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.