The term feeble-minded was used from the late nineteenth century in Europe, the United States and Australasia for disorders later referred to as illnesses or deficiencies of the mind.

At the time, "mental deficiency" encompassed all degrees of educational and social deficiency. Within the concept of mental deficiency, researchers established a hierarchy, ranging from idiocy, at the most severe end of the scale; to imbecility, at the median point; and to feeble-mindedness at the highest end of functioning. The latter was conceived of as a form of high-grade mental deficiency.

The development of the ranking system of mental deficiency has been attributed to Sir Charles Trevelyan in 1876, and was associated with the rise of eugenics. The term and hierarchy had been used in that sense at least ten years previously. "Wild card" terms outside the established hierarchy such as "idiot savant", may have been used as connotations for varying degrees of autism.

Moron is a term once used in psychology and psychiatry to denote mild intellectual disability. The term was closely tied with the American eugenics movement. Once the term became popularized, it fell out of use by the psychological community, as it was used more commonly as an insult than as a psychological term. It is similar to imbecile and idiot.

The term imbecile was once used by psychiatrists to denote a category of people with moderate to moderate intellectual disability, as well as a type of criminal. The word arises from the Latin word "imbecillus", meaning weak, or weak-minded. It included people with an IQ of 26–50, between "idiot" (IQ of 0–25) and "moron" (IQ of 51–70). In the obsolete medical classification (ICD-9, 1977), these people were said to have "moderate mental retardation" or "moderate mental subnormality" with IQ of 35–49.

The meaning was further refined into mental and moral imbecility. The concepts of "moral insanity", "moral idiocy"," and "moral imbecility", led to the emerging field of eugenic criminology, which held that crime can be reduced by preventing "feeble-minded" people from reproducing.

"Imbecile" as a concrete classification was popularized by psychologist Henry H. Goddard and was used in 1927 by United States Supreme Court Justice Oliver Wendell Holmes Jr. in his ruling in the forced-sterilization case "Buck v. Bell", 274 U.S. 200 (1927).

The concept is closely associated with psychology, psychiatry, criminology, and eugenics. However, the term "imbecile" quickly passed into vernacular usage as a derogatory term, and fell out of professional use in the 20th century in favor of "mental retardation".

In recent decades, the phrases "mental retardation", "mentally retarded", and "retarded" initially used in a medical manner, are regarded as derogatory and politically incorrect much like "moron", "imbecile", "cretin", "dolt" and "idiot", formerly used as scientific terms in the early 20th century. On October 5, 2010, President of the United States Barack Obama signed Senate Bill 2781, known as "Rosa's Law", which changed references in many Federal statutes that referred to "mental retardation" to refer instead to "intellectual disability".

"Moron" was coined in 1910 by psychologist Henry H. Goddard from the Ancient Greek word "" ("moros"), which meant "dull" and used to describe a person with a mental age in adulthood of between 8 and 12 on the Binet scale. It was once applied to people with an IQ of 51–70, being superior in one degree to "imbecile" (IQ of 26–50) and superior in two degrees to "idiot" (IQ of 0–25). The word "moron", along with others including, "idiotic", "imbecilic", "stupid", and "feeble-minded", was formerly considered a valid descriptor in the psychological community, but it is now deprecated in use by psychologists.

In the obsolete medical classification (ICD-9, 1977), these people (morons and feeble-minded) were said to have "mild mental retardation", "mild mental subnormality" or "high-grade defect" with IQ 50–70.

Following opposition to Goddard's attempts to popularize his ideas, Goddard recanted his earlier assertions about the moron: "It may still be objected that moron parents are likely to have imbecile or idiot children. There is not much evidence that this is the case. The danger is probably negligible."

The earliest recorded use of the term in the English language dates from 1534, when it appears in one of the first English translations of the New Testament. A biblical injunction to "Comforte the feble mynded" is included in 1 Thessalonians 5:14.

A London "Times" editorial of November 1834 describes the long-serving former Prime Minister Lord Liverpool as a "feeble-minded pedant of office".

By most definitions, intellectual disability is more accurately considered a "disability" rather than a "disease". Intellectual disability can be distinguished in many ways from mental illness, such as schizophrenia or depression. Currently, there is no "cure" for an established disability, though with appropriate support and teaching, most individuals can learn to do many things.

