Asperger Syndrome

In subject area: Neuroscience

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Asperger syndrome (AS) is defined as a pervasive developmental disorder characterized by significant impairments in social interaction and restricted behavior, while language skills remain unaffected. It is considered a milder form of autistic disorder.

AI generated definition based on: Neuroeconomics, 2014

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1. Introduction to Asperger Syndrome in Neuro Science

Asperger syndrome (AS) is a pervasive developmental disorder within the autism spectrum disorders (ASD), characterized by marked impairments in social interaction and restricted, repetitive patterns of behavior, with preserved language skills and cognitive development. Hans Asperger first described the syndrome in 1944, noting a group of boys with advanced knowledge in special areas of interest but significant social ineptitude, using the term "autistic psychopathy" to indicate a personality disorder rather than a psychiatric illness. The classification of AS evolved through its inclusion as a distinct diagnostic subcategory in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) and the International Classification of Diseases, Tenth Revision (ICD-10), with diagnostic criteria emphasizing the absence of clinically significant language delay and cognitive impairment, distinguishing it from other ASD forms.

The DSM-IV criteria for AS require qualitative impairment in social interaction and restricted, repetitive, and stereotyped patterns of behavior, interests, and activities, without significant speech deficits or delays in cognitive development and self-help skills. Core behavioral features include social impairments, focused and circumscribed interests, and motor clumsiness, with individuals often displaying poor prosody, tangential speech, and marked verbosity on specific topics. The mean age for AS diagnosis is relatively high, about 8–11 years, due to the lack of early language delay and the later emergence of social difficulties.

There is ongoing debate regarding the distinction between AS and high-functioning autism (HFA), with many studies failing to demonstrate clear differences in behavioral, cognitive, and neurobiological levels, leading to recommendations for subsuming AS under ASD in the DSM-5. The prevalence of AS is estimated at 0.26–0.71%, with a male preponderance.

2. Neurobiological and Genetic Basis of Asperger Syndrome

Neuroanatomical and neuroimaging studies of AS have identified abnormalities in several brain regions, including the amygdala, hippocampus, cerebellum, prefrontal cortex, and temporoparietal junction. Functional imaging studies have demonstrated reduced activation in brain regions important for mentalising, such as the anterior paracingulate cortex, superior temporal sulci, and temporal poles bilaterally, in individuals with AS during mentalising tasks. Structural magnetic resonance imaging (MRI) studies have confirmed white matter microstructural alterations of the superior cerebellar peduncle, which are associated with social impairment in adults with AS. Positron emission tomography (PET) imaging has shown a lack of normal activation of the left prefrontal area in individuals with AS during theory of mind tasks, with activation of neighboring areas instead, suggesting a nonspecific reasoning mechanism for inferring mental states. Dysfunction has also been observed in brain regions subserving social cognition in AS, including the anterior cingulate cortex, prefrontal cortex, temporoparietal junction, amygdala, and periamygaloid cortex. Evidence from imaging studies indicates problems with functional connectivity among separate brain regions in AS.

Genetic studies indicate that AS is polygenic, with many risk genes implicated and requiring large sample sizes for robust statistical detection. Molecular pathways implicated in synaptic plasticity and connectivity in AS include genes such as SHANK3, DISC1, and IRSp53. Rare variants in DISC1 have been associated with AS, and IRSp53, a postsynaptic density scaffolding protein, interacts with SHANK and is implicated in the regulation of dendritic spines. Neurochemical findings in AS point to alterations in gamma-aminobutyric acid (GABA)ergic systems, with evidence for their involvement in pathophysiology.

3. Cognitive and Behavioral Neuroscience of Asperger Syndrome

Individuals with AS typically exhibit a cognitive profile marked by strengths in verbal abilities, with preserved articulation, verbal output, auditory perception, vocabulary, and verbal memory, while showing deficits in fine and gross motor skills, visual motor integration, visual–spatial perception, nonverbal concept formation, and visual memory. AS is associated with good verbal performance, poor visuo-spatial skills, gauche social behavior, and clumsiness, with many difficulties linked to right-hemisphere dysfunction. Average psychometric intelligence and language skills are preserved in AS. Children with AS show impairments in using and reading non-verbal cues and are often aware of their social isolation but unable to compensate for these deficiencies.

The behavioral manifestations include severe difficulty with social interactions, socially naïve and inappropriate behavior, repetitive, narrow, and unusual patterns of behavior and interests, and clumsiness or delayed motor development. Restricted repetitive and stereotyped patterns of behavior, interests, and activities are key features, with additional symptoms such as hypersensitivity to light, touch, noise, or smell, and lack of conversational reciprocity unless explicitly taught. Motor clumsiness and all-encompassing interests can interfere with functioning and intrude on family life.

Neural mechanisms underlying these features involve dysfunctions in the mirror neuron system, with individuals showing weaker activations in Broca's area and reduced cortical thickness in regions of the mirror neuron system, including Broca's area, the inferior parietal lobule, and the superior temporal sulcus. Deficiencies in theory of mind—the ability to understand that other people have unique perspectives and thoughts—may be linked to social-communicative deficits, while weak central coherence, a deficit in integrating details into a coherent global perception, may be linked to a tendency to focus on parts and miss the bigger picture. Research suggests that the kinds of problems that individuals with AS have in directing their behavior may be different from those observed in autism, for example, their problem may be more one of initiating behavior than moving effectively from one behavior to another, perhaps suggesting that different parts of the prefrontal brain are involved in each disorder.

Impaired social cognition impacts communication and adaptive functioning, with children having difficulty inferring the emotions of others from facial and body language, severely limiting their ability to develop and maintain appropriate social relationships. Autobiographical memory deficits are present, with individuals recalling fewer and less-detailed episodic memories than controls, and showing reduced use of possessive pronouns and family-related vocabulary, which may indicate less self-investment in life experiences and impact recall. Overlap is observed with other neurodevelopmental disorders such as nonverbal learning disabilities syndrome and semantic-pragmatic disorder.

4. Developmental Trajectories, Neuroplasticity, and Neuropsychological Assessment

AS is characterized by the same impairment in social interaction and restricted interests as in autistic disorder; however, language skills are relatively normal, with use of single words by age 2 years and phrases by 3 years, and later language is marked by pragmatic deficits in the social use of language. While cognitive and adaptive skills are described as normal, this may vary, and some studies discuss specific cognitive vulnerabilities; children with AS are usually not recognized until after 4 years of age, when social interactions with peers in preschool settings become a concern. Individuals exhibit deficits in fine and gross motor skills, visual motor integration, visual–spatial perception, nonverbal concept formation, and visual memory, with preserved articulation, verbal output, auditory perception, vocabulary, and verbal memory. Verbal abilities tend to be stronger relative to performance abilities, with particular weakness in visual–spatial organization and graphomotor skills. However, individuals with AS did not consistently demonstrate nonverbal weaknesses or increased spatial or motor problems relative to individuals with high-functioning autism, indicating variability in these deficits.

Fine motor vulnerabilities can be pronounced in some younger children with AS relative to autism, but this finding is not universal; several unusual features in the communication domain are common, including poor prosody, tangential and circumstantial speech, and marked verbosity on specific topics of interest. The process necessary to make an accurate diagnosis of AS is challenging and often involves a team approach, with the Autism Diagnostic Interview–Revised and Module 3 or 4 of the Autism Diagnostic Observation Schedule ideally suited for higher functioning verbal children such as those with AS. A complete battery of standardized tests is needed to differentiate AS from learning disorders with overlapping characteristics.

The NEPSY-II is a pediatric neuropsychological assessment that contains a Social Perception domain including Affect Recognition and Theory of Mind tests, which assess the cognitive processes that facilitate social interactions and may be useful for identifying diagnoses associated with impairments in social behaviors, such as ASD. Differential diagnosis is complicated by similarities between AS and multiple disorders, including semantic-pragmatic disorder, schizoid disorder, right hemisphere learning disabilities (as described in psychiatry and other disciplines), and nonverbal learning disability. AS is even less often associated with a known medical condition than is autistic disorder; nevertheless, a number of mental health conditions (schizophrenia, schizoid personality, anxiety disorder, obsessive-compulsive disorder, oppositional defiant disorder, and selective/elective mutism) may mimic AS or coexist with it.

Individuals with AS present high rates of comorbid disorders such as emotional disorders (anxiety and depression), behavioral disorders (conduct disorder, oppositional defiant disorder), and attention-deficit/hyperactivity disorder (ADHD), which might delay or obscure the diagnosis of AS. Estimates of comorbidity with depression and anxiety are as high as 65 percent, and hyperactivity and inattention are common among children with AS, with initial misdiagnosis with ADHD also reported.

5. Therapeutic Interventions and Neurobiological Outcomes

Behavioral therapies for AS include social skills training and coaching in metacognitive strategies, which are designed to address the major symptoms observed in AS and improve cognitive, emotional, and physical functioning. Neurofeedback, often combined with biofeedback, is a core intervention that aims to normalize electroencephalographic (EEG) patterns and enhance self-regulation and calming, with training goals established by comparison to database norms. Biofeedback, particularly heart rate variability training, is used to decrease sympathetic drive and increase parasympathetic tone, engendering a feeling of calm through increased vagal efferent tone. The polyvagal theory provides a framework for understanding the success of biofeedback and neurofeedback in clients with AS.

Neurofeedback protocols for AS are individualized based on quantitative EEG assessment, targeting abnormal activation and connectivity in cortical areas. Common training sites include Cz in children and FCz in adults, with specific frequency bands addressed according to assessment findings. Training steps may include decreasing slow wave frequencies and enhancing 13–15 Hz activity to address ADHD symptoms, and modulating beta activity to address anxiety and perseverative thinking. For sensory and motor aprosodia, training targets slow wave activity and coherence abnormalities in parietal and temporal/frontal areas. Executive functioning deficits are addressed by normalizing electrical activity over relevant cortical areas while the client engages in learning strategies and biofeedback.

Evidence from neurofeedback interventions indicates improvements in attention, language, and visuo-spatial processing, with gains continuing even after treatment ends. Neurofeedback at FCz has been associated with improved humor comprehension and empathy in individuals with AS. The systems theory of neural synergy posits that interventions at any point in the nervous system can produce changes elsewhere, supporting the combined use of neurofeedback and biofeedback to rebalance mind–body functioning.

Personalized approaches are informed by functional neuroanatomy and EEG findings, with interventions tailored to individual profiles and symptom areas.

