Echolalia (also known as echologia or echophrasia) is defined as the unsolicited repetition of vocalizations made by another person (by the same person is called palilalia). In its profound form it is automatic and effortless. It is one of the echophenomena, closely related to echopraxia, the automatic repetition of movements made by another person; both are "subsets of imitative behavior" whereby sounds or actions are imitated "without explicit awareness". Echolalia may be an immediate reaction to a stimulus or may be delayed.

The word "echolalia" is derived from the Greek , meaning "echo" or "to repeat", and ("laliá") meaning "speech" or "talk" (of onomatopoeic origin, from the verb ("laléo"), meaning "to talk").

Due to advances in modern neuroimaging, scientists have been able to gain a better understanding of how language is learned and comprehended. Based on the new data from the world of neuroscience, improvements can be made in coping with the disorder.

Therapists have been developing multiple methods of improving speech and comprehension. These techniques utilize three general principles: maximizing therapy occurrences, ensuring behavioral and communicative relevance, and allowing patients to focus on the language tools that are still available in his or her repertoire.

Many of the following treatment techniques are used to improve auditory comprehension in patients with aphasia:

- Use common words

- Using concrete nouns is more effective than using adjectives, adverbs, or verbs

- Using action verbs that are easily imagined

- Concise and grammatically simple sentences as opposed to lengthy sentences

- Speaking slowly, repeating oneself several times when conversing with patients who are aphasic

- Using gestures

A relatively new method of language therapy involves coincidence learning. Coincidence learning focuses on the simultaneous learning of two or more events and stipulates that these events are wired together in the brain, strengthening the learning process. Therapists use coincidence learning to find and improve language correlations or coincidences that have been either damaged or deleted by severe cases of aphasia, such as transcortical sensory aphasia. This technique is important in brain function and recovery, as it strengthens associated brain areas that remain unaffected after brian damage. It can be achieved with intensive therapy hours in order to maximize time where correlation is emphasized.

Through careful analysis of neuroimaging studies, a correlation has been developed with motor function and the understanding of action verbs. For example, leg and motor areas were seen to be activated words such as "kick", leading scientists to understand the connection between motor and language processes in the brain. This is yet another example of using relationships that are related in the brain for the purpose of rehabilitating speech and comprehension.

Of huge importance in aphasia therapy is the need to start practicing as soon as possible. Greater recovery occurs when a patient attempts to improve their comprehension and speaking soon after aphasia occurs. There is an inverse relationship between the length of time spent not practicing and level of recovery. The patient should be pushed to their limits of verbal communication in order for them to practice and build upon their remaining language skills.

One effective therapy technique is using what are known as language games in order to encourage verbal communication. One famous example is known as "Builder's Game", where a 'builder' and a 'helper' must communicate in order to effectively work on a project. The helper must hand the builder the tools he or she may need, which requires effective oral communication. The builder succeeds by requesting tools from the assistant by usually using single word utterances, such as 'hammer' or 'nail'. Thus, when the helper hands the tool to the builder, the game incorporates action with language, a key therapy technique. The assistant would then hand the builder the requested tool. Success of the game occurs when the builder's requests are specific to ensure successful building.

Ultimately, regardless of therapy plan or method, improvement in speech does not appear overnight; it requires a significant time investment by the patient as well as a dedicated speech therapist seeking to ensure that the patient is focusing on the correct speech tasks outside of the clinic. Furthermore, the patient must collaborate with friends and family members during their free time in order to maximize the efficacy of the treatment.

Echolalia can be categorized as immediate (occurring immediately after the stimulus) vs. delayed (some time after the occurrence of a stimulus). Immediate echolalia results from quick recall of information from the short-term memory and "superficial linguistic processing". A typical pediatric presentation of immediate echolalia might be as follows: a child is asked "Do you want dinner?"; the child echoes back "Do you want dinner?", followed by a pause, and then a response, "Yes. What's for dinner?"

In delayed echolalia the patient repeats words, phrases, or multiple sentences after a delay that can be anywhere from hours to years later. Immediate echolalia can be indicative that a developmental disorder exists, but this is not necessarily the case. Sometimes echolalia can be observed when an individual echoes back a statement to indicate they are contemplating a response and fully heard the original statement.

