Susceptibility-weighted imaging in the experimental autoimmune encephalomyelitis model of multiple sclerosis indicates elevated deoxyhemoglobin, iron deposition and demyelination

Abstract

SWI lesions exist in EAE mice. Many lesions seen in SWI were a result of deoxyhemoglobin in the blood, and so may indicate areas of hypoxia. A smaller number of SWI lesions coincided with parenchymal iron, demyelination, and/or inflammation.

Phase White Matter Signal Abnormalities in Patients with Clinically Isolated Syndrome and Other Neurologic Disorders

“…13 Results from the present study indicate that the specificity in differentiating patients with CIS versus those with OND is increased by the presence of multiple phase WM-SAs, even exceeding the specificity of using 11 In a recent autoimmune encephalomyelitis mouse-model study, phase WM-SAs correlated with all of these factors independently. 25 A majority of MS WM-SAs have a central vein as seen on MR venography, 36,37 and it stands to reason that some WM-SAs visible on SWI-filtered phase are the result of deoxygenated blood in those veins. The current study included a group of patients with neurologic disorders other than CIS.…”

“…SWI-filtered phase work has mostly focused on patients with MS, 11,[13][14][15]24 high-field-strength imaging, 11,13,24 or histologically validating phase WM-SAs. 11,25 Regardless of what pathology phase WM-SAs represent, it is imperative to identify whether their presence has diagnostic value. In the present study, we assessed WM-SAs visible on T2WI and SWI-filtered phase among patients with CIS and patients with other neurologic disorders (OND) to investigate their prevalence, location, and ability to differentiate disease groups.…”

Current Developments In Mri For Assessing Rodent Models of Multiple Sclerosis

“…SWI hypointense lesions have been demonstrated in EAE mice immunized with MOG 35--55 , complete Freud's adjuvant (CFA) and pertussis toxin (PT) [196]. These lesions were more prevalent in the lumbar spinal cord and cerebellum during the peak of disease severity at around days 16--19, as well as during long--term imaging at day 30 up to 6 months ( figure 10).…”

“…In addition, some of the lesions were no longer visible following perfusion; the percentages of the remaining lesions after perfusion were 60.1 % and 46.6% in the spinal cord and cerebellum respectively. This could be an indicator of the role of deoxyhemoglobin in the lumen vessels, in which they would have disappeared in ex--vivo imaging [196]. Histopathology analyses of SWI hypointense lesions revealed iron deposition, inflammation and demyelination within the white matter of the lumbar spinal cord, and inflammatory perivascular cuffs within the white matter of the cerebellum [196].…”

“…This could be an indicator of the role of deoxyhemoglobin in the lumen vessels, in which they would have disappeared in ex--vivo imaging [196]. Histopathology analyses of SWI hypointense lesions revealed iron deposition, inflammation and demyelination within the white matter of the lumbar spinal cord, and inflammatory perivascular cuffs within the white matter of the cerebellum [196]. [196].…”