is more effective for the treatment of depressive rather than manic episodes. Doses ranging from 100–200 mg have been reported to have the most efficacy, while experimental doses of 400 mg have rendered little response. A large, multicentre trial comparing carbamazepine and lithium over two and a half years found that carbamazepine was superior in terms of preventing future episodes of bipolar II, although lithium was superior in individuals with bipolar I. There is also some evidence for the use of valproate and topiramate, although the results for the use of gabapentin have been disappointing.

- Antidepressants - there is evidence to support the use of SSRI and SNRI antidepressants in bipolar II. Indeed, some sources consider them to be one of the first line treatments. However, antidepressants also pose significant risks, including a switch to mania, rapid cycling, and dysphoria and so many psychiatrists advise against their use for bipolar. When used, antidepressants are typically combined with a mood stabilizer.

- Antipsychotics - there is good evidence for the use of quetiapine, and it has been approved by the FDA for this indication. There is also some evidence for the use of risperidone, although the relevant trial was not placebo controlled and was complicated by the use of other medications in some of the patients.

- Dopamine agonists - there is evidence for the efficacy of pramipexole from one RCT.

Treatment typically includes three things: the treatment of acute hypomania, the treatment of acute depression, and the prevention of the relapse of either hypomania or depression. The main goal is to make sure that patients do not harm themselves.

Prader–Willi syndrome has no cure; however, several treatments are in place to lessen the condition's symptoms. During infancy, subjects should undergo therapies to improve muscle strength. Speech and occupational therapy are also indicated. During the school years, children benefit from a highly structured learning environment as well as extra help. The largest problem associated with the syndrome is severe obesity. Access to food must be strictly supervised and limited, usually by installing locks on all food-storage places including refrigerators.

Because hypotonia can be a symptom of PWS, it is vital to provide proper nutrition during infancy. It is also very important to stress physical activity in individuals with PWS for all ages in order to optimize strength and promote a healthy lifestyle.

Prescription of daily recombinant growth hormone injections are indicated for children with PWS. GH supports linear growth and increased muscle mass, and may lessen food preoccupation and weight gain.

Because of severe obesity, obstructive sleep apnea is a common sequela, and a positive airway pressure machine is often needed. There may come a time when a person who has been diagnosed with PWS may have to undergo surgical procedures. One surgery that has proven to be unsuccessful for treating the obesity is gastric bypass. Patients with Prader–Willi syndrome have a very high tolerance to pain; therefore they may be experiencing significant abdominal symptoms such as acute gastritis, appendicitis, or cholecystitis and not be aware of it until later.

Behavior and psychiatric problems should be detected early for the best results. These issues are best when treated with parental education and training. Sometimes medication is introduced as well. Serotonin agonists have been most effective in lessening temper tantrums and improving compulsivity.

Currently there are no official tests or treatments for ROHHAD. Each child has the symptoms above at different ages, yet most symptoms are eventually present. Many children are misdiagnosed or are never diagnosed until alveolar hypoventilation occurs.

Reactive strategies include:

- Redirection: distracting the person by offering another activity, or changing the topic of conversation. Offer the person a choice of 2 or 3 things, but no more than 3, because this can be overwhelming. In offering a choice, make sure to pause to allow the person time to process the information and give a response.

- Talking to the person and finding out what the problem is

- Working out what the person's behaviour is trying to communicate

- Crisis management

Positive Behaviour Support (PBS) is a treatment approach that looks at the best way to work with each individual with disabilities. A behavioural therapist conducts a functional analysis of behaviour which helps to determine ways to improve the quality of life for the person and does not just deal with problem behaviour.

PBS also acknowledges the needs of support staff and includes strategies to manage crises when they arise. The following model is a brief guide to staff to remind them of key things to think about when planning support for a person with disabilities. There are two main objectives: reacting situationally when the behaviour occurs, and then acting proactively to prevent the behaviour from occurring.

