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14-September-2008 18:02:36 - Epilepsy This article is about the neurological disorder as it affects humans. For veterinary information, see Epilepsy in animals. Epileptic redirects here. For the graphic novel, see Epileptic graphic novel. Epilepsy Classification and external resources ICD-10 G40.-G41. ICD-9 345 DiseasesDB 4366 MedlinePlus 000694 eMedicine neuro/415 MeSH D004827 Epilepsy is a common chronic neurological disorder that is characterized by recurrent unprovoked seizures.12 These seizures are transient signs and/or symptoms due to abnormal, excessive or synchronous neuronal activity in the brain.3 About 50 million people worldwide have epilepsy at any one time.4 Epilepsy is usually controlled, but not cured, with medication, although surgery may be considered in difficult cases. However, over 30% of people with epilepsy do not have seizure control even with the best available medicationscitation needed. Not all epilepsy syndromes are lifelong - some forms are confined to particular stages of childhood. Epilepsy should not be understood as a single disorder, but rather as a group of syndromes with vastly divergent symptoms but all involving episodic abnormal electrical activity in the brain. Contents 1 Classification 2 Diagnosis 3 Precipitants 4 Epidemiology 5 Seizure types 6 Epilepsy syndromes 7 Treatment 7.1 Responding to a seizure 7.2 Pharmacologic treatment 7.3 Surgical treatment 7.4 Other treatment 8 Pathophysiology 9 History and stigma 10 Controversy 11 Notable people with epilepsy 12 Legal implications 13 Important investigators of epilepsy 14 See also 15 References 16 External links Classification Epilepsies are classified in five ways: By their first cause or etiology. By the observable manifestations of the seizures, known as semiology. By the location in the brain where the seizures originate. As a part of discrete, identifiable medical syndromes. By the event that triggers the seizures, as in primary reading epilepsy. In 1981, the International League Against Epilepsy ILAE proposed a classification scheme for individual seizures that remains in common use.5 This classification is based on observation clinical and EEG rather than the underlying pathophysiology or anatomy and is outlined later on in this article. In 1989, the ILAE proposed a classification scheme for epilepsies and epileptic syndromes.6 This can be broadly described as a two-axis scheme having the cause on one axis and the extent of localisation within the brain on the other. Since 1997, the ILAE have been working on a new scheme that has five axes: ictal phenomenon, seizure type, syndrome, etiology and impairment.7 Diagnosis The diagnosis of epilepsy requires the presence of recurrent, unprovoked seizures; accordingly, it is usually made based on the medical history. Imaging and measurement technologies such as electroencephalography EEG, magnetic resonance imaging MRI, single photon emission computed tomography SPECT, positron emission tomography PET, and magnetoencephalography MEG may be useful to discover an etiology for the epilepsy, discover the affected brain region, or classify the epileptic syndrome, but these studies are not useful in making the initial diagnosis. Long-term video-EEG monitoring for epilepsy is the gold standard for diagnosis, but it is not routinely employed owing to its high cost, low availability and inconvenience. Convulsive or other seizure-like activity, non-epileptic in origin, can be observed in many other medical conditions. These non-epileptic seizures can be hard to differentiate and may lead to misdiagnosis. Epilepsy covers conditions with different etiologies, natural histories and prognoses, each requiring different management strategies. A full medical diagnosis requires a definite categorization of seizure and syndrome types.8 Precipitants The diagnosis of epilepsy usually requires that the seizures occur spontaneously. Nevertheless, certain epilepsy syndromes require particular precipitants or triggers for seizures to occur. These are termed reflex epilepsy. For example, patients with primary reading epilepsy have seizures triggered by reading. Photosensitive epilepsy can be limited to seizures triggered by flashing lights. Other precipitants can trigger an epileptic seizure in patients who otherwise would be susceptible to spontaneous seizures. For example, children with childhood absence epilepsy may be susceptible to hyperventilation. In fact, flashing lights and hyperventilation are activating procedures used in clinical EEG to help trigger seizures to aid diagnosis. Finally, other precipitants can facilitate, rather than obligately trigger, seizures in susceptible individuals. Emotional stress, sleep deprivation, sleep itself, and febrile illness are examples of precipitants cited by patients with epilepsy. Notably, the influence of various precipitants varies with the epilepsy syndrome. 9. Likewise, the menstrual cycle in women with epilepsy can influence patterns of seizure recurrence. Catamenial epilepsy is the term denoting seizures linked to the menstrual cycle.10 Epidemiology Epilepsy is one of the most common of the serious neurological disorders.11 Genetic, congenital, and developmental conditions are mostly associated with it among younger patients; tumors are more likely over age 40; head trauma and central nervous system infections may occur at any age. The prevalence of active epilepsy is roughly in the range 5-10 per 1000 people. Up to 5% of people experience nonfebrile seizures at some point in life; epilepsy's lifetime prevalence is relatively high because most patients either stop having seizures or less commonly die of it. Epilepsy's approximate annual incidence rate is 40-70 per 100,000 in industrialized countries and 100-190 per 100,000 in resource-poor countries; socioeconomically deprived people are at higher risk. In industrialized countries the incidence rate decreased in children but increased among the elderly during the three decades prior to 2003, for reasons not fully understood.12 Children with epilepsy are three to nine times more likely to have mental health problems than healthy children. Although the search for risk factors has often produced inconsistent results, there is evidence that the development of mental health problems in children with epilepsy is moderated and mediated by family risk factors. Attention-deficit/hyperactivity disorder ADHD affects three to five times more children with epilepsy than children in the general population, and children with epilepsy also have significantly higher rates of depression and anxiety. 