Skip to main content
NIHPA Author Manuscripts logoLink to NIHPA Author Manuscripts
. Author manuscript; available in PMC: 2015 Jan 15.
Published in final edited form as: J Neurosurg Spine. 2014 Aug;21(2):315–316.

Response

John D Heiss 1, Edward H Oldfield 2
PMCID: PMC4295116  NIHMSID: NIHMS651030  PMID: 25221803

We thank Dr. Mattei for his comments on our paper and his thoughts about syringomyelia associated with cervical spondylosis. We agree with him that syringomyelia caused by cervical spondylosis is quite rare. In fact, the MR images presented by him do not show syringomyelia, before or after surgery. Only a very small portion of the cervical portion of the spinal cord, a short segment behind the body of C-4, has a signal intensity similar to the signal intensity of the subarachnoid CSF shown in the same image. The remainder of the abnormal signal affecting the cervical segments of the spinal cord is consistent with edematous tissue or tissue damaged as a result of cervical myelopathy. Although these MRI changes may represent the edematous changes that occur with the “presyrinx” state, syringomyelia so rarely occurs with cervical degenerative disease that the changes seen cannot be considered to indicate the pending development of syringomyelia.

We agree that, in the rare instances in which it occurs, this type of syringomyelia usually occurs “after obliteration of the anterior spinal subarachnoid cisterns due to intervertebral disc pathology” and that “anterior cervical discectomy and fusion” often results in “reduction in the dimensions of the syrinx.” We do not agree with his statement, “According to the follow-up postoperative images obtained in these patients, although the surgical procedure does not seem to have affected the total anteroposterior diameter of the cervical spinal canal, a posterior shift of the spinal cord was verified.” To evaluate if the anteroposterior diameter of the cervical spinal canal was affected by surgery, we drew a dotted line indicating the anterior extent of the spinal canal before surgery on the postoperative image (Figure 1, response). This image and the measurements on Dr. Mattei’s Figure 1 clearly show that the anteroposterior diameter of the cervical spinal canal was expanded by his ACDF. The second part of his statement, “a posterior shift of the spinal cord was verified” is not confirmed in Figure 1, in which the width of the subarachnoid space dorsal to the spinal cord in the midcervical spine is unchanged from before surgery. An increase in the width of the subarachnoid space anterior to the spinal cord after surgery is consistent with removal of the C4–5 and C5–6 intervertebral discs and expansion of the spinal canal (Fig. 1, here). We agree with him that his surgical procedure likely improved flow through the anterior spinal subarachnoid space after surgery.

Dr. Mattei suggests that “flow jets in the subarachnoid spinal space” have a role in syringomyelia pathogenesis. In his Figure 3, the “flow jets” have a velocity of 10–15 cm/sec but are in the region of the vertebral arteries at the foramen magnum, suggesting that the jets may be due to arterial rather than CSF movement. In contrast to these findings at the foramen magnum, within the cervical subarachnoid space CSF movement is fairly regular (Fig. 3, Mattei). The relevance of the phase-contrast imaging shown in Fig. 3 of Dr. Mattei’s letter to his own case is uncertain, because he does not provide phase-contrast imaging studies for his patient or for other patients with syringomyelia associated with cervical spondylosis. Exuberance for the concept of flow jets must be tempered by the fact that the spinal canal is not an open channel but a partially compliant space, resulting in oscillatory CSF motion at the foramen magnum and in the cervical spinal canal during the cardiac cycle that is limited to 0.4–0.6 ml.1

Dr. Mattei’s letter is a practical reminder that syringomyelia is usually associated with obstruction of normal CSF movement at the foramen magnum or within the spinal canal. Surgical procedures that effectively restore normal CSF flow also resolve syringomyelia.24

Contributor Information

John D. Heiss, National Institute of Neurological Disorders and Stroke, Surgical Neurology Branch, National Institutes of Health, Bethesda, MD

Edward H. Oldfield, University of Virginia, Charlottesville, VA

References

  • 1.Bunck AC, Kroeger JR, Juettner A, Brentrup A, Fiedler B, Crelier GR, et al. Magnetic resonance 4D flow analysis of cerebrospinal fluid dynamics in Chiari I malformation with and without syringomyelia. Eur Radiol. 2012;22:1860–1870. doi: 10.1007/s00330-012-2457-7. [DOI] [PubMed] [Google Scholar]
  • 2.Heiss JD, Patronas N, DeVroom HL, Shawker T, Ennis R, Kammerer W, et al. Elucidating the pathophysiology of syringomyelia. J Neurosurg. 1999;91:553–562. doi: 10.3171/jns.1999.91.4.0553. [DOI] [PubMed] [Google Scholar]
  • 3.Heiss JD, Suffredini G, Smith R, DeVroom HL, Patronas NJ, Butman JA, et al. Pathophysiology of persistent syringomyelia after decompressive craniocervical surgery. Clinical article. J Neurosurg Spine. 2010;13:729–742. doi: 10.3171/2010.6.SPINE10200. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4.Oldfield EH, Muraszko K, Shawker TH, Patronas NJ. Pathophysiology of syringomyelia associated with Chiari I malformation of the cerebellar tonsils. Implications for diagnosis and treatment. J Neurosurg. 1994;80:3–15. doi: 10.3171/jns.1994.80.1.0003. [DOI] [PubMed] [Google Scholar]

RESOURCES