There are thousands of agencies around the world that provide assistance for people with developmental disabilities. They include state-run, for-profit, and non-profit, privately run agencies. Within one agency there could be departments that include fully staffed residential homes, day rehabilitation programs that approximate schools, workshops wherein people with disabilities can obtain jobs, programs that assist people with developmental disabilities in obtaining jobs in the community, programs that provide support for people with developmental disabilities who have their own apartments, programs that assist them with raising their children, and many more. There are also many agencies and programs for parents of children with developmental disabilities.

Beyond that, there are specific programs that people with developmental disabilities can take part in wherein they learn basic life skills. These "goals" may take a much longer amount of time for them to accomplish, but the ultimate goal is independence. This may be anything from independence in tooth brushing to an independent residence. People with developmental disabilities learn throughout their lives and can obtain many new skills even late in life with the help of their families, caregivers, clinicians and the people who coordinate the efforts of all of these people.

There are four broad areas of intervention that allow for active participation from caregivers, community members, clinicians, and of course, the individual(s) with an intellectual disability. These include psychosocial treatments, behavioral treatments, cognitive-behavioral treatments, and family-oriented strategies. Psychosocial treatments are intended primarily for children before and during the preschool years as this is the optimum time for intervention. This early intervention should include encouragement of exploration, mentoring in basic skills, celebration of developmental advances, guided rehearsal and extension of newly acquired skills, protection from harmful displays of disapproval, teasing, or punishment, and exposure to a rich and responsive language environment. A great example of a successful intervention is the Carolina Abecedarian Project that was conducted with over 100 children from low SES families beginning in infancy through pre-school years. Results indicated that by age 2, the children provided the intervention had higher test scores than control group children, and they remained approximately 5 points higher 10 years after the end of the program. By young adulthood, children from the intervention group had better educational attainment, employment opportunities, and fewer behavioral problems than their control-group counterparts.

Core components of behavioral treatments include language and social skills acquisition. Typically, one-to-one training is offered in which a therapist uses a shaping procedure in combination with positive reinforcements to help the child pronounce syllables until words are completed. Sometimes involving pictures and visual aids, therapists aim at improving speech capacity so that short sentences about important daily tasks (e.g. bathroom use, eating, etc.) can be effectively communicated by the child. In a similar fashion, older children benefit from this type of training as they learn to sharpen their social skills such as sharing, taking turns, following instruction, and smiling. At the same time, a movement known as social inclusion attempts to increase valuable interactions between children with an intellectual disability and their non-disabled peers. Cognitive-behavioral treatments, a combination of the previous two treatment types, involves a strategical-metastrategical learning technique that teaches children math, language, and other basic skills pertaining to memory and learning. The first goal of the training is to teach the child to be a strategical thinker through making cognitive connections and plans. Then, the therapist teaches the child to be metastrategical by teaching them to discriminate among different tasks and determine which plan or strategy suits each task. Finally, family-oriented strategies delve into empowering the family with the skill set they need to support and encourage their child or children with an intellectual disability. In general, this includes teaching assertiveness skills or behavior management techniques as well as how to ask for help from neighbors, extended family, or day-care staff. As the child ages, parents are then taught how to approach topics such as housing/residential care, employment, and relationships. The ultimate goal for every intervention or technique is to give the child autonomy and a sense of independence using the acquired skills he/she has.

Although there is no specific medication for intellectual disability, many people with developmental disabilities have further medical complications and may be prescribed several medications. For example, autistic children with developmental delay may be prescribed antipsychotics or mood stabilizers to help with their behavior. Use of psychotropic medications such as benzodiazepines in people with intellectual disability requires monitoring and vigilance as side effects occur commonly and are often misdiagnosed as behavioral and psychiatric problems.

There is no cure for FASD, but treatment is possible. Because CNS damage, symptoms, secondary disabilities, and needs vary widely by individual, there is no one treatment type that works for everyone.

Psychoactive drugs are frequently tried on those with FASD as many FASD symptoms are mistaken for or overlap with other disorders, most notably ADHD.

There is no cure for individuals with DES, but there are therapies to help them cope with their symptoms. DES can affect a number of functions in the brain and vary from person to person. Because of this variance, it is suggested that the most successful therapy would include multiple methods. Researchers suggest that a number of factors in the executive functioning need to be improved, including self-awareness, goal setting, planning, self-initiation, self-monitoring, self-inhibition, flexibility, and strategic behaviour.