6. Conclusion

Asperger syndrome is a complex neurodevelopmental disorder within the autism spectrum characterized by social interaction impairments, restricted interests, and preserved language and cognitive abilities. Neurobiological studies reveal abnormalities in brain regions involved in social cognition and connectivity, supported by genetic findings implicating synaptic plasticity pathways. The cognitive and behavioral profile includes strengths in verbal skills alongside deficits in motor coordination, social cognition, and theory of mind, with significant challenges in adaptive functioning and social communication. Diagnosis requires comprehensive neuropsychological assessment to differentiate AS from overlapping disorders and to identify comorbidities such as anxiety, depression, and attention-deficit/hyperactivity disorder. Therapeutic interventions, particularly behavioral therapies combined with neurofeedback and biofeedback, show promise in improving cognitive, emotional, and social functioning by targeting neural mechanisms and promoting neuroplasticity. Personalized treatment approaches based on neurophysiological assessments are essential for optimizing outcomes. Continued research integrating neurobiological, cognitive, and therapeutic perspectives is critical for advancing understanding and care for individuals with Asperger syndrome.

References (26)

Reference 1
Book Chapter
Understanding Others: Brain Mechanisms of Theory of Mind and Empathy
Singer T., Tusche A.
Neuroeconomics , 2014 pp 513-532
View chapter
Reference 2
Review article
Brief report: Should Asperger syndrome be excluded from the forthcoming DSM-V?
Kaland N.
Research in Autism Spectrum Disorders , 2011 pp 984-989
View article
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"... Abstract Asperger syndrome (AS) is a pervasive developmental disorder , characterized by social impairments and focused, circumscribed interests and activities in the absence of significant language impairment and cognitive delay. Since its inclusion in the DSM-IV, there has been a dramatic increase in its recognition both in children and adults. Some recent studies suggest that there may be differences between AS and high-functioning autism (HFA) on behavioural, cognitive and neurobiological levels. As the majority of studies so far have generally failed to demonstrate a clear distinction between AS and HFA, some researchers have called for eliminating AS from the forthcoming DSM-V. This paper reports some interesting differences between the conditions on different levels and argues for more experimental studies on AS, modifications of its diagnostic criteria, and for its continued retention in the diagnostic manual. 1 ..."
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"... Introduction Since its inclusion in the DSM-IV criteria and in the ICD-10 few childhood-onset disorders have generated as much controversy as Asperger syndrome (AS). Described by Hans Asperger as autistic psychopathy ( Asperger, 1944/1991 ), it is now classified as a pervasive developmental disorder (PDD) or an autism spectrum disorder (ASD), characterized by autistic social impairment and a pattern of restricted, repetitive, and stereotyped behaviours, interests, and activities. According to the DSM-IV (2000) and the ICD-10 , AS occurs without clinically significant impairments or cognitive delays and full criteria for autism are not met. AS is now virtually a household term and Wing (2005) describes how public and professional conceptions about AS have changed since her original writings. During the last decades there has been a dramatic increase in the number of publications dealing with various aspects of AS. Despite the increase in the number of children and adolescents being diagnosed with AS the diagnosis has remained controversial . One reason for this is that we do not know to what extent AS differs from autism with normal intelligence—referred to as high-functioning autism (HFA). It is therefore too early to conclude with final certainty whether the disorders are different or the same . Despite this uncertainty, it has been suggested that AS should be excluded from the forthcoming DSM-V . It is somewhat unclear when a diagnosis of AS can be made , particularly given the different systems in use for diagnosis , in addition to the criteria speciﬁed in the DSM-IV and in the ICD-10. The mean age for making an AS diagnosis is relatively high, about 10–11 years of age . There are at present few appropriate instruments for diagnosing AS at an early age. The purpose of this brief report is to examine recent studies about the core features of AS, suggesting some pertinent differences between AS and autism. The criteria for AS should be substantially revised and this paper argues for the continued retention of the AS diagnosis in the forthcoming DSM-V manual. 1 ..."
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"... Differences in brain structure and function AS is a complex condition and some experimental studies of the brain structure of individuals with AS have been performed . Among the areas of the brain having greatest significance for autistic behaviour are the amygdala, the hippocampus, and the temporal and prefrontal areas . With regard to the abnormal brain processes resulting in pathological brain growth it is not clear whether these processes are specific to autism or whether they also apply to individuals with AS. Recent findings, however, there may be differences in some brain structures between AS and autism. More recently, Jou, Minshew, Keshavan, and Hardan (in press) found that cortical folders were abnormally structured in the left frontal areas of the brain in individuals with autism, but not in those with AS. Variables like age, IQ and brain volume did not have any impact on the differences found between autism and AS with regard to neuropathology. Jou et al. conclude that the validity of AS as a distinct syndrome from autism is not clear, partly because of the paucity of differentiating neurobiological evidence. Moreover, Enticott, Rinehart, Tonge, Bradshaw, and Fitzgerald (2010) reported that cortical inhibition was significantly reduced in an HFA group, but not in an AS and a neurotypical group, suggesting a possible neurobiological dissociation between AS and HFA, based on GABAergic function. 1 ..."
Reference 3
Review article
Asperger syndrome: A simple matter of white matter?
Ellis H.D., Gunter H.L.
Trends in Cognitive Sciences , 1999 pp 192-200
View article
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"... Asperger syndrome (AS) is defined in reports from the World Health Organization (ICD-10; Ref. a ) and the American Psychiatric Association (DSM-IV; Ref. b ) as a cluster of cognitive and social signs including normal verbal development, abnormal social interactions and unusually intense interests. Each report also suggests that motor clumsiness and isolated, special skills are sometimes present. To give a more concrete example of AS, we present the case of Raymond who displays many of the characteristics first described by Asperger’s original paper on ‘autistic psychopathy’ ( Ref. c ). 1 ..."
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"... Asperger syndrome, one of the Pervasive Developmental Disorders, is formally diagnosed on the basis of a cluster of cognitive, social and motor signs. It is also associated with poor visuo-spatial skills, good verbal performance, gauche social behaviour and clumsiness. Many of the difficulties evident in those with Asperger syndrome are closely associated with right-hemisphere dysfunction. In this respect they also resemble signs used to diagnose what has been labelled Nonverbal Learning Disorder. Here, these are treated as being the same or closely-related disorders with a possible common underlying aetiology; that is, a neurodevelopmental abnormality affecting white matter. This review examines the ability of this approach to account for a wide range of characteristics of the Asperger syndrome, and contrasts this with a theory-of-mind approach, which, although able to account for the primary features of Asperger syndrome, is less successful at explaining some of its secondary features. 2 ..."
Reference 4
Book Chapter
Asperger's Syndrome Intervention. Combining Neurofeedback, Biofeedback and Metacognition
Thompson M., Thompson L.
Introduction to Quantitative EEG and Neurofeedback , 2009 pp 365-415
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"... B Historical note In 1944, the Viennese pediatrician Hans Asperger published a description of a group of boys with an unusual constellation of symptoms. They were like little professors with advanced knowledge in their special areas of interest, but they were socially inept. Asperger used the term autistischen Psychopathen ( autistic psychopathies ), borrowing the term autism from Bleuler (1911), and using psychopathy to indicate a personality disorder rather than a psychiatric illness. When his work eventually became more widely known, it was referred to as Asperger’s syndrome . Lorna Wing, a British psychiatrist and autism expert who was largely responsible for bringing this interesting diagnosis to the attention of English-speaking professionals, set out the following criteria for Asperger’s syndrome . Those with AS have well-developed language skills that are, nevertheless, a bit odd with respect to the use of pedantic language, and a lack of normal prosody (rhythm, intonation, and pitch). They show impaired social interaction, and have limited non-verbal communication with little facial expression or use of gesture. They show resistance to change and like routines, repetitive activities, and spending time learning about their special interest areas. They have excellent rote memory for things of interest. They show poor motor coordination, and often have an odd gait and posture. Asperger noted that they did not fit in socially, made their parents’ lives miserable, and drove their teachers to despair . These continue to be the problems that bring them to the attention of mental health professionals today. Asperger died in 1980 without ever meeting Wing, and before his astute observations and eponymous diagnostic grouping really became known in Britain or the USA. His original work was eventually translated into English, and published in a textbook about Asperger’s syndrome and autism written by Ute Frith (1991) . It was 50 years after Asperger’s initial paper was published that the disorder bearing his name was officially recognized in the USA through inclusion in the DSM-IV. By the time Tony Attwood (2007) was writing his second book about AS, however, there were over 2000 publications and 100 books on the subject. 1 ..."
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"... Publisher Summary This chapter aims to broaden practitioners' understanding of Asperger's syndrome (AS), a disorder along the continuum of autistic spectrum disorders (ASD). AS is becoming a relatively common diagnosis in schoolchildren who are very bright intellectually but totally inept socially. They are usually initially misdiagnosed as having attention deficit hyperactivity disorder (ADHD). This chapter emphasizes how to use neurofeedback (NFB) plus biofeedback (BFB), in conjunction with coaching in learning strategies (metacognition) to address the major symptoms observed in AS. It develops an understanding of how feedback can improve a person's cognitive, emotional, and even physical functioning, and has named this a systems theory of neural synergy (STNS). The name underscores the fact that NFB plus BFB influence dynamic circuits, and emphasizes that no matter where one enters the nervous system with an intervention the larger system adjusts as it seeks a new balance. If the intervention is done correctly, the new equilibrium will bring out the individual's potential. This chapter is divided into four sections. The first section gives a general overview of Asperger's syndrome including background, a historical note, information on prevalence, and a description of symptoms that includes the authors' clinical observations. The second section correlates symptoms with functional neuroanatomy and electroencephalographic (EEG) findings. The third section further highlights brain areas found to be dysfunctional in ASD, and cites research findings for each of seven key regions that are repeatedly found to differ when compared to people with typical development. The fourth section is concerned with intervention. It provides an overview of the use of NFB plus BFB for managing the symptoms of AS. It provides a summary of what to do, and a discussion of why it is effective. 3 ..."
