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.

Many medications are used to treat ASD symptoms that interfere with integrating a child into home or school when behavioral treatment fails. More than half of US children diagnosed with ASD are prescribed psychoactive drugs or anticonvulsants, with the most common drug classes being antidepressants, stimulants, and antipsychotics. Antipsychotics, such as risperidone and aripiprazole, have been found to be useful for treating irritability, repetitive behavior, and sleeplessness that often occurs with autism, however their side effects must be weighed against their potential benefits, and people with autism may respond atypically. There is scant reliable research about the effectiveness or safety of drug treatments for adolescents and adults with ASD. No known medication relieves autism's core symptoms of social and communication impairments. Experiments in mice have reversed or reduced some symptoms related to autism by replacing or modulating gene function, suggesting the possibility of targeting therapies to specific rare mutations known to cause autism.

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.

Asperger syndrome treatment attempts to manage distressing symptoms and to teach age-appropriate social, communication and vocational skills that are not naturally acquired during development, with intervention tailored to the needs of the individual based on multidisciplinary assessment. Although progress has been made, data supporting the efficacy of particular interventions are limited.

Several prenatal and perinatal complications have been reported as possible risk factors for autism. These risk factors include maternal gestational diabetes, maternal and paternal age over 30, bleeding after first trimester, use of prescription medication (e.g. valproate) during pregnancy, and meconium in the amniotic fluid. While research is not conclusive on the relation of these factors to autism, each of these factors has been identified more frequently in autistic children compared to their non-autistic siblings and other normally developing youth.

Low vitamin D levels in early development has been hypothesized as a risk factor for autism.

Medications are used to address certain behavioral problems; therapy for children with PDD should be specialized according to the child's specific needs.

Some children with PDD benefit from specialized classrooms in which the class size is small and instruction is given on a one-to-one basis. Others function well in standard special education classes or regular classes with support. Early intervention, including appropriate and specialized educational programs and support services, play a critical role in improving the outcome of individuals with PDD.

Regression in autism spectrum disorders is well documented; attribution of regression to environmental stress factors may result in a delay in diagnosis. The apparent onset of regressive autism is surprising and distressing to parents, who often initially suspect severe hearing loss. A controversy occurred following a fraudulent study linking MMR vaccine to autism, but since then, studies have shown no connection between autism and the MMR vaccine. There are also studies being done to test if certain types of regressive autism have an autoimmune basis.

There are some who believe that regressive autism is simply early-onset autism that was recognized at a later date. Researchers have conducted studies to determine whether regressive autism is a distinct subset of autism spectrum disorders. Over the years, the results of these studies have contradicted one another. Some researchers believe there is still nothing to support a definitive biological difference between early-onset and regressive autism. However, emerging research shows that males with regressive autism have brains that are six percent larger than anyone with early-onset autism. The brains of females with regressive autism show no difference in brain size.

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 no known "cure" for PDD-NOS, but there are interventions that can have a positive influence. Early and intensive implementation of evidence-based practices and interventions are generally believed to improve outcomes. Most of these are individualized special education strategies rather than medical or pharmaceutical treatment; the best outcomes are achieved when a team approach among supporting individuals is utilized.

Some of the more common therapies and services include:

- Visual and environmental supports, visual schedules

- Applied behavior analysis

- Discrete trial instruction (part of applied behavior analysis)

- Social stories and comic strip conversations

- Physical and occupational therapy

Loss of language and skills related to social interaction and self-care are serious. The affected children face ongoing disabilities in certain areas and require long term care. Treatment of CDD involves both behavior therapy, environmental therapy and medications.

- Behavior therapy: The main aim of Applied Behavior Analysis (ABA) is to systematically teach the child to relearn language, self-care and social skills. The treatment programs designed in this respect "use a system of rewards to reinforce desirable behaviors and discourage problem behavior." ABA programs may be designed by a board-certified specialist in behavior analysis called a "BCBA" (Board Certified Behavior Analyst), but ABA is also widely used by a number of other health care personnel from different fields like psychologists, speech therapists, physical therapists and occupational therapists with differing levels of expertise. Parents, teachers and caregivers are instructed to use these behavior therapy methods at all times.

