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Multiple sclerosis (MS): causes, symptoms, therapy

by Josephine Andrews
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Multiple sclerosis (MS, encephalomyelitis disseminata) is a chronic inflammation of the nervous system. Nerve structures are destroyed, which leads to a wide variety of symptoms. The disease often progresses in phases and cannot be cured. However, their progression can usually be slowed down with medication. Read more about the autoimmune disease multiple sclerosis, its causes, symptoms and treatment.

ICD codes for this disease:

ICD codes are internationally valid codes for medical diagnoses. They can be found, for example, in doctor’s letters or on certificates of incapacity for work.

H46 G35

quick overview

  • What is Multiple Sclerosis (MS)? A chronic inflammatory, non-contagious disease of the central nervous system ( brain and spinal cord).
  • Causes: MS is considered an autoimmune disease, the development of which is probably due to several factors (genetic predisposition, infections, smoking, lack of vitamin D , etc.).
  • Symptoms: eg visual disturbances , sensory disturbances (such as tingling), painful paralysis, gait disturbances, persistent tiredness and rapid exhaustion, bladder emptying disorders, sexual dysfunction, concentration problems
  • Examinations: Collection of the medical history, physical and neurological examination, magnetic resonance imaging (MRT), CSF diagnostics, blood and urine tests, if necessary evoked potentials
  • Treatment: Medication (for relapse therapy and for course therapy), symptomatic therapy measures and rehabilitation ( physiotherapy , ergotherapy , psychotherapy , etc.)
  • Prognosis: MS cannot be cured, but its course can be positively influenced by correct and consistent treatment (fewer flare-ups, slower progression of the disease, improved quality of life).

What is multiple sclerosis?

Multiple sclerosis (MS) is a chronic disease of the central nervous system (CNS: spinal cord and brain, including the optic nerve ). It is characterized by relapsing or continuous foci of inflammation in the CNS. Various symptoms are the result, for example visual and sensory disturbances, pain or paralysis. There is currently no cure for multiple sclerosis. The course of the disease can be favorably influenced with medication.

Multiple sclerosis – progressive forms

There are three forms of MS:

  • Relapsing -remitting MS ( RRMS): It is the most common form. The MS symptoms appear here in phases; between the episodes they regress completely or incompletely.
  • Primary progressive MS ( primary progressive MS , PPMS): The disease progresses steadily from the start – the symptoms increase continuously. However, isolated flare-ups can also occur.
  • Secondary progressive MS ( SPMS ): It develops from relapsing-remitting MS. This means: after an initial relapsing course, the symptoms finally progressively increase (as with PPMS) – with or without patch relapses.

You can read more about this in the post Multiple Sclerosis History .

Clinically Isolated Syndrome (HIS)

Doctors describe the presumed first clinical manifestation of multiple sclerosis as “clinically isolated syndrome” (CIS) – i.e. a first-time attack with neurological dysfunctions that are compatible with MS. However, because not all diagnostic criteria are met, multiple sclerosis cannot (yet) be diagnosed.

In the further course, however, this can change, i.e. the clinically isolated syndrome can turn into an actual multiple sclerosis, namely into a relapsing-remitting MS. But that doesn’t have to happen! Sometimes it stays with the one-time boost.

Multiple sclerosis: frequency

More than two million people worldwide suffer from multiple sclerosis. The distribution of the disease varies greatly from region to region. MS is most common in Europe and North America.

Multiple sclerosis usually begins in early adulthood between the ages of 20 and 40. However, it can also break out in children and adolescents as well as in older adults. By far the most common form – relapsing remitting MS – women are affected two to three times more often than men.

Multiple sclerosis: symptoms

Multiple sclerosis is also called the “disease with 1000 faces” because the symptoms can vary greatly from person to person – depending on which nerve structures are affected by the damage.

Most patients initially present with only a single symptom, while others have multiple MS symptoms present at the onset. Frequent first multiple sclerosis symptoms are primarily visual disturbances due to inflammation of the optic nerve (optic neuritis) and/or sensory disturbances of the skin . However, the disease can also appear for the first time with other symptoms. These first signs of multiple sclerosis can also persist as the disease progresses. In addition, other symptoms often accompany it.

Overview of the main MS symptoms

  • Visual disturbances: eg blurred vision, loss of vision and/or pain with eye movements due to inflammation of the optic nerve (optic neuritis), double vision due to impaired coordination of the eye muscles
  • Sensory disorders of the skin (sensitivity disorders) such as tingling, (painful) abnormal sensations (e.g. “pins and needles”) or numbness
  • spasmodic, painful paralysis (spasticity), especially in the legs
  • Movement coordination disorders (ataxias), insecurity when walking or gripping
  • Fatigue (significant persistent weakness and rapid exhaustion)
  • Disorders of bladder and/or bowel emptying (e.g. urinary incontinence, urinary retention, constipation )
  • “slurred” speech
  • dysphagia
  • Involuntary, rhythmic trembling of body parts during purposeful, conscious movements (intention tremor), eg hand trembling when reaching for a glass
  • involuntary, rhythmic eye trembling (nystagmus)
  • cognitive disorders: decreased attention, problems concentrating, impaired short-term memory
  • sexual dysfunctions such as ejaculation problems and impotence in men, orgasm problems in women, decreasing sexual desire ( loss of libido ) in both sexes
  • Pain, e.g. headache , nerve pain (e.g. in the form of trigeminal neuralgia ), back pain
  • dizziness
  • depressed mood, depression

In many cases, exposure to intense heat (such as very hot weather, a fever , a hot bath) temporarily worsens MS symptoms. Doctors refer to this as the Uhthoff phenomenon.

MS relapse

Most patients experience MS symptoms in episodes. An MS flare is defined as an onset of new or a reactivation of previously onset neurological dysfunction, reported subjectively (by the patient) or ascertained objectively by medical evaluation. These dysfunctions must meet the following criteria for the relapse definition:

  • They last at least 24 hours.
  • They have appeared at least 30 days after the onset of the last flare-up.
  • The symptoms were not caused by a change in body temperature (Uhthoff’s phenomenon), infection, or any other physical or organic cause.

Multiple sclerosis: causes

Multiple sclerosis is generally classified as an autoimmune disease . These are diseases in which defense cells of the immune system attack the body’s own tissue due to a malfunction.

In the case of MS, the attack is directed against the central nervous system. Defense cells – especially T-lymphocytes , but also B-lymphocytes – cause inflammation in the area of ​​the nerve cells. The inflammatory damage mainly affects the white matter, which contains the nerve fibers. But the gray matter can also be damaged, especially as the disease progresses. That’s where the nerve cell bodies are.

In multiple sclerosis, the affected nerve cell extensions in the white matter usually lose their myelin sheaths (marrow sheaths). These “covers” enclose sections of the individual nerve fibers in the brain and spinal cord. They serve as electrical insulation and at the same time enable faster excitation transmission.