13 There is a strikingly higher prevalence of epilepsy in children with autism, and evidence suggests that epilepsy is a risk factor for autism, independent of other central nervous system problems.14 Seizure types Main article: Seizure types Seizure types are organized firstly according to whether the source of the seizure within the brain is localized partial or focal onset seizures or distributed generalized seizures. Partial seizures are further divided on the extent to which consciousness is affected. If it is unaffected, then it is a simple partial seizure; otherwise it is a complex partial psychomotor seizure. A partial seizure may spread within the brain - a process known as secondary generalization. Generalized seizures are divided according to the effect on the body but all involve loss of consciousness. These include absence petit mal, myoclonic, clonic, tonic, tonic-clonic grand mal and atonic seizures. Epilepsy syndromes There are many different epilepsy syndromes, each presenting with its own unique combination of seizure type, typical age of onset, EEG findings, treatment, and prognosis. The most widespread classification of the epilepsies 6 divides epilepsy syndromes by location or distribution of seizures as revealed by the appearance of the seizures and by EEG and by cause. Syndromes are divided into localization-related epilepsies, generalized epilepsies, or epilepsies of unknown localization. Localization-related epilepsies, sometimes termed partial or focal epilepsies, arise from an epileptic focus, a small portion of the brain that serves as the irritant driving the epileptic response. Generalized epilepsies, in contrast, arise from many independent foci multifocal epilepsies or from epileptic circuits that involve the whole brain. Epilepsies of unknown localization remain unclear whether they arise from a portion of the brain or from more widespread circuits. Epilepsy syndromes are further divided by presumptive cause: idiopathic, symptomatic, and cryptogenic. Idiopathic epilepsies are generally thought to arise from genetic abnormalities that lead to alteration of basic neuronal regulation. Symptomatic epilepsies arise from the effects of an epileptic lesion, whether that lesion is focal, such as a tumor, or a defect in metabolism causing widespread injury to the brain. Cryptogenic epilepsies involve a presumptive lesion that is otherwise difficult or impossible to uncover during evaluation. Some epileptic syndromes are difficult to fit within this classification scheme and fall in the unknown localization/etiology catagory. People who only have had a single seizure, or those with seizures that occur only after specific precipitants provoked seizures, have epilepsies that fall into this catagory. Febrile convulsions are an example of seizures bound to a particular precipitant. Landau-Kleffner syndrome is another epilepsy which, because of its variety of EEG distributions, falls uneasily in clear catagories. More confusingly, certain syndromes like West syndrome featuring seizures such as Infantile spasms can be classified as idiopathic, syndromic, or cryptogenic depending on cause and can arise from both focal or generalized epileptic lesions. Below are some common seizure syndromes: Benign centrotemporal lobe epilepsy of childhood or Benign rolandic epilepsy is an idiopathic localization-related epilepsy that occurs in children between the ages of 3 and 13 years with peak onset in prepubertal late childhood. Apart from their seizure disorder, these patients are otherwise normal. This syndrome features simple partial seizures that involve facial muscles and frequently cause drooling. Although most episodes are brief, seizures sometimes spread and generalize. Seizures are typically nocturnal and confined to sleep. The EEG may demonstrate spike discharges that occur over the centrotemporal scalp over the central sulcus of the brain the Rolandic sulcus that are predisposed to occur during drowsiness or light sleep. Seizures cease near puberty. 15 Seizures may require anticonvulsant treatment, but sometimes are infrequent enough to allow physicians to defer treatment. Benign occipital epilepsy of childhood BOEC is an idiopathic localization-related epilepsy and consists of an evolving group of syndromes. Most authorities include two subtypes, an early subtype with onset between 3-5 years and an late onset between 7-10 years. Seizures in BOEC usually feature visual symptoms such as scotoma or fortifications brightly colored spots or lines or amaurosis blindness or impairment of vision. Convulsions involving one half the body, hemiconvulsions, or forced eye deviation or head turning are common. Younger patients typically experience symptoms similar to migraine with nausea and headache, and older patients typically complain of more visual symptoms. The EEG in BOEC shows spikes recorded from the occipital back of head regions. Lately, a group of epilepsies termed Panayiotopolous syndrome16 that share some clinical features of BOEC but have a wider variety of EEG findings are classified by some as BOEC. Autosomal dominant nocturnal frontal lobe epilepsy ADNFLE is an idiopathic localization-related epilepsy that is an inheirited epileptic disorder that causes seizures during sleep. Onset is usually in childhood. These seizures arise from the frontal lobes and consist of complex motor movements, such as hand clenching, arm raising/lowering, and knee bending. Vocalizations such as shouting, moaning, or crying are also common. ADNFLE is often misdiagnosed as nightmares. ADNFLE has a genetic basis17. These genes encode various nicotinic acetylcholine receptors. Primary reading epilepsy is a reflex epilepsy classified as an idiopathic localization-related epilepsy. Reading in susceptible individuals triggers characteristic seizures18. Childhood absence epilepsy CEA is an