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group_2_presentation_2_-_epilepsy [2017/11/02 23:43] gaubaa |
group_2_presentation_2_-_epilepsy [2018/01/25 15:18] (current) |
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| + | Link to presentation: https://docs.google.com/a/mcmaster.ca/presentation/d/1dW15LKA4tzy2A1yKkckc6njZKW-URDgH05njQZ8UVXI/edit?usp=sharing | ||
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| ====== Introduction ====== | ====== Introduction ====== | ||
| Epilepsy is a chronic condition that affects the central nervous system and is characterized by a disruption in the normal functioning of neuronal signaling and activity. Epilepsy is characterized by the presence of unprovoked or spontaneously recurring epileptic seizures ranging in severity and occur within a short span of time. There is often no immediately identifiable trigger for epileptic seizures and two or more seizures occurring within a span of 24 hours is considered an isolated event. Seizures that occur during the neonatal period of life, and acute symptomatic seizures linked to substance abuse are not considered epileptic. (Banerjee, Filippi, & Hauser, 2009) (Scharfman, 2007). The spectrum of epileptic seizures range from a lapse in concentration to unconsciousness with regards to severity. In addition, the World Health Organization defines epilepsy as a prevalent and major health concern world wide, and statistics show that over 50 million individuals world-wide present the disorder (World Health Organization, 2015). | Epilepsy is a chronic condition that affects the central nervous system and is characterized by a disruption in the normal functioning of neuronal signaling and activity. Epilepsy is characterized by the presence of unprovoked or spontaneously recurring epileptic seizures ranging in severity and occur within a short span of time. There is often no immediately identifiable trigger for epileptic seizures and two or more seizures occurring within a span of 24 hours is considered an isolated event. Seizures that occur during the neonatal period of life, and acute symptomatic seizures linked to substance abuse are not considered epileptic. (Banerjee, Filippi, & Hauser, 2009) (Scharfman, 2007). The spectrum of epileptic seizures range from a lapse in concentration to unconsciousness with regards to severity. In addition, the World Health Organization defines epilepsy as a prevalent and major health concern world wide, and statistics show that over 50 million individuals world-wide present the disorder (World Health Organization, 2015). | ||
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| ====== Brain Physiology ====== | ====== Brain Physiology ====== | ||
| - | The cortex is primarily composed of two types of neurons, Principle and Interneurons. Principle neurons output action potentials to distal neurons and are excitatory in nature. Interneurons make up the local circuit and influence neighbouring neurons and are inhibitory (Bromfield, 2008). Recurrent inhibition occurs when a principle neurons synapses on an interneuron, once the interneuron has been activated is can elicit an inhibitory effect on the principle cell creating a negative feedback loop. The instigation of a seizure transpires when there is a sudden burst of excitatory activity in a discrete region of the cortex, example the thalamus, which expands to local regions. In order to establish seizure-like symptoms, there needs to be a high-frequency bursts of action potentials from the thalamus and the hyper-synchronization of principle cells (Bromfield, 2008). Each neuron will experience a paroxysmal depolarizing shift which can be characterized by a sustained depolarization (through the release of glutamate and the activation of Ca2+ and Na+ channels), followed by a hyperpolarization (through the opening of K+ channels and influx of Cl- ions via GABA). Propagation of an excitatory response and therefore spreading of seizure-like symptoms occur when this inhibitory response is lost. The loss of this hyperpolarization can occur for a number of reasons such as; a) due to the sustained depolarization, there is