Experts assume that in MS, among other things, certain proteins on the surface of the myelin sheaths are attacked by the autoantibodies. The inflammatory processes triggered in this way gradually destroy the myelin sheath, which is referred to as demyelination or demyelination . The nerve process itself (axon) is also damaged. Researchers have also discovered that in some cases the extension of a nerve cell can be directly damaged. The myelin sheath is still intact.

Nerve cells in comparison – healthy and MS nerve cells
In multiple sclerosis, the nerve sheaths are so damaged that the nerve fibers are partially exposed. This leads to disrupted stimulus transmission.

Over time, MS patients develop numerous (multiple) areas of myelin damage and subsequent scarring (sclerosis) in the brain and spinal cord. These areas are called plaques.

The affected nerve fibers can no longer transmit nerve signals properly – nerve failures occur. These can be very diverse – depending on where in the CNS the foci of inflammation occur. That is why multiple sclerosis is also called ” encephalomyelitis disseminata “. The word “disseminata” means “scattered”, while the term “encephalomyelitis” refers to the basic processes of the disease: “enkephalos” stands for brain, “myelon” for spinal cord and the suffix “-itis” for “inflammation”.

What triggers the autoimmune response in MS?

But why does the immune system get so confused in MS that it attacks its own nerve tissue? The experts don’t know for sure. Presumably, several factors come together in those affected that together trigger the disease ( multifactorial pathogenesis ). The exact interaction of the various factors has not yet been clarified. Experts are currently assuming a genetic predisposition, on the basis of which certain environmental factors can lead to the outbreak of the disease.

genetic factors

Various observations point to a genetic component in the development of multiple sclerosis:

On the one hand, multiple sclerosis occurs more frequently in some families: first-degree relatives (eg mother, son) of MS patients have an increased risk of also developing the chronic nerve disease.

On the other hand, certain genetic constellations appear to be associated with the occurrence of MS. The focus here is particularly on the human leukocyte antigens (HLA). They play a role in immune defense. All other genetic risk factors that have so far been associated with multiple sclerosis are also genes of the immune system.

So to some extent, multiple sclerosis can be heritable – but it’s not the disease itself that’s inherited, it’s the tendency to develop MS. Experts suspect that the disease can only break out in combination with other factors (above all environmental factors such as infections).


Infections (particularly viral and bacterial ) may be involved in the onset of multiple sclerosis. There are corresponding indications, in particular, for the Epstein-Barr virus (EBV) – a representative of the herpes viruses that causes glandular fever .

How exactly an infection with EBV (or other pathogens) could contribute to the development of MS is not yet known. In general, it is possible that the reactions of the immune system to an infection can trigger the development of MS in people who are predisposed to it.

lifestyle and environment

Environmental factors or certain lifestyle factors may also contribute to the development of multiple sclerosis. However, a “bad”, unhealthy lifestyle alone cannot trigger multiple sclerosis.

A critical environmental factor in MS disease appears to be smoking . Smokers have a higher risk of developing multiple sclerosis than non-smokers. In addition, nicotine consumption seems to worsen the course of the disease.

Scientists are also discussing a lack of vitamin D – the “sunshine vitamin” – as a possible risk factor for multiple sclerosis. This suspicion is based on the observation that there is obviously a connection between MS and geographical latitude : the further one moves away from the equator (towards the north or south pole), the more frequently multiple sclerosis occurs in the population. This could be due to decreasing sun exposure: the further away from the equator, the less intense the sun’s rays – and the less sun falls on the skin, the less vitamin D can be produced in the skin.

Other factors

Apparently, gender also plays a role in the development of the disease. Women get multiple sclerosis more often than men. It is not yet known why this is so.

According to research, a high-fat “Western” diet and the associated obesity increase the risk of MS. In addition, increased salt intake and the intestinal flora are discussed as other possible influencing factors on the development of multiple sclerosis .

Ethnicity also seems to have an influence: for example, multiple sclerosis is significantly more common among whites than among other ethnic groups Black males living in the United States are less likely to develop MS than white American males, but more so than black males in Africa. Here again the influence of geographical latitude seems to come into play.

Living with Multiple Sclerosis

As a chronic and serious disease, multiple sclerosis poses many challenges for patients and their families. The disease can affect all areas of life – from partnership, sexuality and family planning to social life and hobbies to training and work.

Can you have children with multiple sclerosis? Are holiday trips possible despite MS? Should your own boss be informed about the illness or should it not? Which jobs are cheap, which rather unfavorable? These and many other questions concern MS patients.

You can read more about how multiple sclerosis affects the everyday life of those affected and how to deal with it in the article Living with multiple sclerosis .

Multiple Sclerosis: Examinations and Diagnosis

Multiple sclerosis is not easy to diagnose : on the one hand, the symptoms are very varied. On the other hand, there are no symptoms that only occur with MS, but most complaints can also have other causes (e.g. circulatory disorders in the brain).

MS is a diagnosis of exclusion : the diagnosis “multiple sclerosis” can only be made if no better explanation can be found for the symptoms that occur or for clinical examination findings (such as spatially distributed foci of inflammation in the CNS).

In order to clarify this, various investigation steps are necessary. Necessary or possible are:

  • Medical history collection
  • neurological examination
  • Magnetic resonance imaging (magnetic resonance imaging, MRI)
  • Examination of the cerebrospinal fluid (liquor diagnostics)
  • neurophysiological investigations (evoked potentials)
  • blood and urine tests

In addition to the medical history, magnetic resonance imaging and CSF diagnostics are of particular importance for the clarification of possible multiple sclerosis. Their results allow a diagnosis of MS using the McDonald criteria , which have been revised several times since their introduction . These relate, among other things, to the number of relapses (in the case of a relapsing course of the disease) and the foci of inflammation in the CNS.

In some cases, neurophysiological examinations (evoked potentials) are also useful. Blood and urine tests are mainly used to rule out other causes of the symptoms and inflammation in the nervous system.

The first point of contact if multiple sclerosis is suspected is the general practitioner. If necessary, he will refer you to a specialist, usually a neurologist.

medical history

The first step towards multiple sclerosis diagnosis is a detailed discussion between the doctor and you as the patient to collect your medical history (anamnesis). For example, the doctor asks:

  • What complaints do you have exactly?
  • When did you first notice the individual symptoms?
  • Have the symptoms changed in any way since the beginning (e.g. increased steadily or decreased in the meantime)?
  • Do you or your close relatives suffer from an autoimmune disease?
  • Are there cases of multiple sclerosis in your family?

Tell the doctor about any complaints you remember – even if you think they are harmless and/or a symptom has long since disappeared. Sometimes you can identify symptoms that were months or even years ago as the first signs of multiple sclerosis. For example, some MS patients recall having a “strange feeling” in an arm or leg for a few days to weeks – a possible indication of a focus of inflammation in the spinal cord area.

