Neuropsychology is an area of psychology that studies the relationships between the brain and the mind and how they affect behavioral control. The traditional approach in neuropsychology involved looking for connections between brain injuries and psychological abnormalities. However, this approach has since changed with the advancement of theoretical models and sophisticated methodologies that elucidate the working of the brain and mind (Keller, 2019). This paper discusses the neuropsychology of autism and describes its etiology, neuropsychological manifestations, treatment recommendations, and areas for future research.
Description of the Neurological Disorder
Autism is a neurodevelopmental disorder that is exemplified by social and communication insufficiencies as well as a constrained and repetitive range of behaviors, activities, or interests. Challenges in social communication often manifest as problems in social-emotional balance and difficulties in using nonverbal exchanges in social interactions and relationships (Matson, 2016; Keller, 2019). Examples of repetitive behaviors include extreme observance of routines, typecast speech, habitual displays of verbal or nonverbal mannerisms, fixated interests, and resistance to change. All these symptoms occur in early childhood, usually before a child reaches 3 years. However, they may not become obvious until social requirements hamper normal functioning. Patients exhibit varying symptoms at different intensities. As a result, the disorder is also referred to as Autism spectrum disorder (ASD) to cater to these differences. Clinically, these differences may be characterized as Asperger syndrome (AS) or high-functioning autism (HFA) individuals among other labels (de Giambattista et al., 2019). The precise presentation often influences the selected treatment option. In this paper, the terms ASD and autism are used interchangeably.
Etiology and Organic Bases
Data on the etiology of autism show that the disorder occurs due to various causal factors, which can be genetic, epigenetic, neurobiological, or environmental. Thus, the causes of ASD are multifaceted and heterogeneous. This section describes each of these etiologies of autism.
Genetic Risk Factors
Some families are more likely to have autism than others because of their inherent genetic makeup. Mutations in specific genes elevate the risk of developing autism. If these mutated genes are passed from parent to offspring, they increase the child’s predisposition to the disorder even if the parent does not suffer from autism. Studies into the genetic causes of ASD indicate that the prevalence of the disorder is higher in males than females, which is attributed to the protective effects of the X chromosome (Loomes et al., 2017). Identical twins are more likely to have ASD than fraternal twins (Yuen et al., 2017). Having an older biological sibling with autism increases the risk of developing the disease. This risk is augmented if more than one older sibling has the disease. Advances in gene sequencing technologies have led to the identification of more than 61 candidate genes associated with ASD.
Epigenetics refers to the investigation of changes in organisms due to alterations in gene expression as opposed to modifications in the genetic sequence. Epigenetic mechanisms such as epimutations, genomic imprinting, and copy number variations (CNVs) are implicated in the development of ASD. Copy number variation occurs when the number of copies of a given gene differs from one person to the next. Clinically important CNVs have been identified in 7 to 14% of patients diagnosed with idiopathic ASD, whereas sporadic autism has been linked to infrequent de novo changes in copy number (Wiśniowiecka-Kowalnik & Nowakowska, 2019). Other epigenetic changes noted in autism include DNA methylation in the PRRT1, FAM181A, CHFR, MAP8KIP3, NALP1L5, and AURKA genes, histone modifications, changes in the expression of epigenetic proteins, transgenerational inheritance, and microRNA dysregulation (Eshraghi et al., 2018).
The environment, particularly prenatal and postnatal factors influence the development of autism in people who are genetically predisposed to the disease. These factors include exposure to drugs (psychotropic medications, antidepressants, misoprostol, paracetamol, beta-adrenergic agonists, thalidomide, and antipyretics), environmental toxins (such as lead, hydrocarbons, insecticides, flame retardants, polychlorinated biphenyls), and dietary factors (iron, folate, thiamine, and vitamin deficiency) (Karimi et al., 2017). Conflicting outcomes have been obtained on advanced parental age with some studies suggesting that having children at the age of 34 or older increases the risk of autism (Wu et al., 2017). However, this assumption has been refuted in other studies (Byars & Boomsma, 2016). Other environmental factors that may influence the development of autism include the physical and mental maternal and familial socioeconomic status. A low socioeconomic standing is associated with a higher risk of autistic children. Natal factors such as very short or prolonged gestation ages (less than 35 weeks and greater than 42 weeks) increase the risk of autism. Furthermore, pregnancy complications such as fetal distress, cesarean delivery, and fetal nuchal cord result in fetal insufficiencies in oxygen (hypoxia), blood, and nutrition, which ultimately increases the risk of autism (Karimi et al., 2017).
