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Is Autism A Neurocognitive Disorder

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Neurocognitive Predictors Of Social And Communicative Developmental Trajectories In Preschoolers With Autism Spectrum Disorders

Five Questions about Autism

Published online by Cambridge University Press: 27 October 2008

Affiliation:University of Washington Autism Center and Center on Human Development and Disability, Seattle, WashingtonDepartment of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington
Affiliation:University of Washington Autism Center and Center on Human Development and Disability, Seattle, WashingtonDepartment of Psychology, University of Washington, Seattle, Washington
Affiliation:Department of Psychology, University of Washington, Seattle, WashingtonInstitute for Learning and Brain Sciences, Seattle, Washington
Affiliation:University of Washington Autism Center and Center on Human Development and Disability, Seattle, WashingtonInstitute for Learning and Brain Sciences, Seattle, Washington
University of Washington Autism Center and Center on Human Development and Disability, Seattle, Washington
Correspondence and reprint requests to: Jeffrey Munson, UW Autism Center, Box 357920 ,

Mild And Major Neurocognitive Disorders Prognosis

Some cases of neurocognitive disorder especially if due to vitamin deficiency, infections, metabolic problems, one-time injuries and temporary hypoxia may be reversible. Others are nonreversible and progressive, but treatments may help manage symptoms and maintain quality of life for months or years.

Association Between Infant Markers And Asd Outcome

When measured at 7 months, the AOSI total score was not a significant predictor of ASD outcome 2 = 4.40, p = 0.11. At 14 months, however, AOSI score did significantly predict ASD outcome 2 = 10.64, p = 0.005, with the HR-ASD group showing higher AOSI scores than LR controls and HR-No ASD .

Seven-month P400 amplitude difference score was a significant overall predictor of the ASD outcome = 12.15, p = 0.002 see Fig. ), with the HR-ASD group differentiating less between the away and towards gaze shifts than LR controls did . HR-ASD and HR-No ASD groups differed only marginally . Results were substantively similar when one outlier was trimmed . Disengagement latency at 14 months also predicted overall ASD outcome = 9.55, p = 0.008 see Fig. ), with the HR-ASD group having significantly longer latencies than both other groups .

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Treatment Options For Asd

Diagnosis and treatment of ASD are difficult because it combines formal and informal treatment processes. Treating autism employs intensive procedures where the entire family and a team of professionals are involved. Treatments take place at homes or in clinics depending on the strength of the disorder. The main treatment methods for Autism involve therapies such as occupation therapy, neurologist, and speech & language therapy. Children are expected to undertake 25 hours each week of full therapy. For example, the Speech & Language Therapy takes a daily duration of 45 minutes. The intervention model plays a significant role in treating children with autism. The model uses psychodynamic theories are commonly combined with the intervention theoretical model. On the other hand, intervention programs aimed at improving communication with patients and making them more open to the society are some forms of autism treatment and therapy. The Chelation process that involves administration of substances that remove heavy metals from the body also helps in treating ASD. The process takes place under the vaccines theory, but these treatments are not 100 percent effective .

Reviewthe Neurocognitive Basis Of Autism

How does Autism impact...

The cognitive study of the underlying mental abnormalities in autism has advanced rapidly, while the biological study of the underlying brain abnormalities and of putative genetic mechanisms is lagging somewhat behind. However, the linking of cognitive and biological studies has become a real possibility. Developmental cognitive neuroscience has transformed our understanding of this enigmatic disorder, which was once misguidedly thought to be caused by maternal rejection. The hypothesis of a specific theory of mind deficit was a crucial step in this process. It explains the puzzle of the characteristic social and communication impairments of autism and allows for the fact that they can coexist with good general abilities. This hypothesis has been widely accepted and a start has been made at pinpointing the brain basis of theory of mind. The non-social impairments of autism have now become a major focus for cognitive research. One theory proposes dysfunction in executive processes, in an attempt to explain repetitive behaviour and inflexibility. Another theory proposes weak information integration, in an attempt to explain narrow interests and special talents. Autism research has thus stimulated ideas on important mind-brain systems that may be dedicated to the development of social awareness, executive functions and integrative processing.

