Guest Post: Is spinal cord volume an independent parameter in MS?


In our recent study, we found significant correlations between the volumes of several brain structures and the spinal cord (SC) in patients with mild disability. However, in patients with moderate to severe disability this correlation was significantly reduced. 

This suggests independent progression of brain and SC volume loss during the transition to the secondary progressive disease phase. Interestingly, in the mild-to-moderate disability group SCV was the only parameter that discriminated between patients with EDSS 2-2.5 and 3-3.5.

Therefore, this gap between brain and SC volume loss could be a hallmark of secondary progression onset in MS. Spinal cord volume could help to identify patients with mild disability who are at risk of disability progression. This hypothesis has to be verified on our longitudinal data.

Could we reduce the clinical-radiological paradox with spinal cord imaging? Or could SC imaging even contribute to a new definition of secondary progression in MS? We believe so. SC pathology has been the focus of research for decades, but nowadays it is feasible to add MRI of the spinal cord to MRI monitoring protocols, because many MRI scanners allow us to investigate SC in the same session as brain imaging. Our preliminary results have to be verified and investigated further longitudinally to understand the individual dynamic in brain and SC volume loss and its relationship with lesion pathology and disability. 

Progression of SC and brain volume loss may be partially independent. SC volume loss may indicate the secondary progressive course, and also be present earlier in the course. The spinal cord pathology is an important piece of the mosaic of MS pathology and an important part of MR monitoring of disease activity. It should be monitored carefully and regularly in MS patients from disease onset. 

Fig 1: Differences in percentage volume loss of several brain structures and spinal
cord volume in the three EDSS groups.
Fig. 2 Spinal
cord volume in
in the three EDSS groups.

Manuela Vaněčková, MD, Ph.D.
MR unit, Departement of Radiology, First Faculty of
Medicine, Charles University and General University Hospital in Prague, Katerinska 30, 128 08 Prague, Czech
E-MAIL:    manuela.vaneckova [at], man.van [at], Manuela.Vaneckova[at],
The lead author
completed her PhD in Neuroscience in 2003. From 2009 she was Associate
Professor of Radiology in Charles University. In 2014 she became Professor of
Radiology in Charles University. Her specialization is Imaging, mainly MRI and
Neuroradiology. She has published more than 180 papers, and 3 monographs on
Neuroradiology, MRI and Multiple sclerosis. So far she has been associated with
13 medical research grants. Her main topics are brain and spinal cord
volumetry, MRI monitoring in daily clinical practice in MS, MRI differential
diagnosis of MS, safety monitoring (PML), neurodegenerative disease, pituitary
MRI and prenatal brain MRI.

About the author

Rebecca Aldam


  • Hasn't this already been known..?
    What is point of papers that don't break new ground or suggest
    new treatments/therapies..?

    "An increase in the size of a cervical cord lesion and the development of multiple new thoracic spinal cord lesions despite rituximab therapy represented the most likely imaging correlate of the progressive neurological deficit. Notably, nearly complete stabilization of brain white matter lesion burden by anti‐CD20 therapy was repeatedly shown on MRI and sustained for nearly a decade.5-7 As expected for a patient with chronic MS, progressive atrophy of total brain and spinal cord volume were also present. These observations are consistent with converging evidence that increasing cortical pathology underlies progressive MS and that these changes are largely independent of underlying white matter lesions but rather might be associated with adjacent overlying meningeal lymphoid aggregates containing B cells and plasma cells.8-13 Could the development of SPMS been the consequence of ectopic lymphoid aggregates in the meninges that are resistant to anti‐CD20 therapy?"

    • "Could the development of SPMS been the consequence of ectopic lymphoid aggregates in the meninges that are resistant to anti‐CD20 therapy"

      Could be, could be. BTK inhibitors now in clinical trial (though looking at RRMS so far) may be the answer to this. A short course could remove plasma cells from the brain as they've been effective in cerebral B cell lymphoma.

    • You argue, that we just state the obvious and that we only contributed more data to already well studied phenomenon. Please note that this dataset is not from a clinical trial. Do you have ability to use spinal cord atrophy in your practice? We have shown, that we are working on implementing spinal cord volumetry in daily clinical practice, on a clinical scanner, on routinely ordered scans, and that is possible. We know that brain pathology does not fully explain disability and that spinal cord is important.
      A question of spinal cord pathology as a biomarker is not clear yet. Some investigators (Kuusisto, Rocca, Rashid, Bieniek) reported no difference in spinal cord volume in healthy controls versus RRMS or CIS, other reported increase in SC volume in RRMS or CIS patients (Klein, Rocca) and some have shown decreased volume in CIS and RRMS patients compared to healthy controls (Liu, Daams, Zivadinov, Brex, Biberacher). Reports on SC atrophy in progressive MS forms have been consistent finding (Rocca, Furby, Lin, Laule, Bieniek, Lucas). The reason for a stronger correlation in PPMS and SPMS is probably the lack of focal inflammation and it further supports the believe, that progression in SPMS is largely driven by the spinal cord involvement.
      We therefore see SC volume as an important biomarker and would like to see it used in clinical practice. Current MR scanners allow examination of brain and cervical cord in one session, which further helps implementation of this biomarker. Healthy control data is needed for obvious reasons.



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