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"... Conclusion This chapter describes the core symptoms of AS, and explains how we assess and intervene to help these clients. The rationale for the training is based on research findings concerning brain function combined with observations of what differs in terms of EEG findings. A combined approach is advocated. Neurofeedback is the core intervention that pulls the brain in the direction of typical functioning, using comparisons to database norms to establish the training goals. We are likely affecting many complex cortical loops by training centrally over the anterior cingulate, including links to the mirror neuron systems. When neurofeedback is augmented by peripheral biofeedback (especially effortless diaphragmatic breathing that enhances heart rate variability), there is a synergistic effect with neural circuits then being influenced not just from the top down (brain changes), but also from the bottom up by way of the complex interactions and connections of the vagal nerve (both its myelinated and unmyelinated fibres). Everything is integrated with complex feedback loops, and thus we explain the results using a systems theory of neural synergy: a change in any part of the system can produce changes elsewhere. When two components of the system are changed in a complementary fashion—as when diaphragmatic breathing is combined with SMR training, for example—the resulting new equilibrium is healthier than if either technique had been learned separately. The experience to date using neurofeedback is encouraging ( Coben, 2007 ; Jarusiewicz, 2002 ; Thompson and Thompson, 1995 ; Thompson et al ., in press). The findings of neuroscience research, including recent work on the mirror neuron system, are supportive of an intervention that allows an individual to exercise their brain and move towards normalization of EEG patterns. Training the brain—bringing inactive areas online and improving communication between different areas of the cortex using neurofeedback—and combining that with biofeedback for further self-regulation and calming will likely become an important component of the tool-kit of interventions for autistic spectrum disorders. It is particularly gratifying to work with those with Asperger’s syndrome because they so often have high intelligence, and there is great potential that can be realized. 3 ..."
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"... A major focus of our work with AS clients has been BFB to decrease sympathetic drive and increase parasympathetic tone by encouraging an increase in heart rate variability (HRV). An increase in vagal efferent tone inhibits the inherent high intrinsic rate of the sinoatrial node slowing the heart, increasing HRV and engendering a feeling of ‘calm.’ The polyvagal theory provides a coherent explanation of why our work using BFB, in particular heart rate variability training, combined with NFB, with its hypothesized effects on AC function, has been successful in clients with Asperger’s syndrome. 3 ..."
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"... In real life a brain–body separation is artificial. For our purpose of explaining why neurofeedback plus biofeedback can rebalance, and thus improve, mind–body functioning, we have developed a systems theory of neural synergy (STNS) which emphasizes that, no matter where we enter the nervous system with our interventions, the neural system will adjust to its own new balance and equilibrium. Whether we train the brain (NFB) or we train the heart (BFB), the neural pathways do connect across the forebrain, the midbrain and the hindbrain as was described under the polyvagal theory above. In particular, the anterior cingulate connects with the brainstem, and that brings all the connections inherent in Porges’ polyvagal theory into play. These considerations support the importance of recognizing the interconnectedness of the entire central nervous system and, in our work with Asperger’s syndrome, they support the combined use of NFB and BFB. The NFB works from the top down. The BFB works from the bottom up in terms of CNS connections. The processes synergistically support each other. 3 ..."
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"... A Neurofeedback + biofeedback: What we do and why it is effective Although we continue to emphasize the importance of diet, sleep, exercise, social skills training, and a good educational and extracurricular program, the primary approach for helping people with AS has become NFB+BFB and cognitive strategies, simply because this has proven most effective. By combining knowledge of functional neuroanatomy with the foregoing theoretical discussions, a picture has emerged concerning the difficulties experienced, both neuroanatomical and functional, by those with ASD. Quantitative electroencephalographic assessment (QEEG) can pinpoint cortical areas with abnormal activation and abnormal connectivity (coherence) as compared to database norms . These areas and/or connections can then be addressed using the neurofeedback approach. It must be emphasized that what follows are some commonly used sites and frequencies but, in all cases, the initial assessment results, either single-channel or 19-channel assessment, lead to the final decision as to the sites and frequencies to be addressed in order to ‘normalize’ cortical functioning. As stated above, we address each of the symptom areas both individually and together. Attention span, impulsivity, and hyperactivity when present, are addressed; firstly, by down-training low-frequency activity between 2 and 10 Hz (whichever range is appropriate for each client, for example, 2–5 Hz, or 3–7 Hz, or 4–8 Hz, and so on) and higher frequency beta, most often somewhere between 19 and 36 Hz at sites that depend on the assessment findings. The most common starting site for clients who have AS is Cz in children, and between Cz and Fz (called FCz in this chapter) in adults. At the same time we frequently up-train SMR at the same site providing, as previously noted, the central site does not evidence high amplitude spindling beta in this frequency range. We may also reward 15–18 Hz beta while the subject is learning and/or carrying out the metacognitive learning strategies that have been taught; for example, while reading and analyzing material that is emotionally descriptive ( Thompson and Thompson, 2003a ). 3 ..."
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"... Typical training session steps for clients with Asperger’s syndrome The training can be conceptualized as a progression of stages that address different aspects of the AS disorder. These are outlined in point form in five steps below. In many cases not all five steps will be needed. Symptoms may resolve after the initial two or three steps. However the actual work of the trainer during the sessions is more complex. It is described as four overlapping processes following the brief outline of steps. Training Steps 1. Address the ADHD symptoms : Begin by helping the client to be more ‘externally’ oriented and calm. Decrease the dominant slow wave frequencies, and enhance 13–15 Hz activity. A common placement is at Cz referenced to the right ear, or C4 to the left ear, respectively. For an excellent discussion of electrode placement, monopolar (referential) as compared to bipolar (sequential), see Les Fehmi and Tom Collura’s article (2007) . 2. Deal with anxiety, (perseveration when present), and internal ruminative thinking Decrease high amplitude19–22 Hz activity (when present). Also, decrease dominant high amplitude beta activity between 23–36 Hz (when present). Usually the electrode is placed at a site that may influence the activity of the cingulate gyrus, that is, between Fz and Cz. In addition, when beta spindling is also observed at another site (sometimes F6 or F5, and occasionally at Pz) then this beta frequency will be decreased at that site. In all adult clients a stress test is carried out, and biofeedback is added to the training program. 3. Deal with the sensory aprosodia : Decrease dominant slow wave activity at P4 and T6, and increase low beta 14–17 Hz. Normalize coherence abnormalities (often hypo-coherence between T6 and F5, and hyper-coherence between parietal and temporal/frontal areas). 4. Deal with the motor aprosodia : Decrease dominant slow wave activity at F6. 3 ..."
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"... Emerich found that the ability of adolescents with Asperger’s syndrome to comprehend humorous material, such as picking funny endings for cartoons and jokes, was significantly impaired . At our Center, a study was done to compare children with AS to a normal school group in terms of reactions to reading happy stories. The Asperger’s group, as measured by self-report using an adjective check list describing their mood, done before and after reading the passage, did not show a shift towards positive emotion. It was found that, after NFB training, the children with Asperger’s did identify more adjectives that signified positive mood in the same way as matched normal controls . An example of these difficulties in an AS client was 19-year-old Brian. In his early sessions Brian would watch people and, if someone told a joke, he would see others smiling and laughing, and then he would burst into a forced laugh. After 40 neurofeedback sessions to decrease high frequency beta activity originating in the anterior cingulate at Brodmann area 24 (seen with LORETA analysis of the 19-channel QEEG and observed in the surface EEG at FCz), Brian not only picked up on humor and laughed appropriately, but he was also telling truly funny stories and jokes. Interestingly, staff were independently commenting to the author that they actually felt that Brian was showing empathy, and truly understanding of how others were feeling. His parents also noted this. Theoretically the FCz NFB might have influenced both the anterior cingulate and the medial prefrontal frontal cortex. Certainly this training would have addressed the beta spindling observed at FCz. The electrode was referenced to the right ear because Brian, similar to the majority of our AS clients, demonstrated high amplitude, low frequency alpha at T6 compared to T5. Our assumption has been that this high amplitude alpha (in some clients it will be low amplitude beta 14–17 Hz) corresponded to relative inactivity at this site in the right hemisphere—an area involved in processing the emotional tone of language and gestures as well as spatial information. 3 ..."
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"... These observations led us to further investigate what was known about the pathophysiology of Asperger’s, and to review where we had been placing the active electrode, and what frequency bands we had been enhancing and inhibiting when our primary objective in these early years had only been to decrease the co-morbid symptoms of ADHD. We were asking the question of what, neurophysiologically, was in common to both ADHD and Asperger’s and, further, what was in common to both these disorders and anxiety? B Brain regions that underlie ADHD symptoms, and appropriate NFB training Beauregard and Levesque (2006) reviewed the literature showing abnormal functioning of the anterior cingulate cortex (ACC), the prefrontal cortex, and the caudate in children with ADHD during tasks involving selective attention. They demonstrated that neurofeedback can normalize these areas as shown by pre- and post-functional magnetic resonance imaging (fMRI) in 15 students diagnosed with ADHD who received neurofeedback training as compared to five control subjects. The anterior cingulate has also been implicated in AS because it is involved in appropriate shifting and fixating of attention. In one study, Landry and Bryson (2004) showed that children with ASDs, when compared to normal children, and even to children with Down’s syndrome, have a distinct difficulty with attention. They demonstrated that, once attention was first engaged on a central fixation stimulus, persons with autistic spectrum disorder had a marked difficulty in disengaging their attention in order to shift attention to a second stimulus. Belmonte’s group studied visual selective attention comparing autistic subjects with normals. They noted that, in autism, physiological indices of selective attention are abnormal even in situations where behavior is intact. They used functional magnetic resonance imaging (fMRI) while subjects performed a bilateral, visual-spatial attention task. In normal subjects, the task evoked activation in a network of cortical regions including the superior parietal lobe. The subjects with ASD differed from normal activation patterns. 3 ..."
Reference 5
Book Chapter
Asperger Syndrome and its Relationships to Autism
McPartland J.C., Volkmar F.R.
The Neuroscience of Autism Spectrum Disorders , 2013 pp 55-67
View chapter