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Treatment Options For Mild Neurocognitive Disorder

Scientists have developed models that enable clinicians use clinical data to test and treat mild Neurocognitive disorders. The dual-retrieval models theoretical tests the diagnostic criteria for testing Mild Neurocognitive Disorder and direct the best treatment option. The model uses a recall based technique that makes it possible to measure processes with clinical memory tests. The model determines the level of memory loss in an individual and determines the type of Neurocognitive Disorder present . Treatment for Mild Neurocognitive Disorder is by use of drugs or therapy. Common drugs proposed for treatment include cholinesterase inhibitors, memantine, and caprylidene. Non-pharmacological treatment options include emotion-oriented treatments, stimulation oriented treatments, and cognition oriented therapy.

Is Autism A Neurocognitive Disorder

In autism spectrum disorder , a number of neurocognitive phenotypes have been identified during childhood that are associated with the core ASD symptom domains of social communication impairments, the presence of restricted and repetitive patterns of behaviour and atypical sensory responses (Diagnostic and …

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Psychopathological And Neurocognitive Studies

The developmental age of all three mosaic carriers was 12 years or older. This maximum score on the clinical interview VABS is in line with the developmental age of the general population. Additionally, all subjects fulfilled the diagnostic criteria for ASD and MDD either currently and/or in the past. In contrast to the ADOS, the mini PAS-ADD did not formally determine ASD as the total subscale scores were just below the cutoff score. Notwithstanding, ASD items scored in the mini PAS-ADD were similar to the clinical observations of the ADOS. During the clinical observation, all participants scored on limited eye contact and minimum use of emotional gestures, when testing was focused on the communication. For social interaction, all three showed impaired social reciprocity, a limited range of facial expressed emotions, and an inadequate description of their role in social relations.

In addition to estimating the degree of psychopathology, we used the CANTAB to measure several cognitive functions of our subjects. The percentages represent the subjects performance compared to the normative group with the same sex and age. Subject 1 had low scores on the PRM and IED. Subject 2 had overall low scores on the tests. Subject 3 experienced problems with the IED. Detailed results are presented in Table all IED scores were lower than 35% of the peer group, indicating an impaired mental flexibility in all three subjects.

Research Autism Before The Autism Spectrum

Autism – Part 2 of 4: Autistic Disorder, CDD, PDD-NOS & Asperger’s

Conserving a distinct line of research dedicated to prototypical autism is still justified, whereas it is at risk of disappearing under the current spectrum approach to diagnosis. For example, studying the gradual improvement of socio-communicative signs between preschool and school age in children with an initial prototypical presentation provides information on the temporal characteristics of these signs . Such knowledge would help improve the specificity of these signs and their contribution to retrospective diagnoses. It is also necessary to preserve a threshold of qualitative similarity with the prototypical autism phenotype, in addition to the non-specific severity threshold.

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Which Is A Common Diagnosis Of A Neurocognitive Disorder Ncd

NCDs commonly result from Alzheimers or Parkinsons disease. In order to be diagnosed with an NCD, a person must exhibit a cognitive decline and some impairment in cognitive functioning. For a diagnosis of mild NCD, the person must still be able to live and perform everyday activities independently.

Disentangling Potentially Artifactual From Genuine Heterogeneity

There is, however, heterogeneity that plausibly belongs to the autism signal when the kinship between a prototypical clinical presentation and an altered version is biologically validated. Examples of this include developmental transformations, some variations in presentation according to intelligence and language level, and the familial aggregation of autism subtypes.

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Indeterminate Nature Of The Clinical Specifiers

The four clinical specifiers of ASD were originally designed to account for the unavoidable heterogeneity of autistic presentation, for example, between nonverbal and hyper-verbal individuals, while preserving the category. These specifiers now exacerbate the heterogeneity of the individuals included in this spectrum, transforming the autism diagnosis into a category as vague as intellectual disability and neurodevelopmental disorders. A common characteristic of the four clinical specifiers is their dimensional, quantitative, and clinically nonspecific nature. Moreover, there are no constraints on how the qualitative properties of the seven criteria are modified according to the expression of each of the specifiers, which misses a major opportunity to increase specificity. For example, a dissociation between advanced knowledge of letters and numbers and poor pragmatic use of verbs would contribute qualitative information to a quantitative language specifier .

