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Related Concept Videos

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...
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...
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...
Spinal Cord Injury ll: Pathophysiology01:14

Spinal Cord Injury ll: Pathophysiology

Spinal cord injury progresses through two interconnected phases: primary injury and secondary injury.Primary InjuryPrimary injury happens at the moment of trauma and involves immediate mechanical damage to the spinal cord.Compression happens when broken vertebrae, herniated discs, or accumulating blood (such as a hematoma) press directly against the spinal cord, distorting its normal shape and function. In cases of contusion, the cord is bruised by a blunt force (like penetrating injuries or...
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...
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...

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Related Experiment Video

Updated: May 20, 2026

A Novel In Vitro Model of Blast Traumatic Brain Injury
08:59

A Novel In Vitro Model of Blast Traumatic Brain Injury

Published on: December 21, 2018

Brain injury risk from primary blast.

Karin A Rafaels1, Cameron R Dale Bass, Matthew B Panzer

  • 1Army Research Laboratory, 328 Hopkins Rd, ATTN RDRL-SLB-W, Aberdeen Proving Ground, MD 21005, USA. kar3k@virginia.edu

The Journal of Trauma and Acute Care Surgery
|July 28, 2012
PubMed
Summary

Understanding blast exposure is crucial for military service members. This study determined blast intensity and duration thresholds for causing mild to severe traumatic brain injuries in ferrets, aiding future protective measures.

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Evaluating Primary Blast Effects In Vitro
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Evaluating Primary Blast Effects In Vitro

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

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Last Updated: May 20, 2026

A Novel In Vitro Model of Blast Traumatic Brain Injury
08:59

A Novel In Vitro Model of Blast Traumatic Brain Injury

Published on: December 21, 2018

Evaluating Primary Blast Effects In Vitro
10:51

Evaluating Primary Blast Effects In Vitro

Published on: September 18, 2017

Low-intensity Blast Wave Model for Preclinical Assessment of Closed-head Mild Traumatic Brain Injury in Rodents
06:09

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

Published on: November 6, 2020

Area of Science:

  • Neuroscience
  • Trauma Research
  • Biomedical Engineering

Background:

  • Military personnel frequently experience explosive events, leading to traumatic brain injuries (TBIs).
  • Limited data exists on the specific blast intensities and durations required to cause TBI.
  • Understanding these parameters is vital for developing effective protective strategies.

Purpose of the Study:

  • To establish primary blast brain injury risk assessments in a gyrencephalic animal model.
  • To determine the relationship between blast intensity/duration and the likelihood of brain injury.
  • To provide data for designing protective gear and evaluating TBI risks.

Main Methods:

  • Anesthetized ferrets were exposed to controlled shock tube blasts of varying intensities focused on the head.
  • Physiological responses, necropsy, and histological examinations were conducted to assess injury.
  • Logistic regression analysis was used to derive injury risk functions for apnea, hemorrhage, and fatality.

Main Results:

  • Increasing blast severity correlated with increased post-blast apnea.
  • Hemorrhages, particularly near the brain stem, were observed at higher blast intensities.
  • Risk functions for apnea, bleeding, and fatality were established based on peak overpressure and positive-phase duration.

Conclusions:

  • This study provides the first risk assessments for mild and moderate/severe primary blast brain injuries in a gyrencephalic model.
  • Mild to moderate brain injury thresholds may be comparable to or lower than those causing pulmonary injury.
  • The derived risk functions offer realistic injury probabilities to guide future TBI research and protective equipment development.