Researchers observed the daily repetitions of an autistic six-year-old in order to examine the differences between triggers for delayed versus immediate echolalia. Researchers further distinguished immediate echos by the sequential context in which they occur: after corrections, after directives, or in indiscernible sequential positions. Delayed echos are distinguished on the basis of ownership: self-echos, other-echos, and impersonal echos. The results showed that nearly all immediate echos produced by the six-year-old were found in sequential contexts, while the delayed echoes also occurred in the basis of ownership.

Although echolalia can be an impairment, the symptoms can involve a large selection of underlying meanings and behaviors across and within subjects. "Mitigated echolalia" refers to a repetition in which the original stimulus is somewhat altered, and "ambient echolalia" refers to the repetition (typically occurring in individuals with dementia) of environmental stimuli such as a television program running in the background.

Examples of mitigated echolalia are pronoun changes or syntax corrections. The first can be seen in the example of asking the patient “Where are you going?” and with patient responding “Where am I going?” The latter would be seen in the clinician asking “Where are I going?” and the patient repeating “Where am I going?” In mitigated echolalia some language processing is occurring. Mitigated echolalia can be seen in dyspraxia and aphasia of speech.

A Japanese case report describes a 20-year-old college student who was admitted to the hospital complaining about headaches and meningitis; however, he also exhibited signs of ambient echolalia. The researchers stated that the young patient's repetition was occurring at approximately the same tempo as his normal speech rate. The patient did not simply repeat words he had heard one after another. The patient reported that his ambient echolalia appeared to be random but appeared when he was distracted. He was also aware of his echolalia, but said he is unable to stop the repetitions.

Echopraxia (also known as echokinesis) is the involuntary repetition or imitation of another person's actions. Similar to echolalia, the involuntary repetition of sounds and language, it is one of the echophenomena ("automatic imitative actions without explicit awareness"). It has long been recognized as a core feature of Tourette syndrome, and is considered a complex tic, but it also occurs in autism spectrum disorders, schizophrenia and catatonia, aphasia, and disorders involving the startle reflex such as Latah. Echopraxia has also been observed in individuals with frontal lobe damage, epilepsy, dementia and autoimmune disorders; the causes of and the link between echopraxia and these disorders is undetermined.

The etymology of the term is from Ancient Greek: " (ēkhō) from (ēkhē "sound") and " (praksis, "action, activity, practice)".

Echopraxia is the involuntary mirroring of an observed action. Imitated actions can range from simple motor tasks such as picking up a phone to violent actions such as hitting another person.

Imitative learning and emulation of physical and verbal actions are critical to early development (up to the age of two or three), but when these behaviors become reactions rather than a means for learning, they are considered echophenomena (copying behaviors).

The exact cause of palilalia is unknown.

Palilalia also occurs in a variety of neurodegenerative disorders, occurring most commonly in Tourette syndrome, Alzheimer's disease, and progressive supranuclear palsy. Such degradation can occur in the substantia nigra where decreased dopamine production results in a loss of function. It can also occur in a variety of genetic disorders including Fragile X syndrome, Prader-Willi syndrome, Asperger's syndrome, autism, and the speaker has no difficulty initiating speech.

Hyperlexia is a syndrome characterized by a child's precocious ability to read. It was initially identified by Norman E. Silberberg and Margaret C. Silberberg (1967), who defined it as the precocious ability to read words without prior training in learning to read, typically before the age of 5. They indicated that children with hyperlexia have a significantly higher word-decoding ability than their reading comprehension levels. Children with hyperlexia also present with an intense fascination for written material at a very early age.

Hyperlexic children are characterized by having average or above-average IQs, and word-reading ability well above what would be expected given their age. First named and scientifically described in 1967 (Silverberg and Silverberg), it can be viewed as a superability in which word recognition ability goes far above expected levels of skill. Some hyperlexics, however, have trouble understanding speech. Some experts believe that most, or perhaps all children with hyperlexia, lie on the autism spectrum. However, one expert, Darold Treffert, proposes that hyperlexia has subtypes, only some of which overlap with autism. Between 5 and 20 percent of autistic children have been estimated to be hyperlexic.

