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 pervasive brain tissue and functional abnormalities, there have arisen theories of pervasive or widespread neural information processing or signal coordination abnormalities (such as weak central coherence, impaired complex processing, and underconnectivity), which are argued to underlie the specific observable behavioral features of autism. This convergence of findings and models suggests that a systems- and chronic disease-based reformulation of function and pathophysiology in autism needs to be considered, and it opens the possibility for new treatment targets.

Transcranial magnetic stimulation produced a specific picture naming deficit. The absence of any effect on word:nonword reading or colour naming, suggests that left hemispheric posterior BA37 is necessary for object recognition.

These data suggest that a continuum of schizophrenic-type traits affect the way a person processes information about the self and that mental state attribution and self-recognition are processed by similar neural substrates.

Compared with age- and sex-matched healthy volunteers, patients with autism spectrum disorders showed significantly decreased metabolism in both the anterior and posterior cingulate gyri.

Temporal lobe epileptics often experience profound interictal (i.e. between seizure) emotional disturbances, such as fear, anxiety, and depression. Partial and short-term kindling produce robust changes in emotional behavior in both cats and rats.

We demonstrated that calculation expertise was not due to increased activity of processes that exist in non-experts; rather, the expert and the non-experts used different brain areas for calculation.

Recent results confirm the prominent role of astrocytes in glutathione metabolism and the defense against reactive oxygen species in brain.

General Hospital (MGH) has identified specific portions of the brain's white matter that are abnormally large in children with autism and developmental language disorder (DLD).

The minicolumn is a continuing source of research and debate more than half a century after it was identified as a component of brain organization. The minicolumn is a sophisticated local network that contains within it the elements for redundancy and plasticity. Although it is sometimes compared to subcortical nuclei, the design of the minicolumn is a distinctive form of module that has evolved specifically in the neocortex. It unites the horizontal and vertical components of cortex within the same cortical space. Minicolumns are often considered highly repetitive, even clone-like, units. However, they display considerable heterogeneity between areas and species, perhaps even within a given macrocolumn. Despite a growing recognition of the anatomical basis of the cortical minicolumn, as well as its physiological properties, the potential of the minicolumn has not been exploited in fields such as comparative neuroanatomy, abnormalities of the brain and mind, and evolution.

In this chapter, specific attributes of faces and their basic parts, i.e. features and configurations will be discussed. The aim is to sensitize the reader to the specific properties of a face and its probable processing.

We present the first assessment of motion sensitivity for persons with autism and normal intelligence using motion patterns that require neural processing mechanisms of varying complexity. Compared to matched controls, our results demonstrate that the motion sensitivity of observers with autism is similar to that of nonautistic observers for different types of first-order (luminance-defined) motion stimuli, but significantly decreased for the same types of second-order (texture-defined) stimuli. The latter class of motion stimuli has been demonstrated to require additional neural computation to be processed adequately. This finding may reflect less efficient integrative functioning of the neural mechanisms that mediate visuoperceptual processing in autism. The contribution of this finding with regards to abnormal perceptual integration in autism, its effect on cognitive operations, and possible behavioral implications are discussed.

Each of the newly discovered nerve growth factors or neurotrophins exerts its effect on very specific brain systems, many of them sensory ones that are known to be deficient in autistic disorders.

Some brain regions are associated with different forms of learning and memory. Right BA46 is commonly engaged by working memory and episodic retrieval tasks. Parietal BA7 is usually activated by working memory, episodic memory, and skill learning tasks.

The major findings to date on the neural basis of autism concern aspects of the limbic system, and functionally related and connected regions of the orbitomedial prefrontal cortex, and visual areas of the temporal lobe.

What brain mechanisms underlie autism and how do they give rise to autistic behavioral symptoms? This article describes a neural model, called the iSTART model, which proposes how cognitive, emotional, timing, and motor processes that involve brain regions like prefrontal and temporal cortex, amygdala, hippocampus, and cerebellum may interact together to create and perpetuate autistic symptoms. These model processes were originally developed to explain data concerning how the brain controls normal behaviors. The iSTART model shows how autistic behavioral symptoms may arise from prescribed breakdowns in these brain processes, notably a combination of underaroused emotional depression in the amygdala and related affective brain regions, learning of hyperspecific recognition categories in temporal and prefrontal cortices, and breakdowns of adaptively timed attentional and motor circuits in the hippocampal system and cerebellum. The model clarifies how malfunctions in a subset of these mechanisms can, though a system-wide vicious circle of environmentally mediated feedback, cause and maintain problems with them all.

