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group_5_presentation_1_-_multiple_sclerosis [2016/09/25 19:40] singhj35 |
group_5_presentation_1_-_multiple_sclerosis [2018/01/25 15:18] (current) |
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| {{:ms-mri_t1_535x314-01.jpg|}} | {{:ms-mri_t1_535x314-01.jpg|}} | ||
| - | Figure 1: A T1-weighted MRI demonstrating permanent lesions in a MS patient. The dark spots | + | **Figure 1**: A T1-weighted MRI demonstrating permanent lesions in a MS patient. The dark spots |
| in the scan are the lesions. (Source: Spinms, 2016) | in the scan are the lesions. (Source: Spinms, 2016) | ||
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| **Evidence Supporting Immune-mediated Pathophysiology:** | **Evidence Supporting Immune-mediated Pathophysiology:** | ||
| - | In an experiment conducted by Tzartos et al. (2008), they wanted to explore specifically which immune system factors and cells were involved in demyelination as well as the role of Interleukin-17 in demyelination (Tzartos et al., 2008). Initially, they wanted to determine whether T cells, astrocytes, microglia/macrophages, oligodendrocytes were able to produce IL-17, since there were earlier reports that IL-17 is present in higher concentrations in MS tissues. They used in situ hybridization and immunofluorescent-labelled IL-17 mRNA (Tzartos et al., 2008). In addition, they also labelled the interested cells and used an overlap imaging technique to show where IL-17 was present and therefore indicating its production . Astrocytes, T cells, oligodendrocytes all overlapped with IL-17 expression while microglia/macrophages did not (Tzartos et al., 2008). ( Fig X- T cells showed the largest expression, while astrocytes and oligodendrocytes showed small amount). In another experiment, they then wanted to see whether there was an increase of activity of CD3 T cell involved ( Th17 cells) in lesions/plaques and compare this to normal nerve tissue. They also looked at IL-17 to assess the activity of the activated Th17 cells (Tzartos et al., 2008). Using tissue samples from the perivascular areas of acute lesions, active borders of chronic active lesions, inactive lesions, inactive areas of chronic active lesions and as well as NAWM in MS patients(normal appearing white matter), they observed that there was increased amount of IL-17 cytokine and CD3 T cells in MS patient tissues samples compared to the non MS brain (control variable) . This indicated that IL-17 is largely involved in the inflammatory response in MS (Tzartos et al., 2008). In addition, they looked at alternative method to quantify the presence of IL-17 in MS patient brain sample. They compared the densities and were able to conclude the similar results as previously reported. Therefore, demonstrating that IL-17 and CD3 T cells were involved in carrying out an inflammatory response leading to demyelination of neurons (Tzartos et al., 2008). | + | In an experiment conducted by Tzartos et al. (2008), they wanted to explore specifically which immune system factors and cells were involved in demyelination as well as the role of Interleukin-17 in demyelination (Tzartos et al., 2008). Initially, they wanted to determine whether T cells, astrocytes, microglia/macrophages, oligodendrocytes were able to produce IL-17, since there were earlier reports that IL-17 is present in higher concentrations in MS tissues. They used in situ hybridization and immunofluorescent-labelled IL-17 mRNA (Tzartos et al., 2008). In addition, they also labelled the interested cells and used an overlap imaging technique to show where IL-17 was present and therefore indicating its production . Astrocytes, T cells, oligodendrocytes all overlapped with IL-17 expression while microglia/macrophages did not, as shown in //Figure 4// (Tzartos et al., 2008). In another experiment, they then wanted to see whether there was an increase of activity of CD3 T cell involved ( Th17 cells) in lesions and compare this to normal nerve tissue. They also looked at IL-17 to assess the activity of the activated Th17 cells (Tzartos et al., 2008). Using tissue samples from the perivascular areas of acute lesions, active borders of chronic active lesions, inactive lesions, inactive areas of chronic active lesions and as well as NAWM in MS patients(normal appearing white matter), they observed that there was increased amount of IL-17 cytokine and CD3 T cells in MS patient tissues samples compared to the non MS brain (control variable), highlighted in //Figure 5// below. This indicated that IL-17 is largely involved in the inflammatory response in MS (Tzartos et al., 2008). In addition, they looked at alternative method to quantify the presence of IL-17 in MS patient brain sample. They compared the densities from //Figure 6// and were able to conclude the similar results as previously reported. Therefore, demonstrating that IL-17 and CD3 T cells were involved in carrying out an inflammatory response leading to demyelination of neurons (Tzartos et al., 2008). |
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| >Glatiramer acetate is thought to alter the immune processes believed to be responsible for the pathogenesis of MS, however its mechanism is not fully known. (Hedley, 2012) Studies have shown that there is delay of progression from CIS to “clinically definite MS” in MS patients for up to three years with use of glatiramer acetate. (Hedley, 2012) This treatment reduces the number and severity of relapses, and the formation of new lesions on a brain MRI, however its effects on long-term progression are not clear. (Hedley, 2012) Adverse effects of glatiramer acetate minor and mainly consist of injection site reactions, seen in 70% of patients. (Hedley, 2012) Other less common side effects include lipoatrophy, flushing, shortness of breath, chest tightness, and palpitations. (Hillman, 2014) | >Glatiramer acetate is thought to alter the immune processes believed to be responsible for the pathogenesis of MS, however its mechanism is not fully known. (Hedley, 2012) Studies have shown that there is delay of progression from CIS to “clinically definite MS” in MS patients for up to three years with use of glatiramer acetate. (Hedley, 2012) This treatment reduces the number and severity of relapses, and the formation of new lesions on a brain MRI, however its effects on long-term progression are not clear. (Hedley, 2012) Adverse effects of glatiramer acetate minor and mainly consist of injection site reactions, seen in 70% of patients. (Hedley, 2012) Other less common side effects include lipoatrophy, flushing, shortness of breath, chest tightness, and palpitations. (Hillman, 2014) | ||