Anomalies in the genes can lead to abnormal mechanisms of brain development, which can result in structural and functional aberrations of the brain, symptomatic mannerisms, and neurobiological oddities (Keller, 2019). Examples of physical and functional irregularities in the developing are a buildup of gray matter in the temporal and frontal lobes, a smaller proportion of white to grey matter by puberty, morphological and operational discrepancies in the limbic system and cerebellum, and synaptic insufficiencies that hamper neuronal circuits and physical structures (Matson, 2016). Additionally, the brain’s response to the environment can generate symptomatic behaviors such as low neural sensitivity to active gaze changes during infancy, an inclination to nonsocial processing, an inclination to hemispheric irregularities, and changes in conventional outlines of social neurodevelopment, which decreases response to social stimuli.
Nevertheless, identifying the cellular nature of autism and comprehending the association between genetic changes and neurobiological upshots is convoluted by several factors. They include variations in brain growth and development, heterogeneity in genetic differences that cause autism, and problems separating major and minor consequences in developmental syndromes. Another common problem is the pleiotropy of candidate genes, which means that a single gene may affect various traits.
Neuropsychological manifestations of autism refer to changes in five domains of intelligence, attention, executive function, social cognition, and praxis. There is a negative correlation between autistic attributes and neuropsychological functioning along a continuum (Hyseni et al., 2019). An increase in autistic traits results in a decrease in neuropsychological performance. This correlation is significant even after making amendments for obfuscating variables such as gender, ethnicity, age, household income, maternal education, and maternal practices such as alcohol and tobacco use during pregnancy.
The Diagnostic and Statistical Manual of Mental Disorders (DSM-5) description of autism indicates that individuals with the disorder have attention aberrances. Furthermore, attention-deficit/hyperactivity disorder (ADHD) can co-occur with autism (Matson, 2016; Zwick, 2017; Keller, 2019). Therefore, this combination can further worsen patients’ adaptive skills more than when one of these disorders occur alone. Attention deficits in autism lead to exhaustion and decelerate the patient’s cognitive performance. Joint attention, which is the common focus of at least two people on one occurrence or object, is another aspect that is hampered in ASD. The manifestations of inadequacies in joint attention include trouble orientating to people in shared surroundings, limited range of expansive functions to obtain reassurance and engagement from others, difficulties identifying and explaining other people’s emotional standing, intents, and perceptions, and trouble focusing on an item or occurrence.
About five facets of attention are usually evaluated in ASD. They include working memory, inhibition, updating, cognitive flexibility, and planning. Working memory holds information temporarily and aids in the manipulation of this information by relating it to longstanding memories. Therefore, working memory has a substantial effect on problem-solving potential, learning, and thinking. It is also needed in social and formal situations, for instance, holding a conversation without forgetting crucial details or executing multiple instructions simultaneously. Inhibition is the capacity to withhold unwanted reactions. This facet is linked to behavioral regulation. Inadequacies in this function cause difficulty in social interactions by failing to react appropriately to stressful conditions (Zwick, 2017). Updating, in contrast, is the capacity to regenerate the contents of memory by in a goal-oriented manner. Anomalies in this function cause unbalanced thinking and difficulties in understanding, which hamper social interaction.
Cognitive flexibility denotes the capacity to change to a different train of thought based on the prevailing circumstances. Anxiety symptoms in autism have a negative effect on cognitive flexibility. Hence, individuals with ASD find it hard to adapt to changing environments accordingly, thereby increasing their stress levels. Planning denotes the process of making multiplex operations that follow a precise sequence, making follow-ups, reassessing, and restructuring. Successful planning cannot take place in the absence of other executive functions (Zwick, 2017). Autism results in planning inadequacies, which hinders the implementation of activities in everyday life, such as running a household or preparing meals without external assistance.
Praxis denotes the capacity to theorize, strategize, and execute resolute motor actions successfully. ASD causes anomalies in motor skills, which may manifest as clumsiness or developmental coordination disorder (DCD), also referred to as dyspraxia (Sokhadze et al., 2016). Issues with praxis can have extensive implications on private and public life. Some of the private facets of life that may be affected include washing, dressing, and using utensils. Conversely, public aspects that suffer due to praxis issues include poor work or academic performance, exhaustion, and excessive slowness. Praxis also affects social skills, for example, social communication and interactions, which are common abnormalities in autism.
