Multiple sclerosis (Encephalomyelitis Disseminata, MS, ed)

Multiple sclerosis is a chronic inflammatory disease of the brain and/or spinal cord (central nervous system, CNS) and mainly affects young adults. It is one of the most common neurological diseases, affecting about 4/100,000 people in Germany every year.

What are the causes of multiple sclerosis?

The cause of this disease is believed to be a Autoimmune response Assumed: Inflammatory and defense cells of the body mistakenly attack the body's own structures. This leads to a degradation of the sheathing layer of nerve fibres (myelin sheaths) and to damage to the nerve fibre itself. In the affected fibres, nerve impulses are transmitted more poorly.

Exactly how multiple sclerosis develops is still not fully understood. There is much to be said for a combination of favourable hereditary factors and environmental influences that lead to a faulty reaction of the body's own defence or immune system. It is possible that several factors must be present at the same time for the disease to occur.

Is multiple sclerosis hereditary?

There are indications that hereditary factors favour the development of MS. However, MS is certainly not a "classic hereditary disease" that is passed on from parent to child. The relative risk of developing multiple sclerosis is only slightly increased in children of a parent with MS compared to the regional population.

Multiple sclerosis and environmental factors

One thing's for sure:

  • that there are areas with high MS risk in areas with low MS risk. For example, the risk of developing MS is higher in the northern hemisphere.
  • that MS is by no means a contagious disease
  • that women fall ill more often than men

is currently being discussed:

  • whether vitamin D metabolism could play a role (in childhood?)
  • viral infections contracted in childhood alter the risk of contracting the disease

Symptoms and course

Multiple sclerosis can cause very different neurological symptoms depending on the site of inflammation in the central nervous system. Possible signs are, for example, sensory disturbances, visual disturbances, bladder disturbances, dizziness or paralysis. The course of the disease also varies, so one speaks of a "relapsing-progressive" form, when individual intermittent attacks are present, the symptoms of which often improve spontaneously after a few days, but which leave a residual disturbance and can be distinguished from a "chronic progressive" form, when the symptoms deteriorate continuously slowly without relapses being evident. There is also a "relapsing-remitting" form, in which the failure symptoms of the relapse completely recover.


To confirm the diagnosis of multiple sclerosis, the doctor must consider the symptoms, course and examination results together. If the neurologist suspects multiple sclerosis on the basis of the symptoms, the medical history and his physical examination, he still has the following options to check or confirm the suspected diagnosis:

In 85 percent of patients with multiple sclerosis, brain images (MRIs) show changes that indicate inflammatory foci even in the early stages. In the advanced stages, this is the case in almost all patients.

McDonald criteria: When is the diagnosis established?

For the diagnosis doctors use the so-called McDonald criteria (current version 2010):
Accordingly, the diagnosis of multiple sclerosis is considered to be confirmed if the medical examination reveals a spatial and temporal distribution of the signs of the disease and symptoms. This can be fulfilled if a second episode of the disease occurs at least one month apart and / or a control MRI scan of the brain shows one or more new so-called foci compared to the previous scan.

MS therapy - current status and treatment/controls

McDonald criteria of 2001 and their revision of 2005 and 2010

In 2001, an international panel of experts proposed new criteria for the diagnosis of MS that emphasized the importance of imaging findings (MRI) in addition to clinical findings (McDonald criteria). Revisions were made in 2005 and 2010. These revised McDonald criteria are characterized overall by an easier diagnosis of MS. Importantly, they state that a diagnosis of MS should not be made if the pathologic findings elicited are better explained by another condition. In 2010, the McDonald criteria were revised again:

Relapsing multiple sclerosis

Drawers Objectifiable clinical manifestations Other required criteria
2 or more 2 or more none; clinical "evidence" sufficient (additional "evidence" desirable, must then be compatible with MS)
2 or more 1
  • spatial dissemination in MRI (see below for definition)
    another clinical episode
  • positive CSF findings and 2 or more MS-type lesions on MRI
1 2 or more
  • temporal dissemination in MRI (see below for definition)
  • second clinical episode
1 1
  • Spatial dissemination in MRI (see below)
  • 2 or more MS-typical lesions on MRI with positive CSF findings and temporal dissemination on MRI (see below)
  • second clinical episode
Zeiltiche Dissemination:

(a) simultaneous detection of asymptomatic gadolinium-enriching lesions and non-enriching lesions at any given time
(b) detection of a new (or gadolinium-enriching) T2 lesion at any time compared with a reference image
(c) a new clinical episode

Note: Gadolinium = contrast agent in MRT

Spatial Dissemination:

Detection of =1 T2 lesion in 2 of the following 4 regions

1. infratentorial (involving the brainstem and cerebellum)
2. juxtacortical (in the cerebrum)
3. periventricular (next to the cerebrospinal fluid chambers = ventricles) in the cerebrum
4. spinal (spinal cord)

(Swanton criteria)
In the case of spinal or brainstem symptomatology, the symptomatic lesions are not counted!

Chronic progressive multiple sclerosis

Neurological progression suggestive of MS
  • One year of disease progression (retrospectively or prospectively determined). and
  • Two out of three of the following criteria:
    • Evidence of spatial dissemination in the gehrin based on =1 T2 lesions in MS-typical regions (infratentorial, juxtacortical, periventricular).
    • Evidence of spatial dissemination of the spinal cord (=2 T2 lesions)
    • Positive CSF findings


In MS research, apart from the treatment of acute relapses, which still consists of the administration of high doses of cortisone i.v., the greatest progress in neurological therapy has been made in recent years and much more can be expected. So it's about the possibility of reducing the rate and intensity of relapses in a preventive way - in other words, a kind of "prophylaxis". Based on the fact that it is a malfunction of the immune system, i.e. an autoimmune chronic inflammatory disease, the effect of all these drugs is based on a positive effect on the immune system (with regard to MS) - they are therefore so-called "prophylactic" drugs.Immunomodulatory" acting drugs.

Treatment goal and management of relapsing-remitting MS (RRMS)

  • Generally early and target à
  • (NEDA = no evidence of disease activity) i.e. no lesions on MRI+no relapse for at least 1 year + no progression + atrophy ? = NEDA -4 → MEDA = Mininmal evidence of d acitivity)
  • Control under therapy every 3 months/1 year, then every 6 months
  • EDSS-score + other neuropsych. tests ( fatigue, cognition ...)
  • MRI initially 3/6 mo, then every 6/12 mo cranial and if necessary spinal à no foci receiving KM

Mild/moderate course → Basic therapy

  • IFN-ß (beta-interferon)
  • Dimethyl fumarate (DMF)
  • Glatimer acetate
  • Terflunomide
  • Azathioprine

The doctor calls it a "Highly active course form" if the following characteristics are observed:

after the diagnosis has been made according to Mc Donald (see above) additional:

  • 2 functionally relevant relapses within one year or
  • Initial manifestation with disabling relapse and marked lesional activity on MRI or
  • Under therapy (> 6 months) occurrence of a clin. Relapse + MRI findings
  • Strong increase in MRI activity

For this purpose, the following drugs are available as so-called "escalation therapy". These are:

  • Alemtuzumab = genetically engineered monoclonal IgG1?-antibodies,
  • Fingolimod = immunosuppressant produced by a fungus that prevents lymphocytes, which play a role in inflammation, from leaving the lymph nodes
  • Natalizumab = monoclonal antibody produced by genetic engineering,
  • Mitoxantrone = cytostatic drug that inhibits the formation of B- and T-lymphocytes

As you can easily see, there are now a number of different medications, the use of which can only be determined by a specialist with specific experience in MS.