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| New diagnoses of epilepsy are approximated at 2.4 million annually (World Health Organization, 2012). | New diagnoses of epilepsy are approximated at 2.4 million annually (World Health Organization, 2012). | ||
| - | In the case of Childhood Absence Epilepsy, the annual incidence has been reported to fall within the range of 2-8% per 100,000 children under the age of 16 years old. Among children that are already afflicted with epilepsy, rates can go up 10% (Crunelli and Leresche, 2002). Furthermore, girls are deemed to be at twice the risk of boys in developing Childhood Absence Epilepsy, however, equal incidences have thus far been reported (Crunelli and Leresche, 2002). | + | In the case of CAE, the annual incidence has been reported to fall within the range of 2-8% per 100,000 children under the age of 16 years old. Among children that are already afflicted with epilepsy, rates can go up 10% (Crunelli and Leresche, 2002). Furthermore, girls are deemed to be at twice the risk of boys in developing CAE, however, equal incidences have thus far been reported (Crunelli and Leresche, 2002). |
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| - | Partial seizures can either be simple or complex in which the later involves a loss in consciousness or cognitive abilities and the former does not (McCormick & Contreras, 2001). Simple partial seizures may also involve an “aura” which is a sensory experience prior to the onset of the seizure (McCandless, 2011). These sensory experiences could involve: perceived buzzing or whistling noises, a bad taste in the mouth, visions of flashing lights, hallucinations, sweating, or nausea, etc., depending on the brain region involved (McCandless, 2011). Clonic movements (constant contraction and relaxation of muscles) of the neck, face or whole extremities may also appear as a symptom in simple partial seizures (McCandless, 2011). Complex partial seizures may involve the experience of an aura prior to the onset of the seizure, motionless staring involving a loss of consciousness or repetitive movements of the extremities (McCandless, 2011). | + | Partial seizures can either be simple or complex in which the latter involves a loss in consciousness or cognitive abilities and the former does not (McCormick & Contreras, 2001). Simple partial seizures may also involve an “aura” which is a sensory experience prior to the onset of the seizure (McCandless, 2011). These sensory experiences could involve: perceived buzzing or whistling noises, a bad taste in the mouth, visions of flashing lights, hallucinations, sweating, or nausea, etc., depending on the brain region involved (McCandless, 2011). Clonic movements (constant contraction and relaxation of muscles) of the neck, face or whole extremities may also appear as a symptom in simple partial seizures (McCandless, 2011). Complex partial seizures may involve the experience of an aura prior to the onset of the seizure, motionless staring involving a loss of consciousness or repetitive movements of the extremities (McCandless, 2011). |
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| **Childhood Absence Epilepsy Diagnosis:** | **Childhood Absence Epilepsy Diagnosis:** | ||
| - | To diagnose childhood absence epilepsy, physicians will start off with asking the caregiver about the history of the symptoms being presented and any other associated health problems (Holmes & Fisher, 2013). They will then proceed in a physical examination to see if there is any bodily damage that could be leading to the seizures (Holmes & Fisher, 2013). An electroencephalogram (EEG) on the child’s brain activity is essential in detecting the presence of seizures. The child will be diagnosed with childhood absence epilepsy if there is generalized neuronal activity at 3 Hz spike and wave discharges as indicated by the EEG (Holmes & Fisher, 2013). This 3 Hz spike is caused by a depolarization via excessive excitatory neuronal activity among pyramidal cells in cortical structures (McCormick & Contreras, 2001). In order to study the child’s seizure episodes with the EEG or to merely observe their symptoms, the child will be asked to intentionally hyperventilate (Holmes & Fisher, 2013). Hyperventilation has been shown to induce an absence seizure in most children diagnosed with CAE (Holmes & Fisher, 2013). CT and MRI scans appear to be normal in these patients, indicating that there doesn’t appear to be anatomical damage or abnormalities in the brains of these children (Holmes & Fisher, 2013). | + | To diagnose childhood absence epilepsy, physicians will start off with asking the caregiver about the history of the symptoms being presented and any other associated health problems (Holmes & Fisher, 2013). They will then proceed in a physical examination to see if there is any bodily damage that could be leading to the seizures (Holmes & Fisher, 2013). An EEG on the child’s brain activity is essential in detecting the presence of seizures. The child will be diagnosed with CAE if there is generalized neuronal activity at 3 Hz spike and wave discharges as indicated by the EEG (Holmes & Fisher, 2013). This 3 Hz spike is caused by a depolarization via excessive excitatory neuronal activity among pyramidal cells in cortical structures (McCormick & Contreras, 2001). In order to study the child’s seizure episodes with the EEG or to merely observe their symptoms, the child will be asked to intentionally hyperventilate (Holmes & Fisher, 2013). Hyperventilation has been shown to induce an absence seizure in most children diagnosed with CAE (Holmes & Fisher, 2013). CT and MRI scans appear to be normal in these patients, indicating that there doesn’t appear to be anatomical damage or abnormalities in the brains of these children (Holmes & Fisher, 2013). |