What brain mechanisms underlie autism and how do they give rise to autistic behavioral symptoms? This article describes a neural model, called the iSTART model, which proposes how cognitive, emotional, timing, and motor processes that involve brain regions like prefrontal and temporal cortex, amygdala, hippocampus, and cerebellum may interact together to create and perpetuate autistic symptoms. These model processes were originally developed to explain data concerning how the brain controls normal behaviors. The iSTART model shows how autistic behavioral symptoms may arise from prescribed breakdowns in these brain processes, notably a combination of underaroused emotional depression in the amygdala and related affective brain regions, learning of hyperspecific recognition categories in temporal and prefrontal cortices, and breakdowns of adaptively timed attentional and motor circuits in the hippocampal system and cerebellum. The model clarifies how malfunctions in a subset of these mechanisms can, though a system-wide vicious circle of environmentally mediated feedback, cause and maintain problems with them all.

The piece consist of five neurons, each arbitrarily assigned a pitch. Each beat corresponds to an action potential. one of the attached files is at full speed and one is at one third speed.

Infantile autism is a behaviorally defined disorder associated with characteristic cognitive, language and behavioral features. Several postmortem studies have highlighted areas of anatomic abnormality in the autistic brain. Consistent findings have been observed in the limbic system, cerebellum and related inferior olive. In the limbic system, the hippocampus, amygdala and entorhinal cortex have shown small cell size and increased cell packing density at all ages, suggesting a pattern consistent with development curtailment. Findings in the cerebellum have included significantly reduced numbers of Purkinje cells, primarily in the posterior inferior regions of the hemispheres. A different pattern of change has been noted in the vertical limb of the diagonal band of broca, cerebellar nuclei and inferior olive with plentiful and abnormally enlarged neurons in the brains of young autistic subjects, and in adult autistic brains, small, pale neurons that are reduced in number. These findings combined with reported age-related changes in brain weight and volume, have raised the possibility that the neuropathology of autism may represent an on-going process.

Focuses primarily on the neuroanatomical and neurophysiological abnormalities found in autistic subjects, particularly those seen in magnetic resonance imaging (MRI) and event-related potential (ERP) studies.

More Information: Links to On-Line Neuroscience Journals; Links to Print Neuroscience Journals; Links to Publishers

The repetitive, stereotyped, and obsessive behaviors that characterizeautism may in part be attributable to disruption of theregion of the fronto-striatal system, which mediates executiveabilities. Neuropsychological testing has shown that childrenwith autism exhibit set-shifting deficiencies on tests such as theWisconsin Card Sorting task but show normal inhibitory abilityon variants of the Stroop color-word test. According to Minshewand Goldstein's multiple primary deficit theory, the complexityof the executive functioning task is important in determining theperformance of individuals with autism. This study employed avisual-spatial task (with a Stroop-type component) to examinethe integrity of executive functioning, in particular inhibition,in autism (n = 12) and Asperger's disorder (n = 12) underincreasing levels of cognitive complexity. Whereas the Asperger'sdisorder group performed similarly to age- and IQ-matched controlparticipants, even at the higher levels of cognitive complexity,the high-functioning autism group displayed inhibitory deficitsspecifically associated with increasing cognitive load.

Data suggest that abnormal neural growth patterns early in development lead to an array of consequences in anatomical and functional organization.

Neuropathologic studies of autism identify abnormalities in regions that may be critical interaction, language, and memory. There is scant evidence, however, to support the hypothesis of a well-localized �Region X� that results in autism when insulted.

The proposed (neurobiological) model is composed of a representational component subserved by posterior brain regions (temporal and parietal) and an application / execution component subserved by prefrontal regions.

There are several structural and neurochemical abnormalities associated with autism that can help to explain the specific behaviors and deficits characteristic of the disorder.

Recent studies have begun to elucidate the roles played in social cognition by specific neural structures, genes, and neurotransmitter systems. Cortical regions in the temporal lobe participate in perceiving socially relevant stimuli, whereas the amygdala, right somatosensory cortices, orbitofrontal cortices, and cingulate cortices all participate in linking perception of such stimuli to motivation, emotion, and cognition. Open questions remain about the domain-specificity of social cognition, about its overlap with emotion and with communication, and about the methods best suited for its investigation.

A neural network capable of defining neural maps simulates the process of neurodevelopment. The computer simulations hint that brain regions responsible for the formation of higher level representations are impaired in autistic patients.