There is no cure for ONH; however, many therapeutic interventions exist for the care of its symptoms. These may include hormone replacement therapy for hypopituitarism, occupational, physical, and/or speech therapy for other issues, and services of a teacher of students with blindness/visually impairment. Special attention should be paid to early development of oral motor skills and acclimation to textured foods for children with texture aversion, or who are otherwise resistant to eating.

Sleep dysfunction can be ameliorated using melatonin in the evening in order to adjust a child's circadian clock.

Treatment for strabismus may include patching of the better eye, which may result in improved vision in the worse eye; however, this should be reserved for cases in which the potential for vision improvement in both eyes is felt to be good. Surgery to align the eyes can be performed once children with strabismus develop equal visual acuity in both eyes, most often after the age of three. Generally surgery results in improved appearance only and not in improved visual function.

Although 1p36 Deletion Syndrome can be debilitating in many ways, patients do respond to various treatments and therapies. These include the following:

American Sign Language: Because few individuals with Monosomy 1p36 develop complex speech, an alternate form of communication is critical to development. Most patients can learn basic signs to communicate their needs and wants. This also appears to reduce frustration and may reduce self-injurious tendencies. Children with hearing loss will often qualify for locally sponsored sign language classes.

Music Therapy: Music has been shown to aid children with 1p36 deletion in various developmental areas. It serves as an excellent auditory stimulus and can teach listening skills. Songs with actions help the child to develop coordination and motor skills.

Physical Therapy: Due to low muscle tone, patients with 1p36 Deletions take a great deal of time to learn to roll over, sit up, crawl and walk. However, regular physical therapy has shown to shorten the length of time needed to achieve each of those developmental milestones.

Occupational Therapy can be helpful to help children with oral motor and feeding difficulties (including dysphagia and transitioning to solid foods) as well as developmental delays in motor, social and sensory domains.

The variable presentation of ROHHAD includes the following main symptoms:

- Hyperphagia and obesity by age of 10 years - (median age 3 years);

- Respiratory Manifestations:

- Alveolar Hypoventilation (median onset age 6.2 years);

- Cardiorespiratory arrest;

- Reduced Carbon Dioxide Ventilatory Response;

- Obstructive sleep apnea.

- Thermal or other hypothalamic dysregulations, with autonomic dysregulation by median age 3.6 years:

- Failed Growth Hormone Stimulation;

- Adipsic hypernatremia (inability to feel thirst to keep normal hydration);

- Hypernatremia;

- Hyperprolactinemia;

- Hyperphagia;

- Diabetes insipidus;

- Ophthalmologic Manifestations;

- Thermal Dysregulation;

- Gastrointestinal dysmotility;

- Altered Perception of Pain;

- Altered Sweating;

- Cold Hands and Feet.

- Neurobehavioral disorders;

- Tumors of neural crest origin.

Clinically overlapping cases exist because CCHS phenotype can also include autonomic nervous system dysregulation, or tumors of neural crest origin.

Serotonin and norepinephrine reuptake inhibitor, venlafaxine, were given to case study KS four months after initial stroke that started symptoms of witzelsucht. Changes back to his original behavior were noticeable after daily dose of 37.5 mg of venlafaxine for two weeks. In subsequent two months, inappropriate jokes and hypersexual behavior were rarely noticed. Due to the rareness of this disorder, not much research into potential treatments has been conducted.

Klüver–Bucy syndrome is a syndrome resulting from bilateral lesions of the medial temporal lobe (including amygdaloid nucleus). Klüver–Bucy syndrome may present with compulsive eating, hypersexuality, insertion of inappropriate objects in the mouth (hyperorality), visual agnosia, and .

Prader–Willi syndrome is frequently associated with a constant, extreme, ravenous insatiable appetite which persists no matter how much the patient eats, often resulting in morbid obesity. Caregivers need to strictly limit the patients' access to food, usually by installing locks on refrigerators and on all closets and cabinets where food is stored. It is the most common genetic cause of morbid obesity in children. There is currently no consensus as to the cause for this symptom, although genetic abnormalities in chromosome 15 disrupt the normal functioning of the hypothalamus. Given that the hypothalamus arcuate nucleus regulates many basic processes, including appetite, there may well be a link. In the hypothalamus of people with PWS, nerve cells that produce oxytocin, a hormone thought to contribute to satiety, have been found to be abnormal.

