Infantile traumatic brain injury with a biphasic clinical course and late reduced diffusion

Nanako Takase1, Noboru Igarashi2, Hiromichi Taneichi3

  • 1Department of Pediatrics, Tokyo Women's Medical University Yachiyo Medical Center, Yachiyo, Japan.

Insights

Infants with traumatic brain injury (TBI) may show delayed white matter diffusion changes, mimicking acute encephalopathy with biphasic seizures and late reduced diffusion (AESD). This suggests excitotoxicity as a potential cause for TBI-related brain injury.

Area of Science:

  • Pediatric Neurology
  • Neuroradiology
  • Neurocritical Care

Background:

  • Traumatic brain injury (TBI) in infants, including abusive head trauma, can present with subcortical white matter lesions.
  • The underlying mechanisms and clinical presentation of these lesions remain unclear.

Observation:

  • Two infants with TBI exhibited biphasic clinical courses and delayed reduced diffusion in the subcortical white matter.
  • Seven similar TBI cases were reviewed, showing consistent clinical and radiological patterns.

Findings:

  • TBI patients displayed secondary neurological symptoms on days 3-6 and delayed reduced diffusion (days 3-6) after initial normal diffusion (days 1-2).
  • These findings closely resemble acute encephalopathy with biphasic seizures and late reduced diffusion (AESD).
  • MR spectroscopy indicated a transient glutamine increase, a marker also seen in AESD, pointing to excitotoxicity.

Implications:

  • The findings suggest excitotoxicity as a potential pathomechanism in TBI-related subcortical white matter injury in infants.
  • This highlights the importance of recognizing biphasic clinical courses and delayed diffusion changes in pediatric TBI.
  • Further research is warranted to elucidate the precise mechanisms and optimize management strategies for these critical cases.

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