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group_3_presentation_1_-_epilepsy-_childhood_absence_epilepsy [2017/02/03 23:39] makdayr |
group_3_presentation_1_-_epilepsy-_childhood_absence_epilepsy [2017/02/04 00:04] makdayr |
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| ====== Prognosis and Prevention ====== | ====== Prognosis and Prevention ====== | ||
| - | Overall, the remission rate for CAE is 80% by early puberty, although these rates vary widely. Approximately, 11-18% of children who have CAE develop tonic-clonic seizures, which begin at puberty. If the child has tonic-clonic seizures as well as absence seizures, these are less likely to go away. However, they are usually easy to control. | + | Overall, the remission rate for CAE is 80% by early puberty, although these rates vary widely. Approximately, 11-18% of children who have CAE develop tonic-clonic seizures, which begin at puberty (Hirsh & Thomas, 2007).. If the child has tonic-clonic seizures as well as absence seizures, these are less likely to go away. However, they are usually easy to control. Early treatment to the anti-epileptic drugs may contribute to the permanent disappearance of the seizures. Drugs may be discontinued if a child has been seizure free for two-three years, but early discontinuation may trigger seizures (Hirsh & Thomas, 2007). |
| - | Early treatment to the anti-epileptic drugs (AEDs) may contribute to the permanent disappearance of the seizures. Drugs may be discontinued if a child has been seizure free for two-three years, but early discontinuation may trigger seizures. | + | |
| - | A study conducted by Wirrell et al found that, in a study size of 81 children, forty-seven (65%) were in remission at the time of follow-up, which was 20.4 years on average. 17% of this population were taking AEDs but continued to have seizures, while 13% were taking AEDs and 15% had progressed to JME. This evidence suggests that when AEDs are taken, chances of remission into adulthood are high. | + | A study conducted by Wirrell et al found that, in a study size of 81 children, forty-seven (65%) were in remission at the time of follow-up, which was 20.4 years on average (Wirrell et al, 1996). 17% of this population were taking AEDs but continued to have seizures, while 13% were taking AEDs and 15% had progressed to JME. This evidence suggests that when AEDs are taken, chances of remission into adulthood are high (Wirrell et al, 1996). |
| - | Of 81 children with CAE, 72 (89%) were contacted for follow-up. Mean age at seizure onset was 5.7 years (range, 1 to 14 years) and at follow-up was 20.4 years (range, 12 to 31 years). Forty-seven (65%) were in remission. Twelve others (17%) were not taking AEDs but continued to have seizures. Thirteen (18%) were taking AEDs; five were seizure-free over the last year (in four of these a trial without AEDs had previously failed). Fifteen percent of the total cohort had progressed to JME. Multiple clinical and EEG factors were examined as predictors of outcome. Factors predicting no remission (p < 0.05) included cognitive difficulties at diagnosis, absence status prior to or during AED treatment, development of generalized tonic clonic or myoclonic seizures after onset of AEDs, abnormal background on initial EEG, and family history of generalized seizures in first-degree relatives. | + | |
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| - | Furthermore, in a retrospective analysis of a cohort of 163 patients, 64 of which had CAE, were followed for a duration of 25.8 years. It was found that 58% of patients with CAE were in remission, and had been seizure free for a period of at least two years. | + | |
| + | Furthermore, in a retrospective analysis of a cohort of 163 patients, 64 of which had CAE, were followed for a duration of 25.8 years. It was found that 58% of patients with CAE were in remission, and had been seizure free for a period of at least two years (Trinka et al 2004). | ||
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| - | For patients who refuse pharmacological treatment, a ketogenic diet, special high fat, low-carbohydrate diet, is available as an alternative regimen to control and manage seizures. The ketogenic diet may prove to be beneficial in comparison to the AEDs. Studies find that approximately 50% reduction in the frequency of seizures. In a recent study of 317 Chinese children, 35.0%, 26.2%, and 18.6% children showed >50% seizure reduction at three, six, and 12 months, respectively. Furthermore, in a systematic review conducted by Keene et al, with a total collective population of 972, an average of 15.6% of the patients had become seizure-free at the 6-month mark, and 33.0% had more than 50% reduction in seizure frequency after incorporating the ketogenic diet. | + | For patients who refuse pharmacological