- Environmental Therapy: Sensory Enrichment Therapy uses enrichment of the sensory experience to improve symptoms in autism, many of which are common to CDD.

- Medications: There are no medications available to directly treat CDD. Antipsychotic medications are used to treat severe behavior problems like aggressive stance and repetitive behavior patterns. Anticonvulsant medications are used to control seizures.

The diagnostic category pervasive developmental disorders (PDD), as opposed to specific developmental disorders (SDD), refers to a group of five disorders characterized by delays in the development of multiple basic functions including socialization and communication. The pervasive developmental disorders are: All autism spectrum disorders and Rett syndrome.

The first four of these disorders are commonly called the autism spectrum disorders; the last disorder is much rarer, and is sometimes placed in the autism spectrum and sometimes not.

The onset of pervasive developmental disorders occurs during infancy, but the condition is usually not identified until the child is around three years old. Parents may begin to question the health of their child when developmental milestones are not met, including age appropriate motor movement and speech production.

There is a division among doctors on the use of the term PDD. Many use the term PDD as a short way of saying PDD-NOS (Pervasive developmental disorder not otherwise specified). Others use the general category label of PDD because they are hesitant to diagnose very young children with a specific type of PDD, such as autism. Both approaches contribute to confusion about the term, because the term PDD actually refers to a category of disorders and is not a diagnostic label.

A 2013 review stated that life expectancy for FXS was 12 years lower than the general population and that the causes of death were similar to those found for the general population.

Treatments for HFA address individual symptoms, rather than the condition as a whole. For instance, to treat anxiety, which is often associated with HFA, the main treatment is cognitive behavior therapy. While this is the tested and approved treatment for anxiety, it does not quite meet the needs associated with the symptoms of HFA. There is very little discussion of the parent's role in anxiety intervention for children and teenagers. A revised version of cognitive behavior therapy has parents and teachers acting in a role as social coaches to help the children or young adults cope with the issues they are facing. There have been several trials proving that the involvement of parents in the lives of the children affected with anxiety associated with HFA is important.

No single intervention exists to aid individuals with high-functioning autism. However, there are proactive strategies, such as self care and self-management, designed to maintain or change behavior to make living with high functioning autism easier. Self-management strategies aim to provide skills necessary to self-regulate behavior, leading to greater levels of independence. Improving self-management skills allows the individual to be more self-reliant rather than having to rely on an external source for supervision or control. Self-monitoring is a framework, not a rigid structure, designed to encourage independence and self-control. Self-monitoring is not for everyone. It requires the attention and dedication of the individual with high-functioning autism as well as the individual overseeing the progress.

A framework for self-monitoring is provided below

- Identify positive target behaviors

- Establish an alternative behavior that is positive/constructive

- Establish a self-recording sheet

- Individuals can make sure to stay on track with intended goals

- Set goals and keep them

The goal of self-monitoring is to enforce self-monitoring independently without prompting.

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.

Current trends in treating the disorder include medications for symptom-based treatments that aim to minimize the secondary characteristics associated with the disorder. If an individual is diagnosed with FXS, genetic counseling for testing family members at risk for carrying the full mutation or premutation is a critical first-step. Due to a higher prevalence of FXS in boys, the most commonly used medications are stimulants that target hyperactivity, impulsivity, and attentional problems. For co-morbid disorders with FXS, antidepressants such as selective serotonin reuptake inhibitors (SSRIs) are utilized to treat the underlying anxiety, obsessive-compulsive behaviors, and mood disorders. Following antidepressants, antipsychotics such as Risperdal and Seroquel are used to treat high rates of self-injurious, aggressive and aberrant behaviors in this population (Bailey Jr et al., 2012). Anticonvulsants are another set of pharmacological treatments used to control seizures as well as mood swings in 13%–18% of individuals suffering from FXS. Drugs targeting the mGluR5 (metabotropic glutamate receptors) that are linked with synaptic plasticity are especially beneficial for targeted symptoms of FXS. Lithium is also currently being used in clinical trials with humans, showing significant improvements in behavioral functioning, adaptive behavior, and verbal memory. Alongside pharmacological treatments, environmental influences such as home environment and parental abilities as well as behavioral interventions such as speech therapy, sensory integration, etc. all factor in together to promote adaptive functioning for individuals with FXS.

