Multiple Sclerosis

Multiple Sclerosis

    * Introduction
    * Clinical
    * Diagnostic Laboratory
    * Evolution and prognosis
    * Clinical Forms
    * Diagnosis
    * Treatment
Multiple sclerosis was first described in terms of clinical and pathological in 1866 by Charcot and Vulpian. Synonymous terms to describe multiple sclerosis are: multiple sclerosis, insular sclerosis, multilocular sclerosis, multiple sclerosis. It is a chronic autoimmune inflammatory disease of the central nervous system characterized by neuronal demyelination localized, multifocal, evolving with the formation of plaques of multiple sclerosis. Demyelinating disease is primary to young adult.
Around the age of onset is 20-30 years. The disease is more common in women. Symptoms vary depending on the location of lesions. In the disease meet visual disturbances, muscular atrophy progressive centripetal evolution of the upper limbs, sensory disturbances and paresthesia that diestezii, motor problems as paralysis, spastic paralysis. Other clinical manifestations of disease are like ataxii cerebellar disorders, nystagmus, intentional tremor, abnormal eye with optic nerve damage, sphincter disturbances and psychiatric disorders. The disease progresses slowly, being marked by temporary remissions and flare outbursts.
Etiopathogenesis There are several theories about the cause of this disease. At present it is considered that multiple sclerosis is due to an unidentified neuroinfectii caused by a virus that acts through a mechanism neuroalergic. Infection usually occurs during childhood and become clinically manifest in adulthood. It was observed that the cerebrospinal fluid of patients with multiple sclerosis existence of measles antibodies. Hence it was concluded that the causative agent of this disease as measles virus.
Pathogenic mechanism of autoimmune disease is a neuroalergic mechanism, mediated and delayed type. After inoculation of virus, viral infection plays a permeabilizant the blood brain barrier. After the disintegration of myelin sheaths, it releases a factor antigen in circulation. In response to this, the body's immune system synthesize humoral and cellular antibodies. These antibodies are infiltrating the central nervous system where it triggers a second phase of demyelination, the myelin sheaths disintegrate and form boards sclerosis. Neuroalergica theory is supported by a series of arguments clinical, anatomical and experimental: - Clinical arguments: different points of nevraxului invasion, taking the appearance of a rash; trend of evolution in relapse, the disease gets worse from intercurrent infections. - Arguments anatomical substrate there is some resemblance pathologically to secondary encefalitele of vaccine and infectious eruptive diseases. - Experimental arguments: they could not obtain experimental demyelinating encephalitis in experimental animals by inoculation of homologous or heterologous brain emulsions.
From anatomical point of view, three fundamental processes overlap and come in multiple sclerosis: demyelination multilocular, glial proliferation and interstitial inflammatory or infiltrative processes around small vessels. Areas of demyelination are found throughout the entire central nervous system, varying sizes and affects mainly the white matter of the oval center, corpus callosum, protuberantei leg, bulbar pyramids and olivele, floor fourth ventricle and posterior spinal cords. The process of demyelination is seen rarely in the cranial nerves, optic nerves were worst affected, oculomotor nerves and cranial nerves VII and VIII.
Macroscopically, tiles may have different sizes and ages. Older cards have a gray color and a high consistency. The latest have a reddish tint, lower consistency, not well defined. Sclerosis plaques size varies from a few millimeters to 4-5 cm.
Microscopically, there is a noticeable damage to the myelin sheath, demyelination is essentially of bulk and discontinuous. Axial filament is not affected. Myelin-forming cells, oligodendrogliile disappear rather quickly after onset. Glial proliferation following demyelination process, of interest for micro and macroglia. Phagocytic microglia participate in the process of breakdown of myelin destruction lipoidica corpus and granular form. These foci of demyelination clean. Macroglia serves to replace damaged tissues and delimit sclerosis plaques. In recent forms of the disease are found inflammatory lesions, especially in the nervous parenchyma, in white matter in the form of infiltrative processes, precapilare around small vessels and capillaries and venules around. MS plates plasmacytoma latest shows infiltration.