Hyperlexic children are often fascinated by letters or numbers. They are extremely good at decoding language and thus often become very early readers. Some hyperlexic children learn to spell long words (such as "elephant") before they are two years old and learn to read whole sentences before they turn three.

An fMRI study of a single child showed that hyperlexia may be the neurological opposite of dyslexia.

Palilalia (from the Greek πάλιν ("pálin") meaning "again" and λαλιά ("laliá") meaning "speech" or "to talk"), a complex tic, is a language disorder characterized by the involuntary repetition of syllables, words, or phrases. It has features resembling other complex tics such as echolalia or coprolalia, but, unlike other aphasias, palilalia is based upon contextually correct speech.

It was originally described by Alexandre-Achille Souques in a patient with stroke that resulted in left-side hemiplegia, although a condition described as auto-echolalia in 1899 by Édouard Brissaud may have been the same condition.

Transcortical sensory aphasia (TSA) is a kind of aphasia that involves damage to specific areas of the temporal lobe of the brain, resulting in symptoms such as poor auditory comprehension, relatively intact repetition, and fluent speech with semantic paraphasias present. TSA is a fluent aphasia similar to Wernicke's aphasia, with the exception of a strong ability to repeat words and phrases. The person may repeat questions rather than answer them ("echolalia").

In all of these ways, TSA is very similar to a more commonly known language disorder, receptive aphasia. However, transcortical sensory aphasia differs from receptive aphasia in that patients still have intact repetition and exhibit echolalia, or the compulsive repetition of words. Transcortical sensory aphasia cannot be diagnosed through brain imaging techniques such as functional magnetic resonance imaging (fMRI), as the results are often difficult to interpret. Therefore, clinicians rely on language assessments and observations to determine if a patient presents with the characteristics of TSA. Patients diagnosed with TSA have shown partial recovery of speech and comprehension after beginning speech therapy. Speech therapy methods for patients with any subtype of aphasia are based on the principles of learning and neuroplasticity. Clinical research on TSA is limited because it occurs so infrequently in patients with aphasia that it is very difficult to perform systematic studies.

TSA should not be confused with transcortical motor aphasia (TMA), which is characterized by nonfluent speech output, with good comprehension and repetition. Patients with TMA have impaired writing skills, difficulty speaking and difficulty maintaining a clear thought process. Furthermore, TMA is caused by lesions in cortical motor areas of the brain as well as lesions in the anterior portion of the basal ganglia, and can be seen in patients with expressive aphasia.

Echophenomenon (also known as echo phenomenon) is "automatic imitative actions without explicit awareness" or pathological repetitions of external stimuli or activities, actions, sounds, or phrases, indicative of an underlying disorder.

The echophenomena include repetition:

- echolalia – of vocalizations (the most common of the echophenomena)

- echopraxia – of actions

- echomimia – of facial expressions

- echographia – of words that are written or typed

- echoplasia – physically or mentally, tracing contours of objects

- echolalioplasia – involving sign language, described in one individual with Tourette syndrome ().

- echologia – of words or sounds in thought

The word hyperlexia is derived from the Greek terms "hyper" ("over") and "léxis" ("diction", "word").

In terms of treatment for frontal lobe disorder, general supportive care is given, also some level of supervision could be needed. The prognosis will depend on the cause of the disorder, of course. A possible complication is that individuals with severe injuries may be disabled, such that, a caregiver may be unrecognizable to the person.

Another aspect of treatment of frontal lobe disorder is speech therapy. This type of therapy might help individuals with symptoms that are associated with aphasia and dysarthria.

Frontal lobe disorder is an impairment of the frontal lobe that occurs due to disease or head trauma. The frontal lobe of the brain plays a key role in higher mental functions such as motivation, planning, social behaviour, and speech production. A frontal lobe syndrome can be caused by a range of conditions including head trauma, tumours, degenerative diseases, neurosurgery and cerebrovascular disease. Frontal lobe impairment can be detected by recognition of typical clinical signs, use of simple screening tests, and specialist neurological testing.

