This study examined brain electrical responses as a physiological measure of speed and specificity of attentional shifting in eight adult males with autism.

Scientists in the United States have found that some stunted regions of the brain may be to blame for the most severe symptoms of the condition, while other undersized regions may cause the milder symptoms often suffered by close relatives of autistics.

Autism has been thought to be characterized, in part, by dysfunction in emotional and social cognition, but the pathology of the underlying processes and their neural substrates remain poorly understood. Several studies have hypothesized that abnormal amygdala function may account for some of the impairments seen in autism, specifically, impaired recognition of socially relevant information from faces. We explored this issue in eight high-functioning subjects with autism in four experiments that assessed recognition of emotional and social information, primarily from faces. All tasks used were identical to those previously used in studies of subjects with bilateral amygdala damage, permitting direct comparisons. All subjects with autism made abnormal social judgments regarding the trustworthiness of faces; however, all were able to make normal social judgments from lexical stimuli, and all had a normal ability to perceptually discriminate the stimuli. Overall, these data from subjects with autism show some parallels to those from neurological subjects with focal amygdala damage. We suggest that amygdala dysfunction in autism might contribute to an impaired ability to link visual perception of socially relevant stimuli with retrieval of social knowledge and with elicitation of social behavior.

Impairments in communication and social interaction are associated with altered perfusion in the medial prefrontal cortex and anterior cingulate gyrus; obsessive desire for sameness with altered perfusion in the right medial temporal lobe.

Individuals with autism spectrum disorders demonstrate a pattern of brain activity during face discrimination that is consistent with feature-based strategies that are more typical of nonface object perception

Higher brain functions are sculpted on the basis of the "hard-wired" primary emotions through the process of Affective Neural Darwinism. Here we make a tentative new proposal as to the nature of the primary emotions, based mainly on a combination of the work of Jaak Panksepp on affective neuroscience, the work of Stevens and Price on evolutionary psychiatry, and data on animal behaviour and neurology. In particular we suggest that in addition to the systems identified by Panksepp, there is substantial evidence for a "hard-wired" Ranking affective system in humans and other mammals, as well as a Disgust system which originally functioned to protect against toxins.

The present study provides additional evidence that the amygdala and hippocampus are structurally abnormal in autism. It will be of interest to determine whether an enlarged amygdala and hippocampus are characteristic of all children with autism or distinguish a particular phenotype. Understanding the genesis and functional implications of an early enlargement may be amenable to molecular neurobiological approaches using animal models. The consequences of an abnormal amygdala and hippocampus in autism, and how these might be effectively treated, will be elucidated by both animal and human studies on the normal function of these structures.

Autism is clearly not a disease that is caused by a defect in only one section of the brain. Many scientists have accepted the idea that autism is caused by a malfunction in the development of the brain which encompasses many regions.

This article discusses and provides examples of successful use of two methods that may be used to incorporate a variety of full-length feature films into neuroscience instruction. One, the "neuro-cinema" pairs the presentation of a film featuring extensive neuroscience content with primary literature reading assignments, group discussion and writing exercises. The second, a neuroscience film series, features group discussion of movies of perhaps more limited relevance to neuroscience.

We find modest associations of several polymorphisms with the efficiency of executive attention but not with overall performance measures such as reaction time.

These findings support a broader concept of cerebellar function, in which the cerebellum is involved in diverse cognitive and noncognitive neurobehavioral systems, including the attention and motor systems.

New research is challenging the long-held belief that autism affects only those regions of the brain that control social interaction, communication, and reasoning -- suggesting, instead, that the disorder affects the entire brain. The government-funded study found that even highly functioning autistic children had difficulty when asked to perform a wide range of complex tasks involving other areas of the brain. This suggests different parts of the autistic brain have difficulty working together to process complex information. This may be the driving component of autism, the researchers say.

