Autism Therapy

Parenting Children With Asperger's And High-functioning Autism

Mark Hutten, M.A is a practicing counseling psychologist and a professional parent-coach with experience of over 20 years in the field of High-Functioning Autism (HFA) and Asperger's. being the executive director of online parent support, LLC, Hutten presents several workshops and conducts numerous training courses for both professionals and parents dealing with HFA and Asperger's; besides, he works with hundreds of teenagers and children with HFA and Asperger's. Hutten is also an author of several articles that highlight parenting techniques based on highly effective research for dealing with children with HFA and Asperger's. The founder of the support group has published 'My out of control Child' and 'My out of control teen' eBooks. Most of Hutten's columns and articles discuss several ways of parenting young ones with conduct disorder, ODD, ADHD, Autism, Asperger's syndrome, Bipolar disorder, reactive attachment disorder, and many more conditions. The helpful parenting toolkit is all about a system that enables parents to minimize the child's meltdowns, low frustration tolerance, and tantrums, physical and verbal aggression, school-related behavior problems, social skills deficits, picky eating, attention difficulties, rigid thinking, problems completing homework, sleep problems, rituals and obsessions, and many more behavioral problems. The eBook is available for download. Read more...

Parenting Children With Aspergers And Highfunctioning Autism Summary


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The Essential Guide to Autism

Here is just some of what you'll learn: 13 common Asd (Autism Spectrum Disorder) misconceptions and the real truth for each this information will greatly help put your mind at ease about this mysterious disorder. The three main signs of autism and how to quickly and easily recognize each. The three broad categories of autism and how to immediately tell in which category someone with autism belongs and what this means for their treatment. The 5 most recent, most accepted theories about the cause of Asds this information may surprise you. 13 questions all concerned parents should ask themselves if they think their child may have autism your responses to these questions will ensure you know what step to take next. 28 additional signs of autism youll know exactly what behaviors to look for when assessing your child or loved one. Common treatments for autism and how to know if a treatment is right for your child or loved one. 18 questions you should always ask before submitting your child or loved one for a particular treatment this information will help ensure your child receives the treatment thats right for him or her. The six most common autism treatments used today plus, whether or not it is good to combine treatments. The positives and negatives of using Applied Behavioral Analysis to treat autism and how to tell if your child is right for an Aba program. How to choose an Aba provider including four things that you should always look for before deciding upon a provider. The five steps involved in a successful Floor Time program if a program doesnt include all five of these steps then it is definitely not right for you child. The effectiveness of the most common alternative autism treatments plus, 14 things that you should always look for before selecting an alternative treatment program. How to use the diet to help control autism naturally diet experts agree that many symptoms can decrease in severity and some may even disappear with a change in diet learn more here. Supplements that have been shown to benefit those with autism and how to ensure your autistic child takes the supplements without having a battle on your hands. 6 tips for a successful supplementation program these tips will help you cut costs and ensure that your child adjusts to the program quickly and easily. How to cope with the stress of raising a child with autism this information will have you feeling better and more relaxed than you have in years. How to ensure the safety of a a child with autism follow these 12 simple tips and your childs safety is practically guaranteed. How to ensure the education needs of your child with autism are being met including seven questions that you should always ask your childs school. How to deal with an adolescent with autism follow these tips to safely navigate your way through this difficult time in anyones life. Read more...

The Essential Guide to Autism Summary

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Author: Rachel Evans
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A Parent's Guide For Reversing Autism

Whilst best results are seen in younger children the seven step plan I have outlined in this book, including the diet, can be applied to any autistic person of any age. Step One details the gluten free/casein free diet and why it is so important for recovery to begin. It also explains why, after only 6 weeks, a particular type of cows milk can be included back into the diet. This milk has a different molecular structure than other milks. You are unlikely to hear about this milk anywhere else in the autistic community as we have been told that all casein is bad. This is simply not true. Your child may be similar to mine and have no reaction to this milk casein whatsoever. I explain how to test your child for this and other food intolerances in step one. If you have a child who is a 'picky eater' or skeptical family members, then doing step one correctly will put an end to all that. This diet is strict and has to be done properly or you will not get the results you are longing for. If you follow my recommendations for diet outlined in this chapter you could see significant improvements in your child in as little as a week.

