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Systems Analysis of the Neuroinflammatory and Hemodynamic Response to Traumatic Brain Injury
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Chronic cerebrovascular dysfunction after traumatic brain injury.

Amandine Jullienne1, Andre Obenaus1,2,3, Aleksandra Ichkova4

  • 1Department of Pediatrics, Loma Linda University School of Medicine, Loma Linda, California.

Journal of Neuroscience Research
|April 28, 2016
PubMed
Summary

Traumatic brain injuries (TBI) disrupt brain blood vessels, causing long-term physiological and cognitive issues. This review details TBI-induced cerebrovascular dysfunctions and their cellular mechanisms.

Keywords:
cerebrovascular dysfunctionneurovascular dysfunctiontraumatic brain injury

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Area of Science:

  • Neuroscience
  • Vascular Biology
  • Trauma Research

Background:

  • Traumatic brain injuries (TBI) frequently result in cerebrovascular dysfunction.
  • These vascular alterations contribute to persistent physiological and cognitive impairments.
  • All cellular components of blood vessels can be affected by TBI.

Purpose of the Study:

  • To review cerebrovascular dysfunctions following TBI.
  • To discuss the mechanisms underlying these dysfunctions.
  • To highlight the roles of cerebral blood vessel cells in secondary injury.

Main Methods:

  • Literature review focusing on TBI and cerebrovascular dysfunction.
  • Analysis of cellular mechanisms involved in secondary injury cascade.
  • Synthesis of current knowledge on vascular alterations post-TBI.

Main Results:

  • TBI induces various cerebrovascular issues: altered cerebral blood flow, impaired autoregulation, subarachnoid hemorrhage, vasospasms, blood-brain barrier disruption, and edema.
  • Mechanisms involve endothelial cells, smooth muscle cells, astrocytes, pericytes, and perivascular nerves.
  • These cellular components play critical roles in the secondary injury process.

Conclusions:

  • Cerebrovascular dysfunction is a significant consequence of TBI.
  • Understanding the cellular mechanisms is crucial for developing therapeutic strategies.
  • Targeting vascular cells may mitigate secondary injury progression after TBI.