It has been said that people with autism suffer from a lack of "central coherence," the cognitive ability to bind together a jumble of separate features into a single, coherent object or concept (Frith, 1989Go). Ironically, the same can be said of the field of autism research, which all too often seems a fragmented tapestry stitched from differing analytical threads and theoretical patterns. Defined and diagnosed by purely behavioral criteria, autism was first described and investigated using the tools of behavioral psychology. More recent years have added brain anatomy and physiology, genetics, and biochemistry, but results from these new domains have not been fully integrated with what is known about autistic behavior. The unification of these many levels of analysis will not only provide therapeutic targets for prevention and remediation of autism but can also provide a test case for theories of normal brain and cognitive development. Autism research therefore has much to learn from and much to offer to the broader neuroscience community.

A substantial body of research exists that shows differences between autistic and non-autistic individuals in the structure of the brain, 'electrical wiring' and the level of certain neurotransmitters in blood and spinal fluid.

Evidence exists for the significance of the limbic system and the amygdala in particular when it comes to regulation of social interaction, and of damage to such brain areas when it comes to impaired social awareness and responsiveness.

During the last decade imaging and autopsy studies of people with autism have found abnormalities in the cerebellum and in other brain regions that are components of the cerebellar system. Particularly striking are findings that lobules VI and VII of the vermis, the central "trunk" of the cerebellum, are abnormal. Whether these are real findings or are methodological artifacts still is in dispute, but even the possibility that this part of the brain is dysfunctional in autism leads down a tantalizing and useful trail. Vermal lobules VI and VII are the phylogenetically oldest part of the mammalian cerebellum, and would be involved in the primitive behaviors that differentiate mammals from reptiles, from whom mammals evolved. These behaviors are nursing in conjunction with maternal care, audiovocal communication for maintaining maternal-offspring contact, and play. Disruption of these behaviors, from the child’s side of the interactions, is the autistic triad.

Many useful interventions use environmental accommodations that provide a consistent pattern of sensory, motor, attentional, emotional, or some other type of modulation, compensating for one actual or potential type of cerebellar disability or another.

Over the past 10 years, high-tech research methods have begun to reveal neurological damage in some autistic individuals. One of the most important findings indicates specific damage in the limbic system, particularly in the amygdala and hippocampus.

Finally, the intriguing possibility that foetal testosterone mediates empathy through testosterone receptors in the amygdala and other parts of the 'social brain' will be an important hypothesis to test when methods become available.

Although the possibility that autism and visual agnosia were dissociable factors in this patient cannot be excluded, the finding of both deficits supports the possibility that occipito-temporal lesions can predispose to the development of autism.

The broad variation in phenotypes and severities within autism spectrum disorders suggests the involvement of multiple predisposing factors, interacting in complex ways with normal developmental courses and gradients. Identification of these factors, and the common developmental path into which theyfeed, is hampered bythe large degrees of convergence from causal factors to altered brain development, and divergence from abnormal brain development into altered cognition and behaviour. Genetic, neurochemical, neuroimaging and behavioural findings on autism, as well as studies of normal development and of genetic syndromes that share symptoms with autism, offer hypotheses as to the nature of causal factors and their possible effects on the structure and dynamics of neural systems. Such alterations in neural properties may in turn perturb activity-dependent development, giving rise to a complex behavioural syndrome many steps removed from the root causes. Animal models based on genetic, neurochemical, neurophysiological, and behavioural manipulations offer the possibility of exploring these developmental processes in detail, as do human studies addressing endophenotypes beyond the diagnosis itself.

Cambridge University professor Simon Baron-Cohen thinks he knows why autism strikes four times as many boys as girls, but his theory of general differences between male and female brains has generated quite a bit of debate.

Mapping of the behavioral, emotional, and social deficits seen in ASD patients is far from being accomplished. Preliminary studies, however, suggest that the language impairment seen in these children may be partly ascribed to a reduced brain response to external sounds, as shown by magnetoencephalography.

