General | October 3, 2014 | Author: The Super Pharmacist
A large proportion of human nerve cells are of a form in which short projections called dendrites (similar to branches in appearance) radiate out from the centre. Nerve cells also possess a long, thin extension, called an axon, which functions to make contact with other cells. Axons carry electrical impulses from the main body of the cell, and end to form an 'axon terminal', where the nerve cell communicates with a dendrite of another nerve cell (this interface is known as a synapse) to carry on the impulse.
Alternatively, if the terminal makes contact with a muscle cell, it will activate its movement in a similar manner. This is the basis of neural system function, which enables conscious and unconscious movement, brain function and physiological processes.
Axons must be insulated, to ensure that the electrical impulses flowing through them are retained within them in order to transmit signals on to the next cell, and also for protection. Insulation is a flexible substance, known as myelin, mostly made up of a fat-like molecule called galactocerebroside. Myelin is produced by cells called Schwann cells, which are located along the axon. Myelin wraps around both the axon and Schwann cell to form the myelin sheath. There may be a large number of separate sheaths along the length of the axon, depending on its size.
The role of myelin in protecting and conserving neural function is not to be discounted. Disorders in which this material degenerates or fails to form around the axon, can take a significant toll on the ability to move or perceive the environment, and even on mental health in some cases.
This condition involves increasing death rates in Schwann cells, and eventual destruction of axons.
Some remyelination may occur in the early stages of the disease, but eventually the loss of this material and the cells that produce it is too extensive to overcome. Lesions in the form of scar tissue (sclera) forms around the damaged axons, which disrupts neural transmission in the affected areas.
Multiple sclerosis presents as a wide range of symptoms affecting motor and/or sensory processes as myelin is lost from an increasing number of neurons in the brain and spinal cord.
The exact cause of multiple sclerosis has not yet been defined. Research into this condition suggests that the most likely factors associated with the disorder are genetic and environmental in nature Some scientists conclude that the disease is caused by immune-system cells that react to myelin as a foreign substance (for unknown reasons) and attack it until sclera appear.
Inflammation may also contribute further to this damage to nervous system tissue.
The effects of multiple sclerosis may include:
The risk of disability as a result of the condition is associated with advanced age. There is some evidence that a history of smoking may affect the progression and severity of symptoms.
Multiple sclerosis may be classified into a number of main subtypes based on the rate of symptom progression and the frequency with which they arise. These are:
As there is no known cause for this condition, there is no cure as of yet. Therapies for multiple sclerosis are mainly directed at the management of symptoms. These include:
This is a relatively new treatment for multiple sclerosis. It modulates the immune response, and may act by preventing immune cells targeting myelin. A randomised controlled trial allocated 1033 patients with relapsing-remitting multiple sclerosis to placebo, 0.5mg or 1.25mg doses of fingolimod daily. The patients on both active doses had a significantly improved rate of relapse in comparison with the placebo group. The groups receiving fingolimod also had significantly less new brain lesions, and exhibited a significantly reduced rate of brain volume loss, in comparison with the patients on placebo. Another randomised trial including 1153 patients comparing the same doses of fingolimod to a weekly 30 microgram dose of interferon beta-1a found that the rate of relapse per year was significantly lower in the fingolimod groups.
These are a class of drugs that may reduce pain (if present), visual symptoms and inflammation in multiple sclerosis patients.
Unlike many treatments for this condition, coritcosteroids are often administered intravenously, whereas others are injected into muscle tissue. An analysis of two studies on corticosteroids in multiple sclerosis treatment found that these drugs achieved significant but short-term (approximately 30 days) improvements in vision problems and disability. The analysis concluded that corticosteroids had no appreciable effects on the rates or risks of relapse.
Interferons are a class of natural immune molecules that play a role in the control of immune cells. Interferon beta-1a is a classic multiple sclerosis treatment, but may cause side-effects related to changes in the immune response induced by this drug. A double-blind trial randomised 311 patients with relapsing-remitting multiple sclerosis to 30 micrograms interferon beta-1a or a placebo weekly. The patients in the treatment group exhibited significantly less progressive disability, and a significantly reduced brain lesion count than the placebo group.
Antibodies are molecules designed to identify and attach to another biological molecule with a high degree of accuracy and efficacy, thus preventing that molecule from carrying out its role in disease progression.There is potential for antibody therapy in multiple sclerosis treatment, as many immune-system molecules may be important factors in the mechanisms underlying demyelination. The antibody alemtuzumab has attracted considerable attention as a candidate for novel multiple sclerosis therapy. A randomised-controlled trial allocated 202 patients to this antibody at intravenous doses of 12 or 24 mg per day for five days, or interferon beta-1a three times weekly. Both alemtuzumab groups experienced significantly fewer relapses than the interferon beta-1a group. A significantly larger proportion of either alemtuzumab group avoided relapsing for 2 years. On the other hand, there were more infections (as a result of immune suppression) in the alemtuzumab groups. This indicates promise for antibody therapy in multiple sclerosis management, despite the risks of adverse effects.
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