Sunday, 13 March 2016

Diagnosis of MS

Diagnosis of MS means the need to identifty lesions in time and space.

So a relapse affecting a different region of the CNS. 
This can be seen with MRI

This can be seen by histology too

Are all lesions round, ovioid?

The uneven shapped lesion is probably the youngest lesion likely to be following the path of a blood vessels, but not  round like the older lesions and the light blue ones are probably repair and these are known as shadow plaques. 
So lesions in different locations (lesions in space) and as the  lesions are different ages  (lesions in time)   

5 comments:

  1. Bit off topic. Is it possible that the initial insult for all MS types is against Na channels (or cause Na channel dysfunction) throughout the CNS and that B & T cells can only access the WM (closer to blood vessels) and not GM thereby accounting for the inflammatory WM lesions vs GM atrophy, which seems to be B or T-cell independent?

    One study has shown that Na channel dysfunction can activate microglia & macrophages causing further neurodegeneration/axonal damage from the start of the MS process. Maybe this is why majority of MS patients transition to progressive MS regardless of any DMD because they mainly effect only B and T-cells but not Na channels/microglia or macrophages? Maybe RRMS is just a secondary autoimmune reaction in the WM to something that is already going on in reaction to axon death through Na channel dysfunction & microglial/macrophage activation? Maybe progressive MS has more Na channel damage and microglial/macrocyte activation with no or minimal secondary autoimmune reaction in the WM by B and T-cells?

    If this was the case, wouldn't it be more prudent in all MS to try to block the original insult resulting in Na channel dysfunction (EBV, low Vitamin D, etc.) or protect Na channels (anti-seizure medications) or stopping/dampening microglia and macrophage activation (MAB?)? This way you would stop disease progression in all MS types (WM & GM) and the secondary autoimmune reaction that is RRMS (mainly WM inflammatory activity)?

    ReplyDelete
  2. According to these guys: http://www.ajnr.org/content/21/6/1039.full.pdf

    "Therefore, the mere presence of (small) veins in MS lesions may not be more than coincidence; only the correspondence of ovoid lesions along a vein is typical of MS."

    You say that MS lesions form out of white cells that exit bloodstream and exercise autoimmune attack. However, in ADEM, the closest cousin of MS, an inflammatory demyelinating disease regarded as autoimmune with a viral trigger (like a twin brother of MS according to this blog!) presents with lesions of completely different morphology and topography:

    http://www.slideshare.net/afmcite2002/ms-vs-adem-basic-differences-and-approach

    In ADEM, lesions are not typically periventricular, are not ovoid, vary considerably in size and shape and don't have clear borders. These and other differences mentioned in the slideshow above are almost proof that ADEM and MS have a totally different pathology. Therefore damage in MS cannot be autoimmune in origin. Therefore white cells in MS lesions do not cause the damage.

    ReplyDelete
    Replies
    1. "Therefore damage in MS cannot be autoimmune in origin. Therefore white cells in MS lesions do not cause the damage."

      That's quite a logic leap there, VV. Guess we'll all have to get new jobs shelf-stacking.

      Delete
    2. Some more differences:
      Inflammation is diffuse in ADEM (random), but focal in MS (not random). ADEM is monophasic, but MS is relapsing.

      MD2, according to you MS is an autoimmune demyelinating disease like ADEM, but shares almost nothing with it. I may be absolute, but you are self-contradictory.

      Delete
    3. Whatever, VV, I've got an interview at Tesco's tomorrow.

      Delete

Please note that all comments are moderated and any personal or marketing-related submissions will not be shown.