| - | Deciding on which treatment to use (interferon beta or glatiramer acetate) depends on patient preference in type and frequency of injection. (See Figure **X**) | + | Deciding on which treatment to use (interferon beta or glatiramer acetate) depends on patient preference in type and frequency of injection. (See Figure 7) |
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| {{:table_01.png|}} | {{:table_01.png|}} | ||
| - |  **Figure X**: The dosing, frequency, and route of administration for the ACB-R therapies. (Source: Hillman & Khorassani, 2014) | + |  **Figure 7**: The dosing, frequency, and route of administration for the ACB-R therapies. (Source: Hillman & Khorassani, 2014) |
| </style> | </style> | ||
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| {{:treadmill_training.jpg|}} | {{:treadmill_training.jpg|}} | ||
| - | **Figure X**: Body weight assisted treadmill training. There is physical assistance for each | + | **Figure 8**: Body weight assisted treadmill training. There is physical assistance for each |
| leg due to impaired walking ability. (Source: http://agelessphysio.com) | leg due to impaired walking ability. (Source: http://agelessphysio.com) | ||
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| __Walking Ability__ | __Walking Ability__ | ||
| - | > A common symptom of MS is impaired walking ability. Dalfampridine (Fampyra or Ampyra) can be used to improve walking ability. Dalfampridine is a potassium channel blocker that enhances conduction along demyelinated nerve fibres. (Hillman, 2014) In phase 3 clinical trials, walking speed was increased by about 25% within weeks in MS patients. (Hedley, 2012) There are, however, side effects such as a greater risk of seizures, anxiety, insomnia, dizziness, and tremor. (Hedley, 2012) In terms of physical therapy, exercise through treadmill training has been shown to improve walking endurance and velocity. (Amato & Portaccio, 2012) (See Figure **X**) | + | > A common symptom of MS is impaired walking ability. Dalfampridine (Fampyra or Ampyra) can be used to improve walking ability. Dalfampridine is a potassium channel blocker that enhances conduction along demyelinated nerve fibres. (Hillman, 2014) In phase 3 clinical trials, walking speed was increased by about 25% within weeks in MS patients. (Hedley, 2012) There are, however, side effects such as a greater risk of seizures, anxiety, insomnia, dizziness, and tremor. (Hedley, 2012) In terms of physical therapy, exercise through treadmill training has been shown to improve walking endurance and velocity. (Amato & Portaccio, 2012) (See Figure 8) |
| __Depression__ | __Depression__ | ||
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| Amato, M. P. & Portaccio, E. (2012). Management options in multiple sclerosis-associated fatigue. Expert Opinion on Pharmacotherapy, 13(2), 207-216 | Amato, M. P. & Portaccio, E. (2012). Management options in multiple sclerosis-associated fatigue. Expert Opinion on Pharmacotherapy, 13(2), 207-216 | ||
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| + | Ascherio A, Munger KL (April 2007). "Environmental risk factors for multiple sclerosis. Part I: the role of infection". Annals of Neurology. 61 (4): 288–99. | ||
| Brosnan, C. F., & Raine, C. S. (1996). Mechanisms of immune injury in multiple sclerosis. Brain Pathology, 6(3), 243-257. | Brosnan, C. F., & Raine, C. S. (1996). Mechanisms of immune injury in multiple sclerosis. Brain Pathology, 6(3), 243-257. | ||
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| + | Compston A, Coles A (October 2008). "Multiple sclerosis". Lancet. 372 (9648): 1502–17 | ||
| de la Fuente AG et al. Vitamin D receptor-retinoid X receptor heterodimer signaling regulates oligodendrocyte progenitor cell differentiation. J Cell Biol. 2015; 211(5):975-85. | de la Fuente AG et al. Vitamin D receptor-retinoid X receptor heterodimer signaling regulates oligodendrocyte progenitor cell differentiation. J Cell Biol. 2015; 211(5):975-85. | ||
| Multiple Sclerosis Clinical Presentation. (2016). Retrieved September 18, 2016, from http://emedicine.medscape.com/article/1146199-clinical | Multiple Sclerosis Clinical Presentation. (2016). Retrieved September 18, 2016, from http://emedicine.medscape.com/article/1146199-clinical | ||
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| + | Dyment DA, Ebers GC, Sadovnick AD (February 2004). "Genetics of multiple sclerosis".Lancet Neurol. 3 (92): 104–10 | ||
| Fowler, C. J., Panicker, J. N., Drake, N., Harris, C., Harrison, S. C. W., Kirby, M., Lucas, M., Macleod, N., Mangnall, J., North, A., et al. (2009). A UK consensus on the management of the bladder in multiple sclerosis. Postgraduate Medical Journal. 85, 552-559. | Fowler, C. J., Panicker, J. N., Drake, N., Harris, C., Harrison, S. C. W., Kirby, M., Lucas, M., Macleod, N., Mangnall, J., North, A., et al. (2009). A UK consensus on the management of the bladder in multiple sclerosis. Postgraduate Medical Journal. 85, 552-559. | ||
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| + | Gilden DH (March 2005). "Infectious causes of multiple sclerosis". The Lancet Neurology. 4 (3): 195–202 | ||
| Hedley, L. (2012). Multiple sclerosis treatment options. The Pharmaceutical Journal. 288, 247-250. | Hedley, L. (2012). Multiple sclerosis treatment options. The Pharmaceutical Journal. 288, 247-250. | ||
