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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...
Degenerative Disc Disease ll: Pathophysiology01:23

Degenerative Disc Disease ll: Pathophysiology

The symptoms of degenerative disc disease arise from a combination of mechanical compression, vascular compromise, and biochemical inflammation, which together disrupt nerve function and produce pain.Mechanical CompressionDisc degeneration reduces height and elasticity, predisposing to herniation of the nucleus pulposus, a major cause of radicular pain. Herniations may be protrusion (bulging with intact annulus), extrusion (nucleus extends beyond disc but remains connected), or sequestration...
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...
Herniated Intervertebral Disc l: Introduction01:29

Herniated Intervertebral Disc l: Introduction

Intervertebral disc herniation refers to the displacement of the nucleus pulposus (the gel-like inner core of the disc) through a tear or weakened area in the annulus fibrosus (the outer fibrous ring). The displaced disc material extends beyond the normal boundaries of the disc space and may compress or irritate nearby spinal nerve roots or, less commonly, the spinal cord.Etiology and Risk FactorsHerniation commonly results from degeneration, in which aging reduces disc hydration and...
Myasthenia Gravis ll: Pathophysiology01:22

Myasthenia Gravis ll: Pathophysiology

The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...

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Related Experiment Video

Updated: May 18, 2026

Modeling Charcot-Marie-Tooth Disease In Vitro by Transfecting Mouse Primary Motoneurons
07:43

Modeling Charcot-Marie-Tooth Disease In Vitro by Transfecting Mouse Primary Motoneurons

Published on: January 7, 2019

Pathophysiology of primary spinal syringomyelia.

John D Heiss1, Kendall Snyder, Matthew M Peterson

  • 1National Institute of Neurological Disorders and Stroke, Surgical Neurology Branch, National Institute of Health, Bethesda, Maryland, USA. heissj@ninds.nih.gov

Journal of Neurosurgery. Spine
|September 11, 2012
PubMed
Summary

Spinal lesions increase pressure waves in the cerebrospinal fluid (CSF) space, leading to syrinx formation and progression in syringomyelia. This study confirms a common mechanism for syrinx development in spinal conditions.

Related Experiment Videos

Last Updated: May 18, 2026

Modeling Charcot-Marie-Tooth Disease In Vitro by Transfecting Mouse Primary Motoneurons
07:43

Modeling Charcot-Marie-Tooth Disease In Vitro by Transfecting Mouse Primary Motoneurons

Published on: January 7, 2019

Area of Science:

  • Neurology
  • Neurosurgery
  • Biomedical Engineering

Background:

  • Syringomyelia pathogenesis, particularly with spinal lesions, remains unclear.
  • A proposed mechanism involves reduced spinal subarachnoid space (SAS) compliance leading to exaggerated CSF pressure waves.
  • These waves may drive CSF into the spinal cord, forming and progressing syrinxes.

Purpose of the Study:

  • To investigate the pathophysiology of syringomyelia in patients with spinal lesions obstructing the SAS.
  • To test the hypothesis that spinal SAS obstruction causes increased CSF pulse pressure, leading to syrinx formation.

Main Methods:

  • Prospective study of 36 adult patients with spinal SAS obstruction.
  • Pre- and post-operative assessments including clinical exams, MRI, CT myelography, and CSF pressure measurements.
  • Comparison with 18 healthy controls.

Main Results:

  • Syringomyelia patients exhibited increased cervical subarachnoid pulse pressure compared to controls.
  • Reduced pressure transmission below the obstruction and decreased spinal CSF compliance were observed.
  • Intraoperative ultrasonography showed pulse pressure waves compressing the spinal cord superior to the obstruction.

Conclusions:

  • Findings support the theory that spinal SAS obstruction increases pulse pressure, causing syrinx formation and progression.
  • A common mechanism for syrinx development is indicated, similar to Chiari Type I malformation.
  • This research elucidates the role of CSF dynamics in syringomyelia pathogenesis.