Intraventricular hemorrhage (IVH) in premature infants is a devastating problem that occurs tens of thousands of times each year in the United States alone. Survivors face numerous neurological concerns, including cognitive deficits, cerebral palsy, and hydrocephalus. As neurosurgeons, we are humbled by our inability to do much more than manage spinal fluid diversion. One mechanism that appears to underlie the neurological troubles is white matter injury caused by demyelination. It has been discovered that hyaluronan (HA), a negatively charged glycosaminoglycan polymer, is abundantly found in white matter lesions with IVH, where an HA receptor known as CD44 is overexpressed, oligodendrocyte precursors (OPCs) show arrested maturation, and there is reduced myelination.1 Because of the growing body of information implicating HA as a potential therapeutic target in IVH, Vinukonda et al2 sought to investigate an HA-dependent mechanism as a possible therapeutic target to improve myelination via the administration of hyaluronidase or HA oligosaccharides.
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