Don’t be afraid to tell them about any sexual dysfunction or problems with bladder or bowel movements. This information is important for the doctor! The more complete and precise your descriptions are, the faster he can assess whether multiple sclerosis is actually the cause of your symptoms.

Neurological examination

The anamnesis interview is followed by a detailed physical neurological examination. Its primary purpose is to check the functioning of your brain and nerves. Among other things, the focus is on:

  • Function of eyes and cranial nerves
  • Sensation of touch, pain and temperature
  • muscle strength and muscle tension
  • coordination and movement
  • Interaction of the nerve conduction for the urinary bladder , rectum and sexual organs
  • Reflexes (e.g. absent abdominal skin reflexes are a common MS sign)

The various parameters are determined and documented in a standardized manner. The “Expanded Disability Status Scale” (EDSS) is often used . With this scale, the degree of disability in multiple sclerosis can be systematically recorded with regard to the walking distance and in eight functional systems ( cerebellum , brain stem, visual disorders, etc.).

Another rating system for neurological deficits in multiple sclerosis is the Multiple Sclerosis Functional Composite Scale (MSFC) . For example, doctors test arm function using a timed pegboard test (“9-hole-peg test”) and the ability to walk a short distance (“timed 25 foot walk”).

Magnetic resonance imaging (MRI)

Magnetic resonance imaging (magnetic resonance imaging, MRI) is very important if multiple sclerosis is suspected. With the help of a contrast medium that is injected into a vein at the beginning of the examination, active foci of inflammation in your brain and/or spinal cord can be visualized on the MRI images.

In the case of relapsing MS, the diagnostic criteria require that these foci of inflammation occur in a spatially and temporally dispersed manner (disseminated), i.e. there must be foci of inflammation in more than one location in the CNS, and new such foci must arise as the disease progresses.

The second criterion – i.e. the temporal distribution (temporal dissemination) of the foci of inflammation – is not only considered to be fulfilled by the corresponding image evidence using MRI. Instead, the detection of certain protein patterns in the cerebrospinal fluid is sufficient (CSF diagnostics – see below).

If MS-typical changes in the CNS can be detected by means of magnetic resonance imaging without the patient showing clinical symptoms of the nerve disease, this is referred to as radiologically isolated syndrome (RIS). It’s not multiple sclerosis!

CSF diagnostics

Another important step on the way to the diagnosis “multiple sclerosis” is the examination of the cerebrospinal fluid ( liquor ). To do this, the doctor carefully sticks a fine hollow needle into the spinal cord canal ( lumbar puncture ) under local anesthesia in order to take a small sample of the cerebrospinal fluid. It is analyzed in more detail in the laboratory (liquor diagnostics):

Chronic inflammatory processes in the central nervous system, such as those that occur in multiple sclerosis, lead to various abnormalities in the cerebrospinal fluid. This includes, among other things, the detection of certain protein patterns, so-called oligoclonal bands (OKB).

CSF diagnostics can also be used to clarify whether the inflammation in the nervous system is possibly caused by germs (such as the borreliosis pathogen) and not by multiple sclerosis.

Neurophysiological Examination

Neurophysiological examinations can be helpful to detect clinically undetectable damage in the central nervous system and to objectively record existing symptoms. This is possible via the so-called evoked potentials. These allow a statement about the excitation transmission to the central nervous system.

To do this, doctors measure electrical voltage differences that occur when certain nerve tracts are stimulated in a targeted manner. The detection takes place using electrodes, mostly by EEG (electroencephalography). The following evoked potentials can be helpful in the context of MS diagnostics:

>> Visual Evoked Potentials (VEP) : The retina is stimulated to assess the visual pathway in the brain . To do this, look at a chessboard pattern on a monitor, for example, whose fields appear in different brightnesses in quick succession. Meanwhile, the potentials triggered in this way and transmitted via the optic nerve and visual pathway are derived and recorded by electrodes on your head.

>> Somatosensitive Evoked Potentials (SSEP) : The doctor stimulates sensitive nerves (e.g. for tactile sensitivity) in your skin with the help of an electric current.

>> Motor evoked potentials (MEP) : Motor nerve pathways in the CNS are stimulated via a special magnetic stimulator in order to trigger twitches of tuned muscles. Attached electrodes measure this motor response. The time that elapses between stimulation and motor response provides information about the functional status of the tested nerve tracts. Since a magnetic field is used here to stimulate the nerves, doctors also speak of transcranial magnetic stimulation.

>> Acoustically evoked potentials (AEP) : This measurement can also be useful in the case of multiple sclerosis. Sounds are played to you through headphones. Doctors then use electrodes to measure how quickly these acoustic stimuli are transmitted to the brain.

blood and urine tests

As mentioned above, blood and urine tests are carried out as part of MS diagnostics primarily to reveal differential diagnoses, i.e. to reveal other possible causes for the symptoms and inflammation in the central nervous system that occur.

The following parameters may be of interest in the blood analysis:

Urine tests can also be informative for clarifying a suspected multiple sclerosis.

Sometimes it can take weeks, months or even years before the multiple sclerosis diagnosis is definitely established. The search for the “disease with 1000 names” is like a puzzle: the more pieces (findings) that fit together, the more certain it is that you actually have MS.

Multiple sclerosis: therapy

Multiple sclerosis therapy is based on various pillars:

  • Relapse therapy : This refers to the acute treatment of MS relapses, preferably with glucocorticoids (“cortisone”). Alternatively, a type of blood washing called plasmapheresis or immune adsorption is sometimes helpful.
  • Course-modifying therapy (basic therapy, immunotherapy): Here, an attempt is made to positively influence the course of multiple sclerosis through the long-term use of certain drugs (immunotherapeutic agents).
  • Symptomatic therapy : This includes measures to relieve various MS symptoms, for example physiotherapy and, if necessary, antispasmodic medication for painful muscle spasms.
  • Rehabilitation procedures : The aim of rehabilitation for multiple sclerosis is to enable those affected to return to their family, professional and social life.

In order to achieve the therapy goals, multiple sclerosis patients are treated by many different therapists and medical specialties. In addition to various doctors (neurologists, ophthalmologists, urologists, general practitioners, etc.) , the treatment team for MS can also include, for example, psychologists, physiotherapists, occupational therapists, speech therapists, nursing staff and/or social workers. The individual needs of a patient are decisive when putting together the treatment team and therapy plan.

Multiple sclerosis: relapse therapy

An MS flare-up should be started as soon as possible after the onset of symptoms. The treatment of choice is the administration of “cortisone” (glucocorticoid, corticosteroid). Alternatively, plasmapheresis is performed in certain cases.

cortisone therapy

As a standard, high- dose cortisone therapy (cortisone shock therapy, cortisone pulse therapy) is carried out over three to five days for MS flare -up therapy. Methylprednisolone is most commonly given as an infusion directly into a vein (intravenously) at a dosage of 500 to 1000 milligrams per day. The cortisone should preferably be given in one dose in the morning because it can cause insomnia.

