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Is periventricular leukomalacia an axonopathy as well as an oligopathy?
O Dammann1, H Hagberg, A Leviton
1Neuroepidemiology Unit, Department of Neurology, Children's Hospital, Boston, Massachusetts 02115, U.S.A.
Insights
Periventricular leukomalacia, a white matter disorder in preterm infants, may involve both oligodendrocyte and axonal damage. Current evidence suggests it is premature to attribute this condition solely to oligodendrocyte injury.
Area of Science:
- Neuroscience
- Neonatal Neurology
- Developmental Pediatrics
Background:
- Periventricular leukomalacia (PVL) is a neonatal white matter disorder.
- Cranial ultrasound findings in PVL predict long-term developmental limitations in preterm infants.
- The prevailing hypothesis suggests primary damage to oligodendrocytes, leading to secondary axonal injury.
Purpose of the Study:
- To discuss the differential roles of oligodendrocytes and axons in the etiology of PVL.
- To explore analogies from multiple sclerosis and hydrocephalus literature.
- To evaluate the current understanding of PVL pathogenesis.
Main Methods:
- Literature review and synthesis.
- Comparative analysis of PVL with other neurological disorders.
- Discussion of oligodendrocyte and axonal contributions to PVL.
Main Results:
- Oligodendrocytes are vulnerable in PVL, supporting the hypothesis of primary damage.
- Axonal damage is recognized as a significant component of PVL.
- Analogies with multiple sclerosis and hydrocephalus offer insights into PVL mechanisms.
Conclusions:
- It is premature to exclusively attribute PVL to oligodendrocyte damage or maldevelopment.
- Both oligodendrocyte and axonal pathology likely contribute to PVL.
- Further research is needed to fully elucidate the complex etiology of PVL.
Abstract:
Periventricular leukomalacia is a white matter disorder, the neonatal cranial ultrasound images of which predict long-term developmental limitations among preterm infants. The vulnerability of oligodendrocytes has led to the hypothesis that oligodendrocytes suffer the primary damage, with axonal damage occurring as a consequence. In this article, we discuss the differential role of oligodendrocytes and axons in this disorder's etiology, offering analogies from the multiple sclerosis and hydrocephalus literature. We conclude that it is too early to view periventricular leukomalacia exclusively as a consequence of oligodendrocyte damage and/or maldevelopment.