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"... Clinical Features In many respects, Asperger’s original (1944) description continues to provide one of the best overviews of the clinical features in AS. The cases he described had major problems in social interaction. This was, and remains, the major similarity to autism. However, other features were also present, such as highly intense, idiosyncratic special interests, trouble in self-awareness, impairments with motor skills, and difficulty with social communication. These special interests became a major focus of the child’s life and often interfered with familial function. Asperger emphasized the intrusiveness of these interests on other facets of the child’s life, such as learning. The first cases were noted to have major difficulties in self-awareness – especially affective self-awareness. They tended to approach highly emotionally laden tasks in an intellectual way and this further compounded their social isolation. Asperger also noted persistent gross and fine motor vulnerabilities. Developmentally, he noted that the cases tended to talk before they walked and that parents were often unconcerned until the child entered preschool or other settings where major problems with peers quickly surfaced. The combination of motor and social problems also made for difficulties in sports. The social presentation of these children, that is, as little professors, served to further isolate them from peers, despite some degree of social interest on their part. Although the cases had excellent basic language skills (e.g., vocabulary), they also had significant problems with nonverbal and social (pragmatic) communication skills. Voice modulation was noted to be odd, as were facial expressions and gestures. Difficulties with rigidity and social isolation also could result in behavioral difficulties, as cases balked at minor changes in routine. Finally, Asperger’s original paper also emphasized the existence of similar personality problems in family members – particularly fathers. AS is often detected later in childhood than other autism spectrum disorders (ASD) because children with AS develop language and self-help skills on time. 1 ..."
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"... History In 1944, a medical student in Vienna, working on his medical school thesis, described four boys with marked social problems and poor motor skills, but highly developed verbal language, and unusual, highly idiosyncratic and circumscribed special interests . This student, Hans Asperger, also observed that the condition seemed familial, and he used the word ‘autism’ in his original description of the condition as ‘Autistic Psychopathy’. Asperger made the important point that the special interests exhibited by these boys were maladaptive both because they interfered with learning in other areas and because they could come to dominate the family’s life. Because of the international academic impasse caused by World War II, he was not familiar with Leo Kanner’s report, published the preceding year (1943), describing the condition of early infantile autism. At that time, the current emphasis on phenomenological, research-based definitions had not yet evolved , and Asperger continued to publish on the topic until the time of his death . Because he published in German journals, his work received relatively little attention in the English language literature at the time. Very few English language publications on Asperger syndrome (AS) appeared for several decades after Asperger’s work. Initial publications included discussion of AS as a type of personality trait/disorder , as well as redescription of some Asperger’s cases , though the significance and relationship to autism was not recognized at the time. Several events in the 1980s increased awareness of AS. First, the American Psychiatric Association (APA) Diagnostic and Statistical Manual (DSM-III) recognized infantile autism as an official diagnostic concept . The following year, a British psychiatrist, Lorna Wing, published a highly influential review of Hans Asperger and his work . Wing’s review summarized Asperger’s account and provided a series of short case reports. She suggested that some aspects of his original description should be modified, for example, the presence in girls, individuals with delayed language, and individuals with intellectual disability. Wing highlighted the diagnostic concept but also greatly emphasized her impression that AS was a condition on the autism spectrum, closely related to autism, if not a variant of it. 1 ..."
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"... Based on the results of the field trial, AS was included as a distinct diagnostic subcategory (within the pervasive developmental disorders) in DSM-IV and ICD - 10 . The publication of the DSM-IV-Text Revision wrought significant changes to descriptive text accompanying the diagnostic criteria for AS, but no changes were made in the diagnostic algorithm. Diagnostic Criteria Current definitions maintain some continuity with Asperger’s original description of the disorder but also differ in several ways . Current diagnostic criteria in the DSM-IV-TR distinguish AS from autism primarily by adding exclusionary criteria . Children with social deficits and restricted interests who do not meet criteria for autism, did not evidence frank language delay, and possess preserved cognitive ability and daily living skills qualify for AS. Specific diagnostic criteria include two areas of impairment from among the following social behaviors: 1. Inability to use multiple nonverbal behaviors, such as eye-to-eye gaze, facial expression, body postures, and gestures to regulate social interaction; 2. Failure to develop peer relationships appropriate to developmental level; 3. Lack of spontaneous seeking to share enjoyment, interests, or achievements with other people (e.g., by a lack of showing, bringing, or pointing out objects of interest to other people); 4. Lack of social or emotional reciprocity. These social impairments must co-occur with at least one area of impairment in terms of the following categories of restricted, repetitive, and stereotyped patterns of behavior, interests, and activities: 1. Encompassing preoccupation with one or more stereotyped and restricted patterns of interest that is abnormal either in intensity or focus; 2. Apparently inflexible adherence to specific, nonfunctional routines or rituals; 3. Stereotyped and repetitive motor mannerisms (e.g., hand or finger flapping or twisting, or complex whole-body movements); 4. Persistent preoccupation with parts of objects. 1 ..."
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"... Functional imaging suggests abnormalities in brain activity associated with face-processing mechanisms in the inferotemporal cortex in ASD , and some of these anomalies have been specifically replicated in subsamples of individuals with AS . SPECT imaging suggests abnormal right hemisphere functioning in AS . Dysfunction has also been observed in brain regions subserving social cognition in AS, e.g., anterior cingulate cortex, prefrontal cortex, temporoparietal junction, amygdala, and periamygaloid cortex . An emerging body of research suggests problems with functional connectivity among separate brain regions in ASD and, specifically, in AS . Despite these isolated examples of AS-specific brain differences, a recent review of 208 imaging studies failed to reveal robust differences between individuals with AS and other autism spectrum disorders . Current brain imaging research fails to present a clear picture of the specific neurobiological underpinnings of AS or factors that distinguish it from other autism spectrum disorders. 1 ..."
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"... Psychological Factors Several studies suggest a distinct neuropsychological profile in AS . Klin and colleagues (1995) compared individuals with AS to those with other high-functioning autism spectrum disorders on a variety of neuropsychological measures, and determined that individuals with AS exhibited deficits in fine and gross motor skills, visual motor integration, visual–spatial perception, nonverbal concept formation, and visual memory with preserved articulation, verbal output, auditory perception, vocabulary, and verbal memory. Individuals with AS have been reported to exhibit stronger verbal abilities relative to performance abilities, with particular weakness in visual–spatial organization and graphomotor skills . Overall, individuals with AS tend to demonstrate higher scores on measures of verbal functioning relative to individuals with autism . However, this study also found that individuals with AS did not consistently demonstrate nonverbal weaknesses or increased spatial or motor problems relative to individuals with HFA. Concordant with this finding, some researchers have argued that individuals with AS evidence overall greater cognitive ability than individuals with HFA, irrespective of verbal versus nonverbal ability . Resolution of this issue is complicated by the employment of heterogeneous diagnostic schemes, which have been shown to directly influence IQ differential . 2 ..."
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"... Differential Diagnosis Given the commonality with autism in terms of severity and persistence of social deficits, the major issue regarding differential diagnosis has been differentiation from autism. In contrast to autism, language is relatively preserved, as are verbally mediated cognitive skills. Fine motor vulnerabilities can be dramatic in younger children relative to autism. For example, in contrast to a child with autism with good drawing abilities but limited vocabulary, the child with AS may produce a rather poor and immature drawing but elaborate verbiage to describe it. Other issues arise from similarities between AS and multiple disorders described in psychiatry and other disciplines, including semantic-pragmatic disorder, schizoid disorder, right hemisphere learning disabilities, and nonverbal learning disability . The concept of nonverbal learning disability , in particular, has been of interest, since it is a syndrome associated with a number of different conditions in addition to AS. This concept focuses on a constellation of symptoms and a specific neuropsychological profile in which, in contrast to more classical autism, nonverbal skills are more impacted than verbal ones; changes in the syndrome manifest themselves over development as individuals are taught, or learn on their own, to use coping strategies bringing the verbal strengths into use in addressing areas of deficit. The DSM-IV and ICD-10 approach has drawn criticism . For these reasons, multiple authors have proposed variant diagnostic criteria to improve upon perceived shortcomings in the current diagnostic operationalization (see Box 1.4.2 ). 3 ..."
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"... Comorbidity AS commonly co-occurs with depression and anxiety, with estimates of comorbidity as high as 65 percent. The common overlap between AS and these mood disorders has been posited to represent a potential distinction between AS and other high-functioning forms of ASD . However, such discrepancies between AS and other ASD are not universally observed . Anxiety in AS may stem from several sources. Concern about possible violations of rigid routines or rituals can be anxiety-provoking for children with AS. They frequently rely on particular schedules or methods of completing daily activities that, when violated, result in significant distress. Conversely, when placed in a context in which no clear schedule or set of expectations is known, anxiety may result. Anxiety in individuals with AS may also manifest similarly to social anxiety, i.e., a preoccupation with failing during social encounters. Depressive symptomatology may also result from chronic frustration with social and romantic failures. Individuals with AS may become isolated over time, further increasing risks for anxiety and depression. In younger children, bullying is noted to contribute to isolation . Ironically, strong language abilities may render developmental difficulties less obvious and decrease the likelihood of obtaining assistance from peers and teachers alike . Hyperactivity and inattention are common among children with AS , and many children with the disorder are often initially misdiagnosed with attention-deficit/hyperactivity disorder. Some studies have associated AS typoTourette’s syndrome , obsessive-compulsive disorder , and psychotic conditions . As described above, the unique neuropsychological profile of nonverbal learning disability has also been associated with AS . 3 ..."
Reference 6
Reference works Chapter
Applications in Diverse Populations
Donald P. Oswald
Comprehensive Clinical Psychology , 1998 pp 19-35
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"... This term includes a variety of behavioral features associated with autism ranging from stereotyped motor movements to difficulty with transitions and preferential (even obsessive) interest in particular topics of conversation. Kanner (1943) originally believed that most children with autism did not manifest mental retardation, a conclusion that was endorsed by others and led to the assertion that these individuals were merely unmotivated to engage in standardized intellectual assessment or that these instruments were somehow inappropriate for the population. Subsequent investigations, however, demonstrated that most individuals with AD also display general intellectual impairment and deficits in adaptive behavior . 9.02.2.2 Asperger's Disorder Asperger's disorder was originally described by Hans Asperger in 1944 and over the next 50 years appeared infrequently in the literature under the designation Asperger's syndrome. Individuals in the contemporary category of Asperger's disorder have been described in the literature under other designations as well, including mild autistic, high-functioning autistic, near-normal autistic, and schizotypal personality disorder. Recent work suggests substantial overlap between Asperger's disorder and two other diagnostic designations in contemporary literature: nonverbal learning disabilities syndrome and semantic-pragmatic disorder . The key features of Asperger's disorder, as described in the Diagnostic and statistical manual of mental disorders are (i) a qualitative impairment in social interaction; and (ii) restricted repetitive and stereotyped patterns of behavior, interests, and activities. Significant speech deficits are not part of the presentation, and persons with Asperger's disorder are less likely to display deficits in nonverbal concept formation, auditory perception, articulation, vocabulary, and verbal output than are high-functioning persons with autism . However, several unusual features in the communication domain are common in individuals with Asperger's disorder, including poor prosody, tangential and circumstantial speech, and marked verbosity on specific topics of interest . In his original case descriptions, Asperger appears to have viewed clumsiness, or some other form of motor impairment, as a defining feature of the syndrome. 1 ..."
