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The vertebral veins drain into the subclavian vein and are adjacent to the jugular vein confluens. i doubt that injury would happen thomo_en wrote:That was a real mind-appetizer. Consequently, makes the next question inevitable: Is there a risk of such vertebral vein damage after ballooning the jugulars in their lowest part? It is there where the VVs end, isn't it?
i think that there is poor development of the vertebral veins. they travel adjacent to the vertebral arteries within the bony canal. at around the sixth vertebra of the neck they exit and travel toward the subclavian vein.Cece wrote:Does incomplete mean that it's partial agenesis of the vertebral veins? I would think a valve issue in the verts might eventually be treatable (you mentioned back in June that Dr. Galleotti had tried treating the verts with negligible or mixed results?) but agenesis would be really tricky. But if it takes two obstructions to cause problems, the clearing of one of the obstructions might yet be enough to relieve the problems.drsclafani wrote: imaging of the vertebral veins illustrates that an outlet of a second system IS present. Both vertebral veins are incomplete.
Thanks for sharing these latest images and case study.
Hi Dr are these problems in the Verts hard to image or assess?drsclafani wrote:i think that there is poor development of the vertebral veins. they travel adjacent to the vertebral arteries within the bony canal. at around the sixth vertebra of the neck they exit and travel toward the subclavian vein.Cece wrote:Does incomplete mean that it's partial agenesis of the vertebral veins? I would think a valve issue in the verts might eventually be treatable (you mentioned back in June that Dr. Galleotti had tried treating the verts with negligible or mixed results?) but agenesis would be really tricky. But if it takes two obstructions to cause problems, the clearing of one of the obstructions might yet be enough to relieve the problems.drsclafani wrote: imaging of the vertebral veins illustrates that an outlet of a second system IS present. Both vertebral veins are incomplete.
Thanks for sharing these latest images and case study.
the upper part of the vein in this case were just poorly developed.
By external stents, do you mean around the vein from the outside, put in surgically? I don't think it would work by the carotid, because internally or externally, an IJV stent would put pressure on the wall of the carotid, possibly causing slow heart beat or other issues.Nunzio wrote:In the future I envision using external stents to prevent extrinsic compression of the Jugular vein. I know Dr.Noda was releasing the scalene muscle to prevent compression.
The same concept goes for people claiming they have the carotid bulb indenting the Jugular vein.
Your problem is that Gazelle have a long neck prone to these misalignment problems. If you were an Hippopotamus with a short neck, you might be just fine even though "lady Hippopotamus" doesn't have the same ring as "lady Gazelle"
Good luck on your new treatment.
i do not usually attempt catheterization and venography of the vertebral artery, although it is not uncommon for the catheter to enter this vessel when attempting catheterization of the internal jugular vein.NZer1 wrote:Hi Dr are these problems in the Verts hard to image or assess?drsclafani wrote:i think that there is poor development of the vertebral veins. they travel adjacent to the vertebral arteries within the bony canal. at around the sixth vertebra of the neck they exit and travel toward the subclavian vein.Cece wrote: Does incomplete mean that it's partial agenesis of the vertebral veins? I would think a valve issue in the verts might eventually be treatable (you mentioned back in June that Dr. Galleotti had tried treating the verts with negligible or mixed results?) but agenesis would be really tricky. But if it takes two obstructions to cause problems, the clearing of one of the obstructions might yet be enough to relieve the problems.
Thanks for sharing these latest images and case study.
the upper part of the vein in this case were just poorly developed.
They have always been of interest to me.
no, these studies are phasic in nature.HappyPoet wrote:Hi Dr. Sclafani,
A quick question: If there is no obstruction reflux into the deep cerebral veins shown on TC DUS, does that mean there never has been and there never will be such reflux?
Thanks!
Yes Cece, That was what I meant, I agree with you about the carotid bulb;if you rub on it you can lower somebody blood pressure significantly; that is why is important to understand that the problem is whatever is on the other side pushing the Jugular vein against the carotid bulb and that could be addressed surgically too, maybe " a la Noda"Cece wrote:By external stents, do you mean around the vein from the outside, put in surgically? I don't think it would work by the carotid, because internally or externally, an IJV stent would put pressure on the wall of the carotid, possibly causing slow heart beat or other issues.Nunzio wrote:In the future I envision using external stents to prevent extrinsic compression of the Jugular vein. I know Dr.Noda was releasing the scalene muscle to prevent compression.
