Autism: Differences in White Matter Fibre Tract Development present from 6-24 months

[Firestormm]

Differences in White Matter Fiber Tract Development Present From 6 to 24 Months in Infants With Autism

February 17 2012: http://ajp.psychiatryonline.org/article.aspx?articleid=668180 Paper available in full.

Abstract

Objective:

Evidence from prospective studies of high-risk infants suggests that early symptoms of autism usually emerge late in the first or early in the second year of life after a period of relatively typical development. The authors prospectively examined white matter fiber tract organization from 6 to 24 months in high-risk infants who developed autism spectrum disorders (ASDs) by 24 months.

Method:

The participants were 92 high-risk infant siblings from an ongoing imaging study of autism. All participants had diffusion tensor imaging at 6 months and behavioral assessments at 24 months; a majority contributed additional imaging data at 12 and/or 24 months. At 24 months, 28 infants met criteria for ASDs and 64 infants did not. Microstructural properties of white matter fiber tracts reported to be associated with ASDs or related behaviors were characterized by fractional anisotropy and radial and axial diffusivity.

Results:

The fractional anisotropy trajectories for 12 of 15 fiber tracts differed significantly between the infants who developed ASDs and those who did not. Development for most fiber tracts in the infants with ASDs was characterized by higher fractional anisotropy values at 6 months followed by slower change over time relative to infants without ASDs. Thus, by 24 months of age, those with ASDs had lower values.

Conclusions:

These results suggest that aberrant development of white matter pathways may precede the manifestation of autistic symptoms in the first year of life. Longitudinal data are critical to characterizing the dynamic age-related brain and behavior changes underlying this neurodevelopmental disorder.

LBRB Article and related video: http://leftbrainrightbrain.co.uk/20...LeftBrain/rightBrain+(Left+Brain/Right+Brain)

 

[natasa778]

If confirmed/replicated etc findings like these would confirm my suspicion that the main insult in most cases happens very early in life. Prenatal infection and placental pathology seem to be crucial.

Placental infection and/or inflammation is already highly suspect as behind autism (and has been partially confirmed - raised cytokines and other markers have been found in kids who later regressed). Very promising area of research imo, especially in terms of prevention and early treatment.

Amniotic fluid inflammatory cytokines: Potential markers of immunologic dysfunction in autism spectrum disorders

Exposure to prenatal inflammation is a known risk factor for long term neurobehavioral disorders including cerebral palsy, schizophrenia, and autism. Models of systemic inflammation during pregnancy have demonstrated an association with an immune response an adverse neurobehavioral outcomes for the exposed fetus. Yet, the most common route for an inflammatory exposure to a fetus is from intrauterine inflammation as occurs with chorioamnionitis... http://www.ncbi.nlm.nih.gov/pubmed/21382466

Interesting case study was published recently - mum had active CMV infection during pregnancy only one of the triplets got infected and later developed autism. The placenta and amniotic fluid of that child showed clear pathology and presence of CMV, which was absent in other two placentas.

It would also tie in neatly with further regressions kids go through vaccination, natural infections, exposure to allergens etc. This is because prenatal immune insult (either as direct infection or through maternal immune activation) dysregulates the immature immune system and makes it less able to fight off infections and more prone to inflammatory 'over-reaction' later on. Perfect fit to what we see in autism.

 

[natasa778]

few more related

Activation of the Maternal Immune System Alters Cerebellar Development in the Offspring

The cerebellar pathology observed in the offspring of influenza- or poly(I:C)-exposed mice is strikingly similar to that observed in autism.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2614890/?tool=pubmed

this one I think correlates closely to the brain findings Firestormm posted above

Brain enlargement and increased behavioral and cytokine reactivity in infant monkeys following acute prenatal endotoxemia
http://www.ncbi.nlm.nih.gov/pubmed/21192986


Innate immune dysfunction in the neonatal rat following prenatal endotoxin exposure
http://www.ncbi.nlm.nih.gov/pubmed/18708268

While the immune system is functionally immature in the neonatal period, these results suggest that prenatal infection may further reduce the capacity of the innate neonatal immune system to respond to endotoxin, leaving offspring more vulnerable to pathogenic invasion in neonatal life.

hence more pathogenic bacteria in the gut?? more herpesviruses, polyomaviruses in the brain etc findings? ineffective response to live virus vaccines?


wondering if this kind of prenatal or early postnatal exposure would play a role in risk of CFS? I think there is some research showing early infections as predisposing factors to MS (could be speculation only, not sure if actual research carried out?).