Multiple sclerosis (MS) Home A-Z Health Information Health Library A-Z Multiple Sclerosis (MS) Overview MS is an inflammatory demyelinating disorder of the central nervous system (CNS). MS occurs rarely before puberty and after the age of 60 years. Peak incidence occurs between 30 and 40 years of age. The episodes are often triggered by smoking, deficiency of vitamins D or B12, and higher altitudes. Causes Exact cause is unknownMay be attributed to a combination of environmental and genetic factors Risk factors Genetics: A gene on chromosome 6p21 is associated with MS, and about 200 genes contribute to the MS riskFamily historyFemale sex Age range 20 to 40 yearsRace: White people, especially those from Northern Europe, are at the highest risk.Climate: MS is more common in temperate climates, such as Canada, the northern United States, and EuropeLow vitamin D levelsObesitySmoking; second-hand smoke exposure may be related to the risk of paediatric MS.Epstein-Barr virus (EBV)Gut dysbiosis Symptoms Symptoms depend on the structure involved in neuraxisTransverse myelitisWeakness, sensory symptomsUrinary urgency and retentionFlexor spasmsSpastic quadra or paraparesisSensory levelBrainstemAtaxiaDiplopiaDysarthriaFacial numbnessInternuclear ophthalmoplegiaGaze palsyRubral tremorCerebellumAtaxiaDysarthriaNystagmusOptic neuritisVisual lossPainful eye movementsRAPD (relative afferent pupillary defect)Impaired colour vision (Ishihara colour plates)Decreased acuityOptic atrophyCerebral hemispheres:Poor memoryDisinhibitionDementiaEpilepsy (rarely)Lhermitte’s symptom (Neck flexion causes current like sensation or tingling)Uhtoff’s phenomenon, which is worsening of symptoms, e.g. vision, when body temperature is raised due to hot shower or exerciseInternuclear ophthalmoplegia (impaired adduction on abducting the other eye) Course of disease 85% of patients experience relapse or disease remittance (RRMS), 50–60% experience the secondary progressive phase (SPMS), and 10% have primary progressive disease (PPMS) with gradual accumulation of disability. Diagnosis MRI to determine T2W high signal changes in the corpus callosum, periventricular white matter, and brainstemMcDonald criteriaEvoked responses evaluation:Visual evoked responses (VER): delayed even after the recovery of optic neuritisSomatosensory evoked potentials (SSEP)- delayed in cases of spinal cord lesions. Specialist to approach Neurologist Treatment CorticosteroidsDisease-modifying therapy (DMT) : Interferons, Glatiramer acetate, Monoclonal antibodies natalizumab, rituximab, alemtuzumabSupportive treatment for spasticity, bladder dysfunction, fatigue