Neurodevelopmental disorders are in their multitude associated with widely varying degrees of difficulty, depending on which there are different degrees of mental, emotional, physical, and economic consequences for individuals, and in turn families, groups and society.

There is some evidence that children with AS may see a lessening of symptoms; up to 20% of children may no longer meet the diagnostic criteria as adults, although social and communication difficulties may persist. As of 2006, no studies addressing the long-term outcome of individuals with Asperger syndrome are available and there are no systematic long-term follow-up studies of children with AS. Individuals with AS appear to have normal life expectancy, but have an increased prevalence of comorbid psychiatric conditions, such as major depressive disorder and anxiety disorder that may significantly affect prognosis. Although social impairment may be lifelong, the outcome is generally more positive than with individuals with lower functioning autism spectrum disorders; for example, ASD symptoms are more likely to diminish with time in children with AS or HFA. Most students with AS/HFA have average mathematical ability and test slightly worse in mathematics than in general intelligence, but some are gifted in mathematics. AS has potentially been linked to some accomplishments, such as Vernon L. Smith winning the Nobel Memorial Prize in Economic Sciences; however, Smith is self-diagnosed.

Although many attend regular education classes, some children with AS may utilize special education services because of their social and behavioral difficulties. Adolescents with AS may exhibit ongoing difficulty with self care or organization, and disturbances in social and romantic relationships. Despite high cognitive potential, most young adults with AS remain at home, yet some do marry and work independently. The "different-ness" adolescents experience can be traumatic. Anxiety may stem from preoccupation over possible violations of routines and rituals, from being placed in a situation without a clear schedule or expectations, or from concern with failing in social encounters; the resulting stress may manifest as inattention, withdrawal, reliance on obsessions, hyperactivity, or aggressive or oppositional behavior. Depression is often the result of chronic frustration from repeated failure to engage others socially, and mood disorders requiring treatment may develop. Clinical experience suggests the rate of suicide may be higher among those with AS, but this has not been confirmed by systematic empirical studies.

Education of families is critical in developing strategies for understanding strengths and weaknesses; helping the family to cope improves outcomes in children. Prognosis may be improved by diagnosis at a younger age that allows for early interventions, while interventions in adulthood are valuable but less beneficial. There are legal implications for individuals with AS as they run the risk of exploitation by others and may be unable to comprehend the societal implications of their actions.

Immune reactions during pregnancy, both maternal and of the developing child, may produce neurodevelopmental disorders. One typical immune reaction in infants and children is PANDAS, or "Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infection". Another disorder is Sydenham's chorea, which results in more abnormal movements of the body and fewer psychological sequellae. Both are immune reactions against brain tissue that follow infection by "Streptococcus" bacteria. Susceptibility to these immune diseases may be genetically determined, so sometimes several family members may suffer from one or both of them following an epidemic of Strep infection.

Although not necessary for the diagnosis, individuals with intellectual disability are at higher risk for SMD. It is more common in boys, and can occur at any age.

Intellectual disability in children can be caused by genetic or environmental factors. The individual could have a natural brain malformation or pre or postnatal damage done to the brain caused by drowning or a traumatic brain injury, for example. Nearly 30 to 50% of individuals with intellectual disability will never know the cause of their diagnosis even after thorough investigation.

Prenatal causes of intellectual disability include:

- Congenital infections such as cytomegalovirus, toxoplasmosis, herpes, syphilis, rubella and human immunodeficiency virus

- Prolonged maternal fever in the first trimester

- Exposure to anticonvulsants or alcohol

- Untreated maternal phenylketonuria (PKU)

- Complications of prematurity, especially in extremely low-birth-weight infants

- Postnatal exposure to lead

Single-gene disorders that result in intellectual disability include:

- Fragile X syndrome

- Neurofibromatosis

- Tuberous sclerosis

- Noonan's syndrome

- Cornelia de Lange's syndrome

These single-gene disorders are usually associated with atypical physical characteristics.

