Related Experiment Video

Updated: Jun 23, 2026

Effects of Blast-induced Neurotrauma on Pressurized Rodent Middle Cerebral Arteries
08:21

Effects of Blast-induced Neurotrauma on Pressurized Rodent Middle Cerebral Arteries

Published on: April 1, 2019

7.7K

Pontine pathology mediates common symptoms of blast-induced chronic mild traumatic brain injury

James S Meabon1,2, Abigail G Schindler2,3, Daniel R Murray1

  • 1VA Northwest Mental Illness Research, Education, and Clinical Center (MIRECC), VA Puget Sound Health Care System (VA Puget Sound), Seattle, WA, USA.

Brain Communications
|March 26, 2026
PubMed

Insights

Repeated mild traumatic brain injury (mTBI) causes chronic myelin damage in the brainstem, leading to persistent post-concussive symptoms (PCS) like sleep disturbance. This pontine white matter pathology is a key driver of long-term disability after blast exposure.

Area of Science:

  • Neuroscience
  • Neuropathology
  • Traumatic Brain Injury Research

Background:

  • Persistent post-concussive symptoms (PCS) following mild traumatic brain injury (mTBI) are common, but the underlying brain mechanisms remain unclear.
  • Fragmented sleep is a prevalent PCS, yet its direct link to specific brain injury sites and cellular changes is not well understood.

Purpose of the Study:

  • To investigate if repeated blast-induced mTBI causes chronic myelin damage and microglial activation in the pontine reticular formation.
  • To determine if this pontine pathology mediates persistent PCS, including sleep disturbances, in a mouse model and in veterans.

Main Methods:

  • Utilized spatially resolved single-cell phenotyping in a mouse model of blast-mTBI.
  • Examined neuropathology and microglial nodules in veterans with a history of blast-mTBI.
  • Employed diffusion tensor imaging (DTI) to assess pontine white matter integrity.

Main Results:

  • Repeated blast-mTBI induced persistent microglial activation and myelin phagocytosis in the mouse pontine reticular formation.
  • Veterans with repeated blast-mTBI showed similar microglial changes decades post-injury.
  • DTI revealed a dose-dependent disruption of pontine myelin that correlated with sleep disturbances and PCS severity.

Conclusions:

  • Pontine white matter pathology, characterized by microglial activation and myelin loss, is a significant biomarker and mechanistic driver of chronic PCS after repeated blast-mTBI.
  • Brainstem microglia and oligodendrocytes are identified as potential therapeutic targets for mitigating long-term consequences of blast-induced TBI.
Keywords:
TBIblastmTBImilitaryoverpressure

More Related Videos

Low-intensity Blast Wave Model for Preclinical Assessment of Closed-head Mild Traumatic Brain Injury in Rodents06:09

Low-intensity Blast Wave Model for Preclinical Assessment of Closed-head Mild Traumatic Brain Injury in Rodents

Published on: November 6, 2020

3.2K
Author Spotlight: Deciphering the Long-Term Effects of Low-Level Blast Exposures in Mice06:00

Author Spotlight: Deciphering the Long-Term Effects of Low-Level Blast Exposures in Mice

Published on: May 24, 2024

1.4K

Related Concept Videos

Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
Traumatic Brain Injury l: Introduction01:28

Traumatic Brain Injury l: Introduction

DefinitionTraumatic brain injury, or TBI, is a disturbance of normal brain function induced by an external mechanical force, such as a direct blow to the head or a penetrating injury. It can affect both brain structure and function, producing a wide range of clinical outcomes. TBI is a heterogeneous condition, meaning its effects may differ based on the type, location, and severity of the injury.Basis of ClassificationTBI is classified based on severity, injury mechanism, or pathophysiology. In...
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

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...