Cognitive deficits in autism may manifest as either social cognition during communal interactions or deficiencies in cognitive functions such as language. Social cognition is a collection of cognitive functions that permit meaningful interactions among people. It can also denote the psychological processes that are used during perception, thinking, or understanding people during social interactions. Autism affects social cognition by impairing core components such as emotion perception, theory of mind, social perception, attributional style, and social knowledge (Lord et al., 2020). Few neuropsychological tests are available for these domains. Therefore, their evaluation is often carried out through qualitative observations.
Theory of mind denotes the ability to ruminate on what is on their minds as well as other people’s thoughts. The inability to imagine other people’s needs or intents often results in misunderstandings in many social dealings, which may ultimately cause self-isolation. Emotion perception refers to being cognizant of other people’s emotions, which is a necessary component of social dealings (Nakagawa & Chiba, 2016). Failure to recognize emotional information leads to misconstrued voice tone, facial expressions, and body language, thereby impairing social discernment.
Conversely, attributional style illustrates people’s elucidation of good and bad events in their lives. Overall, occurrences are attributed to diverse origins. Nonetheless, diminished attributional style results in an exaggeration of causative factors, leading to the attribution of responsibility to one cause. For instance, an individual may hold themselves responsible for adverse events (depressive bias) or extreme suspicion of other people (hostile bias). Shortfalls in social cognition may also encompass difficulties in communal and emotional learning, comprehending and controlling emotions, creating prosocial targets, and using relational skills to deal with developmentally pertinent tasks (Schmitt et al., 2018). Individuals with ASD may find it hard to tell apart between feelings of different parties or to assimilate different information in a given context.
Challenges in cognitive skills such as language may affect a total of 7 areas, including a poor acquisition of vocabulary, phrases, and syntax; challenges in comprehending verbal and nonverbal communication; inadequacies in vocal development; conversational shortfalls, executive function shortcomings; symbolic play deficiencies, and literacy limitations. Impeded acquisition of new words and phrases may present as late attainment of words that denote social impetuses such as nouns and attributes, loss of previously acquired words, and the application of echolalia, which is the reiteration of expressions used by other people (Schmitt et al., 2018). Inadequacies in vocal development may manifest as uncharacteristic reactions to verbal communication of caregivers, unusual voice productions, and aberrant prosody following the emergence of speech, which means that speech may sound mechanical.
Conversation shortfalls may include a limited comprehension and application of conventional norms in conversation, for instance, voice volume, intonation, prosody, and timing of conversations. Redundant or unnecessary information may be included in conversations. In contrast, pertinent details may be omitted during conversations. Taking turns during conversation may be problematic as well as beginning topics of common interest. Instead, patients with ASD may prefer to dwell on conversations on topics of special interests. They may not understand the need for clarification, which may prevent them from asking any questions related to the discussion (Nakagawa & Chiba, 2016). Patients with autism may not realize when they miscommunicate or the need to rectify such errors. Their comprehension of figurative speech, including idioms, sarcasm, or the multiple meanings of words is limited.
Symbolic shortcomings include late attainment of normal and functional use of items, monotonous and rigid inventive play, and restricted cooperative play in collaborative settings. Conversely, literacy insufficiencies include problems in reading, comprehending accounts and expository types of text that need more than one outlook, for example, argumentative, or comparative versus contrastive tests. Other challenges in literacy shortfalls include the inability to identify the main idea and summarize a piece of text, which leads to the provision of inadequate information during writing (Schmitt et al., 2018). Scarcities in executive functioning may manifest as the absence of or poor flexibility, inability to solve problems, poor planning and organization, and poor inhibition.
Neuropsychological Assessment Tools
The diagnosis of autism follows the American Psychiatric Association’s DSM-5 criteria. The patient should present with consistent insufficiencies in social communication and interaction, particularly in socio-emotional reciprocity, non-verbal communication applied in social interactions, and difficulties creating, sustaining, and comprehending relationships (criterion A). The patient should also demonstrate limited, repetitive behaviors by having at least two of the following indications: repetitive movement, dialogue or the use of objects, obsession with specific interests or attachments, unyielding observance to routines, and excessive or very low reactivity to sensory signals (criterion B). The above indications must be evident in the early phases of development (criterion C) and must result in a clinically substantial deficiency in occupational, social, or other functional areas (criterion D). These impairments should not be attributed to developmental delays or intellectual disability (criterion E) (Gardner et al., 2018; Autism Speaks, 2020). The severity of criteria A and B should be indicated, which can be level I (needing support), level II (needing significant support), or level III (needing very significant support).