Autistic adults were more likely than normal adults to offer nothing to the other player. The autists seem incapable of understanding what another player might believe and do; as a result, ironically, they play like self-interested game theorists!

Existing data argue strongly for a role of the amygdala and its collaborating cortical systems in the pathobiology of autism spectrum conditions.

Autism is a neurodevelopmental disorder characterized by impaired communication and social interaction and may be accompanied by mental retardation and epilepsy. Its cause remains unknown, despite evidence that genetic, environmental, and immunological factors may play a role in its pathogenesis. To investigate whether immune-mediated mechanisms are involved in the pathogenesis of autism, we used immunocytochemistry, cytokine protein arrays, and enzyme-linked immunosorbent assays to study brain tissues and cerebrospinal fluid (CSF) from autistic patients and determined the magnitude of neuroglial and inflammatory reactions and their cytokine expression profiles. Brain tissues from cerebellum, midfrontal, and cingulate gyrus obtained at autopsy from 11 patients with autism were used for morphological studies. Fresh-frozen tissues available from seven patients and CSF from six living autistic patients were used for cytokine protein profiling. We demonstrate an active neuroinflammatory process in the cerebral cortex, white matter, and notably in cerebellum of autistic patients. Immunocytochemical studies showed marked activation of microglia and astroglia, and cytokine profiling indicated that macrophage chemoattractant protein (MCP)-1 and tumor growth factor-beta1, derived from neuroglia, were the most prevalent cytokines in brain tissues. CSF showed a unique proinflammatory profile of cytokines, including a marked increase in MCP-1. Our findings indicate that innate neuroimmune reactions play a pathogenic role in an undefined proportion of autistic patients, suggesting that future therapies might involve modifying neuroglial responses in the brain.

Brains are dynamical systems in which learning tends toward isolation by increasing specialization of cognitive skills. Induction of social skills for cooperative behavior requires 'unlearning' in social contexts. A hypothesis is proposed by which oxytocin and related neuropeptides play a key role in meltdown of prior learning, in preparation for new learning. This has implications for clinical management of disorders of the socialization processes in children and psychopathic adults.

Autism is a behaviorally defined life-long disorder of higher cortical function, with onset in early childhood, that affects sociability, language and communication, play, and range of interests and activities.

Stressful events set up a chain of neurochemical changes in the brain that intensify emotions while undermining concentration and intellectual performance. as the 'trigger' event occurs, substances called catecholamines activate the amygdala.

"Costumeless consciousness, that is he" said Emily Dickinson. Was she thinking of a child with autism or Asperger syndrome? These beautiful children may indeed reveal their feelings for all to see; they do share an incompetence for being deceitful. But in many other ways, they can be quite different.Some are gentle and passive while others can become angry or hyperactive; some are quite clumsy and while others are astonishingly graceful and balanced; some stun us with their brilliant savant skills even while otherwise functioning at much lower cognitive levels. Who are these enigmatic children?

The amygdala is an area in the brain that controls emotions and behavior. The hippocampus has to do with learning and memory. It's believed that these two structures (and areas related to them) play some kind of role in autism.

Classic neuropathologic observations are rather consistent in respect to the limbic system, the cerebellum, decreased number of Purkinje cells, and the cerebral cortex.

Autism is currently viewed as a largely genetically determined neurodevelopmental disorder, although its underlying biological causes remain to be established. In this review, we examine the available neuropathological literature on autism and discuss the findings that have emerged. Classic neuropathological observations are rather consistent with respect to the limbic system (nine of 14 studied cases showed increased cell packing density and smaller neuronal size), the cerebellum (21 of 29 studied cases showed a decreased number of Purkinje cells, and in all of five cases that were examined for age-related morphological alterations, these changes were found in cerebellar nuclei and inferior olive) and the cerebral cortex (>50% of the studied cases showed features of cortical dysgenesis). However, all reported studies had to contend with the problem of small sample sizes, the use of quantification techniques not free of bias and assumptions, and high percentages of autistic subjects with comorbid mental retardation (at least 70%) or epilepsy (at least 40%). Furthermore, data from the limbic system and on age-related changes lack replication by independent groups. It is anticipated that future neuropathological studies hold great promise, especially as new techniques such as design-based stereology and gene expression are increasingly implemented and combined, larger samples are analysed, and younger subjects free of comorbidities are investigated.

The consistent message from all of these papers is of the paucity of guidance available to prescribers and of the need for more high-quality, age-specific research, rather than continued reliance upon extrapolation of findings from studies among adults.