The treatment of Tourette's focuses on identifying and helping the individual manage the most troubling or impairing symptoms. Most cases of Tourette's are mild, and do not require pharmacological treatment; instead, psychobehavioral therapy, education, and reassurance may be sufficient. Treatments, where warranted, can be divided into those that target tics and comorbid conditions, which, when present, are often a larger source of impairment than the tics themselves. Not all people with tics have comorbid conditions, but when those conditions are present, they often take treatment priority.

There is no cure for Tourette's and no medication that works universally for all individuals without significant adverse effects. Knowledge, education and understanding are uppermost in management plans for tic disorders. The management of the symptoms of Tourette's may include pharmacological, behavioral and psychological therapies. While pharmacological intervention is reserved for more severe symptoms, other treatments (such as supportive psychotherapy or cognitive behavioral therapy) may help to avoid or ameliorate depression and social isolation, and to improve family support. Educating a patient, family, and surrounding community (such as friends, school, and church) is a key treatment strategy, and may be all that is required in mild cases.

Medication is available to help when symptoms interfere with functioning. The classes of medication with the most proven efficacy in treating tics—typical and atypical neuroleptics including risperidone (trade name Risperdal), ziprasidone (Geodon), haloperidol (Haldol), pimozide (Orap) and fluphenazine (Prolixin)—can have long-term and short-term adverse effects. The antihypertensive agents clonidine (trade name Catapres) and guanfacine (Tenex) are also used to treat tics; studies show variable efficacy, but a lower side effect profile than the neuroleptics. Stimulants and other medications may be useful in treating ADHD when it co-occurs with tic disorders. Drugs from several other classes of medications can be used when stimulant trials fail, including guanfacine (trade name Tenex), atomoxetine (Strattera) and tricyclic antidepressants. Clomipramine (Anafranil), a tricyclic, and SSRIs—a class of antidepressants including fluoxetine (Prozac), sertraline (Zoloft), and fluvoxamine (Luvox)—may be prescribed when a Tourette's patient also has symptoms of obsessive–compulsive disorder. Several other medications have been tried, but evidence to support their use is unconvincing.

Because children with tics often present to physicians when their tics are most severe, and because of the waxing and waning nature of tics, it is recommended that medication not be started immediately or changed often. Frequently, the tics subside with explanation, reassurance, understanding of the condition and a supportive environment. When medication is used, the goal is not to eliminate symptoms: it should be used at the lowest possible dose that manages symptoms without adverse effects, given that these may be more disturbing than the symptoms for which they were prescribed.

Cognitive behavioral therapy (CBT) is a useful treatment when OCD is present, and there is increasing evidence supporting the use of habit reversal (HRT) in the treatment of tics. There is evidence that HRT reduces tic severity, but there are methodological limitations in the studies, and a need for more trained specialists and better large-scale studies.

Relaxation techniques, such as exercise, yoga or meditation, may be useful in relieving the stress that may aggravate tics, but the majority of behavioral interventions (such as relaxation training and biofeedback, with the exception of habit reversal) have not been systematically evaluated and are not empirically supported therapies for Tourette's. Deep brain stimulation has been used to treat adults with severe Tourette's that does not respond to conventional treatment, but it is regarded as an invasive, experimental procedure that is unlikely to become widespread.

, studies on the impact of dietary interventions on the symptoms of Tourette's are scarce and methodologically poor, and a single dietary pattern has not been established. Anecdotal reports suggest that certain dietary interventions may relieve symptoms, such as gluten-free and low-sugar diets.

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.

Although many alternative therapies and interventions are available, few are supported by scientific studies. Treatment approaches have little empirical support in quality-of-life contexts, and many programs focus on success measures that lack predictive validity and real-world relevance. Scientific evidence appears to matter less to service providers than program marketing, training availability, and parent requests. Some alternative treatments may place the child at risk. A 2008 study found that compared to their peers, autistic boys have significantly thinner bones if on casein-free diets; in 2005, botched chelation therapy killed a five-year-old child with autism. There has been early research looking at hyperbaric treatments in children with autism.