Apart from the DSM-5 criteria, the second edition of the Autism Diagnostic Observation Schedule (ADOS-2) is used to diagnose ASD across the lifespan from children aged 12 months to adults. ADOS-2 is considered the gold standard in the assessment of autism in children and adults. It is a semi-structured instrument that evaluates the four critical areas of autism, including play, social interactions, communication, and repetitive behaviors (Sorokin & Davydova, 2017). ADOS-2 comprises five modules based on the chronological age and the patient’s extent of expressive language. The toddler module applies to children aged 12 to 30 months. The administration of the instrument entails observing the patient, coding their behavior, and scoring. This process lasts between 40 to 60 minutes (Maddox et al., 2017). The findings of this tool direct the diagnosis, planning of therapy, and educational adjustments.
Additional tools can be used for a detailed evaluation of other neuropsychological manifestations of ASD. For example, NEPSY-II is used in the neuropsychological assessment of cognitive functions in children aged between 3 and 16 years. NEPSY-II has six domains such as attention and executive functioning, language, memory and learning, sensorimotor, social perception, and visual processing (Hyseni et al., 2019). The instrument has 32 subsets, which includes 23 items from the first edition and 9 new items. The Social Responsiveness Scale (SRS) measures the severity of autism symptoms, particularly those associated with social behavior. It consists of 65 items and is highly sensitive to subtle symptoms, which makes it possible to distinguish between clinical groups (Li et al., 2018). Therefore, SRS can monitor symptoms across varying developmental stages. Intelligence can be measured using the Wechsler Intelligence Scales (WIS), which is available in different versions for various ages. This psychometric test can differentiate between practical and linguistic intelligence, which makes it possible to ascertain a patient’s level of intelligence (Rabiee, 2019). WIS measures four main indices of working memory index (WMI), verbal communication index (VCI), processing speed index (PSI), and perceptual reasoning index (PRI).
Profile of Findings
The scores obtained in modules 1 to 4 of ADOS-2 are likened to cut-off scores, leading to the classification of the diagnosis as autism, autism spectrum, and non-spectrum (Maddox et al., 2017). However, the toddler module only identifies areas of concern as opposed to the classification of the disorder. The NEPSY-II findings are scored based on each of the administered subsets. The outcomes may be at the borderline, at the anticipated level, above the expected level or below the normal level.
Findings from the Wechsler Intelligence Scale for children (WISC) can diagnose high-functioning autism in patients with IQ scores that are greater than 70. There are no substantial differences in the WISC scores between typically developing and children diagnosed with high-functioning autism in terms of matrix reasoning and comprehension (Rabiee et al., 2019). However, children with autism often have slower processing speeds. The VCI scores have a negative correlation with communication deficiencies, whereas WMI totals have a positive correlation with social manifestations in patients with ASD. This finding emphasizes the importance of processing speed (Haigh et al., 2018). Communication capabilities have a positive correlation with processing speed and execution of tasks. However, as processing speed declines, there is a reduction in communication skills and a higher incidence of communication symptoms.
Cognitive profiles of individuals with autism differ according to sex. Male patients with autism often exhibit higher verbal capacities, whereas females with the disorder have better processing speeds and enhanced cognitive functioning (Lehnhardt et al., 2016). The rationale for these differences is that females tend to have better social skills that enable them to camouflage their autistic symptoms more effectively than males (Dean et al., 2017). These discrepancies influence diagnosis and therapy.
Brain connectivity differs across different developmental stages in people with autism (Dajani & Uddin, 2016; Van Rooij et al., 2018). For instance, overconnectivity is commonly observed in children while adults and teenagers present with underconnectivity (Keller, 2019). Therefore, cognitive functions are also likely to differ across the lifespan. An increase in age corresponds to a decline in cognitive functions, particularly in executive functioning, cognitive flexibility, and attentional tasks such as fluency, working memory (Powell et al., 2017; Keller, 2019). However, no differences have been noted between the verbal memory and visual searching tasks between autistic elderly and those with typical development.