Current pharmacological treatment centers on managing problem behaviors and psychiatric symptoms associated with FXS. However, as there has been very little research done in this specific population, the evidence to support the use of these medications in individuals with FXS is poor.

ADHD, which affects the majority of boys and 30% of girls with FXS, is frequently treated using stimulants. However, the use of stimulants in the fragile X population is associated with a greater frequency of adverse events including increased anxiety, irritability and mood lability. Anxiety, as well as mood and obsessive-compulsive symptoms, may be treated using SSRIs, although these can also aggravate hyperactivity and cause disinhibited behavior. Atypical antipsychotics can be used to stabilise mood and control aggression, especially in those with comorbid ASD. However, monitoring is required for metabolic side effects including weight gain and diabetes, as well as movement disorders related to extrapyramidal side effects such as tardive dyskinesia. Individuals with coexisting seizure disorder may require treatment with anticonvulsants.

There is currently no specific treatment for megalencephaly, however periodic head measurements may be assessed to determine the rate of brain growth.

Those individuals who develop neurological disorders may be prescribed anti-epileptic drugs for seizures. Studies have shown that reducing epilepsy can increase cell apoptosis and reduce the proliferation of neurons that ultimately leads to brain overgrowth.

Although little is known about the biological basis of autism, studies have revealed structural abnormalities in specific brain regions. Regions identified in the "social" brain include the amygdala, superior temporal sulcus, fusiform gyrus area and orbitofrontal cortex. Further abnormalities have been observed in the caudate nucleus, believed to be involved in restrictive behaviors, as well as in a significant increase in the amount of cortical grey matter and atypical connectivity between brain regions.

There is a mistaken belief that some vaccinations, such as the MMR, the measles/mumps vaccine, may cause autism. This was based on a research study published by Andrew Wakefield, which has been determined fraudulent and retracted. The results of this study caused some parents to take their children off the vaccines; these diseases can cause intellectual disabilities or death. The claim that some vaccinations cause autism has not been proven through multiple large-scale studies conducted in Japan, the United States, and other countries.

There are no objectively definitive statistics about how many people have savant skills. The estimates range from "exceedingly rare" to one in ten people with autism having savant skills in varying degrees. A 2009 British study of 137 parents of autistic children found that 28% believe their children met the criteria for a savant skill, defined as a skill or power "at a level that would be unusual even for 'normal' people". As many as 50 cases of sudden or acquired savant syndrome have been reported.

Males with savant syndrome outnumber females by roughly 6:1, slightly higher than the sex ratio disparity for autism spectrum disorders of 4.3:1.

Since there are very few treatment methods focused on managing megalencephaly, future research is targeted at inhibiting mutation of the pathway. However, this next step could be met with several complications as understanding the underlying mechanism of the mutation is a difficult task. The genetic coding that initiates a single mutation is sporadic and patterns are hard to detect in many cases.

Even thought very little research has been done to create inhibitors of the PI3K-AKT pathway, several pharmaceutical companies have begun to focus their interests in designing a prevention method for this purpose.

Currently there is no cure for Rett syndrome. Treatment is directed towards improving function and addressing symptoms throughout life. A multi-disciplinary team approach is typically used to treat the person throughout life. This team may include primary care physician, physical therapist, occupational therapist, speech-language pathologist, nutritionist, and support services in academic and occupational settings.