The same concept goes for people claiming they have the carotid bulb indenting the Jugular vein.Your problem is that Gazelle have a long neck prone to these misalignment problems. If you were an Hippopotamus with a short neck, you might be just fine even though "lady Hippopotamus" doesn't have the same ring as "lady Gazelle"
Good luck on your new treatment.
Mechanical blood flow and MSIn a recent review of the role of venous reflux, Simka stated: “It is hypothesized that pathological refluxing venous flow in the cerebral and spinal veins increases the expression of adhesion molecules, particularly ICAM-1, by the cerebrovascular endothelium” [16]. Along these lines, Bergan demonstrated, by occluding a major vein in the rat, that the number of leukocytes migrating across the vessel wall increased progressively during occlusion [17–19]. Multiple microhemorrhages occurred upstream of the occlusion (usually 20–30 µm in diameter, but some as large as 200 µm). “The venular occlusion experiments showed that reduced flow can rapidly set in motion an inflammatory cascade, including hallmarks like leukocyte adhesion to the endothelium, migration into the interstitium, free radical production and parenchymal cell death that begins soon after occlusion…” Bergan goes on to say: “Elevated pressures can also cause the formation of transcellular gaps through endothelial cells, which may be related to the development of microhemorrhages.”
Perfusion Deficits in Multiple SclerosisIn the 1980s, Schelling believed that there was a significant mechanical nature related to the fact that the vascular damage follows a path opposed to the flow [20]. He quotes Carswell as saying: “In inflammation, the local congestion commences in the capillaries, afterwards extends to the small veins, but never to large branches; in mechanical congestion (by venous flow inversion) the blood accumulates first in the venous trunks, which are always conspicuous, and afterwards in the branches and capillaries.” [21]. Further evidence of this mechanical effect comes from observations of Allen, who noticed the widened vascular beds around veins and the central widening of the venous tree indicative of intermittent increases in cerebral pressure [22]. It is also worth looking into Fog’s work. He summarizes his results from a series of cadaver brain studies as “thirty plaques showed that they definitely followed the course of the veins, so that course and dimensions of the veins determine the shape, course and dimension of the plaques.” [23]. He also closes his work with the comment: “Consequently, multiple sclerosis, pathologico-anatomically, must be considered a periphlebitis, as proved by the author in 1948 in the case of plaques of the spinal cord.” [24].
Recently, it has been demonstrated that there is reduced perfusion and even loss of small medullary vein visibility in MS [8]. Juurlink discusses the role of hypoperfusion in MS [25]. He comments that the reduced perfusion can be detrimental to oligodendrocytes, preferentially affects white matter, causes demyelination and leads to microglial activity. He notes that these can be most marked in the optic nerve and tract. He then states: “There is now ample evidence that ischemic insults of sufficient severity can cause upregulation of cell adhesion molecules onto the endothelial cells, thus allowing infiltration of leukocytes into the brain parenchyma, resulting in an inflammatory lesion.” He goes on to point out that hypertension of genetically susceptible lesions leads to vascular damage, which in turn leads to ischemia. There is actually a body of evidence suggesting reduced perfusion in MS patients. Back in the 1980s, Swank et al. found that past the age of 40 years, MS patients had markedly reduced blood flow compared with normal individuals [26]. Using MRI, there has been a thrust in the last 10 years to study perfusion in MS. The work of Meng Law [27] and others [28–32] demonstrates that there is reduced perfusion as a function of severity of disease. Law et al. reported a significant decrease of cerebral blood flow and a prolongation of mean transit time in the normal-appearing white matter (NAWM) at the level of the lateral ventricles in MS patients [27]. These reductions often appear in the basal ganglia and thalamus and have been related to fatigue [30,31,33]. A study of seven patients with relapsing– relapsing–remit- remit remitting MS revealed decreased relative cerebral blood volume (CBV) in chronic lesions and further reduced relative CBV in one acute lesion in white matter compared with that in gray matter [27].
i have not changed my treatments by beginning on the left side. However, i believe I have been able to better assess the global drainage problems and counsel patients better.CuriousRobot wrote:Dr Scalfani:
You once wrote of asking the Italian doctors why they enter through the left iliac femoral venous axis and not the right (something about it being easier, a straight shot, through the right than the left).
Have you found that going through the left is truly warranted in your research so far? Do you feel that by entering through the right, a doctor may miss something?
Thanks,
Przemek