Multiple Sclerosis: When the Immune System Attacks Nerve Insulation

Multiple sclerosis, usually called MS, is an immune mediated disease affecting the brain, spinal cord and optic nerves. Inflammation damages myelin, the protective insulation around nerve fibres, disrupting electrical messages. Symptoms and disease patterns vary widely, and diagnosis requires neurological assessment rather than one symptom or scan.

What multiple sclerosis is Multiple sclerosis, usually called MS, is a long term immune mediated disease of the central nervous system. The central nervous system includes the brain, spinal cord and optic nerves connecting the eyes to the brain. In MS, immune activity attacks myelin, the protective insulation surrounding many nerve fibres. This produces inflammation, demyelination and areas of tissue damage called lesions or plaques. Nerve fibres themselves can also become damaged. This helps explain why some symptoms recover while others persist or progress. What myelin normally does Myelin forms a fatty insulating layer around many nerve fibres. It allows electrical signals to travel rapidly and efficiently between the brain, spinal cord and the rest of the body. When myelin is inflamed or stripped away, nerve messages can become slower, distorted or blocked. The symptoms depend on where the affected nerve pathway is located. Damage in an optic nerve can affect sight, while spinal cord damage can alter strength, sensation or bladder control. Demyelination, repair and scarring The nervous system can sometimes repair damaged myelin through a process called remyelination. This repair may contribute to improvement after an early relapse. Repair is not always complete. Repeated inflammation can leave scarring and permanent nerve fibre loss. Over time, the nervous system may become less able to compensate for accumulated damage. Modern treatment therefore aims to prevent new inflammatory attacks rather than waiting for disability to become established. MS affects the central nervous system MS affects the central nervous system rather than primarily damaging the peripheral nerves outside the brain and spinal cord. However, central damage can still produce numbness, tingling, weakness and pain in the arms, legs or trunk. Similar symptoms can arise from trapped nerves, peripheral neuropathy, vitamin deficiency, migraine or spinal disease. The location of symptoms alone cannot establish whether the cause lies within the central or peripheral nervous system. Symptoms vary widely No two people experience MS in exactly the same way. One person may develop painful visual loss. Another may first notice numbness, imbalance, limb weakness or bladder difficulty. Symptoms can appear during distinct attacks, progress gradually or follow a combination of both patterns. Some symptoms are visible, such as walking difficulty. Others, including fatigue, pain and cognitive change, may be less apparent. Having one common MS symptom does not mean that someone has MS. Optic neuritis Optic neuritis is inflammation of an optic nerve and is a common first demyelinating presentation. Vision usually becomes blurred or dim in one eye over hours or days. Moving the affected eye often causes pain. Colours, particularly red, may appear faded or washed out. A central blurred or missing area can develop within the visual field. Most typical episodes improve, but recovery can take weeks or months and may remain incomplete. Optic neuritis can also occur in neuromyelitis optica spectrum disorder, MOG antibody disease, infection and other conditions. Double vision and eye movement problems Demyelination within brainstem pathways can disrupt coordination between the eyes. This may cause double vision, jerky eye movements or a sensation that the surroundings are moving. Double vision has many possible causes, including stroke, nerve palsy, thyroid eye disease and muscle disorders. Sudden double vision with weakness, speech change or severe imbalance requires emergency assessment. Sensory disturbance Altered sensation is a common early MS symptom. A person may experience numbness, pins and needles, burning, cold sensations or increased sensitivity to touch. Symptoms may affect one limb, both legs, part of the face or a band around the trunk. A spinal cord lesion can cause sensory symptoms that rise upwards from the feet or affect one side below a particular level. Vague brief tingling alone is common and usually has another explanation. Persistent focal neurological symptoms require assessment. Limb weakness MS can interrupt pathways controlling voluntary movement. A leg may drag, a hand may lose dexterity or both legs may feel heavy and weak. Weakness may emerge during a relapse or develop gradually during progressive disease. Pain, fatigue, poor balance and spasticity can also make movement feel weak without complete loss of muscle power. Sudden weakness must be assessed as a possible stroke or another emergency rather than presumed to be MS. Balance and coordination Lesions affecting the cerebellum, brainstem or sensory pathways can impair balance and coordination. A person may feel unsteady, veer while walking, drop objects or struggle with precise movements. Speech can become slurred or broken into unusual rhythms in some people. Vertigo may occur, although most dizziness in the general population is not caused by MS. Falls