About 1/4 of individuals with intellectual disability have a detectable chromosomal abnormality. Others may have small amounts of deletion or duplication of chromosomes, which may go unnoticed and therefore, undetermined.

Frequency estimates vary enormously. In 2015 it was estimated that 37.2 million people globally are affected. A 2003 review of epidemiological studies of children found autism rates ranging from 0.03 to 4.84 per 1,000, with the ratio of autism to Asperger syndrome ranging from 1.5:1 to 16:1; combining the geometric mean ratio of 5:1 with a conservative prevalence estimate for autism of 1.3 per 1,000 suggests indirectly that the prevalence of AS might be around 0.26 per 1,000. Part of the variance in estimates arises from differences in diagnostic criteria. For example, a relatively small 2007 study of 5,484 eight-year-old children in Finland found 2.9 children per 1,000 met the ICD-10 criteria for an AS diagnosis, 2.7 per 1,000 for Gillberg and Gillberg criteria, 2.5 for DSM-IV, 1.6 for Szatmari "et al.", and 4.3 per 1,000 for the union of the four criteria. Boys seem to be more likely to have AS than girls; estimates of the sex ratio range from 1.6:1 to 4:1, using the Gillberg and Gillberg criteria. Females with autism spectrum disorders may be underdiagnosed.

Anxiety disorder and major depressive disorder are the most common conditions seen at the same time; comorbidity of these in persons with AS is estimated at 65%. Reports have associated AS with medical conditions such as aminoaciduria and ligamentous laxity, but these have been case reports or small studies and no factors have been associated with AS across studies. One study of males with AS found an increased rate of epilepsy and a high rate (51%) of nonverbal learning disorder. AS is associated with tics, Tourette syndrome, and bipolar disorder, and the repetitive behaviors of AS have many similarities with the symptoms of obsessive–compulsive disorder and obsessive–compulsive personality disorder. However many of these studies are based on clinical samples or lack standardized measures; nonetheless, comorbid conditions are relatively common.

There are a number of factors that could potentially contribute to the development of feeding and eating disorders of infancy or early childhood. These factors include:

- Physiological – a chemical imbalance effecting the child's appetite could cause a feeding or eating disorder.

- Developmental – developmental abnormalities in oral-sensory, oral-motor, and swallowing can impact the child's eating ability and elicit a feeding or eating disorder.

- Environmental – simple issues such as inconsistent meal times can cause a feeding or eating disorder. Giving the child food that they are not developmentally acquired for can also cause these disorders. Family dysfunction and sociocultural issues could also play a role in feeding or eating disorders.

- Relational – when the child is not securely attached to the mother, it can cause feeding interactions to become disturbed or unnatural. Other factors, such as parental emotional unavailability and parental eating disorders, can cause feeding and eating disorders in their children.

- Psychological and behavioral – these factors include one involving the child's temperament. Characteristics such as being anxious, impulsive, distracted, or strong-willed personality types are ones that could affect the child's eating and cause a disorder. The individual could have learned to reject food due to a traumatic experience such as choking or being force fed.

Developmental coordination disorder is a lifelong neurological condition that is more common in males than in females, with a ratio of approximately four males to every female. The exact proportion of people with the disorder is unknown since the disorder can be difficult to detect due to a lack of specific laboratory tests, thus making diagnosis of the condition one of elimination of all other possible causes/diseases. Approximately 5–6% of children are affected by this condition.

A pervasive developmental disorder not otherwise specified (PDD-NOS) is one of the four autism spectrum disorders (ASD) and also one of the five disorders classified as a pervasive developmental disorder (PDD). According to the DSM-IV, PDD-NOS is a diagnosis that is used for "severe and pervasive impairment in the development of reciprocal social interaction or verbal and nonverbal communication skills, or when stereotyped behavior, interests, and activities are present, but the criteria are not met for a specific PDD" or for several other disorders. PDD-NOS is often called atypical autism, because the criteria for autistic disorder are not met, for instance because of late age of onset, atypical symptomatology, or subthreshold symptomatology, or all of these. Even though PDD-NOS is considered milder than typical autism, this is not always true. While some characteristics may be milder, others may be more severe.