We sketch a hypothesis about autism according to which autistic children use overt behaviour in order to control a malfunctioning autonomic nervous system and suggest that they have learned to avoid using certain processing areas in the temporal lobes

For the first time, according to researchers, a link has been found between a structural abnormality of the brain and autism. The link was discovered by British scientists studying patients with tuberous sclerosis (TS) who were also suspected to have autism. Tuberous sclerosis is an inherited disorder that affects many parts of the body, causing lesions on the skin and in the heart, kidneys, eyes, and brain. It is also associated with mental retardation and autism. Cambridge University researchers studied 18 TS patients with suspected autism. On testing, 9 were, in fact, found to have autism -- the other 9 where found to have other psychiatric disorders. When the researchers examined the brain scans of the 18 patients, they found that 8 of them had tubers -- brain lesions commonly found in tuberous sclerosis -- in the temporal lobes. All of these 8 patients had autism. No tubers were identified in the temporal lobes of patients without autism.

Structural problems in the autistic brain are restricted to the limbic system, which controls our moods, emotions, motivations, and attention, and the vestibular-cerebellar system. Thalamus and neocortex, which control cognitive abilities, are normal.

Researchers are now trying to better understand what constitutes a “normal” brain by studying a newly compiled atlas that contains digitally mapped images of 7,000 of the organs.

As educators and parents become more cognizant of the impact they have on the growing brain, they often begin asking, "How does the human brain work and what can I do to nurture its covert operations?"

Provides accessible, high-quality information about how the brain works and how people learn.

A Johns Hopkins study has failed to link the typical autistic child's fixation on spinning objects and constant whirling around to long-suspected damage to the brain's control center for movement, balance and equilibrium.

The major difference between brain development in a child versus learning an adult is a matter of degree: the brain is far more impressionable (neuroscientists use the term plastic) in early life than in maturity.

A primer on the brain and nervous system, published by the Society for Neuroscience.

We function as a whole as the two halves of us ratchet up their functions to mesh with each other. And that is exciting; no matter what side of the brain you think with!

Single whole-brain image technology provided the first direct pictures of normal brain anatomy in living humans, helping researchers understand the relationship between brain structure, function, and human behavior.

Brain myths reflect people's deep interest in understanding how their own brains work, and that beyond the misconceptions lies an opportunity to convert enthusiasm into knowledge.

Created to introduce basic concepts on early brain research in a way that challenges us to think critically and creatively about what we have heard about the research, facts and misinformation concerning infants and brain development.

Because congenital amusia is the mirror image of the music-savant syndrome described earlier in autism, it provides strong evidence for the presence of early pressures to develop neural networks that are dedicated to music.

In the past, researchers believed that our genes were the main determinants of brain development. Now an increasing number or studies shows that conditions in our surroundings can influence our internal brain plan during early life and in later years.

The study was published in the Archives of General Psychiatry. Researchers examined brain volume and head circumference in 51 children with autism (aged 18 to 35 months) and 25 children in the same age group who were both developmentally delayed and normally developed. Head measurements obtained from medical records were also examined in another larger sample of 113 children with autism and 189 healthy children, aged from 0 to 3 years. The results showed that in children with autism there was significant enlargement in the volume of the brain region known as the cerebral cortex. That region is responsible for processing thought, perception, and memory, among other things. Evidence of brain enlargement was found in both gray and white matter throughout this part of the brain. No enlargement was found in the cerebellum, the region of the brain that deals with balance and coordination of movement.

When persons with autism remember letters, they may use brain areas different from those of nonautistic individuals. This finding adds to the understanding of how autistic individuals process information. A new study offers a glimpse of some of the cerebral "highways" that people with autism may use when trying to remember letters of the alphabet. It has found that when persons with autism try to recall letters they have seen, they may perform as well as individuals without the disorder, but even when their performance is comparable, they may tap brain areas not deployed by the latter.

Practical, applications of current research in the neurosciences to improve and maintain mental skills. Site includes tests of memory, executive planning, emotional response, social interaction, language/computation, and spatial/construction.

Discover how the brain develops, within the context of relationships, from conception through three years of age--with special sections for parents, caregivers, and pediatric and family clinicians.