an increase in extracellular K+ which decreases the electrochemical gradient causing less of a K+ efflux, b) sustained depolarization leads to increased Ca2+ levels which leads to increased vesicle fusion and neurotransmitter release, c) depolarization leads to activation of excitatory NMDA R causing increased Ca2+ influx. Referring to Figure 10, it can be seen propagation of the seizure can be attributed to increased excitatory behaviour and diminished inhibition (Bromfield, 2008). | + | The cortex is primarily composed of two types of neurons, principle and interneurons. Principle neurons output action potentials to distal neurons and are excitatory in nature. Interneurons make up the local circuit and influence neighbouring neurons and are inhibitory (Bromfield, 2008). Recurrent inhibition occurs when a principle neurons synapses on an interneuron, once the interneuron has been activated is can elicit an inhibitory effect on the principle cell creating a negative feedback loop. The instigation of seizure transpires when there is a sudden burst of excitatory activity in a discrete region of the cortex, example the thalamus, and expands to local regions. In order to establish seizure-like symptoms, there needs to be a high-frequency bursts of action potentials from the thalamus and the hyper-synchronization of principle cells (Bromfield, 2008). Each neuron will experience a paroxysmal depolarizing shift which can be characterized by a sustained depolarization (through the release of glutamate and the activation of Ca2+ and Na+ channels), followed by a hyperpolarization (through the opening of K+ channels and influx of Cl- ions via GABA). Propagation of an excitatory response and therefore spreading of seizure-like symptoms occur when this inhibitory response is lost. The loss of this hyperpolarization can occur for a number of reasons such as; a) due to the sustained depolarization, there is an increase in extracellular K+ which decreases the electrochemical gradient causing less of a K+ efflux, b) sustained depolarization leads to increased Ca2+ levels which leads to increased vesicle fusion and neurotransmitter release, c) depolarization leads to activation of excitatory NMDA R causing increased Ca2+ influx. Referring to Figure 10, it can be seen propagation of the seizure can be attributed to increased excitatory behaviour and diminished inhibition (Bromfield, 2008). |
| {{::loss_of_hyperpol.png|}} | {{::loss_of_hyperpol.png|}} | ||
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| **Vagus Nerve Stimulation (VNS)** | **Vagus Nerve Stimulation (VNS)** | ||
| - | VNS is a novel therapy that has become available for epilepsy. This is used for patients with partial onset with or without secondary generalization after the age of 12. It is a system compromised of battery generators which send intermittent electrical stimuli controlled by software and an interrogating wand (Uthman, 2000). The generator is implanted in the left upper chest which connects to the left cervical vagus nerve using two semi-circular helical electrodes. It takes an approximate of 2 hours to complete under general anesthesia. There are some effects that are present during VNS such as vice alteration and tingling sensation in the throat(Uthman, 2000). The intensity of the effects starts to decrease over several weeks. This is one of the less invasive methods for anti-epilepsy. This is however not a replacement for resection surgery which is known to produce seizure-free effects in patients with a chance of 70-90%. (Uthman, 2000) | + | It is a novel therapy that has become available for epilepsy. This is used for patients with partial onset with or without secondary generalization after the age of 12. It is basically a system compromised to battery generators which send intermittent electrical stimuli which is controlled by software and an interrogating wand (Uthman, 2000). The generator is implanted in the left upper chest which connects to the left cervical vagus nerve using two semi-circular helical electrodes. It takes an approximate of 2 hours to complete under general anesthesia. There are some effects that are present during VNS such as vice alteration and tingling sensation in the throat(Uthman, 2000). The intensity of the effects starts to decrease over several weeks. This is one of the less invasive methods for anti-epilepsy. This is however not a replacement for resection surgery which is known to produce seizure-free effects in patients with a chance of 70-90%. (Uthman, 2000) |