It is common for individuals with PDD-NOS to have more intact social skills and a lower level of intellectual deficit than individuals with other PDDs. Characteristics of many individuals with PDD-NOS are:

- Communication difficulties (e.g., using and understanding language)

- Difficulty with social behavior

- Difficulty with changes in routines or environments

- Uneven skill development (strengths in some areas and delays in others)

- Unusual play with toys and other objects

- Repetitive body movements or behavior patterns

- Preoccupation with fantasy, such as imaginary friends in childhood

Intellectual disability affects about 2–3% of the general population. 75–90% of the affected people have mild intellectual disability. Non-syndromic or idiopathic ID accounts for 30–50% of cases. About a quarter of cases are caused by a genetic disorder. Cases of unknown cause affect about 95 million people as of 2013.

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.

Prognosis depends on the severity of the disorder. Recognizing symptoms early can help reduce the risk of self-injury, which can be lessened with meditations. Stereotypic movement disorder due to head trauma may be permanent.

This is an ill-defined disorder of uncertain nosological validity. The category is included here because of the evidence that children with moderate to severe intellectual disability (IQ below 35) who exhibit major problems in hyperactivity and inattention frequently show stereotyped behaviours; such children tend not to benefit from stimulant drugs (unlike those with an IQ in the normal range) and may exhibit a severe dysphoric reaction (sometimes with psychomotor retardation) when given stimulants; in adolescence the overactivity tends to be replaced by underactivity (a pattern that is not usual in hyperkinetic children with normal intelligence). It is also common for the syndrome to be associated with a variety of developmental delays, either specific or global. The extent to which the behavioural pattern is a function of low IQ or of organic brain damage is not known, neither is it clear whether the disorders in children with mild intellectual disability who show the hyperkinetic syndrome would be better classified here or under F90.- (Hyperkinetic disorders); at present they are included in F90-.

Diagnostic guidelines

Diagnosis depends on the combination of developmentally inappropriate severe overactivity, motor stereotypies, and moderate to severe intellectual disability; all three must be present for the diagnosis. If the diagnostic criteria for F84.0 (childhood autism), F84.1 (atypical autism) or F84.2 (Rett's syndrome) are met, that condition should be diagnosed instead.

Tourette syndrome is a spectrum disorder—its severity ranges over a spectrum from mild to severe. The majority of cases are mild and require no treatment. In these cases, the impact of symptoms on the individual may be mild, to the extent that casual observers might not know of their condition. The overall prognosis is positive, but a minority of children with Tourette syndrome have severe symptoms that persist into adulthood. A study of 46 subjects at 19 years of age found that the symptoms of 80% had minimum to mild impact on their overall functioning, and that the other 20% experienced at least a moderate impact on their overall functioning. The rare minority of severe cases can inhibit or prevent individuals from holding a job or having a fulfilling social life. In a follow-up study of thirty-one adults with Tourette's, all patients completed high school, 52% finished at least two years of college, and 71% were full-time employed or were pursuing higher education.

Regardless of symptom severity, individuals with Tourette's have a normal life span. Although the symptoms may be lifelong and chronic for some, the condition is not degenerative or life-threatening. Intelligence is normal in those with Tourette's, although there may be learning disabilities. Severity of tics early in life does not predict tic severity in later life, and prognosis is generally favorable, although there is no reliable means of predicting the outcome for a particular individual. The gene or genes associated with Tourette's have not been identified, and there is no potential "cure". A higher rate of migraines than the general population and sleep disturbances are reported.

