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CSF Volume at 6 Months Correctly Predicts ASD Diagnosis at 24 Months in High Risk Infants

Research Question

Researchers in this article compiled fMRI data from infants of high and low risk for ASD in order to measure extra-axial cerebrospinal fluid (EA-CSF) volume as a possible biomarker for ASD.


A total of 343 infants underwent neuroimaging at 6, 12, and 24 months of age. Infants were designated as either high risk denoting a genetic susceptibility to ASD from an older sibling or low risk denoting no immediate genetic relation to ASD. Subsequent fMRI analysis showed a significant increase in EA-CSF volume for high-risk infants in the 6-24 -month age range. Additionally, EA-CSF volume at 6 months predicted ASD diagnosis at 24 months with an overall accuracy of 69% (66% sensitivity, 68% specificity).


A strength of this experiment is the large sample size. The high number of independent data points allows the author to confidently introduce not only statistically significant results, but also a strong correlation between 6-month EA-CSF volume and 24 mo. ASD diagnosis.

A weakness of this paper is the brief introduction. While the introduction discusses previous lines of EA-CSF research and CSF functioning, it does not mention the natural fluctuation of CSF volume from infancy into adulthood. Without knowledge of the natural fluctuations in CSF, it is difficult to theoretically associate CSF with ASD.


This study shows that EA-CSF volume at 6 months has potential use as a biological marker of ASD or earlier processes of motor impairment. Clinically, if the present findings are rigorously supported, neuroimaging analysis may provide radiologists with a personalized, quantitative tool for labelling ASD risk during infancy. Assessing risk for ASD can ultimately lead to earlier intervention and a higher chance of optimal outcome.

Future Directions

New research can explore the interaction of CSF volume in adults with ASD. Questions such as “does EA-CSF volume stay high after the 24-month mark?” may be tested to further our knowledge of ASD etiology into adulthood.

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