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| A quick review of the normal transmission of the action potential aids in understanding the pathophysiology behind ictogenesis, or the production of a seizure. The resting potential in a neuron that is not firing is -70 millivolts (mV). A higher concentration of sodium (Na+) is found outside the cell, and a higher concentration of potassium (K+) is found inside the cell (Stafstrom, 1998). | A quick review of the normal transmission of the action potential aids in understanding the pathophysiology behind ictogenesis, or the production of a seizure. The resting potential in a neuron that is not firing is -70 millivolts (mV). A higher concentration of sodium (Na+) is found outside the cell, and a higher concentration of potassium (K+) is found inside the cell (Stafstrom, 1998). | ||
| - | Once stimulated, the action potential is an “all-or-none” event. Depolarization occurs as there is an influx of Na+ ions through voltage-gated ion channels (Stafstrom, 1998). The membrane potential at the end of the depolarization stage is +30 mV, at which point K+ ions exit the cell. After repolarization, the membrane reaches a stage of hyperpolarization (Stafstrom, 1998). This stage is dependent of intracellular calcium (Ca2+) levels and is mediated by the action of the Ca2+-dependent K+ channels. These channels regulate the refractory period so that the cell cannot generate another action potential. After the production of one action potential is complete, the cell then enters the refractory period, which restores the normal balance of intracellular and extracellular ions (Stafstrom, 1998). | + | Once stimulated, the action potential is an “all-or-none” event. Depolarization occurs as there is an influx of Na+ ions through voltage-gated ion channels (Stafstrom, 1998). The membrane potential at the end of the depolarization stage is +30 mV, at which point K+ ions exit the cell. After repolarization, the membrane reaches a stage of hyperpolarization (Stafstrom, 1998). This stage is dependent on intracellular calcium (Ca2+) levels and is mediated by the action of the Ca2+-dependent K+ channels. These channels regulate the refractory period so that the cell cannot generate another action potential. After the production of one action potential is complete, the cell then enters the refractory period, which restores the normal balance of intracellular and extracellular ions (Stafstrom, 1998). |
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| ====== Synaptic Transmission ====== | ====== Synaptic Transmission ====== | ||
| - | As action potentials arrive at the end of the axon, the influx of Ca2+ prompts vesicles to release one of two neurotransmitters: glutamate or gamma-amino butyric acid, or GABA. In an inhibitory post-synaptic potential (IPSP), GABA is released into the synapse (Stafstrom, 1998). GABA receptors activate chloride channels. Influx of Cl- ions increases the negative charge of the neuron which results in hyperpolarization, thus inhibiting the passage of the action potential. In an excitatory post-synaptic potential (EPSP), glutamate is released into the synapse (Stafstrom, 1998). Glutamate binds to one of its many receptors on the post-synaptic terminal, which activates another ion channel. Depending on the type of receptor activated, Na+, Mg2+, or Ca2+ may enter the cell and initiate a depolarization event (Stafstrom, 1998). | + | As action potentials arrive at the end of the axon, the influx of Ca2+ prompts vesicles to release one of two neurotransmitters: glutamate or gamma-amino butyric acid, or GABA. In an inhibitory post-synaptic potential (IPSP), GABA is released into the synapse (Stafstrom, 1998). GABA receptors activate chloride channels. Influx of Cl- ions increases the negative charge of the post-synaptic neuron which results in hyperpolarization, thus inhibiting the passage of the action potential. In an excitatory post-synaptic potential (EPSP), glutamate is released into the synapse (Stafstrom, 1998). Glutamate binds to one of its many receptors on the post-synaptic terminal, which activates another ion channel. Depending on the type of receptor activated, Na+, Mg2+, or Ca2+ may enter the cell and initiate a depolarization event (Stafstrom, 1998). |
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| Etiology underlying epilepsy is categorized into three main types: idiopathic, remote symptomatic, and cryptogenic (Berg et al., 1999). | Etiology underlying epilepsy is categorized into three main types: idiopathic, remote symptomatic, and cryptogenic (Berg et al., 1999). | ||
| - | Idiopathic epilepsy contributes to 40% of the diagnoses (Engelborghs et al., 2000). Patients show no neurological abnormalities but have a strong genetic predisposition for the disorder (Berg et al., 1999). The most common examples include benign rolandic epilepsy, juvenile myoclonic epilepsy, and childhood absence epilepsy. Underlying genetic bases for idiopathic epilepsy are not very well understood because of the polygenic nature of its inheritance (Engelborghs et al., 2000). Although there is very little literature on humans with absence epilepsy, studies conducted on rat models have demonstrated an autosomal dominant mode of inheritance of one main gene, the WAG/Rij strain, along with significant interactions of a few other genes (Renier & Coenen, 2000). Various replications of this study have been conducted and literature reviews claim that these studies are validated with similar patterns of inheritance