Cerebral Blood Flow and Red Cell Delivery in Normal Subjects and in Multiple Sclerosis

Swank, Roy L.; Roth, John G.; Woody, David C.

doi:10.1080/01616412.1983.11739631

Cited by 33 publications

(21 citation statements)

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“…Positron Emission Tomography (PET) and Single Photon Emission Computed Tomography (SPECT) studies have shown a decreased cerebral blood flow (CBF) in grey and white matter of MS patients [156,157]. Non conventional magnetic resonance (MR) techniques, such as proton MR spectroscopy and magnetization transfer resonance, have demonstrated diffuse pathological changes affecting both NAWM and NAGM in MS patients.…”

Section: Chronic Hypoperfusion Hypoxia and Angiogenesismentioning

confidence: 99%

Angiogenesis in multiple sclerosis and experimental autoimmune encephalomyelitis

Girolamo

Coppola

Ribatti

et al. 2014

Acta Neuropathologica Communications

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Angiogenesis, the formation of new vessels, is found in Multiple Sclerosis (MS) demyelinating lesions following Vascular Endothelial Growth Factor (VEGF) release and the production of several other angiogenic molecules. The increased energy demand of inflammatory cuffs and damaged neural cells explains the strong angiogenic response in plaques and surrounding white matter. An angiogenic response has also been documented in an experimental model of MS, experimental allergic encephalomyelitis (EAE), where blood-brain barrier disruption and vascular remodelling appeared in a pre-symptomatic disease phase. In both MS and EAE, VEGF acts as a pro-inflammatory factor in the early phase but its reduced responsivity in the late phase can disrupt neuroregenerative attempts, since VEGF naturally enhances neuron resistance to injury and regulates neural progenitor proliferation, migration, differentiation and oligodendrocyte precursor cell (OPC) survival and migration to demyelinated lesions. Angiogenesis, neurogenesis and oligodendroglia maturation are closely intertwined in the neurovascular niches of the subventricular zone, one of the preferential locations of inflammatory lesions in MS, and in all the other temporary vascular niches where the mutual fostering of angiogenesis and OPC maturation occurs. Angiogenesis, induced either by CNS inflammation or by hypoxic stimuli related to neurovascular uncoupling, appears to be ineffective in chronic MS due to a counterbalancing effect of vasoconstrictive mechanisms determined by the reduced axonal activity, astrocyte dysfunction, microglia secretion of free radical species and mitochondrial abnormalities. Thus, angiogenesis, that supplies several trophic factors, should be promoted in therapeutic neuroregeneration efforts to combat the progressive, degenerative phase of MS.

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Section: Chronic Hypoperfusion Hypoxia and Angiogenesismentioning

confidence: 99%

Angiogenesis in multiple sclerosis and experimental autoimmune encephalomyelitis

Girolamo

Coppola

Ribatti

et al. 2014

Acta Neuropathologica Communications

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“…Early measurements of global perfusion in multiple sclerosis using radioactive 133 Xe [31], positron emission tomography (PET) [32], or single photon emission computed tomography (SPECT) techniques [33] suffered from a very low spatial resolution. Findings of a generally lower perfusion in MS patients compared to healthy individuals were contradicted by the demonstration of increased perfusion during the time of acute inflammation in an animal model of MS [34].…”

Section: Cerebral Perfusion Changes Precede Blood-brain Barrier Breakmentioning

confidence: 99%

Cerebral blood perfusion changes in multiple sclerosis

Wuerfel

Paul

Zipp

2007

Journal of the Neurological Sciences

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| The proximity of immune cell aggregations to the vasculature is a hallmark of multiple sclerosis. Furthermore, it is widely accepted that inflammation is able to modulate the microcirculation. Until recently, the detection of cerebral blood perfusion changes was technically challenging, and perfusion studies in multiple sclerosis patients yielded contradictory results. However, new developments in fast magnetic resonance imaging have enabled us to image the cerebral hemodynamics based on the dynamic tracking of a bolus of paramagnetic contrast agents (dynamic susceptibility contrast). This review discusses the technical principles, possible pitfalls, and potential for absolute quantification of cerebral blood volume and flow in a clinical setting. It also outlines recent findings on inflammation associated perfusion changes, which are inseparable from pathological considerations in multiple sclerosis.

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“…Cerebral hypoperfusion associated with MS is widely documented, yet the pathophysiologic mechanisms are not well understood 7 . Contributing factors such as neuronal loss, primary vascular abnormality and metabolic dysregulation have been implicated 4, 5, 7, 12 . Perfusion imaging provides insight into the pathophysiology and disease severity of MS 13 , and correlates with cognitive impairment in patients with secondary progressive MS 12 .…”

Section: Discussionmentioning

confidence: 99%

Comparison of Quantitative Cerebral Blood Flow Measurements Performed by Bookend Dynamic Susceptibility Contrast and Arterial Spin-Labeling MRI in Relapsing-Remitting Multiple Sclerosis

D'Ortenzio

Hojjat

Vitorino

et al. 2016

AJNR Am J Neuroradiol

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Background and Purpose Quantitative CBF usage as a biomarker for cognitive impairment and disease progression in MS is potentially a powerful tool for longitudinal patient monitoring. Dynamic Susceptibility contrast perfusion with Bookend T1-calibration (Bookend Technique) and pseudo-continuous Arterial Spin Labeling have recently been used for CBF quantification in relapsing-remitting MS. The non-invasive nature of pseudo-continuous Arterial Spin Labeling is advantageous over gadolinium-based techniques, but correlation between the techniques is not well established in the context of MS. Materials and Methods We compared pseudo-continuous Arterial Spin Labeling CBF to the Bookend technique in a prospective cohort of 19 healthy controls, 19 relapsing-remitting MS subjects without cognitive impairment and 20 relapsing-remitting MS subjects with cognitive impairment on a voxel-wise and Brodmann regional basis. Linear Pearson correlation, SNR and coefficient of variation were quantified. Results Voxel-wise paired T-tests revealed no significant CBF differences between techniques after normalization of global mean intensities. Highest Pearson correlations were observed in deep GM structures (average r = 0.71 basal ganglia, and r = 0.65 thalamus) but remained robust for cortical GM, WM and WML (average r = 0.51, 0.53, 0.54 respectively). Lower Pearson correlations were observed for CL (average r=0.23). Brodmann regional correlations were significant for all groups. All correlations were maintained in healthy controls and in RRMS disease. Highest SNR was present in Bookend perfusion while the highest coefficient of variation was present in WML. Conclusion Agreement between pseudo-continuous Arterial Spin Labeling and Bookend technique CBF measurements is demonstrated in healthy controls and relapsing-remitting MS patients

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Cerebral Blood Flow and Red Cell Delivery in Normal Subjects and in Multiple Sclerosis

Cited by 33 publications

References 0 publications

Angiogenesis in multiple sclerosis and experimental autoimmune encephalomyelitis

Angiogenesis in multiple sclerosis and experimental autoimmune encephalomyelitis

Cerebral blood perfusion changes in multiple sclerosis

Comparison of Quantitative Cerebral Blood Flow Measurements Performed by Bookend Dynamic Susceptibility Contrast and Arterial Spin-Labeling MRI in Relapsing-Remitting Multiple Sclerosis

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