Neurobehavioral theories of autism have hypothesized core deficits in sensory input or perception, basic attentional abilities or generalized attention to extrapersonal space, anterograde memory, auditory information processing, higher order memory abilities, conceptual reasoning abilities, executive function, control mechanisms of attention, and higher order abilities across domains. A neuropsychologic battery designed to investigate these hypotheses was administered to 33 rigorously diagnosed autistic individuals with IQ scores greater than 80, and 33 individually matched normal controls. Stepwise discriminant function was used to define the profile of neuropsychologic functioning across domains. The neuropsychologic profile in these autistic individuals was defined by impairments in skilled motor, complex memory, complex language, and reasoning domains, and by intact or superior performance in the attention, simple memory, simple language, and visual-spatial domains. This profile is not consistent with mental retardation or with a general deficit syndrome, but rather with a selective impairment in complex information processing that does not involve visual-spatial processing. This profile is not consistent with a single primary deficit, but with a multiple primary deficit model in which the deficit pattern within and across domains is reflective of the complexity of the information processing demands. This neuropsychologic profile is furthermore consistent with the neurophysiologic characterization of autism as a late information processing disorder with sparing of early information processing.

The objectives of neuropsychological assessment in clinical practice are to assess and diagnose disturbances of mentation and behavior and to relate these findings to their neurological implications and to the issues of clinical treatment and prognosis.

What neuropsychological assessment is and why it's important to educators. How educators use neuropsychological assessment and what some of its limitations are. List of information sources.

To call a child learning disabled is to put the burden of responsibility on the wrong person! It is our responsibility to teach much more than it is the responsibility of the child to learn. It is we who should be called teaching disabled.

Although juvenile delinquents can present with a wide range of cognitive impairments, the deficits reported in the literature involve primarily verbal abilities and, to a lesser extent, executive functions.

This article reviews three competing neuropsychological theories of autism: the executive dysfunction hypothesis, the weak central coherence hypothesis, and the limbic system hypothesis.

This study examined the possibility that diagnostic differentiation between children with autism and Asperger syndrome may be enhanced through the use of neuropsychological profiles. Two groups of children, clinically diagnosed as having Asperger syndrome (n = 35) or autism (n = 21), were tested with a neuropsychological battery to assess the propositions that these groups might differ in terms of Wechsler IQ profiles, brain hemispheric strengths and weaknesses, and executive functioning. Clinically diagnosed children with Asperger syndrome and autism were not differentiated on the basis of their neuropsychological profiles. The major difference between them was the overall higher IQ in Asperger syndrome, which was largely due to superior verbal abilities. Differences were also examined using DSM-IV/ICD-10 criteria: children were grouped according to the early history of presence or absence of language delay. No differences between the groups on any neurocognitive measure were found and there was no support for current neuropsychological theories purporting to support differential diagnostic status. It appears that current diagnostic differentiation in clinical practice may be primarily influenced by the child's estimated verbal IQ level.

Meta-source devoted exclusively to the subject of Human Neuropsychology.

The areas most commonly assessed include general intellectual function (i.e., IQ), language, visual spatial ability, memory and learning, attention and concentration, motor/sensory function, abstraction and executive function, and personality.

The analysis of the interaction between social and biological determinants of behavior can best be studied by also having a full understanding of the biological components of behavior.

In conclusion, the present findings of nAChR {alpha}4 and {alpha}7 subunit abnormalities in the cerebellum suggest a role for these receptors in the neurodevelopmental pathological process in autism and in the aetiology of particular clinical symptoms.

NMR signal intensities in five regions of the midsagittal corpus callosum were measured in autism patients and normal controls.

While a number of factors are vital for proper brain development, physical attention appears to play a role in maintaining brain chemistry, brain architecture and possibly some mental functioning.

Serotonergic disturbances may play a role in the pathophysiology of autism. Autism is not associated with alterations in the noradrenergic system. Metabolism of serotonin in humans undergoes significant changes between the ages of 12 and 18 years.

Autists, unlike psychopaths, do adhere to rules, distinguish between merely convential and moral rules, experience feelings of guilt and have a strong sense of justice... they seem to be moral agents in a kantian sense of the term...

The Social Delusion pheromone is produced when a person feels himself to be part of, and accepted by, a group of people. When a person -- for example, an autistic person -- does not feel part of the group, he will not produce the Social Delusion pheromone. The Vomeronasal Organs (VNO's) of people in the group will therefore have no Social Delusion pheromone to react to. Group members will immediately perceive a Social Delusion pheromone non-producer to be an outsider, and will behave accordingly.