treatment, a ketogenic diet, special high fat, low-carbohydrate diet, is available as an alternative regimen to control and manage seizures. The ketogenic diet may prove to be beneficial in comparison to the antiepileptic drugs. Studies find that approximately 50% reduction in the frequency of seizures (Sharma & Jain 2014). In a recent study of 317 Chinese children, 35.0%, 26.2%, and 18.6% children showed greater than a 50% seizure reduction at three, six, and 12 months, respectively. Furthermore, in a systematic review conducted by Keene et al, with a total collective population of 972, an average of 15.6% of the patients had become seizure-free at the 6-month mark, and 33.0% had more than 50% reduction in seizure frequency after incorporating the KD (Sharma & Jain 2014). |
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| + | Furthermore, a study by Neal et al aimed to test the efficacy of the ketogenic diet in a randomised controlled trial. Children were assigned to one of two groups: the control group, or the ketogenic diet group. The control group had no changes to treatment. It was found that after a period of 3 months, the mean percentage of baseline seizures was significantly lower in the ketogenic diet group than in the control group (62.0% vs 136.9%). These results support the use of the ketogenic diet in CAE. (Neal et al, 2008). This diet may be effective due to changing from a glucose substrate to one that is a ketone body (Swink,1997). The ketone body substrate seems to have anticonvulsant properties; this information is especially useful for developing new drugs that can imitate the biochemical effects of a ketone diet in the future (Swink,1997). | ||
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| Crunelli, V., & Leresche, N. (2002). Childhood absence epilepsy: genes, channels, neurons andnetworks. //Nature Reviews Neuroscience//, 3(5), 371-382. | Crunelli, V., & Leresche, N. (2002). Childhood absence epilepsy: genes, channels, neurons andnetworks. //Nature Reviews Neuroscience//, 3(5), 371-382. | ||
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| Devinsky, O., & Sirven, J. I. (2013). Myoclonic Seizures and Tonic-Clonic Seizures. Epilepsy Foundation. Retrieved January 24, 2017, from http://www.epilepsy.com/learn/types-seizures/myoclonic-seizures | Devinsky, O., & Sirven, J. I. (2013). Myoclonic Seizures and Tonic-Clonic Seizures. Epilepsy Foundation. Retrieved January 24, 2017, from http://www.epilepsy.com/learn/types-seizures/myoclonic-seizures | ||
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| Donner, E. J. (2010). Absence Seizures. about kid’s health. Retrieved January 24, 2017 from, http://www.aboutkidshealth.ca/En/ResourceCentres/Epilepsy/UnderstandingEpilepsyDia gnosis/TypesofSeizures/Pages/Absence-Seizures.aspx | Donner, E. J. (2010). Absence Seizures. about kid’s health. Retrieved January 24, 2017 from, http://www.aboutkidshealth.ca/En/ResourceCentres/Epilepsy/UnderstandingEpilepsyDia gnosis/TypesofSeizures/Pages/Absence-Seizures.aspx | ||
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| Epilepsy. (2013, May 31). Mayo Clinic. Retrieved January 21, 2017, from http://www.mayoclinic.org/diseases-conditions/epilepsy/basics/definition/CON-20033721?p=1 | Epilepsy. (2013, May 31). Mayo Clinic. Retrieved January 21, 2017, from http://www.mayoclinic.org/diseases-conditions/epilepsy/basics/definition/CON-20033721?p=1 | ||
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| "Epilepsy". Fact Sheets. World Health Organization. October 2012. Retrieved January 21, 2017. | "Epilepsy". Fact Sheets. World Health Organization. October 2012. Retrieved January 21, 2017. | ||
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| Glauser, T. A., Cnaan, A., Shinnar, S., Hirtz, D. G., Dlugos, D., Masur, D., ... & Adamson, P. C. (2013). Ethosuximide, valproic acid, and lamotrigine in childhood absence epilepsy: initial monotherapy outcomes at 12 months. //Epilepsia//, 54(1), 141-155. | Glauser, T. A., Cnaan, A., Shinnar, S., Hirtz, D. G., Dlugos, D., Masur, D., ... & Adamson, P. C. (2013). Ethosuximide, valproic acid, and lamotrigine in childhood absence epilepsy: initial monotherapy outcomes at 12 months. //Epilepsia//, 54(1), 141-155. | ||
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| Goldenberg, M. M. (2010). Overview of drugs used for epilepsy and seizures: etiology, diagnosis, and treatment. //Pharmacy and Therapeutics,// 35(7), 392. | Goldenberg, M. M. (2010). Overview of drugs used for epilepsy and seizures: etiology, diagnosis, and treatment. //Pharmacy and Therapeutics,// 35(7), 392. | ||
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| Gotman, J. (2008). Epileptic Networks studied with EEG-fMRI. //Epilepsia//. 49 (s3), 42-51. | Gotman, J. (2008). Epileptic Networks studied with EEG-fMRI. //Epilepsia//. 49 (s3), 42-51. | ||
