[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address 35.172.233.215. Please contact the publisher to request reinstatement.
[Skip to Content Landing]
Neurological Review
October 2008

Progress in Periventricular Leukomalacia

Author Affiliations

Author Affiliations: Institute of Pediatric Regenerative Medicine, Shriners Hospital and School of Medicine, University of California, Davis (Drs Deng and D. Pleasure); and Departments of Cell Biology and Human Anatomy (Dr Deng), Pediatrics (Drs J. Pleasure and D. Pleasure), and Neurology (Dr D. Pleasure), UC Davis School of Medicine, Sacramento, California.

Arch Neurol. 2008;65(10):1291-1295. doi:10.1001/archneur.65.10.1291
Abstract

Periventricular leukomalacia (PVL) is the predominant form of brain injury and the leading known cause of cerebral palsy and cognitive deficits in premature infants. The number of low-birth-weight infants who survive to demonstrate these neurologic deficts is increasing. Magnetic resonance imaging–based neuroimaging techniques provide greater diagnostic sensitivity for PVL than does head ultrasonography and often document the involvement of telencephalic gray matter and long tracts in addition to periventricular white matter. The neuropathologic hallmarks of PVL are microglial activation and focal and diffuse periventricular depletion of premyelinating oligodendroglia. Premyelinating oligodendroglia are highly vulnerable to death caused by glutamate, free radicals, and proinflammatory cytokines. Studies in animal models of PVL suggest that pharmacologic interventions that target these toxic molecules will be useful in diminishing the severity of PVL.

×