A Parents Guide For Reversing Autism Summary

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Author: Donna Blackmore
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Challenges for Animal Models of Autism

In recent years, several rodent models of autism have been developed that reflect some behavioral, genetic, and neu-roanatomical alterations associated with this disorder. One of the main problems for the development of a relevant model is to define markers of autism, addressing its complexity and diversity. An ideal rodent model of autism should display symptoms of aberrant social interaction and communication, as well as repetitive behaviors. Tasks that could examine these behavioral symptoms in rodents have been already developed and are summarized in Table 1. However, an animal model of autism based solely on behavioral assays would be incomplete. Animal model should also address a combination of the neuro-pathological, biochemical and genetic factors implicated in autism. Another challenge lies in the fact that many clinical hallmarks of autism are difficult or almost impossible to replicate in rodents, e.g., theory of mind (ability to intuit the feelings and intentions of...

Current Animal Models of Autism

More than a dozen of different rodent models of autism are currently used. They can be classified into three categories (1) models created by neonatal lesions of brain areas shown to be abnormal in autism, e.g., cerebellum, the amygdala, hippocampus, or the medial prefrontal cortex (2) models mimicking environmental factors that increase the risk for autism in humans, e.g., prenatal exposure to valproic acid (VPA) or pre- and neonatal immunological challenges and (3) genetically modified animals, e.g., targeted mutations in genes associated with autism or localized in chromosomal regions identified by linkage analyses.

Autism Spectrum Disorders

Autism spectrum disorders (ASDs) are a group of neu-rodevelopmental disorders that involve qualitative impairments in social interaction and communication, and restricted repetitive and stereotyped patterns of behavior ( stereotypical and repetitive behavior), interests and activities. The ASDs include autism or autistic disorder, Asperger's disorder, and pervasive developmental disorder not otherwise specified (PDD NOS). The category of Pervasive Developmental Disorders (PDDs) is broader and also includes Rett's disorder and childhood disintegrative disorder. All these disorders cause significant impairment in functioning.

Drug Treatments For Autism

Despite many trials to identify drugs that affect social interactions, no medication has been shown to unambiguously modify the core or associated symptoms in individuals with autism. Recent reviews describe drug treatment strategies for various associated symptoms commonly found in autism (Hollander et al., 2003). For instance, a-adrenergic agents, P- blockers and typical and atypical antipsychotic agents are prescribed to decrease aggressive behaviours. Selective serotonin reuptake inhibitors are used for treatment of the anxiety or for stereotypes and repetitive behaviours. Dopamine reuptake blocking agents, stimulants and a-adrenergic agents are used for hyperactive patients, and finally antidepressants, anticonvulsants and melatonin have shown some benefits for sleep disorders. However, none of these treatments can definitely improve the severe symptoms in autistic patients and it is some times necessary to try several of them before to observe a slight effect. Behavioural...

From genomics to proteomics

Although these techniques are easier to apply for diseases with clear-cut lesions, such as ischemia following focal stroke (Wang et al. 2000), their potential interest and application in many psychiatric disorders is important now that large collections of brains from patients who have died are being made in different countries. These will provide samples for applying these techniques. Other developments in proteomics may be of considerable value in the development of new pharmaceutical targets through pharmacogenomics. Gene expression arrays are used to define the mechanism of action for new compounds, or to screen for direct influence of an agent on a specific pathway. Some new techniques may be specifically relevant for psychopharmacogenomics. For example, voxelation, using high-throughput analyses of spatially registered voxels harvested from the brain followed by three dimensions reconstruction, is performed before a Gene Expression Tomography (GET) which employs analyses of sets...