BACKGROUND: Impaired neuropsychological test performance, especially on tests of executive function and attention, is often seen in children diagnosed with autism spectrum disorders (ASD). Structures involved in fronto-striatal circuitry, such as the caudate nucleus, may support these cognitive abilities. However, few studies have examined caudate volumes specifically in children with ASD, or correlated caudate volumes to cognitive ability. METHODS: Neuropsychological test scores and caudate volumes of children with ASD were compared to those of children with bipolar disorder (BD) and of typically developing (TD) children. The relationship between test performance and caudate volumes was analyzed. RESULTS: The ASD group displayed larger right and left caudate volumes, and modest executive deficits, compared to TD controls. While caudate volume inversely predicted performance on the Wisconsin Card Sorting Test in all participants, it differentially predicted performance on measures of attention across the ASD, BD and TD groups. CONCLUSIONS: Larger caudate volumes were related to impaired problem solving. On a test of attention, larger left caudate volumes predicted increased impulsivity and more omission errors in the ASD group as compared to the TD group, however smaller volume predicted poorer discriminant responding as compared to the BD group.

Vermian abnormalities undoubtedly seen in some schizophrenic patients may constitute a subsyndrome, possibly related to autistic disorders in which cerebellar abnormalities are well corroborated.

Lesions of the vermis are related to behavioural and verbal production disturbances, whereas those affecting the cerebellar hemispheres are associated with patterns of side-specic cognitive dysfunctions.

The cerebellum is primarily responsible for motor movements. There is also some recent evidence that the cerebellum is partially responsible for speech, learning, emotions, and attention.

There are really just a handful of processes that a developing brain employs in order to make sense of the world. All generally involve the expansion and elaboration of the nervous system coupled with careful observation and cataloging of environment.

There are several types of dysfunction: Attention; memory; language; organizational skills; neuromotor functioning; higher cognitive functions; social cognition.

The findings do not support previous claims of localized neurodevelopmental abnormalities. They do point to the likely involvement of the cerebral cortex in autism.

Onset of epileptiform activity before language acquisition may cause abnormal or delayed language development and acquired aphasia after acquisition of language. Language disorder associated with seizures appears to be broader than originally thought.

Neurofibromatosis type 1 (NF1) is associated with a broad range of relatively nonspecific cognitive impairments, including low IQ, learning disabilities, and behavioral difficulties.

The ToM hypothesis has explanatory power in relation to the triad symptoms of autism (social, communication, and imagination abnormalities), but has little relevance to the non-triad symptoms (attention to detail, islets of ability, obsessions).

By mapping autism behaviourally in a more comprehensive and useable format, neurophysiology, neuroanatomy and biological neuroscience can target areas and cellular workings more expansively and in greater detail

Narrow neural columns have been suggested to be a neuroanatomical abnormality in autism. A previous hypothetical explanation, an unbalance between excitatory and inhibitory lateral feedback in the neocortex, has been found to be difficult to reconcile with the relatively high comorbidity of autism with epilepsy. Two alternative explanations are discussed, an early low capacity for producing serotonin, documented in autism, and insufficient production of nitric oxide. An early low level of serotonin has in animal experiments caused narrow neural columns. Insufficient nitric oxide is known from neural network theory to cause narrow neural columns.

The idea of a fixed intelligence has given way to a more flexible perception of gradual intellectual development dependent on external stimulation. Our intelligence, therefore, is our singular, collective ability to act and react in an everchanging world.

The number of neural connections in the left temporal lobe is abnormally high in the brains of patients with autism, while connectivity between the frontal lobe and the rest of the brain is decreased. These findings, from a study presented at the 36th annual meeting of the Society for Neuroscience, held this week in Atlanta, Georgia, may explain why autistic patients have difficulty with language and other communication skills.

Considerable evidence exists that mental disorders may correlate with CAPD and this correlation could be revealed through psychoacoustics and neuroaudiology.

Although some experimental data in children with DLD and dyslexia suggest that both disorders may be due to a basic temporal processing impairment, dyslexia seems to be characterized by a more severe deficit in reading decoding than reading comprehension.

The behavioral experiment showed that Asperger and high-functioning autistic subjects have a special deficit of imitation, lacking the natural preference for mitating in a mirror-image fashion. Results support the hypothesis of possible MNS dysfunction.