assessment, physiotherapy and suitable mobility aids can reduce injury and preserve independence. Spasticity and spasms Spasticity is increased muscle tone caused by disruption of motor pathways within the brain or spinal cord. Muscles may feel stiff, resist movement or produce sudden involuntary spasms. Spasticity can cause pain, disturb sleep and affect walking, dressing or transfers. Infection, constipation, bladder problems, skin pressure, pain and poor positioning can make it worse. Some muscle tone may help a person stand or transfer. Treatment must therefore balance reducing stiffness against preserving function. Lhermitte's sign Lhermitte's sign is a brief electric shock or buzzing sensation triggered by bending the neck forwards. The sensation travels down the neck or spine and may extend into the arms or legs. It suggests irritation of sensory pathways within the cervical spinal cord. Lhermitte's sign is associated with MS but is not specific to it. Cervical spinal disease, vitamin B12 deficiency, radiotherapy and other conditions can cause a similar sensation. Fatigue MS related fatigue is more than ordinary tiredness after activity. It can appear suddenly, feel disproportionate to exertion and interfere with thought, movement and everyday tasks. Heat, physical effort, emotional stress and poor sleep can worsen it. Fatigue should not automatically be attributed to MS. Anaemia, thyroid disease, infection, pain, depression, medicine effects and sleep disorders require consideration. Energy conservation, planned rest, exercise and management of contributing symptoms can help. Bladder dysfunction MS can disrupt communication between the brain, spinal cord and bladder. Some people develop urgency, frequency, leakage or waking repeatedly at night to pass urine. Others cannot empty the bladder fully and may develop hesitancy, a weak stream or urinary retention. Incomplete emptying can increase urinary infection risk and may require bladder scanning or specialist assessment. New bladder symptoms should not automatically be blamed on MS. Infection, diabetes, pelvic floor problems and obstruction are common alternatives. Bowel and sexual symptoms Constipation is common and may reflect reduced mobility, altered nerve control, medicines, fluid intake or diet. Bowel urgency or incontinence can also occur. Sexual symptoms may include erectile difficulty, vaginal dryness, reduced genital sensation or difficulty reaching orgasm. Fatigue, pain, mood and relationship factors can contribute alongside neurological dysfunction. These symptoms deserve direct, respectful assessment rather than being omitted from routine care. Pain and unusual sensations MS can cause neuropathic pain through damage to sensory pathways. This may feel burning, stabbing, electric or painfully sensitive to light touch. Trigeminal neuralgia causes sudden severe facial pain and can occur in MS, particularly in younger adults. Musculoskeletal pain may develop from altered walking, weakness, poor posture or spasticity. The treatment depends on the pain mechanism. Ordinary painkillers may not control neuropathic pain effectively. Thinking, memory and mood MS can affect attention, information processing speed, memory and planning. These changes are often subtle and do not mean that dementia is inevitable. Fatigue, pain, poor sleep, anxiety and depression can worsen cognitive performance. Depression and anxiety are common and should be recognised and treated. Sudden confusion or major behavioural change requires urgent assessment for infection, medicines, seizures or another neurological illness. Heat sensitivity and temporary worsening Heat can temporarily worsen existing MS symptoms by slowing conduction through previously damaged nerve pathways. This is sometimes called Uhthoff's phenomenon. Fever, hot weather, exercise or a hot bath may briefly worsen sight, weakness, fatigue or coordination. Symptoms usually improve when body temperature returns to normal. This temporary worsening does not necessarily represent new inflammation or a new relapse. Infection causing fever must still be identified and treated. What a lesion is An MS lesion is an area where inflammation, demyelination and tissue injury have occurred within the central nervous system. MRI can identify many lesions that never caused a recognised symptom. The clinical effect depends on the lesion's location, size and effect on important nerve pathways. A small strategically located lesion may cause obvious symptoms, while several other lesions may remain clinically silent. Not every bright area seen on an MRI is an MS lesion. Dissemination in space Dissemination in space means that characteristic damage has occurred in different central nervous system locations. These locations can include particular regions of the brain, spinal cord and optic nerve. Different symptoms at different times may provide clinical evidence of separate affected pathways. MRI often provides more direct evidence by showing lesions in characteristic anatomical regions. Dissemination in space is essential to the concept of MS because one isolated site may represent another condition. Dissemination in time Dissemination in time means that inflammatory disease has been active on more than one occasion. This may be shown by separate clinical attacks occurring at different times. MRI can also show old and new lesions together or