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group_5_presentation_1_-_multiple_sclerosis [2016/09/25 19:45] 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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| >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) |
| </style> | </style> | ||
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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. | ||
| + | |||
| + | 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. | ||