idiopathic generalized epilepsy that affects children between the ages of 4 and 12 years of age, although peak onset is around 5-6 years old. These patients have recurrent absence seizures, brief episodes of unresponsive staring, sometimes with minor motor features such as eye blinking or subtle chewing. The EEG finding in CAE is generalized 3 Hz spike and wave discharges. Some go on to develop generalized tonic-clonic seizures. This condition carries a good prognosis because children do not usually show cognitive decline or neurological deficits, and the seizures in the majority cease spontaneously with onging maturation. Generalized 3 Hz spike and wave discharges in EEG Generalized 3 Hz spike and wave discharges in EEG Juvenile absence epilepsy is an idiopathic generalized epilepsy with later onset that CAE, typically in prepubertal adolescence, with the most frequent seizure type being absence seizures. Generalized tonic-clonic seizures can occur. 3 Hz spike-wave or muliple spike discharges can be seen on EEG. Prognosis is mixed, with some patients going on to a syndrome that is poorly distinguishable from JME. Juvenile myoclonic epilepsy JME is an idiopathic generalized epilepsy that occurs in patients aged 8 to 20 years. Patients have normal cognition and are otherwise neurologically intact. The most common seizures are myoclonic jerks, although generalized tonic-clonic seizures and absence seizures may occur as well. Myoclonic jerks usually cluster in the early morning after awakening. The EEG reveals generalized 4-6 Hz spike wave discharges or multiple spike discharges. Interestingly, these patients are often first diagnosed when they have their first generalized tonic-clonic seizure later in life when they experience sleep deprivation e.g., freshman year in college after staying up late to study for exams. Alcohol withdrawal can also be a major contributing factor in breakthrough seizures as well. The risk of the tendency to have seizures is lifelong; however, the majority have well-controlled seizures with anticonvulsant medication and avoidance of seizure precipitants. Symptomatic localization-related epilepsies Symptomatic localization-related epilepsies are divided by the location in the brain of the epileptic lesion, since the symptoms of the seizures are more closely tied to the brain location rather than the cause of the lesion. Tumors, atriovenous malformations, cavernous malformations, trauma, and cerebral infarcts can all be causes of epileptic foci in different brain regions. Temporal lobe epilepsy TLE, a symptomatic localization-related epilepsy, is the most common epilepsy of adults who experience seizures poorly controlled with anticonvulsant medications. In most cases, the epileptogenic region is found in the midline mesial temporal structures e.g., the hippocampus, amygdala, and parahippocampal gyrus. Seizures begin in late childhood and adolescence. Most of these patients have complex partial seizures sometimes preceded by an aura, and some TLE patients also suffer from secondary generalized tonic-clonic seizures. If the patient does not respond sufficiently to medical treatment, epilepsy surgery may be considered. Frontal lobe epilepsy, usually a symptomatic or cryptogenic localization-related epilepsy, arises from lesions causing seizures that occur in the frontal lobes of the brain. These epilepsies can be difficult to diagnose because the symptoms of seizures can easily be confused with nonepileptic spells and, because of limitations of the EEG, be difficult to see with standard scalp EEG. Rasmussen's encephalitis is a symptomatic localization-related epilepsy that is a progressive, inflammatory lesion affecting children with onset before the age of 10. Seizures start as separate simple partial or complex partial seizures and may progress to epilepsia partialis continuata simple partial status epilepticus. Neuroimaging shows inflammatory encephalitis on one side of the brain that may spread if not treated. Dementia and hemiparesis are other problems. The cause is hypothesized to involve an immulogical attack against glutamate receptors, a common neurotransmitter in the brain. 19 West syndrome is a triad of developmental delay, seizures termed infantile spasms, and EEG demonstrating a pattern termed hypsarrhythmia. Onset occurs between 3 months and 2 years, with peak onset between 8-9 months. West syndrome may arise from idiopathic, symptomatic, or cryptogenic causes. The most common cause is tuberous sclerosis. The prognosis varies with the underlying cause. In general most surviving patients remain with significant cognitive impairment and continuing seizures and may evolve to another eponymic syndrome, Lennox-Gastaut syndrome. Dravet's syndrome Severe myoclonic epilepsy of infancy SMEI. This generalized epilepsy syndrome is distinguished from benign myoclonic epilepsy by its severity and must be differentiated from the Lennox-Gastaut syndrome and Doose's myoclonic-astatic epilepsy. Onset is in the first year of life and symptoms peak at about 5 months of age with febrile hemiclonic or generalized status epilepticus. Boys are twice as often affected as girls. Prognosis is poor. Most cases are sporadic. Family history of epilepsy and febrile convulsions is present in around 25 percent of the cases.20 Progressive myoclonic epilepsies define a group of symptomatic generalized epilepsies characterized by progressive dementia and myoclonic seizures. Tonic-clonic seizures may occur as well. Diseases usually classified in this group are Unverricht-Lundborg disease, myoclonus epilepsy with ragged red fibers, Lafora disease, neuronal ceroid lipofucinosis, and sialdosis. Lennox-Gastaut syndrome LGS is a generalized epilepsy that consists of a triad of developmental delay or childhood dementia, mixed generalized seizures, and EEG demonstating a pattern of approximately 2 Hz slow spike-wave. Onset occurs between 2-18 years. As in West syndrome, LGS result from idiopathic, symptomatic, or cryptogenic causes, and many patients first have West syndrome. Authorities emphasize different seizure types as important in LGS, but most have astatic seizures drop attacks, tonic seizures, tonic-clonic seizures, atypical absence seizures, and sometimes, complex