Inflammation could be defined as a means by which body tissues respond to all types of injury (Roitt, 1997). It is a defense mechanism against infections caused by injuries. Physical stimuli such as temperature changes, UV radiation or skin irritation can cause the release of inflammatory mediators such as cytokines that ensure the immune system has an adequate defense, chemokines that bring leukocytes to the site of inflammation, eicosanoids, neuropeptides, etc. The inflammation could be acute or chronic. Acute inflammation is an immediate response to trauma; in which the body fights against foreign bodies and heals wounds. Inflammatory mediators are released from the cell, provoking the immune response. Vassolidation is another stage of acute inflammation; it causes an increase in blood flow and therefore an increase in blood vessel permeability, which then leads to the release of plasma proteins in the affected tissues (Spector & Willoughby, 1963). It may be characterized by redness, swelling, and increased warmth in the affected area. After vasolidation, inflammatory cells penetrate the damaged tissue due to increased permeability. Mast cells are responsible for the release of mediators such as cytokines and chemokines that eliminate dead cells and toxins. This is followed by the release of other important mediators from endothelial cells. To make the inflammatory response effective, leukocytes, other mediators such as leukotrienes and kinins. The chemokine brings leukocytes to the site of inflammation, plasma proteins capable of destroying pathogens are activated, the lesion begins to heal, and then acute inflammation ceases. Under normal conditions, the inflammatory response is turned off by anti-inflammatory mechanisms to avoid...... half of article ......NJ & Gibson, RM (2006). The role of inflammation in central nervous system injuries and diseases. The British Journal of Pharmacology. 1 Inflammation in multiple sclerosis: the good, the bad and the complex47, S232–S240. Martino, G., Furlan, R. & Poliani, PL The pathogenic role of inflammation in multiple sclerosis. Rev. Neurol. 2000 June 16-30; 30(12):1213-7.Rooks, A. & Burns, T. (2010). Rook's Textbook of Dermatology. Vol 4 (chapter 12). John Wiley and Sons. Roitt, I. M. (1997). Essential immunology (9th edition). Blackwell Scientific, Oxford. Spector, W. G. and D. A. Willoughby (1963). Inflammatory responses. J. Pathol. Bacteriol. 27:118-149. Martino, G., Adorini, L., Rieckmann, P., Hillert, J. Kallmann, B. Comi, G. & Filippi, M. Inflammation in multiple sclerosis: the good, the bad, and the complex. Lancet Neurology. Volume 1, number 8, December 2002, pages 499-509