Magnetic Resonance Imaging in Multiple Sclerosis
Since its introduction to medical practice in the 1980s, magnetic resonance imaging (MRI) has become an indispensable imaging technique. It exploits differences in relaxation times (T1 and T2) between nuclei that have an odd number of nucleons (protons and neutrons) – usually hydrogen protons from water molecules present in bodily tissues. When these nuclei are subjected to a homogeneous magnetic field and stimulated by radiofrequency pulses they return to an equilibrium state at different relaxation rates generating variable resonance signals. Differences between water-containing tissues affect the relaxation rates and allow the generation of an image revealing structural differences within these tissues. Initially used for chemical and physical analyses, it rapidly evolved into a fundamental medical imaging procedure that revealed to be particularly useful in the detection of lesions of the central nervous system (CNS).1 This high-resolution technique allows detection of focal and diffuse abnormalities in the white and grey matter and has become an established tool in the diagnosis of multiple sclerosis (MS) at clinical centres worldwide. It has also proved valuable in monitoring disease activity and progression, and treatment response in the research setting.2
Gadolinium-based compounds markedly decrease the T1 relaxation time of adjacent mobile water protons. As a result, after intravenous gadolinium administration, there is a locally increased signal on T1-weighted images from CNS tissues where, normally, there is no blood brain barrier (e.g., the circumventricular organs, meninges and choroid plexus) or where it is abnormally compromised or even absent. Thisoccurs in many types of tumoural, inflammatory and infective lesions.
Longitudinal and cross-sectional magnetic resonance (MR) studies have shown that contrast-enhancement occurs in almost all new MS plaques in patients with relapsing-remitting MS (RRMS) or secondary progressive MS (SPMS). This enhancement correlates with altered blood brain barrier permeability in the setting of acute perivascular inflammation, discriminating acute active from chronic inactive lesions (see Figure 1). The gadolinium enhancement varies in size and shape, and usually lasts from a few days to weeks with an average duration of three weeks. New contrast-enhancing lesions are nearly always associated with a hyperintense lesion in the samelocation on T2-weighted images. The extent of these new T2 lesions usually contract over time (three–five months) and their intensity is reduced as oedema resolves and some tissue repair occurs, leaving a much smaller T2 permanent ‘footprint’ of the prior inflammatory event (see Figure 2).
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