The drugs of choice in treating this condition are Glatiramer acetate (GA) and interferon (IFN) which poses different mechanism of actions (MOA). In cerebrospinal fluid (CSF) IFN is usually passive but it controls the basement of vascular system from allowing inflammatory cells from going to the brain. GA acts by reacting with the T. cells which mainly come together with APC and shift the T. cell balance to TH2 anti inflammatory. GA does not affect the blood-brain barrier (BBB) as compared to damage caused by other steroids and IFN administration.
GA portrays robust immunological activities earlier during administration. IFN has great effect on the periphery since it reduces BB disruption and penetration which results in reduction of influx of the inflammatory cells from the CNS and consequently it leads to reduction of Matrix metalloproteinase (MMP) activity. IFN also reduces the trafficking of inflammatory cells into the CNS by regulating the adhesion molecules and therefore reducing the inflammatory cells influx which consequently affects the brain.
IFN can also interfere with chemokines which reduces influx in CSF cells. GA has great affinity of grooving in MCH which leads to generation of specific T cells which does not inhibit the trafficking of T. cell through BBB. MS can be effectively treated by understanding the way drugs works and the clinical manifestation of the disease. Drug should have efficacy tolerability and safety multiple drugs with different mechanisms of action need to be used in MS due to its prevalence in multiple anatomical sites (Pollard, 2006).
MS is a neurological disorder which affects central nervous system (brain and the spinal cord). This results to debilitating motor and sensory dysfunction. Disease is quite variable during its onset and progression. Mostly in the earlier stages the disease can not be diagnosed since it lacks symptoms which can help in detecting the condition. Some of the clinical features noted in this disease are:- – Sensory deficit which can result to parathesias and numbness of body cells.
– Motor- An individual experience a lot of difficulties in fine movements and gaits. – Other clinical features include lack of balance, unable to regulate bladder and sexual functions. In MS influx of mononuclear cells mainly occurs in blood brain barrier which cause immune prevalence in central nervous system. Various secretions such as cytokines and chemokines can result to loss of myelin, disruption of oligodendrocyte integrity and also loss of axonal. These events are quite influential in the disease and they affect neural athropathy progression.
Brain inflammation activities can also affect migration of leucocytes in transendothelial region and then enters the brain which consequently alters the process of myelination which is quite an important process in determining MS (http://www. labtestsonline. org/understanding/conditions/autoimmune. html as retrieved on 5 Mar 2008 18:58:04 GMT) . Clinically MS is a multifunction disease and it’s most diversified by its many clinical features some of its symptoms include: Impaired vision due to neuritis of optic nerve this is mainly evidenced by the inflammation of optic nerve.
Other symptoms include peresis and paralysis, lack of sensation or over sensation felt as burning or prickling, ataxia, fatigue and also incontinence at some extents. Cognitive impairment and other mental in ability can occur in some instances which can result to difficult in maintaining memory and concentration. The disease mainly effects young female more than males which shows that the prevalence rate for female is higher than that of male amounting to a ration of 2:1 (Dudek, 2006).
Another diagnosis that can be made on MS can be focused on clinical grounds which are determined by the multiple neurological deficits which are mainly explained by localized CNS pathology. Symptoms are seen to disseminate in different times and at different locations and are seen to occur in more than one occasion. For diagnosis to be reached, these symptoms must be evaluated to determine the clinical manifestation of MS. In acute stage the disease is polysymptomatic and therefore physicians have a great difficult in determining disease condition due to its manifestation of symptoms in different forms
During the acute phase of the disease the disorder can progress and results to permanent disability or even death in some occasions. When the disease is in benign state there are usually occurrences of relapse but there is no evidence of significant residues neurological deficit even after some years of its manifestation. All these observations when taken into account show that the disease is surely a multifunctional disease. The main underlying features in this condition are evidence by the immune attack of myelin and production of cells, the oligoderdrocyte (Volpe, 1990).
With all these ideas about immunological and clinical aspect of MS the disease’s future trend is not well known since the primary target which is the myelin does not give a clear understanding of whether the oligodednocyte destruction mainly occurs prior or post myelin loss. Viral and other genetic factors also contributes a lot to the etiology of MS but in most cases the main central features of disease takes place around the cellular immune system. CD4+ and CD8+ T cells and macrophages have their central features in the pathogenecity of the disease.
Cytokines mainly plays a major role in inducing disease which is key factor in deciphering complexity of immunopathogenesis of MS. MS is basically believed that it involves relationship between the brain’s immune system and the ability of the brain to induce alteration in myelin and axonal integrity or the functioning of the disease. Therefore, the disease is multifunctional due to its many causative agents, different clinical manifestation and its presence in many sites in the body.
Reference:
Robert Volpe, (1990), autoimmune Disorders of Endocrine System, CRC Press, New York, pg 224. https://labtestsonline.org/understanding/conditions/autoimmune.html