MS Pathology: Dawson’s fingers

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For those of you have been confused about comments in relation to Dawson’s fingers the following is a brief account of this anatomical feature, that is considered unique to MS.

Dawson’s Fingers” refers to MS lesions around the veins that radiate out from the ventricles (fluid filled spaces in the centre of the brain). “Dawson’s Fingers” are supposed  to be the result of inflammation or mechanical damage by blood pressure along the space around veins; these are called Virchow-Robin spaces. 

Dawson’s Fingers appearing on MRI; please note how they appear as perpendicular fingers to the ventricle (black slit).
Dawson’s fingers spread along, and from, large periventricular collecting veins, and are attributed to so called perivenular inflammation. 

A cartoon demonstrating the perivenular inflammatory infiltrates that cause MS lesion formation and enlarged perivenular spaces (Virchow-Robin spaces) in MS. The prominent perivenular spaces can be with (bottom vessel) or without (top vessel) lesion association. Image from AJNR.
Who was Dawson? He was a Scottish pathologist who described these lesions. 


Please note Virchow-Robin spaces, are not necessarliy synonymous with perivenular spaces; the term refers to enlarged perivascular spaces that surround blood vessels for a short distance as they enter the brain. The term is used for spaces around both arteries and veins. 


“Why are Dawson’s fingers important? Firstly, they are relatively easy to see and are not found in other diseases. Their location suggests that the cerebrospinal fluid from the ventricles may have something to do with their formation. However, perivenular inflammation or inflammatory cuffs occurs in locations away from the ventricles with no connection with CSF pathways; for example in the deep white matter of the brain and even in the retina of the eyes. The latter observation is very important as their is no myelin in the rentina. This latter observation is why I personally don’t think myelin per se is necessarily the main target of immunological attack in MS.”

“The problem I have with cherry picking Dawson’s fingers as the pathological feature of MS that supports the concept of venous flow problems in MS is that it does not explain the deep perivenular lesions. Nor does it explain why Dawson’s fingers are not the same as the venous lesions we seen in conditions associated with venous stasis; i.e. the lesions that occur from a thrombosis or clot in the draining veins of the brain.”

“When we talk about a possible cause of MS it has to explain everything; we can’t cherry pick or select some aspects of the disease that fit our theory and discard other aspects that don’t.”

“My world of MS is data and Bradford-Hill’s theory of causation. In my opinion at the moment, the only facts that partially conform to Bradford-Hill’s criteria and can explain some of the epidemiological observations is an infectious disease. This opinion may change with time, but to change it will require hard reproducible scientific data.”

About the author

Prof G

Professor of Neurology, Barts & The London. MS & Preventive Neurology thinker, blogger, runner, vegetable gardener, husband, father, cook and wine & food lover.

10 comments

  • This would seem to suggest that MS is a group of diseases with similar symptoms and pathology, but different causes. Why don't PPMS er's have meningeal Bcell follicles? Just like cancer is seen as being a genetic susceptibilty together with environmental issues, it's the same for MS, and this is a catch all. Why is it hereditary in some, and out of the blue in others? The EBV may have an influence in some, but what other viruses are at play?

  • RE: "This latter observation is why I personally don't think myelin per se is necessarily the main target of immunological attack in MS."

    Then what is the primary target in MS?

  • Re: "Why don't PPMS er's have meningeal B cell follicles?"

    PPMS does; the fact that the recent literature has focused on SPMS does not mean that PPMS does not have follicles. Our group has looked at several cases with PPMS and have found follicle-like structures. In addition, MS'ers with PPMS have OCBs in their CSF.

  • Re: "Why is it hereditary in some, and out of the blue in others?"

    Not all MS'ers have a family history of the disease; only 1 in 7 do. Having the genetic risk factor only increases your risk of getting the disease by between 3 and 6x. In addition, many people without the genetic risk factor develop this disease. It is not an all or nothing phenomenon. What is needed are studies to try and work out how the genetic and environmental risk factors interact with each other. This is something we are planning to do.

  • Re: "EBV may have an influence in some, but what other viruses are at play?"

    I think a group of viruses called human endogenous retroviruses or HERVs may have a role to play. These viruses have integrated into our DNA and can be activated by various stimuli; EBV is on such stimulus. I will do a series of posts on HERVS to inform you in more detail of their potential role.

    • Please notify me with any info on HERVS that you have found, just diagnosed with MS and my MRI shows Dawson Fingers. Thanks

  • Re: "Then what is the primary target in MS?"

    I wish I knew. It could be the cell that makes myelin, the oligodenrocyte, rather than the myelin or even the nerve processes call the axon. I am not convinced with any of the data on the current putative auto-antigens; totally unconvincing.

  • Re: "Then what is the primary target in MS?"
    Re "I wish I knew."

    Why should there be any target? By a priori endorsing the existence of a target, the range of possible explanations gets diminished to those concerning blood-borne agents, namely viruses and lymphocytes. It has led nowhere, so far.

  • Re "…the concept of venous flow problems in MS is that it does not explain the deep perivenular lesions. Nor does it explain why Dawson's fingers are not the same as the venous lesions we seen in conditions associated with venous stasis"

    They are not the same because they are induced by swift retrograde venous blood flow, not by venous stasis. This also explains the formation of deep perivenular lesions (Steiner's splashes) as they are upstream from the Dawson's fingers.

  • Patient with bilateral cerebral small foci with abnormal signal likely demyelination
    impressive plaques of m.s …I would know diagnosis and treatment of this case

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