Multiple Sclerosis (MS) is a chronic inflammatory autoimmune disease that affected approximately 2.5 million people worldwide (Pietrangelo, A & Higuera, V, 2015). It typically manifests in people between the ages of 15-50 years of age. In 2011 it was estimated that there were approximately 100 000 Canadians living with MS, which has steady been rising (Multiple Sclerosis Society of Canada, 2016). In recent years Canada has become known as having one of the highest incidence rates worldwide with an estimated 291 people per 100 000 diagnosed each year (Multiple Sclerosis Society of Canada, 2016; Pietrangelo, A & Higuera, V, 2015). Although the reason behind Canada’s high incidence rates are unclear researcher are exploring potential factors. According to the Multiple Sclerosis Society of Canada, MS is not considered to be a fatal disease and those with it can be expected to live near-normal lifespans, due to various forms of symptom management (Multiple Sclerosis Society of Canada, 2016).
Etiology
Currently research is unclear to the initial cause of MS. Most research leads us to believe that it is a combination of one's genetics and their environment. Some research studies also point to an infectious etiology, which include possible pathogens like the human herpes virus, Epstein Barr virus and mycoplasm pneumoniae, being possible triggers for the autoimmune reaction (Loma, I., & Heyman, R, 2011).
Pathophysiology Facts
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- ,MS is an autoimmune disease that causes the degeneration of the neurons in the CNS which includes the brain and spinal cord
- Damage caused through the mechanisms of both the innate and adaptive immune system
- Immune system attacks the myelin sheath surrounding the neurons causing inflammation and leads to the progress deterioration of the neuron
- Myelin sheath is necessary for the transmission of nerve impulses throughout the body
- Mild damage to the myelin sheath results in mild symptoms
- increasing damage or scar tissue that forms can cause permanent damage and severe symptoms
- (Loma, I., & Heyman, R, 2011)
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Innate Immune system
- Governs the antigen nonspecific response through the activation of specific receptors called toll-like receptors (TLRs)
- Activation of TLRs results in the production of cytokines
- For example: TLRs activate dendritic cells which activates T cells causing cytokines such as IL-10, to be released, which causes inflammation and damage to the neurons
- (Loma, I., & Heyman, R, 2011)
- Activated by specific antigens being presented to T lymphocytes by antigen presenting cells (APCs)
- APCs include B cells, dendritic cells, microglia and macrophages
- Once the APCs is presented to the T cell, activation and response of CD4 and CD8 cells occur
- CD4 cells come from Th1, Th2, or Th17 which secrete cytokines and cause inflammation and nerve damage
- Decrease in the number of regulatory T cells, which means there is a no regulation on the number of Th1, Th2 and Th17 cytokines released
- Lack of regulation leads to more inflammation and further nerve damage
- CD8 cells kill glial cells, leaving axons exposed, transecting axons, promoting vascular permeability and activating oligodendrocyte death which leads to MS lesions
- More research needs to be completed to fully understand the mechanism behind the disease
- (Loma, I., & Heyman, R, 2011)
TYPES OF MULTIPLE SCLEROSIS
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- Relapsing/Remitting Multiple Sclerosis (RRMS): Most common type, approximately 85% of cases. Characterized by discrete attacks that evolve over days to weeks followed by a period of remission where the patient does not experience worsening function.
- Secondary Progressive Multiple Sclerosis (SPMS): Initial relapses, followed by gradual neurological deterioration without acute attacks.
- Primary Progressive Multiple Sclerosis (PPMS): Steady functional decline from the onset of the disease. No relapses ever.
- Progressive Relapsing Multiple Sclerosis: Steady functional decline from the onset of the disease with later acute attacks. Only distinguished from PPMS later on in the disease
- (Loma, I., & Heyman, R., 2011)