Multiple Sclerosis Pathophysiology
Multiple sclerosis tends to be an inflammatory demyelinating disease that affects the central nervous system, particularly when the immune cells attack the central nervous system causing neuron degeneration, tissue damage, and inflammation. Multiple sclerosis pathophysiology involves many co-existing and interrelated stages that are usually depicted in a uniquely simplified stepwise manner. In this condition, acute relapse tends to be a clear indicator of the new inflammatory activity that occurs in the central nervous system, and they tend to be driven by the autoreactive T-cells that usually trigger an attack in the myelin-producing oligodendrocytes. The loss of the impaired remyelination and oligodendrocytes may result in accumulation of the relapse related disability. The inflammatory lesions that occur are also linked to the axonal transaction loss that usually occur early during the disease course and tends to get worse with time. The high dosage corticosteroids are mainly used to reduce acute central nervous inflammation. This short term advantage tend to occur at the expense of the optimal demyelination since the animal models have accurately demonstrated that the corticosteroids could cause oligodendrocyte loss in various brain regions. Further animal model information or data tend to suggest that the corticosteroids tend to restrict the development of body neurons and tend to increase the apoptosis of the body neurons that usually form the optic nerve. As the multiple sclerosis disease progress or evolve, the expected outcome of the high dose corticosteroids on the neurons and oligodendrocytes may cause depression, steroid resistance, and disability
The signs and symptoms of multiple sclerosis tend to differ depending on the level of damage that the nerves have caused, and the location of the affected nerve fibers. Individuals with severe nerve damage tend to lose their ability to walk on their own while then other individuals tend to experience the long periods of remissions without experiencing new symptoms. The most common signs and symptoms of multiple sclerosis include; first, weakness or numbness of one or more body limbs. These symptoms mainly occur on one side of the body at a time. Secondly, electric shock sensations that tend to occur together with certain neck movements, particularly when bending the neck forward. Thirdly, tremor, which results in lack of body coordination. Fourth, development of vision problems, for instance, having blurry vision, and prolonged double vision. Other signs and symptoms include; dizziness, fatigue, and slurred speech.
There is no known specific cause of multiple sclerosis; however, there are various risk factors that are likely to cause or increase the chances of acquiring the disease. These risk factors include, first, age, multiple sclerosis may occur at any age, but it mainly affects the individuals that are between the age of sixteen to sixty-five years. Secondly, Gender. Women tend to be at a higher chance of acquiring the disease. According to research, women are two to three times more likely to get the disease as compared to men (Dendrou, Fugger, & Friese, 2015). Thirdly, race, the white population, mainly those with the northern European descent, tend to be at a higher risk of developing the disease. Fourth, climate, multiple sclerosis tends to be common, particularly in the nations with temperate climates such as Canada, New Zealand, and Europe.
Amyotrophic Lateral Sclerosis
Amyotrophic lateral sclerosis is considered to be a progressive neurodegenerative condition that is characterized or identified through the death of the pyramidal neurons that occur in the motor neurons and motor cortex in the central spinal cord and brain stem.
The mechanism that exists in the neurodegeneration of the amyotrophic lateral sclerosis tend to be multifactorial, and they usually operate through the interrelated genetic and molecular pathways. In most cases, the neurodegeneration in amyotrophic lateral sclerosis occurs due to the complex interaction of the generation of the free radicals, glutamate excitotoxicity SOD1 enzymes, cytoplasmic protein aggregate, and the disruption of the axonal transport processes through accumulating the neurofilament intracellular aggregates. The mutation of FUS and TARDBP leads to the formation of the intracellular aggregates that tend to be harmful to the body neurons (Brown, & Al-Chalabi, 2017). Also, the activation of the microglia leads to the production of pro-inflammatory cytokines that trigger further toxicity. Ultimately, the motor neuron degeneration happens as a result of activation of the calcium-dependent enzymatic pathways.
Amyotrophic lateral sclerosis is manifested by various signs and symptoms that tend to differ among individuals. This signs and symptoms include, difficulties walking, hand weakness, slurred speech, falling and tripping, twisting in the arm, muscle cramps, and having difficulty holding the head upright. The signs and symptoms of the amyotrophic disease usually start in the hands, limbs, or feet and later spread to other body parts. However, as the disease progress, other body nerve cells are destroyed, and the body muscle continues to weaken.
The amyotrophic lateral sclerosis is caused by various factors that include, first, gene mutation. Human genetic mutation can trigger the inherited ALS, which tends to cause almost the same signs and symptoms as the non-inherited ALS. Secondly, chemical imbalance. Individuals with ALS tend to have higher levels of glutamate, which is considered toxic to certain nerve cells. Thirdly, protein mishandling, the mishandled proteins that exist within the nerve cells may result in the gradual accumulation of the abnormal forms of protein in the cells, thus affecting the nerve cells. Fourth, the disorganized body immune response. In some situations, a person’s body immune system may begin to attack some of his or her normal body cells, which may result in the death of nerve body nerve cells.
Brown, R. H., & Al-Chalabi, A., (2017). Amyotrophic lateral sclerosis. New England Journal of Medicine, 377(2), 162-172. Retrieved from https://www.nejm.org/doi/full/10.1056/NEJMra1603471
Dendrou, C. A., Fugger, L., & Friese, M. A. (2015). Immunopathology of multiple sclerosis. Nature Reviews Immunology, 15(9), 545. Retrieved from https://www.researchgate.net/profile/Manuel_Friese2/publication/280910740_Immunopathology_of_multiple_sclerosis/links/57cb446708aedb6d6d9a2519.pdf
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