| **Deep Brain Stimulation (DBS)** | **Deep Brain Stimulation (DBS)** | ||
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| **Brain Surgery** | **Brain Surgery** | ||
| - | The goal of surgery is to find the epileptogenic focus which is not eloquent cortex and resect it without causing any neurological deficits. The most common focus point in adults is the temporal lobe (mainly the hippocampus). There are many ways to discover the area of epileptogenic focus: Video and scalp EEG, fMRI, MEG (magnetoencephalography), or seizure semiology. | + | The goal of surgery is to find the epileptogenic focus which is not eloquent cortex and resect it without causing any neurological deficits. The most common focus point in adults is the temporal lobe (mainly the hippocampus). There are many ways to discover the area of epileptogenic focus: Video and scalp EEG, fMRI, MEG (magnetoencephalography), or seizure semiology. (Kawai, 2015) |
| Surgery can be divided into either palliative or curative procedures. Curative procedures include lesional resection, lobectomy, and multiple subpial transections. For the treatment of temporal love epilepsy a gamma knife radiosurgery is used. | Surgery can be divided into either palliative or curative procedures. Curative procedures include lesional resection, lobectomy, and multiple subpial transections. For the treatment of temporal love epilepsy a gamma knife radiosurgery is used. | ||
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| Surgery is either used to define and resect an area of epileptogenic focus or disrupt the spread of seizure activity which in turn reduces the likelihood of seizures. Electrodes are used to record from the surface of the brain. One of the most common procedures is for medial temporal lobe epilepsy where the hippocampus is the main target for surgery. | Surgery is either used to define and resect an area of epileptogenic focus or disrupt the spread of seizure activity which in turn reduces the likelihood of seizures. Electrodes are used to record from the surface of the brain. One of the most common procedures is for medial temporal lobe epilepsy where the hippocampus is the main target for surgery. | ||
| - | + | (Bromfield, 2006) | |
| - | (Bromfield, 2006) (Kawai, 2015) | + | |
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| Banerjee, P. N., Filippi, D., & Hauser, W. A. (2009). The descriptive epidemiology of epilepsy-a review. Epilepsy Research, 85(1), 31–45. http://doi.org/10.1016/j.eplepsyres.2009.03.003 | Banerjee, P. N., Filippi, D., & Hauser, W. A. (2009). The descriptive epidemiology of epilepsy-a review. Epilepsy Research, 85(1), 31–45. http://doi.org/10.1016/j.eplepsyres.2009.03.003 | ||
| - | Bhalla, D., Godet, B., Druet-Cabanac, M., Preux, P.M. (2011). Etiologies of epilepsy: a comprehensive review. Expert Review of Neurotherapeutics. 11(6):861-76 | + | Bhalla, D., Godet, B., Druet-Cabanac, M., Preux, P.M. (2011). Etiologies of epilepsy: a comprehensive review. Expert Review of Neurotherapeutics. 11(6):861-76. Retrieved from https://journals-scholarsportal-info.libaccess.lib.mcmaster.ca/pdf/14737175/v11i0006/861_eoeacr.xml |
| - | https://journals-scholarsportal-info.libaccess.lib.mcmaster.ca/pdf/14737175/v11i0006/861_eoeacr.xml | + | |
| BRADFORD, H.F. (1995). Glutamate, GABA and epilepsy. Prog. Neurobiol., 47, 477–511. | BRADFORD, H.F. (1995). Glutamate, GABA and epilepsy. Prog. Neurobiol., 47, 477–511. | ||
| - | Bromfield EB, Cavazos JE, Sirven JI, editors. An Introduction to Epilepsy [Internet]. West Hartford (CT): American Epilepsy Society; 2006. Chapter 1, Basic Mechanisms Underlying Seizures and Epilepsy.Available from: https://www.ncbi.nlm.nih.gov/books/NBK2510/ | + | Bromfield EB, Cavazos JE, Sirven JI, editors. An Introduction to Epilepsy [Internet]. West Hartford (CT): American Epilepsy Society; 2006. Chapter 1, Basic Mechanisms Underlying Seizures and Epilepsy. Retrieved from: https://www.ncbi.nlm.nih.gov/books/NBK2510/ |
