Cool papers Cheer!!
what a great thread to have begun...
Both of these studies are looking at venous issues in which the veins are stressed by excessive blood flow and both result in myelopathy---
myelopathy= disease or degeneration of the spinal cord with resultant neurological deficits. MSers have myelopathy.
It makes me crazy when I hear a neurologist who has been presented this idea has declared this "can't" be the cause of MS. A look at the literature and en effort to study this shows it most certainly can cause demyelination and inflammation and in legs we know we get lesions. So based on what scientific principle is it rejected out of hand? And given that we seem to have these stenoses it seems to me perhaps it is up to them to show that such an anomaly CAN'T harm the MS brain before they tell us to ignore it.
I really appreciated the note that it took some years for the lady with the altered blood flow to develop neuro problems after her repair. It may show how it can be that people can have a jugular removed and they seem "fine" at least if you check them the next week. Question is does the body cope with that over years? MY guess is no and in around a decade you see these issues.
HERE"S another one
along the same "veins"
Spinal dural arteriovenous fistula: the pathology of venous hypertensive myelopathy
RW Hurst, LC Kenyon, E Lavi, EC Raps and P Marcotte
Department of Radiology, University of Pennsylvania Medical Center, Philadelphia, USA.
Spinal dural arteriovenous fistulas (SDAVFs) are the most common type of spinal vascular malformation. The arteriovenous shunts, located entirely outside the spinal cord, cause a clinical picture of chronic progressive myelopathy believed to arise from the effects of increased venous pressure and impaired venous drainage on the spinal cord. Despite their well-described clinical and angiographic features, no reports have documented the spinal cord pathology in a case of angiographically or pathologically proven SDAVF. We report such a patient in whom a spinal cord biopsy supported increased venous pressure as a mechanism of neurologic dysfunction.
So increased pressure caused this neurologic problem for this patient.
The question is can this kindof injury cause demyelination?Paper here
Evidence of Acute Demyelination Around a Developmental Venous Anomaly: Magnetic Resonance Imaging Findings
JUNG, GREGOR MD; SCHRÖDER, RITA MD; LANFERMANN, HEINER MD; JACOBS, ANDREAS MD; SZELIES, BRIGITTE MD; SCHRÖDER, ROLAND MD
The authors report on the occurrence of a focal demyelination showing a mass effect around a developmental venous anomaly in the cerebellum. Because the latter presented as a single lesion, the differentiation from intraparenchymal neoplasms or infarction was difficult. Follow-up magnetic resonance imaging and histology from a biopsy specimen give useful information to find the appropriate diagnosis.
Another oneFound here
Cerebral venous thrombosis in the rhesus monkey
W. D. Sheffield, R. A. Squire and J. D. Strandberg
Cerebral venous thrombosis was identified in four rhesus monkeys. Two initially showed neurologic signs and three had diarrhea or dysentery. All four had severe intestinal disease, including three cases of ulcerative colitis complicated by extracerebral thromboembolic disease. Central nervous system lesions, confined to the centrum semiovale, were multiple thrombi of internal cerebral veins, perivenular demyelination, and gemistocytic astrocytosis. The lesions resembled those found in people with cerebral venous thrombosis, and support the hypothesis that perivenular demyelination may occur as a sequela to venous occlusion. The lesions were identical to those found in "leukoencephalosis and perivascular myelosis," an entity of unknown cause previously described in monkeys.
The monkeys had actual clots and sudden complete occlusion but the fact remains; demyelination as a result of venous changes.
And then here is something to addCLICK HERE
Evidence for subacute fat embolism as the cause of multiple sclerosis.James PB.
The neurological features of decompression sickness, which is thought to be due to gas embolism, are similar to those of multiple sclerosis (MS). This similarity suggested the re-examination of a concept, first proposed in 1882, that the demyelination in MS is due to venous thrombosis. Unfortunately, although the plaques of MS are often perivenular, thromboses are not always present. Nevertheless, vascular theories can explain the topography of the lesions in MS. Embolism is generally associated with arterial rather than venous damage, and with neuronal infarction rather than loss of myelin. However, the intra-arterial injection of a range of substances can cause venous damage and perivenous demyelination in the brain, although it does not exactly reproduce the plaques seen in man. There is also evidence in man that fat may lodge in the microcirculation of the nervous system and cause distal perivenous oedema with the loss of myelin from axons. Since acute fat embolism may produce lesions not only in the white matter of the brain, but also in the cord, the retina, the meninges, and the skin, and since all these have been described in MS, subacute fat embolism may be the cause of MS.
That guy was close he is almost there if only he'd known about the venous stenoses and backups............... The kinds of injuries that happen to tissue secondary to the CVI (in legs) are similar to thromobsis so if he'd have known...........
So many years ago............