Differences

This shows you the differences between two versions of the page.

Link to this comparison view

Both sides previous revision Previous revision
Next revision
Previous revision
group_3_presentation_1_-_epilepsy-_childhood_absence_epilepsy [2017/02/03 12:36]
javedaa
group_3_presentation_1_-_epilepsy-_childhood_absence_epilepsy [2018/01/25 15:18] (current)
Line 32: Line 32:
 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).
  
 <​HTML>​ <​HTML>​
Line 53: Line 53:
    
  
-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).
    
  
Line 71: Line 71:
 **Tonic-clonic seizures:** this type of generalized seizures has two phases associated with it. First is the tonic phase in which the individual’s muscles will tighten and then they will lose consciousness. Second is the clonic phase where the individual’s muscles will contract and relax in a rhythmic fashion. These seizures typically last for 1 to 3 minutes, however if prolonged to over 5 minutes this becomes a medical emergency. (Mayo Clinic, 2017; Devinsky & Sirvin, 2013) **Tonic-clonic seizures:** this type of generalized seizures has two phases associated with it. First is the tonic phase in which the individual’s muscles will tighten and then they will lose consciousness. Second is the clonic phase where the individual’s muscles will contract and relax in a rhythmic fashion. These seizures typically last for 1 to 3 minutes, however if prolonged to over 5 minutes this becomes a medical emergency. (Mayo Clinic, 2017; Devinsky & Sirvin, 2013)
    
 +
 +
 +**Childhood Absence Epilepsy Symptoms:**
  
 The symptoms reported for childhood absence epilepsy in particular are a result of the absence seizures experienced. The seizures present as staring spells lasting approximately 10 to 20 seconds as a result of a brief lack of consciousness (Holmes and Fisher, 2013). The child will not know that they have experienced the seizure and will continue with the activity they were previously involved in or they may experience some brief confusion (Donner, 2010). These seizures could occur up to one hundred times daily and are typically spurred on by exercise (Holmes and Fisher, 2013). A child may also experience automatisms,​ which are actions performed by the body unintentionally (Donner, 2010). These actions may include, tongue movement, chewing, swallowing, raising eyelids and fiddling with hands (Donner, 2010). ​ The symptoms reported for childhood absence epilepsy in particular are a result of the absence seizures experienced. The seizures present as staring spells lasting approximately 10 to 20 seconds as a result of a brief lack of consciousness (Holmes and Fisher, 2013). The child will not know that they have experienced the seizure and will continue with the activity they were previously involved in or they may experience some brief confusion (Donner, 2010). These seizures could occur up to one hundred times daily and are typically spurred on by exercise (Holmes and Fisher, 2013). A child may also experience automatisms,​ which are actions performed by the body unintentionally (Donner, 2010). These actions may include, tongue movement, chewing, swallowing, raising eyelids and fiddling with hands (Donner, 2010). ​
Line 112: Line 115:
  
  
-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 (EEGon 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). ​+ 
 +**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 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). ​
  
 <​HTML>​ <​HTML>​
Line 118: Line 124:
 </​HTML>​ </​HTML>​
  
 +====== The Action Potential ======
 +
 +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 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). ​
 +
 +<​HTML>​
 +<br>
 +</​HTML>​
 +
 +====== 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 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). ​
 +
 +<​HTML>​
 +<br>
 +</​HTML>​
  
 ====== Etiology ====== ====== Etiology ======
  
-**ENTER HERE YUMNA**+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 (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). 
 + 
 +Finally, some types of epilepsy have no known causes or underlying mechanisms and these are known as cryptogenic (Berg et al., 1999). ​
  
 <​HTML>​ <​HTML>​
Line 129: Line 158:
 ====== Pathophysiology ====== ====== Pathophysiology ======
  