Current Concepts and State of Knowledge Concepts for In Vivo Modeling

There is an ongoing discussion about the criteria to be used in the evaluation of animal models. It has been suggested that the only meaningful initial evaluating criterion for an animal model is its ability to lead to accurate predictions (predictive validity). Other authors stressed that the demonstration of construct validity (similarity to the underlying causes of the disease) represents the most important and necessary component in validation of an animal model. Others claim that the modeling of symptoms (face validity) must remain the primary goal of animal models of psychiatric disorders. The resolution of this puzzling controversy depends on the desired purpose of the model that one wishes to validate. Although, regarding complex psychiatric disorders such as autism, a multidimensional approach should be used as an optimal strategy.

Behavioral Tests for Autistic Like Aberrations in Rodents

As an important prerequisite, it is necessary to use appropriate behavioral test batteries for the validation of an animal model of autism. The three core symptoms of autism should be targeted first Autism Animal Models. Table 1. Rodent behavioral tasks relevant to autism (for references see Crawley 2007). Tests analogous to core autistic symptoms Tests analogous to associated symptoms Tests analogous to core autistic symptoms Tests analogous to associated symptoms

Lesion Induced Models

The exact locus of brain dysfunction in autism remains a point of debate (Bauman and Kemper 2005). Many brain regions, ranging from brainstem and cerebellum to association areas of the neocortex, have been suggested as potential candidates. Nevertheless, converging lines of evidence suggest that dysfunctions and morphological abnormalities in the medial temporal lobe, especially amygdala, and the prefrontal cortex (PFC) might underlie social deficits in autism. On that basis several models of autism have been proposed (Tordjman et al. 2007). For example, neonatal ibotenic acid lesion of the amygdala on PND 7 in rat produces a spectrum of behavioral abnormalities resembling those described in autism decreased social interaction, increased stereotypic-like activity and decreased exploratory behavior. Similarly, neonatal ventral hippocampus lesion in rats leads to impaired social behaviors, motor hyperresponsiveness to stress, enhanced stereotypies, deficits in pre-pulse and latent...

Models Created by Environmental and Immune Factors

An exposure during embryogenesis to at least three ter-atogens appears to be a risk factor for autism thalidomide, VPA, and misoprostol (Arndt et al. 2005). Accordingly, one of the best validated animal models of autism is induced by prenatal exposure to VPA on the twelfth day of gestation (reviewed in Markram et al. 2007). VPA rats show several brainstem and cerebellar abnormalities resembling those found in autistic patients. At the behavioral level, VPA rats exhibit decreased social interactions, increased repetitive behaviors, enhanced anxiety, locomotor hyperactivity combined with lower exploratory activity, lower sensitivity to pain, higher sensitivity to non-painful sensory stimulation, impaired pre-pulse inhibition, and faster acquisition of eye-blink conditioning. Interestingly, behavioral aberrations described in VPA rats are observed mostly in males and can be reversed by environmental enrichment procedure. These might resemble both disproportion in boys to girls ratio in...

Genetically Induced Models

To date, several genetically induced mouse models of autism have been proposed (Moy and Nadler 2008). They were created using three general approaches. One approach is to induce mutations in genes regulating social behavior. For example, oxytocin gene knockout pups display reduced exploration, less separation distress calls, and later on a diminished social recognition. Reduced social interaction and decreased exploration were also observed in serotonin transporter-null mice. A third approach uses gene mutations relevant to loci for autism susceptibility, identified by association or linkage studies. For example, Relnrl + mice show lower rates of separation distress calls, impairments in reversal learning, increased anxiety, decreased pre-pulse inhibition, and a progressive loss of Purkinje cells. Similarly, Gabrb3 gene deficient mice exhibit impaired social and exploratory behaviors, deficits in non-selective attention and hypopla-sia of cerebellar vermal lobules. Another example,...