Study Autism Subgroups Separately Then Compare Them

Cognitive Challenges

Instead of an a priori assumption that all presentations of ASD represent the same condition, it would be beneficial to study potential autism subgroups separately and merge them only if they are similar for targeted variables. Beyond non-syndromic autism with and without SOD, candidate subgroups include syndromic autism, and validated and non-validated subthreshold individuals. Excluding the aspect of speech from the diagnostic criteria accounts for much heterogeneity and increases the risk of losing the information conveyed by speech to the diagnosis. Having or not a history of SOD has a lifelong impact, not only on language and speech but also on the nature of peaks of abilities , intelligence subtest profiles , motor difficulties , domains of interest , lateralization of brain structures and functions , gyrification , white matter , and neural activity during speech-like processing , which are unavoidably blurred when the two subgroups are analyzed together.

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Dissociative Identity Disorder Autism And A Conversation

Dissociative Identity Disorder is on the same spectrum as Post Traumatic Stress Disorder . They are both DISSOCIATIVE disorders. Those who develop DID have over developed abilities in dissociating, a skill very commonly overdeveloped in children with autism. Dissociation is a natural process in children under the age of 5 but most children grow out of it. Those with developmental disabilities may have stronger motivations to dissociate from what they find sensorily overwhelming or too hard to process and so those with autism may be predisposed to dissociation but also other dissociative processes, such as depersonalisation and derealisation. Some personality traits can also predispose some children to overdeveloping these dissociative processes.

When someone already predisposed to skills in dissociation grows up in conditions of severe neglect, trauma and chronic abuse before the ages of 3-5 years old, that person is at risk of their dissociative skills getting in the way of cohesive identity development. Instead the person grows up with different parts of the self compartmentalised and eventually each part so differentiated from each other they can lose awareness of any relatedness to each other and essentially become alters within a DID system.


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DONNA:50 is a massive team. How do you keep track of them? Do you use external ways to represent each to help the therapist track who is thinking/feeling what?



Mild And Major Neurocognitive Disorders Diagnosis

Diagnosing major or mild neurocognitive disorder requires a thorough physical, psychological and neurological evaluation. Your physician will use the criteria for neurocognitive disorders listed in the Diagnostic and Statistical Manual of Mental Disorders , published by the American Psychiatric Association, to determine if your symptoms indicate the condition.

Diagnostic tests include:

Brain scans: A CT scan or MRI can help your physician determine if a specific brain condition is causing your symptoms, such as a stroke, a tumor or hydrocephalus . A PET scan can show patterns of brain activity and identify if an amyloid protein found in Alzheimers disease is present.

Cognitive and neuropsychological tests: These tests measure skills such as memory, orientation, reasoning and judgment, language and attention.

Lab tests: Blood tests can detect health issues that can affect brain function, such as a vitamin B-12 deficiency or an underactive thyroid. Spinal fluid may also be examined for signs of infection, inflammation or markers of some degenerative diseases.

Neurological evaluation: Your physician will evaluate your memory, language skills, visual perception, attention, problem-solving, movement, senses, balance, reflexes and more.

Physical examination: A physician will perform a physical exam and ask questions about your health to determine if your symptoms could be linked to an underlying physical health problem or medication side effect.

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Prevalence Rates And Causes For Asd

PrevalenceExperts are still researching about ASD to determine its prevalence and specific symptoms. The year 1997 recorded more cases of children suffering from ASD in Brick Township compared to any other prevalence. The report by Centers for Disease Control and Prevention showed the prevalence to be 6.7 per 1000 children. Additionally, CDC realized 7.8 percent of children between ages of 4 and 17 falls at greater risks of developing ASD. On the other hand, it is not known how many parents out there house children with autism.

Identifying Autism From Neural Representations Of Social Interactions: Neurocognitive Markers Of Autism

Challenging Behaviors in Children with Autism Spectrum Disorders
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    Affiliation Department of Psychology and Center for Cognitive Brain Imaging, Carnegie Mellon University, Pittsburgh, Pennsylvania, United States of America

  • Affiliation Department of Psychology and Center for Cognitive Brain Imaging, Carnegie Mellon University, Pittsburgh, Pennsylvania, United States of America

  • Affiliations Department of Psychology and Center for Cognitive Brain Imaging, Carnegie Mellon University, Pittsburgh, Pennsylvania, United States of America, Brain Institute of Rio Grande do Sul , Pontifical Catholic University of Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil

  • Affiliation Department of Psychology and Center for Cognitive Brain Imaging, Carnegie Mellon University, Pittsburgh, Pennsylvania, United States of America

  • Affiliation Machine Learning Department, Carnegie Mellon University, Pittsburgh, Pennsylvania, United States of America

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Acknowledging The Effect Of Artifactual Heterogeneity In Clinical Settings And Research Programs

The decrease in effect-sizes in neurocognitive autism research over time is likely due to increased artifactual heterogeneity, which affects our ability to construct neurobiological models of autism. We propose that these problems may be mitigated by modifying the diagnostic criteria and prevalent research strategies.

