Mother-Child Relationship for Families of Children with Autism in Cognitively

Monique Crawley*

Department of Clinical Neurosciences, Kings College Hospital, Denmark Hill, London, United Kingdom

*Corresponding Author:
Monique Crawley
Department of Clinical Neurosciences, Kings College Hospital, Denmark Hill, London, United Kingdom
E-mail:monicrawl@yahoo.com

Received date: December 30, 2022, Manuscript No. IPCDD-23-15841; Editor assigned date: January 02, 2023, PreQC No. IPCDD-23-15841 (PQ); Reviewed date: January 12, 2023, QC No. IPCDD-23-15841; Revised date: January 23, 2023, Manuscript No. IPCDD-23-15841 (R); Published date: January 30, 2023, DOI: 10.36648/2471-1786.9.1.049
Citation: Crawley M (2022) Mother-Child Relationship for Families of Children with Autism in Cognitively. J Child Dev Disord Vol.9 No.1: 49.

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Description

Asperger's syndrome and classic autism share three fundamental diagnostic characteristics: 1) difficulties in social development and communication development, as well as unusually strong, narrow interests and behavior that repeats itself Since social communication is always necessary, it might be more beneficial to consider autism and Asperger's Syndrome (AS) to share two main characteristics: difficulties in social and communication, as well as narrow interests and repetitive actions. The child must have started talking on time and have an IQ of at least average to qualify for the diagnosis of AS. At various stages of development, these characteristics take on different manifestations. The "mind-blindness" theory, which was developed in the 1980s and 1990s and has been a remarkable success in explaining autism's social and communication issues, is summarized at the beginning of this article. The "Empathizing-Systemizing" (E-S) theory, a more recent two-factor theory, is then criticized, arguing that it is superior to this theory.

As background, it's important to remember why we need a cognitive theory of autism. Behavior-related and diverse are the characteristics of Autism Spectrum Conditions (ASC), of which classic autism and as are the most distinct subgroups. There are dozens or even hundreds of behavioral characteristics that can be identified depending on how these are counted. These are attempted to be broken down into one or two fundamental mental processes by a cognitive theory. This is not a substitute for a neurobiological theory because we need both to comprehend how abnormal neural structure or functioning can lead to abnormal behavior. The cognitive level effectively acts as a mediator between the neurobiological and behavioral levels of description.

Sensory and Arousal Modulation

A nonverbal child with severe mental retardation and self-injury to a high-functioning college student with an above-average IQ despite impaired language use and inadequate social skills are examples of the highly variable cognitive manifestations of ASDs. Although some cognitive abilities are characteristically affected by autism, mental retardation is not a defining characteristic of autism; however, the mean distribution of IQs is lower than average, and the likelihood of retardation increases with more widespread brain dysfunction. Mental retardation is a disorder of complex human abilities, defined by behavior, with numerous genetic and nongenetic causes. The more severe the retardation, the more likely it is that the dysfunction in the brain underneath will have an effect on the many different networks that are responsible for social skills like language and flexibility in thinking. Autism, like mental retardation, is a behavioral disorder characterized by a wide range of genetic and nongenetic causes. There is currently no evidence that any particular genetic or nongenetic disorder is connected to any of the other DSM-IV subtypes of autism, with the exception of Rett syndrome, which is typically brought on by de novo mutations or microdeletions of the methyl-CpG-binding protein 2 (MeCP2) gene on Xq28.13 With the exception of Rett syndrome, the entire spectrum of behaviorally defined autism is referred to as autism in this article. The majority of cases of autism are caused by multiple genetic factors, according to current evidence.

Autism may also be linked to genetic mutations that cause a number of other diseases that can be diagnosed. Angelman Syndrome (AS) and Prader-Willi Syndrome (PWS) typically result from genetic deletions or uniparental disomy (inheritance of both chromosomes from one parent) of the chromosome 15q11-q13 locus, with abnormal imprinting or genetic mutations found in up to 5.1% of PWS cases and up to 15% of AS cases. Neurofibromatosis, a common autosomal dominant disorder with neurologic and cutaneous manifestation PWS is caused by the loss of genes that come from the father, whereas AS, which is more frequently associated with autism than PWS, can be caused by the loss or mutation of the ATP10C or UBE3A genes, which come from the mother.

The Mind-blindness Theory

A surprising number of boys who have Duchenne muscular dystrophy fall into the autistic spectrum. In case studies, numerous other uncommon single-gene defects, such as those found in Sotos syndrome, Williams syndrome, hypomelanosis of Ito, Cowden syndrome, and Moebius syndrome, have been linked to autism. For a more comprehensive list of rare genetic conditions that occasionally cause autism, we recommend The Biology of the Autistic Syndromes. Lastly, abnormal cellular metabolism, such as mitochondrial disease or dysfunction, may also cause autism. It is well known that untreated phenylketonuria is a metabolic cause of autism; However, it is unclear whether this is due to the specific dopamine pathway deficit or the severe mental retardation that results. Up to a quarter of autism patients have high levels of uric acid secretion, according to some clinic-based studies, and antihyperuricosuric metabolic therapy improves some symptoms. Although it has not been widely replicated, this represents a significant portion of these clinical samples, and the genes that are responsible for this kind of "purine autism" have yet to be identified.

Eisenberg, recalling that he found three autistic siblings among 131 autistic children but failed to identify the genetic cause, emphasized that our conclusions always reflect prevailing concepts and ideas in a review of child and adolescent psychiatry over the past 50 years. Our conceptions of autism, as well as the education and treatment provided to those who are affected by it, have been influenced by cultural shifts and research findings. Kanner realized that the long-term institutionalization of psychiatric patients and those with learning disabilities "cut short any prospects of improvement" during his lifetime. However, even Kanner was caught up in the psychoanalytic era, when all childhood disorders were attributed to poor parenting, and held that this was a contributing cause. Kanner had always stressed the constitutional basis of autism.

While early intervention can significantly improve the behavioral adjustment of children with autism, there is currently no effect on long-term prognosis, according to reviews of the education and treatment of autistic children. The administration of educational and medical services is another factor that influences interventions.

Over 50% of children with autism take vitamins or drugs in the United States, where managed care limits the intensity and duration of psychiatric treatments. This is very different from what happens in the United Kingdom.

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