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Introduction Multiple Sclerosis (ms) Is A Chronic Inflammatory Disease Of ...

Introduction
Multiple sclerosis (MS) is a chronic inflammatory disease of unknown cause, affecting the central nervous system (CNS). It affects more than 2 million people worldwide and 85% of patients experience at least 1 relapse, followed by partial or complete recovery (Neuhaus, Kieseier & Hartung 2006). Hence MS is often referred to as a relapsing remitting disease. Without adequate therapeutic intervention over half of all MS patients will enter a second disease phase, involving a progressively worsening disability, often in conjunction with superimposed relapses.
The histopathology of MS involves the pathological infiltration of immune cells across the blood brain barrier (Javed, Reder 2006) and demyelination of CNS axons. It usually involves a cycle of relapse and remission, with the therapeutic aim to increase the proportion of remission time and lower or stop relapse occurrences. Many therapies centre around targeting the immune response and aiming to prevent both immune cells from reaching the CNS and stopping the immune response that results if they do. MS is incurable at the current time so drug therapy aims to modify the disease course or treat the symptoms of the disease. Therefore the drugs licensed for therapy in MS so far include those that address symptoms including pain relief, depression, anxiety, digestive and excretory problems and the symptoms of immune response, but also now include newer drugs such as interferons, which address the specific disease pathology. In addition to drug therapy there are various kinds of complementary therapy, which will be dealt with briefly, following a review of the more traditional drug treatments. First, however, the immune response in MS which forms the target for many newly developed drugs is discussed, as is a rather significant issue relating to data about drug treatment.
The pathogenesis of MS
Figure 1 below indicates the hypothetical pathogensis of MS, although it should be recognised that it is only hypothetical.
Figure 1. The hypothetical pathogenesis of multiple sclerosis, indicating the potential role of immune cells (Neuhaus, Kieseier & Hartung 2006) Key

Ordinarily Th1 cells release pro-inflammatory cytokines, including Interferon-? and interleukin-2, but are reciprocally modulated by the Th2 mediated anti-inflammatory response, leading to an appropriate inflammatory response. Unlike the normal immune response, unfortunately patients with MS show over activity in Th1 cells, leading to an excessive production of Th1 pro-inflammatory cytokines (Javed, Reder 2006), which is not balanced by the Th2 response, which is abnormally low.
MS is associated with axonal transection leading to neurological deficits (Khan et al. 2005). Indeed it is believed that it is this axonal degeneration that underlies the worsening neurological deficits and brain atrophy and chronic disability observed as the disease progresses (Kreitman, Blanchette 2004).

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