People with Prader–Willi syndrome have high ghrelin levels, which are thought to directly contribute to the increased appetite, hyperphagia, and obesity seen in this syndrome. Cassidy states the need for a clear delineation of behavioral expectations, the reinforcement of behavioural limits and the establishment of regular routines.

The main mental health difficulties experienced by people with PWS include compulsive behaviour (usually manifested in skin picking) and anxiety. Psychiatric symptoms, for example, hallucinations, paranoia and depression, have been described in some cases and affect approximately 5–10% of young adults. Patients are also often extremely stubborn and prone to anger. Psychiatric and behavioural problems are the most common cause of hospitalization.

It is typical for to 70–90% of affected individuals to develop behavioral patterns in early childhood. Aspects of these patterns can include stubbornness, temper tantrums, controlling and manipulative behavior, difficulty with change in routine, and compulsive-like behaviors.

The list of symptoms differs somewhat by source. Generally included are the following:

1. Amnesia. Characterised by an inability to recall memories. Its nature is both anterograde and retrograde, meaning new memories cannot be formed and old memories cannot be recalled. The level of amnesia is considered to be profound.

2. Docility. Characterized by exhibiting diminished fear responses or reacting with unusually low aggression. This has also been termed "" or "tameness".

3. Dietary changes and hyperphagia. Characterized by eating inappropriate objects (pica), or overeating, or both.

4. Hyperorality. This was described by Ozawa et al. as "an oral tendency, or compulsion to examine objects by mouth".

5. Hypersexuality. Characterized by a heightened sex drive or a tendency to seek sexual stimulation from unusual or inappropriate objects.

6. Visual agnosia. Characterized by an inability to recognize familiar objects or people.

While this cluster of syndromes is common to such sources as 1997's "The Neuropsychiatry of Limbic and Subcortical Disorders", 2005's "Functional Neuroanatomy: Text and Atlas" and 1997's "Single-Photon Emission CT and MR Findings in Klüver-Bucy after Reye syndrome", an article in the "American Journal of Neuroradiology", the three vary thereafter.

Inconsistent criteria include:

- Hypermetamorphosis, characterized by Ozawa et al. as "an irresistible impulse to notice and react to everything within sight". This is included under the classification systems described by "The Neuropsychiatry of Limbic and Subcortical Disorders" and "Single-Photon Emission CT and MR Findings in Klüver-Bucy".

- Lack of emotional response, diminished emotional affect. This is a symptom under "The Neuropsychiatry of Limbic and Subcortical Disorders" and is included under "Single-Photon Emission CT and MR Findings in Klüver-Bucy" along with apathy under docility.

Witzelsucht (from the German "witzeln", meaning to joke or wisecrack, and "sucht", meaning addiction or yearning) is a set of rare neurological symptoms characterized by a tendency to make puns, or tell inappropriate jokes or pointless stories in socially inappropriate situations. A less common symptom is hypersexuality, the tendency to make sexual comments at inappropriate times or situations. Patients do not understand that their behavior is abnormal, therefore are nonresponsive to others' reactions. This disorder is most commonly seen in patients with frontal lobe damage, particularly right frontal lobe tumors or trauma. The disorder remains named in accordance with its reviewed definition by German neurologist Hermann Oppenheim; its first description as the less focused "Moria" ("stupidity"), by German neurologist Moritz Jastrowitz, was in 1888.

Due to similarity of symptoms of the disorder to the mannerisms of Batman's arch-rival Joker, it is sometimes known as 'The Joker Syndrome'

The visual prognosis in optic nerve hypoplasia is quite variable. Occasionally, optic nerve hypoplasia may be compatible with near-normal vision; in other cases, one or both eyes may be functionally, or legally blind. Although most patients with only optic nerve involvement lead normally productive lives, those with accompanying endocrine dysfunction or other midline cerebral abnormalities are more at risk for on-going intellectual and other disabilities.