Acute spinal cord lesions on MRI

Spinal cord lesions may behave differently to brain lesions.

Neurol Clin Pract. 2017 Oct;7(5):401-403. doi: 10.1212/CPJ.0000000000000309.

Reduced diffusion in acute cervical cord multiple sclerosis lesions.

Eisele P, Alonso A, Szabo K, Gass A

Several studies have reported reduced water diffusion in acute inflammatory-demyelinating lesions in multiple sclerosis (MS) on brain MRI.1–4 Spinal cord (SC) MRI represents an important part of diagnostic examinations in MS as 80% to 90% of patients with MS show focal and/or diffuse signal abnormalities. Acute SC lesions frequently show contrast enhancement because of an increased vascular permeability. We report 2 patients with acute relapses who showed symptomatic SC lesions with reduced diffusion.

Figure: A: Hyperintense cervical cord lesion, B: hyperintense on diffusion-weighted image (yellow arrow), C: reduced apparent diffusion coefficient values (red arrow)

Over the past year I have wondered whether MRI research in MS has stagnated? The turn of phrase ‘beating a dead horse’ comes to mind (however, unpalatable that may sound). An alternative (more positive analogy) might be ‘I hate to drive this nail into the wall’, but some lateral thinking may help (wink)? Precisely what is needed is anyone’s guess; but a starting point might be to seek out ideas in the most unlikeliest corners of research publications – other scientific areas, low impact but well reviewed articles, abstracts from past conferences…

The authors here discuss a form of imaging which has been around for many years but only used in stroke. I’ve been vegetating about acute MS lesions in the spinal cord for some time now, particularly because our radiology colleagues commonly interpret these changes as a stroke and not MS activity (the authors touch on this but don’t have an answer for this). Moreover, since it’s a lottery as to whether there is a contrast enhancement of lesions or not, adding diffusion weighted imaging to our protocol may increase likelihood of assigning an individual as demonstrating active disease than previously.

What is diffusion-weighted imaging (DWI)? DWI uses the diffusion of water molecules in tissues to generate contrast in images. In tissues which demonstrate cellular swelling, and hence reduced water mobility, there is high signal demonstrated from stationary water molecules on DWI maps referred to as “restricted diffusion”.

The authors suggest that in the very early phase of MS lesion development where contrast enhancement may be absent, restriction is present (see figure above). They consider this to be a transient phenomenon, present for a few days before pseudonormalization (although I think this may be variable from lesion to lesion from personal experience). Equally, it’s uncertain whether all lesions go through this step-wise process or only a sub-set of them demonstrate this phenomenon.

About the author

Neuro Doc Gnanapavan


    • It got declined by NICE, but you can leave a comment at the bottom of their findings. Gavin has a link to this on an earlier tweet.

    • I don't read his tweets – I read the blog for thoughts theories and explanations.

      So I was surprised to learn about the NHS refusal to list from other sources and even more surprised at the lack of indignation?

    • Price negotiations I suspect in an already saturated market. Innovative, I’ll let you decide. Rituximab in that regard should have been made available ages ago.

    • Yes, I know and I agree.

      My question is – where is Barts' indignation (or a post) about it?

      I'm not referring to the tweets the above poster referred to.

    • Frankly, beyond cogitating and now comatose…I try to do my bit by driving interest in MS topics beyond the same old 😉

  • Diffusion before enhancement means swelling before vessel leakage, right?

    1. If the lesion was the result of autoimmunity, then either super-microglia of the spinal cord went mad only locally and managed to breakdown local tissue within hours, or immune cells from the blood passed through BBB without leakage, created an ovoid, local and contained havoc and then went silent.

    2. If the lesion was the result of some process involving EBV and B-cells, then some EBV-immortalised-B-cells teleported from the blood inside the spinal cord at that spot only, broke the hell loose and then went silent.

    3. If the lesion was the result of trauma, then something having to do with the anatomy of spot caused tissue injury and swelling. Then BBB opened up and immune cells went in to clear debris and investigate.

    Now, dear readers, apply Occam's razor and choose the simplest and most plausible explanation.

    • I'm afraid for such a complex disease with interactions between the the two most complex systems in the body, ie nervous system and immune system to try and apply Occam's razor and come up with a simple explanation is a fool's errand.
      I'm afraid point 3 which presumably is your favoured explanation is a non-starter.
      The good news is we're now getting much closer to understanding MS with the latest B cell data.

    • MD2, please explain to us how was this lesion created and why there is diffusion prior to BBB disruption.

    • Ok, while waiting for MD2 to answer my question (which should be fairly easy for him since "…we're now getting much closer to understanding MS with the latest B cell data"), i'll proceed with another comment.

      Is it a fool's errand to choose the explanation that best fits available data? Applying Occam's razor is the task of selecting the simplest (comparative degree) between available explanations, which by no means means that the selected answer is simple (positive degree) or simplistic.

      MD2 dismisses explanation 3 as a non-starter, but provides no justification. Everybody knows that trauma is the most common cause of spinal cord injuries and it hasn't been proved that MS is NOT traumatic. So where does that certainty comes from? Did MD2 perform an biopsy of the specific lesion and found no evidence of trauma? No, he is just speculating based on "latest B cell data", that is the "efficacy" of B-cell depleting agents.

      But don't listen to me, I'm not a doctor. Check out this:

      "If one asks what kinds of disturbance might cause local defects in the blood-brain barrier, the obvious suggestions are (a) a local rise in venous pressure,
      (b) focal inflammation and
      (c) mechanical stresses, especially longitudinal stretching of vessels."

      The cervical cord in multiple sclerosis (1977)
      D.R. Oppenheimer

      So, I'm not completely off topic talking about trauma. Forty years ago, a neuropathologist proposed longitudinal mechanical stresses.

      And now the best part: Do you notice the longitudinal reduction of diffusion coefficients in picture C above?



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