Psychological Manifestations (Behavioral and Emotional)
Some of the notable behavioral and emotional challenges in patients include difficulties handling changes in normal routines or transitioning from one activity to another as well as simplifying acquired skills. Patients with ASD may tend to use objects in unconventional ways and develop rare attachments to objects. Other unusual behaviors include unwarranted anger or laughing at inappropriate times. They may experience anxiety and social withdrawal because of cognitive shortfalls that hamper their social interactions, for example, misconceptions of social events or the inability to recognize pertinent information. Consequently, depression may ensue due to problems with socialization. Other symptoms include trouble sleeping, poor self-management, limited and repetitive manners, interests, or actions, utilizing eccentric behavioral stratagems and emotive expressions such as belligerence, throwing tantrums, and running away from situations (Lord et al., 2020). Patients with ASD may also use idiosyncratic approaches to self-regulation, for example, flapping of hands, chewing on clothing, rocking, or production of strange sounds.
Psychosocial manifestations may also present as sensory and feeding problems. Examples of sensory problems include overreaction and under-responsiveness or mixed pattern reactions to sounds, touch, smell, movement, and visual disorder. There may be mixed reactions to social cues such as voice, social touch, and closeness of other people. Patients with autism may be inclined to nonsocial stimuli, which may bring about string interests with the sensory features of items and occurrences (Lord et al., 2020). In contrast, feeding challenges may include habitually rejecting or accepting certain foods based on their texture or how it is presented. As a result, such patients may end up with a limited variety of foods.
The goal of treatment in ASD is to maximize the patient’s strengths and solve weaknesses associated with the main features of the disease. Therapy also aims at promoting normal life by enhancing communication skills and physical activity. Other treatment goals include changing contextual factors to eliminate obstacles and boost the enablers of successful communication by making pertinent adaptations. The current treatment options in ASD can be classified broadly as psychosocial or behavioral, pharmacological, and complementary alternative medicine.
Behavioral or Psychosocial Therapies
The gold-standard treatment for behavioral manifestations in autism is behavioral interventions commenced in the early stages of life using a rigorous delivery approach. Applied behavior analysis (ABA) is a form of therapy that is founded on operant conditioning and learning theories (Roane et al., 2016). It entails the use of precise intervention targets alongside positive reinforcement such as edible incentives, verbal compliments, or tokens. Reiteration of learning-trials forms a major constituent in the treatment. Prompt, rigorous ABA intermediation is assumed to elicit positive outcomes such as substantial improvements in lead intelligence quotient (IQ) points (DeFilippis & Wagner, 2016).
Another behavioral intermediation is Pivotal Response Treatment (PRT), which entails a true-to-life behavioral technique that is directed at precise skills and motivations (pivotal areas). The rationale for PRT is that it elicits more widespread benefits in additional areas that the therapy does not target directly, for example, joint attention. The main advantage of PRT is that it takes a shorter time than ABA treatments. Findings from a randomized, controlled trial indicated that PRT enhanced practical and adaptive communication dexterities in children between the ages of 2 to 6 years who had diagnoses of ASD and language delay (Ona et al., 2020). PRT generates better outcomes than ABA in terms of improvements in verbal expressive communication following three months of treatment. An additional benefit of PRT is that it reduces disruptive behaviors in the course of PRT treatment as opposed to ABA. Psychosocial interventions are useful in managing the behavioral symptoms associated with ASD. However, their benefits are curtailed by prolonged treatment durations and high costs, which are inaccessible to most families with low incomes.
The US Food and Drug Administration (FDA) approved two pharmacological agents for the treatment of autism symptoms. These drugs are risperidone and aripiprazole (Ichikawa et al., 2017). Risperidone is an antipsychotic medication that is used in adults. It was authorized in 2006 to manage symptoms such as belligerence, irritability, tantrums, and premeditated injury in children and teenagers with autism. Risperidone exerts its effects by impeding the brain’s receptors for dopamine and serotonin. The safety and efficacy of this drug have been demonstrated in short-term use, with improvements in hyperactivity and monotonous behavior (Masi et al., 2017). Nonetheless, treatment with risperidone results in undesired consequences such as excessive sleepiness and an increase in weight. There is an elevated production of the hormone prolactin from the pituitary gland, which may produce feminizing upshots in males and females (Scahill et al., 2016; Maneeton et al., 2018). The magnitude of the side effects is proportional to the dose administered. Most patients on risperidone therapy discontinue the treatment due to somnolence.
Aripiprazole, a third-generation atypical antipsychotic agent, is approved for the treatment of irritability in children and teenagers with ASD (Bartram et al., 2019). However, this drug is also associated with adverse events such as exhaustion, sedation, vomiting, shaking, excessive sleepiness, and augmented appetite. Treatment discontinuation usually happens as a result of weight gain and aggression. Aripiprazole stabilizes the dopamine system and has a lower chance of increasing serum prolactin concentrations. Therefore, the extrapyramidal indications noted with the use of risperidone are unlikely with aripiprazole.