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| Ha, H., & Bellanger, R. (2013). Epilepsy: treatment and management. //US Pharm//, 38(1), 35-39. | Ha, H., & Bellanger, R. (2013). Epilepsy: treatment and management. //US Pharm//, 38(1), 35-39. | ||
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| Holmes, G. L. & Fisher, R. S. (2013). Childhood Absence Epilepsy. Epilepsy Foundation. Retrieved January 24, 2017, from http://www.epilepsy.com/learn/types-epilepsy-syndromes/childhood-absence-epilepsy | Holmes, G. L. & Fisher, R. S. (2013). Childhood Absence Epilepsy. Epilepsy Foundation. Retrieved January 24, 2017, from http://www.epilepsy.com/learn/types-epilepsy-syndromes/childhood-absence-epilepsy | ||
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| Loiseau, P., Panayiotopoulos, C. P., & Hirsch, E. (2002). Childhood absence epilepsy and related syndromes. //Epileptic syndromes in infancy, childhood and adolescence//, 3, 285-304. | Loiseau, P., Panayiotopoulos, C. P., & Hirsch, E. (2002). Childhood absence epilepsy and related syndromes. //Epileptic syndromes in infancy, childhood and adolescence//, 3, 285-304. | ||
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| McCandless, D. W. (2011). Epilepsy. Simple Partial Seizures (143-152) Chicago. IL: Springer Science+Business Media. | McCandless, D. W. (2011). Epilepsy. Simple Partial Seizures (143-152) Chicago. IL: Springer Science+Business Media. | ||
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| McCormick, D. A., & Contreras D. (2001). On the Cellular and Network Bases of Epileptic Seizures. //Annul. Rev. Physiol,// 63: 815-846. | McCormick, D. A., & Contreras D. (2001). On the Cellular and Network Bases of Epileptic Seizures. //Annul. Rev. Physiol,// 63: 815-846. | ||
| + | Neal, E. G., Chaffe, H., Schwartz, R. H., Lawson, M. S., Edwards, N., Fitzsimmons, G., ... & Cross, J. H. (2008). The ketogenic diet for the treatment of childhood epilepsy: a randomised controlled trial. The Lancet Neurology, 7(6), 500-506. | ||
| Peterson, S. L., & Albertson, T. E. (Eds.). (1998). Neuropharmacology methods in epilepsy research. CRC Press. | Peterson, S. L., & Albertson, T. E. (Eds.). (1998). Neuropharmacology methods in epilepsy research. CRC Press. | ||
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| Pillai, J. & Sperling, M. R. (2006). Interictal EEG and the Diagnosis of Epilepsy. //Epilepsia//. 47 (s1), 14-22. | Pillai, J. & Sperling, M. R. (2006). Interictal EEG and the Diagnosis of Epilepsy. //Epilepsia//. 47 (s1), 14-22. | ||
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| Sander, J. W. (2003). The epidemiology of epilepsy revisited.// Current opinion in neurology//, 16(2), 165-170. | Sander, J. W. (2003). The epidemiology of epilepsy revisited.// Current opinion in neurology//, 16(2), 165-170. | ||
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| + | Sharma, S., & Jain, P. (2014). The ketogenic diet and other dietary treatments for refractory epilepsy in children. Annals of Indian Academy of Neurology, 17(3), 253-258. | ||
| Stafstrom, C. E. (1998). Back to Basics: The Pathophysiology of Epileptic Seizures: A Primer For Pediatricians. Pediatrics in Review, 19 (10). | Stafstrom, C. E. (1998). Back to Basics: The Pathophysiology of Epileptic Seizures: A Primer For Pediatricians. Pediatrics in Review, 19 (10). | ||
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| Stafstrom, C. E., Rho, J. M. (2016). Pathophysiology of seizures and epilepsy. URL: https://www.uptodate.com/contents/pathophysiology-of-seizures-and-epilepsy | Stafstrom, C. E., Rho, J. M. (2016). Pathophysiology of seizures and epilepsy. URL: https://www.uptodate.com/contents/pathophysiology-of-seizures-and-epilepsy | ||
| - | What Is Epilepsy? (2014, January). Epilepsy Foundation. Retrieved January 21, 2017, http://www.epilepsy.com/learn/epilepsy-101/what-epilepsy | + | Swink, T. D., Vining, E. P., & Freeman, J. M. (1996). The ketogenic diet: 1997. Advances in pediatrics, 44, 297-329. |
| + | Trinka, E., Baumgartner, S., Unterberger, I., Unterrainer, J., Luef, G., Haberlandt, E., & Bauer, G. (2004). Long-term prognosis for childhood and juvenile absence epilepsy. Journal of neurology, 251(10), 1235-1241. | ||
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| + | What Is Epilepsy? (2014, January). Epilepsy Foundation. Retrieved January 21, 2017, http://www.epilepsy.com/learn/epilepsy-101/what-epilepsy | ||
| - | What is Epilepsy? (2016). Epilepsy Ontario. Retrieved January 21, 2017, from http://epilepsyontario.org/about-epilepsy/what-is-epilepsy/ | + | Wirrell, E. C., Camfield, C. S., Camfield, P. R., Gordon, K. E., & Dooley, J. M. (1996). Long-term prognosis of typical childhood absence epilepsy Remission or progression to juvenile myoclonic epilepsy. Neurology, 47(4), 912-918. |
