Posted: Wed Dec 17, 2008 7:50 pm
Here are couple of other related, non-Zamboni Pubmed abstracts:
Seven-Tesla magnetic resonance imaging: new vision of microvascular abnormalities in multiple sclerosis.
Arch Neurol. 2008 Jun;65(6):812-6.
Comment in: Arch Neurol. 2008 Nov;65(11):1547-8; author reply 1548.
Ge Y, Zohrabian VM, Grossman RI.
Department of Radiology, Center for Biomedical Imaging, New York University School of Medicine, 650 First Ave, Room 615, New York, NY 10016, USA. yulin.ge@nyumc.org
BACKGROUND: Although the role of vascular pathology in multiple sclerosis (MS) lesions was suggested long ago, the derivation of these lesions from the vasculature has been difficult to assess in vivo. Ultrahigh-field (eg, 7-T) magnetic resonance imaging (MRI) has become a tool for assessing vascular involvement in MS lesions owing to markedly increased image resolution and susceptibility contrast of venous blood.
OBJECTIVE: To describe the perivenous association of MS lesions on high-resolution and high-contrast 7-T susceptibility-sensitive MRI.
DESIGN: Case study.
SETTING: University hospital.
PATIENTS: Two women with clinically definite relapsing-remitting MS.
RESULTS: We demonstrated markedly enhanced detection of unique microvascular involvement associated with most of the visualized MS lesions with abnormal signals on and around the venous wall on 7-T compared with 3-T MRI.
CONCLUSIONS: These findings, which have never been shown on conventional fields of MRI, not only allow for direct evidence of vascular pathogenesis in MS in vivo but also have important implications for monitoring lesion activity and therapeutic response.
Raised venous pressure as a factor in multiple sclerosis.
Med Hypotheses. 2008;70(6):1112-7.
Comment in: Med Hypotheses. 2008 Oct;71(4):619.
Talbert DG.
Institute of Reproductive and Developmental Biology, Imperial College School of Medicine, Du Cane Road, London W12 ONN, United Kingdom. d.talbert@imperial.ac.uk
It is hypothesised that the inflammatory condition seen in MS and the progressive myelopathy that is being successfully halted by obliteration of dural arteriovenous fistulas (DAVFs), may actually be two sides of the same coin.
Excessive venous hypertension can stretch vein walls sufficiently to separate the tight junctions between endothelial cells forming the blood-brain-barrier (BBB). Colloids, etc., but not necessarily erythrocytes, could then pass through the exposed porous basement membranes. The resulting changes in osmotic pressure, etc. would disrupt the axon and dendrite internal transport systems, leading to their disintegration. The normal inflammatory processes which would follow, might be indistinguishable from those associated with autoimmune disease.
Ascending progressive myelopathy and disablement are associated with an intracranial DAVF when its outflow enters the spinal venous system and descends past the cervical region. This can be arrested, and some degree of recovery produced, if the DAVF can be successfully eliminated or blocked. However, if the DAVF outflow is entirely into the spine, intracranial venous pressure may be normal and so there is nothing to alert the clinician to the presence of an intracranial DAVF.
It is suggested that where spinal MS has been diagnosed from clinical observations, patients should be referred for angiological investigation to search for DAVFs within the head to identify any treatable subjects.
Seven-Tesla magnetic resonance imaging: new vision of microvascular abnormalities in multiple sclerosis.
Arch Neurol. 2008 Jun;65(6):812-6.
Comment in: Arch Neurol. 2008 Nov;65(11):1547-8; author reply 1548.
Ge Y, Zohrabian VM, Grossman RI.
Department of Radiology, Center for Biomedical Imaging, New York University School of Medicine, 650 First Ave, Room 615, New York, NY 10016, USA. yulin.ge@nyumc.org
BACKGROUND: Although the role of vascular pathology in multiple sclerosis (MS) lesions was suggested long ago, the derivation of these lesions from the vasculature has been difficult to assess in vivo. Ultrahigh-field (eg, 7-T) magnetic resonance imaging (MRI) has become a tool for assessing vascular involvement in MS lesions owing to markedly increased image resolution and susceptibility contrast of venous blood.
OBJECTIVE: To describe the perivenous association of MS lesions on high-resolution and high-contrast 7-T susceptibility-sensitive MRI.
DESIGN: Case study.
SETTING: University hospital.
PATIENTS: Two women with clinically definite relapsing-remitting MS.
RESULTS: We demonstrated markedly enhanced detection of unique microvascular involvement associated with most of the visualized MS lesions with abnormal signals on and around the venous wall on 7-T compared with 3-T MRI.
CONCLUSIONS: These findings, which have never been shown on conventional fields of MRI, not only allow for direct evidence of vascular pathogenesis in MS in vivo but also have important implications for monitoring lesion activity and therapeutic response.
Raised venous pressure as a factor in multiple sclerosis.
Med Hypotheses. 2008;70(6):1112-7.
Comment in: Med Hypotheses. 2008 Oct;71(4):619.
Talbert DG.
Institute of Reproductive and Developmental Biology, Imperial College School of Medicine, Du Cane Road, London W12 ONN, United Kingdom. d.talbert@imperial.ac.uk
It is hypothesised that the inflammatory condition seen in MS and the progressive myelopathy that is being successfully halted by obliteration of dural arteriovenous fistulas (DAVFs), may actually be two sides of the same coin.
Excessive venous hypertension can stretch vein walls sufficiently to separate the tight junctions between endothelial cells forming the blood-brain-barrier (BBB). Colloids, etc., but not necessarily erythrocytes, could then pass through the exposed porous basement membranes. The resulting changes in osmotic pressure, etc. would disrupt the axon and dendrite internal transport systems, leading to their disintegration. The normal inflammatory processes which would follow, might be indistinguishable from those associated with autoimmune disease.
Ascending progressive myelopathy and disablement are associated with an intracranial DAVF when its outflow enters the spinal venous system and descends past the cervical region. This can be arrested, and some degree of recovery produced, if the DAVF can be successfully eliminated or blocked. However, if the DAVF outflow is entirely into the spine, intracranial venous pressure may be normal and so there is nothing to alert the clinician to the presence of an intracranial DAVF.
It is suggested that where spinal MS has been diagnosed from clinical observations, patients should be referred for angiological investigation to search for DAVFs within the head to identify any treatable subjects.