Multiple Sclerosis
Multiple sclerosis (MS) is a chronic disease of the central nervous system, which includes the brain, spinal cord and optic nerves. It is the most common neurological disease in young adults, affecting approximately two million people worldwide.
Currently there is no cure for MS, but the condition has become increasingly manageable with the help of disease modifying drugs (DMDs). These therapies can change the course of the disease by reducing the number, frequency and severity of attacks as well as the number and volume of lesions in the brain. Some DMDs have also been shown to delay the progression of disability in patients with MS. Studies indicate that drug therapy should be started as early as possible following diagnosis to give the patient the best possible long-term prognosis.
Multiple sclerosis at a glance:
Multiple sclerosis at a glance:
- MS is a complex, multifaceted disease of the central nervous system (CNS) with multiple pathways.
- MS interferes with the brain’s ability to control such functions as seeing, walking and talking. It is unpredictable and every person with MS will have his or her unique set of symptoms.
- It can be difficult to diagnose, although technologies such as magnetic resonance imaging (MRI) and optical coherence tomography (OCT) are improving the ability to diagnose and treat MS earlier.
- MS is usually diagnosed between the ages of 20 and 40, and is twice as common among women as it is among men.
- Symptoms vary, ranging from mild to more severe, but most commonly include: blurred vision, problems with strength and coordination, and numbness or tingling in the limbs.
While the exact cause of MS is unknown, it is believed to be an autoimmune disease.
Normally, the immune system defends the body against foreign invaders such as viruses or
bacteria. In autoimmune diseases, the body attacks its own tissue. In MS, a type of white
blood cell, called T lymphocytes, are activated and start to multiply and cross the blood-brain
barrier (BBB) to the brain and spinal cord. The T lymphocytes then begin to attack the
protective coating on the axons of nerve cells (neurons), called myelin. The loss of myelin leaves behind scar tissue called sclerosis. These damaged areas are also known as plaques or lesions. When this occurs, nerve “communication” along the axon (and consequently along the nerve) is disrupted. Damage can also occur in the underlying nerve cell, leading to permanent symptoms and disability.
Scientists do not yet know what triggers the immune system to begin attacking myelin.
Most agree that several factors are involved, including:
1. Mackay RP, Myrianthopoulos NC, Multiple sclerosis in twins and their relatives. Arch Neuro. 1966; 15:449-462.
2. Williams A, et al. Multiple sclerosis in twins. Neurology. 1980;30:1139-1147.
3. Ebers GC, et al. A population-based study of multiple sclerosis and twins. N. Engl J Med. 1986;315:1638-1642.
4. Duquette P. The increased susceptibility of women to multiple sclerosis. Mult Scler. 1998: 4: 511-512.
5. Dean G, McLoughlin H, Brady R, Adelstein AM, Tallet-Williams J. Multiple sclerosis among immigrants in greater London. Br Med J. 1976: 1:861-864.
6. Krtzke JF, Gudmundsson KR and Bergmann S. MS in Iceland.- Evidence of a post-war epidemic. Neurology. 1982;32: 143-150.
Normally, the immune system defends the body against foreign invaders such as viruses or
bacteria. In autoimmune diseases, the body attacks its own tissue. In MS, a type of white
blood cell, called T lymphocytes, are activated and start to multiply and cross the blood-brain
barrier (BBB) to the brain and spinal cord. The T lymphocytes then begin to attack the
protective coating on the axons of nerve cells (neurons), called myelin. The loss of myelin leaves behind scar tissue called sclerosis. These damaged areas are also known as plaques or lesions. When this occurs, nerve “communication” along the axon (and consequently along the nerve) is disrupted. Damage can also occur in the underlying nerve cell, leading to permanent symptoms and disability.
Scientists do not yet know what triggers the immune system to begin attacking myelin.
Most agree that several factors are involved, including:
- Genetics1,2,3
- Gender4
- Environmental factors5,6
2. Williams A, et al. Multiple sclerosis in twins. Neurology. 1980;30:1139-1147.
3. Ebers GC, et al. A population-based study of multiple sclerosis and twins. N. Engl J Med. 1986;315:1638-1642.
4. Duquette P. The increased susceptibility of women to multiple sclerosis. Mult Scler. 1998: 4: 511-512.
5. Dean G, McLoughlin H, Brady R, Adelstein AM, Tallet-Williams J. Multiple sclerosis among immigrants in greater London. Br Med J. 1976: 1:861-864.
6. Krtzke JF, Gudmundsson KR and Bergmann S. MS in Iceland.- Evidence of a post-war epidemic. Neurology. 1982;32: 143-150.
There are several clinical patterns of MS:
1. Wingerchuk, D. Lucchinetti, C. Noseworthy, J. Multiple Sclerosis: Current Pathophysiological Concepts. Lav Invest. 2001; 81: 263-281.
2. Wehman-Tubbs, K. Yale, S. Rolak, L. Insight into Multiple Sclerosis. Clinical Medicine & Research. 2005; 3: 41-44.
- Relapsing-Remitting MS (RRMS) is the most common form of MS, and affects approximately
85% of people with the disease.1 RRMS follows a course of relapses where
there is an increased level of symptoms, followed by recovery periods (remissions) where
there are fewer or no evident symptoms.2 - Secondary-Progressive MS (SPMS) starts when people with RRMS begin to experience
worsening of their symptoms and disability, generally without developing new relapses. In some cases, people with SPMS continue to experience relapses. Research has shown that about two thirds of patients with RRMS go on to develop SPMS.1 - Primary-Progressive MS (PPMS) occurs in about 10 percent of patients with MS. It is
defined by a steady accumulation of disability from the onset of the disease.1 - Progressive-Relapsing MS (PRMS) is very rare (occurs in approximately 5% of MS
patients) and involves a steady increase in disability with interspersed acute attacks. 1
2. Wehman-Tubbs, K. Yale, S. Rolak, L. Insight into Multiple Sclerosis. Clinical Medicine & Research. 2005; 3: 41-44.