Several studies have demonstrated that the condition in most children improves with maturity. Tics may be at their highest severity at the time that they are diagnosed, and often improve with understanding of the condition by individuals and their families and friends. The statistical age of highest tic severity is typically between eight and twelve, with most individuals experiencing steadily declining tic severity as they pass through adolescence. One study showed no correlation with tic severity and the onset of puberty, in contrast with the popular belief that tics increase at puberty. In many cases, a complete remission of tic symptoms occurs after adolescence. However, a study using videotape to record tics in adults found that, although tics diminished in comparison with childhood, and all measures of tic severity improved by adulthood, 90% of adults still had tics. Half of the adults who considered themselves tic-free still displayed evidence of tics.

Many people with TS may not realize they have tics; because tics are more commonly expressed in private, TS may go unrecognized or undetected. It is not uncommon for the parents of affected children to be unaware that they, too, may have had tics as children. Because Tourette's tends to subside with maturity, and because milder cases of Tourette's are now more likely to be recognized, the first realization that a parent had tics as a child may not come until their offspring is diagnosed. It is not uncommon for several members of a family to be diagnosed together, as parents bringing children to a physician for an evaluation of tics become aware that they, too, had tics as a child.

Children with Tourette's may suffer socially if their tics are viewed as "bizarre". If a child has disabling tics, or tics that interfere with social or academic functioning, supportive psychotherapy or school accommodations can be helpful. Because comorbid conditions (such as ADHD or OCD) can cause greater impact on overall functioning than tics, a thorough evaluation for comorbidity is called for when symptoms and impairment warrant.

A supportive environment and family generally gives those with Tourette's the skills to manage the disorder. People with Tourette's may learn to camouflage socially inappropriate tics or to channel the energy of their tics into a functional endeavor. Accomplished musicians, athletes, public speakers, and professionals from all walks of life are found among people with Tourette's. Outcomes in adulthood are associated more with the perceived significance of having severe tics as a child than with the actual severity of the tics. A person who was misunderstood, punished, or teased at home or at school will fare worse than children who enjoyed an understanding and supportive environment.

Education, and a "watch and wait" strategy, are the only treatment needed for many, and the majority of individuals with tics do not seek treatment; treatment of tic disorders is similar to treatment of Tourette syndrome.

Tourette syndrome is found among all social, racial and ethnic groups and has been reported in all parts of the world; it is three to four times more frequent among males than among females. The tics of Tourette syndrome begin in childhood and tend to remit or subside with maturity; thus, a diagnosis may no longer be warranted for many adults, and observed prevalence rates are higher among children than adults. As children pass through adolescence, about one-quarter become tic-free, almost one-half see their tics diminish to a minimal or mild level, and less than one-quarter have persistent tics. Only 5 to 14% of adults experience worse tics in adulthood than in childhood.

Up to 1% of the overall population experiences tic disorders, including chronic tics and transient tics of childhood. Chronic tics affect 5% of children, and transient tics affect up to 20%. Prevalence rates in special education populations are higher.

The reported prevalence of TS varies "according to the source, age, and sex of the sample; the ascertainment procedures; and diagnostic system", with a range reported between .4% and 3.8% for children ages 5 to 18. Robertson (2011) says that 1% of school-age children have Tourette's. According to Lombroso and Scahill (2008), the emerging consensus is that .1 to 1% of children have Tourette's, with several studies supporting a tighter range of .6 to .8%. Bloch and Leckman (2009) and Swain (2007) report a range of prevalence in children of .4 to .6%, Knight et al. (2012) estimate .77% in children, and Du et al. (2010) report that 1 to 3% of "Western" school-age children have Tourette's.

Singer (2011) states the prevalence of TS in the overall population at any time is .1% for impairing cases and .6% for all cases, while Bloch and colleagues (2011) state the overall prevalence as between .3 and 1%. Robertson (2011) also suggests that the rate of Tourette's in the general population is 1%. Using year 2000 census data, a prevalence range of .1 to 1% yields an estimate of 53,000–530,000 school-age children with Tourette's in the US, and a prevalence estimate of .1% means that in 2001 about 553,000 people in the UK age 5 or older would have Tourette's.