seen in patients with absence epilepsy (Coenen & Van Luijtelaar, 2003). Underlying changes in the biochemical microenvironment can also play a role in the etiology of epilepsy. These include increase in glutamate levels, decrease in GABA, and in some cases, blockage of the Na+-K+ pump (Engelborghs et al., 2000). Genetic alterations in T-type calcium channels have been associated with most generalized epilepsy syndromes, including childhood absence epilepsy (Stafstrom & Rho, 2016). | + | Idiopathic epilepsy contributes to 40% of the diagnoses (Engelborghs et al., 2000). Patients show no neurological abnormalities but have a strong genetic predisposition for the disorder (Berg et al., 1999). The most common examples include benign rolandic epilepsy, juvenile myoclonic epilepsy (JME), and CAE. Underlying genetic bases for idiopathic epilepsy are not very well understood because of the polygenic nature of its inheritance (Engelborghs et al., 2000). Although there is very little literature on humans with absence epilepsy, studies conducted on rat models have demonstrated an autosomal dominant mode of inheritance of one main gene, the WAG/Rij strain, along with significant interactions of a few other genes (Renier & Coenen, 2000). Various replications of this study have been conducted and literature reviews claim that these studies are validated with similar patterns of inheritance seen in patients with absence epilepsy (Coenen & Van Luijtelaar, 2003). Underlying changes in the biochemical microenvironment can also play a role in the etiology of epilepsy. These include increase in glutamate levels, decrease in GABA, and in some cases, blockage of the Na+-K+ pump (Engelborghs et al., 2000). Genetic alterations in T-type calcium channels have been associated with most generalized epilepsy syndromes, including CAE (Stafstrom & Rho, 2016). |
| Remote symptomatic epilepsy is less common and has no known genetic bases. This type of epilepsy is characterized by the presence of a neurological abnormality, a history of brain injury, or comorbidities with other disorders. Patients are diagnosed with symptomatic epilepsy if they have had more than one sporadic, unprovoked seizure (Berg et al., 1999). Symptomatic mechanisms may be caused by a process known as “kindling” (Engelborghs et al., 2000). Kindling refers to the process of permanently decreasing the threshold potential for normal neuronal transmission. This causes the membrane to depolarize at a lower potential charge and may lead to structural and functional changes in glutamatergic synapses (Engelborghs et al., 2000). | Remote symptomatic epilepsy is less common and has no known genetic bases. This type of epilepsy is characterized by the presence of a neurological abnormality, a history of brain injury, or comorbidities with other disorders. Patients are diagnosed with symptomatic epilepsy if they have had more than one sporadic, unprovoked seizure (Berg et al., 1999). Symptomatic mechanisms may be caused by a process known as “kindling” (Engelborghs et al., 2000). Kindling refers to the process of permanently decreasing the threshold potential for normal neuronal transmission. This causes the membrane to depolarize at a lower potential charge and may lead to structural and functional changes in glutamatergic synapses (Engelborghs et al., 2000). | ||
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| Another factor that characterizes a seizure is when the action potential reaches the end of the axon. Due to the presence of genetically altered T-type calcium, a large number of Ca2+ enters the cell, which induces the release of a large amount of neurotransmitters into the synapse. Epileptic neurons also tend to have chronically elevated Ca2+ levels inside the cell to begin with (Stafstrom & Rho, 2016). This, in combination with the excess of glutamate and low GABA levels, leads to overstimulation and depolarization of a multitude of surrounding neurons (Engelborghs et al., 2000). All components of normal neurotransmission are intricately linked together in a delicate balance of electric potential within the brain. A disruption in any one of these checkpoints can have a devastating domino effect which may lead to the production of an epileptic seizure. | Another factor that characterizes a seizure is when the action potential reaches the end of the axon. Due to the presence of genetically altered T-type calcium, a large number of Ca2+ enters the cell, which induces the release of a large amount of neurotransmitters into the synapse. Epileptic neurons also tend to have chronically elevated Ca2+ levels inside the cell to begin with (Stafstrom & Rho, 2016). This, in combination with the excess of glutamate and low GABA levels, leads to overstimulation and depolarization of a multitude of surrounding neurons (Engelborghs et al., 2000). All components of normal neurotransmission are intricately linked together in a delicate balance of electric potential within the brain. A disruption in any one of these checkpoints can have a devastating domino effect which may lead to the production of an epileptic seizure. | ||