We present a novel data smoothing and analysis framework for cortical thickness data defined on the brain cortical manifold. Gaussian kernel smoothing, which weights neighboring observations according to their 3D Euclidean distance, has been widely used in 3D brain images to increase the signal-to-noise ratio. When the observations lie on a convoluted brain surface, however, it is more natural to assign the weights based on the geodesic distance along the surface. We therefore develop a framework for geodesic distance-based kernel smoothing and statistical analysis on the cortical manifolds. As an illustration, we apply our methods in detecting the regions of abnormal cortical thickness in 16 high functioning autistic children via random field based multiple comparison correction that utilizes the new smoothing technique.

Dopamine exerts a major role in regulating neuronal motor control, cognition, event prediction, emotion and vascular function and has been implicated in the maintenance and expression of neuro-psychiatric disease states such as Parkinson's, TS and ADHD.

Genetic and neurofunctional research in autism has highlighted the need for improved characterization of the core social disorder defining the broad spectrum of syndrome manifestations. This article reviews the advantages and limitations of current methods for the refinement and quantification of this highly heterogeneous social phenotype. The study of social visual pursuit by use of eye-tracking technology is offered as a paradigm for novel tools incorporating these requirements and as a research effort that builds on the emerging synergy of different branches of social neuroscience. Advances in the area will require increased consideration of processes underlying experimental results and a closer approximation of experimental methods to the naturalistic demands inherent in real-life social situations.

Interest regarding neural information processing in autism is growing because atypical perceptual abilities are a characteristic feature of persons with autism. Central to our review is how characteristic perceptual abilities, referred to as perceptual signatures, can be used to suggest a neural etiology that is specific to autism. We review evidence from studies assessing both motion and form perception and how the resulting perceptual signatures are interpreted within the context of two main hypotheses regarding information processing in autism: the pathway- and complexity-specific hypotheses. We present evidence suggesting that an autism-specific neural etiology based on perceptual abilities can only be made when particular experimental paradigms are used, and that such an etiology is most congruent with the complexity-specific hypothesis.

The multiple interactions between all levels, invoked by the neuroconstructivist approach, highlight why it is essential to start studies of developmental disorders in early infancy and then to trace the subsequent processes of development itself.

Autism is a severe developmental disorder marked by a triad of deficits, including impairments in reciprocal social interaction, delays in early language and communication, and the presence of restrictive, repetitive and stereotyped behaviors. In this review, it is argued that the search for the neurobiological bases of the autism spectrum disorders should focus on the social deficits, as they alone are specific to autism and they are likely to be most informative with respect to modeling the pathophysiology of the disorder. Many recent studies have documented the difficulties persons with an autism spectrum disorder have accurately perceiving facial identity and facial expressions. This behavioral literature on face perception abnormalities in autism is reviewed and integrated with the functional magnetic resonance imaging (fMRI) literature in this area, and a heuristic model of the pathophysiology of autism is presented. This model posits an early developmental failure in autism involving the amygdala, with a cascading influence on the development of cortical areas that mediate social perception in the visual domain, specifically the fusiform "face area" of the ventral temporal lobe. Moreover, there are now some provocative data to suggest that visual perceptual areas of the ventral temporal pathway are also involved in important ways in representations of the semantic attributes of people, social knowledge and social cognition. Social perception and social cognition are postulated as normally linked during development such that growth in social perceptual skills during childhood provides important scaffolding for social skill development. It is argued that the development of face perception and social cognitive skills are supported by the amygdala-fusiform system, and that deficits in this network are instrumental in causing autism.

We show that despite putative processing similarities at the cognitive level, binding in Williams syndrome and autism can be dissociated at the neurophysiological level by different abnormalities in underlying brain oscillatory activity.

