Radshare is all about sharing knowledge in radiology.
Inculcating interest in students is our motto.
we strongly believe that most of the times radiologic morphology clinches a diagnosis. However there can always be histologic surprises.So all the cases published in the blog are either histologically proven or radiologically diagnostic.
Wednesday, 30 May 2012
Mid Sagittal T2 wt image: Ill defined linear mild hyperintensity in the cervical cord at the level of C2. A small well defined hyperintensity in the body of corpus callosum.
Parasagittal T2 wt image: well defined hyperintensity in fronto parietal periventricular location, perpendicular to the ventricle.
TYPICAL DAWSON'S FINGER Parasagittal T2 wt image: Oval hyperintensity in posterior parietal periventricular white matter, oriented perpendicular to ventricle
Multiple sclerosis is considered an inflammatory, autoimmune neurologic disease that is characterised by demyelination and axonal injury.
Although MS lesion plaques can be found throughout the brain, they have a predilection for periventricular white matter and tend to have an ovoid configuration with the major axes perpendicular to the ventricular surface.
At the initial stage, the lesions are typically thin and appear to be linear (Dawson’s fingers),which is probably associated with the inflammatory changes around the long axis of the medullary vein that create the dilated perivenular space.
In addition to the periventricular region, the corpus callosum,subcortical region, brain stem, U-fibers, optic nerves, and visual pathway are also regions where lesions are frequently located.
The abnormalities of the corpus callosum, U-fibers, and optic nerves, however, may allow for the differentiation of MS from cerebrovascular disease.
Although MS is a disease that predominantly affects white matter, lesions can and do occur in gray matter and are better detected on FLAIR imaging.
Optic neuritis, which appears early and may be the only presentation in the initial stage of MS, can be detected by using a fat-suppression technique combined with contrast-enhanced imaging or by using long-echo short-tau inversion recovery (STIR) imaging.
The accumulation of hypointense lesions on T1(so-called black holes) may correlate with disease progression and disability.
In the acute inflammatory phase, the lesion may disrupt the BBB, leading to gadolinium enhancement that is believed to be the first detectable event on conventional MR imaging and may last from days to weeks.
Enhancing lesions, which may vary in shape and size, usually start as homogeneous enhancing nodules and subsequently progress to ringlike enhancements.
Contrast-enhanced T1WI is now routinely used in the study of MS and provides one in vivo measure of inflammatory activity. It is able to detect disease activity 5–10 times more frequently than the clinical evaluation of relapses which suggests that most of the enhancing lesions are clinically silent.
Overall, T2 lesion load is significantly higher and enhancing T1 lesion load is lower in Secondary Progressive MS than in Relapsing Remitting MS.
Another imaging hallmark of MS is brain atrophy, which is considered to be a net accumulative disease burden as the ultimate consequence of all types of pathologic processes found in the brain.
Brain atrophy in MS usually appears as enlarged ventricles and the reduced size of the corpus callosum.
Reference: AJNR Am J Neuroradiol 27:1165–76 u Jun-Jul 2006