demonstrate a new lesion on a later scan. Certain cerebrospinal fluid or specialised MRI findings can now provide alternative evidence in selected diagnostic pathways. The exact rules belong to specialist diagnostic criteria and should not be used as a self assessment checklist. The McDonald criteria Neurologists use the McDonald criteria to diagnose MS accurately and as early as evidence permits. NICE now refers clinicians to the 2024 revised McDonald criteria. The criteria combine the symptoms and background, neurological examination, MRI pattern and selected laboratory findings. They usually seek evidence that characteristic central nervous system damage is disseminated in space and time. Updated criteria can sometimes establish MS after one clinical attack when sufficient MRI or cerebrospinal fluid evidence is present. Before applying the criteria, the neurologist must consider and exclude a better alternative diagnosis. Clinically isolated syndrome Clinically isolated syndrome, usually called CIS, is a first episode of neurological symptoms caused by central demyelination. Examples include optic neuritis, a spinal cord syndrome or a brainstem episode lasting more than 24 hours. CIS is diagnosed when there is insufficient evidence to confirm MS under current criteria. Some people with CIS later develop further evidence and receive an MS diagnosis. Others never have another attack and never meet the criteria for MS. MRI and cerebrospinal fluid findings help estimate risk, but they cannot predict one person's future with certainty. CIS is not automatically MS The symptoms of CIS and an MS relapse can be identical. The distinction concerns the total evidence available, not whether the original episode was genuine or severe. A person with CIS needs follow up and clear instructions about reporting new neurological symptoms. Selected people at higher risk may be offered disease modifying treatment before another clinical attack occurs. The term should not be interpreted as either a definite lifelong MS diagnosis or complete reassurance. Radiologically isolated syndrome Radiologically isolated syndrome describes MRI lesions resembling MS in someone without recognised demyelinating symptoms. Many such lesions are found when imaging is performed for an unrelated reason. Some people later develop symptoms or meet MS diagnostic criteria, while others do not. A neurologist reviews whether the MRI pattern is genuinely characteristic and whether another cause is more likely. An incidental scan report alone should not be interpreted as a diagnosis of MS. Relapsing remitting MS Relapsing remitting MS causes distinct attacks of new or worsening neurological symptoms. These attacks are followed by partial or complete recovery, called remission. Symptoms may disappear, improve substantially or leave some lasting impairment. New MRI activity can occur without a noticeable relapse. Disease modifying treatment aims to reduce inflammatory attacks and silent MRI activity early in the disease course. Secondary progressive MS Secondary progressive MS develops after an earlier relapsing remitting course in some people. Neurological disability gradually worsens over time, whether or not clear relapses continue. The transition is often gradual rather than occurring on one identifiable date. Secondary progressive MS can still be described as active when relapses or new inflammatory MRI lesions occur. Some disease modifying treatments are available when there is continuing inflammatory activity. Rehabilitation and symptom management remain important regardless of inflammatory activity. Primary progressive MS Primary progressive MS causes gradual neurological worsening from the beginning rather than an initial pattern of distinct relapses and remissions. Walking, balance and leg function are commonly affected, although the presentation varies. Small temporary fluctuations can occur and do not necessarily represent relapses. Diagnosis requires evidence of sustained progression and characteristic neurological, MRI or cerebrospinal fluid findings. A disease modifying treatment is available for selected people with early primary progressive MS and inflammatory imaging activity. Active disease and progression Modern care also describes MS as active or not active, and with or without progression. Active disease means that relapses or new inflammatory MRI lesions have occurred. Progression means that disability is worsening independently of a clear relapse. Inflammation and progression can coexist rather than representing completely separate diseases. These descriptions help guide treatment and are reviewed over time. What counts as an MS relapse A relapse involves new neurological symptoms or worsening of existing symptoms lasting more than 24 hours. The person should previously have been stable for at least one month. There must be no better explanation such as infection, fever, overheating or another illness. Relapse symptoms commonly develop over hours or days rather than becoming maximal within seconds. Every suspected relapse should be reported because relapse frequency can affect disease modifying treatment decisions. Pseudo relapse and symptom fluctuation A pseudo relapse is temporary worsening of previous symptoms without new inflammatory nerve damage. Urinary or respiratory infection, fever, heat, stress, exhaustion and poor sleep can