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Multiple sclerosis. Contrast-enhanced MRI in patients with multiple sclerosis show that increased permeability of the blood-brain barrier commonly occurs with this disease. Lymphocyte recruitment into the brain across endothelial cells of the blood-brain barrier, which is otherwise restricted and well regulated, represents a critical event in pathogenesis of multiple sclerosis (Correale and Villa 2007). The changes in capillary permeability often precede T2-weighted MRI evidence of tissue damage. Increased gelatinase B (a type of matrix metalloproteinase) is associated with an open blood-brain barrier on MRI. Steroids may improve capillary function by reducing activity of gelatinase B.

Various inflammatory factors produced by perivascular cells in multiple sclerosis affect the permeability of the blood-brain barrier. One of these, the intercellular adhesion molecule-1, binds to its leukocyte ligands and allows activated leukocytes entry into the central nervous system. According to 1 hypothesis, pathological reflux of venous flow in the cerebral and spinal veins increases the expression of intercellular adhesion molecule-1 by the cerebrovascular endothelium, which, in turn, could lead to increased permeability of the blood-brain barrier (Simka 2009).

pathological reflux of venous flow in the cerebral and spinal veins increases the expression of intercellular adhesion molecule-1 y the cerebrovascular endothelium, which, in turn, could lead to increased permeability of the blood-brain barrier (Simka 2009).

Perhaps, in addition to or instead of pharmacotherapy, surgical correction could be an option in some anatomical variants of pathological venous outflow, such as in the localized occlusion of the azygous vein.
Hopefully, a hemodynamic approach to the multiple sclerosis pathogenesis can open a new chapter of investi- gations and treatment of this debilitating neurologic disease.

Clinical assessment of the blood-brain barrier. Two main approaches are used for studying the integrity of human blood-brain barrier in vivo: (1) structural imaging employs contrast agents that only penetrate the blood-brain barrier at sites of damage, and (2) functional imaging is used to study the transport of substances across the blood-brain barrier- both intact and damaged. Structural imaging employs contrast agents with CT scanning and is relatively insensitive. MRI with the contrast agent gadolinium is more sensitive. Hyperintense acute reperfusion injury marker (HARM) is gadolinium enhancement of cerebrospinal fluid on fluid-attenuated inversion recovery MRI and may be a useful imaging biomarker to evaluate matrix metalloproteinase-9, which may play a role in blood-brain barrier disruption after ischemic stroke (Barr et al 2010).

Cece wrote: Is HARM present in MS patients?
If MRIs with gadolinium enhancement measure blood brain barrier integrity, then the results we heard awhile back about 12 out of 13 MS patients having no enhancement on their MRIs done post-CCSVI treatment mean that we go from leaky blood-brain barriers to intact blood-brain barriers post-treatment. And that is a wonderful thing.

Post-Gd-DTPA FLAIR identification of HARM has been confirmed in subsequent studies of stroke and multiple sclerosis, identifying its utility in clinical practice as a marker of BBB disruption.

In vitro investigation of poor cerebrospinal fluid suppression on fluid-attenuated inversion recovery images in the presence of a gadolinium-based contrast agent.

Magnetic resonance imaging (MRI) blindly demonstrates a trend for fewer T2 lesions in the ITG (p = 0.081), corresponding to a 10% decrease in the ITG compared with a 23% increase in the DTG over the first 6 months of the study.