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Using a philosophical approach or deductive reasoning, we challenge the dominant clinico-radiological worldview that defines multiple sclerosis (MS) as a focal inflammatory disease of the central nervous system (CNS). We provide a range of evidence to argue that the ‘real MS’ is in fact driven primarily by a smouldering pathological disease process. In natural history studies and clinical trials, relapses and focal activity revealed by magnetic resonance imaging (MRI) in MS patients on placebo or on disease-modifying therapies (DMTs) were found to be poor predictors of long-term disease evolution and were dissociated from disability outcomes. In addition, the progressive accumulation of disability in MS can occur independently of relapse activity from early in the disease course. This scenario is underpinned by a more diffuse smouldering pathological process that may affect the entire CNS. Many putative pathological drivers of smouldering MS can be potentially modified by specific therapeutic strategies, an approach that may have major implications for the management of MS patients. We hypothesise that therapeutically targeting a state of ‘no evident inflammatory disease activity’ (NEIDA) cannot sufficiently prevent disability accumulation in MS, meaning that treatment should also focus on other brain and spinal cord pathological processes contributing to the slow loss of neurological function. This should also be complemented with a holistic approach to the management of other systemic disease processes that have been shown to worsen MS outcomes.

Background Plasma exchange (PE) is increasingly undertaken in diseases involving humoral factors and is proven to be beneficial in acute demyelinating diseases. Spinal attacks in relapsing neuromyelitis optica (NMO) and in extensive transverse myelitis (ETM) – a truncated form of NMO with spinal involvement – are usually devastating. Objective We retrospectively studied the outcome of PE-treated versus steroid-only treated spinal attacks in relapsing NMO and ETM. Methods We included 96 severe spinal attacks in 43 Afro-Caribbean patients. PE was given as an add-on therapy in 29 attacks. Expanded disability status score (EDSS) was obtained before attack, during the acute and residual stage. We defined the ΔEDSS as the rise from basal to residual EDSS. Results The ΔEDSS was found to be lower in the PE-treated group (1.2 ± 1.6 vs 2.6 ± 2.3; P < 0.01). A low basal impairment is associated with a better outcome. Improvement was obtained in both NMO-IgG negative and positive NMO attacks. Minor adverse events manifested in seven PE sessions (24%). Conclusion PE appears to be a safe add-on therapy that may be employed early in severe spinal attacks in the NMO spectrum disorders in order to maximize improvement rate. PE efficiency is independent of NMO-IgG positivity.

Neuromyelitis optica (NMO) is an inflammatory demyelinating disease of the central nervous system (CNS) with a poor prognosis in terms of the optic-spinal function. Recently, a serum autoantibody (NMO-IgG) binding to the blood–brain barrier region was detected exclusively in patients with NMO and its high risk group. We treated six NMO-IgG-positive patients (all female; age 21–67 years old, median 41; three with optic neuritis and three with myelitis) who were unresponsive to high-dose intravenous methylprednisolone (HIMP), with plasma exchange (PE) (three to five exchanges, 2–3 L each). Three of the patients(one with optic neuritis and two with myelitis) showed definite functional improvement following PE. The clinical improvement started to appear after one or two exchanges, while there was little or no improvement in the other three patients. Such quick clinical responses to PE suggest a pathogenetic role of humoral immune factors in NMO, although delayed responses to the corticosteroid therapy might have contributed to the therapeutic efficacy, in part. Further clinical and in vitro studies are needed to determine whether the removal of NMO-IgG is directly relevant to the therapeutic efficacy. PE may hasten the functional recovery from corticosteroid-resistant relapses in some NMO-IgG-positive patients with NMO.