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Cognition and behavior: White matter shows delays in autism

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Alla Katsnelson
6 December 2013

Sturdy nerves: A brain imaging method called diffusion tensor imaging can be used to evaluate the integrity of the brain’s nerve fibers.

A difference in how auditory nerve fibers develop may explain why children with autism process sounds a fraction of a second more slowly than typically developing children do. The result, published in September in Brain Research, also suggests that a widely used method for assessing nerve fiber structure may not be appropriate for autism research1.

The brain’s response to sound speeds up as children age. This boost in speed is known to be accompanied by the maturation of white matter — the nerve fibers that connect brain regions. Specifically, there is an age-related change in myelin, the fatty coating that helps neurons transmit signals.

In children with autism, however, the brain’s response to sound is known to be delayed. To determine whether this delay is associated with abnormal white matter, the researchers examined the structure of the nerve fibers in 53 children with autism and 39 age-matched controls, all aged 5 to 17 years.

The researchers used a technique called magnetoencephalography, which maps magnetic fields generated by neurons to map brain activity patterns. They found that although response time in children with autism is on average slower than in the controls, it increases at the same rate with age in both groups.   

The researchers then looked at the structure of the white matter using diffusion tensor imaging, which measures how water molecules diffuse along nerve fibers. They found that, based on a widely used measure called fractional anisotropy, white matter in the brains of children with autism does not mature with age as it does in controls.

However, a closer look at the data reveals that this interpretation is incorrect: White matter in children with autism does mature, but differently than it does in controls.

Fractional anisotropy is a composite of two individual measurements: axial diffusivity, which assesses how water diffuses along nerve fibers, and radial diffusivity, which measures how it diffuses across the fibers. Radial diffusivity decreases with age in both groups, but more slowly in the children with autism. Meanwhile, axial diffusivity decreases only in the children with autism, in whom the fibers are still immature.

Taken together for children with autism, however, these two measures cancel each other out, incorrectly suggesting that the children’s nerve fibers do not mature over time.

The findings suggest that fractional anisotropy may not be a good way to assess white matter structure in autism, the authors say. They add that because both the response to sound and white matter structure vary widely, even among the children within each group, unpacking the exact relationship between them will require following individual children over long periods of time.

News and Opinion articles on SFARI.org are editorially independent of the Simons Foundation.

References:

1. Roberts T.P. et al. Brain Res. 1537, 79-85 (2013) PubMed

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Comments

Name: Eileen Nicole Simon
11 December 2013 - 11:43AM

Evidence has been available for decades that nuclei in the brainstem auditory pathway are fully myelinated by 29 weeks gestation, and this is the age when the fetus firsts responds to sounds [1, 2]. It is common knowledge that brain maturation follows an orderly course, and that this orderly course can be disrupted by prenatal exposure to alcohol and other substances [3].

Evidence has also been available for decades that nuclei in the brainstem auditory pathway are selectively injured by asphyxia at birth [4]. This evidence was obtained by subjecting monkeys to asphyxia at birth, and then it was found that postnatal maturation of the brain was disrupted [5]. This evidence has for too long been forgotten.

Evidence of difficult birth with asphyxia evidenced by low Apgar scores has been reported more often than any other etiological factor for autism. Asphyxia at birth is dismissed in almost all of these reports as deriving from some preexisting problem with the child or the mother. How outrageously unscientific!!! The monkeys subjected to asphyxia had no preexisting problems.

The monkey experiments should be repeated, and brain maturation followed by all of the modern imaging techniques. No one expects a monkey to learn to speak, but language development in the human species begins with the ability to distinguish syllable and word boundaries in rapid streams of speech [6]. I am glad that auditory dysfunction is finally being recognized as a serious predisposition for autism.

Clamping the umbilical cord before the first breath will cause asphyxia if resuscitation cannot be accomplished quickly. There is no health benefit from clamping off placental blood flow after birth. Use of a clamp on the umbilical cord is a clear medical error, and it should be stopped. This error has been inflicted as an obstetric protocol since the mid 1980s. Stop this procedure, and the autism epidemic will likely be stopped.

[1] Yakovlev PI and Lecours A-R. The myelogenetic cycles of regional maturation of the brain. In A. Minkowski (Ed.), Regional Development of the Brain in Early Life (pp. 3-70). Oxford: Blackwell Scientific Publications, 1967.
[2] Moore JK, Perazzo LM, Braun A. Time course of axonal myelination in the human brainstem auditory pathway. Hear Res. 1995 Jul;87(1-2):21-31.
[3] Roebuck TM, Mattson SN, Riley EP. A review of the neuroanatomical findings in children with fetal alcohol syndrome or prenatal exposure to alcohol. Alcohol Clin Exp Res. 1998 Apr;22(2):339-44.
[4] Windle WF. Brain damage by asphyxia at birth. Sci Am. 1969 Oct;221(4):76-84.
[5] Faro MD, Windle WF. Transneuronal degeneration in brains of monkeys asphyxiated at birth. Exp Neurol. 1969 May;24(1):38-53.
[6] Brown R. A First Language: The Early Stages. Cambridge, MA: Harvard University Press, 1973.

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