Preliminary data suggest hyper-activation of occipitotemporal visual areas and hypo-activation of parietal attention areas consistent with a model in which a generalised, non-selective arousal partially compensates for impairment of selective attention.

All parts of the brain are concerned with simple behavior. Only the prefrontal lobes in the foremost section have been liberated from having to do with sensation and movement.

For some reason the brainstem structures that control social behavior do not function properly and as a result allow behaviors such as hyperactivity, lack of attention, listening, facial expression and vocalization to not be properly regulated.

The mRNA levels of several genes were significantly increased in autism, including excitatory amino acid transporter 1 and glutamate receptor AMPA 1, two members of the glutamate system.

Artificial neural networks were trained to predict behavioural performance from single-trial EEG in autistic and normal subjects in a task involving response to rare stimuli and shifting of attention between vision and audition.

The prefrontal cortex may be as a five-member Executive Committee, as the pre-frontal control extensions of five: The Perceiver, the Verbalizer, Motivator, the Attender, the Organizer.

Abnormalities in anatomy and function of the cranial nerve motor nuclei have been demonstrated in some people with autism and can be modeled in rats by exposure to valproic acid during neural tube closure.

The incidence of autism has risen 10-fold since the early 1980s, with most of this rise not explainable by changing diagnostic criteria. The rise in autism is paradoxical in that autism is considered to be one of the most genetically determined of the major neurodevelopmental disorders and should accordingly either be stable or even declining. Because a variety of epigenetic influences, particularly those occurring during the prenatal period, can override or masquerade as genetic influences, these should be considered as prime contributors to the recent increase of autism. Prenatal influences on dopamine activity are especially well-documented, including the effects of maternal psychosocial stress, maternal fever, maternal genetic and hormonal status, use of certain medications, urban birth, and fetal hypoxia. All of these factors have been implicated in the genesis of autism, which is characterized by a �hyperdopaminergic� state based on evidence from monkey and human behavioral studies, pharmacological studies in humans, and a left-hemispheric predominance of both dopamine and autistic-like symptoms. Chronically high maternal levels of dopamine caused by the pressures of increasingly urbanized societies and by changing maternal demographics such as increased workforce participation, educational achievement level, and age at first birth, may be especially significant epigenetic contributors to the recent autism rise.

Last summer Clay Bassett died tragically and unexpectedly at age 14 and his parents did something they never imagined they would do: they donated their son's brain to a tissue bank and became key players in the emerging field of brain research.

There may be a face pathway in the occipitotemporal region. Prosopagnosia, depending on the nature of the damage, can involve facial recognition impairments in general, not just inability to recognize familiar faces.

There is now some evidence that interferon-a-based immunotherapy induces the cytokine network, decreases serotonergic turnover in the brain, and induces catabolism of tryptophan.

We present a new model of remembering in the context of conditional discrimination. It is a behavioral model in that choice is determined by its reinforcement history.

In this thesis, visual and auditory selective attention tasks are described in groups of high functioning autistic children and adolescents. It was found that autistic children show profoundly smaller P3 amplitudes than controls, but that these abnormalities were not preceded by abnormalities in selective attention. However, autistic children already showed abnormalities in visual processing around 100 milliseconds after stimulus presentation, as seen in much smaller P1 amplitudes. In autistic adolescents such amplitude reductions were not observed, but this group did show abnormal selective attention. These abnormalities in selective attention were interpreted as compensatory mechanisms, normalizing P3.

Whenever we, as researchers, write about autistics or Jews or women, we must be cognizant that we are discussing and describing members of our society. Indeed, I submit that whenever we write for the public, we must be more not less circumspect. We can't depend on stereotype, a Hollywood movie, or a casual conversation with a colleague to provide us with knowledge of the phenotypes that NIH cares about. Instead, we must research the implication of our findings with the same rigor that we research our basic phenomena. Relevance is a prized commodity these days, but let's not buy relevance at the cost of scientific inaccuracy and societal stigma.

Some recent evidence has suggested abnormalities of the dorsal stream and possibly the mirror neuron system in autism, which may be responsible for impairments of joint attention, imitation, and secondarily for language delays. The current study investigates functional connectivity along the dorsal stream in autism, examining interregional blood oxygenation level dependent (BOLD) signal cross-correlation during visuomotor coordination. Eight high-functioning autistic men and eight handedness and age-matched controls were included. Visually prompted button presses were performed with the preferred hand. For each subject, functional connectivity was computed in terms of BOLD signal correlation with the mean time series in bilateral visual area 17. Our hypothesis of reduced dorsal stream connectivity in autism was only in part confirmed. Functional connectivity with superior parietal areas was not significantly reduced. However, the autism group showed significantly reduced connectivity with bilateral inferior frontal area 44, which is compatible with the hypothesis of mirror neuron defects in autism. More generally, our findings suggest that dorsal stream connectivity in autism may not be fully functional.

