tsoft wrote:Just wondering if anyone has measured the brain blood flow in 24 hour basis and of course to compare it with healthy controls.
I remember that night blood pressure may decrease causing effects like TIA and etc.
Introduction: Recently, there has been an increased interest in the role of poor venous flow in patients with multiple sclerosis (MS) (1). The goal of this work is to understand the flow characteristics of both the major arteries and veins in the neck in an MS population. By using phase contrast MR imaging, we can evaluate the flow in a variety of locations to examine the total cardiovascular input/output to and from the brain. In
this preliminary study, we will examine a total of 127 MS cases and present a variety of quantitative measures of the arterial and venous flow.
Methods: Institutional review board approval was obtained for the human imaging protocols performed. A total of 127 MS patients were scanned with a variety of conditions. These include relapsing remitting, secondary progressive, primary progressive, and progressive relapsing. Blood flow is measured with two dimensional PCMRI imaging on a 3T Siemens Magnetom Tim Trio with the following parameters:
repetition time = 14.4ms, echo time = 4.41ms, flip angle = 25o , field of view = 256mmx256mm, acquisition matrix size = 448x448, in-plane resolution = 0.57mmx0.57mm, slice thickness = 4mm and velocity encoding (VENC) = 50cm/sec. Pulse gating was used to monitor and trigger the data acquisition. Images were acquired for a total of 25 time points during the cardiac cycle. The imaging plane was chosen to
be at the cervical 6/7 level at the lower neck and perpendicular to the internal jugular veins (IJV). Our in-house software (written in MATLAB) was used to segment vessels and compute flow. Vessel segmentation was achieved manually. In some cases the blood flow velocity exceeded our VENC and resulted in phase aliasing. This was corrected by running a simple phase unwrapping algorithm that takes into account the phase values of all the voxels throughout the cardiac cycle inside the vessel. Blood flow velocities through both veins and arteries were measured throughout the cardiac cycle. The volume flow rates at individual time points were computed by multiplying the spatial average velocity with the vessel lumen area. Then average volume flow rate was computed for the whole the cardiac cycle. The distribution of both arterial and venous
blood flow in different vessels was computed after the flow was quantified. The mismatch between arterial flow and venous flow was computed via: VA mismatch (%) = (arterial flow – venous flow)/arterial flow * 100. The ratio of blood flow between the dominant vein that carries most of the venous blood and the 2nd dominant vein was calculated for each patient. Reflux blood flow for internal jugular veins was calculated by: reverse flow/forward flow * 100. Finally, the pulsatility index (PI) for both internal
jugular veins was computed by: (Vmax-Vmin) / Vmean, where Vmax, Vmin and Vmean are the maximum, minimum and mean of the spatial average velocities for all the time points over the cardiac cycle.
On average, the left and right common carotid arteries carry almost the same amount of blood (6.37±1.32 mL/sec for LCCA vs. 6.32±1.59 mL/sec for RCCA). The same is true for the vertebral arteries (1.72±0.72 mL/sec vs. 1.51±0.65 mL/sec). However, the distribution of blood flow through the VAs is much more spread out than the CCAs. The blood flow through the RIJV (-6.12±2.88 mL/sec) is significantly more than the
LIJV (-3.74±2.52 mL/sec). This is consistent with the findings of others.
The spread between the left and right IJVs is also much more pronounced than that of the CCAs (see Fig. 1 left). Similar findings are shown for the total left and right arterial and venous flow rates. In general, arteries on both sides carry almost the same amount of blood while the right side veins carry more blood than the left side veins. Vessel crosssectional
area is found to have more variability than the vessel flow rate, especially for the IJVs (58.4±38.2 mm 2 for LIJV and 78.4±45.6 mm2 for RIJV).
The average percentage of IJV blood flow out of the total venous flow is measured to be 71.9±19.2%. Using the categorization method in , out of the 127 MS patients, 42.5% were type I, 48.8% were type II and 8.7% were type III. This is significantly different from the categorization in  for normals. The venous-arterial mismatch is measured to
be 14.0 ±11.1%. The ratio of sub-dominant vs. dominant venous flow is 0.50±0.25. Figure 1 (right) shows the plot of subdominant flow/dominant flow ratio vs. dominant flow rate. Reflux flow was found to be 4.9±14.8% for LIJV and 1.5±6.0% for RIJV (cases with zero reflux flow were not included when calculating these measures).
Finally, the pulsatility indices of the IJVs are 2.1±1.1 for LIJV and 1.9±1.0 for RIJV (cases with pulsatility index higher than 10 were not included when calculating these measures).
Discussion and Conclusions: The pronounced spread of blood flow through the left and right vertebral arteries and the left and right internal jugular veins is worth noting. It means that the blood distribution between the left and right sides can be significantly disproportionate for some patients. This could be due to various anatomical or physiological conditions. An example could be vessel stenosis on one side. Compared to the findings in , our measurements show that in more MS patients (48.8% for type II compared to only 22% in ) the internal jugular veins carry less blood out of the brain. This could be caused by CCSVI and other veins or collaterals serve as alternative pathways. It is also interesting that about 1/4 of all the MS patients have a significantly more dominant vein (meaning that the 2nd dominant vein only carries less than 20% of the blood through the dominant vein).
tsoft wrote:Thank you Cheer!