partial seizures. Anticonvulsants are usually only partially successful in treatment. Treatment Epilepsy is usually treated with medication prescribed by a physician; primary caregivers, neurologists, and neurosurgeons all frequently care for people with epilepsy. In some cases the implantation of a stimulator of the vagus nerve, or a special diet can be helpful. Neurosurgical operations for epilepsy can be palliative, reducing the frequency or severity of seizures; or, in some patients, an operation can be curative. Responding to a seizure In most cases, the proper emergency response to a generalized tonic-clonic epileptic seizure is simply to prevent the patient from self-injury by moving him or her away from sharp edges, placing something soft beneath the head, and carefully rolling the person into the recovery position to avoid asphyxiation. In some cases the person may seem to start snoring loudly following a seizure, before coming to. This merely indicates that the person is beginning to breathe properly and does not mean he or she is suffocating. Should the person regurgitate, the material should be allowed to drip out the side of the person's mouth by itself. If a seizure lasts longer than 5 minutes, or if the seizures begin coming in 'waves' one after the other - then Emergency Medical Services should be contacted immediately. Prolonged seizures may develop into status epilepticus, a dangerous condition requiring hospitalization and emergency treatment. Objects should never be placed in a person's mouth by anybody - including paramedics - during a seizure as this could result in serious injury to either party. Despite common folklore, it is not possible for a person to swallow their own tongue during a seizure. However, it is possible that the person will bite their own tongue, especially if an object is placed in the mouth. With other types of seizures such as simple partial seizures and complex partial seizures where the person is not convulsing but may be hallucinating, disoriented, distressed, or unconscious, the person should be reassured, gently guided away from danger, and sometimes it may be necessary to protect the person from self-injury, but physical force should be used only as a last resort as this could distress the person even more. In complex partial seizures where the person is unconscious, attempts to rouse the person should not be made as the seizure must take its full course. After a seizure, the person may pass into a deep sleep or otherwise they will be disoriented and often unaware that they have just had a seizure, as amnesia is common with complex partial seizures. The person should remain observed until they have completely recovered, as with a tonic-clonic seizure. After a seizure, it is typical for a person to be exhausted and confused. Often the person is not immediately aware that they have just had a seizure. During this time one should stay with the person - reassuring and comforting them - until they appear to act as they normally would. Seldom during seizures do people lose bladder or bowel control. In some instances the person may vomit after coming to. People should not eat or drink until they have returned to their normal level of awareness, and they should not be allowed to wander about unsupervised. Many patients will sleep deeply for a few hours after a seizure - this is common for those having just experienced a more violent type of seizure such as a tonic-clonic. In about 50% of people with epilepsy, headaches may occur after a seizure. These headaches share many features with migraines, and respond to the same medications. It is helpful if those present at the time of a seizure make note of how long and how severe the seizure was. It is also helpful to note any mannerisms displayed during the seizure. For example, the individual may twist the body to the right or left, may blink, might mumble nonsense words, or might pull at clothing. Any observed behaviors, when relayed to a neurologist, may be of help in diagnosing the type of seizure which occurred. Pharmacologic treatment Main article: Anticonvulsant Mechanisms of Drug Action:- 1- Sodium channel blockers voltage dependent 2- Calcium channel blockers T-type 3- Potentiate the effect of GABA inhibitory 4- Decrease the excitatory transmission glutaminic Some medications can be taken daily in order to prevent seizures altogether or reduce the frequency of their occurrence. These are termed anticonvulsant or antiepileptic drugs sometimes AEDs. All such drugs have side effects that are idiosyncratic and others that are dosage-dependent. It is not possible to predict who will suffer from side effects or at what dose the side effects will appear. Some people with epilepsy will experience a complete remission when treated with an anticonvulsant medication. If this does not occur, the dose of medication may be increased, or another medication may be added to the first. The general strategy is to increase the medication dose until either the seizures are controlled, or until dose-limiting side effects appear; at which point the medication dose is reduced to the highest amount that does not produce undesirable side effects. A study found that in 83% of patients on a two drug regime to control their epilepsy could be slowly transferred completely off of one of the drugs and be controlled with a single drug regime without any increase in seizure frequency. Surprisingly it was found that 36% of patients showed greater seizure control on a single drug regime for epilepsy control than on a two drug regime. Side effects were also decreased in those taking a single drug regime. It was concluded that overall a reduction in polypharmacy may be benefitial for most patients who have intractable epilepsy.21 Serum levels of AEDs can be checked to determine medication compliance and to assess the effects of drug-drug interactions; some physicians do not use serum levels to fine tune medication, but other physicians believe that serum levels provide excellent data for tailoring medications to suit an individual's specific and relatively variable body chemistry. For example, therapeutic doses the dose at which seizures are controlled and side effects are minimal and tolerable may vary widely