If intravenous cortisone administration is not possible for an MS patient, one can switch to cortisone tablets.

The cortisone shock therapy can shorten the duration of the relapse and promote the remission of the symptoms. If it works insufficiently, experts recommend increasing (escalating) the therapy :

Ultra-high cortisone doses of up to 2000 mg/day for three to five days are possible. Depending on the severity and duration of the symptoms, plasmapheresis or immune adsorption (see below) can be considered as an alternative or subsequently.

Side effects :

In addition to the sleep disorders mentioned above, possible side effects of cortisone shock therapy for multiple sclerosis include slight mood changes, upset stomach, facial flushing and weight gain .

Plasmapheresis or immune adsorption

A so-called plasmapheresis (PE) or immune adsorption (IA) can be considered if:

  • Disabling neurological functional disorders persist after completion of the cortisone shock therapy or
  • progressive, particularly severe MS flare-ups occur during cortisone shock therapy.

Plasmapheresis or IA is a type of blood washing . Using a special device, blood is drawn out of the patient’s body via a catheter, filtered, and then returned to the body. The purpose of filtering is to remove immunoglobulins from the blood, which are responsible for the inflammatory process during an MS attack.

The difference between plasmapheresis and immunoadsorption:

During plasmapheresis , non-specific plasma (including the immunoglobulins it contains) is filtered out of the patient’s bloodstream and replaced with a protein solution (administering albumin). In contrast, with immunoadsorption , only the immunoglobulins responsible for the inflammatory processes are “fished out” of the patient’s blood. In both cases, the “blood wash” is repeated several times.

It is unclear whether one method is superior to the other or both are equally effective for MS patients.

Plasmapheresis or immune adsorption should be carried out on an inpatient basis in specialized MS centers. It should be done in the first six to eight weeks after the onset of an MS flare-up. However, the best possible period has not yet been clarified in scientific studies. Under certain circumstances, PE/IA can also be considered at an earlier point in time, for example when ultra-high-dose cortisone infusions are not possible in an MS patient.

Side effects and complications of plasmapheresis (PE) or immune adsorption (IA) are, for example:

  • Blood pressure regulation disorders
  • kidney damage
  • Tetany symptoms (= motor disorders and sensitivity caused by overexcitable muscles, such as muscle cramps, tingling and other abnormal sensations), caused by a disturbed balance of blood salts (electrolytes) [in PE]
  • Coagulation disorders [esp. with PE]
  • Side effects and complications of a possibly necessary medicinal “blood thinning” (anticoagulation) such as increased tendency to bleed
  • allergic reactions (e.g. to the added albumin in PE or to the membranes used to filter the blood)
  • mechanical irritation or complications from using large catheters (e.g. bleeding or clotting)
  • Infections in the area of ​​catheter access (up to ” blood poisoning ” = sepsis)
  • very rare: pulmonary edema / transfusion-related active lung failure [in PE]

Multiple sclerosis: course-modifying therapy

A course-modifying therapy (immunotherapy, basic therapy, course therapy) consists of the long-term administration of so-called immunotherapeutic agents . These include active ingredients that suppress the activity of the immune system (immunosuppressants) or can specifically change immune reactions (immunomodulators).

Immunotherapy cannot cure multiple sclerosis, but it can have a positive effect on the course. It shows the greatest effect in relapsing MS, i.e. in relapsing remitting MS (RRMS) and active secondary progressive MS (active SPMS). “Active” refers to the occurrence of relapses and/or new or increasing damage caused by inflammation in the CNS. In these cases, therapy with MS immunotherapeutics can reduce the rate of relapses and counteract progressive disabilities caused by relapses.

Immunotherapy is less effective in non-active SPMS and in primary progressive MS (PPMS). However, the use of certain immunotherapy drugs can sometimes be helpful. Read more about this below.

Types of immunotherapy drugs

The following immunotherapeutic agents are currently used to treat multiple sclerosis:

  • Beta interferons (incl. peg interferon)
  • glatiramer acetate
  • dimethyl fumarate
  • teriflunomide
  • S1P receptor modulators: fingolimod, siponimod, ozanimod, ponesimod (no approval for MS in Switzerland)
  • cladribine
  • Natalizumab
  • Ocrelizumab
  • Ofatumumab
  • Rituximab (not approved for multiple sclerosis)
  • Alemtuzumab
  • other immunotherapeutics

The selection of suitable MS immunotherapeutic agents in an individual case depends on many different factors such as the course of multiple sclerosis, the disease activity and any previous treatments with immunotherapeutic agents. Individual factors also play a role, for example how old a patient is, how well he/she tolerates a medication and whether there is a specific concomitant disease or pregnancy.

The current medical guideline for multiple sclerosis divides MS immunotherapeutics into three categories of effectiveness – according to their relative reduction in inflammatory activity (relapse rate, inflammatory activity in the MRI, relapse-related progression of the disease). These effectiveness categories replace the previous step-by-step scheme for MS therapy. For example, in relapsing-remitting MS, which is unlikely to be highly active, Category 1 agents (such as beta interferons or dimethyl fumarate) are indicated.

Below you will find brief descriptions of the various immunotherapeutic agents:

beta interferons

Beta interferons (also interferon-beta) belong to the group of cytokines. These are signaling proteins that occur naturally in the body and can, among other things, modulate immune reactions. It has not yet been clarified exactly how beta interferons administered as medication work in multiple sclerosis.

The active ingredients are applied as an injection – depending on the preparation under the skin and/or in a muscle. The frequency of use also depends on the preparation: MS patients have to inject most preparations once or several times a week. However, a preparation is also available that only has to be injected every two weeks because the beta interferon it contains is coupled with polyethylene glycol. This pegylated interferon has a longer duration of action than unpegylated interferon.

Side effects : Flu-like symptoms are most common, especially at the beginning of therapy (e.g. headache, muscle pain, chills, fever). To prevent this, “creeping in” the therapy (slow increase in dose) and administering the injection in the evening help. In addition, taking anti-inflammatory paracetamol or ibuprofen half an hour before the injection can counteract the flu-like symptoms.

Interferon beta injections given under the skin (subcutaneously) can cause reactions at the injection site, ranging from redness, pain and itching to local inflammation and tissue death (necrosis).

In multiple sclerosis patients with a history of depression, treatment with interferon beta may increase depression.

Patients receiving interferon therapy often develop a deficiency in neutrophilic granulocytes and blood platelets as well as increased blood values ​​for transaminases.

