Asperger Syndrome
Autistic Disorder
Child Development Disorders, Pervasive
Language Development Disorders
Nerve Fibers, Unmyelinated
The functional neuroanatomy of social behaviour: changes in cerebral blood flow when people with autistic disorder process facial expressions. (1/149)
Although high-functioning individuals with autistic disorder (i.e. autism and Asperger syndrome) are of normal intelligence, they have life-long abnormalities in social communication and emotional behaviour. However, the biological basis of social difficulties in autism is poorly understood. Facial expressions help shape behaviour, and we investigated if high-functioning people with autistic disorder show neurobiological differences from controls when processing emotional facial expressions. We used functional MRI to investigate brain activity in nine adults with autistic disorder (mean age +/- standard deviation 37 +/- 7 years; IQ 102 +/- 15) and nine controls (27 +/- 7 years; IQ 116 +/- 10) when explicitly (consciously) and implicitly (unconsciously) processing emotional facial expressions. Subjects with autistic disorder differed significantly from controls in the activity of cerebellar, mesolimbic and temporal lobe cortical regions of the brain when processing facial expressions. Notably, they did not activate a cortical 'face area' when explicitly appraising expressions, or the left amygdala region and left cerebellum when implicitly processing emotional facial expressions. High-functioning people with autistic disorder have biological differences from controls when consciously and unconsciously processing facial emotions, and these differences are most likely to be neurodevelopmental in origin. This may account for some of the abnormalities in social behaviour associated with autism. (+info)Dissociation between 'theory of mind' and executive functions in a patient with early left amygdala damage. (2/149)
There have been recent suggestions that the amygdala may be involved in the development or mediation of 'theory of mind'. We report a patient, B.M., with early or congenital left amygdala damage who, by adulthood, had received the psychiatric diagnoses of schizophrenia and Asperger's syndrome. We conducted a series of experimental investigations to determine B.M.'s cognitive functioning. In line with his diagnoses, B.M. was found to be severely impaired in his ability to represent mental states. Following this, we conducted a second series of studies to determine B.M.'s executive functioning. In the literature, there have been frequent claims that theory of mind is mediated by general executive functioning. B.M. showed no indication of executive function impairment, passing 16 tests assessing his ability to inhibit dominant responses, create and maintain goal-related behaviours, and temporally sequence behaviour. The findings are discussed with reference to models regarding the role of the amygdala in the development of theory of mind and the degree of dissociation between theory of mind and executive functioning. We conclude that theory of mind is not simply a function of more general executive functions, and that executive functions can develop and function on-line, independently of theory of mind. Moreover, we conclude that the amygdala may play some role in the development of the circuitry mediating theory of mind. (+info)A genomewide screen for autism susceptibility loci. (3/149)
We report the analysis of 335 microsatellite markers genotyped in 110 multiplex families with autism. All families include at least two "affected" siblings, at least one of whom has autism; the remaining affected sibs carry diagnoses of either Asperger syndrome or pervasive developmental disorder. Affected sib-pair analysis yielded multipoint maximum LOD scores (MLS) that reach the accepted threshold for suggestive linkage on chromosomes 5, X, and 19. Nominal evidence for linkage (point-wise P<.05) was obtained on chromosomes 2, 3, 4, 8, 10, 11, 12, 15, 16, 18, and 20, and secondary loci were found on chromosomes 5 and 19. Analysis of families sharing alleles at the putative X chromosomal linked locus and one or more other putative linked loci produced an MLS of 3.56 for the DXS470-D19S174 marker combination. In an effort to increase power to detect linkage, scan statistics were used to evaluate the significance of peak LOD scores based on statistical evidence at adjacent marker loci. This analysis yielded impressive evidence for linkage to autism and autism-spectrum disorders with significant genomewide P values <.05 for markers on chromosomes 5 and 8 and with suggestive linkage evidence for a marker on chromosome 19. (+info)Episodic memory and autonoetic consciousness: a first-person approach. (4/149)
Episodic memory is identified with autonoetic consciousness, which gives rise to remembering in the sense of self-recollection in the mental re-enactment of previous events at which one was present. Autonoetic consciousness is distinguished from noetic consciousness, which gives rise to awareness of the past that is limited to feelings of familiarity or knowing. Noetic consciousness is identified not with episodic but with semantic memory, which involves general knowledge. A recently developed approach to episodic memory makes use of 'first-person' reports of remembering and knowing. Studies using this approach have revealed many independent variables that selectively affect remembering and others that selectively affect knowing. These studies can also be interpreted in terms of distinctiveness and fluency of processing. Remembering and knowing do not correspond with degrees of confidence in memory. Nor does remembering always control the memory response. There is evidence that remembering is selectively impaired in various populations, including not only amnesic patients and older adults but also adults with Asperger's syndrome. This first-person approach to episodic memory represents one way in which that most elusive aspect of consciousness, its subjectivity, can be investigated scientifically. The two kinds of conscious experiences can be manipulated experimentally in ways that are systematic, replicable and intelligible theoretically. (+info)Brain anatomy and sensorimotor gating in Asperger's syndrome. (5/149)
