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

Causes of increased appetite include:

- Anxiety

- Stress

- Depression

- Certain drugs

- Diabetes mellitus

- Hyperthyroidism

- Hypoglycemia

- Fatigue

- Depression

- Premenstrual syndrome

- Prader–Willi syndrome

- Bulimia

- Graves' disease

- Kleine–Levin syndrome

Exclusive breast-feeding is recommended in all newborn infants for its nutritional and other beneficial effects. Parents changing the diet and lifestyle of their offspring by offering appropriate food portions, increasing physical activity, and keeping sedentary behaviors at a minimum may also decrease the obesity levels in children.

If children were more mobile and less sedentary, the rate of obesity would decrease. Parents should recognize the signs and encourage their children to be more physically active. By walking or riding a bike, instead of using motorised transport or watching television, will reduce sedentary activity.

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.

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."

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.

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.

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.

KLS can be diagnosed when there is confusion, apathy, or derealization in addition to frequent bouts of extreme tiredness and prolonged sleep. The earliest it can be diagnosed is the second episode, this is not common. The condition is generally treated as a diagnosis of exclusion. Because KLS is rare, other conditions with similar symptoms are usually considered first.

MRIs can determine if the symptoms are caused by certain brain disorders, stroke, and multiple sclerosis. Lumbar puncture can determine if encephalitis is the cause. KLS must be differentiated from substance abuse by toxicology tests. The use of Electroencephalography (EEG) can exclude temporal status epilepticus from consideration. EEGs are normal in about 70% of KLS patients, but background slowing may sometimes be detected. In addition, low-frequency high-amplitude waves can be observed during waking hours.

Initially, KLS appears similar to bipolar depression. Patients with frontal-lobe syndromes and Klüver-Bucy syndrome also display similar symptoms, but these conditions can be differentiated by the presence of brain lesions. KLS should also be distinguished from very rare cases of menstruation-caused hypersomnia.

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 "Diagnostic and Statistical Manual of Mental Disorders" (DSM-IV) recognizes two types of bipolar disorders—bipolar I and bipolar II. People with bipolar I disorder suffer from at least one manic or mixed episode, and may experience depressive episodes. On the contrary, as noted above, people with bipolar II disorder experience a milder form of a manic episode, known as a hypomanic episode as well as major depressive episodes. Although bipolar II is thought to be less severe than bipolar I in regards to symptom intensity, it is actually more severe and distressing with respect to episode frequency and overall course. Those with bipolar II often experience more frequent bouts of depressive episodes. Specific criteria defined by the DSM-IV for a bipolar II diagnosis is as follows:

- The presence of a hypomanic or major depressive episode.

- If currently in major depressive episode, history of a hypomanic episode. If currently in a hypomanic episode, history of a major depressive episode. No history of a manic episode.

- Significant stress or impairment in social, occupational, or other important areas of functioning.

Studies have identified major differences between bipolar I and bipolar II in regards to their clinical features, comorbidity rates and family histories. According to Baek et al. (2011), during depressive episodes, bipolar II patients tend to show higher rates of psychomotor agitation, guilt, shame, suicidal ideation, and suicide attempts. Bipolar II patients have shown higher lifetime comorbidity rates of DSM axis I diagnoses such as phobias, anxiety disorders, substance & alcohol abuse, and eating disorders and there is a higher correlation between bipolar II patients and family history of psychiatric illness, including major depression and substance-related disorders. The occurrence rate of psychiatric illness in first degree relatives of bipolar II patients was 26.5%, versus 15.4% in bipolar I patients.

Screening instruments like the Mood Disorders Questionnaire (MDQ) are helpful tools in determining a patient's status on the bipolar spectrum and getting families involved can also improve chances of an accurate diagnosis and acknowledgment of hypomanic episodes. In addition, there are certain features that have been shown to increase the chances that depressed patients are suffering from a bipolar disorder including atypical symptoms of depression like hypersomnia and hyperphagia, a family history of bipolar disorder, medication-induced hypomania, recurrent or psychotic depression, antidepressant refractory depression, and early or postpartum depression.

It is traditionally characterized by hypotonia, short stature, hyperphagia, obesity, behavioral issues (specifically OCD-like behaviors), small hands and feet, hypogonadism, and mild intellectual disability. However, with early diagnosis and early treatment (such as with growth hormone therapy), the prognosis for persons with PWS is beginning to change. Like autism, PWS is a spectrum disorder and symptoms can range from mild to severe and may change throughout the person's lifetime. Various organ systems are affected.

