Multiple Sclerosis (MS) causes a patient's immune system to attack it's own myelin, which is a function that insulates a layer of the brain nerves. Myelin enables a fast conduction of impulses in the brain. MS affects 30 to 80 people per 100,000 inhabitants.
MS is most likely a result of environmental and genetic factors. There are multiple suspected risk factors; various theories cite infections with viruses, retroviruses, spirochetes, chlamydia as well as the lack of Vitamin D in childhood.
MS appears predominantly in Caucasians and women are affected twice as often as men. It is most prevalent in Northern Europe, Canada and the northern parts of the USA. Strangely, the commonality of the disease directly correlates with how close it is to the equator. The reason for this is not entirely clear yet. The climate, sunlight, diet, infections and genetic factors are all thought to play a role. The environmental factors in childhood supposedly play an important role in the disease development which appears years later.
Although the disease is not considered hereditary, studies with identical twins have shown that if one of the siblings falls ill with multiple sclerosis, the other twin has a 30% chance of also developing this disease. The HLA (human leukocyte antigen) system plays an important role. It is a genetically determined protein that affects the immune system.
Disease beginning and its formation
The course of the disease involves exacerbations followed by remissions. Such a disease form is called the relapsing-remitting type. Between attacks, the symptoms may completely disappear, although permanent neurological problems often remain when the disease progresses. During an exacerbation, the following neurological symptoms may appear: decreased visual acuity in one eye, diplopia (double vision) and sensory deficits in various parts of the body, muscle weakness in certain extremities, clumsiness of the hands and disturbances in urination. In 15% of patients with primary-progressive form of disease, the disease progresses smoothly without acute exacerbations.
In selected patients the symptoms tend to gradually accumulate from the very beginning. Many patients start in a relapsing-remitting stage and later progress to a progressive stage.
The signs and symptoms are varied and differ greatly among the patients. They depend on the location of the inflammatory focus in the brain. The initial attack is characterized by the following disturbances appearing singly or in combination: visual disturbances in one eye, diplopia, sensory disturbances in different body parts, muscle weakness in certain extremities as well as clumsiness of the hands, disturbed movement coordination and balance, fatigue and difficulties with urination and defecation. When an attack subsides, the symptoms may disappear completely in a few weeks although a residual neurological disability can remain.
According to the immunologic explanation, the inflammatory process in the brain is triggered by the activated T-lymphocytes. However, these cells enter the brain only after the blood-brain barrier has been damaged, for instance by a viral infection. Upon entering the brain, T lymphocytes fail to recognize the patient's own myelin and thus they attack it. An immune process is triggered, attracting other inflammatory cells activating additional inflammatory mediators such as cytokines and metalloproteinases, which then damage the blood-brain barrier. A vicious cycle is created, but the inflammation nevertheless subsides with time. Despite this however, some scars remain in the tissue. A phase of repair and remyelinization follows, but the initial state is never attained. Some axons also suffer permanent damage. The signs and symptoms are thus the result of the accumulation and location of such lesions in the brain and the spinal cord.
Diagnosis is made on the basis of diagnostic criteria. Nowadays, the McDonald criteria is used which take into consideration the clinical picture (the number of attacks and neurological disturbances). They also consider the number of inflammatory foci revealed by the magnetic resonance imaging (MRI) of the brain and the spinal cord. In essence, it is still about determining the course of disease "in time and space".
Prevention and therapy
Multiple sclerosis still cannot be cured or prevented. It is only possible to influence its progression and reduce the number of flare-ups. A general rule that applies in case of this disease is the need to avoid excessive physical and psychological stressors, and especially situations that can aggravate the immune system, such as colds because an infection may trigger a flare-up.
Research has shown that the flu vaccination does not hurt these patients, nor does it cause new flare-ups. Nutrition must be varied; it is extremely important that a well-balanced diet is consumed to provide all of the essential vitamins and minerals. High temperatures such as those found in a sauna or hot baths may transiently worsen the symptoms; thus, exposure to heat is not recommended. Adequate physical exercise and keeping fit is also beneficial as fatigue is a prominent symptom of this disease.
Acute exacerbations or flare-ups are treated with corticosteroids that act fast to contain the flare-ups. In addition, the aim is to prevent new flare-ups and disease progression. To this effect, biological medicines that suppress the immune system have been used in the past years, mainly the interferon-beta and glatiramer acetate. A novel and very potent drug is natalizumab which prevents inflammatory cells to cross the blood-brain barrier and cause brain lesions typical of multiple sclerosis. Natalizumab is used for rapidly progressing cases where interferons are not sufficiently effective. There are numerous other drugs on their way, currently in the last phase of clinical trials.