Asperger's syndrome (an autistic disorder) is characterized by stereotyped and obsessional behaviours, and pervasive abnormalities in socio-emotional and communicative behaviour. These symptoms lead to social exclusion and a significant healthcare burden; however, their neurobiological basis is poorly understood. There are few studies on brain anatomy of Asperger's syndrome, and no focal anatomical abnormality has been reliably reported from brain imaging studies of autism, although there is increasing evidence for differences in limbic circuits. These brain regions are important in sensorimotor gating, and impaired 'gating' may partly explain the failure of people with autistic disorders to inhibit repetitive thoughts and actions. Thus, we compared brain anatomy and sensorimotor gating in healthy people with Asperger's syndrome and controls. We included 21 adults with Asperger's syndrome and 24 controls. All had normal IQ and were aged 18-49 years. We studied brain anatomy using quantitative MRI, and sensorimotor gating using prepulse inhibition of startle in a subset of 12 individuals with Asperger's syndrome and 14 controls. We found significant age-related differences in volume of cerebral hemispheres and caudate nuclei (controls, but not people with Asperger's syndrome, had age-related reductions in volume). Also, people with Asperger's syndrome had significantly less grey matter in fronto-striatal and cerebellar regions than controls, and widespread differences in white matter. Moreover, sensorimotor gating was significantly impaired in Asperger's syndrome. People with Asperger's syndrome most likely have generalized alterations in brain development, but this is associated with significant differences from controls in the anatomy and function of specific brain regions implicated in behaviours characterizing the disorder. We hypothesize that Asperger's syndrome is associated with abnormalities in fronto-striatal pathways resulting in defective sensorimotor gating, and consequently characteristic difficulties inhibiting repetitive thoughts, speech and actions. (+info)Autism, Asperger syndrome and brain mechanisms for the attribution of mental states to animated shapes. (6/149)
Ten able adults with autism or Asperger syndrome and 10 normal volunteers were PET scanned while watching animated sequences. The animations depicted two triangles moving about on a screen in three different conditions: moving randomly, moving in a goal-directed fashion (chasing, fighting), and moving interactively with implied intentions (coaxing, tricking). The last condition frequently elicited descriptions in terms of mental states that viewers attributed to the triangles (mentalizing). The autism group gave fewer and less accurate descriptions of these latter animations, but equally accurate descriptions of the other animations compared with controls. While viewing animations that elicited mentalizing, in contrast to randomly moving shapes, the normal group showed increased activation in a previously identified mentalizing network (medial prefrontal cortex, superior temporal sulcus at the temporo-parietal junction and temporal poles). The autism group showed less activation than the normal group in all these regions. However, one additional region, extrastriate cortex, which was highly active when watching animations that elicited mentalizing, showed the same amount of increased activation in both groups. In the autism group this extrastriate region showed reduced functional connectivity with the superior temporal sulcus at the temporo-parietal junction, an area associated with the processing of biological motion as well as with mentalizing. This finding suggests a physiological cause for the mentalizing dysfunction in autism: a bottleneck in the interaction between higher order and lower order perceptual processes. (+info)Oxytocin infusion reduces repetitive behaviors in adults with autistic and Asperger's disorders. (7/149)
Autism is a neurodevelopmental disorder characterized by dysfunction in three core behavioral domains: repetitive behaviors, social deficits, and language abnormalities. There is evidence that abnormalities exist in peptide systems, particularly the oxytocin system, in autism spectrum patients. Furthermore, oxytocin and the closely related peptide vasopressin are known to play a role in social and repetitive behaviors. This study examined the impact of oxytocin on repetitive behaviors in 15 adults with autism or Asperger's disorder via randomized double-blind oxytocin and placebo challenges. The primary outcome measure was an instrument rating six repetitive behaviors: need to know, repeating, ordering, need to tell/ask, self-injury, and touching. Patients with autism spectrum disorders showed a significant reduction in repetitive behaviors following oxytocin infusion in comparison to placebo infusion. Repetitive behavior in autism spectrum disorders may be related to abnormalities in the oxytocin system, and may be partially ameliorated by synthetic oxytocin infusion. (+info)Impaired mirror-image imitation in Asperger and high-functioning autistic subjects. (8/149)