BACKGROUND: The precise mechanisms underlying the pathophysiology of autism are currently unknown. Given the key role of brain-derived neurotrophic factor (BDNF) in brain development, we hypothesized that BDNF may play a role in the pathophysiology of autism. In this study, we studied whether serum levels of BDNF are altered in patients with autism. METHODS: We measured serum levels of BDNF in 18 adult male patients with autism and 18 age-matched healthy male control subjects. RESULTS: The serum levels of BDNF in patients with autism (25.6+/-2.15 ng/ml (mean+/-S.D.)) were significantly (z=-4.42, p<0.001) lower than those of normal controls (61.6+/-10.9 ng/ml (mean+/-S.D.)). Nevertheless, we found no correlations between BDNF levels and clinical variables in autistic patients. CONCLUSIONS: This study suggests that reduced BDNF levels may play a role in the pathophysiology of autism.

Studies looking at changes in regional metabolism after treatment and baseline predictors of treatment response are particularly important in helping to understand the neurobiology of the autism spectrum disorders.

Results from neuroimaging studies of childhood-onset psychiatric disorders suggest consistency in the structures found to be abnormal, but inconsistencies in the nature of these abnormalities. (JAACAP)

With increased recognition in the media, heightened prevalence, and advances in research technologies, investigation into the causes of autism has broadened in recent years. Studies at the molecular, structural, and behavioral levels have resulted in significant findings, linking autism to qualitative differences in neurological function and an alteration of early development. Familial aggregation of autism demonstrate a strong genetic factor, although genetics can not completely account for its pathogenesis. Studies show autism having one of the most complex pathologies among neurodevelopmental disorders. Future studies applying sophisticated methodologies in new areas may shed light on current mysteries surrounding the disorder.

Examine the mechanisms whereby acetylcholine might induce synaptic plasticity; considers the neural circuitry implicated in these studies, namely pathways that are susceptible to cholinergic plasticity and the neural regulation of the cholinergic system.

In two linked functional magnetic resonance imaging (fMRI) studies of healthy young adults, we show here that the FFA is engaged by a social attribution task (SAT) involving perception of human-like interactions among three simple geometric shapes. The amygdala, temporal pole, medial prefrontal cortex, inferolateral frontal cortex and superior temporal sulci were also significantly engaged. Activation of the FFA to a task without faces challenges the received view that the FFA is restricted in its activities to the perception of faces.

Reasoning about social exchange is a specialized and separable component of human social intelligence. The brain processes information about the social world differently from other types of information.

Children with LKSV and ASD have a greater frequency of serum antibodies to brain endothelial cells and to nuclei than children with NNIs or healthy children. Autoimmunity may play a role in pathogenesis of language and social developmental abnormalities

Excerpted from Brain Facts, a 52-page primer on the brain and nervous system.

In both schizophrenia and autism, the fusiform gyrus and amygdala are consistently implicated during emotion perception tasks. Theory of mind tasks appear to involve the frontal cortex, in particular the medial frontal and medial prefrontal regions.

Social cognitive neuroscience is a rapidly emerging field that utilizes cognitive neuroscientific techniques (e.g., lesion studies, neuroimaging) to address concepts traditionally in the social psychological realm (e.g., attitudes, stereotypes). The purpose of this article is to review published neuroscientific and neuropsychological research into social cognition. The author focuses on the role of the prefrontal cortex in social behavior and presents a framework that provides cohesion of this research. The article proposes that this framework will be useful in guiding future social cognitive neuroscientific research.

The field of social cognitive neuroscience is still relatively new but builds on a variety of well established disciplines including social, developmental and cognitive psychology, evolutionary biology, neuropsychology and computer science, each providing a solid basis of relevant research. In the past few years, interest in the neurological underpinnings of social cognition has burgeoned, as demonstrated by at least four special issues of major journals in this field. What drives this interest in social cognitive neuroscience? And what is the future of this flourishing discipline? In this article, we pick out several areas of social cognitive neuroscience and focus on where we believe each area might head in terms of future research.