-**ENTER HERE YUMNA**+The pathophysiology of epilepsy is characterized by two distinct but related hallmarks: hyperexcitability and hypersynchrony. Hyperexcitability is when a neuron abnormally responds to incoming excitatory stimuli and fires multiple discharges at once instead of just one (Stafstrom, 1998). Hypersynchrony is when a large number of neighboring neurons discharge into one neuron simultaneously. Epilepsy is the result of a combination of both these characteristics (Stafstrom, 1998).  
 +  
 +The main distinguishing factor of a seizure from a normal depolarization event can be seen in an EEG. Normally, excitation and inhibition are balanced and when neurons are not needed, they are silent (Stafstrom, 1998). Normal brain activity is low-voltage and desynchronized. If neurons start firing discharges at an abnormal rate, this classifies as a paroxysmal depolarization shift (PDS) and can be seen in an EEG as a “spike” of electrical activity. This is known as the interictal state (Stafstrom, 1998). In the ictal state, there is a flood of repeated EEG spikes which may continue for several second and can last up to a few minutes (Stafstrom, 1998).  
 + 
 +<​HTML>​ 
 +<​br>​ 
 +</​HTML>​ 
 + 
 +====== Ictogenesis ====== 
 + 
 +Abnormal excitation of neurons may be attributed to a combination of factors. In the axonal membrane, there may be an abnormally large amount of K+ ions outside the cell, which switches around the normal concentration gradient (Stafstrom, 1998). After depolarization,​ there will be no efflux of K+ and Na+ would remain within the cell. The cell membrane will then remain in a state of depolarization,​ during which an abnormal number of action potentials will discharge within one large depolarization event (Stafstrom, 1998). This shift in depolarization is what characterizes the PDS, depicted in the EEG as the interictal spike. In some cases, the PDS is followed by a state of “post-PDS hyperpolarization” during which the cell may temporarily hyperpolarize (Stafstrom, 1998). However, if the PDS progresses, it leads to the barrage of synchronized neuronal firing characteristic of the ictal state (Stafstrom, 1998).  
 +  
 +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 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).  
 + 
 +<​HTML>​ 
 +<​br>​ 
 +</​HTML>​ 
 + 
 +====== Susceptibility of the Immature Brain ====== 
 + 
 +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).  
 + 
 +- Early in development,​ GABA actually induces an excitatory effect rather than an inhibitory effect (Stafstrom & Rho, 2016). 
 + 
 +- There are more synapses found in the immature brain than the mature one. This increases the amount of fast-acting electrical signals to be transmitted that may facilitate the production of seizures (Stafstrom & Rho, 2016).  
 + 
 +These are just some examples that may increase a child’s susceptibility to developing epilepsy. Each of these factors alters the brain’s delicate balance of excitation and inhibition, in the favor of excitation (Stafstrom & Rho, 2016).  
  
 <​HTML>​ <​HTML>​
Line 137: Line 197:
 ====== Prognosis and Prevention ====== ====== Prognosis and Prevention ======
  
-**ENTER HERE KRITIKA**+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). 
 + 
 +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).  
 + 
 +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). 
  
 <​HTML>​ <​HTML>​
Line 149: Line 214:
 **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)**.
    
  
Line 164: Line 229:
  
  
-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. ​**(KRITIKA ADD STUFF HERE)**+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). 
  
 <​HTML>​ <​HTML>​
Line 179: Line 247:
  
 ====== References ====== ====== References ======
 +
 +Berg, A. T., Shinnar, S., Levy, S. R., & Testa, F. M. (1999). Newly diagnosed epilepsy in children: presentation at diagnosis. Epilepsia, 40(4), 445-452.
  
 Buchhalter, J. (2011). Treatment of Childhood Absence Epilepsy—An Evidence-Based Answer at Last!. //Epilepsy Currents//, 11(1), 12-15. Buchhalter, J. (2011). Treatment of Childhood Absence Epilepsy—An Evidence-Based Answer at Last!. //Epilepsy Currents//, 11(1), 12-15.
  
 +Coenen, A. M. L., & Van Luijtelaar, E. L. J. M. (2003). Genetic animal models for absence epilepsy: a review of the WAG/Rij strain of rats. Behavior genetics,​ 33(6),​ 635-655.
  
 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.
- 
  
 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
- 
  
 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
  
 +Engelborghs,​ S., D’hooge, R., & De Deyn, P. P. (2000). Pathophysiology of epilepsy. Acta neurologica belgica, 100(4), 201-213.
  
 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
- 
  
 "​Epilepsy"​. Fact Sheets. World Health Organization. October 2012. Retrieved January 21, 2017. "​Epilepsy"​. Fact Sheets. World Health Organization. October 2012. Retrieved January 21, 2017.
- 
  
 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.
- 
  
 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.
- 
  
 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. ​
- 
  
 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.
- 
  
 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
- 
  
 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.
- 
  
 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.
- 
  
 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.
- 
  
 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.  ​
  
 +Renier, W. O., & Coenen, A. M. L. (2000). Human absence epilepsy: the WAG/Rij rat as a model. Neuroscience Research Communications,​ 26(3),​ 181-191.
  
 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.
  
 +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.
  
-What Is Epilepsy? (2014January)Epilepsy FoundationRetrieved January 21, 2017, http://www.epilepsy.com/​learn/​epilepsy-101/​what-epilepsy+StafstromCE(1998). Back to BasicsThe Pathophysiology of Epileptic Seizures: A Primer For PediatriciansPediatrics in Review, 19 (10).
  
 +Stafstrom, C. E., Rho, J. M. (2016). Pathophysiology of seizures and epilepsy. URL: https://​www.uptodate.com/​contents/​pathophysiology-of-seizures-and-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.
 +
 +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 OntarioRetrieved January 212017from http://​epilepsyontario.org/about-epilepsy/what-is-epilepsy/+Wirrell, EC., CamfieldCS., 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.
  
  
Print/export
QR Code
QR Code group_3_presentation_1_-_epilepsy-_childhood_absence_epilepsy (generated for current page)