from among patients. The therapeutic ranges provided by pharmaceutical companies are only ranges and by using blood serum levels and seizures diaries, better seizure control can sometimes be reached. In some cases such as a seizure flurry serum levels can be useful to know if the level is very high or very low. If a person's epilepsy cannot be brought under control after adequate trials of two or three experts vary here different drugs, that person's epilepsy is generally said to be 'medically refractory.' Various drugs may prevent seizures or reduce seizure frequency: these include carbamazepine common brand name Tegretol, clobazam Frisium, clonazepam Klonopin, ethosuximide Zarontin, felbamate Felbatol, fosphenytoin Cerebyx, gabapentin Neurontin, lamotrigine Lamictal, levetiracetam Keppra, oxcarbazepine Trileptal, phenobarbital Luminal, phenytoin Dilantin, pregabalin Lyrica, primidone Mysoline, sodium valproate Epilim, tiagabine Gabitril, topiramate Topamax, valproate semisodium Depakote, Epival, valproic acid Depakene, Convulex, vigabatrin Sabril, and zonisamide Zonegran. Other drugs are commonly used to abort an active seizure or interrupt a seizure flurry; these include diazepam Valium and lorazepam Ativan. Drugs used only in the treatment of refractory status epilepticus include paraldehyde Paral, midazolam Versed, and pentobarbital Nembutal. Bromides were the first of the effective anticonvulsant pure compounds, but are no longer used in humans22 due to their toxicity and low efficacy. It has been found that taking valproates while pregnant can have high chances of reduced IQ towards children.2324 Many epileptics have found that marijuana is an effective medical treatment of epilepsy, and a telephone survey conducted in 2003 revealed that more than twice as many epileptics use marijuana than the general population.2526 Surgical treatment Surgical treatment can be an option for epilepsy when an underlying brain abnormality, such as a benign tumor or an area of scar tissue e.g. hippocampal sclerosis can be identified. The abnormality must be removable by a neurosurgeon. Surgery is usually only offered to patients when their epilepsy has not been controlled by adequate attempts with multiple medications. Before surgery is offered, the medical team conducts many tests to assess whether removal of brain tissue will result in unacceptable problems with memory, vision, language or movement, which are controlled by different parts of the brain. These tests usually include a neuropsychological evaluation, which sometimes includes an intracarotid sodium amobarbital test Wada test - although this invasive procedure is being replaced by non-invasive functional MRI in many centres. Resective surgery, as opposed to palliative, successfully eliminates or significantly reduces seizures in about 50-90% of the patients who undergo it the exact percentage depends on the particulars of the case and surgeon in question. Many patients decide not to undergo surgery owing to fear or the uncertainty of having a brain operation. The most common form of resective surgical treatment for epilepsy is to remove the front part of either the right or left temporal lobe. A study of 48 patients who underwent this operation, anterior temporal lobectomy, between 1965 and 1974 determined the long-term success of the procedure. Of the 48 patients, 21 had had no seizures that caused loss of consciousness since the operation. Three others had been free of seizures for at least 19 years. The rest had either never been completely free of seizures or had died between the time of the surgery and commencement of the study.27 Palliative surgery for epilepsy is intended to reduce the frequency or severity of seizures. Examples are callosotomy or commissurotomy to prevent seizures from generalizing spreading to involve the entire brain, which results in a loss of consciousness. This procedure can therefore prevent injury due to the person falling to the ground after losing consciousness. It is performed only when the seizures cannot be controlled by other means. Resective surgery can be considered palliative if it is undertaken with the expectation that it will reduce but not eliminate seizures. Hemispherectomy is a drastic operation in which most or all of one half of the cerebral cortex is removed. It is reserved for people suffering from the most catastrophic epilepsies, such as those due to Rasmussen syndrome. If the surgery is performed on very young patients 2-5 years old, the remaining hemisphere may acquire some rudimentary motor control of the ipsilateral body; in older patients, paralysis results on the side of the body opposite to the part of the brain that was removed. Because of these and other side effects it is usually reserved for patients who have exhausted other treatment options. Other treatment The ketogenic diet can be effective and is mainly used in children whose epilepsy has not been controlled with medication. As with anticonvulsant drugs, the mechanism behind the effect is not fully understood. The ketogenic diet is very high in fat and very low in carbohydrates. This treatment was developed in the 1920s at the Mayo clinic, but was largely forgotten with the discovery of modern anti-epileptic drugs. Since the 1990s, it has returned to the anti-epileptic treatment arsenal and is available from most paediatric epilepsy centres. Now proven effective with infants, too: http://www.physorg.com/news140111291.html A study conducted by Johns Hopkins reported that 50% of those patients starting the Ketogenic diet reported a decrease in seizures of 50% or more, with 29% of patients reporting a 90% reduction in symptoms; these patients had previously tried an average of six anticonvulsant drugs. Vagus nerve stimulation VNS is a recently developed form of seizure control which uses an implanted electrical device, similar in size, shape and implant location to a heart pacemaker, which connects to the vagus nerve in the neck. Once in place the device can be set to emit electronic pulses, stimulating the vagus nerve at pre-set intervals and milliamp levels. Treatment studies have shown that approximately 50% of those treated in this fashion will show significant seizure frequency reduction. The