Free Shipping on orders over $99

Multiple Sclerosis: Current and emerging treatments for MS

General | October 3, 2014 | Author: The Super Pharmacist

general

Multiple Sclerosis: Current and emerging treatments for MS

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.

Multiple sclerosis

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 demyelination (progressive lack of myelin) is a hallmark of a particular disease known as encephalomyelitis disseminata, or, more popularly, as multiple sclerosis.

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 symptoms

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

The effects of multiple sclerosis may include:

  • Tingling and/or pins and needles in the extremities
  • Numbness
  • Irregular reflex reactions, often resulting in apparently superior reflexes
  • Poor balance and/or coordination
  • Muscle spasms
  • Difficulty in swallowing
  • Speech difficulties
  • Visual abnormalities, including double vision, involuntary eye movements or deterioration of vision
  • Pain (acute or chronic)
  • Fatigue
  • Depressive symptoms (in rare cases)

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:

  • Primary progressive: Symptoms start gradually and progress regularly to severity.
  • Secondary progressive: Symptoms begin as above, but may then appear to recede and return in increasingly severe 'waves'. There may be a number of these, after which the condition may stabilise at a constant level of severity
  • Progressive-relapsing: A regular increase of symptoms punctuated by 'attacks' of increased severity.
  • Relapsing-remitting: Infrequent severe 'attacks', between which symptoms may be relatively mild or moderate, but tending towards more severity as time passes.

Current and Emerging Treatments for Multiple Sclerosis

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:

Fingolimod

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.

Corticosteroids

These are a class of drugs that may reduce pain (if present), visual symptoms and inflammation in multiple sclerosis patients. 

CorticosteroidsUnlike 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.

Interferon beta-1a

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.

Antibody therapy

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.

www.superpharmacy.com.au  Australia's best online pharmacy

References

Compston A, Coles A. Multiple sclerosis. The Lancet.2008;372(9648):1502-1517.

Hensiek AE, Seaman SR, Barcellos LF, et al. Familial effects on the clinical course of multiple sclerosis. Neurology.2007;68(5):376-383.

Bartholomaus I, Kawakami N, Odoardi F, et al. Effector T cell interactions with meningeal vascular structures in nascent autoimmune CNS lesions. Nature.2009;462(7269):94-98.

Kurtzke JF. Rating neurologic impairment in multiple sclerosis: An expanded disability status scale (EDSS). Neurology.1983;33(11):1444.

Rovaris M, Barkhof F, Calabrese M, et al. MRI features of benign multiple sclerosis: Toward a new definition of this disease phenotype. Neurology.2009;72(19):1693-1701.

Scalfari A, Neuhaus A, Daumer M, Ebers GC, Muraro PA. Age and disability accumulation in multiple sclerosis. Neurology.2011;77(13):1246-1252.

Gholipour T, Healy B, Baruch NF, Weiner HL, Chitnis T. Demographic and clinical characteristics of malignant multiple sclerosis. Neurology.2011;76(23):1996-2001.

Brusaferri F, Candelise L. Steriods for multiple sclerosis and optic neuritis: a meta-analysis of randomized controlled clinical trials. J Neurol.2000;247(6):435-442.

Jacobs LD, Cookfair DL, Rudick RA, et al. Intramuscular interferon beta-1a for disease progression in relapsing multiple sclerosis. Annals of Neurology.1996;39(3):285-294.

Freedman MS. Long-term follow-up of clinical trials of multiple sclerosis therapies. Neurology.2011;76(1 Supplement 1):S26-S34.

Mandala S, Hajdu R, Bergstrom J, et al. Alteration of Lymphocyte Trafficking by Sphingosine-1-Phosphate Receptor Agonists. Science.2002;296(5566):346-349.

Kappos L, Radue E-W, O'Connor P, et al. A Placebo-Controlled Trial of Oral Fingolimod in Relapsing Multiple Sclerosis. New England Journal of Medicine.2010;362(5):387-401.

Cohen JA, Barkhof F, Comi G, et al. Oral Fingolimod or Intramuscular Interferon for Relapsing Multiple Sclerosis. New England Journal of Medicine.2010;362(5):402-415.

Saidha S, Eckstein C, Calabresi PA. New and emerging disease modifying therapies for multiple sclerosis. Annals of the New York Academy of Sciences.2012;1247(1):117-137.

Coles AJ, Twyman CL, Arnold DL, et al. Alemtuzumab for patients with relapsing multiple sclerosis after disease-modifying therapy: a randomised controlled phase 3 trial. The Lancet.2012;380(9856):1829-1839.

backBack to Blog Home