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"... Asperger's Disorder Asperger's disorder was originally described by Hans Asperger in 1944 and over the next 50 years appeared infrequently in the literature under the designation Asperger's syndrome. Individuals in the contemporary category of Asperger's disorder have been described in the literature under other designations as well, including mild autistic, high-functioning autistic, near-normal autistic, and schizotypal personality disorder. Recent work suggests substantial overlap between Asperger's disorder and two other diagnostic designations in contemporary literature: nonverbal learning disabilities syndrome and semantic-pragmatic disorder . The key features of Asperger's disorder, as described in the Diagnostic and statistical manual of mental disorders are (i) a qualitative impairment in social interaction; and (ii) restricted repetitive and stereotyped patterns of behavior, interests, and activities. Significant speech deficits are not part of the presentation, and persons with Asperger's disorder are less likely to display deficits in nonverbal concept formation, auditory perception, articulation, vocabulary, and verbal output than are high-functioning persons with autism . However, several unusual features in the communication domain are common in individuals with Asperger's disorder, including poor prosody, tangential and circumstantial speech, and marked verbosity on specific topics of interest . In his original case descriptions, Asperger appears to have viewed clumsiness, or some other form of motor impairment, as a defining feature of the syndrome. Using high-functioning persons with autism as a comparison group, Asperger's disorder individuals have been reported to have greater difficulties with some motor tasks . Reports of clumsiness in Asperger's disorder were sufficiently convincing that the feature was included among the diagnostic criteria for the syndrome in the International classification of diseases (10th ed., ICD-10), the most recent World Health Organization (1993) classification of diseases and health problems. Recent research findings differ on the question of whether motor skills deficits reliably distinguish individuals with Asperger's disorder from high-functioning individuals with autism . 1 ..."
Reference 7
Book Chapter
Asperger syndrome and adolescent girl: understanding the rhythm of emotions towards the struggle with social relationships—cognitive-behavioral and narrative therapy
Carla Vale Lucas, Luísa Soares, Filipa Oliveira
Emerging Programs for Autism Spectrum Disorder , 2021 pp 411-423
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"... Asperger’s syndrome The diagnosis of Asperger’s disorder was first added to the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, 4th edition as a pervasive developmental disorder belonging to the family of autism spectrum disorders ( American Psychiatric Association (APA), 1994; Portway & Johnson, 2003 ). Diagnosing individuals with AS is complex as there isn’t any biological test to aid diagnosis . Thus it is made solely on the basis of developmental and behavioral characteristics . Moreover individuals with AS present high rates of comorbid disorders (such as emotional disorders—anxiety and depression; as well as behavioral disorders—conduct disorder, oppositional defiant disorder; and attention-deficit/hyperactivity disorder), which might delay or obscure the diagnose of AS , leaving the child at risk of negative encounters, developing low self-esteem, anxiety, and depression . The mean age for a diagnosis of AS is approximately 8 years old . The difficulties presented are age-related, and need to be targeted in intervention. During elementary school, social skill deficits became more prominent. In middle school, children begin feeling their differences and express sadness, anxiety, and rejection. Teenagers faced increased anxiety, obsessive-compulsive, and ever-changing social skill deficiencies . In DSM-5, an explicit diagnostic category “Asperger syndrome” will no longer exist. That doesn’t mean that individuals with milder autistic symptoms, good cognitive and language abilities will disappear . People with AS are affected to different degrees in the way they think, communicate, relate to others, and understand the world around them . Individuals with AS have been identified as having difficulty with “theory of mind” tasks. That is, they lack an understanding and appreciation of the feelings, thoughts, needs, and intentions of others, how their behavior impacts others, and the meaning of reciprocity in relationships . Due to these social deficits, the attempts made in social contexts are often clumsy and inappropriate. 1 ..."
Reference 8
Book Chapter
Pervasive Developmental Disorders: Autism, Asperger's Syndrome, and Pervasive Developmental Disorder-Not Otherwise Specified
Morley D. Glicken
Evidence-Based Practice with Emotionally Troubled Children and Adolescents , 2009 pp 229-241
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"... Asperger's disorder or high-level autism? The validity of Asperger's syndrome as a diagnosis separate and distinct from autism remains an ongoing issue in the literature. Using the DSM-IV criteria for autism, Eisenmajer et al. (1996) and Howlin (2000) among a host of researchers, have shown that most, if not all, children diagnosed with AS actually meet DSM-IV criteria for autism. Much of the current literature indicates that Asperger's syndrome is at the high-functioning or mild end of the autism continuum. In fact, one of the early Asperger's syndrome researchers now writes, “Asperger syndrome and high-functioning autism are not distinct conditions”. Tryon et al. (2006) argue that “According to the DSM-IV , if an individual meets criteria for autism, the individual cannot have Asperger's disorder” (p. 2). Tryon et al. (2006) studied a sample of children diagnosed with AD, and using the DSM-IV-TR criteria ruled out Asperger's disorder in 85% of the cases and could not be confirmed in the other 15%. The author's believe there is “mounting empirical evidence that Asperger's disorder is high-functioning autism and that Asperger's disorder should be deleted from the next version of the DSM. High and low-functioning autism would continue to be indicated” (p. 6). According to the DSM-IV-TR , a child can still have autism even without language or cognitive delays. A diagnosis of autism takes precedence over Asperger's syndrome. The authors note that “If a child meets DSM-IV-TR autism criteria, the child cannot have Asperger's disorder” (p. 6). 1 ..."
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"... Asperger's syndrome The term Asperger's syndrome (AS) is a widely misunderstood and misused diagnostic term. Incorrectly applied to a number of otherwise normal people who may be shy, socially awkward, or heavily invested in subjects (we often incorrectly think of geeks as having AS), this section deals with the research on correct diagnosis of AS and its relationship to other disorders. Asperger's syndrome (AS) is a form of PDD characterized by two primary areas of deficit: (a) social interaction (e.g., gaze avoidance; failure to develop normal peer relations; failure to spontaneously share enjoyment, interest, and achievements; lack of social or emotional reciprocity) and (b) restricted repetitive and stereotyped patterns of behavior, interests, and activities (e.g., stereotyped and repetitive motor mannerisms, rigid adherence to nonfunctional routines, persistent preoccupation with parts of objects) . Children with AS also have difficulty inferring the emotions of others from facial and body language . These social difficulties severely limit the child's ability to develop and maintain appropriate social relationships. In contrast to the substantial cognitive and language deficits characterized by autism, children with AS experience no unusual delays in cognition or language . Additional symptoms of AS include the following : Severe difficulty with social interactions; socially naïvety, inappropriate and awkward behavior. Repetitive, narrow and unusual patterns of behavior and interests. No clinically-significant delays in language or cognition, unlike classic autism. Appearance of clumsiness or delayed motor development. Appearance of eccentricity to other children. Behavior of a loner, but intense desire to be included by other children and to be sociable, but lack of appropriate social skills. Frequent difficulty with written language. Hypersensitivity to light, touch, noise, or smell. Lack of conversational reciprocity, unless explicitly taught. 2 ..."
Reference 9
Reference works Chapter
Childhood Mental Disorders
Scarpa A., Wilson L.
Encyclopedia of Human Behavior , 2012 pp 467-475
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"... Autism Spectrum Disorders Together, autism, Asperger's disorder, and PDD-NOS are referred to as autism spectrum disorders (ASDs). They are considered spectrum disorders because children vary in the symptoms they display and the severity of the disorder. High functioning autism and Asperger's disorder are often similar in presentation and there is a controversy over whether they are truly distinct disorders. Autism is thought to be the fastest growing developmental disability in the country. Recent statistics from the Centers for Disease Control and Prevention indicate that as many as 1 in 110 children are affected with an ASD. As such, more children are being recognized and require services. The diagnosis of autism requires impairments in three key areas – social functioning, communication, and repetitive behaviors, interests or activities – with onset prior to age three. The primary difference between the diagnosis of autism and Asperger's disorder is that Asperger's disorder does not require delays in communication. Also, in Asperger's disorder, there is no clinically significant delay in cognitive development, self-help skills, adaptive behavior, and curiosity about the environment. However, research has not clearly shown distinctions between Asperger's disorder and high functioning autism in outcome, course/outcome, etiology, neurocognitive profile, or treatment needs. As such, current recommendations are that Asperger's disorder be subsumed under the autism category in future editions of the DSM. Impairments in social interaction include nonverbal behaviors (e.g., eye contact, gestures) to regulate social interaction, peer relationships, spontaneous sharing of enjoyment, and social or emotional reciprocity. Impairments in communication include delay or lack of spoken language, initiating or sustaining a conversation, stereotyped or repetitive language, make-believe or social imitative play. Impairments in behaviors include preoccupation with an interest that is abnormal in intensity or focus, inflexible adherence to routines or rituals, motor mannerisms (e.g., hand-flapping, twisting), and persistent preoccupation with parts of objects. 1 ..."
Reference 10
Review article
'Nurturing the brain' as an emerging research field involving child neurology
Ito M.
Brain and Development , 2004 pp 429-433
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"... Asperger syndrome is characterized by impairment in social understanding and interaction and apathy, while average psychometric intelligence and language skills are preserved . This syndrome resembles autism, but these two disorders are distinguishable from each other in their presentation, prognosis and treatment requirements. Children with Asperger syndrome show impairments in their ability to both use and read non-verbal cues when conversing or interacting with others. These children are aware of the social isolation resulting from these impairments, but they are often unsuccessful in compensating for these deficiencies to form and maintain social relationships. They are often targets of bullying. Asperger syndrome occurs at a rate of 0.26–0.71%. There is no known cause of Asperger syndrome, but its genetic background seems to be evident. A likely suggestion is that it involves brain dysfunction induced by pre-, peri, or postnatal disorders. 1 ..."
Reference 11
Book Chapter
