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Updated: Jun 29, 2026
Mouse Models of Periventricular Leukomalacia
Published on: May 18, 2010
Progress in periventricular leukomalacia
Wenbin Deng1, Jeanette Pleasure, David Pleasure
1Department of Neurology, UC Davis School of Medicine, 2425 Stockton Blvd, Sacramento, CA 95817, USA.
Insights
Periventricular leukomalacia (PVL) is a major brain injury in premature infants, leading to cerebral palsy. Research suggests targeting toxic molecules may reduce PVL severity in animal models.
Area of Science:
- Neuroscience
- Neonatal Medicine
- Developmental Pediatrics
Background:
- Periventricular leukomalacia (PVL) is the primary brain injury in premature infants.
- PVL is the leading cause of cerebral palsy and cognitive deficits in survivors.
- The incidence of PVL-related neurological deficits in surviving low-birth-weight infants is rising.
Purpose of the Study:
- To review the neuropathology of PVL.
- To discuss advanced neuroimaging techniques for PVL diagnosis.
- To explore potential therapeutic targets for PVL.
Main Methods:
- Review of neuropathologic hallmarks of PVL.
- Comparison of diagnostic sensitivity between MRI and ultrasonography.
- Analysis of animal models for therapeutic strategies.
Main Results:
- PVL involves microglial activation and loss of premyelinating oligodendroglia.
- MRI offers higher sensitivity for PVL detection than ultrasonography.
- Premyelinating oligodendroglia are susceptible to excitotoxicity, oxidative stress, and inflammation.
- Animal studies indicate pharmacologic interventions targeting toxic molecules may mitigate PVL.
Conclusions:
- PVL is a significant concern in premature infant neurology.
- Advanced neuroimaging improves PVL detection and characterization.
- Understanding PVL pathophysiology points to potential therapeutic avenues targeting specific molecular pathways.
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.
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