Tourette syndrome was once thought to be rare: in 1972, the US National Institutes of Health (NIH) believed there were fewer than 100 cases in the United States, and a 1973 registry reported only 485 cases worldwide. However, multiple studies published since 2000 have consistently demonstrated that the prevalence is much higher than previously thought. Discrepancies across current and prior prevalence estimates come from several factors: ascertainment bias in earlier samples drawn from clinically referred cases, assessment methods that may fail to detect milder cases, and differences in diagnostic criteria and thresholds. There were few broad-based community studies published before 2000 and until the 1980s, most epidemiological studies of Tourette syndrome were based on individuals referred to tertiary care or specialty clinics. Individuals with mild symptoms may not seek treatment and physicians may not confer an official diagnosis of TS on children out of concern for stigmatization; children with milder symptoms are unlikely to be referred to specialty clinics, so prevalence studies have an inherent bias towards more severe cases. Studies of Tourette syndrome are vulnerable to error because tics vary in intensity and expression, are often intermittent, and are not always recognized by clinicians, patients, family members, friends or teachers; approximately 20% of persons with Tourette syndrome do not recognize that they have tics. Newer studies—recognizing that tics may often be undiagnosed and hard to detect—use direct classroom observation and multiple informants (parent, teacher, and trained observers), and therefore record more cases than older studies relying on referrals. As the diagnostic threshold and assessment methodology have moved towards recognition of milder cases, the result is an increase in estimated prevalence.

Tourette's is associated with several comorbid conditions, or co-occurring diagnoses, which are often the major source of impairment for an affected child. Most individuals with tics do not seek medical attention, so epidemiological studies of TS "reflect a strong ascertainment bias", but among those who do warrant medical attention, the majority have other conditions, and up to 50% have ADHD or OCD.

Overactive disorder associated with mental retardation and stereotyped movements is a pervasive developmental disorder (PDD) listed in Chapter V(F) of the tenth revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-10); its diagnostic code is F84.4.

Developmental coordination disorder is classified (by doctors) in the fifth revision of the "Diagnostic and Statistical Manual of Mental Disorders" (DSM-5) as a motor disorder, in the category of neurodevelopmental disorders.

Tic disorders are more common among males than females.

A large, community-based study suggested that over 19% of school-age children have tic disorders; the children with tic disorders in that study were usually undiagnosed.

As many as 1 in 100 people may experience some form of tic disorder, usually before the onset of puberty. Tourette syndrome is the more severe expression of a spectrum of tic disorders, which are thought to be due to the same genetic vulnerability. Nevertheless, most cases of Tourette syndrome are not severe. Although a significant amount of investigative work indicates genetic linkage of the various tic disorders, further study is needed to confirm the relationship.

The term "multisystem developmental disorder" has also been used to describe various developmental disorders. These include:

- Alagille syndrome, an autosomal dominant disorder with a wide range of features and manifestations. Its five most significant features are chronic cholestasis, a condition where bile cannot flow from the liver to the duodenum, occurring in 95% of cases; heart abnormalities (over 90%); butterfly vertebrae; posterior embryotoxon and a distinctive face (prominent forehead, deep-set eyes, and a pointed chin).

- Rubinstein-Taybi syndrome, a mental retardation syndrome characterized by broad thumbs, facial abnormalities, and big toes alongside mental retardation.

- Williams syndrome, a neurodevelopmental disorder characterized by a unique profile of strengths and deficits; most with the condition have mild mental retardation but have grammatical and lexical abilities above what would be expected from their IQs. They are hypersocial and empathetic, but social isolation is commonly experienced.

- Proteus syndrome, a congenital disorder causing disproportionate growth of skin, bone, and other tissues.

- Asphyxiating thoracic dysplasia, a autosomal recessive skeletal disorder with an estimated prevalence of between 1 in 100,000 and 1 in 130,000 live births.

