The most frequent demyelinating disease. There are about 2.1 million people affected. The incidence of MS is 2-150:100000 depending on the country.
Etiology and pathophysiology
It’s likely that MS is an autoimmune disease, which attacks people with genetic predisposition after an exposure to specific environmental factors. The immune system attacks the structures of CNS which is the cause of damage. Typically, lesions are localized in the white matter of the brain, periventricularly, in the brainstem, basal ganglia and in the spinal cord, as also lesions are found in optic nerves.
Damage to nervous system in MS is due to destruction of oligodendrocytes – the cells that produce myelin. There is a concurrent process of inflammation simultaneously with demyelization. T lymphocytes are the main cells witch participate in the inflammatory process, they are crossing the blood-brain barrier and trigger the inflammation of the CNS’s myelin. A lot of different cytokines and antibodies are participating in the inflammatory process. There is evidence of concurrent activation of B lymphocytes in the process of MS.
Diagnosis of MS is relatively complicated because symptoms and signs are very similar to other demyelinating diseases. The specific diagnostic criteria are developed (McDonald criteria) and reviewed in 2010. The criteria are based on clinical, radiological and laboratory findings.
Radiological criteria are based on the dissemination of lesions in time and localization, so the diagnosis can’t be made after the first episode of the disease. Sometimes repeated MRI is needed to make the MS diagnosis. There are oligoclonal (IgG) bands of antibodies found in cerebrospinal liquor of patient if there is a chronic inflammatory process. 85% of patients with MS have positive oligoclonal antibodies in their blood.
Symptoms of MS depend on the localization of lesions in the CNS. Internuclear ophthalmoplegia, Lermitte’s sign, wire-type sensory disturbances, pyramidal signs, neurogenic bladder and optic neuritis are the classical signs of MS. The occurrence of the symptoms of MS is unpredictable usually takes about 24 hours. Reduction of symptoms takes a lot of time and remissions are not complete usually. Every infection can provoke a pseudorelapse.
MS is divided to categories by type of progression of the disease. The type of progression is diagnosed clinically and further therapeutic decisions are based on the type of disease.
The types of progression are:
- Relapsing-remitting MS (RRMS) – Patients suffer from relapses with complete/non-complete resolution of symptoms. There are no signs between relapses. (50% of patients convert to the secondary progressive type)
- Secondary progressive MS – starts like RRMS but there is stable progression of the disease and symptoms between relapses.
- Primary progressive MS – there are no remissions from the first sign. Approximately 15% of patients.
Multiple sclerosis is not a fully curable disease.
The treatment of MS consists of specific therapy of relapses, immunomodulatory therapy, symptomatic treatment and rehabilitation.
The main goal of the treatment is to reduce inflammatory process and demyelinization, make relapses to occur less frequently and to reduce the disability.
Methylprednisolon 1000mg/day in 3-5 days is used to treat acute relapse of MS. Plasmapheresis is used some times when there is no effect with methylprednisolon.
Immunomodulatory drugs are targeting the frequency of relapses in RRMS. The main immunomodulatory drugs are Interferon beta1a (Avonex, Rebif), Interferon beta 1b (Betaferon, Extavia), Glatiramer acetate (Copaxone). Natalizumab (Tysabril) and Mytoxantrone are commonest immunosuppressive drugs used is MS treatment.
There are specific inclusion criteria for patients who can get state-funded drugs after counsilium based decision.
All this drugs have side effects which can cause patients to stop taking the drugs.
The treatment of MS is complex team based process which is participated by neurologist, neuroradiologist, neuroophtalmologist and rehabilitation specialist.