One method for individuals to improve in these areas is to help them plan and carry out actions and intentions through a series of goals and sub-goals. To accomplish this, therapists teach patients a three-step model called the General Planning Approach. The first step is Information and Awareness, in which the patients are taught about their own problems and shown how this affects their lives. The patients are then taught to monitor their executive functions and begin to evaluate them. The second stage, Goal Setting and Planning, consists of patients making specific goals, as well as devising a plan to accomplish them. For example, patients may decide they will have lunch with a friend (their goal). They are taught to write down which friend it may be, where they are going for lunch, what time they are going, how they will get there, etc. (sub-goals). They are also taught to make sure the steps go in the correct order. The final stage, named Initiation, Execution, and Regulation, requires patients to implement their goals in their everyday lives. Initiation can be taught through normal routines. The first step can cue the patient to go to the next step in their plan. Execution and regulation are put into action with reminders of how to proceed if something goes wrong in the behavioural script. This treatment method has resulted in improved daily executive functioning, however no improvements were seen on formal executive functioning tests.

Since planning is needed in many activities, different techniques have been used to improve this deficit in patients with DES. Autobiographical memories can be used to help direct future behaviour. You can draw on past experiences to know what to do in the future. For example, when you want to take a bus, you know from past experience that you have to walk to the bus stop, have the exact amount of change, put the change in the slot, and then you can go find a seat. Patients with DES seem to not be able to use this autobiographical memory as well as a normal person. Training for DES patients asks them to think of a specific time when they did an activity previously. They are then instructed to think about how they accomplished this activity. An example includes "how would you plan a holiday". Patients are taught to think of specific times they went on a holiday and then to think how they may have planned these holidays. By drawing on past experiences patients were better able to make good decisions and plans.

Cognitive Analytic Therapy (CAT) has also been used to help those with DES. Because individuals with this syndrome have trouble integrating information into their actions it is often suggested that they have programmed reminders delivered to a cell phone or pager. This helps them remember how they should behave and discontinue inappropriate actions. Another method of reminding is to have patients write a letter to themselves. They can then read the letter whenever they need to. To help patients remember how to behave, they may also create a diagram. The diagram helps organize their thoughts and shows the patient how they can change their behaviour in everyday situations.

The use of auditory stimuli has been examined in the treatment of DES. The presentation of auditory stimuli causes an interruption in current activity, which appears to aid in preventing "goal neglect" by increasing the patients' ability to monitor time and focus on goals. Given such stimuli, subjects no longer performed below their age group average IQ.

Among children, the cause of intellectual disability is unknown for one-third to one-half of cases. About 5% of cases are inherited from a person's parents. Genetic defects that cause intellectual disability but are not inherited can be caused by accidents or mutations in genetic development. Examples of such accidents are development of an extra chromosome 18 (trisomy 18) and Down syndrome, which is the most common genetic cause. Velocariofacial syndrome and fetal alcohol spectrum disorders are the two next most common causes. However, doctors have found many other causes. The most common are:

- Genetic conditions. Sometimes disability is caused by abnormal genes inherited from parents, errors when genes combine, or other reasons. The most prevalent genetic conditions include Down syndrome, Klinefelter syndrome, Fragile X syndrome (common among boys), neurofibromatosis, congenital hypothyroidism, Williams syndrome, phenylketonuria (PKU), and Prader–Willi syndrome. Other genetic conditions include Phelan-McDermid syndrome (22q13del), Mowat–Wilson syndrome, genetic ciliopathy, and Siderius type X-linked intellectual disability () as caused by mutations in the "PHF8" gene (). In the rarest of cases, abnormalities with the X or Y chromosome may also cause disability. 48, XXXX and 49, XXXXX syndrome affect a small number of girls worldwide, while boys may be affected by 49, XXXXY, or 49, XYYYY. 47, XYY is not associated with significantly lowered IQ though affected individuals may have slightly lower IQs than non-affected siblings on average.

- Problems during pregnancy. Intellectual disability can result when the fetus does not develop properly. For example, there may be a problem with the way the fetus' cells divide as it grows. A pregnant person who drinks alcohol (see fetal alcohol spectrum disorder) or gets an infection like rubella during pregnancy may also have a baby with intellectual disability.

- Problems at birth. If a baby has problems during labor and birth, such as not getting enough oxygen, he or she may have developmental disability due to brain damage.

- Exposure to certain types of disease or toxins. Diseases like whooping cough, measles, or meningitis can cause intellectual disability if medical care is delayed or inadequate. Exposure to poisons like lead or mercury may also affect mental ability.

