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Diagnosis of Multiple Sclerosis
There are several diagnostic tests used to detect Multiple Sclerosis (referred to as MS). An MRI (multilple resonance imaging) can confirm a diagnosis by showing lesions and sites of inflammation in the brain. Although the presence of lesions is common in Multiple Sclerosis sufferers, the absence of lesions is not a sign that the disease is not active. An electroencephalogram (EEG) can isolate changes in brain waves when introduced to audio or visual stimuli. The Evoked Potential test measures the speed with which nerve impulses travel. Demyelination significantly reduces the speed of nerve signal transmission and can be detected with this test. Lumbar punctures and spinal taps are also used to test spinal fluids for the presence of certain immuno-proteins present in Multiple Sclerosis sufferers.
Facts about Multiple Sclerosis
Multiple sclerosis is an inflammatory and demyelinating disease of the central nervous system and is believed to be immune mediated. This debilitating disorder affects at least 350,000 people in the United States. The disease occurs in young adults with the mean age of onset of 30 years. Women make up 70% of the MS population. This gender preference remains unexplained.
The symptoms of MS may be mild or severe, of short or long duration and may appear in various combinations, depending on the area of the nervous system affected. Complete or partial remission of symptoms, especially in the early stages of the disease occurs in approximately 70% of MS patients.
The initial symptoms of MS are often blurred or double vision, red-green color distortion, or even blindness in one eye.
However, visual problems tend to clear up in the later stages of MS. Inflammatory problems of the optic nerve may be diagnosed as retrobulbar or optic neuritis. MS patients will have an attack of optic neuritis at some time or other and it will be the first symptom of MS in approximately 15 percent. This has led to general recognition of optic neuritis as an early sign of MS, especially if test also reveals abnormalities in the patient's spinal fluid.
Most MS patients experience muscle weakness in their extremities and difficulty with coordination and balance at some time during the course of the disease.
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Most people with MS also exhibit paresthesias, transitory abnormal sensory feelings such as numbness, prickling, or "pins and needles" sensations; uncommonly some may experience pain. Loss of sensation may occur. Speech impediments, tremors, and dizziness are other frequent complaints. Occasionally, hearing loss is exhibited as well.
Approximately, half of all people with MS experience cognitive impairments such as poor concentration, attention, memory, and poor judgement. However, such symptoms are often overlooked and are only detectable through comprehensive testing.
All in the family or not? Genetic and Non-Genetic Risk Factors
Genetic predisposition is found to be involved in MS. A recent study found that familial clustering of MS cases was explained solely by genetic factors. The familial rate of MS (combining first, second, and third degree relatives) is as high as 20%. The risk of developing MS increases if there is a close relative with the disease. It is greatest for the sister of a female patient, who has a 25-fold increased chance of developing MS compared to the general population. Despite these data supporting the importance of genetic factors in MS, no abnormal genes have been found. MS twin studies find the concordance rate of monozygotic twins no more than 21-40%. However, it has been argued that incomplete penetrance of MS susceptibility genes in monozygotic twins argues in favor of environmental factors superimposed on genetic predisposition.
It is likely that MS disease susceptibility is polygenic. To date, the only clear-cut gene locus linked to MS has been the MHC, with the class II alleles in particular have the strongest association.
The earliest pathological change in MS is the penetration of lymphocytes from the systemic blood compartment into the CNS. This penetration occurs across endothelial cells, particularly the venules within white matter. Initially, CD4 lymphocytes predominate in the perivascular exudate. This cell penetration is the beginning of a cascade that culminates in formation of the demyelinated plaque, the neuropathologic lesion of MS. Diverse cells follow, including CD8 and other T cells; B cells and plasma cells; and macrophages/monocytes expressing class II histocompatibility complex (MHC) antigens. Local activation of adjacent glial and endothelial cells occurs with resident CNS macrophages (microglia) expressing class II antigen, as well as occasional astrocytes. There is local production of cytokines, immunoglobulins, and enzymes such as proteinases and lipases. Myelin damage occurs within 1 or 2 days of initial cell penetration. The macrophages begin to strip myelin from axons, leading to demyelination and to a lesser extent axonal injury. Oligodendroyctes initially proliferate and remyelinate, but ultimately oligodendrocytes disappear from the plaque lesion.
Antibodies to MBP and less commonly PLP can be found in the CSf and the brain of MS patients. MBP antibodies appear to correlate with more prominent inflammatory changes. Studies have looked at the lymphocytes within MS brain tissue, in particular T cells and their receptors, and T cell receptor variable (V), diversity (D), and junctional (J) gene rearrangements.
Although no definitive drug cure is available, various drugs are used to subdue symptoms and reduce the frequency of relapses. These treatments cannot totally arrest the disease. However, they do make it possible for many sufferers to live normal functioning lives. Synthetic interferon is also used to slow disabling factors and reduce relapses. Corticosteroids or ACTH, can shorten the duration of attacks and reduce inflammation. Non-drug treatments such as exercise and physical therapy may be beneficial in maintaining coordination and strengthening muscles, while speech therapy can help with difficulties swallowing and speaking.
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Clark, C.A.; Werring, D.J.; & Miller, D.H. (2000). Diffusion imaging of the spinal cord in vivo: Estimation of the principal diffusivities and application to multiple sclerosis. Magnetic Resonance in Medicine. 43:1; 133-138.
Coyle, P.K. (1996). The neuroimmunology of Multiple sclerosis. Advances in Neuroimmunology. 6; 143-154.
Guterman, H.; Nehmadi, Y.; Chistyakov, A.; Soustiel, J.; Hafner, H.; & Feinsod, M. (2000). Classification of brain-stem trigeminal evoked potentials in multiple sclerosis, minor head injuries and post-concussion syndrome pathologies by similarity measurements. International Journal of Medical Informatics. 60:3; 303 - 318.
For information regarding Multiple Sclerosis: http://www.msnet.org/