Multiple sclerosis is a pathology of enormous social importance because it is one of the most frequent causes of disability due to neurological disease in young people. In fact, it is a disease of youth: 70% of multiple sclerosis patients are between 21 and 40 years of age. Within the evolutionary forms of the disease, progressive forms tend to appear later in life (45 years) and relapsing remitting forms between 25 and 30 years of age. The prevalence of the disease in Spain is 50-60 cases per 100,000 inhabitants.
On the other hand, it is one of the diseases that has been most studied epidemiologically, without identifying the etiological factors.
In order to diagnose a patient with multiple sclerosis, the prerequisite must be met: the patient must have physically and temporally spaced lesions of the neuroaxis.
Why does multiple sclerosis occur?
The etiopathogenesis of this disease is autoimmune, i.e. the immune defense system mediated by antibodies attacks the organism itself, as if it were the antigen. Specifically, it attacks the myelin of the white matter of the neural axis that covers the axons.
The immunopathogenic mechanism is supported by several facts, such as the presence in acute inflammatory demyelinating inflammatory plaques of T lymphocytes, the activation of B lymphocytes with intrathecal production of immunoglobulins and the abnormal expression of antigens, as well as the association to certain HLA haplotypes. Likewise, some so far unknown environmental factor would induce changes on oligodendroglia antigens, being these the targets of the immune response.
Viruses, especially of the herpes family and retroviruses, have been studied. However, it has not been possible to detect viral genetic material in demyelinating plaques.
The genetic hypothesis shows a concordance of 30% in monozygotic twins and 5% in dizygotic twins, so there seems to be an oligogenetic inheritance pattern.
Effects of demyelination in multiple sclerosis
The main effect of demyelination is the interruption of electrical conduction, so that nerve conduction in the neural axis will be interrupted and blocked. However, there is not always a correlation between inflammatory lesions or active demyelinating plaques seen on MRI and symptomatology. Conduction slowing does not always explain the deficit symptoms, but fatigue does.
Sometimes the potentials are generated spontaneously, giving rise to acute symptoms such as tonic convulsions when resting the feet, dysarthria and ataxia, provoked when speaking. The increase of temperature in summer decreases the conduction velocity, worsening the symptoms.
Classification and symptomatology of multiple sclerosis
In 1983 Poser devised a diagnostic protocol that includes clinical and paraclinical data, and classifies multiple sclerosis as possible, probable and definite. In this regard, symptomatology is divided into:
– Deficient
– Framed in outbreaks
– Paroxysmal phenomena that are short-lived and leave no sequelae.
To define a focal neurological dysfunction as an outbreak it must last more than 24 hours, and to recognize a second outbreak it must be spaced in time more than one month, and be topographically separated.
There are four different evolutionary types, according to the distribution and progression of the disease:
1) Relapsing-remitting outbreaks.
2) Primarily progressive
3) Secondarily progressive
4) Relapsing-progressive
70% of patients present the relapsing-remitting form. The majority of controlled patients present one flare-up per year, an incidence that decreases over the following 10 years. The degree of disability is assessed by the EDSS (Expanded Disability Status Scale).
The onset symptomatology varies according to the series, including, among others:
– Sensory disorder
– Motor defect
– Optic neuritis
– Diplopia
– Trigeminal disorder
– Facial paresis
– Vertigo
– Sphincter disorder
– Mental disorder
– Subcortical dementia
Diagnosis of multiple sclerosis
Magnetic resonance imaging of the brain was a real revolution in the diagnosis and follow-up of the disease. However, the low specificity of this MRI is due to the fact that other inflammatory lesions (sarcoidosis, acute disseminated encephalomyelitis), vasculitic lesions (SLE, Behcet’s disease) and small ischemic lesions offer similar images. The clinical radiological correlation is not as good as expected. Gadolinium contrast uptake indicates acute demyelinating plaque activity with clinical symptomatology.
Visual, somesthetic and auditory truncal evoked potentials are affected in 65% (auditory in 30%), and contribute to the diagnosis of multiple sclerosis.
In multiple sclerosis, the cellularity is clear, with normal cellularity and normal proteins. 90% of patients show intrathecal synthesis of immunoglobulins, with 95% of patients showing oligoclonal bands.
Treatment of multiple sclerosis
Neurology experts propose treatment for multiple sclerosis at three levels:
1) Treatment of the acute flare, with high doses of a potent glucocorticoid, which are both natural and synthetic adrenocortical steroids.
2) Maintenance treatment, with research with immunomodulators: interferon beta 1 (protein produced naturally by the immune system), glatiramed acetate, immunosuppressants (some of them of recent application). Plasmapheresis (removing blood from the body and processing it to separate white blood cells, red blood cells and platelets from the plasma) and immunoglobulins have not shown great efficacy.
3) Symptomatic rehabilitative treatment. It consists of the treatment of spasticity, sexual impotence, sphincteric symptomatology, depression, pain and possible deterioration, which is absolutely necessary for the patient’s improvement.
4) New avenues of research. New avenues of research have recently opened up in short-term scientific studies that seem promising for treating the disease.