- Iodine deficiency, affecting approximately 2 billion people worldwide, is the leading preventable cause of intellectual disability in areas of the developing world where iodine deficiency is endemic. Iodine deficiency also causes goiter, an enlargement of the thyroid gland. More common than full-fledged cretinism, as intellectual disability caused by severe iodine deficiency is called, is mild impairment of intelligence. Certain areas of the world due to natural deficiency and governmental inaction are severely affected. India is the most outstanding, with 500 million suffering from deficiency, 54 million from goiter, and 2 million from cretinism. Among other nations affected by iodine deficiency, China and Kazakhstan have instituted widespread iodization programs, whereas, as of 2006, Russia had not.

- Malnutrition is a common cause of reduced intelligence in parts of the world affected by famine, such as Ethiopia.

- Absence of the arcuate fasciculus.

Before beginning treatment for mania, careful differential diagnosis must be performed to rule out secondary causes.

The acute treatment of a manic episode of bipolar disorder involves the utilization of either a mood stabilizer (valproate, lithium, or carbamazepine) or an atypical antipsychotic (olanzapine, quetiapine, risperidone, or aripiprazole). Although hypomanic episodes may respond to a mood stabilizer alone, full-blown episodes are treated with an atypical antipsychotic (often in conjunction with a mood stabilizer, as these tend to produce the most rapid improvement).

When the manic behaviours have gone, long-term treatment then focuses on prophylactic treatment to try to stabilize the patient's mood, typically through a combination of pharmacotherapy and psychotherapy. The likelihood of having a relapse is very high for those who have experienced two or more episodes of mania or depression. While medication for bipolar disorder is important to manage symptoms of mania and depression, studies show relying on medications alone is not the most effective method of treatment. Medication is most effective when used in combination with other bipolar disorder treatments, including psychotherapy, self-help coping strategies, and healthy lifestyle choices.

Lithium is the classic mood stabilizer to prevent further manic and depressive episodes. A systematic review found that long term lithium treatment substantially reduces the risk of bipolar manic relapse, by 42%. Anticonvulsants such as valproate, oxcarbazepine and carbamazepine are also used for prophylaxis. More recent drug solutions include lamotrigine, which is another anticonvulsant. Clonazepam (Klonopin) is also used. Sometimes atypical antipsychotics are used in combination with the previous mentioned medications as well, including olanzapine (Zyprexa) which helps treat hallucinations or delusions, Asenapine (Saphris, Sycrest), aripiprazole (Abilify), risperidone, ziprasidone, and clozapine which is often used for people who do not respond to lithium or anticonvulsants.

Verapamil, a calcium-channel blocker, is useful in the treatment of hypomania and in those cases where lithium and mood stabilizers are contraindicated or ineffective. Verapamil is effective for both short-term and long-term treatment.

Antidepressant monotherapy is not recommended for the treatment of depression in patients with bipolar disorders I or II, and no benefit has been demonstrated by combining antidepressants with mood stabilizers in these patients.

Although there is no cure for NM, it is possible, and common for many people live healthy active lives even with moderate to severe cases. Research continues to seek ways to ameliorate debilitating symptoms and lengthen the life-span in quality ways for those affected. Some people have seen mild improvements in secretion handling, energy level, and physical functioning with supplemental L-tyrosine, an amino acid that is available through health centers. Some symptoms may worsen as the patient ages. Muscle loss increases with age naturally, but it is even more significant with nemaline myopathy.

At present, Nemaline myopathy does not have a cure. Nemaline myopathy is a very rare disease that only effects 1 out of 50,000 on average, although recent studies show that this number is even smaller. There are a number of treatments to minimize the symptoms of the disease. The treatments and procedures to help patients with nemaline myopathy vary depending on the severity of the disease. A possible accommodation could be the use of a stabilizer, such as a brace. Other means include moderate stretching and moderate exercise to help target muscles maintain maximum health.

As people with NM grow and develop throughout their lives, it is important for them to see a variety of health professionals regularly, including a neurologist, physical therapist, and others, such as speech therapists and psychologists, to help both the patient and family adjust to everyday life.

Alexithymia is a personality construct characterized by the inability to identify and describe emotions in the self. The core characteristics of alexithymia are marked dysfunction in emotional awareness, social attachment, and interpersonal relating. Furthermore, people with alexithymia have difficulty in distinguishing and appreciating the emotions of others, which is thought to lead to unempathic and ineffective emotional responding. Alexithymia occurs in approximately 10% of the population and can occur with a number of psychiatric conditions.

