Sensory aphasia cannot be diagnosed through the use of imaging techniques. Differences in cognition between asymptomatic subjects and affected patients can be observed via functional magnetic resonance imaging (fMRI). However, these results only reveal temporal differences in cognition between control and diagnosed subjects. The degree of progression during therapy can also be surveyed through cognition tests monitored by fMRI. Many patients’ progress is assessed over time via repeated testing and corresponding cerebral imaging by fMRI.

Sensory aphasia is typically diagnosed by non-invasive evaluations. Neurologists, neuropsychologists or speech pathologists will administer oral evaluations to determine the extent of a patient’s comprehension and speech capability. Initial assessment will determine if the cause of linguistic deficiency is aphasia. If the diagnosis is then confirmed, testing will next address the type of aphasia and its severity. The Boston Diagnostic Aphasia Examination specializes in determining the severity of a sensory aphasia through the observation of conversational behaviors. Several modalities of perception and response are observed in conjunction with the subject’s ability to process sensory information. The location of the brain lesion and type of the aphasia can then be inferred from the observed symptoms. The Minnesota Test for Differential Diagnosis is the most lengthy and thorough assessment of sensory aphasia. It pinpoints weaknesses in the auditory and visual senses, as well as reading comprehension. From this differential diagnosis, a patient’s course of treatment can be determined. After treatment planning, the Porch Index of Communicative Ability is used to evaluate prognosis and the degree of recovery.

There is no formal test for diagnosing echopraxia. It is easier to distinguish in individuals over the age of five, because younger children frequently imitate others' actions.

Imitation can be divided into two types: imitative learning and automatic imitation. Imitative learning occurs when a person consciously mimics an observed action in order to learn the mechanism behind that action and perform it himself or herself. Babies begin copying movements soon after birth; this behavior begins to diminish around the age of three. Before that, it is not possible to diagnose echopraxia, because it is difficult to differentiate between imitative learning and automatic imitation. If the imitative behavior continues beyond infanthood, it may be considered echopraxia.

Echopraxia may be more easily distinguished in older individuals, because their behaviors in relation to prior behaviors can be differentiated. They report feeling an uncontrollable urge to perform an action after seeing it being performed. Automatic behavior is occasionally present in healthy adults (for example, when a person observes someone yawning, he or she may do the same); these behaviors are not considered echopraxia.

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").

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 is a typical symptom of Tourette syndrome but causes are not well elucidated.

One theoretical cause subject to ongoing debate surrounds the role of the mirror neuron system (MNS), a group of neurons in the inferior frontal gyrus (F5 region) of the brain that may influence imitative behaviors, but no widely accepted neural or computational models have been put forward to describe how mirror neuron activity supports cognitive functions such as imitation.

The diagnosis of frontal lobe disorder can be divided into the following three categories:

- Clinical history

Frontal lobe disorders may be recognized through a sudden and dramatic change in a person's personality, for example with loss of social awareness, disinhibition, emotional instability, irritability or impulsiveness. Alternatively the disorder may become apparent because of mood changes such as depression, anxiety or apathy.

- Examination

On mental state examination a person with frontal lobe damage may show speech problems, with reduced verbal fluency. Typically the person is lacking in insight and judgment, but does not have marked cognitive abnormalities or memory impairment (as measured for example by the mini-mental state examination). With more severe impairment there may be echolalia or mutism. Neurological examination may show primitive reflexes (also known as frontal release signs) such as the grasp reflex. Akinesia (lack of spontaneous movement) will be present in more severe and advanced cases.

- Further investigation

A range of neuropsychological tests are available for clarifying the nature and extent of frontal lobe dysfunction. For example, concept formation and ability to shift mental sets can be measured with the Wisconsin Card Sorting Test, planning can be assessed with the Mazes subtest of the WISC. Individuals with Pick's disease will show frontal cortical atrophy on MRIs. Frontal impairment due to head injuries, tumours or cerebrovascular disease will also be apparent on brain imaging.

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.

Palilalia is considered an aphasia, a disorder of language, and is not to be confused with speech disorders, as there is no difficulty in the formation of internal speech. Palilalia is similar to speech disorders such as stuttering or cluttering, as it tends to only express itself in spontaneous speech, such as answering basic questions, and not in automatic speech such as reading or singing; however, it distinctively affects words and phrases rather than syllables and sounds.

