The relative contribution of CSF malabsorption and obstruction in three different etiological groups of neonatal high-pressure hydrocephalus (HC) was assessed in a study at University of Bonn, Germany, and University of Groningen, The Netherlands. CSF biomarkers, transforming growth factor beta-1 (TGF B-l), and aminoterminal propeptide of type 1 collagen (PC1NP), indicative of growth factor- and fibrosis-related CSF malabsorption, were assessed and compared in neonates with post-hemorrhagic HC (n=6), non-hemorrhagic triventricular HC (n=4) and spina bifida (SB) HC (n=12). CSF interleukin-6 (IL-6) cytokines, indicative of inflammation, were low and did not differ between groups. TGF B-l concentrations were significantly higher in post-hemorrhagic HC cases (median 355 pg/ml) than in SB HC (median 103) and non-hemorrhagic HC (median 120); p=0.01 and 0.03, respectively. Median CSF PC1NP concentrations were significantly lower in SB HC (180 ng/ml) than in post-hemorrhagic HC (1,060 ng/ml); p=0.002. Neonatal posthemorrhagic HC is associated with high concentrations of CSF malabsorption-related biomarkers whereas SB and non-hemorrhagic HC have lower concentrations, indicating that CSF obstruction contributes more to the development of these cases than malabsorption. [1]

COMMENT. High TGF B-l and PC1NP CSF concentrations in neonatal post-hemorrhagic HC are indicative of a fibrosis-related malabsorption as the cause of the HC, contrasting with relatively low levels of malabsorption biomarkers in SB and non-hemorrhagic triventricular HC. CSF obstruction, rather than malabsorption, plays a major role in the pathogenesis of high-pressure SB and non-hemorrhagic HC.