Hints Of Phenotypes For Variant Sert Alleles From Genetic Studies In Mouse And

Although functional coding variants have yet to be identified in hSERTs, functional variants in promoter and intronic regions have been investigated for their relationship to clinical syndromes. As noted above, the s alleles of the 5HTTLPR have been found to associate with reduced transcriptional activity of the SERT promoter and with neuroticism and anxiety traits (Lesch et al., 1996). However, the degree to which the 5-HTTLPR influences SERT expression is at present controversial, with both supportive (Little et al., 1998 Heinz et al., 2000) and contradictory (Willeit et al., 2001) evidence. Recently, Du and co-workers (Du et al., 2000) were able to replicate the finding of Lesch of an association between 5-HTTLPR s alleles and neuroticism, but only in a male population, the gender of the original Lesch studies. These findings suggest that gender-specific expression of phenotypes may need to be considered in evaluation of SERT variants and that neuroti-cism and anxiety continue to...

Diffusion Tensor Imaging and Tractography

Most of the previously described volumetric methods focus on gray matter structures as opposed to diffusion tensor imaging (DTI) and associated techniques that image white matter. DTI technologies image water diffusion to study the directionality and integrity of white matter connections between different locations of the brain (Kubicki et al. 2007). These studies advance the hypothesis that psychiatric disorders are characterized by altered connectivity ( disconnection syndromes ). These studies are beginning to help us understand the basis of cerebral organization and connectivity and how it might be affected in psychiatric disorders such as autism (Alexander et al. 2007), late-life depression

Neurotransmitter Transporters

Plasma membrane transporters have long been recognized as important components of the machinery for neural signaling. Reuptake inhibitors increase the levels of neuro-transmitter in the synapse, thus enhancing synaptic transmission, and provide important targets for therapeutic intervention. Indeed, the importance of neurotransmitter transporters is highlighted by the broad spectrum of drugs targeting these proteins, including those used to treat depression, anxiety, obesity and epilepsy, in addition to drugs of abuse, such as cocaine, amphetamine, and ecstasy (2). Furthermore, it is well established that neurotransmitter transporters have roles in several neurological and psychiatric diseases, including amyotrophic lateral sclerosis, severe orthostatic hypotension, obsessive-compulsive disorder, Asperger's syndrome, anorexia, and autism (3).

Neurobehavioral Interpretations and Clinical Importance of Stereotypy

Stereotyped behaviors are generally thought to reflect the dysfunction of the central nervous system (Robbins et al. 1990 Teitelbaum et al. 1990). Persons with mental retardation, autism, schizophrenia, Tourette's syndrome, Hun-tington's disease, or obsessive compulsive disorder (OCD) often exhibit excessively repetitious and apparently purposeless behaviors as do persons who have used excessive amounts of amphetamine over multi-day periods. Substantial clinical and experimental evidence points to dopamine as the brain neurotransmitter with a major role in the expression of stereotyped behavior in the aforementioned clinical abnormalities. In rodent studies of the behavioral effects of psychomotor stimulants, links have been established between dopaminergically innervated subcortical structures and expression of increased locomotor activation and stereotypy induction. Dopa-mine agonists are thought to induce locomotor activity by acting on the nucleus accumbens, while actions of the...

Physiological Role of Shank Proteins

The relatively strong effect of mutations in the human SHANK3 gene argues for a specific functional role of this protein, as similar disease-associated mutations in the other SHANK genes have not been detected so far. The SHANK3 gene is located on the distal arm of chromosome 22q13.3 and may be lost due to chromosomal translocations (Bonaglia et al. 2001) or deletions (in the 22q13.3 microdeletion syndrome, a disorder that affects about 1 in 200,000 people). In addition, point mutations leading to frame shifts or alterations in the protein sequence have been described recently (Durand et al. 2007). Affected patients suffer from severe mental retardation, delayed speech and autism. The current view is that the haploinsuffi-ciency of the SHANK3 gene leads to a lack of functional Shank proteins, which may be critical for the maturation of dendritic spines and formation of synapses.