Palilalia may occur in conditions affecting the pre-frontal cortex or basal ganglia regions, either from physical trauma, neurodegenerative disorders, genetic disorders, or a loss of dopamine in these brain regions. Palilalia occurs most commonly in Tourette syndrome and may be present in neurodegenerative disorders like Alzheimer's disease and progressive supranuclear palsy.

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

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

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.

About half of parents of children with ASD notice their child's unusual behaviors by age 18 months, and about four-fifths notice by age 24 months. According to an article, failure to meet any of the following milestones "is an absolute indication to proceed with further evaluations. Delay in referral for such testing may delay early diagnosis and treatment and affect the long-term outcome".

- No babbling by 12 months.

- No gesturing (pointing, waving, etc.) by 12 months.

- No single words by 16 months.

- No two-word (spontaneous, not just echolalic) phrases by 24 months.

- Any loss of any language or social skills, at any age.

The United States Preventive Services Task Force in 2016 found it was unclear if screening was beneficial or harmful among children in whom there is no concerns. The Japanese practice is to screen all children for ASD at 18 and 24 months, using autism-specific formal screening tests. In contrast, in the UK, children whose families or doctors recognize possible signs of autism are screened. It is not known which approach is more effective. Screening tools include the Modified Checklist for Autism in Toddlers (M-CHAT), the Early Screening of Autistic Traits Questionnaire, and the First Year Inventory; initial data on M-CHAT and its predecessor, the Checklist for Autism in Toddlers (CHAT), on children aged 18–30 months suggests that it is best used in a clinical setting and that it has low sensitivity (many false-negatives) but good specificity (few false-positives). It may be more accurate to precede these tests with a broadband screener that does not distinguish ASD from other developmental disorders. Screening tools designed for one culture's norms for behaviors like eye contact may be inappropriate for a different culture. Although genetic screening for autism is generally still impractical, it can be considered in some cases, such as children with neurological symptoms and dysmorphic features.

While infection with rubella during pregnancy causes fewer than 1% of cases of autism, vaccination against rubella can prevent many of those cases.

ASD can be detected as early as 18 months or even younger in some cases. A reliable diagnosis can usually be made by the age of two years. The diverse expressions of ASD symptoms pose diagnostic challenges to clinicians. Individuals with an ASD may present at various times of development (e.g., toddler, child, or adolescent), and symptom expression may vary over the course of development. Furthermore, clinicians must differentiate among pervasive developmental disorders, and may also consider similar conditions, including intellectual disability not associated with a pervasive developmental disorder, specific language disorders, ADHD, anxiety, and psychotic disorders.

Considering the unique challenges in diagnosing ASD, specific practice parameters for its assessment have been published by the American Academy of Neurology, the American Academy of Child and Adolescent Psychiatry, and a consensus panel with representation from various professional societies. The practice parameters outlined by these societies include an initial screening of children by general practitioners (i.e., "Level 1 screening") and for children who fail the initial screening, a comprehensive diagnostic assessment by experienced clinicians (i.e. "Level 2 evaluation"). Furthermore, it has been suggested that assessments of children with suspected ASD be evaluated within a developmental framework, include multiple informants (e.g., parents and teachers) from diverse contexts (e.g., home and school), and employ a multidisciplinary team of professionals (e.g., clinical psychologists, neuropsychologists, and psychiatrists).

After a child shows initial evidence of ASD tendencies, psychologists administer various psychological assessment tools to assess for ASD. Among these measurements, the Autism Diagnostic Interview-Revised (ADI-R) and the Autism Diagnostic Observation Schedule (ADOS) are considered the "gold standards" for assessing autistic children. The ADI-R is a semi-structured parent interview that probes for symptoms of autism by evaluating a child's current behavior and developmental history. The ADOS is a semistructured interactive evaluation of ASD symptoms that is used to measure social and communication abilities by eliciting several opportunities (or "presses") for spontaneous behaviors (e.g., eye contact) in standardized context. Various other questionnaires (e.g., The Childhood Autism Rating Scale, Autism Treatment Evaluation Checklist) and tests of cognitive functioning (e.g., The Peabody Picture Vocabulary Test) are typically included in an ASD assessment battery.