Although popularly used as an alternative treatment for people with autism, there is no good evidence that a gluten-free diet is of benefit. In the subset of people who have gluten sensitivity there is limited evidence that suggests that a gluten free diet may improve some autistic behaviors.

Educational interventions can be effective to varying degrees in most children: intensive ABA treatment has demonstrated effectiveness in enhancing global functioning in preschool children and is well-established for improving intellectual performance of young children. Similarly, teacher-implemented intervention that utilizes an ABA combined with a developmental social pragmatic approach has been found to be a well-established treatment in improving social-communication skills in young children, although there is less evidence in its treatment of global symptoms. Neuropsychological reports are often poorly communicated to educators, resulting in a gap between what a report recommends and what education is provided. It is not known whether treatment programs for children lead to significant improvements after the children grow up, and the limited research on the effectiveness of adult residential programs shows mixed results. The appropriateness of including children with varying severity of autism spectrum disorders in the general education population is a subject of current debate among educators and researchers.

No medications directly treat the core symptoms of AS. Although research into the efficacy of pharmaceutical intervention for AS is limited, it is essential to diagnose and treat comorbid conditions. Deficits in self-identifying emotions or in observing effects of one's behavior on others can make it difficult for individuals with AS to see why medication may be appropriate. Medication can be effective in combination with behavioral interventions and environmental accommodations in treating comorbid symptoms such as anxiety disorder, major depressive disorder, inattention and aggression. The atypical antipsychotic medications risperidone and olanzapine have been shown to reduce the associated symptoms of AS; risperidone can reduce repetitive and self-injurious behaviors, aggressive outbursts and impulsivity, and improve stereotypical patterns of behavior and social relatedness. The selective serotonin reuptake inhibitors (SSRIs) fluoxetine, fluvoxamine, and sertraline have been effective in treating restricted and repetitive interests and behaviors.

Care must be taken with medications, as side effects may be more common and harder to evaluate in individuals with AS, and tests of drugs' effectiveness against comorbid conditions routinely exclude individuals from the autism spectrum. Abnormalities in metabolism, cardiac conduction times, and an increased risk of type 2 diabetes have been raised as concerns with these medications, along with serious long-term neurological side effects. SSRIs can lead to manifestations of behavioral activation such as increased impulsivity, aggression, and sleep disturbance. Weight gain and fatigue are commonly reported side effects of risperidone, which may also lead to increased risk for extrapyramidal symptoms such as restlessness and dystonia and increased serum prolactin levels. Sedation and weight gain are more common with olanzapine, which has also been linked with diabetes. Sedative side-effects in school-age children have ramifications for classroom learning. Individuals with AS may be unable to identify and communicate their internal moods and emotions or to tolerate side effects that for most people would not be problematic.

There is no known cure for autism, although those with Asperger syndrome and those who have autism and require little-to-no support are more likely to experience a lessening of symptoms over time. The main goals of treatment are to lessen associated deficits and family distress, and to increase quality of life and functional independence. In general, higher IQs are correlated with greater responsiveness to treatment and improved treatment outcomes. Although evidence-based interventions for autistic children vary in their methods, many adopt a psychoeducational approach to enhancing cognitive, communication, and social skills while minimizing problem behaviors. It has been argued that no single treatment is best and treatment is typically tailored to the child's needs.

Intensive, sustained special education programs and behavior therapy early in life can help children acquire self-care, social, and job skills. Available approaches include applied behavior analysis, developmental models, structured teaching, speech and language therapy, social skills therapy, and occupational therapy. Among these approaches, interventions either treat autistic features comprehensively, or focus treatment on a specific area of deficit. Generally, when educating those with autism, specific tactics may be used to effectively relay information to these individuals. Using as much social interaction as possible is key in targeting the inhibition autistic individuals experience concerning person-to-person contact. Additionally, research has shown that employing semantic groupings, which involves assigning words to typical conceptual categories, can be benevficial in fostering learning.