Integration Of Different Evidence Disease Gene Predictor

It is often the case that one does not have enough known high-confident disease genes available. In this scenario, simple intersection or presence absence analysis can be applied. For each type of source, score 1 is assigned to a gene if it carries certain property similar to known disease genes. Then the total score from different sources is used for ranking genes. This scoring system is simple and easy-to-use. Although the scores are not weighted for different genes or different types of evidence, it has been successfully and efficiently applied to identify a novel breast cancer gene, HMMR (Pujana et al., 2007). We also used this ranking procedure in the autism network study (manuscript in preparation). Firstly, we assigned score of 1 to a gene if (1) it has high topological overlap with a known autism gene in human gene expression network, or (2) it has high topological overlap with a known autism gene in mouse gene expression network, or (3) it is directly connected to a known...

Discussions And Conclusion

To identify what functional characteristics are significantly over-represented in a list of genes, the list of the control genes is often needed. Due to the nature of the data, most lists of candidate genes are derived from a set of regions detected by linkage or association studies, or by copy number variation analysis. It was observed that genes in close genomic neighborhood may have similar expressions and functional annotations (Su et al. 2002). Thus appropriate control datasets need to be chosen to correct for such bias. In our study of identifying pathways and networks using copy number variable regions in autism patients, two types of control sets were used for an unbiased comparison (1) randomly permuted CNV regions across human genome (2) naturally occurring human CNVs in normal individuals extracted from Database of Genomic Variants (DGV, http varia-tion ). Using these two types of control sets, an increased connectivity among brain-expressed genes from...

Stereotypical and Repetitive Behavior Definition

Stereotypical and repetitive behavior is commonly seen in individuals with autism spectrum disorders (ASDs) and mental retardation (MR). In lower functioning individuals with ASDs or MR, this usually consists of self-stimulatory, nonfunctional, motor behaviors. However, in mild MR or higher functioning individuals with ASDs, this can consist of verbal and motor rituals, obsessive questioning, rigidly held routines, preoccupation with details, and desire for sameness and completeness. Autism Spectrum Disorders and Mental Retardation

Proteinassociated Cns Diseases

Autism and autistic disorders Autism is a childhood behavioral and neurological disorder with onset prior to three years of age. The main features of autism spectrum disorders (ASD) are deficits in language, social, and emotional functioning, with significantly variable secondary symptoms of aggression, self-injurious behavior and impulsivity. Autism now affects 62-67 per 10,000 births, with boys being affected four times more frequently than girls (Bertrand 2001 Chakrabarti 2001). While the exact cause of autism is unknown, an abnormal functioning of neurotransmitter receptors may be one mechanism involved. The theory of vaccine-related autism is actually related to the pertussis toxin found in the diphtheria, pertussis, and tetanus (DPT) vaccine. The toxin in the vaccine uncouples Ga proteins from retinoid receptors in the brain, thereby functionally uncoupling receptors from their intracellular signaling proteins (Megson 2000). A pre-existing family history of defects in Ga...

Faulty Epigenetics Germline Mutations

Neurodevelopmental disorder of infant girls with a variable clinical phenotype characterized by loss of motor and language skills, microcephaly, autistic features, and stereotypic hand movements Mental retardation affecting males primarily other diagnostic criteria long face, large everted ears, autism, hand biting, hyperactivity and macroorchidism (large testicles)

Neuroimaging Synonyms

Neuroimaging is a family of techniques used for obtaining images of the structure or the function of the human brain. Neuroimaging studies investigate structural and functional brain maturation in health or in diseases of the brain, such as schizophrenia, bipolar disorder, depression, ADHD, drug dependence, and autism. These studies often aim to find genetic and environmental markers of variance in brain structure and function over time. Through additions to diagnostic radiology, neuroimaging has broadened to become a distinct field in neuroscience. The neuroimaging techniques that are currently used in research include single-photon emission computerized tomography (SPECT), positron emission tomography (PET), distinct forms of magnetic resonance imaging (MRI) including structural and functional MRI, MR spectroscopy (MRS), and diffusion tensor imaging (DTI).

