PATHOLOGY, ETIOLOGY AND EPIDEMIOLOGY
In May 1868, Jean Martin Charcot (1825–93) described ‘sclerosed plaques’ in the periventricular area, pons and spinal cord [1]. The characteristic pathological hallmark of MS is perivenular inflammatory lesions, resulting in demyelinating plaques [2]. New data shows that in patients with multiple sclerosis, mitochondrial dysfunction is at the root of pathological cascade leading to brain damage [3].
The exact etiology of MS is not fully understood, although epidemiological data suggests that genetic and environmental factors are important [4]. Genetic vulnerability is generally considered primary risk determinant [5]. The EBV infection has been proven to increase the risk of MS [6]. There is also growing evidence that lower levels of vitamin D are associated with increased risk of MS and higher activity in ongoing disease [7].
MS typically affects young and middle-aged adults, with females being 2-3 times more susceptible than males. Rarely, the disease can manifest in children and elderly. Prevalence of MS varies substantially from high number of cases in North America and Europe (>100/100,000 inhabitants) to low figures in Eastern Asia and sub-Saharan Africa (2/100,000 population) [8].
THE TYPES OF MULTIPLE SCLEROSIS
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Radiologically isolated syndrome (RIS) : MRI suspicious lesions without clinical syndromes
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Clinically isolated syndrome (CIS): The first neurological episode indicative of multiple sclerosis but still does not meet the criteria for MS diagnosis
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Relapse-remitting MS (RRMS) : the most common disease course – characterized by clearly defined attacks of new or increasing neurologic symptoms. These attacks are followed by periods of partial or complete recovery (remissions) and relapses.
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Secondary progressive MS (SRMS): Most people with RRMS will eventually transition to a secondary progressive deterioration of neurological functions after 10-15 years.
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Primary progressive MS (PRMS): PRMS is characterized by accumulation of disability without early recurrence or remission. [9].
CLINICAL FEATURE
Typical clinical features of multiple sclerosis include absence of abdominal reflexes, weakness, paresthesia, visual impairment, urinary incontinence, dysarthria. In advanced cases, progressive spastic paraparesis, sensory ataxia, cerebellar ataxia and cognitive and progressive visual failure can be present.
DIAGNOSTIC CRITERIA
Diagnosis of MS is based on clinical picture, laboratory findings and imaging methods, according to McDonald's criteria, with the last revision in 2017 (Table 1.)
IMAGING IN MULTIPLE SCLEROSIS
MR imaging plays a key role in the diagnosis and follow up of MS.
The MRI protocol used for MS imaging in our department can be found in Table 2.
TREATMENT
The treatment of MS can be divided into disease‐modifying (DMD) therapies like immunosuppressive (fingolimod, natalizumab, ocrelizumab) or immunomodulatory (such as interferon beta, glatiramer acetate, teriflunomide) and symptomatic therapies (including medication and physical interventions that address symptoms arising from damage to the CNS).
Immune reconstitution therapies (including alemtuzumab and cladribine) may be offered as short courses in order to produce lasting immunological activity – this is at present the closest possible therapy for MS.
Disease-modifying drugs are available only to patients with clinically relapsing disease and a subset of those patients with progressive disease with high levels of inflammatory disease on MRI [10].