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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...
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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...
Neurogenesis and Regeneration of Nervous Tissue01:15

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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...
Hemorrhagic Stroke ll: Pathophysiology01:29

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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...

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A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation
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Published on: June 10, 2020

Trauma with neurologic sequelae.

Brett S Tennent-Brown1

  • 1Department of Clinical Studies, University of Pennsylvania School of Veterinary Medicine, New Bolton Center, Kennett Square, PA 19348, USA. tennentb@vet.upenn.edu <tennentb@vet.upenn.edu>

The Veterinary Clinics of North America. Equine Practice
|March 24, 2007
PubMed
Summary

Spinal cord injury (SCI) in horses results from trauma, leading to secondary events like inflammation and ischemia that hinder recovery. Optimizing oxygen delivery and exploring human-tested therapies are crucial for equine SCI management.

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Area of Science:

  • Equine veterinary medicine
  • Neurology
  • Trauma research

Background:

  • Spinal cord injury (SCI) in horses is frequently caused by accidents such as rearing and falling, collisions, or slips.
  • The pathophysiology involves a primary mechanical trauma followed by secondary injury cascades, including ischemia, oxidative stress, excitotoxicity, ion dysregulation, and inflammation.
  • The severity of these secondary events significantly impacts the potential for neurological function restoration.

Purpose of the Study:

  • To outline the pathophysiology of equine spinal cord injury.
  • To describe clinical signs based on lesion location and damage severity.
  • To discuss acute management strategies and potential therapeutic interventions from human medicine applicable to horses.

Main Methods:

  • Review of the pathophysiology of spinal cord injury in horses.
  • Correlation of clinical signs with lesion location and tissue damage.
  • Discussion of current and potential therapeutic strategies.

Main Results:

  • Secondary injury events (ischemia, inflammation, etc.) are critical determinants of neurological outcome.
  • Clinical signs vary with the site and extent of spinal cord damage.
  • Acute management should prioritize oxygen delivery to the injured spinal cord.

Conclusions:

  • Understanding the secondary injury cascade is vital for managing equine SCI.
  • Optimizing oxygenation is a key component of acute care.
  • Investigating therapies successful in human SCI may offer new treatment avenues for horses.