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Updated: Oct 12, 2026
Mouse Models of Periventricular Leukomalacia
Published on: May 18, 2010
Ventriculomegaly, delayed myelination, white matter hypoplasia, and "periventricular" leukomalacia: how are they
Insights
Lateral ventricular enlargement in preterm infants may indicate white matter damage, not always hydrocephalus. This finding aids in preventing overtreatment and guides efforts to protect developing white matter.
Area of Science:
- Neonatal neurology
- Neurodevelopmental disorders
- Pediatric neuroimaging
Background:
- Preterm infants are at high risk for lateral ventricular enlargement.
- This enlargement can be associated with intracranial hemorrhage and diffuse white matter damage.
- Ventriculomegaly without macrocephaly often signifies hypoplastic white matter or reduced axonal density.
Purpose of the Study:
- To investigate the relationship between ventriculomegaly and white matter damage in preterm infants.
- To differentiate ventriculomegaly caused by white matter damage from that due to cerebrospinal fluid dynamics.
- To understand the underlying mechanisms of myelinogenesis disturbances in preterm newborns.
Main Methods:
- Observational study analyzing neuroimaging findings in preterm infants.
- Correlation of ventricular size with white matter integrity and myelination status.
- Review of potential etiological factors including growth factors, toxins, and physiological perturbations.
Main Results:
- Many cases of ventriculomegaly in preterm infants reflect diffuse white matter damage, not impaired cerebrospinal fluid flow.
- Hypoplastic white matter and inadequate axonal density are key indicators.
- Disturbances in myelinogenesis, affecting oligodendroglia or axons, are hypothesized to cause both ventriculomegaly and delayed myelination.
Conclusions:
- Ventriculomegaly in preterm infants can be a marker of underlying white matter damage.
- Distinguishing this from hydrocephalus is crucial to avoid overtreatment.
- Further research into the causes of white matter damage may lead to preventative strategies.
Abstract:
Preterm infants, including some who have sustained intracranial hemorrhage, appear to be at increased risk of lateral ventricular enlargement. Although some occurrences might be due to an impairment of cerebrospinal fluid flow or absorption, many instances of ventriculomegaly without accompanying macrocephaly reflect diffuse white matter damage resulting in diminished (i.e., hypoplastic) white matter or an inadequate density of axons. Perinatally acquired widespread white matter damage is sometimes associated with the focal white matter necrosis. We hypothesize that in some infants both ventriculomegaly and delayed myelination are consequences of disturbances to myelinogenesis that result from an impairment of cells destined to become oligodendroglia or of disturbances to rapidly growing axons. The vulnerability of developing white matter in preterm newborns might, in part, reflect the diminished availability of growth/ survival factors, or a vulnerability to toxins or physiologic perturbations. Awareness that some ventriculomegaly reflects widely distributed white matter damage should prevent overtreatment of what might appear to be hydrocephalus, but is not due to impaired cerebrospinal fluid dynamics. Increased understanding of the phenomena leading to ventriculomegaly related to paucity of white matter should lead to successful efforts to prevent white matter damage in preterm newborns.
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