Article Figures & Data
Figures
- Fig 1.
The normal process of leukocyte migration out of blood vessels into tissue involves interactions between leukocytes and endothelial cells including rolling (A), adhesion (B), and extravasation (C). The adhesion molecules α4β1 and α4β7 found on leukocytes are integral in the adhesion process to endothelial cells.
- Fig 2.
A, Natalizumab blocks the adhesion of leukocytes to endothelial cells by blocking the interaction of the α4-integrin subunit of α4β1 with VCAM-1 and of α4β7 with mucosal MAdCAM-1. B, This prevents autoreactive leukocytes from exiting blood vessels and entering target organs to cause inflammation.
- Fig 3.
A 27-year-old man presented with numbness and weakness of both upper extremities and the left lower extremity, with multiple enhancing MR imaging lesions. He was prescribed high-dose β interferon (Rebif) soon after his initial clinical exacerbation but was switched to glatiramer acetate 1 year later due to breakthrough radiologic disease activity. The patient developed new right-sided paresthesias 3 years after his initial presentation. The MR imaging in this figure was performed when the new symptoms developed. A, FLAIR-weighted sagittal FSE image of the brain shows patchy high-signal-intensity areas involving the corpus callosum, brain stem structures, and cerebellum. B, FLAIR-weighted axial FSE image shows multiple patchy areas of high FLAIR signal intensity involving the corpus callosum and bilateral periventricular white matter with the presence of edema around a large right periatrial lesion. C, Postcontrast T1-weighted axial FSE image shows that a majority of the larger lesions exhibit intense patchy enhancement, suggestive of active demyelination.
- Fig 4.
Within 1 month of the MR imaging shown in Fig 3, the patient was started on a course of natalizumab (Tysabri), 300 mg administered intravenously every 4 weeks. Repeat MR imaging after 6 months was performed. A, FLAIR-weighted sagittal FSE image of the brain shows improvement in the patchy high-signal-intensity area of the corpus callosum with resolution of lesions involving the brain stem structures and cerebellum. B, FLAIR-weighted axial FSE image shows marked improvement in the areas of demyelination involving the corpus callosum and bilateral periventricular white matter. C, Postcontrast T1-weighted axial FSE image shows only 1 small area of enhancement in the right periventricular white matter, with lack of enhancement of the rest of the enhancing lesions.
