Related Experiment Video
Updated: Jul 15, 2026

Isolating Central Nervous System Tissues and Associated Meninges for the Downstream Analysis of Immune cells
Published on: May 19, 2020
Pathogenetic role of myelitis for syringomyelia
Sabrina Ravaglia1, Enver I Bogdanov, Anna Pichiecchio
1Institute of Neurology C. Mondino, University of Pavia, Pavia, Italy. sabrina.ravaglia@mondino.it <sabrina.ravaglia@mondino.it>
Inflammatory spinal cord lesions can cause syringomyelia through mechanisms other than cerebrospinal fluid (CSF) flow obstruction. Intrinsic spinal cord factors, like edema, play a significant role in syrinx development, especially during acute myelitis.
Area of Science:
- Neuroscience
- Neurology
- Pathology
Background:
- Syringomyelia is typically linked to cerebrospinal fluid (CSF) flow obstruction.
- However, syringomyelia can occur without evident CSF obstruction, particularly with inflammatory spinal cord lesions (myelitis).
- Vasogenic edema and interstitial fluid accumulation are hypothesized as alternative mechanisms.
Observation:
- A prospective case series examined transient syringomyelia in patients with non-infectious myelitis (sarcoidosis, post-infectious, Devic's, MS).
- Syringes developed during acute myelitis, resolved with steroids, involved the central canal, and localized to the affected spinal segment.
- CSF flow obstruction was noted in only one patient; others lacked anatomical predispositions.
Findings:
- Syringomyelia associated with myelitis often lacks structural CSF flow block.
- Intrinsic medullary factors, including blood-spinal cord barrier breakdown and impaired fluid drainage, are implicated.
- Inflammation-triggered intramedullary processes are key drivers of syrinx formation.
Implications:
- This challenges the sole reliance on CSF obstruction models for syringomyelia.
- Highlights the importance of intrinsic spinal cord mechanisms in inflammatory conditions.
- Suggests new therapeutic targets focusing on spinal cord inflammation and edema management.
Related Concept Videos
Poliomyelitis
Encephalitis ll: Pathophysiology
Bacterial Meningitis II: Pathophysiology
Myasthenia Gravis ll: Pathophysiology
Myocarditis I: Introduction
Viral Meningitis