Multisystem developmental disorder (MSDD) is a term used by Stanley Greenspan to describe children under age 3 who exhibit signs of impaired communication as in autism, but with strong emotional attachments atypical of autism. It is described in the DC:0-3R manual as an optional diagnosis for children under two years of age.

Examples of psychomotor retardation include the following:

- Unaccountable difficulty in carrying out what are usually considered "automatic" or "mundane" self-care tasks for healthy people (i.e., without depressive illness) such as taking a shower, dressing, self-grooming, cooking, brushing one's teeth and exercising.

- Physical difficulty performing activities which normally would require little thought or effort such as walking up a flight of stairs, getting out of bed, preparing meals and clearing dishes from the table, household chores or returning phone calls.

- Tasks requiring mobility suddenly (or gradually) and inexplicably seem to be "impossible". Activities such as shopping, getting groceries, caring for the daily needs of one's children and meeting the demands of employment or school are commonly affected. Individuals experiencing these symptoms typically sense that something is wrong, and may be confused about their inability to perform these tasks.

- Activities usually requiring little mental effort can become challenging. Balancing one's checkbook, making a shopping list or making decisions about mundane tasks (such as deciding what errands need to be done) are often difficult.

In schizophrenia, activity level may vary from psychomotor retardation to agitation; the patient will experience periods of listlessness and may be unresponsive, and at the next moment be active and energetic.

Psychomotor retardation (also known as "psychomotor impairment" or "motormental retardation") involves a slowing-down of thought and a reduction of physical movements in an individual. Psychomotor retardation can cause a visible slowing of physical and emotional reactions, including speech and affect. This is most-commonly seen in people with major depression and in the depressed phase of bipolar disorder; it is also associated with the adverse effects of certain drugs, such as benzodiazepines. Particularly in an inpatient setting, psychomotor retardation may require increased nursing care to ensure adequate food and fluid intake and sufficient personal care. Informed consent for treatment is more difficult to achieve in the presence of this condition.

Tardive dyskinesia most commonly occurs in patients with psychiatric conditions who are treated with antipsychotic medications for many years. The average prevalence rate has been estimated to be around 30% for individuals taking antipsychotic medication, such as that used to treat schizophrenia. A study being conducted at the Yale University School of Medicine has estimated that "32% of patients develop persistent tics after 5 years on major tranquilizers, 57% by 15 years, and 68% by 25 years." More drastic data was found during a longitudinal study conducted on individuals 45 years of age and older who were taking antipsychotic drugs. According to this research study, 26% of patients developed tardive dyskinesia after just one year on the medication. Another 60% of this at-risk group developed the disorder after 3 years, and 23% developed "severe" cases of tardive dyskinesia within 3 years. According to these estimates, the majority of patients will eventually develop the disorder if they remain on the drugs long enough.

Elderly patients are more prone to develop tardive dyskinesia, and elderly women are more at-risk than elderly men. The risk is much lower for younger men and women, and also more equal across the sexes. Patients who have undergone electro-convulsive therapy or have a history of diabetes or alcohol abuse also have a higher risk of developing tardive dyskinesia.

Several studies have recently been conducted comparing the prevalence rate of tardive dyskinesia with second generation, or more modern, antipsychotic drugs to that of first generation drugs. The newer antipsychotics appear to have a substantially reduced potential for causing tardive dyskinesia. However, some studies express concern that the prevalence rate has decreased far less than expected, cautioning against the overestimation of the safety of modern antipsychotics.

A physician can evaluate and diagnose a patient with tardive dyskinesia by conducting a systematic examination. The physician should ask the patient to relax, and look for symptoms like facial grimacing, eye or lip movements, tics, respiratory irregularities, and tongue movements. In some cases, patients experience nutritional problems, so a physician can also look for a gain or loss in weight.

Apart from the underlying psychiatric disorder, tardive dyskinesia may cause afflicted people to become socially isolated. It also increases the risk of dysmorphophobia and can even lead to suicide. Emotional or physical stress can increase the severity of dyskinetic movements, whereas relaxation and sedation have the opposite effect.