Paul MacLean has investigated integrated brain functioning through selected brain lesions in animals that disturb circuits necessary for complex behaviors, such as social displays. MacLean is unique in his comparative neurobehavioral approach that emphasizes the evolutionary origins of parenting and social behaviors and the implications of brain changes in the evolution from reptiles (social displays) to mammals (nursing, audiovocal communication, play) to man (self-awareness, intentionality, social context) that link affect and cognition. Subjectively, how "looking with feeling toward others," the basic element in empathy, evolved has been a central concern of his. Neuroimaging studies of social cognition, mother-infant communication, moral behavior, forgiveness, and trust are consistent with particular brain systems being activated in cooperative social behaviors. The identification of mirror neurons is pertinent to MacLean's model of isopraxis and studies of thalamocortical resonances may be pertinent to his neurobehavioral models. Studies of behavioral phenotypes in human neurodevelopmental disorders are consistent with MacLean's model of brain circuits being linked to complex behaviors during development. In autistic disorder, the behavioral phenotype involves disrupted social communication, deviant imaginative play, and motor stereotypies. In Lesch-Nyhan syndrome (LNS), self-injury occurs in individuals with normal sensory systems intact who require and request physical restraint to prevent self-injury; they ask for assistance from others to prevent them from harming themselves. Autism involves the lack of subjective awareness of others intentions and LNS involves a failure in self-regulation and self-control of self-injurious behavior. MacLean's models laid the groundwork for studies focused on understanding brain functioning in these conditions.

This article will review cognitive deficits that can lead to moderate to profound social awkwardness and ineptitude in children.

The world's largest organization of scientists and physicians dedicated to understanding the brain, spinal cord and peripheral nervous system.

The cerebellum may serve to prepare internal systems for upcoming events based on predictions computed from continuous tracking of and learning from sensory, cognitive, and motor information.

While it is possible to say that 'no studies have shown that SPECT scans or the radiation levels used in them cause cancer,' it is a bit disingenuous: the only reason one could say that is that no such studies have ever been done.

Increasing cognitive capacity during childhood may coincide with a gradual loss rather than formation of new synapses and presumably a strengthening of remaining synaptic connections.

Intellectual disability, a common but under-researched condition, is strongly associated with autism spectrum disorders (ASD). Although studies have investigated the neural correlates of intelligence quotient (IQ) and ASD in intellectually unimpaired subjects, these issues have not been addressed in intellectually impaired subjects. We studied 63 intellectually disabled adolescents receiving additional learning support and 72 controls using whole brain tissue volumes extracted from native space and voxel-based morphometry (VBM) in normalised space. We applied a qualitative and quantitative review of VBM preprocessing and modified the optimised method to establish optimum co-registration of the brains in normalised space. We report tissue density differences at cluster level with adjustment for underlying smoothness. Individuals with intellectual disability had smaller total white matter and total brain tissue volumes than controls, as well as reduced grey matter density in the right cerebellar hemisphere and left temporo-parietal cortex, and reduced white matter density in the posterior corpus callosum. Intellectually disabled subjects were additionally subgrouped according to their degree of reported autistic features. Reduced grey matter density was detected in the thalamus of subjects with autistic features scoring within the pervasive developmental disorder range as compared to subjects below the threshold for ASD, and increased white matter density was detected in the left superior temporal gyrus of subjects scoring above the threshold for autism as compared to subjects below the threshold for ASD.

Synesthesia is abnormal only in being statistically rare. It is, in fact, a normal brain process that is prematurely displayed to consciousness in a minority of individuals.

Autism is a behaviorally defined disorder characterized by a broad constellation of symptoms. Numerous studies directed to the biological substrate demonstrate clear effects of neurodevelopmental differences that will likely point to the etiology, course, and long-term outcomes of the disorder. Consistently replicated research on the neural underpinnings of autism is reviewed. In general, results suggest several main conclusions: First, autism is a heterogeneous disorder and is likely to have multiple possible etiologies; second, structural brain studies have indicated a variety of diffuse anatomical differences, reflective of an early developmental change in the growth or pruning of neural tissue, rather than localized lesions; similarly, neurochemical studies suggest early, neuromodulatory discrepancies rather than gross or localized abnormalities; and finally, there are a number of limitations on studies of brain activity that to date preclude definitive answers to questions of how the brain functions differently in autism. The large number of active research programs investigating the cognitive neuroscience of autism spectrum disorders, in combination with the exciting development of new methodologies and tools in this area, indicates the drama and excitement of work in this area.

