To review the evidence for the presence of prenatal and perinatal factors that affect the risk of autism and autism spectrum disorders.
Relevant articles were identified by searching MEDLINE, screening reference lists of original studies, and searching major journals likely to publish epidemiological studies on the topic.
For inclusion in this review, studies required (1) a well-defined sample of cases drawn from population-based registers or cohorts; (2) standardized, prospectively collected obstetric information from birth records or registers; (3) comparison subjects drawn from the general population with information on obstetric complications collected from the same source; and (4) a standardized format for presentation of data, allowing for comparisons among studies. Main Exposures Parental characteristics and obstetric complications.
Rates of autism and autism spectrum disorders.
Seven epidemiological studies were identified that fulfilled inclusion criteria. The parental characteristics associated with an increased risk of autism and autism spectrum disorders included advanced maternal age, advanced paternal age, and maternal place of birth outside Europe or North America. The obstetric conditions that emerged as significant fell into 2 categories: (1) birth weight and duration of gestation and (2) intrapartum hypoxia.
Evidence to suggest that parental age and obstetric conditions are associated with an increased risk of autism and autism spectrum disorders is accumulating. Although not proven as independent risk factors for autism, these variables should be examined in future studies that use large, population-based birth cohorts with precise assessments of exposures and potential confounders.
"In this study, history of low birth weight was found to be highly significant among autistic children than controls. Kolevzon et al.  suggested the presence of non heritable prenatal and perinatal risk factors for autism. An association is suggested between autism and obstetric complications, prenatal or intrapartum use of medications . "
[Show abstract][Hide abstract] ABSTRACT: Classical autism belongs to a group of heterogeneous neurobehavioral disorders known as autism spectrum disorders (ASDs) characterized by abnormalities in social interaction, impaired communication, and repetitive stereotypic behaviors. Overall, there is an increased risk of ASDs associated with common mutations affecting the folate/methylation cycle. This study aimed at identification of the C677T polymorphic genotypes of MTHFR gene among the Egyptian children with autism and to correlate them with different phenotypes.
Egyptian Journal of Medical Human Genetics 06/2014; 15(4). DOI:10.1016/j.ejmhg.2014.05.004
"ogy of ASD and a first report stating that environmental factors may be more important than genetic factors has been pub - lished ( Hallmayer et al . , 2011 ) . In the last few years specific envi - ronmental factors , especially prenatal and perinatal , have been implicated in increased ASD risk ( Gardener et al . , 2011 ; Kinney et al . , 2008 ; Kolevzon et al . , 2007 ; Newschaffer et al . , 2007 ) . The environmental factors that could potentially have a sex - specific effect are discussed here ."
[Show abstract][Hide abstract] ABSTRACT: The male predominance of autism spectrum disorders (ASD) is one of the best-known, and at the same time, one of the least understood characteristics of these disorders. In this paper we review genetic, epigenetic, hormonal, and environmental mechanisms underlying this male preponderance. Sex-specific effects of Y-linked genes (including SRY expression leading to testicular development), balanced and skewed X-inactivation, genes that escape X-inactivation, parent-of-origin allelic imprinting, and the hypothetical heterochromatin sink are reviewed. These mechanisms likely contribute to etiology, instead of being simply causative to ASD. Environments, both internal and external, also play important roles in ASD's etiology. Early exposure to androgenic hormones and early maternal immune activation comprise environmental factors affecting sex-specific susceptibility to ASD. The gene-environment interactions underlying ASD, suggested here, implicate early prenatal stress as being especially detrimental to boys with a vulnerable genotype.
Frontiers in Neuroendocrinology 04/2014; 35(3). DOI:10.1016/j.yfrne.2014.03.006 · 7.04 Impact Factor
"The onset of the clinical features of autism is gradual in many children, but in other children, a functional regression has been reported in the first 1–2 years [65,66]. Some studies suggest a prenatal onset of developmental abnormalities leading to autism [67,68]. The pattern of changes seen in the cerebellum suggests that the pathology was acquired early in development . "
[Show abstract][Hide abstract] ABSTRACT: Several morphometric studies have revealed smaller than normal neurons in the neocortex of autistic subjects. To test the hypothesis that abnormal neuronal growth is a marker of an autism-associated global encephalopathy, neuronal volumes were estimated in 16 brain regions, including various subcortical structures, Ammon's horn, archicortex, cerebellum, and brainstem in 14 brains from individuals with autism 4 to 60 years of age and 14 age-matched control brains. This stereological study showed a significantly smaller volume of neuronal soma in 14 of 16 regions in the 4- to 8-year-old autistic brains than in the controls. Arbitrary classification revealed a very severe neuronal volume deficit in 14.3% of significantly altered structures, severe in 50%, moderate in 21.4%, and mild in 14.3% structures. This pattern suggests desynchronized neuronal growth in the interacting neuronal networks involved in the autistic phenotype. The comparative study of the autistic and control subject brains revealed that the number of structures with a significant volume deficit decreased from 14 in the 4- to 8-year-old autistic subjects to 4 in the 36- to 60-year-old. Neuronal volumes in 75% of the structures examined in the older adults with autism are comparable to neuronal volume in age-matched controls. This pattern suggests defects of neuronal growth in early childhood and delayed up-regulation of neuronal growth during adolescence and adulthood reducing neuron soma volume deficit in majority of examined regions. However, significant correction of neuron size but limited clinical improvements suggests that delayed correction does not restore functional deficits.
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