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Imaging in multiple sclerosis and related disorders
  1. Shelley Renowden
  1. Correspondence to Dr Shelley Renowden, Department of Neuroradiology, Frenchay Hospital, NHS Trust, Bristol, UK

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Demyelinating disorders of the central nervous system (CNS) may be divided into primary (cause unknown, eg, multiple sclerosis (MS)) and secondary (eg, infective, hypoxic–ischaemic, metabolic, toxic) processes. The underlying cause damages the myelin sheath and/or oligodendrocyte. MRI is the imaging modality of choice because of its high spatial and contrast resolution, but imaging features are often non-specific.

The most common causes of multifocal white matter lesions are perivascular spaces (not discussed here), ischaemia (small vessel disease) and MS. Small vessel disease is much more common than MS, hence, their distinguishing features are discussed first.

Small vessel disease

Vascular white matter lesions are age-related, asymptomatic foci of ischaemic demyelination (unidentified bright objects or ‘UBOs’), myelin pallor or gliosis. They are uncommon in those below age 40 years (figure 1), thereafter, increasing in frequency with age. These white matter changes occur in 5–10% of those aged 20–40 years. Most patients are neurologically normal. At all ages, the incidence and lesion load increase with cardiovascular risk factors (figure 2). The white matter lesions are small and have high T2 signal but differ from MS plaques because of their irregular shape, poor definition and peripheral location and are most common in the frontal and parietal lobes. Posterior fossa lesions are uncommon, and callosal lesions are rare because of a dual blood supply.

Figure 1

T2W axial MR image of a neurologically normal 45-year-old shows small ill-defined foci of high T2 signal in the frontal subcortical white matter. These are almost certainly age-related changes of no significance.

Figure 2

T2W axial (A) and axial apparent diffusion coefficient MR images (B) in a 63-year-old man with sudden onset right hemiparesis, showing multiple small peripheral, poorly defined foci of high T2 signal in the frontal lobes and adjacent to the trigones of both lateral ventricles—more numerous than in the patient in figure 1. He is …

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