Monday, 17 April 2017

DrK the Star with abit of Flair

Campion T, Smith RJ, Altmann DR, Brito GC, Turner BP, Evanson J, George IC, Sati P, Reich DS, Miquel ME, Schmierer K. FLAIR* to visualize veins in white matter lesions: A new tool for the diagnosis of multiple sclerosis? Eur Radiol. 2017. doi: 10.1007/s00330-017-4822-z.

OBJECTIVE:To explore the potential of a post-processing technique combining FLAIR and T2* (FLAIR*) to distinguish between lesions caused by multiple sclerosis (MS) from cerebral small vessel disease (SVD) in a clinical setting.
METHODS:FLAIR and T2* head datasets acquired at 3T of 25 people with relapsing MS (pwRMS) and ten with pwSVD were used. After post-processing, FLAIR* maps were used to determine the proportion of white matter lesions (WML) showing the 'vein in lesion' sign (VIL), a characteristic histopathological feature of MS plaques. Sensitivity and specificity of MS diagnosis were examined on the basis of >45% VIL+ and >60% VIL+ WML, and compared with current dissemination in space (DIS) MRI criteria.
RESULTS:All pwRMS had >45% VIL+ WML (range 58-100%) whilst in pwSVD the proportion of VIL+ WML was significantly lower (0-64%; mean 32±20%). Sensitivity based on >45% VIL+ was 100% and specificity 80% whilst with >60% VIL+ as the criterion, sensitivity was 96% and specificity 90%. DIS criteria had 96% sensitivity and 40% specificity.
CONCLUSION:FLAIR* enables VIL+ WML detection in a clinical setting, facilitating differentiation of MS from SVD based on brain MRI.

KEY POINTS:
• FLAIR* in a clinical setting allows visualization of veins in white matter lesions. 
• Significant proportions of MS lesions demonstrate a vein in lesion on MRI. 
• Microangiopathic lesions demonstrate a lower proportion of intralesional veins than MS lesions. 
• Intralesional vein-based criteria may complement current MRI criteria for MS diagnosis.

Fluid-attenuated inversion recovery (FLAIR) is a pulse sequence used in magnetic resonance imaging.  The pulse sequence is an inversion recovery technique that nulls fluids. For example, it can be used in brain imaging to suppress cerebrospinal fluid (CSF) effects on the image, so as to bring out the periventricular hyperintense lesions, such as multiple sclerosis (MS) plaques.


T2 is defined as a time constant for the decay of transverse magnetization arising from natural interactions at the atomic or molecular levels. (Don't worry I can't understand this either:-) used as a measurement of those processes contributing to the transverse decay of the MR signal that arise from natural interactions at the atomic and molecular levels within the tissue or substance of interest.  In any real experiment, however, the transverse magnetization decays much faster than would be predicted by natural atomic and molecular mechanisms; this rate is denoted T2* ("T2-star"). T2* can be considered an "observed" or "effective" T2, whereas the first T2 can be considered the "natural" or "true" T2 of the tissue being imaged. T2* is always less than or equal to T2.

T2* results principally from inhomogeneities in the main magnetic field. These inhomogeneities may be the result of intrinsic defects in the magnet itself or from susceptibility-induced field distortions produced by the tissue or other materials placed within the field.

T2* decay refers to an exponential decrease in Mxy (i.e. signal strength) following the initial excitation pulse as a function of time constant T2*.

Whilst the CCSVIers were shouting its all about the veins, so was DrK, but this time using yet another imaging sequence, which is used to detect blood vessels at the heart of MS lesion. This may help in MS diagnosis.

CoI: This is work from TeamG

8 comments:

  1. Does drK see fewer of those lesions in older/SPMS patients?

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    1. This paper focused on the "diagnostic" use of FLAIR* in relatively early/relapsing MS. In pwPMS the diagnostic question is often less relevant though one advantage of the "vein-in-lesion" sign could be to distinguish lesion caused by vascular risk factors from MS even in advanced MS thereby supporting NEDA in more advanced disease. We'll keep working on this.

      In an earlier study using 7T MRI a group from Amsterdam described a significantly lower percentage of perivascular deep white matter lesions (73%) in pwMS over 40 years of age compared with younger patients (92%): Kilsdonk ID, et al. Morphological features of MS lesions on FLAIR* at 7 T and their relation to patient characteristics. J Neurol 2014;261:1356–64.

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    2. I suppose this supports the "from outside-in" theory of MS - and as the person ages and the immune response changes there should be fewer new lesions of this type? Or?
      (I find it rather puzzling that as we still function OK and the MS is RR, the number of lesions on MRI increases - then when MRI lesions are no longer increasing a crisis hits and the person turns SP).

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    3. I don't think one can make much in terms of pathophysiology out of fewer MS lesions showing veins when we age. I rather suspect with age pwMS also accumulate non-specific or micro-angiopathic (small vessel disease) lesions leading - quite literally - to a more mixed picture. Alas, even in later stage disease there is accumulation of lesions, we just can't see them all, particularly in the grey matter, and other factors (neuro-axonal loss exhausting reserve capacity, etc) become more apparent.

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  2. I don't know if it would be a silly question, but since there is such a link between MS lesions and veins could there be a relationship also with atherosclerosis?

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    Replies
    1. No silly questions there are. Atherosclerosis affects the arterial side of the vascular bed, MS lesions emerge around veins.

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    2. Since there are no silly questions I have a 'rogue gene' that causes raised factor viii levels does this figure in any of this or am I barking up the wrong tree?

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