Myelin and Neuropsychological Impact of Multiple Sclerosis which Causes Demyelination - Term Paper Example

Function of Myelin and Neuropsychological Impact of Multiple Sclerosis which Causes Demyelination Murtaza, Muhammad Junaid Islamabad, Pakistan Abstract This paper explores the specialized function of myelin and a disorder that causes degeneration of myelin sheath or demyelination. Axons are wrapped in cells with a high concentration of a white, fatty substance called Myelin.Myelin sheath not only serve as a fatty insulating material covering the axon, but also speeds up the transmission of that moves along axon. Myelinated neurons differ with unmyelinated neurons because of its size and functionality. The myelin sheath is derived from special type of Glial cell that provides various type of support for neurons, because of certain disorders it can be degenerated. The factor which hinders them to regenerate is the inappropriate muscle neuron that is paired with the corresponding damaged motor neurons. Thus, regeneration may sometimes fail. If myelin regeneration fails, some neurons die without being regenerated which is known as demyelination.Martin et al. s (2001) termed Multiple Sclerosis (MS) as one of the biggest factors that may trigger demyelination. This essay examines impact of MS on Myelin sheath and causes of demyelination. Keywords: Multiple Sclerosis Function of Myelin and Neuropsychological Impact of Multiple Sclerosis which Causes Demyelination Myelin is an insulating material made up of protein and fat where the myelins sheath is made of. Myelin, on the other hand it is an outgrowth of glial cells, which are specialised cells that surround neurons, providing mechanical and physical support and electrical insulation. The myelin sheath is usually found in the axon of a neuron. This helps in the functioning of the nervous system as a whole. Its production is called myelination, which occurs during the fourteenth week of fetal development. Myelination occurs rapidly during the infancy period of an individual, thus, requiring him to eat food rich in fats. The myelin sheath’s main function is to speed up the impulses that were sent along the fiber that has myelin sheath (myelinated fiber). Impulses are nerve signals received by our various senses like the sense of hearing, touch, taste, smell, and sight. In myelinated fibers, these impulses hop on one Ranvier node to the other. On the other hand, impulses were sent by waves on unmyelinated fibers. If a single peripheral fiber has been damaged, the myelins sheath gives off a track that is responsible for its regeneration. The myelin sheath does not always attain the perfect regeneration for each fiber. Sometimes, the correct muscles fibers are nowhere to be found so some motor neurons of the peripheral nervous system die. When the myelin layer is damaged, the individual may be prone to a higher level of dysfunctionality. Unmyelinated fibers and myelinated axons of the mammalian central nervous system do not regenerate. The reason for this is that the CNS of mammals in enclosed in the spinal column, which has a lesser deal of trauma rather than the peripheral nervous system. Research shows that optic nerve fibers in postnatal rats can regroup. But its regeneration often depends on two conditions namely: axonal die-back has to be prevented with appropriate neurotrophic factors and neurite growth inhibitory components have to be inactivated. This led the scientists to further understand the regeneration of nerve fibers in mammalian CNS. For invertebrates, propagation of action potentials in unmyelinated axons is sufficient to run fast. To accelerate the speed, the axon should be a little larger. Increasing the speed of action potentials and increasing the diameter of the axon is not possible in vertebrates. Angeli et al. s (2010) mentions that Squid giant axons spread up to 1 mm in diameter and have a great speed. Mammalian nerves have about 400 fibers in the same cross-sectional area as the squid giant axon. So if every nerve fiber is size of the squid giant axon, every nerve in mammals would be about 2 cm in diameter. Thus a different mechanism for vertebrate nerve conduction increase has been developed: the insulating sheath of axons in the membranes of the myelin sheath. Some axons are not less than 150 rounds of Schwann cells, the effective thickness of the axon membrane ion leakage and eliminate increases 100 times through cell membranes, except for the periodic gaps called nodes of Ranvier. Goodman et al. s (2002) mentions that the physiological importance of saltatory nerve conduction are often difficult to understand for common people, especially students. A clever analogy of these events has recently been published, but the mechanism of mediation saltatory nerve conduction was not included. The mechanism of mediation saltatory nerve conduction, the propagation of action potentials on the activation of voltage-gated sodium channels depends on different factors. Think again, that the non-medullated axon sodium channel voltage depends on the length of the membrane. In contrast, myelinated axons of voltage-gated sodium channels in nodal areas. Nodes rooms (Ranvier nodes) are spaces ~ 2 microns long and unmyelinated. Unmyelinated spaces are located at ~ 1 mm intervals along the surface of axons (internodes rooms: myelinated wraps). Propagation of action potentials along the