In addition, persistent neutralizing antibodies against the drug can develop during beta interferon treatment, which can make it less effective.

glatiramer acetate

Glatiramer acetate (GLAT) is also an immunomodulator. Its mode of action is not exactly known. Various mechanisms are discussed. Among other things, GLAT could promote the formation of regulatory T-suppressor cells (a subgroup of lymphocytes ).

Depending on the dosage, GLAT is injected under the skin once a day or three times a week.

Side effects : GLAT injections very often cause local reactions at the injection site (redness, pain, wheal formation, itching). Local lipoatrophy, which is cosmetically disturbing, often occurs, i.e. the local loss of subcutaneous fatty tissue, which shows up as a dent.

In the pivotal study of the GLAT preparation, 15 percent of patients developed at least one whole-body (systemic) post-injection reaction involving vasodilatation, chest pain, shortness of breath, or palpitations immediately after a GLAT injection.

dimethyl fumarate

Dimethyl fumarate (DMF) has an immunomodulating and anti-inflammatory effect. Its exact mode of action has not yet been fully elucidated. It is known so far that dimethyl fumarate reduces, among other things, the formation of pro-inflammatory cytokines. It may also have a protective effect on nerve cells and myelin sheaths (neuro- and myelin-protective).

The active ingredient is taken twice a day as a capsule.

Side effects : The most common causes of taking DMF are itching, a feeling of heat or “flush” (skinny reddening with a feeling of heat), gastrointestinal complaints (such as diarrhea , nausea, pain in the stomach or abdomen) and a lack of lymphocytes (lymphopenia) . The reduction in these important immune cells makes sufferers more susceptible to infections.

Very rarely, this can be a so-called progressive multifocal leukoencephalopathy (PML): By the end of 2020, eleven multiple sclerosis patients under DMF therapy developed this life-threatening viral disease of the brain. PML is caused by the JC virus and has a poor prognosis. The risk of contracting it basically exists when the immune system is disturbed. This can be caused by medication (such as DMF) or illnesses such as cancer or AIDS.

Patients who take dimethyl fumarate are also more likely to get shingles. There is also an increased risk of proteinuria – increased excretion of protein in the urine.


Teriflunomide has an immunosuppressive effect. It inhibits the regeneration of an enzyme that is important for cell proliferation – the rapid growth of cells – particularly in lymphocytes. These white blood cells are involved in the abnormal immune responses in multiple sclerosis.

People with MS take teriflunomide as a pill once a day.

Side effects : Very often, teriflunomide causes an increase in certain liver values ​​(transaminases, including ALT in particular), headaches, thinning hair, diarrhea and nausea.

Typical effects of teriflunomide therapy are a reduction in white blood cells by around 15 percent and platelets by up to 10 percent. In addition, other changes in the blood picture occur as frequent side effects (lack of neutrophils, anemia). Infections, such as those of the upper respiratory tract or cold sores , also occur frequently .

Peripheral nerve disorders (peripheral neuropathies), such as carpal tunnel syndrome , occasionally develop with teriflunomide .


Fingolimod is what is known as an S1P receptor modulator: it reduces the number of lymphocytes in the blood by blocking a special receptor (sphingosine 1-phosphate receptor). As a result, fewer lymphocytes can get from the lymph nodes into the blood and thus further into the central nervous system, where they contribute to the disease process in multiple sclerosis.

The active ingredient is taken once a day as a capsule.

Side effects : Due to the mechanism of action described, a lack of lymphocytes (lymphopenia) is a typical therapeutic effect.

The most serious side effects include disturbances in the conduction of impulses in the heart , which can manifest themselves, for example, as an AV block . Therefore, patients must take the first fingolimod capsule under ECG control. This also applies if someone stopped taking fingolimod for more than 14 days after using fingolimod for more than a month and now wants to start it again.

Infections can also be serious under fingolimod: flu and sinusitis are very common, bronchitis, bran lichen (form of skin fungus) and herpes infections often develop. Cryptococcosis (a fungal infection), such as cryptococcal meningitis ( meningitis ), is sometimes also observed.

As with dimethyl fumarate, there have also been a few cases of JC virus-related brain disease, i.e. progressive multifocal leukoencephalopathy, with fingolimod (40 cases by the end of August 2020 in more than 307,000 MS patients treated with fingolimod).

Macular edema is a serious but only occasionally occurring side effect of fingolimod . This eye disease can lead to blindness if left untreated.

Another undesirable effect of fingolimod therapy is the increased risk of certain cancer tumors: for example, basal cell carcinoma (type of white skin cancer) and occasionally black skin cancer (malignant melanoma) often develop under fingolimod.

A common side effect is the increase in liver enzymes – sometimes a sign of relevant liver damage.

In addition, there were individual cases of a posterior reversible encephalopathy syndrome (neurological condition with brain swelling), a hemophagocytic syndrome (disease with an uncontrolled overshooting immune reaction) and atypical multiple sclerosis courses under fingolimod.


Like fingolimod, siponimod is a sphingosine-1-phosphate receptor modulator (S1P receptor modulator) that has received approval for MS therapy (but only for the treatment of active secondary progressive MS – see below).

Siponimod is taken in tablet form daily.

Before starting therapy, a genetic examination of the patient is necessary. Genetic factors are determined that influence the metabolism of the active substance in the body. Based on the test result, it is decided how siponimod is dosed or whether it may be given at all.

Side effects : They do not differ significantly with siponimod from those with fingolimod (cardiac side effects such as AV block, macular edema, potentially increased risk of infection, etc.).


Ozanimod is another S1P receptor modulator that can be used in MS therapy. It is taken as a capsule once a day.

Side Effects : Again, side effects are generally the same as fingolimod. However, certain undesirable effects are less common with ozanimod. In addition to pathologically elevated liver enzymes, this also includes, for example, AV blockages. Therefore, in the case of ozanimod – in contrast to fingolimod – the first intake only has to be medically monitored in MS patients with certain heart diseases.


In May 2021, a fourth S1P receptor modulator was approved in the EU for multiple sclerosis therapy: ponesimod. Like the other representatives of this drug class, it is taken once a day.

Side Effects : Some of the most common side effects include upper respiratory tract infections, elevated liver enzymes, and high blood pressure . Other undesirable effects include urinary tract infections and shortness of breath ( dyspnea ).


Cladribine is an immunosuppressive drug that was first developed (as a solution for injection) to treat a certain type of blood cancer ( hairy cell leukemia ). A few years ago it was also approved for multiple sclerosis therapy. Via various mechanisms, the active substance causes cell death (apoptosis), mainly in lymphocytes.

Cladribine therapy for multiple sclerosis consists of two therapy cycles that extend over two years. Two short-term intake phases are planned per year: In two consecutive months, the patient takes one or two cladribine tablets on four to five days.

Side effects : Very often, treatment with cladribine tablets causes a lack of lymphocytes (lymphopenia). A reduced number of neutrophils often develops. Shingles also occurs frequently, especially in connection with a lack of lymphocytes.