Given that ASD patients may exhibit some indications that are common in other psychiatric ailments, it is necessary to look into the efficacy of other pharmacotherapeutic agents in managing these overlapping symptoms. For example, the use of antidepressants to manage autism symptoms has been investigated due to the occurrence of symptoms such as monotonous, ritualistic behaviors and persistence on limited routine patterns, which are also observed in depression. Some of the drugs that have been tested include selective serotonin reuptake inhibitors and tricyclic antidepressants, and mood stabilizers such as divalproex sodium. These medications have led to improvements in autism symptoms (Masi et al., 2017). Furthermore, the efficacy of methylphenidate, atomoxetine, and clonidine, which are ADHD medications, is proven for signs such as a lack of attention, impetuosity, and overactivity.
Complementary Alternative Medicine
The use of complementary alternative medicine (CAM) for the treatment of autism has also been explored. For instance, the use of controlled-release melatonin for sleep disturbances in children and adolescents alone and combined with cognitive-behavioral therapy (CBT) has yielded positive outcomes with high levels of safety and tolerability (DeFilippis & Wagner, 2016). Varying effects have been obtained with the use of omega-3 fatty acids and methyl B12 with some studies reporting significant improvements (Cheng et al., 2017; Hendren et al., 2016; DeFilippis & Wagner, 2016). Implementing dietary restrictions and administration of digestive enzymes is useful in improving the gastrointestinal symptoms associated with autism but does not resolve the core symptoms.
Findings from systematic reviews show that cognitive, environmental, social, and genetic differences result in highly diverse autism phenotypes, which ultimately introduces significant variations in study samples. Consequently, the potential effect size of interventions is reduced. Therefore, future research should consider conducting trials that focus on the effect of treatments in groups of patients who exhibit similar social, environmental, genetic, and cognitive characteristics. A notable area of interest is that autism in children poses a significant caregiver burden. It would be interesting to conduct a study on the views and perceptions of caregivers of autism patients to determine ways in which healthcare providers can help them to manage their patients more effectively.
Autism is a range of disorders that are typified by deficits in communication and learning. The etiology of the condition is linked to diverse genetic, epigenetic, environmental, and neurobiological factors. As a result, the disorder is highly heterogeneous because different etiological causes elicit varying neuropsychological manifestations. Furthermore, the heterogeneity of autism influences the choice and efficacy of different treatment modalities. Currently, the disorder can be managed through behavioral interventions, pharmacological agents, or complementary alternative medicine. The application of behavioral interventions is limited by cost, which makes it inaccessible to patients from low socioeconomic backgrounds. Risperidone and aripiprazole are the two main drugs approved by the FDA for the treatment of autism. However, due to the overlap of symptoms with other mental health disorders, many other drugs such as antidepressants and antipsychotic agents have been tested in the treatment of precise symptoms. Trials on different medications or treatment modes often yield different outcomes due to the heterogeneity of the disease, which limits the study samples. Future studies could consider investigating new medications in standardized patient groups.
Autism Speaks. (2020). Autism diagnosis criteria: DSM-5. Web.
Bartram, L. A., Lozano, J., & Coury, D. L. (2019). Aripiprazole for treating irritability associated with autism spectrum disorders. Expert Opinion on Pharmacotherapy, 20(12), 1421-1427. Web.
Byars, S. G., & Boomsma, J. J. (2016). Opposite differential risks for autism and schizophrenia based on maternal age, paternal age, and parental age differences. Evolution, Medicine, and Public Health, 2016(1), 286-298. Web.
Cheng, Y. S., Tseng, P. T., Chen, Y. W., Stubbs, B., Yang, W. C., Chen, T. Y., Wu, C. K., & Lin, P. Y. (2017). Supplementation of omega 3 fatty acids may improve hyperactivity, lethargy, and stereotypy in children with autism spectrum disorders: A meta-analysis of randomized controlled trials. Neuropsychiatric Disease and Treatment, 13, 2531-2543. Web.
Dajani, D. R., & Uddin, L. Q. (2016). Local brain connectivity across development in autism spectrum disorder: A cross‐sectional investigation. Autism Research, 9(1), 43-54. Web.
de Giambattista, C., Ventura, P., Trerotoli, P., Margari, M., Palumbi, R., & Margari, L. (2019). Subtyping the autism spectrum disorder: Comparison of children with high functioning autism and Asperger syndrome. Journal of Autism and Developmental Disorders, 49(1), 138-150. Web.