Responsive Neurostimulator System RNS is currently undergoing clinical study prior to FDA approval. This system relies upon a device implanted just under the scalp. The leads attached to the device are implanted either on the brain surface or in the brain area itself and are located close to the area where the seizures are believed to start. When a seizure begins, small amounts of electrical stimulation are delivered to suppress it. This system is different from the VNS system in that the RNS relies on direct brain stimulation and the RNS is a responsive system. The VNS pulses at predetermined intervals previously set by medical personnel. The RNS system is designed to respond to detected signs that a seizure is about to begin and can record events and allow customized response patterns which may provide a greater degree of seizure control.28 A seizure response dog is a form of service dog that is trained to summon help or ensure personal safety when a seizure occurs. These are not suitable for everybody and not all dogs can be so trained. Rarely, a dog may develop the ability to sense a seizure before it occurs.29 A number of systematic reviews by the Cochrane Collaboration into treatments for epilepsy looked at acupuncture,30 psychological interventions,31 vitamins32 and yoga33 and found there is no reliable evidence to support the use of these as treatments for epilepsy. Further studies are needed on the subject. Pathophysiology Mutations in several genes have been linked to some types of epilepsy. Several genes that code for protein subunits of voltage-gated and ligand-gated ion channels have been associated with forms of generalized epilepsy and infantile seizure syndromes.34 Several ligand-gated ion channels have been linked to some types of frontal and generalized epilepsies. Epilepsy-related mutations in some non-ion channel genes have also been identified. Epileptogenesis is the process by which a normal brain develops epilepsy after an insult. One interesting finding in animals is that repeated low-level electrical stimulation to some brain sites can lead to permanent increases in seizure susceptibility: in other words, a permanent decrease in seizure threshold. This phenomenon, known as kindling by analogy with the use of burning twigs to start a larger fire was discovered by Dr. Graham Goddard in 1967. Chemical stimulation can also induce seizures; repeated exposures to some pesticides have been shown to induce seizures in both humans and animals. One mechanism proposed for this is called excitotoxicity. The roles of kindling and excitotoxicity, if any, in human epilepsy are currently hotly debated. Other causes of epilepsy are brain lesions, where there is scar tissue or another abnormal mass of tissue in an area of the brain. History and stigma The word epilepsy is derived from the Greek epilepsia, which in turn can be broken into epi- upon and lepsis to take hold of, or seizure35 In the past, epilepsy was associated with religious experiences and even demonic possession. In ancient times, epilepsy was known as the Sacred Disease because people thought that epileptic seizures were a form of attack by demons, or that the visions experienced by persons with epilepsy were sent by the gods. Among animist Hmong families, for example, epilepsy was understood as an attack by an evil spirit, but the affected person could become revered as a shaman through these otherworldly experiences.36 However, in most cultures, persons with epilepsy have been stigmatized, shunned, or even imprisoned; in the Salpêtrière, the birthplace of modern neurology, Jean-Martin Charcot found people with epilepsy side-by-side with the mentally retarded, those with chronic syphilis, and the criminally insane. In Tanzania to this day, as with other parts of Africa, epilepsy is associated with possession by evil spirits, witchcraft, or poisoning and is believed by many to be contagious.37 In ancient Rome, epilepsy was known as the Morbus Comitialis 'disease of the assembly hall' and was seen as a curse from the gods. Stigma continues to this day, in both the public and private spheres, but polls suggest it is generally decreasing with time, at least in the developed world; Hippocrates remarked that epilepsy would cease to be considered divine the day it was understood.38 Controversy There has been some relatively mild controversy surrounding the standards for diagnosis for partial-complex seizures and how these standards are applied in practice, both among some surrealists1 and in particular as regards Mary Baker Eddy, founder of Christian Science. In April 2003, the BBC TV science programme Horizon featured discussion of research by American neurologist Gregory Holmes indicating that Ellen G. White, spiritual founder of the Seventh-day Adventist Church, may have suffered from temporal lobe epilepsy as a result of brain damage due to an accident suffered at age nine - the epilepsy supposedly being responsible for her powerful religious experiences. Temporal lobe epilepsy is known to be associated with such experiences. Notable people with epilepsy Main article: List of people with epilepsy Many notable people, past and present, have carried the diagnosis of epilepsy. In many cases, their epilepsy is a footnote to their accomplishments; for some, it played an integral role in their fame. Historical diagnoses of epilepsy are not always certain; there is controversy about what is considered an acceptable amount of evidence in support of such a diagnosis. Legal implications Main article: Epilepsy and driving Most people diagnosed with epilepsy are forbidden by their local laws from operating vehicles. However, there are usually exceptions for those who can prove that they have stabilized their condition. Those few whose seizures do not cause impairment of consciousness, or whose seizures only arise from sleep, may be exempt from such restrictions, depending on local laws. There is an ongoing debate in bioethics over who should bear the burden of ensuring that an epilepsy patient does not drive a car or fly an airplane. In the U.S., people with epilepsy can drive if their seizures are controlled with treatment and they meet the licensing requirements in their state. How long they have to be free