Human Genetic Variation

Duplications of the long arm of chromosome 15 (15q11-13) are the most frequent cytogenetic anomalies in autism spectrum disorders, occurring in approximately 1 -2 of cases (Cook 2001). This duplication syndrome cannot be clinically differentiated from idiopathic autism spectrum disorders (Veenstra-VanderWeele and Cook 2004), indicating that a complete workup of autism should include testing for this cytogenetic abnormality, as well as for several others (Martin and Ledbetter 2007). Interestingly, deletion of this same region of 15q is associated with Angelman syndrome when the deletion occurs on the maternal copy of chromosome 15, and with Prader-Willi syndrome when the deletion occurs on the paternal chromosome (or more rarely, when two maternal copies of chromosome 15 are present, and the paternal chromosome is missing entirely, a condition known as maternal disomy). Both syndromes manifest as quite distinct but dramatic neurobehavioral disorders (Nicholls and Knepper 2001 Vogels...


The advantage of animal models of autism is to study developmental and behavioral deficits in context of a whole organism. We can use such models to clarify complex relationships between genetic, behavioral and environmental variables to better understand and potentially cure autism. What we need now is to combine these different approaches into multidisciplinary studies determining the consequences of environmental factors (e.g., stress, teratogenic substances, enriched environment) on the development of autistic-like behavioral changes in genetically modified animals, and vice versa, to determine the genetic basis of negative and positive effects of environmental factors in animal models. It is also critical to facilitate the process of identifying reliable measures of the human phenomenon, as better understanding of the neuropathology of autism will be essential to continue to build and improve animal models in the future.

Tamya Kolachana

Badner JA, Gershon ES Meta-analysis of whole-genome linkage scans of bipolar disorder and schizophrenia. Mol Psychiatry 7 405-411, 2002 PubMed Bailey A, Le Couteur A, Gottesman I, et al Autism as a strongly genetic disorder evidence from a British twin study. Psychol Med 25 63-77, 1995 PubMed Barrett JC, Cardon LR Evaluating coverage of genome-wide association studies. Nat Genet 38 659-662, 2006 PubMed Cook EH Jr Genetics of autism. Child Adolesc Psychiatr Clin N Am 10 333-350, 2001 PubMed Folstein SE, Rosen-Sheidley B Genetics of autism complex aetiology for a heterogeneous disorder. Nat Rev Genet 2 943-955, 2001 PubMed Marshall CR, Noor A, Vincent JB, et al Structural variation of chromosomes in autism spectrum disorder. Am J Hum Genet 82 477-488, 2008 PubMed Martin CL, Ledbetter DH Autism and cytogenetic abnormalities solving autism one chromosome at a time. Curr Psychiatry Rep 9 141-147, 2007 PubMed Rutter M Genetic studies of autism from the 1970s into the millennium. J Abnorm...


Thus, in schizophrenia, individuals with an affected sibling were found to have a 9 risk, compared with a 1 lifetime risk in the general population. This risk increases to 16 if both an affected sibling and parent are known within the family. Similarly, although non-identical twins have increased risks similar to that of normal siblings, monozygotic twins (who in principle have identical genes) have a 46-48 lifetime risk of schizophrenia (Karayiorgou and Gogos, 1997). In Alzheimer's disease, family studies are complicated by late onset of the condition, but sibling risk is estimated at 3-14 , whereas among monozygotic twins between 40 and 50 concordance has been observed. A strong genetic effect has also been observed in autism, for which sibling risk is 2.9 , but concordance among monozygotic twins can be as high as 60 . In contrast, concordance among dizy-gotic twins is very low, indicating that several loci are likely to be involved as well as...

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Learn How to Help, Understand amp Cope with your Aspergers Child from a UK Chartered Educational Psychologist. Before beginning any practice relating to Aspergers it is highly recommended that you first obtain the consent and advice of a qualified health,education or social care professional.

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