Dean, M., Harwood, R., & Kasari, C. (2017). The art of camouflage: Gender differences in the social behaviors of girls and boys with autism spectrum disorder. Autism, 21(6), 678-689. Web.
DeFilippis, M., & Wagner, K. D. (2016). Treatment of autism spectrum disorder in children and adolescents. Psychopharmacology Bulletin, 46(2), 18-41.
Eshraghi, A. A., Liu, G., Kay, S. I. S., Eshraghi, R. S., Mittal, J., Moshiree, B., & Mittal, R. (2018). Epigenetics and autism spectrum disorder: Is there a correlation? Frontiers in Cellular Neuroscience, 12, 78. Web.
Gardner, L. M., Campbell, J. M., Keisling, B., & Murphy, L. (2018). Correlates of DSM-5 autism spectrum disorder levels of support ratings in a clinical sample. Journal of Autism and Developmental Disorders, 48(10), 3513-3523. Web.
Haigh, S. M., Walsh, J. A., Mazefsky, C. A., Minshew, N. J., & Eack, S. M. (2018). Processing speed is impaired in adults with autism spectrum disorder, and relates to social communication abilities. Journal of Autism and Developmental Disorders, 48(8), 2653-2662. Web.
Hendren, R. L., James, S. J., Widjaja, F., Lawton, B., Rosenblatt, A., & Bent, S. (2016). Randomized, placebo-controlled trial of methyl B12 for children with autism. Journal of Child and Adolescent Psychopharmacology, 26(9), 774-783. Web.
Hyseni, F., Blanken, L. M., Muetzel, R., Verhulst, F. C., Tiemeier, H., & White, T. (2019). Autistic traits and neuropsychological performance in 6-to-10-year-old children: A population-based study. Child Neuropsychology, 25(3), 352-369. Web.
Ichikawa, H., Mikami, K., Okada, T., Yamashita, Y., Ishizaki, Y., Tomoda, A., Ono, H., Usuki, C. & Tadori, Y. (2017). Aripiprazole in the treatment of irritability in children and adolescents with autism spectrum disorder in Japan: A randomized, double-blind, placebo-controlled study. Child Psychiatry & Human Development, 48(5), 796-806. Web.
Karimi, P., Kamali, E., Mousavi, S. M., & Karahmadi, M. (2017). Environmental factors influencing the risk of autism. Journal of Research in Medical Sciences: The Official Journal of Isfahan University of Medical Sciences, 22. Web.
Keller, R. (Ed.) (2019). Psychopathology in adolescents and adults with autism spectrum disorders. Springer.
Lehnhardt, F. G., Falter, C. M., Gawronski, A., Pfeiffer, K., Tepest, R., Franklin, J., & Vogeley, K. (2016). Sex-related cognitive profile in autism spectrum disorders diagnosed late in life: Implications for the female autistic phenotype. Journal of Autism and Developmental Disorders, 46(1), 139-154. Web.
Li, C., Zhou, H., Wang, T., Long, S., Du, X., Xu, X., Yan, W., & Wang, Y. (2018). Performance of the autism spectrum rating scale and social responsiveness scale in identifying autism spectrum disorder among cases of intellectual disability. Neuroscience Bulletin, 34(6), 972-980. Web.
Loomes, R., Hull, L., & Mandy, W. P. L. (2017). What is the male-to-female ratio in autism spectrum disorder? A systematic review and meta-analysis. Journal of the American Academy of Child & Adolescent Psychiatry, 56(6), 466-474. Web.
Lord, C., Brugha, T. S., Charman, T., Cusack, J., Dumas, G., Frazier, T., Jones, E.J., Jones, R.M., Pickles, A., State, M.W., & Taylor, J. L. (2020). Autism spectrum disorder. Nature Reviews Disease Primers, 6(1), 1-23. Web.
Maddox, B. B., Brodkin, E. S., Calkins, M. E., Shea, K., Mullan, K., Hostager, J., Mandell, D. S., & Miller, J. S. (2017). The accuracy of the ADOS-2 in identifying autism among adults with complex psychiatric conditions. Journal of Autism and Developmental Disorders, 47(9), 2703-2709. Web.
Maneeton, N., Maneeton, B., Putthisri, S., Woottiluk, P., Narkpongphun, A., & Srisurapanont, M. (2018). Risperidone for children and adolescents with autism spectrum disorder: A systematic review. Neuropsychiatric Disease and Treatment, 14, 1811-1820. Web.