of seizures varies in different states, but it is most likely to be between three months and a year.3940 The majority of the 50 states place the burden on patients to report their condition to appropriate licensing authorities so that their privileges can be revoked where appropriate. A minority of states place the burden of reporting on the patient's physician. After reporting is carried out, it is usually the driver's licensing agency that decides to revoke or restrict a driver's license. In the UK, it is the responsibility of the patients to inform the Driver and Vehicle Licensing Agency DVLA if they have epilepsy.41 The DVLA rules are quite complex,42 but in summary,43 those continuing to have seizures or who are within 6 months of medication change may have their licence revoked. A doctor who becomes aware that a patient with uncontrolled epilepsy is continuing to drive has, after reminding the patient of their responsibility, a duty to break confidentiality and inform the DVLA. The doctor should advise the patient of the disclosure and the reasons why their failure to notify the agency obliged the doctor to act. The Epilepsy Foundation's Jeanne A. Carpenter
 Epilepsy Legal Defense Fund is dedicated to advancing the rights of people with epilepsy by changing discriminatory practices, policies and laws and to ending epilepsy-related discrimination and injustice through education and increased access to legal services for individuals with epilepsy through a system of managed referrals and legal support to a nationwide network of attorneys committed to this cause. Additionally, the Epilepsy Foundation is a vigorous advocate for people with epilepsy. In the United States, the Foundation has been active in Congress, the executive branch, and the courts, focusing attention on the needs of those with epilepsy. Priorities for the Foundation include: the availability of affordable quality health care, the search for the cure, and the protection of civil rights for people with epilepsy. Important investigators of epilepsy Jean-Martin Charcot John Hughlings Jackson Hans Berger Herbert Jasper Wilder Penfield H. Houston Merritt William G. Lennox Fritz E. Dreifuss See also Non-epileptic seizures Epilepsy in animals Seizure response dog Jacksonian seizure Photosensitive epilepsy Post-traumatic epilepsy Temporal lobe epilepsy Abdominal epilepsy Generalised epilepsy ISAS Ictal-Interictal SPECT Analysis by SPM Postictal state References ^ Commission on Epidemiology and Prognosis, International League Against Epilepsy 1993. Guidelines for epidemiologic studies on epilepsy. Commission on Epidemiology and Prognosis, International League Against Epilepsy. Epilepsia 34 4: 592-6. doi:10.1111/j.1528-1157.1993.tb00433.x. PMID 8330566. ^ Blume W, Lüders H, Mizrahi E, Tassinari C, van Emde Boas W, Engel J 2001. Glossary of descriptive terminology for ictal semiology: report of the ILAE task force on classification and terminology. Epilepsia 42 9: 1212-8. doi:10.1046/j.1528-1157.2001.22001.x. PMID 11580774. ^ Fisher R, van Emde Boas W, Blume W, Elger C, Genton P, Lee P, Engel J 2005. Epileptic seizures and epilepsy: definitions proposed by the International League Against Epilepsy ILAE and the International Bureau for Epilepsy IBE. Epilepsia 46 4: 470-2. doi:10.1111/j.0013-9580.2005.66104.x. PMID 15816939. ^ Epilepsy: aetiogy sic, epidemiology and prognosis. World Health Organization February 2001. Retrieved on 2007-06-14. ^ Proposal for revised clinical and electroencephalographic classification of epileptic seizures. From the Commission on Classification and Terminology of the International League Against Epilepsy 1981. Epilepsia 22 4: 489-501. doi:10.1111/j.1528-1157.1981.tb06159.x. PMID 6790275. ^ a b Proposal for revised classification of epilepsies and epileptic syndromes. Commission on Classification and Terminology of the International League Against Epilepsy 1989. Epilepsia 30 4: 389-99. doi:10.1111/j.1528-1157.1989.tb05316.x. PMID 2502382. ^ Jerome Engel. A Proposed Diagnostic Scheme For People With Epileptic Seizures And With Epilepsy: Report Of The Ilae Task Force On Classification And Terminology. ILAE. Retrieved on 2006-07-18. ^ C P Panayiotopoulos and M Koutroumanidis September 2005. The significance of the syndromic diagnosis of the epilepsies. National Society for Epilepsy. ^ Frucht MM, Quigg M, Schwaner C, Fountain NB. 2000. Distribution of seizure precipitants among epilepsy syndromes.. Epilepsia 41 12: 1534-1539.. ^ Herzog AG, Harden CL, Liporace J, Pennell P, Schomer DL, Sperling M, et al. 2004. Frequency of catamenial seizure exacerbation in women with localization-related epilepsy. Annals Neurology 56 3: 431-434.. ^ Hirtz D, Thurman DJ, Gwinn-Hardy K, Mohamed M, Chaudhuri AR, Zalutsky R 2007-01-30. How common are the 'common' neurologic disorders?. Neurology 68 5: 326-37. doi:10.1212/01.wnl.0000252807.38124.a3. PMID 17261678. ^ Sander JW 2003. The epidemiology of epilepsy revisited. Curr Opin Neurol 16 2: 165-70. doi:10.1097/00019052-200304000-00008. PMID 12644744. ^ Plioplys S, Dunn DW, Caplan R 2007. 10-year research update review: psychiatric problems in children with epilepsy. J Am Acad Child Adolesc Psychiatry 46 11: 1389-402. doi:10.1097/chi.0b013e31815597fc. PMID 18049289. ^ Levisohn PM 2007. The autism-epilepsy connection. Epilepsia 48 Suppl 9: 33-5. PMID 18047599. ^ cite journal | author = Loiseau P, Duche B, Cordova S, et al | title = Prognosis of benign childhood epilepsy with centro-temporal spikes. A follow-up of 168 patients | journal = Epilepsia | volume = 29 | pages = 229-235 | year =1988 ^ cite journal | author = Panayiotopolous CP | title = Benign childhood epileptic syndromes with occipital spikes: New classification proposed by the ILAE | journal = J Child Neurol | volume = 15 | pages = 548-552 | year = 2000 ^ Bertrand D, Picard F, Le Hellard S, Weiland S, Favre I, Phillips H, et al. 2002. How mutations in the nAChRs can cause ADNFLE epilepsy.. Epilepsia 43 Supple 5: 112-122. ^ Koutroumanidis M, Koepp MJ, Richardson MP, Camfield C, Agathonikou A, Ried S, et al 1998. The variants of reading epilepsy. A clinical and video-EEG study of 17 patients with reading-induced seizures. Brain 121: 1409-1427. ^ Rogers et al 1994. Autoantibodies to glutamate