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Autism social abnormalities

If there is an association between the extent or severity of abnormal neurotransmitter functioning and the global measure of severity of autism, the direction and mechanism of causality may still be unclear (as has been discussed in mental retardation). However, neurotransmitter correlates of specific aspects of autism, such as social isolation or obsessional behaviour, are likely to be more revealing and of greater relevance to the study of consciousness. [Pg.314]

The dorsal and ventral hippocampus is involved in the formation of social memory (van Wimersma Greidanus and Maigret, 1996). Neonatal ablations of hippocampal regions can lead to decreased and abnormal social behavior in rhesus monkeys that is reminiscent of severe neuropsychiatric disorders in humans such as autism and schizophrenia (Bachevalier et ah, 1999). These monkeys are often withdrawn socially and will develop locomotoric stereotypies a pattern similar to that found in autistic children. [Pg.197]

Serotonin involvement. There is substantial evidence supporting abnormal 5-HT function in autism, particularly with regard to both the social deficit and repetitive behavior dimensions of this disorder. Many studies of the neurobiology of autism have focused on 5-HT, which is implicated in the regulation of many functions relevant to autism, such as learning, memory. [Pg.205]

MacLean (1985, 1990) has hypothesized that the history of the evolution of the limbic system is the history of the evolution of mammals. The deficits in the limbic structures of autistic individuals appear to ontogenetically mirror a phylogenetic deficiency in paleomammalian brain evolution. Behaviors at the basic core of autistic symptomatology - the expression of affection, social-emotional reciprocity, attachment behaviors, and the capacity to play - that are impaired in individuals with autism represent behaviors that evolved during the transition from reptiles to mammals. These abnormalities of limbic structures have profound human consequences in what is one of the most severe psychiatric disorders and undermine the essence of personality qualities we value as being human. [Pg.41]

Adolphs R, Sears L, Riven J (2001) Abnormal processing of social information from faces in autism. J Cogn Neurosci 13 232-240. [Pg.170]

Following our characterization of NL3 R451C mutants, mice lacking NL4 were also found to exhibit autism-related behavioral abnormalities including social interaction abnormalities and ultrasonic vocalizations (Jamain et al., 2008). The functional consequences of NL4 deletion on synapses have yet to be determined. [Pg.211]

Cerebellar abnormalities may result in disturbances in a neural network involved in the motivation and organization of emotion. Abnormalities in the cerebellar nuclei may play a role in the affective disturbance, abnormal language development, and inappropriate social and psychological behaviors in autism. [Pg.271]

Researchers at the Kennedy Krieger Institute in Baltimore, MD, found that children with autism have increased white matter in the motor region of the brain. In normally developing children, increased white matter is correlated with improved motor skills, but later may contribute to motor dysfunction, as well as abnormal socialization and communication. [Pg.201]


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