The term "alexithymia" was coined by psychotherapist Peter Sifneos in 1973. The word comes from Greek α ("a", "no", the negating alpha privative), λέξις ("léxis", "word"), and θυμός ("thymos", "emotions", but understood by Sifneos as having the meaning "mood"), literally meaning "no words for mood".

Some researchers have suggested that DES is mislabelled as a syndrome because it is possible for the symptoms to exist on their own. Also, there is not a distinct pattern of damage that leads to the syndrome. Not all patients with frontal lobe damage have DES and some patients with no damage at all to the frontal lobe exhibit the necessary pattern of symptoms. This has led research to investigate the possibility that executive functioning is broken down into multiple processes that are spread throughout the frontal lobe. Further disagreement comes from the syndrome being based on Baddeley and Hitch's model of working memory and the central executive, which is a hypothetical construct.

The vagueness of some aspects of the syndrome has led researchers to test for it in a non-clinical sample. The results show that some dysexecutive behaviours are part of everyday life, and the symptoms exist to varying degrees in everyone. For example, absent-mindedness and lapses in attention are common everyday occurrences for most people. However, for the majority of the population such inattentiveness is manageable, whereas patients with DES experience it to such a degree that daily tasks become difficult.

Alexithymia is considered to be a personality trait that places affected individuals at risk for other medical and psychiatric disorders while reducing the likelihood that these individuals will respond to conventional treatments for the other conditions. Alexithymia is not classified as a mental disorder in the fourth edition of the "Diagnostic and Statistical Manual of Mental Disorders". It is a dimensional personality trait that varies in severity from person to person. A person's alexithymia score can be measured with questionnaires such as the Toronto Alexithymia Scale (TAS-20), the Bermond-Vorst Alexithymia Questionnaire (BVAQ), the Online Alexithymia Questionnaire (OAQ-G2) or the Observer Alexithymia Scale (OAS). It is distinct from the psychiatric personality disorders, such as antisocial personality disorder or borderline personality disorder, with which it shares some characteristics, and is likewise distinct from the abnormal conditions of sociopathy or psychopathy.

Alexithymia is defined by:

1. difficulty identifying feelings and distinguishing between feelings and the bodily sensations of emotional arousal

2. difficulty describing feelings to other people

3. constricted imaginal processes, as evidenced by a scarcity of fantasies

4. a stimulus-bound, externally oriented cognitive style.

In studies of the general population the degree of alexithymia was found to be influenced by age, but not by gender; the rates of alexithymia in healthy controls have been found at: 8.3%; 4.7%; 8.9%; and 7%. Thus, several studies have reported that the prevalence rate of alexithymia is less than 10%. A less common finding suggests that there may be a higher prevalence of alexithymia amongst males than females, which may be accounted for by difficulties some males have with "describing feelings", but not by difficulties in "identifying feelings" in which males and females show similar abilities.

Psychologist R. Michael Bagby and psychiatrist Graeme J. Taylor have argued that the alexithymia construct is strongly related (negatively) to the concepts of psychological mindedness and emotional intelligence and there is "strong empirical support for alexithymia being a stable personality trait rather than just a consequence of psychological distress". Other opinions differ and can show evidence that it may be state-dependent.

Bagby and Taylor also suggest that there may be two kinds of alexithymia, "primary alexithymia" which is an enduring psychological trait that does not alter over time, and "secondary alexithymia" which is state-dependent and disappears after the evoking stressful situation has changed. These two manifestations of alexithymia are otherwise called "trait" or "state" alexithymia.

Between 0.3% and 10% of people have refractory disease, which means that they have persistent villous atrophy on a gluten-free diet despite the lack of gluten exposure for more than 12 months. Nevertheless, inadvertent exposure to gluten is the main cause of persistent villous atrophy, and must be ruled out before a diagnosis of refractory disease is made. People with poor basic education and understanding of gluten-free diet often believe that they are strictly following the diet, but are making regular errors. Also, a lack of symptoms is not a reliable indicator of intestinal recuperation.

If alternative causes of villous atrophy have been eliminated, steroids or immunosuppressants (such as azathioprine) may be considered in this scenario.