Psychiatric disorders in childhood and adolescence
Peter Hoare, Andrew Stanfield
Companion to Psychiatric Studies , 2010 pp 595-633
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"... Asperger syndrome This condition, originally described by Hans Asperger in 1944 , shows some similarities to childhood autism in that there is an impairment of social relationships, with a lack of reciprocal social interaction and a restricted repertoire of interests and activities. However, the children differ diagnostically from those with childhood autism in two important respects: there is no global intellectual impairment; and the language development is normal, although impairment in pragmatic language may be seen. Other characteristics include male preponderance and poor motor coordination with marked clumsiness. The condition is now regarded as one of the autistic spectrum disorders , although the dividing line between Asperger syndrome and childhood autism remains unclear. The impairment in social relationships persists into adult life, and owing to the lack of significant language impairment, diagnosis may not be made until later in life when social or occupational demands increase. Transitions (change of school, school to higher education, education to work etc.) may be particularly difficult for individuals with Asperger syndrome. Psychiatric disorder is common, particularly neurotic and depressive conditions. Older individuals may experience brief psychotic disorders. Management is primarily supportive, with a focus on the individual's educational and occupational choices. Maximising routine is often beneficial, and comorbid psychiatric disorders should be treated. Social skills training has shown benefit for some, although a solid evidence base for this is lacking . 1 ..."
Reference 12
Review article
Executive dysfunction in autism
Hill E.L.
Trends in Cognitive Sciences , 2004 pp 26-32
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"... Neuroimaging studies have identified a network of brain regions active during mentalising. This network centres on the anterior paracingulate cortex, the superior temporal sulci and the temporal poles bilaterally . When undertaking mentalising tasks, individuals with Asperger syndrome show significantly less activation in the brain regions important for mentalising in normal individuals [9,10] . 1 ..."
Reference 13
Handbook Chapter
Cerebellar involvement in autism and ADHD
Bruchhage M.M.K., Bucci M.-P., Becker E.B.E.
Handbook of Clinical Neurology , 2018 pp 61-72
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"... Structural neuroimaging in ASD Studies investigating structural differences in the cerebellum in vivo using magnetic resonance imaging (MRI) have confirmed that abnormal cerebellar development and injury contribute to the development of ASD. Specifically, disruption of prenatal cerebellar development during specific developmental “sensitive periods” can lead to key autism features and in turn affect maturation of both cerebellar structures and connected cerebral regions . Cerebellar injury in preterm infants has been associated with ASD symptom onset, with most severe deficits connected to vermal injury . Underdevelopment of the cerebellar vermis (vermal hypoplasia) has been detected in ASD patients as young as 2 years , as well as in adults diagnosed with infantile autism . Furthermore, meta-analyses discovered vermal hypoplasia to be restricted to the posterior vermis (lobules VI–VII) in later childhood , and cerebellar undergrowth, particularly in the vermis, has been associated with increased frontal lobe volume and increased repetitive behavior in autistic children . In addition to posterior vermal hypoplasia, an anatomic likelihood estimate meta-analysis identified reduced volume of the right crus I and left VIIIb to be ASD-specific across developmental stages ; differences in shape , and reduced right crus I/II volume were increasingly pronounced with ASD symptom severity in children with autism , paralleling postmortem findings of reduced Purkinje cell density in lobules crus I and II . In addition, tuberculosis patients with cerebellar lesions exhibited more severe ASD features than those without cerebellar lesions and increased volume of lobules VI–VII has been shown in FXS with comorbid ASD, but not without the double diagnosis . These cerebellar gray matter differences are accompanied by white matter microstructural alterations of the middle and superior cerebellar peduncle , with the latter being associated with decreased motor functioning in children with ASD and social impairment in adults with Asperger syndrome . 1 ..."
Reference 14
Review article
Autism
Tuchman R.
Neurologic Clinics , 2003 pp 915-932
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"... The role of the amygdala and related structures in autism also has been documented by functional MRI (fMRI) studies in patients with autism or Asperger syndrome in whom activation of the front temporal regions, but not the amygdala, occurs when making mentalistic (theory of mind) inferences from the eyes . This is in contrast to control patients who did show activation of the superior temporal gyrus and amygdala, which is the brain system proposed to be at the core of the “social brain network.” Positron emission tomography (PET) findings in autistic subjects include modest and not always significant global increase in resting cerebral glucose use, mostly in the basal ganglia, frontal, temporal and parietal lobes, whereas others have found no significant differences between autistic and control subjects . The lack of consistent abnormalities in PET studies of autism may be the result of the heterogeneous nature of the disorder that makes comparisons of group differences unreliable. A PET study of a group of five high-functioning autistic males (compared with a control group) showed (1) reversed hemispheric dominance during verbal auditory stimulation; (2) a trend toward reduced activation of auditory cortex during acoustic stimulation; and (3) reduced cerebellar activation during nonverbal auditory perception . PET using “theory of mind” tasks in control subjects and in subjects with Asperger syndrome have demonstrated a lack of normal activation of the left prefrontal area in those with Asperger syndrome. Instead, children with Asperger syndrome activated neighboring areas of the brain, suggesting a nonspecific reasoning mechanism for inferring mental states . 1 ..."
Reference 15
Review article
Imaging data in autism: From structure to malfunction
Acosta M.T., Pearl P.L.
Seminars in Pediatric Neurology , 2004 pp 205-213
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"... The orbitofrontal cortex has also been implicated as a plausible locus in the pathophysiology of autism and, in particular, the theory of mind. Patients with Asperger syndrome, who may perform ably on simple neuropsychologic paradigms testing the theory of mind, have difficulties with more complex tasks that mimic daily activities and lead to errors in social interaction. This domain has been related to connections between the orbitofrontal cortex and amygdala and concerns the interpretation of the significance of others’ actions or intentions and its emotional components. 69 In summary, neuroimaging findings to date appear to suggest a network of regions involved in attribution of mental state to others, i.e. theory of mind. These regions include frontal lobe, temporal lobe and cerebellum. 1 ..."
Reference 16
Book Chapter
Genome-wide association studies and neurodevelopment
Rita M. Cantor, Jennifer K. Lowe
Factors Affecting Neurodevelopment , 2021 pp 27-37
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"... Motivation and implementation The current consensus is that ASDs and related traits are polygenic, with as many as 1000 risk genes . With so many genes, each is very likely to have a small effect, and one needs large sample sizes to detect such small effects statistically. Current ASDs’ sample sizes are small compared with 150,000 for schizophrenia and 250,000 for GWAS of coronary artery disease . Current ASDs GWASs lack robust replications. To address this and prioritize genes, we searched for concordance of genetic associations of ASDs and related traits in two publicly available databases under the hypothesis that associations meeting stringent criteria in two databases that take complementary approaches to curation are more likely to be robust. The Human Gene Module of the Simons Foundation Autism Research Initiative (SFARI) Gene database has a panel of scientists who evaluate the published evidence for genes implicated in ASDs and related traits ( https://gene.sfari.org/about-human-gene ). SFARI is organized by category (rare, syndromic, association, functional) and prioritized by gene score (six groups ranging from 1 = high confidence to 6 = not supported). We selected genes in the category “Association” and with gene score of 1–3. The NIH/NHGRI-EBI GWAS Catalog (GC), reports all genes published in the GWAS literature, their p-values, and other information relevant to the studies ( https://www.ebi.ac.uk/gwas/home ) . We searched on “Autism,” “Autism Spectrum Disorder,” “Autism Spectrum Disorder Symptom,” “Social Communication Impairment,” “Asperger Syndrome,” and “Behavior or Behavioral Disorder Measurement.” We explored their overlap and prioritized genes for ASDs by requiring a score of three or smaller in SFARI and a p-value of 5 × 10 −8 or smaller in GC. 2 ..."
Reference 17
Review article
Dendritic spine actin cytoskeleton in autism spectrum disorder
Joensuu M., Lanoue V., Hotulainen P.
Progress in Neuro-Psychopharmacology and Biological Psychiatry , 2018 pp 362-381
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"... In support of this, deficiency or autism-related mutations of Shank3 , the most prevalent of the three, result in altered cortactin, Abp1, cofilin and Rac1 expression or activity, increased integrin activation and a reduction in dendritic spines and synaptic dystrophy . Furthermore, rare de novo CNVs, deletions and duplications in genes encoding SHANK interacting proteins such as Disk large-associated protein 2 ( DLGAP2 ) have been associated with ASD . In line with SHANK mice models, Dlgap2 −/− mice show reduced spine density and a downregulation of synaptic proteins such as HOMER1 . Another postsynaptic density scaffolding protein, linking regulation of the synaptic actin cytoskeleton to ASD, is DISC1 (disrupted in schizophrenia 1) ( DISC1 ). DISC1 plays a major role in early brain development by regulating a number of essential neurodevelopmental events including cell proliferation, neurite outgrowth, synapse formation and neuronal migration . DISC1 maintains spine morphology and function by regulating Rac-1 activator, Kalirin-7 (Kal-7), access to Rac1 ( Fig. 5 ). Kal-7/Rac1 cascade and Rac-1 activation in response to NMDA receptor activation in both neuronal cultures and rat brain in vivo are important for the activity–dependent spine morphology and functional plasticity . In addition to schizophrenia, genetic association and rare variants in DISC1 have been associated with autism and Asperger's syndrome . IRSp53 (also known as brain-specific angiogenesis inhibitor 1-associated protein 2, BAIAP2 ) is a multi-domain scaffolding and adaptor protein that has been implicated in the regulation of membrane and actin dynamics in dendritic spines, filopodia and lamellipodia. 2 ..."
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"... Furthermore, rare de novo CNVs, deletions and duplications in genes encoding SHANK interacting proteins such as Disk large-associated protein 2 ( DLGAP2 ) have been associated with ASD . In line with SHANK mice models, Dlgap2 −/− mice show reduced spine density and a downregulation of synaptic proteins such as HOMER1 . Another postsynaptic density scaffolding protein, linking regulation of the synaptic actin cytoskeleton to ASD, is DISC1 (disrupted in schizophrenia 1) ( DISC1 ). DISC1 plays a major role in early brain development by regulating a number of essential neurodevelopmental events including cell proliferation, neurite outgrowth, synapse formation and neuronal migration . DISC1 maintains spine morphology and function by regulating Rac-1 activator, Kalirin-7 (Kal-7), access to Rac1 ( Fig. 5 ). Kal-7/Rac1 cascade and Rac-1 activation in response to NMDA receptor activation in both neuronal cultures and rat brain in vivo are important for the activity–dependent spine morphology and functional plasticity . In addition to schizophrenia, genetic association and rare variants in DISC1 have been associated with autism and Asperger's syndrome . IRSp53 (also known as brain-specific angiogenesis inhibitor 1-associated protein 2, BAIAP2 ) is a multi-domain scaffolding and adaptor protein that has been implicated in the regulation of membrane and actin dynamics in dendritic spines, filopodia and lamellipodia. Accumulating evidence indicates that IRSp53 is an abundant component of multi-protein complexes on the postsynaptic side of excitatory synapses and directly binds to PSD-95 and Shank/ProSAP ( Fig. 5 ). IRSp53 has been suggested to form a platform-like structure that organizes synaptic signaling to regulate dendritic spines through its ability to interact with F-actin and actin regulatory proteins . 2 ..."