Imitation is crucial for proper development of social and communicative skills. Here, we argue that, based on an error analysis of a behavioral imitation task, adult Asperger and high-functioning autistic subjects suffer from an intriguing deficit of imitation: they lack the natural preference for imitation in a mirror-image fashion. The imitation task consisted of a simple movement sequence of putting a pen with the left or right hand into a green or a blue cup using one of two possible grips. The subjects were asked to imitate the experimenter's hand movements either using the crossed hand (e.g., the subject's right hand corresponding to the experimenter's right hand) for imitation or to imitate as if looking in a mirror (e.g., the subject's left hand corresponding to the experimenter's right hand). When people normally view other persons face-to-face, they prefer to imitate as in a mirror, and observation of mirror-image-like movements speeds up performance in nonimitative tasks. However, our autistic subjects, defective in social cognition, did not profit from mirror-image movements of others. These results provide a new insight into the difficulties that autistic subjects face in viewing and understanding actions of others. (+info)Asperger Syndrome is a developmental disorder that is part of the autism spectrum disorders (ASDs). It is characterized by significant difficulties in social interaction and nonverbal communication, as well as restricted and repetitive patterns of behavior and interests. However, people with Asperger Syndrome usually have normal or above-average intelligence and language development.
The following are some of the diagnostic criteria for Asperger Syndrome according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-5):
1. Persistent deficits in social communication and social interaction across multiple contexts, including:
* Deficits in social-emotional reciprocity;
* Deficits in nonverbal communicative behaviors used for social interaction;
* Deficits in developing, maintaining, and understanding relationships.
2. Restricted, repetitive patterns of behavior, interests, or activities, as manifested by at least two of the following:
* Stereotyped or repetitive motor movements, use of objects, or speech;
* Insistence on sameness, inflexible adherence to routines, or ritualized patterns of verbal or nonverbal behavior;
* Highly restricted, fixated interests that are abnormal in intensity or focus;
* Hyper- or hyporeactivity to sensory input or unusual interest in sensory aspects of the environment.
3. Symptoms must be present in early childhood but may not become fully manifest until social demands exceed limited capacities or may be masked by learned strategies in later life.
4. Symptoms cause clinically significant impairment in social, occupational, or other important areas of functioning.
5. These disturbances are not better explained by intellectual disability (intellectual developmental disorder) or global developmental delay.
It's worth noting that the term "Asperger Syndrome" is no longer used in the DSM-5, and it has been subsumed under the broader category of autism spectrum disorder. However, many people still use the term to describe a particular presentation of ASD with normal language development and intelligence.
Autistic Disorder, also known as Autism or Classic Autism, is a neurodevelopmental disorder that affects communication and behavior. It is characterized by:
1. Persistent deficits in social communication and social interaction across multiple contexts, including:
* Deficits in social-emotional reciprocity;
* Deficits in nonverbal communicative behaviors used for social interaction;
* Deficits in developing, maintaining, and understanding relationships.
2. Restricted, repetitive patterns of behavior, interests, or activities, as manifested by at least two of the following:
* Stereotyped or repetitive motor movements, use of objects, or speech;
* Insistence on sameness, inflexible adherence to routines, or ritualized patterns of verbal or nonverbal behavior;
* Highly restricted, fixated interests that are abnormal in intensity or focus;
* Hyper- or hyporeactivity to sensory input or unusual interest in sensory aspects of the environment.
3. Symptoms must be present in the early developmental period (but may not become fully manifest until social demands exceed limited capacities) and limit or impair everyday functioning.
4. Symptoms do not occur exclusively during the course of a schizophrenia spectrum disorder or other psychotic disorders.
Autistic Disorder is part of the autism spectrum disorders (ASDs), which also include Asperger's Syndrome and Pervasive Developmental Disorder Not Otherwise Specified (PDD-NOS). The current diagnostic term for this category of conditions, according to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), is Autism Spectrum Disorder.
Pervasive developmental disorders (PDD) are a group of conditions that affect the development and functioning of the brain, leading to delays in many areas of development. The American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) has replaced the term "pervasive developmental disorders" with "autism spectrum disorder" and "other neurodevelopmental disorders."
Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by persistent deficits in social communication and interaction across multiple contexts, as well as restricted, repetitive patterns of behavior, interests, or activities. The symptoms of ASD can range from mild to severe, and the condition affects approximately 1 in 54 children in the United States.
Other neurodevelopmental disorders that were previously classified as PDDs include:
1. Intellectual disability (ID): a condition characterized by significant limitations in intellectual functioning and adaptive behavior, which covers many everyday social and practical skills. This disorder used to be referred to as "mental retardation."
2. Communication disorders: these are disorders that affect an individual's ability to communicate, including language disorders, speech sound disorders, and stuttering.
3. Attention-deficit/hyperactivity disorder (ADHD): a neurodevelopmental disorder characterized by symptoms of inattention, hyperactivity, and impulsivity.
4. Specific learning disorder: a neurodevelopmental disorder that affects an individual's ability to learn and use specific academic skills, such as reading, writing, or mathematics.
5. Motor disorders: these are disorders that affect an individual's movement and coordination, including developmental coordination disorder, stereotypic movement disorder, and tic disorders.
The medical definition of 'Child Development Disorders, Pervasive' has been replaced with more specific diagnoses in the DSM-5 to better reflect the diverse nature of these conditions and improve diagnostic accuracy and treatment planning.
The Wechsler Scales are a series of intelligence and neuropsychological tests used to assess various aspects of cognitive functioning in individuals across the lifespan. The scales include:
1. Wechsler Preschool and Primary Scale of Intelligence (WPPSI): Designed for children aged 2 years 6 months to 7 years 3 months, it measures verbal (e.g., vocabulary, comprehension) and performance (e.g., visual-motor integration, spatial reasoning) abilities.
2. Wechsler Intelligence Scale for Children (WISC): Developed for children aged 6 to 16 years, it evaluates verbal comprehension, perceptual reasoning, working memory, and processing speed.
3. Wechsler Adult Intelligence Scale (WAIS): Created for adults aged 16 to 90 years, it assesses similar domains as the WISC but with more complex tasks.
4. Wechsler Memory Scale (WMS): Designed to measure various aspects of memory functioning in individuals aged 16 to 89 years, including visual and auditory immediate and delayed recall, working memory, and attention.
5. Wechsler Abbreviated Scale of Intelligence (WASI): A brief version of the WAIS used for quicker intelligence screening in individuals aged 6 to 89 years.
These scales are widely used in clinical, educational, and research settings to identify strengths and weaknesses in cognitive abilities, diagnose learning disabilities and other neurodevelopmental disorders, monitor treatment progress, and provide recommendations for interventions and accommodations.
Language development disorders, also known as language impairments or communication disorders, refer to a group of conditions that affect an individual's ability to understand and/or use spoken or written language in a typical manner. These disorders can manifest as difficulties with grammar, vocabulary, sentence structure, word finding, following directions, and/or conversational skills.
Language development disorders can be receptive (difficulty understanding language), expressive (difficulty using language to communicate), or mixed (a combination of both). They can occur in isolation or as part of a broader neurodevelopmental disorder, such as autism spectrum disorder or intellectual disability.
The causes of language development disorders are varied and may include genetic factors, environmental influences, neurological conditions, hearing loss, or other medical conditions. It is important to note that language development disorders are not the result of low intelligence or lack of motivation; rather, they reflect a specific impairment in the brain's language processing systems.
Early identification and intervention for language development disorders can significantly improve outcomes and help individuals develop effective communication skills. Treatment typically involves speech-language therapy, which may be provided individually or in a group setting, and may involve strategies such as modeling correct language use, practicing targeted language skills, and using visual aids to support comprehension.
Unmyelinated nerve fibers, also known as unmyelinated axons or non-myelinated fibers, are nerve cells that lack a myelin sheath. Myelin is a fatty, insulating substance that surrounds the axon of many nerve cells and helps to increase the speed of electrical impulses traveling along the nerve fiber.
In unmyelinated nerve fibers, the axons are surrounded by a thin layer of Schwann cell processes called the endoneurium, but there is no continuous myelin sheath. Instead, the axons are packed closely together in bundles, with several axons lying within the same Schwann cell.
Unmyelinated nerve fibers tend to be smaller in diameter than myelinated fibers and conduct electrical impulses more slowly. They are commonly found in the autonomic nervous system, which controls involuntary functions such as heart rate, blood pressure, and digestion, as well as in sensory nerves that transmit pain and temperature signals.