This article will summarise aspects of 'modern approaches to multiple sclerosis (MS)' , focusing on areas where there has been significant change in practice within the last decade, and in particular the new therapeutic agents available for relapsing MS which have posed new dilemmas for neurologists prescribing disease modifying therapies (DMT) for the condition.The basics: aetiology, pathology, and classification MS is a common cause of neurological disability in young and middle age adults, second only to trauma in the UK. Approximately 80,000 individuals in the UK have MS. MS is considered to be a predominantly autoimmune, T-cell mediated disease occurring in genetically predisposed individuals after one or more environmental 'triggers' . The identity of the trigger(s) remains unknown, but currently favoured candidates include childhood Epstein-Barr virus infection, and low vitamin D levels. The result is the onset, usually in adulthood, of lesions affecting the white matter of the central nervous system (CNS), as in the brain, spinal cord and optic nerves. The pathology is characterised by demyelination and axonal loss in the CNS white matter (Fig 1). 1 MS is classified into subtypes according to a simple, but useful scheme: it is purely clinical, based upon the observations of the patient's pattern of disease (Fig 2).Most patients present with a relapsing-remitting disease (RRMS), with relapses ('attacks') followed by recovery (partial or complete), with marked variability in both severity of relapses, and interval between them. A large proportion of patients with RRMS will eventually develop 'secondary progressive' disease (SPMS), characterised by a reduction or cessation of acute relapses but instead a gradual worsening of disability (Fig 2). The length of time spent in the relapsing phase is markedly variable, but once secondary progression is established the rate of progression is fairly predictable, and essentially irreversible. 2 There are no DMT for progressive forms of MS.
Diagnosis of multiple sclerosisThe diagnosis of MS (in its relapsing forms) has long been based upon clinical observation of 'lesions disseminated in both space and time': that is to say, symptoms and signs (consistent with inflammatory demyelination) occurring in different areas of the CNS and at different times (for example an optic neuritis in 2001 and partial myelitis in 2003). The diagnosis is usually confirmed by typical abnormalities on magnetic resonance imaging (MRI) of the brain (Fig 3) and/or cord: other investigations including lumbar puncture, evoked responses and blood testing can all be useful if the clinical or radiological presentation is atypical.The current 'McDonald criteria' 3 have introduced one significant change to the way we can confirm a diagnosis: although still crucial to demonstrate 'dissemination in time' , this can now be done radiologically rather than clinically. In other words, following a first attack of demyelination (for example optic neuritis), and with an abnormal MRI scan, the clinician and ...