In the UK, there is some diagnostic use of the Diagnostic Interview for Social and Communication Disorders (DISCO) was which was developed for use at The Centre for Social and Communication Disorders, by Lorna Wing and Judith Gould, as both a clinical and a research instrument for use with children and adults of any age. The DISCO is designed to elicit a picture of the whole person through the story of their development and behaviour. In clinical work, the primary purpose is to facilitate understanding of the pattern over time of the specific skills and impairments that underlie the overt behaviour. If no information is available, the clinician has to obtain as much information as possible concerning the details of current skills and pattern of behaviour of the person. This type of dimensional approach to clinical description is useful for prescribing treatment.

According to the fifth edition of the "Diagnostic and Statistical Manual of Mental Disorders" (DSM-5), Tourette’s may be diagnosed when a person exhibits both multiple motor and one or more vocal tics over the period of a year; the motor and vocal tics need not be concurrent. The onset must have occurred before the age of 18, and cannot be attributed to the effects of another condition or substance (such as cocaine). Hence, other medical conditions that include tics or tic-like movements—such as autism or other causes of tourettism—must be ruled out before conferring a Tourette's diagnosis. Since 2000, the DSM has recognized that clinicians see patients who meet all the other criteria for Tourette's, but do not have distress or impairment.

There are no specific medical or screening tests that can be used in diagnosing Tourette's; it is frequently misdiagnosed or underdiagnosed, partly because of the wide expression of severity, ranging from mild (the majority of cases) or moderate, to severe (the rare, but more widely recognized and publicized cases). Coughing, eye blinking, and tics that mimic unrelated conditions such as asthma are commonly misdiagnosed.

The diagnosis is made based on observation of the individual's symptoms and family history, and after ruling out secondary causes of tic disorders. In patients with a typical onset and a family history of tics or obsessive–compulsive disorder, a basic physical and neurological examination may be sufficient.

There is no requirement that other comorbid conditions (such as ADHD or OCD) be present, but if a physician believes that there may be another condition present that could explain tics, tests may be ordered as necessary to rule out that condition. An example of this is when diagnostic confusion between tics and seizure activity exists, which would call for an EEG, or if there are symptoms that indicate an MRI to rule out brain abnormalities. TSH levels can be measured to rule out hypothyroidism, which can be a cause of tics. Brain imaging studies are not usually warranted. In teenagers and adults presenting with a sudden onset of tics and other behavioral symptoms, a urine drug screen for cocaine and stimulants might be necessary. If a family history of liver disease is present, serum copper and ceruloplasmin levels can rule out Wilson's disease. Most cases are diagnosed by merely observing a history of tics.

Secondary causes of tics (not related to inherited Tourette syndrome) are commonly referred to as tourettism. Dystonias, choreas, other genetic conditions, and secondary causes of tics should be ruled out in the differential diagnosis for Tourette syndrome. Other conditions that may manifest tics or stereotyped movements include developmental disorders, autism spectrum disorders, and stereotypic movement disorder; Sydenham's chorea; idiopathic dystonia; and genetic conditions such as Huntington's disease, neuroacanthocytosis, Hallervorden-Spatz syndrome, Duchenne muscular dystrophy, Wilson's disease, and tuberous sclerosis. Other possibilities include chromosomal disorders such as Down syndrome, Klinefelter syndrome, XYY syndrome and fragile X syndrome. Acquired causes of tics include drug-induced tics, head trauma, encephalitis, stroke, and carbon monoxide poisoning. The symptoms of Lesch-Nyhan syndrome may also be confused with Tourette syndrome. Most of these conditions are rarer than tic disorders, and a thorough history and examination may be enough to rule them out, without medical or screening tests.

Although not all people with Tourette's have comorbid conditions, most Tourette's patients presenting for clinical care at specialty referral centers may exhibit symptoms of other conditions along with their motor and phonic tics. Associated conditions include attention-deficit hyperactivity disorder (ADD or ADHD), obsessive–compulsive disorder (OCD), learning disabilities and sleep disorders. Disruptive behaviors, impaired functioning, or cognitive impairment in patients with comorbid Tourette's and ADHD may be accounted for by the comorbid ADHD, highlighting the importance of identifying and treating comorbid conditions. Disruption from tics is commonly overshadowed by comorbid conditions that present greater interference to the child. Tic disorders in the absence of ADHD do not appear to be associated with disruptive behavior or functional impairment, while impairment in school, family, or peer relations is greater in patients who have more comorbid conditions and often determines whether therapy is needed.

