Research: Cognitive Impairment and Blood flow

R
Francis PL et al. Robust Perfusion Deficits in Cognitively Impaired Patients with Secondary-Progressive Multiple Sclerosis.AJNR Am J Neuroradiol. 2012 Jun 14. [Epub ahead of print]

BACKGROUND AND PURPOSE:Cognitive impairment is a common, disabling symptom of MS. We investigated the impact of cerebral perfusion and brain and lesion volumetry on cognitive performance in 45 patients with SPMS by using MR imaging.


MATERIALS AND METHODS: Cognition was assessed by using a standard battery, the Minimal Assessment of Cognitive Function in Multiple Sclerosis. MRI was used to assess cerebral blood volume and MRI was used to assess the volume of the grey matter, the white matter and the white matter lesion volume
RESULTS: There was reduced blood volume in the the superior medial frontal cortex of impaired MSers.  There was also lower blood volume in the bilateral thalami and caudate nuclei of impaired patients.

Performance on the Symbol Digit Modalities Test, which assesses information-processing speed, correlated most strongly overall with cerebral perfusion. Focal analyses of grey matter, white matter and the white matter lesion volume revealed no significant differences between patients with and without cognitive impairment, though global GM volume was significantly decreased and global WML volume was significantly increased in impaired patients.

CONCLUSIONS:These results suggest that cognitively impaired patients with SPMS exhibit robust perfusion deficits in cortical and subcortical GM and impaired processing speed.
This study suggests that there may be reduced blood flow in certain areas of the brains of MSers that have problem of with mental processing/cognition during secondary progression. Such people have evidence of reduced nerve content in the grey matter and more MS lesions in the white matter. However it is not clear what this reduced perfusion (blood flow) is due to.

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11 comments

  • Friend was recently prescribed Clexane for a venous clot, she remarked that whilst she was taking it her 'brain fog' disappeared. Curious, as to whether you would have an opinion as to why blood thinning may have ' caused' this observed side effect.

  • Re: "Curious, as to whether you would have an opinion as to why blood thinning may have ' caused' this observed side effect."

    No idea! There is some data that the coagulation pathway is involved in MS inflammation. There is a clotting factor called tissue factor that is involved in tissue inflammation and inhibiting it may have a positive effect!

  • Could be that improved blood flow really helps cog fog? Almost everybody says that after venoplasty. It may not be just a placebo effect.

  • Re: "Almost everybody says that after venoplasty."

    Not sure about this; all of the MSers who I look after who have had CCSVI procedures, against my advice, have not described this phenomenon. I suspect it is selective reporting, i.e. those who have a positive experience report it those who don't keep quite. In the scientific field we call this publication bias. It is a big problem. This is why we need controlled trials,

  • Perhaps there is something in anti-coagulants and MS brain fog? Look at this link between Hughes syndrome and relief from memory loss with appropriate blood thinner warfarin dosage…?

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1742609/pdf/v079p00081.pdf

    The antiphospholipid syndrome (APS, Hughes’ syndrome), first described in 1983, is a prothrombotic disease in which neurological events feature prominently. Strokes, transient ischaemic attacks, and headaches (including migraine) are important complications. However, it is clear that other neurological symptoms, including diplopia, memory loss, ataxia, and “multiple sclerosis-like” features are common. A notable feature of Hughes’ syndrome is the clinical response to anticoagulants; features such as headache and memory loss often improving dramatically with appropriate warfarin dosage. APS may well become recognised as an important (and potentially treatable) cause of neurological disease.

  • Interestingly, too, perhaps is that the Marshall Protocol is a firm believer that Olmesartan – an anti-inflammatory and a drug used to reduce blood pressure – seems to have some impact on MS.

    It is a Vitamin D Receptor agonist too.

    http://mpkb.org/home/mp/olmesartan

  • Gavin,

    about Hughes syndrome i have a question. in agressive rrms with intrathecal synthesis of igM-anti phosphatidilcoline, do you think that hughes syndrome could be a cause? what are the technical differences between ms and hughes?in hughes there are oligoclonal bands in LCR?
    thank you very much for your work.
    regards from spain, Alvaro

  • Re: "about Hughes syndrome i have a question. in agressive rrms with intrathecal synthesis of igM-anti phosphatidilcoline, do you think that hughes syndrome could be a cause?"

    No Hughes' syndrome is different to MS and a good neurologist should be able to distinguish the two. The former is due to blood clots and causes mini strokes.

  • More should be done about blood flow. What about Huperzine A? It's an acetylcholinesterase inhibititor and NMDA receptor antagonist…… The later includes donezipil and revastigmine (sic) both that might have cognitive benefit to MS patients.

    But who will trial Huperzine A? Sigh. Not me.

  • "Friend was recently prescribed Clexane for a venous clot, she remarked that whilst she was taking it her 'brain fog' disappeared."

    "Could be that improved blood flow really helps cog fog? Almost everybody says that after venoplasty."

    My thinking seemed much clearer for some time after venoplasty. Maybe it even was objectively better if you think the PASAT measures something useful (my only perfect score). Now I wonder, though, maybe it was the Plavix and not the balloon? Or perhaps the stars just aligned?

  • Re: "Now I wonder, though, maybe it was the Plavix and not the balloon? Or perhaps the stars just aligned?"

    Without randomised blind sham-controlled trials you will never know. I hope you understand why we need class 1 evidence.

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