J Korean Med Assoc.  2009 Jul;52(7):665-676. 10.5124/jkma.2009.52.7.665.

Multiple Sclerosis

• Kim W
• Kim HJ

• KMID: 2188027
• DOI: http://doi.org/10.5124/jkma.2009.52.7.665

Abstract

Multiple sclerosis (MS) is an inflammatory autoimmune disorder of the central nervous system (CNS) and one of the most common disabling neurological diseases of young adults. Although the exact mechanisms involved in MS pathogenesis remain unclear, MS is believed to be caused by interactions between as yet unidentified environmental factors and susceptibility genes. Symptoms commonly occurred in MS include visual disturbance; weakness; spasticity; sensory disturbances; ataxia; bladder, bowel, and sexual dysfunction; fatigue; affective symptoms; and cognitive impairment. Most patients initially undergo a relapsing-remitting course, however, without treatment, the majority of them make a transition to the secondary progressive form. The clinical diagnosis is based on demonstrating neurological lesions, predominantly in the white matter, that are disseminated over space with the lapse of time. The key to the successful MS management is to prevent disability. Although there is no effective cure for MS, therapies are available that mitigate the course of the disease, treat relapses and improve symptoms, all of which place a significant impact on patients' quality of life. Recent clinical trials suggest that early identification and treatment are critical to optimize the treatment benefit. Currently six agents have been specifically approved for mitigating the course of MS. These include three formulations of interferon beta, glatiramer acetate, mitoxantrone, and natalizumab. Recent advances in understanding of immune pathogenesis lead us to new therapeutic approaches focused on precise target mechanisms. Many ongoing clinical trials will provide better treatment protocols in near future.

Keyword

Multiple sclerosis; Epidemiology; Immunopathology; Diagnosis; Treatment

MeSH Terms

Antibodies, Monoclonal, Humanized
Central Nervous System
Humans
Hypogonadism
Interferon-beta
Mitochondrial Diseases
Mitoxantrone
Multiple Sclerosis
Natalizumab
Ophthalmoplegia
Peptides
Quality of Life
Recurrence
Urinary Bladder
Young Adult
Antibodies, Monoclonal, Humanized
Hypogonadism
Interferon-beta
Mitochondrial Diseases
Mitoxantrone
Ophthalmoplegia
Peptides

Figure

• 

  Figure 1 APC = antigen presenting cell, IFN = interferon, MBP = myelin basic protein, MHC = major histocompatibility complex, MMP = matrix metalloproteinase, NOI = nitric oxide intermediates, ROI = reactive oxygen intermediates, TCR = T cell receptor, TNF = tumor necrosis factor, VCAM = vascular cell adhesion molecule, VLA = very late antigen. The five key immunopathogenic processes in multiple sclerosis (MS) targeted by MS therapies (10). (A) T cell activation and differentiation into T-helper (Th) -1 cells, (B) interleukin (IL)-2-induced proliferation of activated Th1 cells, (C) recruitment of B cells and monocytes by activated Th1 cells, (D) activated Th1 cell trafficking across the blood- brain barrier (BBB), (E) T cell reactivation and induction of immune cell-mediated demyelination.

• 

  Figure 2 Diagram representing the different types of multiple sclerosis.

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  Figure 3 Representing MRI of multiple sclerosis. (A) Fluid-attenuated inversion recovery (FLAIR) MRI demonstrates typical multiple perpendicular-axis periventricular white matter lesions called "Dawson's fingers". (B) Gadolinium enhanced T1-weighted MRI shows well-enhancing MS plaque.

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