Treatment of Rett syndrome includes:

Because of the increased risk of sudden cardiac death, when long QT syndrome is found on an annual screening EKG it is treated with an anti-arrhythmic such as a beta-blocker. There is some evidence that phenytoin may be more effective than a beta-blocker.

Mind-blindness is a cognitive disorder where an individual is unable to attribute mental states to others. As a result of this kind of social and empathetic cognitive deficit, the individual is incapable in putting himself "into someone else's shoes" and cannot conceptualize, understand or predict knowledge, thoughts and beliefs, emotions, feelings and desires, behaviour, actions and intentions of another person. Such an ability to develop a mental awareness of what is in the other minds is known as the theory of mind (ToM), and the "Mind-blindness" Theory asserts that children who delay in this development often are or will be autistic and Asperger's syndrome (AS) patients. In addition to autism and AS, ToM and mind-blindness research has recently been extended to other disorders such as schizophrenia, dementia, bipolar disorders, antisocial personality disorders as well as normal aging.

Males with pathogenic "MECP2" mutations usually die within the first 2 years from severe encephalopathy, unless they have an extra X chromosome (often described as Klinefelter syndrome), or have somatic mosaicism.

Male fetuses with the disorder rarely survive to term. Because the disease-causing gene is located on the X chromosome, a female born with an MECP2 mutation on her X chromosome has another X chromosome with an ostensibly normal copy of the same gene, while a male with the mutation on his X chromosome has no other X chromosome, only a Y chromosome; thus, he has no normal gene. Without a normal gene to provide normal proteins in addition to the abnormal proteins caused by a MECP2 mutation, the XY karyotype male fetus is unable to slow the development of the disease, hence the failure of many male fetuses with a MECP2 mutation to survive to term.

Females with a MECP2 mutation, however, have a non-mutant chromosome that provides them enough normal protein to survive longer. Research shows that males with Rett syndrome may result from Klinefelter's syndrome, in which the male has an XXY karyotype. Thus, a non-mutant "MECP2" gene is necessary for a Rett's-affected embryo to survive in most cases, and the embryo, male or female, must have another X chromosome.

There have, however, been several cases of 46,XY karyotype males with a MECP2 mutation (associated with classical Rett syndrome in females) carried to term, who were affected by neonatal encephalopathy and died before 2 years of age. The incidence of Rett syndrome in males is unknown, partly owing to the low survival of male fetuses with the Rett syndrome-associated MECP2 mutations, and partly to differences between signs caused by MECP2 mutations and those caused by Rett's.

Females can live up to 40 years or more. Laboratory studies on Rett syndrome may show abnormalities such as:

- EEG abnormalities from 2 years of age

- atypical brain glycolipids

- elevated CSF levels of "beta"-endorphin and glutamate

- reduction of substance P

- decreased levels of CSF nerve growth factors

A high proportion of deaths are abrupt, but most have no identifiable cause; in some instances death is the result most likely of:

- spontaneous brainstem dysfunction

- cardiac arrest, likely due to long QT syndrome, ventricular tachycardia or other arrhythmias

- seizures

- gastric perforation

Developmental disorders comprise a group of psychiatric conditions originating in childhood that involve serious impairment in different areas. There are several ways of using this term. The most narrow concept is used in the category "Specific Disorders of Psychological Development" in the ICD-10. These disorders comprise language disorders, learning disorders, motor disorders and autism spectrum disorders. In broader definitions ADHD is included, and the term used is neurodevelopmental disorders. Yet others include antisocial behavior and schizophrenia that begins in childhood and continues through life. However, these two latter conditions are not as stable as the other developmental disorders, and there is not the same evidence of a shared genetic liability.

Developmental disorders are present from early life. They usually improve as the child grows older, but they also entail impairments that continue through adult life. There is a strong genetic component, and more males are afflicted than females.