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Published on: September 28, 2022
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.
Objective:
MRI and CT scans are usually normal in mild traumatic brain injury (mTBI) although 15-20% of such patients suffer for months from fatigue, headache, anxiety, sleep and other disorders. mTBI is suspected to be a cerebrovascular injury, similar to moderate and severe TBI. Brain SPECT is more sensitive and shows perfusion abnormalities immediately after mTBI. This work explores the perfusion abnormalities for young patients suffering from fatigue several months after mTBI.
Patients And Methods:
Twelve mTBI patients (age:8-36 yr, 4 male) with no history of fatigue prior to trauma were prospectively studied following onset of fatigue 6-12 months after mTBI utilizing 99 m-Tc ECD brain SPECT with early and delayed radiotracer imaging.
Results:
The perfusion pattern in the mTBI + fatigue group included left hemispheric deficits in frontal lobes (early phase: 15.2 ± 4.2%, delayed phase: 9.9 ± 2.2%) and medial temporal lobes (early phase 11.2 ± 3.7%, delayed phase: 9.0 ± 2.3%). Seven patients additionally showed excess tracer accumulation in the parenchyma surrounding internal jugular bulb inferior to temporal lobe. This was modeled as due to increased cellular permeability from TBI induced oxidative stress affecting endothelial tight junctions and consequent tracer leakage across jugular bulbs. Prolonged posture changes from erect to supine position during imaging increase jugular cross-sectional area and venous wall pressure as has been observed in other disease processes and seem to be responsible for tracer leakage from jugular bulbs in our study.
Conclusion:
This work supports an oxidative stress and BBB disruption model for mTBI. The frontal and temporal lobe perfusion deficits are attributed to anatomical vulnerabilities of these lobes. During a mild TBI both of these lobes are susceptible to grazing impacts with underlying bony ridges. We propose a relation between mTBI and fatigue arising from oxidative stress in mTBI affecting ATP generation and altering endothelial homeostasis for both micro-and-large vasculatures. The tracer leakage observed around jugular veins is due to posture induced changes in venous cross-sections and wall pressure as well as from compromised endothelium post TBI induced oxidative stress.
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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