There has been increasing attention to the development of evidence-based interventions for young children with ASD. Two theoretical frameworks outlined for early childhood intervention include applied behavioral analysis (ABA) and the developmental social-pragmatic model (DSP). Although ABA therapy has a strong evidence base, particularly in regard to early intensive home-based therapy. ABA's effectiveness may be limited by diagnostic severity and IQ of the person affected by ASD. The Journal of Clinical Child and Adolescent Psychology has deemed two early childhood interventions as “well-established”: individual comprehensive ABA, and focused teacher-implemented ABA combined with DSP.

Another evidence-based intervention that has demonstrated efficacy is a parent training model, which teaches parents how to implement various ABA and DSP techniques themselves. Various DSP programs have been developed to explicitly deliver intervention systems through at-home parent implementation.

A multitude of unresearched alternative therapies have also been implemented. Many have resulted in harm to autistic people and should not be employed unless proven to be safe.

In October 2015, the American Academy of Pediatrics (AAP) proposed new evidence-based recommendations for early interventions in ASD for children under 3. These recommendations emphasize early involvement with both developmental and behavioral methods, support by and for parents and caregivers, and a focus on both the core and associated symptoms of ASD.

The ideal treatment for AS coordinates therapies that address core symptoms of the disorder, including poor communication skills and obsessive or repetitive routines. While most professionals agree that the earlier the intervention, the better, there is no single best treatment package. AS treatment resembles that of other high-functioning ASDs, except that it takes into account the linguistic capabilities, verbal strengths, and nonverbal vulnerabilities of individuals with AS. A typical program generally includes:

- A positive behavior support procedure includes training and support of parents and school faculty in behavior management strategies to use in the home and school;

- An applied behavior analysis (ABA) technique called social skills training for more effective interpersonal interactions;

- Cognitive behavioral therapy to improve stress management relating to anxiety or explosive emotions and to cut back on obsessive interests and repetitive routines;

- Medication, for coexisting conditions such as major depressive disorder and anxiety disorder;

- Occupational or physical therapy to assist with poor sensory processing and motor coordination;

- Social communication intervention, which is specialized speech therapy to help with the pragmatics of the give and take of normal conversation.

Of the many studies on behavior-based early intervention programs, most are case reports of up to five participants and typically examine a few problem behaviors such as self-injury, aggression, noncompliance, stereotypies, or spontaneous language; unintended side effects are largely ignored. Despite the popularity of social skills training, its effectiveness is not firmly established. A randomized controlled study of a model for training parents in problem behaviors in their children with AS showed that parents attending a one-day workshop or six individual lessons reported fewer behavioral problems, while parents receiving the individual lessons reported less intense behavioral problems in their AS children. Vocational training is important to teach job interview etiquette and workplace behavior to older children and adults with AS, and organization software and personal data assistants can improve the work and life management of people with AS.

Thought disorder (TD) or formal thought disorder (FTD) refers to disorganized thinking as evidenced by disorganized speech. Specific thought disorders include derailment, poverty of speech, tangentiality, illogicality, perseveration, and thought blocking.

Psychiatrists consider formal thought disorder as being one of two types of disordered thinking, with the other type being delusions. The latter involves "content" while the former involves "form". Although the term "thought disorder" can refer to either type, in common parlance it refers most often to a disorder of thought "form" also known as formal thought disorder.

Eugen Bleuler, who named schizophrenia, held that thought disorder was its defining characteristic. However, formal thought disorder is not unique to schizophrenia or psychosis. It is often a symptom of mania, and less often it can be present in other mental disorders such as depression. Clanging or echolalia may be present in Tourette syndrome. Patients with a clouded consciousness, like that found in delirium, also have a formal thought disorder.

However, there is a clinical difference between these two groups. Those with schizophrenia or psychosis are less likely to demonstrate awareness or concern about the disordered thinking. Clayton and Winokur have suggested that this results from a fundamental inability to use the same type of Aristotelian logic as others. On the other hand, patients with a clouded consciousness, referred to as "organic" patients, usually do demonstrate awareness and concern, and complain about being "confused" or "unable to think straight"; Clayton and Winokur suggest that this is because their thought disorder results, instead, from various cognitive deficits.

In considering whether an individual has thought disorder, patterns of their speech are closely observed. Although it is normal to exhibit some of the following during times of extreme stress (e.g. a cataclysmic event or the middle of a war) it is the degree, frequency, and the resulting functional impairment that leads to the conclusion that the person being observed has a thought disorder.