unmyelinated axons requires activation of voltage-gated sodium channels along the length of the axon. On the contrary, this requires the propagation of action potentials along myelinated axons to activate voltage-gated sodium channels in nodal areas. Giuliodori et al. s(2004) mentions that with this understanding, people would be able to recognize that the spread of the action potential along myelinated axons is much faster. To further underscore this point, here is an example; consider a myelinated axon 1.5 million microns in length. Only 0.2% of the axons (to 2994), contains the nodes of Ranvier, where the depolarization occurs. Similarly, a myelinated axon with a total area of ​​1.1781 million μm2 membrane is only 2352 (0.2%), which produces a depolarization. Assuming that the time constants equal to the activation of voltage-gated sodium channels along myelinated axons and unmyelinated, the myelin sheath, the length of the field and the surface, which produces a depolarization and reduced speed of propagation of action potentials, will increase. The myelin, like any other major parts of the body, has no escape from diseases. When a myelinated neuron loses its myelin sheath, this is called demyelination. Demyelination occurs when the nerves lose the myelin sheath that insulates them. This hallmarks different neurodegenerative autoimmune diseases such as multiple sclerosis (MS).When myelin degenerates, conduction of impulses can be severely damaged and the nerve eventually withers. Multiple sclerosis is an inflammatory disease, damage to myelin sheaths around axons, brain and spinal cord, causing demyelination and healing and a wide range of signs and symptoms. The onset of the disease usually occurs in young adults and is more common in women. It has an occurrence of 2 to 150 per 100,000 people. MS was described in 1868 by Jean-Martin Charcot. Demyelination due to MS can result in different symptoms determined by the uses of the damaged nerves. It prohibits the signal to travel between the brain and other parts of the body. Symptoms may be different from one patient to another. Usual symptoms include: Blurriness in the central visual field that affects only one eye; may be accompanied by pain upon eye movement, double vision; Difficulty controlling bowel movements or urination; Odd sensation in legs, arms, chest, or face, such as tingling or numbness, heat sensitivity, weakness of limbs; Loss of dexterity, speech and memory impairment; Heat sensitivity; Difficulty coordinating movement or balance disorder, fatigue. MS affects the ability of nerve cells in the brain and spinal cord, in communication with each other. Nerve cells communicate by electrical signals called action potentials on long-fiber axons that are wrapped in an insulating substance called myelin. In MS, the immune system attacks and damages the myelin. In case of loss of myelin, axons can no longer effectively carry signals. Name comes from multiple sclerosis, scarring (sclerosis, better known as plaques or lesions) and in particular in the white matter of the brain and spinal cord, which consists mainly of myelin. Although much is known about the procedures involved in the disease, the cause remains unknown. Theories include genetics or infections. Many environmental risk factors have been found. Almost all of the neurological symptoms may occur with the disease and often progresses to physical and cognitive disabilities. MS takes several forms, with new symptoms occurring either accumulates in discrete attacks (relapsing forms) or slowly over time (progressive forms). Between attacks, symptoms may disappear completely, but neurological problems are common, particularly as the disease progresses. There is no known cure for multiple sclerosis. Treatment attempted return of function after an attack, preventing new attacks and prevent disability. MS drugs can have side effects or bad to be tolerated and many patients pursue alternative treatments, despite the lack of support for scientific studies. The prognosis is difficult to predict, depending on the subtype of disease, disease characteristics of each patient; the first symptoms and the degree of disability the person experiences as time advances, the life expectancy of patients 5-10 years younger with respect to the affected population. References Angeli, E., Wagner, J., Lawrick, E., Moore, K., Anderson, M., Soderland, L., & Brizee, A. (2010, May 5). General format. Retrieved from http://owl.english.purdue.edu/owl/resource/560/01/ Calabrese, P. (2006) Neuropsychology of Multiple Sclerosis: An Overview. Journal of Neurology. ( SUPPL 1 ): 1/10-1/15 Chiaravalloti, N.D., Deluca, J. (2008) Cognitive Impairment in Multiple Sclerosis. Lancet Neurology. 7: 1139-51 Dowling J.E. Neurons and Network: An Introduction to Neuroscience. Cambridge, MA: Harvard Univ. Press, 1992, p. 44. Giuliodori, M.J., DiCarlo, S.E. (2004) Myelinated vs. Unmyelinated Nerve Conduction: A Novel Way of Understanding the Mechanisms. Universidad Nacional de La Plata: La Plata, Argentina. Goodman, B.E., and Waller, S.B. Propagation of action potentials in myelinated vs. unmyelinated neurons. Advan Physiol Educ 26: 223, 2002. Martin G.N., Buskist, W., Carlson, N.R. (2009) Psychology. Pearson: USA. Siegert, R.J., Abernethy, D.A. (2005) Depression in Multiply Sclerosis: A Review. Journal of Neurology, Neuropsychology, and Psychiatry. 76: 469-475. Read More