Reference 18
Book Chapter
Autism and Related Disorders
Volkmar F., Wiesner L.
Developmental-Behavioral Pediatrics , 2009 pp 675-685
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"... Unusual affective responses (e.g., throwing a tantrum in response to a small change) may be a source of great distress to parents. Play skills tend to remain underdeveloped, with objects used more for simple sensorimotor or functional play, rather than more symbolic activities , and are important areas for early intervention . Cognitive development in autism is unusual. Generally, children with autism do best with tasks that involve perceptual-motor or motor abilities, and do poorly with tasks that involve social judgment, abstract thinking, and use of symbolic information or verbal abilities . When the highly discrepant results of various subtests are averaged, IQ scores are often within the range of intellectual disability/intellectual deficiency . With earlier intervention, there seems to have been a trend toward decreased rates of associated intellectual disability, likely reflecting changes in diagnostic practice and the results of earlier intervention . As children with autism reach school age, scores become more stable. Unusual islets of ability are sometimes observed (e.g., children with autism may have amazing abilities to do calendar calculation or drawing abilities) . Such individuals (usually referred to as autistic savants ) can be quite impaired in other areas. Although children with Asperger syndrome also are severely socially disabled, they usually are highly verbal, and their difficulties are not a source of concern until the child is exposed to peers (i.e., typically in the preschool years). In contrast to autism, motor clumsiness is frequent, as are all-encompassing interests; the latter interfere with functioning and often intrude on family life. The pattern on cognitive testing also is different: In contrast to autism, verbal skills are often an area of significant strength for the child; this pattern sometimes is referred to as nonverbal learning disability (see vignette) . Individuals with Asperger syndrome are much less likely to function in the intellectual disability range. From Volkmar FR, Klin A, Schultz RT Asperger’s disorder: Clinical case conference. Am J Psychiatry 157:262-267, 2000. Vignette VignetteAutobiographical Statement of a 10-year-old Boy with Asperger Disorder ∗ ∗ Name changed. 2 ..."
Reference 19
Review article
From music making to speaking: Engaging the mirror neuron system in autism
Wan C.Y., Demaine K., Zipse L., Norton A., Schlaug G.
Brain Research Bulletin , 2010 pp 161-168
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"... Given that the mirror neuron system is believed to involve both sensorimotor integration and speech representation, it is likely to underlie some of the communication deficits in individuals with autism spectrum disorder (ASD). Recent research has provided preliminary support for this hypothesis. Because individuals with high-functioning autism are over-represented in this literature, the work reviewed here should be viewed with caution when extrapolated to individuals with low-functioning autism, especially those who are nonverbal. Nonetheless, published research studies represent a good starting point for understanding the mechanisms underlying speech-motor impairments in individuals with ASD. For example, Nishitani et al. used magnetoencephalography (MEG) and electromyograms (EMG) to measure brain activity and lip movement when individuals with Asperger's syndrome were asked to imitate orofacial gestures. Compared to controls, the ASD group had EMGs that lasted almost twice as long. Moreover, the ASD group showed weaker activations in Broca's area, which was delayed by 45–60 ms. Similarly, when imitating facial expressions inside the MRI scanner, children with autism showed decreased activity in Broca's area relative to controls . Although behavioral performance between these two groups did not differ, Broca's area activity in the autism group correlated with severity of autism as measured by the social subscales of standardized tests [71,72] . In another study, Theoret et al. used TMS and found that the level of excitability in the primary motor cortex during action observation was lower in individuals with ASD compared to controls. A structural imaging study found that compared to controls, individuals with autism had reduced cortical thickness (decreased gray matter) in regions of the mirror neuron system, including Broca's area, the inferior parietal lobule and the superior temporal sulcus . Moreover, the extent of the reduction in cortical thickness in these regions correlated with the severity of communicative and social symptoms in autism. 2 ..."
Reference 20
Reference works Chapter
Neurodevelopmental disorders
Klimkeit E., Rinehart N., Bradshaw J.
International Encyclopedia of Public Health , 2008 pp 512-521
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"... Neuropsychology There are three main cognitive theories of autism and Asperger's disorder: theory-of-mind, the executive dysfunction theory, and the theory of weak central coherence. Deficiencies in theory-of-mind – that is, the ability to understand that other people have unique perspectives and thoughts that are sometimes contextually independent – may be linked to the social-communicative deficits. Weak central coherence, a deficit in the ability to integrate details into a coherent global perception, may be linked to the tendency to be preoccupied with parts of objects and to miss the ‘bigger picture.’ Executive functioning refers to the role of the frontostriatal circuits in coordinating cognitive-motor output so that behavior is well timed, planned, adaptable, appropriate, and relevant. The repetitive, stereotyped, and restricted behaviors may be due, in part, to deficient executive functioning. Movement abnormalities in ASDs, in particular gait (walking) abnormalities, may be underpinned by disruption to neural circuitry involving the basal ganglia and cerebellum. 2 ..."
Reference 21
Reference works Chapter
Neurodevelopmental Disorders in Children
Rinehart N.J., Tonge B.J.
Encyclopedia of Stress , 2007 pp 844-850
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"... A poor theory of mind refers to problems with understanding that other people have their own perspectives and thoughts; it is believed to be a reason why people with ASDs have difficulties understanding and relating to other people. The executive dysfunction theory accounts for the problems that people with ASDs experience with timing and planning and producing appropriate and relevant behavior (e.g., coping with changes in the school timetable, planning homework). This breakdown in the ability to effectively direct one's behavior is also thought to be related to the repetitive, stereotyped, and restricted behavioral patterns of ASDs. Weak central coherence refers to a problem with being unable to see the forest for the trees and is thought to be responsible for why people with ASDs tend to be obsessed with details and often miss the bigger picture. Standardized tests have demonstrated that the neuropsychological profile of autism is characterized primarily by deficient cognitive flexibility and planning, but without problems in the ability to sustain and direct attention (problems attributed to the prefrontal regions of the brain). Research suggests that the kinds of problems that individuals with Asperger's disorder have in directing their behavior may be different from those observed in autism, for example, their problem may be more one of initiating behavior than moving effectively from one behavior to another, perhaps suggesting that different parts of the prefrontal brain are involved in each disorder. Neuromotor testing has found that the walking and upper body postural alignment of people with ASDs is similar to that observed in patients who have Parkinson's disease and patients with cerebellar ataxia, indicating the role of the basal ganglia and cerebellum in these disorders. Again, autism and Asperger's disorder may be associated with different kinds of motor problems, which would suggest the differential involvement of these brain regions. 2 ..."
Reference 22
Review article
Episodic memory and self-awareness in Asperger Syndrome: Analysis of memory narratives
Chaput V., Amsellem F., Urdapilleta I., Chaste P., Leboyer M., Delorme R., Gousse V.
Research in Autism Spectrum Disorders , 2013 pp 1062-1067
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"... Abstract Previous findings from researchers on individuals with Asperger Syndrome (AS) suggest peculiarities of autobiographical memory (AM). They have shown a personal episodic memory deficit in the absence of a personal semantic memory impairment. The primary aim of this study was to explore AM in individuals with AS, and more specifically to investigate the link between episodic memory, self-awareness, and autonoetic consciousness through language analysis. We asked fifteen adults with AS and fifteen age- and IQ-matched controls to recall autobiographical memories from three life periods. Recorded interviews were processed using Alceste software. We found that participants with AS recalled fewer and less-detailed episodic memories than did controls. A content analysis revealed that family-related vocabulary as well as possessive pronouns was significantly less frequent in AS interviews than in those of controls. In conclusion, our results support the hypothesis that a deficiency of episodic memory may be due to poor awareness of the self in social relationships. Reduced use of possessive pronouns may also indicate less self-investment in life experiences, which would in turn impact recall. 2 ..."
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"... Autobiographical memory task Overall subjects with AS produced fewer autobiographical memories ( M = 23.3, SD = 6.7) than did control participants ( M = 29.7, SD = 4.4) ( U = 180, p = 0.005). In addition, individuals with AS recalled fewer episodic memories ( M = 9.3, SD = 8) than did controls ( M = 17.6, SD = 9.2) ( U = 170, p = 0.017). The group with AS also recalled fewer episodic memories that were located in time and space and accompanied by contextual details linked to emotional and sensory feelings. Also, among subjects with AS, eight (53.3%) were unable to produce any memory in response to some TEMPau questions, versus one subject in the control group. 2 ..."
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"... Highlights We study links between episodic memory, self-awareness and autonoetic consciousness in AS. Patients with AS produced fewer episodic memories than controls. Patients with AS used less possessive pronouns and family-related vocabulary than did controls. Deficiency of episodic memory may be due to poor awareness of the self in social relationships. This may indicate less self-investment in life experiences, which would impact recall. 2 ..."
Reference 23
Book Chapter
Autism spectrum disorders
Johnson C.P., Myers S.M.
Developmental-Behavioral Pediatrics , 2008 pp 519-577
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"... Asperger Syndrome Asperger syndrome is characterized by the same impairment in social interaction and restricted interests as in autistic disorder; however, language skills are relatively normal (defined as use of single words by age 2 years and phrases by 3 years) ( Table 15-2 ). 20 Later language is characterized by pragmatic deficits (problems with the social use of language). In addition, cognitive and adaptive skills are normal. Depending on the child's age, it is sometimes quite challenging to distinguish between children with Asperger syndrome and children with autistic disorder and normal intelligence. Because of this, controversy exists as to whether Asperger syndrome represents a high-functioning form of autism or a separate entity. 26, 27 Children with Asperger syndrome are usually not recognized until after 4 years of age, when social interactions with peers in preschool settings become a concern. 2 ..."