Refractory coeliac disease should not be confused with the persistence of symptoms despite gluten withdrawal caused by transient conditions derived from the intestinal damage, which generally revert or improve several months after starting a gluten-free diet, such as small intestinal bacterial overgrowth, lactose intolerance, fructose, sucrose, and sorbitol malabsorption, exocrine pancreatic insufficiency, and microscopic colitis, among others.

At present, the only effective treatment is a lifelong gluten-free diet. No medication exists that will prevent damage or prevent the body from attacking the gut when gluten is present. Strict adherence to the diet allows the intestines to heal, leading to resolution of all symptoms in most cases and, depending on how soon the diet is begun, can also eliminate the heightened risk of osteoporosis and intestinal cancer and in some cases sterility. The diet can be cumbersome; failure to comply with the diet may cause relapse.

Dietitian input is generally requested to ensure the person is aware which foods contain gluten, which foods are safe, and how to have a balanced diet despite the limitations. In many countries, gluten-free products are available on prescription and may be reimbursed by health insurance plans. Gluten-free products are usually more expensive and harder to find than common gluten-containing foods. Since ready-made products often contain traces of gluten, some coeliacs may find it necessary to cook from scratch.

The term "gluten-free" is generally used to indicate a supposed harmless level of gluten rather than a complete absence. The exact level at which gluten is harmless is uncertain and controversial. A recent systematic review tentatively concluded that consumption of less than 10 mg of gluten per day is unlikely to cause histological abnormalities, although it noted that few reliable studies had been done. Regulation of the label "gluten-free" varies. In the European Union, the European Commission issued regulations in 2009 limiting the use of "gluten-free" labels for food products to those with less than 20 mg/kg of gluten, and "very low gluten" labels for those with less than 100 mg/kg. In the United States, the FDA issued regulations in 2013 limiting the use of "gluten-free" labels for food products to those with less than 20 ppm of gluten. The current international Codex Alimentarius standard allows for 20 ppm of gluten in so-called "gluten-free" foods. Several organisations, such as the Gluten-Free Certification Organization (GFCO), the Celiac Sprue Association (CSA), and the National Foundation for Celiac Awareness (NFCA), also certify products and companies as gluten-free.

Gluten-free diet improves healthcare-related quality of life, and strict adherence to the diet gives more benefit than incomplete adherence. Nevertheless, gluten-free diet doesn't completely normalise the quality of life.

Mania, also known as manic syndrome, is a state of abnormally elevated arousal, affect, and energy level, or "a state of heightened overall activation with enhanced affective expression together with lability of affect." Although mania is often conceived as a "mirror image" to depression, the heightened mood can be either euphoric or irritable; indeed, as the mania intensifies, irritability can be more pronounced and result in violence, or anxiety.

The symptoms of mania include heightened mood (either euphoric or irritable); flight of ideas and pressure of speech; and increased energy, decreased need for sleep, and hyperactivity. They are most plainly evident in fully developed hypomanic states; in full-blown mania, however, they undergo progressively severe exacerbations and become more and more obscured by other signs and symptoms, such as delusions and fragmentation of behavior.

Mania is a syndrome of multiple causes. Although the vast majority of cases occur in the context of bipolar disorder, it is a key component of other psychiatric disorders (as schizoaffective disorder, bipolar type) and may also occur secondary to various general medical conditions, as multiple sclerosis; certain medications, as prednisone; or certain substances of abuse, as cocaine or anabolic steroids. In current DSM-5 nomenclature, hypomanic episodes are separated from the more severe full manic episodes, which, in turn, are characterized as either mild, moderate, or severe, with specifiers with regard to certain symptomatic features (e.g. catatonia, psychosis). Mania, however, may be divided into three stages: hypomania, or stage I; acute mania, or stage II; and delirious mania, or stage III. This "staging" of a manic episode is, in particular, very useful from a descriptive and differential diagnostic point of view.

Mania varies in intensity, from mild mania (hypomania) to delirious mania, marked by such symptoms as disorientation, florid psychosis, incoherence, and catatonia. Standardized tools such as Altman Self-Rating Mania Scale and Young Mania Rating Scale can be used to measure severity of manic episodes. Because mania and hypomania have also long been associated with creativity and artistic talent, it is not always the case that the clearly manic bipolar person needs or wants medical help; such persons often either retain sufficient self-control to function normally or are unaware that they have "gone manic" severely enough to be committed or to commit themselves. Manic persons often can be mistaken for being under the influence of drugs.