Multiple Sclerosis: Origins of Spasticity and Weakness in Voluntary Movement

Current Treatments
BETASERON® (interferon beta-1b) is indicated for the treatment of relapsing forms of multiple sclerosis to reduce the frequency of clinical exacerbations. Patients with multiple sclerosis in whom efficacy has been demonstrated include patients who have experienced a first clinical episode and have MRI features consistent with multiple sclerosis

AVONEX® (Interferon beta-1a) is a 166 amino acid glycoprotein with a predicted molecular weight of approximately 22,500 daltons. It is produced by recombinant DNA technology using genetically engineered Chinese Hamster Ovary cells into which the human interferon beta gene has been introduced. The amino acid sequence of AVONEX® is identical to that of natural human interferon beta.

COPAXONE is the brand name for glatiramer acetate (formerly known as copolymer-1). Glatiramer acetate, the active ingredient of COPAXONE, consists of the acetate salts of synthetic polypeptides, containing four naturally occurring amino acids: L-glutamic acid, L-alanine, L-tyrosine, and L-lysine with an average molar fraction of 0.141, 0.427, 0.095, and 0.338, respectively. The average molecular weight of glatiramer acetate is 5,000 – 9,000 daltons. Glatiramer acetate is identified by specific antibodies.

Rebif® (interferon beta-1a) is a purified 166 amino acid glycoprotein with a molecular weight of approximately 22,500 daltons. It is produced by recombinant DNA technology using genetically engineered Chinese Hamster Ovary cells into which the human interferon beta gene has been introduced. The amino acid sequence of Rebif® is identical to that of natural fibroblast derived human interferon beta. Natural interferon beta and interferon beta-1a (Rebif®) are glycosylated with each containing a single N-linked complex carbohydrate moiety.

Tysabri is a monoclonal antibody that affects the actions of the body's immune system. Monoclonal antibodies are made to target and destroy only certain cells in the body. This may help to protect healthy cells from damage. Tysabri is used to treat relapsing forms of multiple sclerosis.

Gilenya™ is a new class of medication called a phingosine 1-phosphate receptormodulator, which is thought to act by retaining certain white blood cells (lympohcytes) in the lymph nodes, thereby preventing those cells from crossing the blood-brain barrier into the central nervous system (CNS). Preventing the entry of these cells into the CNS reduces inflammatory damage to nerve cells.

Early Symptoms
The most common early symptoms of MS include:
* Tingling * Numbness
* Loss of balance
* Weakness in one or more limbs
* Blurred or double vision

Less common symptoms of MS may include
* Slurred speech
* Sudden onset of paralysis
* Lack of coordination
* Cognitive difficulties

Listed above, the early symptoms. I tend to be a poster child for these. The symptoms that occur later on are too numerous just to list. There will be a link included that will get you to a site where these symptoms are listed and explained. Keep in mind that someone may have some of these or many of these, there is no way to tell.

Multiple sclerosis statistics show that approximately 250,000 to 350,000 people in the United States have been diagnosed with this disease. The life expectancy for people with multiple sclerosis is nearly the same as for those without MS. Because of this, multiple sclerosis statistics place the annual cost of MS in the United States in the billions of dollars. MS is five times more prevalent in temperate climates -- such as those found in the northern United States, Canada, and Europe -- than in tropical regions. Furthermore, the age of 15 seems to be significant in terms of risk for developing the disease. Some studies indicate that a person moving from a high-risk (temperate) to a low-risk (tropical) area before the age of 15 tends to adopt the risk (in this case, low) of the new area and vice versa. Other studies suggest that people moving after age 15 maintain the risk of the area where they grew up.

The National MS Society

Tuesday, September 22, 2009

Origins of Spasticity and Weakness in Voluntary Movement

Muscle groups normally work together: when one is flexed, its opposing muscle is relaxed. This complementary muscle action depends on the transmission of signals along pathways connecting the brain, motor neurons in the spinal cord, and muscles ( Figure 3.1). The CNS damage caused by MS disrupts this communication, allowing the persistent contraction of the muscle fibers that produces spasticity.

Spasticity is associated with sprouting of descending motor pathways to form new synaptic connections with spinal neurons and with hypersensitivity caused by denervation.107 Damage to descending motor pathways also causes slowness of movement and weakness. The spinal plaques occurring in many types of spinal MS are associated with a progressive loss of axons and a reduction in diameter or a loss of myelination of residual axons passing through or close to the plaque.103 There can also be alterations in the numbers and types of excitable sodium membrane channels exposed by the membrane demyelination, further altering the conduction capacity of the damaged axons.

Although the mechanisms leading to spasticity and muscle weakness in MS are not fully understood, knowledge about the mechanisms operating in other conditions may be helpful. For example, the mechanisms related to the spinal cord pathology known to occur in MS may be similar to those in incomplete spinal cord injury. The symptoms of spasticity and weakness in MS can also result from plaques in the supraspinal brain and brainstem, which would suggest a comparison with the results of stroke or intracapsular hemorrhage. However, considerably more is known about the effects of incomplete spinal cord injury. Thus, it is more likely to provide instructive parallels for understanding the pathology and pathophysiology of MS. FIGURE 3.1 Functions controlled by nerves at different levels of the spine. Damage at a particular level of the spine usually impairs functions controlled by all nerves at lower levels.

This is an excerpt from published material found on the NIS website.

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