Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

52
Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
52
Neurogenesis and Regeneration of Nervous Tissue01:15

Neurogenesis and Regeneration of Nervous Tissue

2.1K
In the CNS, neurogenesis, the birth of new neurons from stem cells, is limited to the hippocampus in adults. In other regions of the brain and spinal cord, neurogenesis is almost non-existent due to inhibitory influences from neuroglia, especially oligodendrocytes, and the absence of growth-stimulating cues. The myelin produced by oligodendrocytes in the CNS inhibits neuronal regeneration. Furthermore, astrocytes proliferate rapidly after neuronal damage, forming scar tissue that physically...
2.1K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Brain age gap as a diffusion MRI-based marker of traumatic brain injury-related brain changes and associated outcomes.

Brain communications·2026
Same author

PIGMENT: A deep learning framework for Porcine Immunohistochemistry seGMENTation.

bioRxiv : the preprint server for biology·2026
Same author

Features predicting data exclusion in imaging studies of Alzheimer's disease.

Alzheimer's & dementia (Amsterdam, Netherlands)·2026
Same author

Widespread siderophore production among Symbiodiniaceae-associated bacteria.

FEMS microbiology letters·2026
Same author

Tau topography subtypes account for clinical heterogeneity and longitudinal trajectories in early-onset Alzheimer's disease.

Brain communications·2026
Same author

Gray Matter Morphological Networks are Associated with Neurobiological Features, Cognitive Status and Clinical Recovery in Traumatic Brain Injury.

medRxiv : the preprint server for health sciences·2026

Related Experiment Video

Updated: May 1, 2026

Development of an Uncomplicated Mild Traumatic Brain Injury Model Modified by Weight-Drop Method and Evidenced by Magnetic Resonance Imaging
08:27

Development of an Uncomplicated Mild Traumatic Brain Injury Model Modified by Weight-Drop Method and Evidenced by Magnetic Resonance Imaging

Published on: April 11, 2025

1.0K

Longitudinal white matter changes after traumatic axonal injury.

Alison M Perez1, Justin Adler, Nimay Kulkarni

  • 11 Center for BrainHealth at the University of Texas at Dallas , Dallas, Texas.

Journal of Neurotrauma
|April 18, 2014
PubMed
Summary

Diffusion tensor imaging (DTI) reveals white matter (WM) changes after traumatic axonal injury (TAI). Acutely, axial and radial diffusivity increase, while chronic stages show reduced fractional anisotropy and axial diffusivity.

Keywords:
axonal injurybiomarkersbrain edemadiffusion tensor imagingtraumatic brain injury

More Related Videos

A Versatile Murine Model of Subcortical White Matter Stroke for the Study of Axonal Degeneration and White Matter Neurobiology
08:36

A Versatile Murine Model of Subcortical White Matter Stroke for the Study of Axonal Degeneration and White Matter Neurobiology

Published on: March 17, 2016

7.7K
Advanced Diffusion Imaging in The Hippocampus of Rats with Mild Traumatic Brain Injury
10:33

Advanced Diffusion Imaging in The Hippocampus of Rats with Mild Traumatic Brain Injury

Published on: August 14, 2019

8.2K

Related Experiment Videos

Last Updated: May 1, 2026

Development of an Uncomplicated Mild Traumatic Brain Injury Model Modified by Weight-Drop Method and Evidenced by Magnetic Resonance Imaging
08:27

Development of an Uncomplicated Mild Traumatic Brain Injury Model Modified by Weight-Drop Method and Evidenced by Magnetic Resonance Imaging

Published on: April 11, 2025

1.0K
A Versatile Murine Model of Subcortical White Matter Stroke for the Study of Axonal Degeneration and White Matter Neurobiology
08:36

A Versatile Murine Model of Subcortical White Matter Stroke for the Study of Axonal Degeneration and White Matter Neurobiology

Published on: March 17, 2016

7.7K
Advanced Diffusion Imaging in The Hippocampus of Rats with Mild Traumatic Brain Injury
10:33

Advanced Diffusion Imaging in The Hippocampus of Rats with Mild Traumatic Brain Injury

Published on: August 14, 2019

8.2K

Area of Science:

  • Neuroimaging
  • Traumatic Brain Injury Research
  • White Matter Integrity

Background:

  • Diffusion tensor imaging (DTI) is valuable for assessing chronic white matter (WM) damage post-traumatic axonal injury (TAI).
  • Understanding WM compromise evolution from acute to chronic TAI stages requires further investigation.

Purpose of the Study:

  • To longitudinally examine WM integrity changes in patients with TAI from acute to chronic stages using DTI.
  • To correlate DTI metrics with injury severity in the acute phase of TAI.

Main Methods:

  • Longitudinal DTI scans were acquired from 13 TAI patients (average 1 day and 7 months post-injury) and 10 healthy controls.
  • Whole-brain and voxel-based analyses of DTI metrics (FA, MD, AD, RD) were performed using tract-based spatial statistics.

Main Results:

  • Acutely, increased axial diffusivity (AD) and radial diffusivity (RD) were observed, with RD correlating positively with injury severity.
  • Longitudinal analysis revealed significant reductions in fractional anisotropy (FA) and AD (p<0.01) over seven months, while RD remained unchanged.

Conclusions:

  • WM microstructural changes occur dynamically from acute to chronic stages following TAI.
  • The observed longitudinal changes in FA and AD suggest ongoing neurodegenerative processes or resolution of acute edema after TAI.