We propose the hypothesis that the features of autism associated with weak central coherence result from a reduction in the integration of specialized local neural networks in the brain caused by a deficit in temporal binding. The visuoperceptual anomalies associated with weak central coherence may be attributed to a reduction in synchronization of high-frequency gamma activity between local networks processing local features. The failure to utilize context in language processing in autism can be explained in similar terms. Temporal binding deficits could also contribute to executive dysfunction in autism and to some of the deficits in socialization and communication.

The synchrony between the individual brain and its environment is maintained by a system of internal clocks that together reflect the temporal organization of the organism. Extending the theoretical work of Edelman and others, the temporal organization of the brain is posited as functioning through ''re-entry'' and ''temporal tagging'' and binds the wide range of possible times to a unified cognitive experience which is held in unison with the outside world.

Together with a patient's general health and mental status, simple neurological examinations can reveal volumes of information about damage to the brain resulting from stroke, edema, disease, and injury.

In practice, the consequences of a ToM impairment or, in particular, the inability to profit from knowledge which implies that another person holds a false belief, would include misunderstanding other people's behaviour when it is based on false belief. More generally, the ability to make, and take into account, attributions regarding other people's mental states is crucial in interacting in a socially appropriate and sensitive manner. Difficulties in this regard have been reported repeatedly in case studies of patients with frontal lobe damage.

Discusses problems people with autistic conditions show in their understanding of time and chronology and, more rarely, their intense dislike of seeing their own reflection in a mirror or window pane.

MEG studies can contribute to the understanding of cerebral activation sequences in healthy subjects and in patients with neurological or psychiatric diseases, as well as in persons with special cognitive abilities.

Subjective Response Audiometry methods assess hearing at the level of cortical perception and the processing of auditory information using attention and orienting responses.

The behavioral phenotype includes characteristic developmental, cognitive, and linguistic deficits, and psychiatric disorders, including childhood abnormalities of attention, mood, and anxiety.

Balance relies on at least three signals coming from the body: sight, and information coming from the vestibular and proprioceptive systems.

Impairment of metabolism in the auditory system and other brain areas affected in Wernicke's encephalopathy could be shared in common by all of the etiologies of autism.

Social maladjustment has been repeatedly suggested to be accompanied by deficient parasympathetic (vagal) modulation processes involved in the individual's autonomic response to environmental demands.

Collectively, these results indicate disorganized processing of face stimuli in autistic individuals and suggest a mechanism that may subserve the social information processing deficits that characterize autism spectrum disorders.

Individuals with autism do use meaning, like matched participants to assist their recall of words. There was no evidence to suggest that individuals with autism processed information presented pictorially any better than comparison participants.

The idea that the brain, like a muscle, might respond to cerebral exercise with physical growth was surprising to many, and gave strength to an increasingly powerful theory suggesting that all aspects of the mind might have physical correlates.

The cerebellum is the guru of coordinated movement and possibly even some forms of cognitive learning.

There's a pretty good chance that all babies who are later diagnosed as autistic are cognitively/sensorially autistic from birth, and that the adults in the child's life would know that if they knew what to look for. Yes, it's true that a minority of autistic children start out as relatively normal babies and are later diagnosed as autistic following a �regression,� usually at about eighteen months. Some of these toddlers actually hit a temporary developmental plateau and sort of stay at developmental level. Those children don't actually lose any skills. Autistic children are usually described as if they fall into one of two distinct categories, they are either those that experience a regression or those who are obviously autistic from birth. But it may be that there is a continuum of developmental trajectories grading from smooth to more bumpy and with some seeming to backslide. That's a very simplistic view of what might be going on in the child's reality though.

An information resource for brain imaging which integrates clinical information with multimodality imaging data.

Although it has long been thought that frontal lobe abnormality must play an important part in generating the severe impairment in higher-order social, emotional and cognitive functions in autism, only recently have studies identified developmentally early frontal lobe defects. At the microscopic level, neuroinflammatory reactions involving glial activation, migration defects and excess cerebral neurogenesis and/or defective apoptosis might generate frontal neural pathology early in development. It is hypothesized that these abnormal processes cause malformation and thus malfunction of frontal minicolumn microcircuitry. It is suggested that connectivity within frontal lobe is excessive, disorganized and inadequately selective, whereas connectivity between frontal cortex and other systems is poorly synchronized, weakly responsive and information impoverished. Increased local but reduced long-distance cortical-cortical reciprocal activity and coupling would impair the fundamental frontal function of integrating information from widespread and diverse systems and providing complex context-rich feedback, guidance and control to lower-level systems.