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Pathophysiology of persistent syringomyelia after decompressive craniocervical surgery. Clinical article.
J Neurosurg Spine. 2010 Dec; 13(6):729-42.JN

Abstract

OBJECT

Craniocervical decompression for Chiari malformation Type I (CM-I) and syringomyelia has been reported to fail in 10%-40% of patients. The present prospective clinical study was designed to test the hypothesis that in cases in which syringomyelia persists after surgery, craniocervical decompression relieves neither the physiological block at the foramen magnum nor the mechanism of syringomyelia progression.

METHODS

The authors prospectively evaluated and treated 16 patients with CM-I who had persistent syringomyelia despite previous craniocervical decompression. Testing before surgery included the following: 1) clinical examination; 2) evaluation of the anatomy using T1-weighted MR imaging; 3) assessment of the syrinx and CSF velocity and flow using cine phase-contrast MR imaging; and 4) appraisal of the lumbar and cervical subarachnoid pressures at rest, during a Valsalva maneuver, during jugular compression, and following the removal of CSF (CSF compliance measurement). During surgery, ultrasonography was performed to observe the motion of the cerebellar tonsils and syrinx walls; pressure measurements were obtained from the intracranial and lumbar intrathecal spaces. The surgical procedure involved enlarging the previous craniectomy and performing an expansile duraplasty with autologous pericranium. Three to 6 months after surgery, clinical examination, MR imaging, and CSF pressure recordings were repeated. Clinical examination and MR imaging studies were then repeated annually.

RESULTS

Before reexploration, patients had a decreased size of the CSF pathways and a partial blockage in CSF transmission at the foramen magnum. Cervical subarachnoid pressure and pulse pressure were abnormally elevated. During surgery, ultrasonographic imaging demonstrated active pulsation of the cerebellar tonsils, with the tonsils descending during cardiac systole and concomitant narrowing of the upper pole of the syrinx. Three months after reoperation, patency of the CSF pathways was restored and pressure transmission was improved. The flow of syrinx fluid and the diameter of the syrinx decreased after surgery in 15 of 16 patients.

CONCLUSIONS

Persistent blockage of the CSF pathways at the foramen magnum resulted in increased pulsation of the cerebellar tonsils, which acted on a partially enclosed cervical subarachnoid space to create elevated cervical CSF pressure waves, which in turn affected the external surface of the spinal cord to force CSF into the spinal cord through the Virchow-Robin spaces and to propel the syrinx fluid caudally, leading to syrinx progression. A surgical procedure that reestablished the CSF pathways at the foramen magnum reversed this pathophysiological mechanism and resolved syringomyelia. Elucidating the pathophysiology of persistent syringomyelia has implications for its primary and secondary treatment.

Authors+Show Affiliations

Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-1414, USA. heissj@ninds.nih.govNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Intramural

Language

eng

PubMed ID

21121751

Citation

Heiss, John D., et al. "Pathophysiology of Persistent Syringomyelia After Decompressive Craniocervical Surgery. Clinical Article." Journal of Neurosurgery. Spine, vol. 13, no. 6, 2010, pp. 729-42.
Heiss JD, Suffredini G, Smith R, et al. Pathophysiology of persistent syringomyelia after decompressive craniocervical surgery. Clinical article. J Neurosurg Spine. 2010;13(6):729-42.
Heiss, J. D., Suffredini, G., Smith, R., DeVroom, H. L., Patronas, N. J., Butman, J. A., Thomas, F., & Oldfield, E. H. (2010). Pathophysiology of persistent syringomyelia after decompressive craniocervical surgery. Clinical article. Journal of Neurosurgery. Spine, 13(6), 729-42. https://doi.org/10.3171/2010.6.SPINE10200
Heiss JD, et al. Pathophysiology of Persistent Syringomyelia After Decompressive Craniocervical Surgery. Clinical Article. J Neurosurg Spine. 2010;13(6):729-42. PubMed PMID: 21121751.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Pathophysiology of persistent syringomyelia after decompressive craniocervical surgery. Clinical article. AU - Heiss,John D, AU - Suffredini,Giancarlo, AU - Smith,René, AU - DeVroom,Hetty L, AU - Patronas,Nicholas J, AU - Butman,John A, AU - Thomas,Francine, AU - Oldfield,Edward H, PY - 2010/12/3/entrez PY - 2010/12/3/pubmed PY - 2011/1/12/medline SP - 729 EP - 42 JF - Journal of neurosurgery. Spine JO - J Neurosurg Spine VL - 13 IS - 6 N2 - OBJECT: Craniocervical decompression for Chiari malformation Type I (CM-I) and syringomyelia has been reported to fail in 10%-40% of patients. The present prospective clinical study was designed to test the hypothesis that in cases in which syringomyelia persists after surgery, craniocervical decompression relieves neither the physiological block at the foramen magnum nor the mechanism of syringomyelia progression. METHODS: The authors prospectively evaluated and treated 16 patients with CM-I who had persistent syringomyelia despite previous craniocervical decompression. Testing before surgery included the following: 1) clinical examination; 2) evaluation of the anatomy using T1-weighted MR imaging; 3) assessment of the syrinx and CSF velocity and flow using cine phase-contrast MR imaging; and 4) appraisal of the lumbar and cervical subarachnoid pressures at rest, during a Valsalva maneuver, during jugular compression, and following the removal of CSF (CSF compliance measurement). During surgery, ultrasonography was performed to observe the motion of the cerebellar tonsils and syrinx walls; pressure measurements were obtained from the intracranial and lumbar intrathecal spaces. The surgical procedure involved enlarging the previous craniectomy and performing an expansile duraplasty with autologous pericranium. Three to 6 months after surgery, clinical examination, MR imaging, and CSF pressure recordings were repeated. Clinical examination and MR imaging studies were then repeated annually. RESULTS: Before reexploration, patients had a decreased size of the CSF pathways and a partial blockage in CSF transmission at the foramen magnum. Cervical subarachnoid pressure and pulse pressure were abnormally elevated. During surgery, ultrasonographic imaging demonstrated active pulsation of the cerebellar tonsils, with the tonsils descending during cardiac systole and concomitant narrowing of the upper pole of the syrinx. Three months after reoperation, patency of the CSF pathways was restored and pressure transmission was improved. The flow of syrinx fluid and the diameter of the syrinx decreased after surgery in 15 of 16 patients. CONCLUSIONS: Persistent blockage of the CSF pathways at the foramen magnum resulted in increased pulsation of the cerebellar tonsils, which acted on a partially enclosed cervical subarachnoid space to create elevated cervical CSF pressure waves, which in turn affected the external surface of the spinal cord to force CSF into the spinal cord through the Virchow-Robin spaces and to propel the syrinx fluid caudally, leading to syrinx progression. A surgical procedure that reestablished the CSF pathways at the foramen magnum reversed this pathophysiological mechanism and resolved syringomyelia. Elucidating the pathophysiology of persistent syringomyelia has implications for its primary and secondary treatment. SN - 1547-5646 UR - https://www.unboundmedicine.com/medline/citation/21121751/Pathophysiology_of_persistent_syringomyelia_after_decompressive_craniocervical_surgery__Clinical_article_ L2 - https://thejns.org/doi/10.3171/2010.6.SPINE10200 DB - PRIME DP - Unbound Medicine ER -