Traditionally, Prader–Willi syndrome was diagnosed by clinical presentation. Currently, the syndrome is diagnosed through genetic testing; testing is recommended for newborns with pronounced hypotonia. Early diagnosis of PWS allows for early intervention as well as the early prescription of growth hormone. Daily recombinant growth hormone (GH) injections are indicated for children with PWS. GH supports linear growth and increased muscle mass, and may lessen food preoccupation and weight gain.

The mainstay of diagnosis is genetic testing, specifically DNA-based methylation testing to detect the absence of the paternally contributed Prader–Willi syndrome/Angelman syndrome (PWS/AS) region on chromosome 15q11-q13. Such testing detects over 97% of cases. Methylation-specific testing is important to confirm the diagnosis of PWS in all individuals, but especially those who are too young to manifest sufficient features to make the diagnosis on clinical grounds or in those individuals who have atypical findings.

Prader–Willi syndrome is often misdiagnosed as other syndromes due to many in the medical community's unfamiliarity with PWS. Sometimes it is misdiagnosed as Down syndrome, simply because of the relative frequency of Down syndrome compared to PWS.

There have been very few studies conducted to examine the possible causes of Bipolar II. Those that have been done have not considered Bipolar I and Bipolar II separately and have had inconclusive results. Researchers have found that patients with either Bipolar I or II may have increased levels of blood calcium concentrations, but the results are inconclusive. The studies that have been conducted did not find a significant difference between those with Bipolar I or Bipolar II. There has been a study looking at genetics of Bipolar II disorder and the results are inconclusive; however, scientists did find that relatives of people with Bipolar II are more likely to develop the same bipolar disorder or major depression rather than developing Bipolar I disorder.

Central hypoventilation syndrome is a heterogeneous group of seemingly overlapping diseases. Paired-like homeobox 2B (PHOX2B) was confirmed in 2009 as the disease-causing gene in patients with congenital central hypoventilation syndrome (CCHS), a condition present in newborns. This genetic mutation is not present though in those with late-onset central hypoventilation syndrome and hypothalamic dysfunction.

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.

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

Proactive strategies to prevent problems can include:

- Change the environment: This can include increasing opportunities for access to a variety of activities, balancing cognitively and physically demanding activities with periods of rest, providing a predictable environment in order to reduce the level of cognitive demands on the person, trying to provide consistent routines (be mindful of events that may not occur, try not to make promises that cannot be kept, if unable to go out at a particular time then say so), checking for safety in the home environment (e.g. changing/moving furniture).

- Teach a skill: These can include general skills development of useful communication strategies, coping skills (e.g. teach the person what to do when feeling angry, anxious)

- Individual behaviour support plans: These involve reinforcing specific desirable behaviour and ignoring the specific undesirable behaviour (unless it is dangerous, the priority is to keep both people safe through a crisis plan which might involve removing sharp objects or weapons, escaping to a safe place, giving the person time to calm down), avoiding things you know upsets the person, strategies to increase engagement in activities.

Broadly speaking, when the behaviour occurs, assertively in a nonjudgemental, clear, unambiguous way provide feedback that the behaviour is inappropriate, and say what you prefer instead. For example, "Jane, you're standing too close when you are speaking to me, I feel uncomfortable, please take a step back", or "I don't like it when you say I look hot in front of your wife, I feel uncomfortable, I am your Attendant Carer/Support Worker, I am here to help you with your shopping". Then re-direct to the next activity. Any subsequent behaviour ignore. Then generally, as almost all behaviour is communication, understand what the behaviour is trying to communicate and look at ways to have the need met in more appropriate ways.

ONH is diagnosed by ophthalmoscopic examination. Patients with ONH exhibit an optic nerve that appears smaller than normal and different in appearance from small optic nerves caused by other eye conditions such as optic (nerve) atrophy.

DM:DD ratio has proven to be a clinically useful measurement to help diagnose optic nerve hypoplasia. Where "DM" represents the distance from Disk to Macula, and "DD" represents Disc Diameter.

The mean disc diameter (DD) is (Vertical diameter of Disc+Horizontal diameter of Disc)divided by 2. The distance between the center of the disc and the macula is DM.

"Interpretation:" When the ratio of DM to DD is greater than 3, ONH is suspected, and when it is greater than 4, Optic Nerve Hypoplasia is definite.

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 .

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 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.

The following should be taken into account when pronouncing a diagnosis for this condition:

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.

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'