In studies of MS patients, severe infections also occurred more frequently with cladribine than in the placebo group (comparative patients who received a placebo = dummy drug instead of cladribine). In isolated cases, such infections led to death (about one in three patients with tuberculosis ).

In addition, clinical trials and long-term follow-up of patients treated with cladribine have been shown to develop cancerous tumors more frequently than placebo-treated patients.


The genetically engineered antibody natalizumab blocks a special protein on the cell surface, particularly in lymphocytes. As a result, the immune cells can no longer migrate into the central nervous system and trigger the inflammation that is typical of multiple sclerosis.

Natalizumab is usually given as an infusion every four weeks.

Side effects : Very common side effects are urinary tract infections, nasopharyngitis, headache, dizziness, nausea, fatigue (excessive exhaustion) and joint pain . Hives (urticaria), vomiting and feveroften developOccasionally, severe allergic reactions to the drug are observed.

Particular attention must be paid to the risk of developing progressive multifocal leukoencephalopathy (PML). By the end of August 2020, more than 800 cases of this dangerous viral brain disease had been registered in patients receiving natalizumab. Therefore, the use of this active ingredient is carefully considered and closely monitored.

Another rare infectious complication that can arise with natalizumab therapy is herpesvirus-associated infections.


Ocrelizumab is also a genetically engineered antibody and is one of the so-called anti-CD20 antibodies: it binds to a specific surface protein (CD20) of B lymphocytes, causing them to dissolve. The B lymphocytes are involved in damage to the nerve sheaths (myelin sheaths) and nerve cell processes in multiple sclerosis.

It is used in the form of infusions. Therapy begins with two infusions of 300 mg ocrelizumab 14 days apart. Thereafter, MS patients receive an infusion of 600 mg every six months.

Side effects : Infusion reactions are mentioned as the most common side effects (eg itching, rash, nausea, vomiting, headache, fever, chills, slight increase or decrease in blood pressure). They are mostly mild.

A few cases of progressive multifocal leukoencephalopathy (PML) have been observed in patients who have recently been switched to ocrelizumab. Most of these have previously been treated with natalizumab (see above).

Basically, during treatment with anti-CD-20 antibodies, attention must be paid to opportunistic infections (= infections that occur as a result of an impaired immune system) and the reactivation of hepatitis B viruses after the infection has healed.


Ofatumumab is another anti-CD20 antibody. Multiple sclerosis patients can inject the drug themselves under the skin using a pre-filled pen. The therapy is initiated with three injections at intervals of seven days. After a one-week break, the next injection follows, and then another every four weeks.

Side effects : The most common side effects of ofatumumab include upper respiratory tract infections, urinary tract infections, local reactions at the injection site (redness, pain, itching, swelling) and injection-related reactions throughout the body (fever, headache, myalgia, chills, fatigue).

As mentioned above, all anti-CD20 antibodies generally carry the risk of opportunistic infections or recurrence of a hepatitis B infection that has healed.


Rituximab is also an anti-CD20 antibody and is sometimes used in the therapy of multiple sclerosis – however, it is not approved for this area of ​​application (neither in the EU nor in Switzerland), so it is used “off label” here.

You can find out more about the use, side effects and interactions of rituximab here .


Alemtuzumab is another genetically engineered antibody that targets a specific surface protein (CD52) of lymphocytes. By binding to this protein, it triggers the dissolution of the immune cells.

The active substance is administered as an infusion – in the first year on five consecutive days and a year later on three consecutive days. If necessary, alemtuzumab can also be given a third and fourth time on three consecutive days, each time at least 12 months after the previous dose. In total, a maximum of four therapy cycles are possible.

Side effects : Alemtuzumab very often causes infusion reactions (headaches, skin reactions, fever, vomiting, etc.), infections (eg with herpes viruses) and autoimmune thyroid disorders. A common side effect is ITP (idiopathic thrombocytopenic purpura), a rare autoimmune disease. Occasionally, multiple sclerosis patients develop disorders of the white and red blood count during therapy. Autoimmune kidney disease is rare.

After new, sometimes severe side effects became known, the use of alemtuzumab was restricted and linked to certain precautionary measures. These side effects include new immune-mediated diseases (such as autoimmune hepatitis , hemophilia A) and acute cardiovascular side effects (such as heart attack, stroke, pulmonary hemorrhage), which so far have mainly occurred one to three days after an alemtuzumab infusion.

Other immunotherapeutics

>> Azathioprine : This immunosuppressant is approved for the treatment of various diseases – in the EU (but not in Switzerland) also for the treatment of multiple sclerosis. Due to the poor study situation, however, it should only be used in exceptional cases – for example if an MS patient also suffers from an illness that can be treated well with azathioprine (eg Crohn’s disease). You can read more about the effects, use and side effects of azathioprine here .

>> Mitoxantrone : This drug, which has an immunosuppressive effect, among other things, is approved in the EU and Switzerland for the treatment of multiple sclerosis. Because of the poor study situation and its high toxicity, it should only be given as a reserve drug in exceptional cases. Its most serious side effects include heart damage and an increased risk of blood cancer ( leukemia ).

>> Methotrexate : The active ingredient is used in low doses as an anti-inflammatory and immunosuppressant for various diseases. However, he is not licensed for multiple sclerosis therapy. However, methotrexate is rarely given in MS. However, this is only recommended for MS patients who also suffer from a disease that requires treatment with methotrexate due to insufficient evidence of its effectiveness and the lack of approval. You can read more about this active ingredient here .

>> Cyclophosphamide : This immunosuppressive drug is also given in rare cases for multiple sclerosis, although it is not licensed for this and its effectiveness in this disease has not been sufficiently proven. The same applies here as for methotrexate: cyclophosphamide should only be administered to MS patients who have a dual disease that needs to be treated with this drug. You can read more about cyclophosphamide here .

Immunotherapy for Primary Progressive MS (PPMS)

To date, only one drug has been approved for the treatment of primary progressive multiple sclerosis – ocrelizumab. According to the current guideline, rituximab can also be used if necessary, even if it is not approved for multiple sclerosis at all. It is therefore used here in “off label use” (= outside of its approval).

In elderly patients, the effectiveness of these two anti-CD20 antibodies decreases while the complication rate increases. According to the guideline, the use of ocrelizumab or rituximab in PPMS patients over the age of 50 should be considered very carefully – especially if no inflammatory activity in the central nervous system can be detected on the MRI.

In individual cases, however, immunotherapy can also be tried in this age group (limited to two years) if a patient’s degree of disability increases rapidly and there is a risk of loss of independence.