Fmri Study Of The Amygdala

In the second fMRI experiment, we explored the functional neural networking patterns underlying atypical processing of dynamic facial expressions .

However, the coupling patterns between the subcortical and neocortical regions during observation of emotional facial expressions in individuals with ASD remain unclear. A previous study investigated this issue in TD individuals by analyzing fMRI data while the participants observed dynamic facial expressions using dynamic causal modeling this allows inferences to be drawn about the causal and directional effects among brain regions . The models compared included those considering a modulatory effect of dynamic expressions from the amygdala to the neocortical network, from the neocortical network to the amygdala, and a joint effect. The optimal model was that featuring a modulatory effect from the amygdala to the neocortical network. This result is compatible with anatomical findings in monkeys specifically, the amygdala receives inputs via subcortical visual pathways that bypass the neocortical visual pathways , and it sends projections to many neocortical regions, including the visual and motor cortices . Based on these data and the above-described psychological findings on reduced emotional modulation of facial expression processing in individuals with ASD, we hypothesized that modulation of the neocortical network by the amygdala during observation of dynamic facial expressions may be reduced in individuals with ASD.

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Neurocognitive Mechanisms Underlying Social Atypicalities In Autism: Weak Amygdalas Emotional Modulation Hypothesis

  • 1Psychological Process Team, BZP, RIKEN, Kyoto, Japan
  • 2Organization for Promoting Neurodevelopmental Disorder Research, Kyoto, Japan
  • 3Department of Developmental Disorders, National Institute of Mental Health, National Center of Neurology and Psychiatry, Tokyo, Japan
  • 4Brain Activity Imaging Center, ATR-Promotions, Kyoto, Japan

Autism spectrum disorder is a neurodevelopmental condition associated with atypicalities in social interaction. Although psychological and neuroimaging studies have revealed divergent impairments in psychological processes and neural activity related to the processing of social stimuli, it remains difficult to integrate these findings. In an effort to resolve this issue, we review our psychological and functional magnetic resonance imaging findings and present a hypothetical neurocognitive model. Our psychological study showed that emotional modulation of reflexive joint attention is impaired in individuals with ASD. Our fMRI study showed that modulation from the amygdala to the neocortex during observation of dynamic facial expressions is reduced in the ASD group. Based on these findings and other evidence, we hypothesize that weak modulation from the amygdala to the neocortexthrough which emotion rapidly modulates various types of perceptual, cognitive, and motor processing functionsunderlies the social atypicalities in individuals with ASD.

Is A Stroke A Neurocognitive Disorder


Poststroke neurocognitive disorder occurs in the majority of patients affected by stroke with associated cerebral infarct or hemorrhage, according to a study published in Stroke. A shortened summary cognitive score consisting of action speed, executive function, and language may help diagnose poststroke NCD.

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Aging Fathers Selfish Testes And Neurocognitive Disorders


Copy errors: The likelihood of an error, or mutation, in sperm DNA rises steadily with age, but this may not fully explain the increased risk of certain disorders.

There is robust evidence from epidemiological studies that the risk of developing neurocognitive disorders, including autism and schizophrenia, increases with the age of the father at the time of conception.

Among others, a 2011 Swedish study describes a two-fold increase in relative risk of autism for a child born to a father over 55 years of age compared with a father younger than 29 years1. Studies have consistently reported similar risk factors for schizophrenia2.

Despite this well-documented paternal-age effect, the biological basis for the association remains poorly understood. The prevailing explanation is that this effect is mediated by an increase in de novo, or spontaneous, mutations in the sperm of aging men.

An additional mechanism may be at play in the testes of men as they age: This process, known as selfish selection, predicts that certain mutations may hijack the normal mechanisms of sperm production to their own advantage. This enriches for sperm that carry harmful mutations3.

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