trigger this pattern. Symptoms often resemble an earlier relapse and improve after the trigger is addressed. A pseudo relapse still matters because infection or another cause may require treatment. New neurological symptoms should not automatically be dismissed as heat sensitivity or fatigue. How clinicians assess possible MS The clinician asks exactly when symptoms began, how they evolved and how long they lasted. They look for previous episodes that may have resolved, including visual loss, numbness, weakness or unexplained imbalance. Questions cover infections, fever, headache, migraine, medicines, vitamin deficiency and other autoimmune or neurological conditions. A neurological examination assesses vision, eye movements, strength, sensation, reflexes, coordination, balance and walking. The pattern determines whether neurological referral is routine or urgent. MRI in diagnosis MRI is the central imaging test used when MS is suspected. It can examine the brain, spinal cord and, in selected cases, the optic nerves. Special sequences reveal lesions in locations and shapes characteristic of demyelination. Contrast may identify areas where the blood brain barrier is currently disrupted by active inflammation. Follow up MRI can show new lesions and provide evidence that disease has been active at different times. MRI limitations MRI does not diagnose MS by itself. Migraine, ageing, vascular disease, previous infection and several inflammatory conditions can produce white matter abnormalities. The number, shape and anatomical distribution of lesions matter more than simply finding white spots. A normal brain MRI makes typical MS less likely but does not answer every spinal cord or optic nerve question. Scans require interpretation by clinicians experienced in demyelinating disease and within the clinical context. Lumbar puncture A lumbar puncture collects cerebrospinal fluid from the lower back. Cerebrospinal fluid surrounds the brain and spinal cord and can show evidence of immune activity within the central nervous system. The laboratory compares patterns in cerebrospinal fluid with a blood sample. The procedure does not sample the spinal cord itself. A lumbar puncture may help when the history or MRI does not provide enough diagnostic evidence. Oligoclonal bands Oligoclonal bands are antibody patterns produced within the central nervous system. Bands present in cerebrospinal fluid but not matched in blood support ongoing central immune activity. They are found in many people with MS and can contribute to the McDonald diagnostic pathway. They are not specific to MS. Infections and other inflammatory neurological diseases can also produce them. Their absence does not absolutely exclude MS, but an unexpected negative result may prompt careful review of the diagnosis. No one should be diagnosed from oligoclonal bands alone. Other cerebrospinal fluid markers Updated diagnostic criteria also recognise raised kappa free light chains as evidence of central immune activity in selected pathways. These proteins reflect antibody producing cell activity within the nervous system. Like oligoclonal bands, they support but do not independently establish an MS diagnosis. Availability and laboratory methods vary, so specialist interpretation is required. Other tests Blood tests help exclude conditions that can resemble MS. Possible investigations include vitamin B12, folate, thyroid, infection and autoimmune tests, selected according to the presentation. Visual evoked potentials measure how quickly visual signals reach the brain. Optical coherence tomography measures retinal nerve fibre structures and can support assessment of optic nerve damage. These tests add evidence but are not standalone diagnostic tests for MS. Important alternative diagnoses Several conditions can imitate aspects of MS. These include migraine, stroke, vitamin B12 deficiency, cervical spinal cord compression and inherited neurological disease. Neuromyelitis optica spectrum disorder and MOG antibody disease can cause optic neuritis and spinal inflammation but require different treatment. Infection, sarcoidosis, lupus, vasculitis and some cancers can also affect the central nervous system. Functional neurological disorder can produce genuine neurological symptoms through a different mechanism and may coexist with other illness. Accurate diagnosis requires actively considering these alternatives. Why one symptom is not enough Fatigue, dizziness, tingling and poor concentration are common within the general population. NICE advises against routinely suspecting MS when vague fatigue, dizziness, depression or sensory symptoms occur without focal neurological evidence. A convincing demyelinating episode usually evolves over more than 24 hours and persists for days or weeks. Brief symptoms lasting seconds may occur in established MS but rarely establish a first diagnosis by themselves. The diagnostic question concerns the neurological pattern, examination, imaging and exclusion of alternatives. The aims of treatment MS treatment has several distinct purposes. Disease modifying therapies reduce future inflammatory activity. High dose steroids can speed recovery from a significant acute relapse. Symptom treatments address fatigue, spasticity, pain, bladder dysfunction and other consequences. Rehabilitation supports mobility, independence, participation and adaptation. None