Immunotherapy for Secondary Progressive MS (SPMS)

Effective immunotherapeutic agents are currently only available for active SPMS – i.e. for secondary progressive MS with relapses or new inflammatory nerve damage in the MRI. According to the guideline, siponimod, beta-interferons, cladribine and the anti-CD20 antibodies ocrelizumab and rituximab can be considered for affected patients. Arguments for immunotherapy with these active substances are, for example, young age, short duration of illness and low degree of disability.

Only in exceptional cases should mitoxantrone be given to active SPMS because this active ingredient can cause significant side effects (see above).

Immunotherapy should not be started in untreated patients with inactive SPMS . Treatment with an anti-CD20 antibody can only be attempted in individual cases (initially limited to two years) if the disability is increasing rapidly and there is a risk of losing independence. Although there is no evidence that such a treatment helps here, there is no other therapy option for such patients.

Immunotherapy for Clinically Isolated Syndrome (HIS)

Immunotherapy should be given to patients who experience a first flare with symptoms of multiple sclerosis without meeting all diagnostic criteria for MS. To date, only a few beta interferons and glatiramer acetate have been approved for the treatment of such a clinically isolated syndrome (CIS).

If necessary, one can – with close monitoring of the patient – wait with immunotherapy for HIS if one can assume that the course will be mild (e.g. because the flare-up symptoms are only mildly pronounced).

duration of immunotherapy

Studies have not yet adequately investigated when immunotherapy for multiple sclerosis can or should be stopped. However, it is assumed that the inflammatory disease activity tends to decrease with increasing age or the duration of the disease – the effect of immunotherapy is reduced as a result. In addition, the risk of side effects with many immunotherapy drugs is higher the older a patient is.

Therefore, in certain cases, after a certain period of time, the doctor and patient can jointly decide to interrupt the immunotherapy on a trial basis. Such a therapy break can be considered, for example, after at least five years of administration of beta interferons or glatiramer acetate if the patient showed only low disease activity (e.g. few relapses, low inflammatory activity in the MRI) before the start of immunotherapy and there was no disease activity during therapy came.

With some other immunotherapeutic agents such as natalizumab, fingolimod or ocrelizumab – if patients do not show any disease activity – the decision to discontinue therapy should be made on an individual basis. There are no studies on this question.

The duration of therapy is limited from the outset for alemtuzumab (max. four therapy cycles) and cladribine (max. two therapy cycles). If patients show no disease activity after the end of such treatment, no other immunotherapeutic agents should initially be given. However, regular check-ups are recommended.

Other therapies

A few decades ago, researchers came up with the idea that the autoimmune disease multiple sclerosis could possibly be treated by “rebooting” the immune system with autologous stem cell therapy (autologous hematopoietic stem cell transplantation , aHSCT). Put simply, the therapy works as follows:

Blood stem cells are obtained from the body of the MS patient – that is, stem cells that produce the various blood cells (including lymphocytes). Then the patient’s immune system is destroyed with drugs (such as drugs used in chemotherapy for cancer). The patient then gets the stem cells that were removed back via an infusion. These then build a new blood-forming system – and with it a new cellular immune system.

aHSCT is said to be particularly useful in relapsing forms of multiple sclerosis with high disease activity. Several studies on autologous stem cell transplantation in multiple sclerosis are currently underway worldwide, including in Germany.

In Germany, Austria and some other EU countries, aHSCT is currently not approved for the treatment of MS, but it is in some other countries (eg Sweden). In Switzerland, aHSCT received approval for MS therapy in 2018 subject to certain conditions.

In the case of multiple sclerosis, a balanced diet is generally advisable (so far there is no evidence that certain types of diet have a positive effect). Patients should also be aware of the negative impact of being overweight and smoking.

A proven vitamin D deficiency should be compensated for in multiple sclerosis patients, for example with a vitamin D preparation . Taking such a preparation can also be considered if there is no vitamin D deficiency . However, patients should be aware that vitamin D intake has not yet been proven to have a positive effect on the course of multiple sclerosis.

Experts advise against extremely high doses of vitamin D preparations (vitamin D ultra high dose therapy) because health risks cannot be ruled out.

Multiple sclerosis: symptomatic therapy

Multiple sclerosis can cause a wide variety of symptoms (impaired bladder function, fatigue, muscle cramps, etc.). Targeted measures help to alleviate these symptoms and thus improve the quality of life of those affected. The symptomatic therapy is therefore an indispensable part of multiple sclerosis therapy. In addition to medication, it also includes non-medication measures (physiotherapy, ergotherapy, speech therapy , psychotherapy, etc.). Here are some examples:

physical therapy

Physiotherapy with its wide range of techniques and methods can help against a wide variety of MS symptoms, for example in the following cases:

Spasticity – that is, pathologically tense, stiff, cramped muscles that often hurt – are a common symptom of multiple sclerosis. Regular physical therapy can help. It is therefore a central element of the non-drug treatment of spasticity (in addition to avoiding spasticity-triggering factors).

Patients with impaired movement coordination (ataxia) also benefit from regular physiotherapy. The aim is to promote coordination, for example through coordinated gait training/standing up.

If multiple sclerosis causes disorders of the intestinal function (chronic constipation and/or fecal incontinence ), physiotherapy including pelvic floor training can be tried in addition to other non-drug methods.

It often makes sense for MS patients to do the various exercises that they train with their physiotherapist regularly at home (eg pelvic floor training or exercises to relieve muscle cramps). The therapist provides appropriate instructions for independent training.

occupational therapy

Ergotherapy wants to ensure that multiple sclerosis patients can manage their everyday life without outside help and remain independent for as long as possible. All exercises are based on the needs of the patient in everyday life.

For example, ergotherapy is recommended – in addition to physiotherapy – for impaired movement coordination ( ataxia ) and involuntary, rhythmic shaking ( tremor ). With the help of the therapist, patients can, among other things, practice normal, energy-saving movements and practice reaching for objects (such as a cup). In the case of an existing handicap, patients learn to deal with it and to avoid “substitute movements”.

If necessary, therapists also try out and train their patients in using aids such as walking frames or wrist weights (for tremors in the hands).

Occupational therapy usually cannot reverse the impairments of the body and brain. However, it helps those affected to remain independent for as long as possible. For this, people with MS need patience and have to practice – with and without a therapist.

medication for symptoms

If necessary, medication can also be used to relieve various MS symptoms – usually in addition to non-medication measures. Some examples:

  • Antispastic drugs (such as baclofen , tizanidine) for spasticity
  • Fampridine for gait disorders
  • Anticholinergics (e.g. trospium chloride, tolterodine, oxybutynin) for overactive bladder
  • Desmopressin against the urge to urinate at night (nocturia) / frequent urination with usually only small amounts of urine (pollakiuria)
  • Analgesics (painkillers), eg for headaches, nerve pain
  • PDE-5 inhibitors (such as sildenafil ) for erectile dysfunction (erectile dysfunction)
  • Antidepressants (especially SSRIs = selective serotonin reuptake inhibitors) for depressive moods

Multiple Sclerosis: Rehabilitation

While symptomatic therapy is aimed at improving individual multiple sclerosis symptoms, rehabilitation is about more – namely that MS patients can participate better in everyday life overall.