I am familiar with the work of Dr. Hackee, mostly because of your posts and your articles in the Facebook. I am looking forward to his results and believe that this will be a huge step in the right direction.
Yet my wondering was related to whether the state of the jugular veins, arteries and cerebral blood flow at all are constant state or could they be changed, eg during the night, on relapse or other circumstances.
Saying again that I'm just wondering. Maybe i'm saying just nosense...
ikulo wrote:I also see this as more support for the "primary hypoperfusion in MS" hypothesis. The study states that the more highly perfused regions allow for remyelination. This implies that perfusion plays a direct, causal role in (de/re)myelination.
I don't see how myelination itself would cause increased perfusion.
CEREBRAL BLOOD-FLOW IN POLYCYTHÆMIA
D.J. Thomas , John Marshall , R.W. Ross Russell , G. Wetherley-Mein , G.H. Du Boulay , T.C. Pearson , L. Symon , E. Zilkha
Cerebral blood-flow (C.B.F.) has been measured in 16 patients with polycythæmia of differing severity. The mean C.B.F. was 37.9 ml/100 g/min, which is significantly below the normal level of 69.1 (S.D. 9.3) ml/100 g/min (p<0.001). C.B.F. measurement was repeated after venesection in 15 of the patients. Lowering the hæmatocrit from a mean of 0.536 to a mean of 0.455 was associated with a 73% increase in mean C.B.F. (P<0.001) and a 30% reduction in whole-blood viscosity. Low C.B.F. was found at hæmatocrit levels between 0.46 and 0.52. Hæmatocrit levels that are currently considered acceptable in the management of polycythæmia may therefore be too high.
Polycythemia and chorea.
Marvi MM, Lew MF.
Polycythemia vera is a sporadic myeloproliferative disorder of increased red blood cell mass affecting multiple organ systems. Associated thrombosis, hemorrhaging, and hyperviscosity commonly result in neurological manifestations, sometimes in the form of chorea and ballism. Resultant choreiform movements have been mainly described as generalized with orofaciolingual and appendicular muscle involvement, hypotonia, and hyporeflexia. Chorea has also been uncommonly reported as arising from secondary causes of polycythemia; however, the underlying pathophysiology has not been clearly elucidated. Proposed mechanisms for basal ganglia dysfunction include hypoperfusion due to venous stasis, receptor hypersensitivity in a setting of reduced catecholamine levels, and altered platelet dopamine metabolism. Magnetic resonance imaging and single-photon emission computed tomography perfusion studies have failed to reveal an anatomical or physiological basis for polycythemia vera-associated chorea, yet rare pathological examinations of deceased patients have shown signs of cerebral venous thrombosis and perivenous demyelination. Administration of neuroleptics may suppress abnormal choreiform movement; however, effective management of polycythemia vera requires serial venesections in conjunction with chemotherapy. Appropriate treatment may prolong survival to more than 10 years, although chorea may spontaneously remit, re-emerge with resurgence of disease, or continue indefinitely despite maintenance therapy.
To examine the vascular changes occurring in three archival cases of acute multiple sclerosis, and to provide immunohistochemical evidence of early endothelial cell activation and vascular occlusion in this condition.
Early vascular endothelial cell activation which may progress to vasculitis and vascular occlusion including class II antigen expression and fibrin deposition were identified.
The vascular changes were seen prior to cerebral parenchymal reaction and demyelination, and were not seen in control cerebral tissues.
It is proposed that vascular endothelial cell activation may be an early and pivotal event in the evolution of multiple sclerosis, and that demyelination may have an ischaemic basis in this condition. The vascular endothelium may contain an early element in the evolution of multiple sclerosis.
Restoration of blood flow following removal of the stimulus would produce a rapid clinical improvement.
Animal studies have revealed the molecular cascades that are initiated with hypoxia/ischemia in the cells forming the neurovascular unit and that contribute to cell death. Matrix metalloproteinases cause reversible degradation of tight junction proteins early after the onset of ischemia, and a delayed secondary opening during a neuroinflammatory response occurring from 24 to 72 hours after. Cyclooxygenases are important in the delayed opening as the neuroinflammatory response progresses. An early opening of the BBB within the 3-hour therapeutic window for tissue-type plasminogen activator can allow it to enter the brain and increase the risk of hemorrhage. Chronic hypoxic hypoperfusion opens the BBB, which contributes to the cognitive changes seen with lacunar strokes and white matter injury in subcortical ischemic vascular disease. This review will describe the molecular and cellular events associated with BBB disruption and potential therapies directed toward restoring the integrity of the neurovascular unit.
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