- "Alogia" (also "poverty of speech") – A poverty of speech, either in amount or content; it can occur as a negative symptom of schizophrenia.

- "Blocking" – An abrupt stop in the middle of a train of thought; the individual may or may not be able to continue the idea. This is a type of formal thought disorder that can be seen in schizophrenia.

- "Circumstantiality" (also "circumstantial thinking", or "circumstantial speech") – An inability to answer a question without giving excessive, unnecessary detail. This differs from tangential thinking, in that the person does eventually return to the original point.

- "Clanging" or "Clang association" – a severe form of flight of ideas whereby ideas are related only by similar or rhyming sounds rather than actual meaning. This may be heard as excessive rhyming and/or alliteration. e.g. "Many moldy mushrooms merge out of the mildewy mud on Mondays." "I heard the bell. Well, hell, then I fell." It is most commonly seen in bipolar affective disorder (manic phase), although it is often observed in patients with primary psychoses, namely schizophrenia and schizoaffective disorder.

- "Derailment" (also "loose association" and "knight's move thinking") – Thought and/or speech move, either spontaneously or in response to an internal stimulus (distinguishing derailment from "distractible speech," "infra"), from the topic's track onto another which is obliquely related or unrelated. e.g. "The next day when I'd be going out you know, I took control, like uh, I put bleach on my hair in California."

- "Distractible speech" – During mid speech, the subject is changed in response to an external stimulus. e.g. "Then I left San Francisco and moved to... where did you get that tie?"

- "Echolalia" – Echoing of another's speech that may only be committed once, or may be continuous in repetition. This may involve repeating only the last few words or last word of the examiner's sentences. This can be a symptom of Tourette's Syndrome. e.g. "What would you like for dinner?", "That's a good question. "That's a good question". "That's a good question". "That's a good question"."

- "Evasive interaction" – Attempts to express ideas and/or feelings about another individual come out as evasive or in a diluted form, e.g.: "I... er ah... you are uh... I think you have... uh-- acceptable erm... uh... hair."

- "Flight of ideas" – a form of formal thought disorder marked by abrupt leaps from one topic to another, albeit with discernable links between successive ideas, perhaps governed by similarities between subjects or, in somewhat higher grades, by rhyming, puns, and word plays (clang associations), or innocuous environmental stimuli – e.g., the sound of birds chirping. It is most characteristic of the manic phase of bipolar illness.

- "Illogicality" – Conclusions are reached that do not follow logically (non-sequiturs or faulty inferences). e.g. "Do you think this will fit in the box?" draws a reply like "Well duh; it's brown, isn't it?"

- "Incoherence (word salad)" – Speech that is unintelligible because, though the individual words are real words, the manner in which they are strung together results in incoherent gibberish, e.g. the question "Why do people comb their hair?" elicits a response like "Because it makes a twirl in life, my box is broken help me blue elephant. Isn't lettuce brave? I like electrons, hello please!"

- "Loss of goal" – Failure to follow a train of thought to a natural conclusion. e.g. "Why does my computer keep crashing?", "Well, you live in a stucco house, so the pair of scissors needs to be in another drawer."

- "Neologisms" – New word formations. These may also involve elisions of two words that are similar in meaning or in sound. e.g. "I got so angry I picked up a dish and threw it at the geshinker."

- "Perseveration" – Persistent repetition of words or ideas even when another person attempts to change the topic. e.g. "It's great to be here in Nevada, Nevada, Nevada, Nevada, Nevada." This may also involve repeatedly giving the same answer to different questions. e.g. "Is your name Mary?" "Yes." "Are you in the hospital?" "Yes." "Are you a table?" "Yes." Perseveration can include palilalia and logoclonia, and can be an indication of organic brain disease such as Parkinson's.

- "Phonemic paraphasia" – Mispronunciation; syllables out of sequence. e.g. "I slipped on the lice and broke my arm."

- "Pressure of speech" – Unrelenting, rapid speech without pauses. It may be difficult to interrupt the speaker, and the speaker may continue speaking even when a direct question is asked.

