On 2017 Sep 25, Franz Schelling commented:
What appears rather strange is, besides, this fact: The massive changes found to affect the MS lesions' central veins themselves as well as their perivascular spaces are hardly anywhere taken into account
On 2017 Sep 25, Franz Schelling commented:
It is a pity this study offers no explanation for the following: (a) the prominent involvement of the inner cerebral veins (Zeng ea 2013); (b) the abrupt respectively gradual destruction of large subependymal collecting veins (Adams 1989); (c) the extension of these changes on certain segments of mainly the cerebral hemispheres' periventricular veins, first shown by Charcot in 1866, explicitly pointed out by Bruce in 1911, traced in 3D reconstructions by Putnam Adler in 1937 and the most thoroughly and comprehensively by Fog in 1964/5; (d) the absence of any evidence regarding a vein-dependent development of the lesions affecting the spinal cord in MS; and, above all, (e) the lesion dynamics revealed at http://www.msdiscovery.org/news/news_synthesis/322-more-meets-eye. References on request.
On 2017 Sep 18, David Hubbard commented:
Reposted from ResearchGate A new model of MS pathogenesis is reviewed in which the primary mechanism is not immunopathology but instead blood-brain barrier disruption and hypoperfusion: “The focus on the peripheral immune system alone may be limiting our understanding of the disease and the success of developing therapies.” The authors note that all current immunomodulatory therapies act on downstream immune-mediated pathology and provide no treatment for progressive disease or cure. A review of research demonstrates that BBB disruption is present at the earliest stages of disease, preceding symptoms, enhancing lesions, or other MRI changes. Global hypoperfusion is present before any grey matter volume loss and is out of proportion to reduced metabolic demand associated with axonal loss. They propose that oxidative stress secondary to chronic hypoxia causes oligodendrocyte degeneration and selective myelin loss which then leads to immune cell infiltration secondarily.
Finally, the diagnosis and treatment of MS shifts from suppressing T-cells and to perfusing oligodendrocytes.
On 2017 Sep 14, Alessandro Rasman commented:
Giampiero Avruscio MD and Alessandro Rasman
We read with interest the paper from Spencer et al. titled "Vascular pathology in multiple sclerosis: reframing pathogenesis around the blood-brain barrier" (1). Nice review but no mention of pressure, flow, gradient, G-lymphatics. And we find it really curious that the authors are now acting as though it's a surprise there is a vascular pathogenesis in MS. We know the blood brain barrier breaksdown occurs before demyelination. There’s a paper on this from 1990 (2). This ain't new.
References: 1. Spencer, Jonathan I., Jack S. Bell, and Gabriele C. DeLuca. "Vascular pathology in multiple sclerosis: reframing pathogenesis around the blood-brain barrier." J Neurol Neurosurg Psychiatry (2017): jnnp-2017. 2. Kermode, A. G., et al. "Breakdown of the blood-brain barrier precedes symptoms and other MRI signs of new lesions in multiple sclerosis: pathogenetic and clinical implications." Brain 113.5 (1990): 1477-1489.
On 2017 Sep 14, Alessandro Rasman commented:
Giampiero Avruscio MD and Alessandro Rasman
We read with interest the paper from Spencer et al. titled "Vascular pathology in multiple sclerosis: reframing pathogenesis around the blood-brain barrier" (1). Nice review but no mention of pressure, flow, gradient, G-lymphatics. And we find it really curious that the authors are now acting as though it's a surprise there is a vascular pathogenesis in MS. We know the blood brain barrier breaksdown occurs before demyelination. There’s a paper on this from 1990 (2). This ain't new.
References: 1. Spencer, Jonathan I., Jack S. Bell, and Gabriele C. DeLuca. "Vascular pathology in multiple sclerosis: reframing pathogenesis around the blood-brain barrier." J Neurol Neurosurg Psychiatry (2017): jnnp-2017. 2. Kermode, A. G., et al. "Breakdown of the blood-brain barrier precedes symptoms and other MRI signs of new lesions in multiple sclerosis: pathogenetic and clinical implications." Brain 113.5 (1990): 1477-1489.
On 2017 Sep 18, David Hubbard commented:
Reposted from ResearchGate A new model of MS pathogenesis is reviewed in which the primary mechanism is not immunopathology but instead blood-brain barrier disruption and hypoperfusion: “The focus on the peripheral immune system alone may be limiting our understanding of the disease and the success of developing therapies.” The authors note that all current immunomodulatory therapies act on downstream immune-mediated pathology and provide no treatment for progressive disease or cure. A review of research demonstrates that BBB disruption is present at the earliest stages of disease, preceding symptoms, enhancing lesions, or other MRI changes. Global hypoperfusion is present before any grey matter volume loss and is out of proportion to reduced metabolic demand associated with axonal loss. They propose that oxidative stress secondary to chronic hypoxia causes oligodendrocyte degeneration and selective myelin loss which then leads to immune cell infiltration secondarily.
Finally, the diagnosis and treatment of MS shifts from suppressing T-cells and to perfusing oligodendrocytes.
On 2017 Sep 25, Franz Schelling commented:
It is a pity this study offers no explanation for the following: (a) the prominent involvement of the inner cerebral veins (Zeng ea 2013); (b) the abrupt respectively gradual destruction of large subependymal collecting veins (Adams 1989); (c) the extension of these changes on certain segments of mainly the cerebral hemispheres' periventricular veins, first shown by Charcot in 1866, explicitly pointed out by Bruce in 1911, traced in 3D reconstructions by Putnam Adler in 1937 and the most thoroughly and comprehensively by Fog in 1964/5; (d) the absence of any evidence regarding a vein-dependent development of the lesions affecting the spinal cord in MS; and, above all, (e) the lesion dynamics revealed at http://www.msdiscovery.org/news/news_synthesis/322-more-meets-eye. References on request.
On 2017 Sep 25, Franz Schelling commented:
What appears rather strange is, besides, this fact: The massive changes found to affect the MS lesions' central veins themselves as well as their perivascular spaces are hardly anywhere taken into account