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Y. Narita1, Y. Watanabe1, T. Hoshino2, M. Okada2, Y. Yamamoto2 and S. Kuzuhara3

(1) Department of Neurology, Matsusaka Chuo Hospital, Mie, Japan
(2) Department of Neurosurgery, Matsusaka Chuo Hospital, Mie, Japan
(3) Department of Neurology, Mie University Hospital, Mie, Japan
Received: 12 June 1991

Summary A 45-year-old woman developed a myelopathy 9 years after a spontaneous left caroticocavernous fistula (CCF) was treated by a trapping procedure, with clipping distal to the fistula and ligation of the common carotid artery. Spinal MRI and vertebral angiography revealed recurrence of the CCF and gigantic tortuous veins draining through the brain stem down to the midcervical spinal cord. The abnormal veins and myelopathy disappeared after surgical closure of the CCF.

Venous drainage may be anterior via the SOV or posterior via the (IPS) and superior petrosal sinus (SPS). Contralateral venous drainage may also occur via the circular sinus. The latter situation can create contralateral symptoms.

Improvement of paraplegia caused by spinal dural arteriovenous fistula by surgical obliteration more than 6 years after symptom onset
O Kaut, H Urbach and T Klockgether

University of Bonn, Bonn, Germany

Correspondence to:
Dr O Kaut, University of Bonn, Sigmund-Freud-Strasse 25, Bonn 53105, Germany; oliver.kaut@ukb.uni-bonn.de
Spinal dural arteriovenous fistulae (SDAVF) are acquired spinal vascular malformations, in which a small connection between a radicular artery and radicular vein causes venous hypertension, congestive myelopathy and infarction of the spinal cord. Here the case of a 47-year-old man is presented who had pain in his back irradiating to his right leg, numbness of his right leg as well as weakness of both legs. Urination was disturbed with detection of residual urine. Six weeks later he developed a progressive paraparesis of the legs. A T2 weighted MRI of the lower back showed intramedullary hyperintensity. A myelitis was assumed and treatment with acyclovir and dexamethasone was started. Nevertheless, he developed total paralysis of his legs. Six years later, re-evaluation of the initial MRI and a new MRI showed abnormal blood vessels on the dorsal side of the spinal cord, which had been overlooked at the first MRI examination. Spinal angiography demonstrated an arteriovenous fistula. Fistula obliteration was performed. Six months later he was able to stand with canes for 2 min and showed improvement in sensibility. The remarkable aspect of this case of SDAVF is the relevant improvement of complete paraplegia by surgical obliteration 78 months after onset of symptoms. The delay of more than 6 years between onset of first symptoms and final diagnosis underlines the difficulties in making a correct diagnosis of SDAVF. However, even after delayed diagnosis, surgical obliteration should be done, as improvement of neurological function can still be achieved.

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.

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

Abstract
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.

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.

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.

mrhodes40 wrote: 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............

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.

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.

Marie and I are thrilled to have so many medical journals on line for FREE!

cheerleader wrote: ...snip...
but as you can see, Marie and I are thrilled to have so many medical journals on line for FREE! This is only in the last ten years they've been published online, so it's good timing-
cheer

daniel wrote:Every time I search google for titles of medical papers, I get results wanting me to pay $20-30 for access to the full paper. Which sites do you use to get access to and search through the papers for free?