Related Experiment Video

Updated: Sep 5, 2026

Mouse Models of Periventricular Leukomalacia
06:24

Mouse Models of Periventricular Leukomalacia

Published on: May 19, 2010

Brain injury in the premature infant--from pathogenesis to prevention

J J Volpe1

  • 1Harvard Medical School, Boston, MA, USA. volpe-j@al.tch.harvard.edu

Brain & Development
|January 24, 1998
PubMed

Insights

Preventing brain lesions like periventricular hemorrhagic infarction and periventricular leukomalacia in premature infants is achievable. Strategies focus on preventing germinal matrix-intraventricular hemorrhage and protecting against impaired cerebral blood flow.

Area of Science:

  • Neonatal neurology
  • Pediatric neuropathology

Background:

  • Brain injury is a significant concern in premature infants, leading to long-term neurological deficits.
  • Periventricular hemorrhagic infarction and periventricular leukomalacia are the primary brain lesions observed.

Purpose of the Study:

  • To review the neurology, neuropathology, and pathogenesis of these critical brain lesions.
  • To explore potential preventative strategies for these injuries.

Main Methods:

  • Review of existing literature on neonatal brain injury.
  • Analysis of neuropathological findings.
  • Discussion of pathogenetic mechanisms.

Main Results:

  • Periventricular hemorrhagic infarction may be prevented by addressing germinal matrix-intraventricular hemorrhage.
  • Periventricular leukomalacia prevention involves detecting impaired cerebrovascular autoregulation and cerebral blood flow.
  • Interruption of oligodendroglial cell death pathways is a potential therapeutic target.

Conclusions:

  • Prevention of major brain lesions in premature infants is a realistic goal.
  • Targeted interventions can mitigate the risk of periventricular hemorrhagic infarction and periventricular leukomalacia.
  • Further research into neuroprotective agents is warranted.

More Related Videos

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats07:36

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Published on: November 20, 2015

Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats04:12

Modeling Posthemorrhagic Hydrocephalus of Prematurity in Rats

Published on: March 28, 2025

Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Spinal Cord Injury ll: Pathophysiology01:14

Spinal Cord Injury ll: Pathophysiology

Spinal cord injury progresses through two interconnected phases: primary injury and secondary injury.Primary InjuryPrimary injury happens at the moment of trauma and involves immediate mechanical damage to the spinal cord.Compression happens when broken vertebrae, herniated discs, or accumulating blood (such as a hematoma) press directly against the spinal cord, distorting its normal shape and function. In cases of contusion, the cord is bruised by a blunt force (like penetrating injuries or...
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...