- "Self-reference" – Patient repeatedly and inappropriately refers back to self. e.g. "What's the time?", "It's 7 o'clock. That's my problem."

- "Semantic paraphasia" – Substitution of inappropriate word. e.g. "I slipped on the coat, on the ice I mean, and broke my book."

- "Stilted speech" – Speech characterized by the use of words or phrases that are flowery, excessive, and pompous. e.g. "The attorney comported himself indecorously."

- "Tangentiality" – Wandering from the topic and never returning to it or providing the information requested. e.g. in answer to the question "Where are you from?", a response "My dog is from England. They have good fish and chips there. Fish breathe through gills."

- "Word approximations" – Old words used in a new and unconventional way. e.g. "His boss was a ."

The U.S. Center for Disease Control's most recent estimate is that 1 out of every 68 children, or 14.7 per 1,000, have some form of ASD as of 2010. Reviews tend to estimate a prevalence of 6 per 1,000 for autism spectrum disorders as a whole, although prevalence rates vary for each of the developmental disorders in the spectrum. Autism prevalence has been estimated at 1-2 per 1,000, Asperger syndrome at roughly 0.6 per 1,000, childhood disintegrative disorder at 0.02 per 1,000, and PDD-NOS at 3.7 per 1,000. These rates are consistent across cultures and ethnic groups, as autism is considered a universal disorder.

While rates of autism spectrum disorders are consistent across cultures, they vary greatly by gender, with boys affected far more frequently than girls. The average male-to-female ratio for ASDs is 4.2:1, affecting 1 in 70 males, but only 1 in 315 females. Females, however, are more likely to have associated cognitive impairment. Among those with an ASD and intellectual disability, the sex ratio may be closer to 2:1. Prevalence differences may be a result of gender differences in expression of clinical symptoms, with autistic females showing less atypical behaviors and, therefore, less likely to receive an ASD diagnosis.

The causes of developmental disabilities are varied and remain unknown in a large proportion of cases. Even in cases of known etiology the line between "cause" and "effect" is not always clear, leading to difficulty in categorizing causes.

Genetic factors have long been implicated in the causation of developmental disabilities. There is also a large environmental component to these conditions, and the relative contributions of nature versus nurture have been debated for decades.

Current theories on causation focus on genetic factors, and over 1,000 known genetic conditions include developmental disabilities as a symptom.

Developmental disabilities affect between 1 and 2% of the population in most western countries, although many government sources acknowledge that statistics are flawed in this area. The worldwide proportion of people with developmental disabilities is believed to be approximately 1.4%. It is twice as common in males as in females, and some researchers have found that the prevalence of mild developmental disabilities is likely to be higher in areas of poverty and deprivation, and among people of certain ethnicities.

Developmental disability is a diverse group of chronic conditions that are due to mental or physical impairments. Developmental disabilities cause individuals living with them many difficulties in certain areas of life, especially in "language, mobility, learning, self-help, and independent living". Developmental disabilities can be detected early on, and do persist throughout an individual's lifespan. Developmental disability that affects all areas of a child's development is sometimes referred to as global developmental delay.

Most common developmental disabilities:

- Down syndrome is a condition in which people are born with an extra copy of chromosome 21. Normally, a person is born with two copies of chromosome 21. However, if they are born with Down syndrome, they have an extra copy of this chromosome. This extra copy affects the development of the body and brain, causing physical and mental challenges for the individual.

- Fragile X syndrome (FXS) is thought to cause autism and intellectual disability, usually among boys.

- Pervasive developmental disorders (PDD) are a group of developmental disabilities that can cause significant social, communication and behavioral challenges.

- Fetal alcohol spectrum disorders (FASD) are a group of conditions that can occur in a person whose mother drank alcohol during pregnancy.

- Cerebral palsy (CP) is a group of disorders that affect a person’s ability to move and maintain balance and posture. CP is the most common motor disability in childhood.

- Intellectual disability, also (sometimes proscriptively) known as mental retardation, is defined as an IQ below 70 along with limitations in adaptive functioning and onset before the age of 18 years.