For example, attempts are made to eliminate or at least improve existing impairments in everyday activities (e.g. walking, dressing, personal hygiene). Impending impairments (e.g. at work) are to be avoided. In addition, rehabilitation for multiple sclerosis aims to promote the independence and mobility of patients and to maintain or improve their social integration (in the family, social environment and work).

Accordingly, MS patients should be offered rehabilitation in the following situations:

  • with persistent, functionally significant impairment after an MS relapse
  • if there is a risk of losing important functions and/or independence and/or a significant increase in physical or psychosomatic functional disorders during the course of the disease
  • if there is a threat of loss of social and/or professional integration
  • in functionally less affected people, to support the management of the disease and to educate the patient in a structured way about the background of the disease, the necessary therapies and possible self-help measures (psychoeducation)
  • in severely disabled MS patients with clearly defined therapy goals and the need for an interdisciplinary approach

Multi-week and multimodal

In order to be able to achieve these goals, a multi-modal rehabilitation lasting several weeks is required. “Multimodal” means that the rehabilitation program is made up of different components – individually adapted to each MS patient. Common building blocks of MS rehabilitation include:

  • physical therapy
  • occupational therapy
  • Movement and training therapies
  • speech therapy
  • Disease management techniques
  • activating therapeutic care to promote everyday skills
  • Training and information (on illness, therapies, etc.)

Outpatient or inpatient

In principle, MS rehabilitation is possible on an outpatient or inpatient basis in appropriate rehabilitation facilities. The extent of existing impairments and the individual rehabilitation goals are decisive in individual cases.

Anyone who is still sufficiently mobile and only has minor functional limitations can receive regular functional therapy on an outpatient basis. In contrast, inpatient rehabilitation is advisable for multiple sclerosis patients with moderate to severe impairments (particularly limited mobility).

Sometimes treatment in a specialist clinic for multiple sclerosis makes sense, where intensive multimodal therapy is also carried out (MS complex treatment). This is the case with complex symptoms and/or concomitant diseases that need to be medically clarified promptly and/or require further medical treatment measures (e.g. administration of medication such as baclofen directly into the spinal cord canal = intrathecal).

Multiple Sclerosis: Complementary and Alternative Cures

“Complementary” and “alternative” healing methods are not clearly and universally defined terms. In general, they are viewed as a supplement (complementary procedures) or an alternative (alternative procedures) to the conventional (orthodox) treatment of a disease.

Complementary and alternative healing methods often arouse particular interest in people with chronic diseases such as multiple sclerosis. Homeopathy, herbal medicine (phytotherapy), acupuncture – many MS patients place great hopes in these and other procedures.

The effectiveness of complementary and alternative healing methods (generally or for multiple sclerosis) is usually not scientifically proven. There are also risks associated with some methods.

Multiple sclerosis patients should therefore always first discuss with their doctor if they want to use other healing methods (i.e. complementary methods) in addition to conventional multiple sclerosis treatment. On the other hand, it is not advisable to replace conventional medical treatment with alternative healing methods.

In the following table you will find a selection of alternative/complementary procedures that are used in multiple sclerosis:

method judgement
acupuncture Very often used as a supplement (complementary) to MS therapy. Trying to use it to relieve pain, for example, can be useful.
acupressure The same applies here as for acupuncture.
amalgam removal The mercury escaping from the fillings is said to be involved in the development of MS. There is no scientific evidence for this.
Certain forms of nutrition/diets So far, no type of nutrition or diet has been proven to have a positive effect on the course and symptoms of MS. Experts generally recommend a varied, balanced diet with lots of fresh vegetables, fruit, fish and unsaturated fatty acids, but little meat and fat .
Bee venom therapy (apitherapy) Bee venom is said to trigger anti-inflammatory processes in the body. However, there is no scientific evidence of its effectiveness in MS. There is also a risk of severe allergic reactions. It is therefore considered dangerous and not advisable!
Enzyme combinations / enzyme therapy Should break down disease-causing immune complexes. However, a large-scale study could not prove any effectiveness in MS.
fresh cell therapy Risk of severe allergies (including circulatory failure) and risk of infection. It is therefore considered dangerous and not advisable!
homeopathy According to some MS patients, symptoms such as dizziness, bladder and bowel problems, concentration problems, lack of resilience and general well-being improve.
Immune augmentation (boosting the immune response) Possesses a risk of infection and allergies, and a risk of MS getting worse. So it ‘s dangerous and not advisable!
Intrathecal stem cell therapy Injection of the patient’s own stem cells into the spinal canal. Carries a risk of serious to fatal side effects. So it ‘s dangerous and not advisable!
snake venom Carries the risk of severe allergies. It is therefore considered dangerous and not advisable!
Pig brain implantation in the abdominal wall Can worsen MS, cause severe allergic reactions and cause death. So it ‘s dangerous and not advisable!
tai chi The exercises, which are carried out slowly and deliberately, can have a positive effect on some MS symptoms, eg impaired coordination of movements (ataxia).
qigong Part of Traditional Chinese Medicine (TCM). The exercises have a stress-relieving and relaxing effect, which can support MS therapy.
Hyperbaric oxygen therapy (hyperbaric oxygen) Supposed to stop the progression of MS, but this has not been proven in studies.
incense Anti-inflammatory effect. Good results, for example, in inflammatory bowel diseases and rheumatoid arthritis. But there are no studies on its effectiveness in MS.
yoga The various exercises (e.g. for movement, coordination, relaxation) can have a positive effect on symptoms such as spasticity and fatigue.

Multiple sclerosis: prognosis

Many people fear that MS will inevitably end up in a wheelchair sooner or later. Thanks to improved therapies, multiple sclerosis is taking a more favorable course in many patients today than in previous years.

The prognosis for multiple sclerosis in individual cases cannot be predicted. However, there are some clues. For example, the following factors speak for a rather unfavorable course of the disease:

  • male gender
  • later onset of illness
  • Disease onset with multiple symptoms
  • early motor symptoms (e.g. ataxia), cerebellar – i.e. affecting the cerebellum – symptoms (such as intention tremor) or sphincter symptoms (sphincter muscle symptoms such as urinary incontinence)
  • incomplete resolution of relapse symptoms
  • high thrust frequency

One thing is certain: the course of the disease can be positively influenced if the patient receives professional and consistent treatment and the support of their social environment . Equally important is the cooperation of the patient in the various therapeutic measures. However, a sense of proportion is required: If multiple sclerosis patients are too ambitious and want “too much”, their limited strength will wear out and their energy reserves will be exhausted prematurely.

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