The modular arrangement of the neocortex is based on the cell minicolumn: a self-contained ecosystem of neurons and their afferent, efferent, and interneuronal connections. The authors’ preliminary studies indicate that minicolumns in the brains of autistic patients are narrower, with an altered internal organization. More specifically, their minicolumns reveal less peripheral neuropil space and increased spacing among their constituent cells. The peripheral neuropil space of the minicolumn is the conduit, among other things, for inhibitory local circuit projections. A defect in these GABAergic fibers may correlate with the increased prevalence of seizures among autistic patients. This article expands on our initial findings by arguing for the specificity of GABAergic inhibition in the neocortex as being focused around its mini- and macrocolumnar organization. The authors conclude that GABAergic interneurons are vital to proper minicolumnar differentiation and signal processing (e.g., filtering capacity of the neocortex), thus providing a putative correlate to autistic symptomatology.

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.

There is growing evidence that the process of learning, as a general phenomenon, is capable of remodeling brain circuits. the load presented by learning a task is able to drive the process of remodeling the brain, even beyond the childhood years.

These findings suggest that the concept, beliefs, develops as a domain-specific notion that is not equatable with "having a picture (map or diagram) in the head."

By studying the codevelopment of brain and language in the first few years of life, we may able to identify some of the neural mechanisms that permit the emergence of language in our species.

Information on how literacy skills begin in the early years in relation to the developing brain.

The actual effects that serotonin has on the manifestation of autistic symptoms and the debates that surround the relevance of serotonin to autism. (Student term paper)

Neuroscience meetings these days have numerous papers on the role of the brain in emotion, affect, hedonic tone, and the like. Unless these vague concepts can be operationalized, they are likely to impede, if not recede, the progress.

It is concluded that endogenous opioids may play a role in the vulnerability to certain diseases, such as addiction and autism, but also when the disease is present, such as alcoholism.

No one knows whether increased brain size plays a role in the symptoms of autism, but results such as these make investigators wonder whether this could be an example of a deficit in pruning

To explore the contribution of nicotinic receptors to complex cognitive functions, we developed an automated method to investigate sequential locomotor behavior in the mouse and an analysis of social behavior.

One intriguing possibility is that eye gaze stimuli adversely stimulate the autonomic nervous system in autism, perhaps inhibiting the normal development of theory of mind.

Most adolescents with autism form a normal configuration-based face representation, but the absence of the composite effect indicates that they ageless prone to use the contextual information of the face in a visual-search.

The identification of a specific brain system that processes fear is spurring a great interest in the field. New discoveries could explain the mystery behind many mental disorders and prompt the development of new treatments.

Based on NeuroSPECT findings, implications are that medications or efforts to calm the brain and child down, may further shut down the areas in which we want to improve blood flow and function and down regulated blood flow.

An intimate profile of the neurologist-author of Awakenings, The Man Who Mistook His Wife for a Hat, An Anthropologist on Mars, and other tales from the borderlands of the mind. A comprehensive look at Dr. Sacks' work in the context of the role of anecdote in medical practice and evolving models of the brain.

When attentional selection is impaired developmentally, compensatory cognitive strategies may be brought into play in order to achieve functional behavioural performance.

In autism, physiological indices of selective attention have been shown to be abnormal even in situations where behaviour is intact. This divergence between behaviour and physiology suggests the action of some compensatory process of attention, one which may hold clues to the aetiology of autism's characteristic cognitive phenotype. Six subjects with autism spectrum disorders and six normal control subjects were studied with fMRI while performing a bilateral visual spatial attention task. In normal subjects, the task evoked activation in a network of cortical regions including superior parietal lobe (p<0.001), left middle temporal gyrus (p=0.002), left inferior (p<0.001) and middle (p<0.02) frontal gyri, and medial frontal gyrus (p<0.02). Autistic subjects, in contrast, showed activation in bilateral ventral occipital cortex (p<0.03) and striate cortex (p<0.05). Within the task condition, a region-of-interest comparison of attend-left versus attend-right conditions indicated that modulation of activation in the autistic brain as a function of the lateral focus of spatial attention was abnormally decreased in left ventral occipital cortex (p<0.03), abnormally increased in left intraparietal sulcus (p<0.01), and abnormally variable in superior parietal lobe (p<0.03). These results are discussed in terms of a model of autism in which a pervasive defect of neural and synaptic development produces over-connected neural systems prone to noise and crosstalk, resulting in hyper-arousal and reduced selectivity. These low-level attentional traits may be the developmental basis for higher-order cognitive styles such as weak central coherence.