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"... 290, 291 Developing a consensus statement may be more challenging for several reasons: (1) There remains controversy about whether Asperger syndrome is a distinct entity versus a subtype of high-functioning autism 27 ; (2) there are several sets of criteria for Asperger syndrome 36, 340 ; (3) because these children's skills are more complex and differentiated, a wider variety of tests is necessary to quantify the skills 323 ; and (4) most instruments lack sensitivity in identifying more subtle social communication deficits. 290, 291 For these reasons, the process necessary to make an accurate diagnosis of Asperger syndrome is challenging and almost always involves a team approach. The Autism Diagnostic Interview–Revised and Module 3 or 4 of the ADOS are ideally suited for higher functioning verbal children such as those with Asperger syndrome. In addition to historical aspects of the child's early development (particularly language development), a complete battery of standardized tests is needed to differentiate Asperger syndrome from learning disorders with overlapping characteristics (e.g., nonverbal learning disability, pragmatic disorder, semantic-pragmatic language disorder, hyperlexia). Asperger syndrome is even less often associated with a known medical condition than is autistic disorder 18 ; nevertheless, a number of mental health conditions (i.e., schizophrenia, schizoid personality, anxiety disorder, obsessive-compulsive disorder, oppositional defiant disorder, and selective/elective mutism) may mimic Asperger syndrome or coexist with it. Thus, a physician with expertise in ASD and mental health conditions should be involved in the diagnostic process. Table 15-6 lists similar and contrasting characteristics of some of these learning and mental health disorders. ASSESSMENT OF FAMILY FUNCTIONING AND AVAILABLE RESOURCES An important part of the comprehensive evaluation of a child with a suspected ASD is the assessment of the family. It should begin with an assessment of the parents' current understanding of ASD in order to determine both the family's ability to advocate effectively for their child and the appropriate level of training activities needed. 3 ..."
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"... Asperger syndrome is even less often associated with a known medical condition than is autistic disorder 18 ; nevertheless, a number of mental health conditions (i.e., schizophrenia, schizoid personality, anxiety disorder, obsessive-compulsive disorder, oppositional defiant disorder, and selective/elective mutism) may mimic Asperger syndrome or coexist with it. Thus, a physician with expertise in ASD and mental health conditions should be involved in the diagnostic process. Table 15-6 lists similar and contrasting characteristics of some of these learning and mental health disorders. ASSESSMENT OF FAMILY FUNCTIONING AND AVAILABLE RESOURCES An important part of the comprehensive evaluation of a child with a suspected ASD is the assessment of the family. It should begin with an assessment of the parents' current understanding of ASD in order to determine both the family's ability to advocate effectively for their child and the appropriate level of training activities needed. Sometimes parents may need assistance in evaluating the information they already have, especially if it is not peer reviewed and has been accessed from the Internet. The developmental-behavioral pediatrician should also assess the family's coping strategies, resources (financial, childcare, health insurance), and support systems, including family, friends, neighbors, and religious and local community agencies. On the basis of these considerations, the developmental-behavioral pediatrician or, when available, a team social worker or nurse coordinator can formulate a family support plan. 341–343 Referrals to local or Internet-based sources of information, advocacy, and support should be provided. Sleep deprivation, depression, physical well-being, and emotional conditions resulting from stress are more likely to occur in members of families with children with ASD. 344–347 These problems should be considered and referrals made when appropriate. LABORATORY INVESTIGATION The final challenge in the evaluation of ASD, and perhaps the most controversial, is determining the extent of the etiological “search.” Published etiological yields vary and generally are more highly correlated with the presence or absence of coexisting mental retardation rather than with ASD itself. The majority of reports describe finding an underlying cause in 2% to 10% of patients. 3 ..."
Reference 24
Review article
Understanding facial expressivity in autism spectrum disorder: An inside out review of the biological basis and clinical implications
Deutsch S.I., Raffaele C.T.
Progress in Neuro-Psychopharmacology and Biological Psychiatry , 2019 pp 401-417
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"... Moreover, in a research poster presented at the 2010 International Neuropsychological Society Conference, Holdnack & Drozdick reported on a study that compared 800 non-ASD controls to 43 participants with a diagnosis of Autism or Asperger's on the ACS social perception test. Results found that those in the ASD group showed general deficits in social perception, which validated the use of this test for an ASD population . The NEPSY- II is a pediatric neuropsychological assessment that contains a Social Perception domain that includes the Affect Recognition and Theory of Mind (TOM) tests . Specifically, these tests assess the cognitive processes that facilitate social interactions and it may be useful for identifying diagnoses that are associated with impairments in social behaviors, such as ASD . The Affect Recognition test is a three part sub-test within the Social Perception domain of the NEPSY-II that is designed to determine the child's ability to recognize and understand other people's emotional facial expressions . For the first task, the child is presented two pictures of actors portraying facial expressions (happy, sad, fear, angry, disgust, neutral) and asked if the actors are portraying the same or differing emotion(s). For the second task, the child is shown three or four pictures of different actors portraying facial emotions and asked to point out the actors within the series who are expressing the same emotion. For the third task, the examinee is briefly shown a picture of an actor portraying a facial emotion. They are then asked to identify, from memory, one picture out of a series of a different page that portrays that same emotion. The TOM test assesses a child's ability to infer what another person is thinking and if he understands this other person's point of view . 3 ..."
Reference 25
Book Chapter
Asperger’s syndrome intervention: combining neurofeedback, biofeedback, and metacognition
Michael Thompson, Lynda Thompson
Introduction to Quantitative EEG and Neurofeedback , 2023 pp 343-374
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"... Abstract Asperger's syndrome, which constitutes a distinct sub-set of symptoms subsumed under the spectrum of autistic disorders, is increasingly being recognized, not only by clinicians, but also by the general public, due to the portrayal of people with Asperger's in media productions. This chapter details the symptoms and the underlying neuroanatomical findings of Asperger's and then goes on to explain appropriate interventions that combine neurofeedback with biofeedback especially heart rate variability (HRV) training and coaching in metacognitive strategies. 3 ..."
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"... You join in what he is doing, then introduce what you are now going to do together. Meet their dependency needs while allowing some independence and a feeling of control. D Possible addition for dealing with learning difficulties In addition to specific spatial reasoning, verbal interpretation and comprehension difficulties, executive functioning for clients with AS includes the synthesis, integration, and appropriate modulation of all sensory information input: auditory, visual, and kinesthetic. Deficiencies in these executive functions are addressed by careful assessment and then NFB. The identification of specific verbal and NVLD is aided by psycho-educational testing. Deficiencies can then be linked to EEG findings. Then an NFB intervention is designed to normalize the electrical activity over the appropriate cortical areas while the client is learning appropriate strategies, and also doing BFB. Usually, the EEG feedback involves placement over Wernicke’s area for comprehension difficulties, and right parietal areas for NVLD symptoms. The specific frequency ranges for enhance and inhibit are set according to assessment findings for each case. For improving social awareness, the metacognitive strategies portion of the training can use social stories. One can also use short videos with themes that help social understanding. Whether it be comprehension or NVLD, or whether, as in the autistic child, it appears to be a lack of appropriate cingulate and prefrontal modulation of the sensory input from the parietal areas, the connectivity (coherence and/or comodulation) will usually be outside the database norms. Commonly in Asperger’s and in NVLD, we observe a “disconnect” with hypo-coherence between right parietal-temporal region (T4, T6 updated nomenclature T8, P8) and the left frontal lobe (F5) combined with hyper-coherence in the right hemisphere between parietal and temporal, temporal and frontal areas. Thus, the differences from the normal database can be either too much or too little communication between specific sites. Hyper-coherence between regions is an abnormality that is interpreted as resulting from a lack of appropriate differentiation of functioning between regions. 3 ..."
Reference 26
Book Chapter
Enduring Effects of Neurofeedback in Children
Coben R., Arns M., Kouijzer M.E.J.
Neurofeedback and Neuromodulation Techniques and Applications , 2011 pp 403-422
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"... Enduring Behavioral and Neuropsychological Benefits of Neurofeedback in ASD A similar study with findings that can be considered complementary to those of Kouijzer and colleagues was recently conducted by Coben at his New York clinic. This study assessed 20 patients with ASD in order to investigate long-term clinical effects of neurofeedback in terms of behavioral and neuropsychological measures. The subject pool for this study was predominately male (male 16; female 4) and all Caucasian. The mean age was 9.53, with a range of 5–10. Most subjects (80%) were medication-free, with only one subject taking more than two medications. Handedness was mostly right-handed (N=16) with one left-handed and three ambidextrous subjects. Subjects were administered parent rating scales, including the Autism Treatment Evaluation Checklist , the Personality Inventory for Children , the Behavior Rating Inventory of Executive Function , and the Gilliam Asperger's Disorder Scale . Subjects were also administered neuropsychological assessments covering domains of attention/executive functioning, language, and visuo-spatial processing. After baseline assessments were collected all subjects underwent at least 40 sessions of neurofeedback training, with an average of 64.5 completed sessions among all subjects. Upon completion of therapy, subjects were re-evaluated and pre- and post-treatment scores were compared for significance. After re-evaluation, neurofeedback was withheld for 5–22 months (M=10.1 months) while no other treatments were administered. Following this break in treatment, subjects were evaluated once again in the same fashion as previously described. Their latter scores were then compared to scores obtained at the end of active neurofeedback training (Time 2). All statistical computations were performed in the statistical package SPSS. Scores prior to treatment on parent rating scales were compared for significance to scores obtained after treatment had ended. 3 ..."
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"... These occurred in the areas of attention (two-sample t test, t=−3.021, d.f. 19, p <0.007), language (two-sample t test, t=−2.347, d.f. 10, p <0.041) and visuo-spatial processing (two-sample t test, t=−3.568, d.f. 18, p <0.002) (see Figure 15.7 ). This would suggest that neurofeedback training not only led to objective gains in neuropsychological functioning, but that these enhancements in functioning continued to improve over the follow-up period when no treatment was being received. The results of this present study were quite interesting. First, our findings add to the wealth of studies that have shown that from pre- to post-treatment conditions, neurofeedback is an effective therapy for treating individuals with autistic spectrum disorders. Additionally, these results show that this treatment was effective in limiting autistic behavioral deficits as well as deficits of a more neuropsychological nature. Furthermore, as our analysis shows, there were no significant increases in autistic pathology when subjects were re-evaluated after neurofeedback was withheld. This finding supports previously found evidence that neurofeedback is capable of creating stable changes within autistic subjects that are not likely to rapidly degrade when treatment ends . Of potentially even greater interest, this study found that during the period in which subjects were receiving no treatment, positive clinical neuropsychological gains were still being manifested within the domains of attention, executive functioning, language, and visuo-spatial processing. Thus, even without continued treatment subjects apparently were continuing to improve in these realms. An important implication of this finding is that neurofeedback may indeed change the autistic brain to work in novel and more efficient ways, and these changes may continue to progress even after the treatment has ended. This finding helps further the claim that neurofeedback creates specific neurophysiological changes within the autistic brain ( Coben, Sherlin, Hudspeth & McKeon, 2009 [study under review]). This is in stark contrast to other commonly administered treatments for autism. 3 ..."

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