| - | In childhood absence epilepsy, these events take place in thalamocortical circuitry. Specific pathogenesis of an absence seizure results from the effects of a few abnormalities listed previously (Stafstrom & Rho, 2016). Namely, the T-type Ca2+ channels are altered, so that they are activated by smaller membrane depolarizations. Changes in other subtypes of channels that play a role in normal transmission of potentials in the thalamus are also seen in this type of epilepsy. Other synaptic influences include antagonists of GABA and agonists of glutamate (Stafstrom & Rho, 2016). | + | In CAE, these events take place in thalamocortical circuitry. Specific pathogenesis of an absence seizure results from the effects of a few abnormalities listed previously (Stafstrom & Rho, 2016). Namely, the T-type Ca2+ channels are altered, so that they are activated by smaller membrane depolarizations. Changes in other subtypes of channels that play a role in normal transmission of potentials in the thalamus are also seen in this type of epilepsy. Other synaptic influences include antagonists of GABA and agonists of glutamate (Stafstrom & Rho, 2016). |
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| ====== Susceptibility of the Immature Brain ====== | ====== Susceptibility of the Immature Brain ====== | ||
| - | Seizure incidence is highest in the early years of life and in some cases, especially childhood absence epilepsy, the disorder seems to disappear right after puberty. This is a result of multiple physiological factors that contribute to increased susceptibility (Stafstrom & Rho, 2016). | + | Seizure incidence is highest in the early years of life and in some cases, especially CAE, the disorder seems to disappear right after puberty. This is a result of multiple physiological factors that contribute to increased susceptibility (Stafstrom & Rho, 2016). |
| - Ion channels that mediate depolarization events usually develop earlier than those that are responsible for repolarization. In conjuncture with this, excitatory neurotransmitters are produced earlier in development than inhibitory neurotransmitters (Stafstrom & Rho, 2016). | - Ion channels that mediate depolarization events usually develop earlier than those that are responsible for repolarization. In conjuncture with this, excitatory neurotransmitters are produced earlier in development than inhibitory neurotransmitters (Stafstrom & Rho, 2016). | ||
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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 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 juvenile myoclonic epilepsy (JME). This ecidence 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 juvenile myoclonic epilepsy (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. | + | |
| - | + | ||
| - | 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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| **Childhood Absence Epilepsy and AEDs:** | **Childhood Absence Epilepsy and AEDs:** | ||
| - | The three medications of choice commonly used as initial monotherapy to treat childhood absence epilepsy are **Ethosuximide (Zarontin), Valporic acid (Epilim),** and** Lamotrigine (Lamictal)**. | + | The three medications of choice commonly used as initial monotherapy to treat CAE are **Ethosuximide (Zarontin), Valporic acid (Epilim),** and** Lamotrigine (Lamictal)**. |
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| - | However, as of a double blind, randomized control trial conducted in 2013, Ethosuximide is now the recommended first-line therapy in children with childhood absence epilepsy (Glauser et al., 2013). The study looked at the efficacy, tolerability and neuropsychological effects of ethosuximide, valproic acid, and lamotrigine in children diagnosed with CAE. 435 children were eligible and randomly assigned to one of three groups; drug doses were titrated for clinical response (until the child was free of seizures). The primary outcome was freedom from treatment failure (a defined criterion) after 16 weeks of therapy; the secondary outcome was attentional dysfunction. | + | However, as of a double blind, randomized control trial conducted in 2013, Ethosuximide is now the recommended first-line therapy in children with CAE (Glauser et al., 2013). The study looked at the efficacy, tolerability and neuropsychological effects of ethosuximide, valproic acid, and lamotrigine in children diagnosed with CAE. 435 children were eligible and randomly assigned to one of three groups; drug doses were titrated for clinical response (until the child was free of seizures). The primary outcome was freedom from treatment failure (a defined criterion) after 16 weeks of therapy; the secondary outcome was attentional dysfunction. |
| - | The researchers found that Ethosuximide and Valproic acid are more effective than Lamotrigine in the treatment of childhood absence epilepsy. Ethosuximide was also associated with fewer adverse attentional effects (in 33%) where as attentional dysfunction was more common with valproic acid (in 49% children). | + | The researchers found that Ethosuximide and Valproic acid are more effective than Lamotrigine in the treatment of CAE. Ethosuximide was also associated with fewer adverse attentional effects (in 33%) where as attentional dysfunction was more common with valproic acid (in 49% children). |
| This study address the ambiguity clinicians experienced when treating patients and is the first of its kind providing an evidence-based standpoint to initiate Ethosuximide as a first line drug choice. Valproic acid and lamotrigine are options when seizures are refractory to Ethosuximide (Glauser et al., 2013). | This study address the ambiguity clinicians experienced when treating patients and is the first of its kind providing an evidence-based standpoint to initiate Ethosuximide as a first line drug choice. Valproic acid and lamotrigine are options when seizures are refractory to Ethosuximide (Glauser et al., 2013). | ||
| - | 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. 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). |
| + | |||
| + | 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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