The methods demonstrated here might be used with normal or clinical subjects to assess cognitive function.

Research is confirming that the brains of men and women are subtly different. The findings could lead to sex-specific alterations in treatments for diseases such as depression.

There appear to be four phases to abnormal brain growth in autism: 1. slight undergrowth of the brain before birth compared to averages; 2. sudden and excessive increase in head size between 1-2 months and 6-14 months; 3. a gradual slowing in rate of brain growth between ages 2-4 so that by ages 4-5 brain size in autism reaches its near maximum (8 years sooner than that of non-autistic children); 4. a gradual decline in overall brain size extending from middle or late childhood to adults so that by those ages brain size in autism is not significantly different from the healthy average.

Clinical symposia included in-depth reviews of neuroimmunology, outcomes research, quality-of-life issues, central nervous system infections, sports-related neurology, genetics of epilepsy, and new approaches to cerebral palsy.

Face recognition abnormalities in autism are not fully explained by an impairment of holistic face processing, and that there is an unusual significance accorded to the mouth region when children with autism process information from people's faces.

Neuron communication is under intense investigation by researchers because when it goes out of balance ailments ranging from epilepsy to memory disorders can occur.

BACKGROUND: Inhibiting prepotent responses is critical to optimal cognitive and behavioral function across many domains. Several behavioral studies have investigated response inhibition in autism, and the findings varied according to the components involved in inhibition. There has been only one published functional magnetic resonance imaging (fMRI) study so far on inhibition in autism, which found greater activation in participants with autism than control participants. METHODS: This study investigated the neural basis of response inhibition in 12 high-functioning adults with autism and 12 age- and intelligence quotient (IQ)-matched control participants during a simple response inhibition task and an inhibition task involving working memory. RESULTS: In both inhibition tasks, the participants with autism showed less brain activation than control participants in areas often found to be active in response inhibition tasks, namely the anterior cingulate cortex. In the more demanding inhibition condition, involving working memory, the participants with autism showed more activation than control participants in the premotor areas. In addition to the activation differences, the participants with autism showed lower levels of synchronization between the inhibition network (anterior cingulate gyrus, middle cingulate gyrus, and insula) and the right middle and inferior frontal and right inferior parietal regions. CONCLUSIONS: The results indicate that the inhibition circuitry in the autism group is activated atypically and is less synchronized, leaving inhibition to be accomplished by strategic control rather than automatically. At the behavioral level, there was no difference between the groups.

Autism is a neurodevelopmental disorder with strong genetic influences. Clinical experience and limited empirical evidence support the view that autism may be associated with aberrant interhemispheric information transfer. This empirical controlled study examined whether, at neuropsychological testing, children with autism showed problems with interhemispheric information transfer. The study included auditory, visual, and motor measures covering information transfer within, as well as across, modalities. Thirty children (24 males, 6 females; mean age 12 years 8 months, SD 2 years 8 months; range 9 years 5 months to 17 years 5 months) without learning disability but with autism spectrum disorders were compared with 30 children from a mainstream school matched for age, sex, and IQ>75. Children with autism spectrum disorder performed significantly worse than the comparison group on most of the tests (p=0.02 for auditory perception and attention, p=0.005 for visual perception, p=0.0001 for motor control, p=0.04 for tactile perception). Results support the notion that aberrant interhemispheric transfer may be involved in the pathogenesis or clinical course of autism. The findings were not accounted for by lower IQ in the group with autism.

Findings are discussed in terms of the need to take note of the heterogeneity of the learning disabled population and the particular vulnerability to social imperception of children with nonverbal deficits.

The idea of “post-natal” has to do with the macro-encephalopathy. The phenomenon of pathological overgrowth of the brain is taking place after birth, in the first year of life in children with autism. So that is why I call it post-natal. It is transient, because the overgrowth occurs for only a short period of time, leading the brain to be larger than normal for only about three to five years. At that point, the growth tends to stop and the normal brain catches up and surpasses it. There is still a very interesting question about what is happening pre-natally. There is a good possibility that whatever is triggering the post-natal overgrowth might have some connection to what is happening pre-natally. I think this is a very important question: whether pre-natal events are setting up this post-natal phenomenon?