| Cho, C.-H. (2013). New mechanism for glutamate hypothesis in epilepsy. Frontiers in Cellular Neuroscience, 7, 127. http://doi.org/10.3389/fncel.2013.00127 | Cho, C.-H. (2013). New mechanism for glutamate hypothesis in epilepsy. Frontiers in Cellular Neuroscience, 7, 127. http://doi.org/10.3389/fncel.2013.00127 | ||
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| Dostrovsky, J. O. and Lozano, A. M. (2002), Mechanisms of deep brain stimulation. Mov. Disord., 17: S63–S68. doi:10.1002/mds.10143 | Dostrovsky, J. O. and Lozano, A. M. (2002), Mechanisms of deep brain stimulation. Mov. Disord., 17: S63–S68. doi:10.1002/mds.10143 | ||
| - | Epilepsy Support Centre. (2015). Diagnosing Epilepsy. Available at: http://epilepsysupport.ca/seizure-education/about/diagnosing | + | Epilepsy Support Centre. (2015). Diagnosing Epilepsy. Retrieved from http://epilepsysupport.ca/seizure-education/about/diagnosing |
| Fisher, R.S. (2017). The New Classification of Seizures by the International League Against Epilepsy 2017. Current Neurology and Neuroscience Reports, 17(48). https://doi.org/10.1007/s11910-017-0758-6 | Fisher, R.S. (2017). The New Classification of Seizures by the International League Against Epilepsy 2017. Current Neurology and Neuroscience Reports, 17(48). https://doi.org/10.1007/s11910-017-0758-6 | ||
| - | Gilmour, H., Ramage-Morin, P., & Wong, S.L. (2016). Epilepsy in Canada: Prevalence and impact. Statistics Canada. http://www.statcan.gc.ca/pub/82-003-x/2016009/article/14654-eng.htm | + | Gilmour, H., Ramage-Morin, P., & Wong, S.L. (2016). Epilepsy in Canada: Prevalence and impact. Statistics Canada. Retrieved from http://www.statcan.gc.ca/pub/82-003-x/2016009/article/14654-eng.htm |
| Goldberg, E. M., & Coulter, D. A. (2013). Mechanisms of epileptogenesis: a convergence on neural circuit dysfunction. Nature Reviews. Neuroscience, 14(5), 337–349. http://doi.org/10.1038/nrn3482 | Goldberg, E. M., & Coulter, D. A. (2013). Mechanisms of epileptogenesis: a convergence on neural circuit dysfunction. Nature Reviews. Neuroscience, 14(5), 337–349. http://doi.org/10.1038/nrn3482 | ||
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| Banerjee, P. N., Filippi, D., & Hauser, W. A. (2009). The descriptive epidemiology of epilepsy-a review. Epilepsy Research, 85(1), 31–45. http://doi.org/10.1016/j.eplepsyres.2009.03.003 | Banerjee, P. N., Filippi, D., & Hauser, W. A. (2009). The descriptive epidemiology of epilepsy-a review. Epilepsy Research, 85(1), 31–45. http://doi.org/10.1016/j.eplepsyres.2009.03.003 | ||
| - | Sills, G.J.(2006). The mechanisms of action of gabapentin and pregabalin. Current Opinions in Pharmacology.6(1);108-126. https://doi.org/10.1016/j.coph.2005.11.003. (http://www.sciencedirect.com/science/article/pii/S1471489205001906) | + | Sills, G.J.(2006). The mechanisms of action of gabapentin and pregabalin. Current Opinions in Pharmacology.6(1);108-126. https://doi.org/10.1016/j.coph.2005.11.003. |
| - | 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). Retrieved from http://pedsinreview.aappublications.org.libaccess.lib.mcmaster.ca/content/19/10/342.long |
| Treiman DM.(2001). GABAergic mechanisms in epilepsy. Epilepsia;42:Suppl 3:8-12 | Treiman DM.(2001). GABAergic mechanisms in epilepsy. Epilepsia;42:Suppl 3:8-12 | ||
| - | World Health Organization. Epilepsy. Fact Sheet No. 999. Geneva: World Health Organization, 2015. Available at: http://www.who.int/mediacentre/factsheets/fs999/en/index.html | + | World Health Organization. Epilepsy. Fact Sheet No. 999. Geneva: World Health Organization, 2015. Retrieved from http://www.who.int/mediacentre/factsheets/fs999/en/index.html |
| - | Uthman, B. M. (n.d.). (2000). Vagus nerve stimulation for seizures. Retrieved October 27, 2017, from https://www.ncbi.nlm.nih.gov/pubmed/11036181 | + | Uthman, B. M. (n.d.). (2000). Vagus nerve stimulation for seizures. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/11036181 |
