Microvascular and large vein abnormalities in young patients after mild head trauma and associated fatigue: A brain

Tiffany Crider1, Derrick Eng2, Pooja R Sarkar3

  • 1HackensackUMC Palisades, North Bergen, NJ, United States.

Abstract

Insights

Mild traumatic brain injury (mTBI) can cause long-term fatigue due to cerebrovascular changes. Brain SPECT imaging reveals perfusion deficits in the frontal and temporal lobes, supporting an oxidative stress model for mTBI-related fatigue.

Area of Science:

  • Neuroscience
  • Radiology
  • Pathophysiology

Background:

  • Mild traumatic brain injury (mTBI) often presents with normal MRI/CT scans, yet 15-20% of patients experience persistent symptoms like fatigue.
  • mTBI is increasingly recognized as a cerebrovascular injury, similar to moderate and severe TBI.
  • Brain SPECT imaging demonstrates higher sensitivity than MRI/CT in detecting immediate perfusion abnormalities post-mTBI.

Purpose of the Study:

  • To investigate perfusion abnormalities in young patients experiencing fatigue several months after mTBI.
  • To explore the relationship between mTBI, cerebrovascular changes, and persistent fatigue.

Main Methods:

  • Prospective study of twelve mTBI patients (ages 8-36) who developed fatigue 6-12 months post-injury.
  • Utilized 99mTc ECD brain SPECT with early and delayed imaging to assess cerebral blood flow.

Main Results:

  • Identified left hemispheric perfusion deficits in the frontal lobes (early phase: 15.2%, delayed phase: 9.9%) and medial temporal lobes (early phase: 11.2%, delayed phase: 9.0%) in mTBI patients with fatigue.
  • Observed excess radiotracer accumulation around the internal jugular bulb in seven patients, suggesting increased vascular permeability.
  • Linked tracer leakage to oxidative stress, compromised endothelial tight junctions, and posture-induced changes in jugular venous pressure.

Conclusions:

  • Findings support an oxidative stress and blood-brain barrier disruption model for mTBI.
  • Frontal and temporal lobe perfusion deficits are attributed to the anatomical vulnerability of these brain regions to impact.
  • Proposed a link between mTBI-induced oxidative stress, impaired ATP generation, altered endothelial homeostasis, and persistent fatigue.

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