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Related Concept Videos

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...
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...
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...
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...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
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...

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Establishing a Mouse Contusion Spinal Cord Injury Model Based on a Minimally Invasive Technique
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Published on: September 7, 2022

Spinal cord contusion causes acute plasma membrane damage.

Crystal M Simon1, Shan Sharif, Richard P Tan

  • 1The Wallace H. Coulter Department of Biomedical Engineering at Georgia Institute of Technology and Emory University, Laboratory for Neuroengineering, and Parker H. Petit Institute for Bioengineering and Bioscience, Atlanta, Georgia, USA.

Journal of Neurotrauma
|March 6, 2009
PubMed
Summary

Spinal cord injury (SCI) causes acute plasma membrane damage, with severity correlating to impact force. This study quantifies membrane defects, revealing insights into cellular dysfunction post-injury.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Biomedical Engineering

Background:

  • Spinal cord injury (SCI) initiates a cascade of damage, leading to functional loss.
  • Acute plasma membrane damage is a critical early event following SCI.
  • Understanding the extent and nature of this damage is crucial for developing treatments.

Purpose of the Study:

  • To quantify acute plasma membrane damage after SCI.
  • To investigate the relationship between injury severity and membrane defect size.
  • To explore the pathophysiological alterations associated with membrane compromise.

Main Methods:

  • Adult male rats underwent contusion SCI with varying impact forces (100-200 kdyn).
  • Fluorescent dyes (Lucifer yellow, FITC-dextran) were used to assess membrane permeability.
  • Dye uptake in neurons and axons was quantified anatomically.

Main Results:

  • Lucifer yellow uptake positively correlated with impact force, indicating greater membrane damage with increased severity.
  • Following moderate SCI, neurons and axons absorbed more dextran molecules (3-10 kDa) up to 2-3 mm from the injury epicenter.
  • Damaged neurons showed morphological changes like pericellular blebbing.

Conclusions:

  • Acute plasma membrane damage is directly related to SCI severity.
  • The size of membrane defects can be approximated using permeability markers.
  • These findings offer targets for novel therapeutic strategies to mitigate SCI-induced damage.