of these approaches currently provides a universal cure. Disease modifying therapies Disease modifying therapies are usually shortened to DMTs. They alter immune activity to reduce inflammatory attacks within the brain, spinal cord and optic nerves. DMTs can reduce relapse frequency, reduce new MRI lesions and lower the risk of accumulating disability over time. They cannot reliably reverse established severe nerve damage. Most available DMTs treat relapsing forms of MS, while selected treatments are available for active secondary progressive or early active primary progressive disease. DMTs are not symptom medicines A DMT may be working even when an existing symptom remains unchanged. Its main purpose is to reduce future inflammatory disease rather than immediately relieve fatigue, pain or stiffness. Conversely, a symptom medicine may improve daily life without reducing new lesions or relapses. A person may need both disease modifying and symptom directed treatment. Treatment success is assessed using relapses, MRI findings, disability change, safety results and individual goals. Choosing a DMT DMTs are available as injections, tablets, infusions and time limited immune reconstitution treatments. Options include interferons, glatiramer acetate, fumarates, teriflunomide, sphingosine 1 phosphate modulators, cladribine and monoclonal antibodies. The choice depends on disease activity, likely effectiveness, safety, monitoring, route, pregnancy plans and personal preference. Some approaches begin with a lower risk medicine and escalate when disease remains active. Others use a higher efficacy medicine earlier when expected benefits justify its risks. Shared decision making with an MS specialist is essential. Early treatment Current ABN guidance supports discussing DMT treatment promptly when someone is eligible. Inflammatory activity can cause silent MRI damage before obvious disability develops. Delaying effective treatment may allow preventable lesions and relapses to accumulate. Early treatment does not guarantee that progression will never occur. The purpose is to improve the probability of better long term disease control. Monitoring DMT safety DMTs have different effects on infection risk, blood cells, liver function and immune responses. Baseline assessment may include blood counts, liver and kidney tests, pregnancy testing and infection screening. Some treatments require tuberculosis, hepatitis, chickenpox or JC virus assessment. Vaccination should be reviewed before significant immune suppression when possible. Blood tests, clinical review and MRI monitoring continue during and sometimes after treatment. Do not stop or delay a DMT without specialist advice because some treatments can produce rebound disease activity. Rare serious treatment complications Progressive multifocal leukoencephalopathy, usually called PML, is a rare brain infection associated with particular immune suppressing treatments. Possible features include progressive weakness, visual change, altered coordination, cognitive change, speech difficulty or seizures. Other infections, MS activity and stroke can cause similar symptoms. New progressive neurological symptoms during DMT treatment require prompt specialist assessment rather than waiting for routine review. The absolute risk depends strongly on the specific treatment and individual risk factors. Treating an acute relapse Not every relapse requires steroid treatment. NICE recommends considering treatment when a relapse affects usual tasks or wellbeing. High dose methylprednisolone is the standard steroid treatment, usually given as tablets over several days. Intravenous treatment may be used when oral treatment fails, is not tolerated or hospital monitoring is needed. Infection, particularly urinary or respiratory infection, should be excluded before a relapse is confirmed. Steroids should not be kept at home for unsupervised future relapses. What steroids can and cannot do Steroids reduce inflammation and can speed recovery from a relapse. They do not cure MS and do not prevent future relapses. They do not usually improve the final long term recovery achieved after that relapse. Mild sensory symptoms or fatigue alone may not justify the risks of treatment. Possible short term effects include insomnia, mood change, agitation, indigestion and raised blood glucose. Repeated courses contribute to infection, osteoporosis and other steroid related harm. Rehabilitation after a relapse Recovery may require more than medication. Physiotherapy can address weakness, balance, mobility and deconditioning. Occupational therapy can support daily activities, work, equipment and home adaptations. Speech and language therapy may help speech or swallowing problems. Neuropsychology or cognitive rehabilitation may help attention and processing difficulties. Severe relapses or unmet care needs may require inpatient rehabilitation or social care support. Managing fatigue The team first looks for infection, anaemia, thyroid disease, sleep problems, depression, pain and medicine effects. Energy management strategies include prioritising activities, planning rest, pacing and reducing unnecessary physical effort. Aerobic, resistance and balance exercise can improve fatigue and general health when adapted appropriately. Cognitive behavioural approaches can help people manage the practical impact of