Friday, May 17,1996 Fresh Air

The comprehensive approach to making inferences and drawing conclusions used by the clinical neuropsychologist is felt to be superior to more traditional psychological methods in the diagnosis and description of brain dysfunction.

Von Economo neurons (VENs) are a recently evolved cell type which may be involved in the fast intuitive assessment of complex situations. As such, they could be part of the circuitry supporting human social networks. We propose that the VENs relay an output of fronto-insular and anterior cingulate cortex to the parts of frontal and temporal cortex associated with theory-of-mind, where fast intuitions are melded with slower, deliberative judgments. The VENs emerge mainly after birth and increase in number until age 4 yrs. We propose that in autism spectrum disorders the VENs fail to develop normally, and that this failure might be partially responsible for the associated social disabilities that result from faulty intuition.

In this paper, we report the results of a series of novel experimental investigations focusing on the structure and function of the amygdala in a group of children with autism... Surprisingly, there were no significant differences between the patterns of emotional modulation of the startle response in the autistic group compared with the controls.

Social cognitive neuroscience is a fledgling discipline that has already accrued an impressive body of data, but important questions remain regarding the theoretical constructs and methodological approaches that it utilizes. An overview of the papers in this special issue points to several key issues facing the field. We need a theoretical vocabulary that bridges three domains: our intuitive "folk" conceptions of other people, the explanations offered by social psychology, and the explanations offered by cognitive neuroscience. And we need a method that can extract common patterns across multiple studies, to complement strict hypothesis testing of individual studies. These issues can be addressed, in part, by giving theory and experiment equal time, and by fostering an interdisciplinary approach that includes neuroscience, psychology, philosophy, anthropology and allied disciplines.

We give a somewhat idiosyncratic history of the development of neural network models of face processing, concentrating on work at UCSD, and show how these models have led to a novel hypothesis concerning processing of facial expression.

I argue autism is due to the knock-on effects of a defect in the extraction of information from second and higher-order context upon the active learning required for full cognitive, linguistic, affective, social, motor and sensory development. These knock-on effects arise from the link between higher-order context extraction and active learning. Development in children requires them to activity create responses (behavioural sonar) in developmental areas as diverse as intellect, language, motor control, sensory adjustment, stress regulation and 'self' and sociability.

Language deficits are among the core impairments of autism. We previously reported asymmetry reversal of frontal language cortex in boys with autism. Specific language impairment (SLI) and autism share similar language deficits and may share genetic links. This study evaluated asymmetry of frontal language cortex in a new, independent sample of right-handed boys, including a new sample of boys with autism and a group of boys with SLI. Language impaired boys with autism and SLI both had significant reversal of asymmetry in frontal language-related cortex; larger on the right side in both groups of language impaired boys and larger on the left in both unimpaired language groups, strengthening a phenotypic link between ALI and SLI. Thus, we replicated the observation of reversed asymmetry in frontal language cortex reported previously in an independent autism sample, and observed similar reversal in boys with SLI, further strengthening a phenotypic link between SLI and a subgroup of autism. Linguistically unimpaired boys with autism had similar asymmetry compared with the control group, suggesting that Broca's area asymmetry reversal is related more to language impairment than specifically to autism diagnosis.

The most replicated finding in autism neuroanatomy—a tendency to unusually large brains—has seemed paradoxical in relation to the specificity of the abnormalities in three behavioral domains that define autism. We now know a range of things about this phenomenon, including that brains in autism have a growth spurt shortly after birth and then slow in growth a few short years afterward, that only younger but not older brains are larger in autism than in controls, that white matter contributes disproportionately to this volume increase and in a nonuniform pattern suggesting postnatal pathology, that functional connectivity among regions of autistic brains is diminished, and that neuroinflammation (including microgliosis and astrogliosis) appears to be present in autistic brain tissue from childhood through adulthood. Alongside these p