Masi, A., DeMayo, M. M., Glozier, N., & Guastella, A. J. (2017). An overview of autism spectrum disorder, heterogeneity and treatment options. Neuroscience Bulletin, 33(2), 183-193. Web.
Matson, J. L. (Ed.) (2016). Handbook of assessment and diagnosis of autism spectrum disorder. Springer.
Nakagawa, Y., & Chiba, K. (2016). Involvement of neuroinflammation during brain development in social cognitive deficits in autism spectrum disorder and schizophrenia. Journal of Pharmacology and Experimental Therapeutics, 358(3), 504-515. Web.
Ona, H. N., Larsen, K., Nordheim, L. V., & Brurberg, K. G. (2020). Effects of pivotal response treatment (PRT) for children with autism spectrum disorders (ASD): A systematic review. Review Journal of Autism and Developmental Disorders, 1-13. Web.
Powell, P. S., Klinger, L. G., & Klinger, M. R. (2017). Patterns of age-related cognitive differences in adults with autism spectrum disorder. Journal of Autism and Developmental Disorders, 47(10), 3204-3219. Web.
Rabiee, A., Samadi, S. A., Vasaghi-Gharamaleki, B., Hosseini, S., Seyedin, S., Keyhani, M., Mahmoodizadeh, A., & Ranjbar Kermani, F. (2019). The cognitive profile of people with high-functioning autism spectrum disorders. Behavioral Sciences, 9(2), 20. Web.
Roane, H. S., Fisher, W. W., & Carr, J. E. (2016). Applied behavior analysis as treatment for autism spectrum disorder. The Journal of Pediatrics, 175, 27-32. Web.
Scahill, L., Jeon, S., Boorin, S. J., McDougle, C. J., Aman, M. G., Dziura, J., McCracken, J.T., Caprio, S., Arnold, L.E., Nicol, G., & Deng, Y. (2016). Weight gain and metabolic consequences of risperidone in young children with autism spectrum disorder. Journal of the American Academy of Child & Adolescent Psychiatry, 55(5), 415-423. Web.
Schmitt, L. M., White, S. P., Cook, E. H., Sweeney, J. A., & Mosconi, M. W. (2018). Cognitive mechanisms of inhibitory control deficits in autism spectrum disorder. Journal of Child Psychology and Psychiatry, 59(5), 586-595. Web.
Sokhadze, E. M., Tasman, A., Sokhadze, G. E., El-Baz, A. S., & Casanova, M. F. (2016). Behavioral, cognitive, and motor preparation deficits in a visual cued spatial attention task in autism spectrum disorder. Applied Psychophysiology and Biofeedback, 41(1), 81-92. Web.
Sorokin, A. B., & Davydova, E. Y. (2017). Autism diagnostic evaluation schedule (ADOS-2) for evaluation of behavior and communication in toddlers with concern of autism spectrum disorder. Autism and Developmental Disorders, 15(2), 38-44. Web.
Van Rooij, D., Anagnostou, E., Arango, C., Auzias, G., Behrmann, M., Busatto, G. F., Calderoni, S., Daly, E., Deruelle, C., Di Martino, A., & Dinstein, I. (2018). Cortical and subcortical brain morphometry differences between patients with autism spectrum disorder and healthy individuals across the lifespan: Results from the ENIGMA ASD Working Group. American Journal of Psychiatry, 175(4), 359-369. Web.
Wiśniowiecka-Kowalnik, B., & Nowakowska, B. A. (2019). Genetics and epigenetics of autism spectrum disorder—current evidence in the field. Journal of Applied Genetics, 60(1), 37-47. Web.
Wu, S., Wu, F., Ding, Y., Hou, J., Bi, J., & Zhang, Z. (2017). Advanced parental age and autism risk in children: A systematic review and meta‐analysis. Acta Psychiatrica Scandinavica, 135(1), 29-41. Web.
Yuen, R. K., Merico, D., Bookman, M., Howe, J. L., Thiruvahindrapuram, B., Patel, R. V., Whitney, J., Deflaux, N., Bingham, J., Wang, Z., & Pellecchia, G. (2017). Whole genome sequencing resource identifies 18 new candidate genes for autism spectrum disorder. Nature Neuroscience, 20(4), 602-611. Web.
Zwick, G. P. (2017). Neuropsychological assessment in autism spectrum disorder and related conditions. Dialogues in Clinical Neuroscience, 19(4), 373-379.