fatigue. Selected medicines may be considered by a specialist, but benefits are variable and safety requires review. No specific diet has been shown to treat MS related fatigue. Managing spasticity Management begins by treating factors that worsen spasticity, including infection, constipation, pain and skin pressure. Stretching, positioning, physiotherapy and appropriate activity are important. Oral baclofen is commonly considered first when stiffness or spasms cause pain or functional difficulty. Other medicines or specialist interventions may be used when initial treatment is ineffective. Baclofen should not be stopped suddenly because withdrawal can be dangerous. Complex spasticity requires assessment by an experienced multidisciplinary team. Managing bladder symptoms Urine testing helps identify infection when symptoms change suddenly. A bladder scan can show whether urine remains after voiding. Urgency may be managed through fluid review, bladder training, pelvic floor support and selected medicines. Incomplete emptying may require intermittent self catheterisation after specialist assessment and training. Treatment should protect kidney health, reduce infections and support sleep and participation. Persistent blood in urine, pain or recurrent infection requires investigation for other urinary disease. Managing mobility and balance Physiotherapy can improve strength, endurance, balance and confidence with movement. Walking aids, orthoses, functional electrical stimulation or wheelchairs may increase independence and safety. Using equipment does not mean that rehabilitation has failed. Falls assessment considers vision, sensation, medicines, home hazards and osteoporosis risk. Exercise is generally beneficial and does not cause MS progression. Activity plans should account for fatigue, heat sensitivity and individual ability. Managing pain and sensory symptoms Neuropathic pain may respond to medicines used for nerve pain rather than ordinary analgesics. Musculoskeletal pain requires attention to posture, movement, seating, spasticity and joint strain. Trigeminal neuralgia and painful spasms may need specific neurological treatment. New severe pain should not automatically be assumed to be MS. Chest pain, abdominal pain and painful swollen joints require assessment for common medical causes. Pregnancy and reproductive planning MS does not usually prevent pregnancy or require a particular delivery method. Pregnancy planning should include a detailed review of the current DMT and symptom medicines. Some DMTs can continue in selected circumstances, while others require planned timing, contraception or withdrawal. Stopping certain medicines abruptly can allow severe or rebound inflammatory activity. A disabling relapse can be treated with high dose methylprednisolone during pregnancy after infection is excluded. Contact the MS team before conception or promptly after an unexpected pregnancy rather than stopping treatment independently. Lifestyle and general health Smoking increases the risk of developing MS and is associated with worse disease outcomes after diagnosis. Stopping smoking supports neurological, cardiovascular, respiratory and bone health. Regular physical activity improves fitness, strength, mood and several MS symptoms. A balanced diet supports general health, but no particular diet cures MS. Vitamin D may be prescribed to correct deficiency, but NICE does not recommend it solely as an MS treatment. Vaccination decisions should consider the planned or current DMT. Ongoing review People with MS need regular comprehensive review by a coordinated multidisciplinary service. Review covers relapses, progression, MRI activity, treatment safety and new neurological symptoms. It should also address mobility, falls, fatigue, pain, cognition, mood, bladder, bowel and sexual function. Employment, driving, pregnancy plans, social care and carer needs may also be relevant. A period without relapses does not remove the need for monitoring or treatment review. Living with uncertainty The course of MS varies greatly and cannot be predicted precisely from one scan or early relapse. Some people remain independently mobile for decades. Others develop more substantial disability despite treatment. Modern DMTs and multidisciplinary care have improved long term prospects. Prognostic discussions should be individualised and avoid presenting population averages as one person's future. Support should include emotional wellbeing, work, relationships and practical independence. What this lesson should not be used for This lesson cannot diagnose MS from tingling, fatigue, an MRI report or oligoclonal bands alone. It cannot distinguish a relapse from stroke, infection, spinal compression, migraine or another neurological disease. Do not start steroids, stop a DMT or undertake treatment changes without specialist advice. Seek medical assessment for persistent focal neurological symptoms and emergency help for sudden or severe neurological change.

MS is an immune mediated demyelinating disease of the brain, spinal cord and optic nerves. Diagnosis requires a characteristic neurological pattern and evidence that central nervous system damage is distributed across locations and, in most pathways, across time. DMTs reduce future relapses and lesions but do not cure MS, while steroids mainly speed recovery from selected acute relapses.