Learn about the latest data on autism. April 30, Act early on developmental concerns to make a real difference for your child and you!
In recent years, some researchers suggest that ASD is the result of complex interactions between genetic and environmental risk factors [ 37 ]. Understanding the interaction between genetic and environmental factors in the pathogenesis of ASD will lead to optimal treatment strategy.
Clinical features and Diagnosis ASD is typically noticed in the first 3 years of life, with deficits in social behaviors and nonverbal interactions such as reduced eye contact, facial expression, and body gestures [ 1 ].
Children also manifest with non-specific symptoms such as unusual sensory perception skills and experiences, motor clumsiness, and insomnia. Associated phenomena include mental retardation, emotional indifference, hyperactivity, aggression, self-injury, and repetitive behaviors such as body rocking or hand flapping.
Repetitive, stereotyped behaviors are often accompanied by cognitive impairment, seizures or epilepsy, gastrointestinal complaints, disturbedd sleep, and other problems. Differential diagnosis includes childhood schizophrenia, learning disability, and deafness [ 3839 ].
ASD is diagnosed clinically based on the presence of core symptoms. However, caution is required when diagnosing ASD because of non-specific manifestations in different age groups and individual abilities in intelligence and verbal domains.
The earliest nonspecific signs recognized in infancy or toddlers include irritability, passivity, and difficulties with sleeping and eating, followed by delays in language and social engagement. In the first year of age, infants later diagnosed with ASD cannot be easily distinguished from control infants.
At 12 months of age, individuals with ASD show atypical behaviors, across the domains of visual attention, imitation, social responses, motor control, and reactivity [ 40 ]. There is also report about atypical language trajectories, with mild delays at 12 months progressing to more severe delays by 24 months [ 40 ].
ASD can be easily differentiated from other psychosocial disorders Autism review late preschool and early school years. In particular, the role of amygdala in cognition and ASD has been proved in numerous neuropathological and neuroimaging studies.
The amygdala located the medial temporal lobe anterior to the hippocampal formation has been thought to have a strong association with social and aggressive behaviors in patients with ASD [ 4142 ]. The amygdala is a major component of the limbic system and affective loop of the cortico-striato-thalamo-cortical circuit [ 43 ].
The amygdala has 2 specific functions including eye gaze and face processing [ 44 ].
The lesion of the amygdala results in fear-processing, modulation of memory with emotional content, and eye gaze when looking at human face [ 454647 ]. The findings in individuals with amygdala lesion are similar to the phenomena in ASD.
The amygdala receives highly processed somatosensory, visual, auditory, and all types of visceral inputs. It sends efferents through two major pathways, the stria terminalis and the ventral amygdalofugal pathway.
The amygdala comprises a collection of 13 nuclei. Based on histochemical analyses, these 13 nuclei are divided into three primary subgroups: The BL group attributes amygdala to have a role as a node connecting sensory stimuli to higher social cognition level. It links the CM and superficial groups, and it has reciprocal connection with the orbitofrontal cortex, anterior cingulate cortex ACCand the medial prefrontal cortex mPFC [ 48 ].
The BL group contains neurons responsive to faces and actions of others, which is not found in the other two groups of amygdala [ 4950 ]. The CM group consists of the central, medial, cortical nuclei, and the periamygdaloid complex. It innervates many of the visceral and autonomic effector regions of the brain stem, and provides a major output to the hypothalamus, thalamus, ventral tegmental area, and reticular formation [ 51 ].
The superficial group includes the nucleus of the lateral olfactory tract [ 42 ].
It also includes serotonergic, dopaminergic, cholinergic, and noradrenergic cell bodies and pathways [ 52 ].
Since some patients with temporal epilepsy and aggressive behavior experienced improvement in aggressiveness after bilateral stereotactic ablation of basal and corticomedial amygdaloid nuclei, the role of amygdala in emotional processing, especially rage processing has been investigated [ 53545556 ].
Some evidences for the amygdala deficit in patients with ASD have been suggested. Post-mortem studies found the pathology in the amygdala of individuals with ASD compared to age- and sex-matched controls [ 575859 ].
Small neuronal size and increased cell density in the cortical, medial, and central nuclei of the amygdala were detected in ASD patients. Several studies proposed the use of an animal model to confirm the evidence for the association between amygdala and ASD [ 6061 ].
Despite the limitation which stems from the need to prove higher order cognitive disorder, the studies suggested that disease-associated alterations in the temporal lobes during experimental manipulations of the amygdala in animals have produced some symptoms of ASD [ 62 ].
Especially, the Kluver-Bucy syndrome, which is caused by bilateral damage to the anterior temporal lobes in monkeys, has characteristic manifestations similar to ASD [ 6364 ].
Monkeys with the Kluver-Bucy syndrome shows absence of social chattering, lack of facial expression, absence of emotional reactions, repetitive abnormal movement patterns, and increased aggression.
On the contrary, lesioning of the amygdala or blocking amygdala excitability with glutamate antagonist increased dyadic social interactions [ 60 ]. Besides animals, humans who underwent lesioning of the amygdala showed impairments in social judgment.
This phenomenon is called acquired ASD [ 666768 ].
The pattern of social deficits was similar in idiopathic and acquired ASD [ 69 ].The Review Journal of Autism and Developmental Disorders publishes original articles that provide critical reviews of topics across the broad interdisciplinary research fields of autism spectrum disorders.
Topics range from basic to applied and include but are not limited to genetics, neuroscience, diagnosis, applied behavior analysis. Page 2 AUTISM RESEARCH REVIEW INTERNATIONAL Vol.
25, No. 1, Help for parents implementing a GF/CF diet Gluten-free, casein-free diets benefit many children and adults on the autism spectrum, but implement -. Jan 28, · Autism spectrum disorder (ASD) is a set of neurodevelopmental disorders characterized by a deficit in social behaviors and nonverbal interactions such as reduced eye contact, facial expression, and body gestures in the first 3 years of life.
Autism, Asperger's & Theory of Mind A Literature Review Abstract: This literature review examines the history and pertinent research on Autism, a brain development. high-functioning children with a normal appearance and IQ and moderate social and language impairments.
Ge-netic counseling justifies testing, but until autism genes. Autism spectrum disorders are a group of neurodevelopmental disorders characterized by impaired verbal and/or nonverbal communication in addition to repetitive stereotypical behaviors.