Because comorbid conditions such as OCD and ADHD can be more impairing than tics, these conditions are included in an evaluation of patients presenting with tics. "It is critical to note that the comorbid conditions may determine functional status more strongly than the tic disorder," according to Samuel Zinner, MD. The initial assessment of a patient referred for a tic disorder should include a thorough evaluation, including a family history of tics, ADHD, obsessive–compulsive symptoms, and other chronic medical, psychiatric and neurological conditions. Children and adolescents with TS who have learning difficulties are candidates for psychoeducational testing, particularly if the child also has ADHD. Undiagnosed comorbid conditions may result in functional impairment, and it is necessary to identify and treat these conditions to improve functioning. Complications may include depression, sleep problems, social discomfort, self-injury, anxiety, personality disorders, oppositional defiant disorder, and conduct disorders.

Parents of children with Asperger syndrome can typically trace differences in their children's development to as early as 30 months of age. Developmental screening during a routine check-up by a general practitioner or pediatrician may identify signs that warrant further investigation. The United States Preventive Services Task Force in 2016 found it was unclear if screening was beneficial or harmful among children in whom there are no concerns.

The diagnosis of AS is complicated by the use of several different screening instruments, including the Asperger Syndrome Diagnostic Scale (ASDS), Autism Spectrum Screening Questionnaire (ASSQ), Childhood Autism Spectrum Test (CAST) (previously called the Childhood Asperger Syndrome Test), Gilliam Asperger's disorder scale (GADS), Krug Asperger's Disorder Index (KADI), and the Autism-spectrum quotient (AQ; with versions for children, adolescents and adults). None have been shown to reliably differentiate between AS and other ASDs.

Standard diagnostic criteria require impairment in social interaction and repetitive and stereotyped patterns of behavior, activities and interests, without significant delay in language or cognitive development. Unlike the international standard, the DSM-IV-TR criteria also required significant impairment in day-to-day functioning; DSM-5 eliminated AS as a separate diagnosis in 2013, and folded it into the umbrella of autism spectrum disorders. Other sets of diagnostic criteria have been proposed by Szatmari "et al." and by Gillberg and Gillberg.

Diagnosis is most commonly made between the ages of four and eleven. A comprehensive assessment involves a multidisciplinary team that observes across multiple settings, and includes neurological and genetic assessment as well as tests for cognition, psychomotor function, verbal and nonverbal strengths and weaknesses, style of learning, and skills for independent living. The "gold standard" in diagnosing ASDs combines clinical judgment with the Autism Diagnostic Interview-Revised (ADI-R)—a semistructured parent interview—and the Autism Diagnostic Observation Schedule (ADOS)—a conversation and play-based interview with the child. Delayed or mistaken diagnosis can be traumatic for individuals and families; for example, misdiagnosis can lead to medications that worsen behavior.

Underdiagnosis and overdiagnosis may be problems. The cost and difficulty of screening and assessment can delay diagnosis. Conversely, the increasing popularity of drug treatment options and the expansion of benefits has motivated providers to overdiagnose ASD. There are indications AS has been diagnosed more frequently in recent years, partly as a residual diagnosis for children of normal intelligence who are not autistic but have social difficulties.

There are questions about the external validity of the AS diagnosis. That is, it is unclear whether there is a practical benefit in distinguishing AS from HFA and from PDD-NOS; the same child can receive different diagnoses depending on the screening tool. The debate about distinguishing AS from HFA is partly due to a tautological dilemma where disorders are defined based on severity of impairment, so that studies that appear to confirm differences based on severity are to be expected.

Developmental disabilities can be initially suspected when a child does not reach expected child development stages. Subsequently, a differential diagnosis may be used to diagnose an underlying disease, which may include a physical examination and genetic tests.

The degree of disability can be quantified by assigning a "developmental age" to a person, which is age of the group into which test scores place the person. This, in turn, can be used to calculate a "" (DQ) as follows:

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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.

Hospitalization may be necessary during the acute phase of symptoms, and psychiatric care if the patient is a danger to self or others. A neurological consult is advised to rule out any organic cause.

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.

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.