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Pediatrics · Chapter 2. Neonatology

Diagnostic Imaging of Perinatal CNS Lesion Sequelae

Magnetic resonance imaging is the primary diagnostic imaging modality for severe structural brain changes in neonatal practice. These pathological conditions develop predominantly as a sequel to hypoxic-ischemic injuries, logically dividing into white matter damage and concomitant atrophic processes.

EtiologyPredominantly a sequel to hypoxic-ischemic injuries
LocalizationPeriventricular white matter, cortex, and subcortical structures
Key sign«Scalloped» contour of the lateral ventricle walls
Replacement processHydrocephalus ex vacuo due to brain tissue loss
3 min readFor medical studentsUpdated Sep 20, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Periventricular leukomalacia (PVL)

Periventricular leukomalacia is a classic variant of brain injury in newborns, characterized by necrosis of the white matter immediately adjacent to the lateral ventricles. Axial MRI slices are traditionally used for optimal visualization of these changes.

The main imaging signs of PVL include:

  • Change in tissue volume: a pronounced deficit of periventricular white matter is visualized, indicating massive cell death.
  • Ventricle deformation: the walls of the lateral ventricles lose their normal smoothness. Due to the loss of adjacent white matter, they acquire a characteristic uneven, so-called «scalloped» contour.
  • Focal MR signal changes: gliotic changes form in the areas of prior necrosis. On tomograms, this manifests as areas with altered signal intensity in the periventricular regions.

Atrophic changes in the brain parenchyma

Periventricular leukomalacia very rarely occurs in isolation. Most often, it is accompanied by or naturally leads to a secondary loss of brain tissue volume. On MRI scans, this process is recorded as various variants of cerebral atrophy.

Two main patterns of volume loss are distinguished:

  1. Corticosubcortical atrophy. This variant is characterized by diffuse changes. The scans clearly show widening of the subarachnoid spaces, as well as significant deepening of the cerebral hemispheric sulci. Such a picture is direct evidence of a massive decrease in volume of both the cortex itself and the underlying white matter.
  2. Local (regional) atrophy. In contrast to the diffuse process, there is a selective decrease in brain tissue volume here. Typical examples are changes in the temporal and temporoparietal regions, where pronounced widening of the corresponding sulci and fissures is visualized.
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Alterations in adjacent anatomical structures

The marked brain tissue deficit resulting from necrosis and subsequent atrophy inevitably leads to secondary deformation of adjacent anatomical structures of the brain.

  • Ventriculomegaly. There is a marked widening of the entire ventricular system. It is important to understand that in this context, ventriculomegaly is exclusively of a replacement nature (hydrocephalus ex vacuo develops). Cerebrospinal fluid passively fills the excess space formed due to progressive cortical and white matter atrophy.
  • Corpus callosum hypoplasia. Sagittal slices are optimal for assessing this sign, visualizing a sharp thinning of the corpus callosum structure. This phenomenon is a direct consequence of PVL and cortical atrophy: there is massive death of commissural nerve fibers that normally run from the cortex to the opposite hemisphere and form the bulk of the corpus callosum.

Class and exam questions

Why does the shape of the ventricles change in periventricular leukomalacia?

The shape of the ventricles changes due to necrosis and the subsequent loss of adjacent white matter tissue. As a result, the walls of the lateral ventricles collapse unevenly and acquire an irregular, «scalloped» contour.

What does the term «hydrocephalus ex vacuo» mean in the context of CNS lesions?

Hydrocephalus ex vacuo refers to compensatory enlargement of the ventricular system (ventriculomegaly). The ventricles expand passively to fill the intracranial dead space created by brain tissue deficit and atrophy.

What is the cause of corpus callosum hypoplasia in hypoxic-ischemic injuries?

Corpus callosum hypoplasia is a consequence of periventricular leukomalacia and cortical atrophy. It arises due to secondary death of the commissural nerve fibers that form this structure.

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What else to study on this topic

  • MRI signal characteristics of gliotic changes at the site of prior necrosis
  • Differential imaging diagnostics of regional and diffuse corticosubcortical atrophy
  • Evaluation of corpus callosum hypoplasia on sagittal MRI slices
  • Visualization of local atrophy in the temporal and temporoparietal regions
  • Morphological differences between replacement ventriculomegaly and hypertensive hydrocephalus

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