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Related Concept Videos

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...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Neurogenesis and Regeneration of Nervous Tissue01:15

Neurogenesis and Regeneration of Nervous Tissue

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...

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Spinal Cord Lateral Hemisection and Asymmetric Behavioral Assessments in Adult Rats
08:46

Spinal Cord Lateral Hemisection and Asymmetric Behavioral Assessments in Adult Rats

Published on: March 24, 2020

Spinal neuronal dysfunction after stroke.

Michèle Hubli1, Marc Bolliger, Esther Limacher

  • 1Spinal Cord Injury Center, Balgrist University Hospital, University of Zurich, Forchstrasse 340, 8008 Zurich, Switzerland. mhubli@paralab.balgrist.ch

Experimental Neurology
|January 10, 2012
PubMed
Summary
This summary is machine-generated.

Central nervous system lesions like stroke cause spinal neuronal reorganization. Stroke patients show altered spinal reflexes, but unlike spinal cord injury, leg muscle activity doesn't exhaust during locomotion.

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Determining the Functional Status of the Corticospinal Tract Within One Week of Stroke
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Determining the Functional Status of the Corticospinal Tract Within One Week of Stroke
09:10

Determining the Functional Status of the Corticospinal Tract Within One Week of Stroke

Published on: February 22, 2020

Area of Science:

  • Neuroscience
  • Rehabilitation Medicine
  • Neurology

Background:

  • Central nervous system (CNS) lesions, including stroke and spinal cord injury (SCI), induce significant neuronal reorganization.
  • Chronic severe SCI is characterized by spinal neuronal dysfunction, evidenced by muscle electromyographic (EMG) activity exhaustion during locomotion and a shift in spinal reflex (SR) dominance.

Purpose of the Study:

  • To investigate spinal neuronal function changes following severe stroke, specifically unilateral supraspinal input deprivation.
  • To compare spinal neuronal reorganization in stroke survivors with that observed in SCI patients.

Main Methods:

  • Assessed locomotor and spinal reflex (SR) behavior in 30 hemiparetic stroke subjects.
  • Evoked SR responses in the tibialis anterior muscle via tibial nerve stimulation.
  • Recorded leg muscle EMG activity during assisted locomotion in nine subjects.

Main Results:

  • Severely affected chronic stroke subjects (>12 months post-incidence) exhibited a prominent late SR component in the affected leg, contrasting with an early component in the unaffected leg.
  • The late SR component correlated significantly with muscle paresis (rho=0.714) and walking ability (rho=0.493).
  • Unlike SCI patients, no EMG activity exhaustion was observed in affected leg muscles during prolonged assisted locomotion.

Conclusions:

  • Spinal neuronal circuits undergo functional changes post-stroke, sharing similarities and differences with SCI.
  • These distinct spinal adaptations suggest the need for tailored rehabilitative strategies for stroke recovery.