receptor GluR3 in Rasmussen's encephalitis. Science 265: 648-651. ^ Dravet Syndrome. Retrieved on 2007-12-16. ^ Schmidt D Jun 1983. Reduction of two-drug therapy in intractable epilepsy. Epilepsia 24 3: 368-76. doi:10.1111/j.1528-1157.1983.tb04900.x. PMID 6406214. ^ Clemmons DVM, PhD, R.M. 1997. Seizure Disorders in Dogs and Cats. The Neurology Service at the VMTH. University of Florida's Veterinary Medical Teaching Hospital. Retrieved on 2006-03-29. ^ Cassels, Caroline December 8, 2006. NEAD: In Utero Exposure To Valproate Linked to Poor Cognitive Outcomes in Kids. Medscape. Retrieved on 2007-05-23. ^ Meador KJ, Baker GA, Finnell RH, et al 2006. In utero antiepileptic drug exposure: fetal death and malformations. Neurology 67 3: 407-12. doi:10.1212/01.wnl.0000227919.81208.b2. PMID 16894099. ^ Epilepsy and marijuana | epilepsy.com ^ http://www.medscape.com/viewarticle/465891 ^ Kelley K, Theodore WH 2005. Prognosis 30 years after temporal lobectomy. Neurology 64 11: 1974-6. doi:10.1212/01.WNL.0000163998.01543.CF. PMID 15955959. ^ Patient FAQ. RNS System. NeuroPace. Retrieved on 2007-11-02. ^ Barriaux, Marianne 2006-10-16. Dogs trained to warn of an imminent epileptic fit, The Guardian. Retrieved on 2006-11-24. ^ Cheuk D, Wong V 2006. Acupuncture for epilepsy. Cochrane Database Syst Rev 2: CD005062. doi:10.1002/14651858.CD005062.pub2. PMID 16625622. ^ Ramaratnam S, Baker GA, Goldstein LH 2005. Psychological treatments for epilepsy. Cochrane Database Syst Rev 4: CD002029. doi:10.1002/14651858.CD002029.pub2. PMID 16235293. ^ Ranganathan LN, Ramaratnam S 2005. Vitamins for epilepsy. Cochrane Database Syst Rev 2: CD004304. doi:10.1002/14651858.CD004304.pub2. PMID 15846704. ^ Ramaratnam S, Sridharan K 2000. Yoga for epilepsy. Cochrane Database Syst Rev 3: CD001524. doi:10.1002/14651858.CD001524. PMID 10908505. ^ Miriam H. Meisler and Jennifer A. Kearney 2005. Sodium channel mutations in epilepsy and other neurological disorders. Journal of Clinical Investigation 115 8: 2010-2017. doi:10.1172/JCI25466. PMID 16075041 doi:10.1172/JCI25466. ^ Harper, Douglas 2001. epilepsy. Online Etymological Dictionary. Retrieved on 2005-06-05. ^ When Epilepsy Goes By Another Name | epilepsy.com ^ Morbus sacer in Africa: some religious aspects of epilepsy in traditional cultures. Jilek-Aall L. PMID: 10080524 Retrieved 8 October 2006. ^ Hippocrates quotes ^ Epilepsy Foundation Driving and You - Can you drive an automobile if you have epilepsy?. ^ Epilepsy Foundation Driver Information by State ^ UK Epilepsy Action: Driving and Epilepsy, I've had a seizure. What should I do? ^ UK Driver and Vehicle Licensing Agency Guide to the Current Medical Standards Of Fitness to Drive. Full details for doctors regarding epilepsy are given in the Appendix. Information for drivers can be found in Medical Rules - Group 1 Licence Holders ^ UK Epilepsy Action: booklet with further details about driving PDF External links Epilepsy at the Open Directory Project v d e Pathology of the nervous system, primarily CNS G00-G47, 320-349 Inflammatory Meningitis Arachnoiditis, Aseptic meningitis, Tuberculous meningitis - Encephalitis - Myelitis - Encephalomyelitis Acute disseminated - Tropical spastic paraparesis - Cavernous sinus thrombosis Systemic atrophies Huntington's disease - Spinocerebellar ataxia Friedreich's ataxia, Ataxia telangiectasia, Herary spastic paraplegia - Spinal muscular atrophy: Werdnig-Hoffman - Kugelberg-Welander - Fazio-Londe - MND ALS, PMA, PBP, PP, PLS Extrapyramidal and movement disorders Parkinson's disease - Neuroleptic malignant syndrome - Postencephalitic parkinsonism - Pantothenate kinase-associated neurodegeneration - Progressive supranuclear palsy - Striatonigral degeneration - Dystonia/Dyskinesia Spasmodic torticollis, Meige's, Blepharospasm - Essential tremor - Myoclonus - Lafora - Chorea Choreoathetosis - Restless legs - Stiff person Other degenerative/ demyelinating diseases dementia: Alzheimer's - Pick's - Dementia with Lewy bodies - Frontotemporal lobar degeneration mitochondrial disease: Leigh's demyelinating: Multiple sclerosis - Devic's - Central pontine myelinolysis - Transverse myelitis - Marchiafava-Bignami disease - CAMFAK syndrome - Alpers' Seizure/epilepsy Focal - Generalised - Status epilepticus - Myoclonic epilepsy Headache Migraine Familial hemiplegic - Cluster - Vascular - Tension Vascular Transient ischemic attack Amaurosis fugax, Transient global amnesia Cerebrovascular disease MCA, ACA, PCA, Foville's, Millard-Gubler, Lateral medullary, Weber's, Lacunar stroke Sleep disorders Insomnia - Hypersomnia - Sleep apnea Obstructive, Ondine's curse - Narcolepsy - Cataplexy - Kleine-Levin - Circadian rhythm sleep - Delayed sleep phase - Advanced sleep phase Intracranial hypertension Hydrocephalus Normal pressure - Idiopathic intracranial hypertension Other encephalopathy Brain herniation - Cerebral edema - Reye's Other spinal cord disease Syringomyelia - Syringobulbia - Morvan's syndrome - Spinal cord compression v d e Seizures and epilepsy Focal Simple partial · Complex partial · Temporal lobe epilepsy · Frontal lobe epilepsy · Jacksonian seizure Generalised Tonic-clonic · Absence seizure · Atonic seizure · Benign familial neonatal · Lennox-Gastaut · West · Todd's paresis Status epilepticus Epilepsia partialis continua · Complex partial status epilepticus Myoclonic epilepsy Progressive myoclonic epilepsy Dentatorubral-pallidoluysian atrophy · Unverricht-Lundborg disease · Juvenile myoclonic epilepsy Retrieved from http://en..org/wiki/Epilepsy Categories: Medical terms | Neurological disorders | Neurology | Epilepsy | Greek loanwordsHidden categories: All articles with statements | Articles with statements since July 2008 Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages العربية Aymar বাংলা Bosanski Brezhoneg БългарÑ?ки Català Česky Dansk Deutsch Eesti Ελληνικά Español Esperanto Euskara Français Galego Hrvatski Ido Bahasa Indonesia Ã?slenska Italiano עברית Kurdî / كوردی Lietuvių Magyar മലയാളം Nederlands 日本語 ‪Norsk bokmÃ¥l‬ Nouormand Polski Português РуÑ?Ñ?кий Shqip Simple English SlovenÄ?ina SlovenÅ¡Ä?ina СрпÑ?ки / Srpski Suomi Svenska Türkçe УкраїнÑ?ька ä¸æ–‡ This page was last modified on 12 September 2008, at 09:29
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