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Este artículo trata sobre las convulsiones epilépticas. Para otros tipos de convulsiones, consulte Convulsiones no epilépticas . Para otros usos, consulte Convulsión (desambiguación) .
Ataque epiléptico
Otros nombresAtaque epiléptico, [1] convulsiones, ataques, convulsiones [2]
Spike-waves.png
Descargas de ondas y picos generalizados de 3 Hz en el electroencefalograma
EspecialidadNeurología , medicina de emergencia
SíntomasVariable [3]
DuraciónNormalmente <2 minutos [4]
TiposProvocado, no provocado [5]
CausasProvocado : Azúcar en la sangre , la abstinencia de alcohol , bajo contenido de sodio en la sangre , fiebre , infección cerebral , conmoción cerebral [3] [5]
, no provocado : Desconocido, lesión cerebral , tumor cerebral , anterior accidente cerebrovascular [4] [3] [5] [6]
Método de diagnósticoBasado en síntomas, análisis de sangre, imágenes médicas , electroencefalografía [6]
Diagnóstico diferencialSíncope , convulsiones psicógenas no epilépticas , temblor , migraña , ataque isquémico transitorio [3] [4]
TratamientoMenos de 5 min : coloque a la persona de lado, retire los objetos peligrosos cercanos [7]
Más de 5 min : trate según el estado epiléptico [7]
Frecuencia~ 10% de las personas (en un momento determinado) [4] [8]

Una convulsión , formalmente conocida como convulsión epiléptica , es un período de síntomas debido a una actividad neuronal anormalmente excesiva o sincrónica en el cerebro . [5] Los efectos externos varían desde movimientos de agitación incontrolados que involucran gran parte del cuerpo con pérdida de conciencia ( convulsión tónico-clónica ), movimientos de agitación que involucran solo una parte del cuerpo con niveles variables de conciencia ( convulsión focal ), hasta una pérdida momentánea sutil de conciencia ( crisis de ausencia ). [3] La mayoría de las veces, estos episodios duran menos de 2 minutos y lleva algún tiempo volver a la normalidad.[4] [7] Puede ocurrir pérdida del control de la vejiga . [3]

Las convulsiones pueden ser provocadas y no provocadas. [5] Las convulsiones provocadas se deben a un evento temporal como bajo nivel de azúcar en sangre , abstinencia de alcohol , abuso de alcohol junto con medicamentos recetados, bajo nivel de sodio en sangre , fiebre , infección cerebral o conmoción cerebral . [3] [5] Las convulsiones no provocadas ocurren sin una causa conocida o reparable, de modo que es probable que continúen las convulsiones. [4] [3] [5] [6] Las convulsiones no provocadas pueden ser provocadas por el estrés o la falta de sueño . [3]Las enfermedades del cerebro, donde ha habido al menos una convulsión y un riesgo a largo plazo de más convulsiones, se conocen colectivamente como epilepsia . [5] Las condiciones que se parecen a las convulsiones epilépticas pero que no lo son incluyen: desmayos , convulsiones psicógenas no epilépticas y temblores . [3]

Una convulsión que dura más de un breve período es una emergencia médica . [9] Cualquier convulsión que dure más de 5 minutos debe tratarse como estado epiléptico . [7] Una primera convulsión generalmente no requiere un tratamiento a largo plazo con medicamentos anticonvulsivos, a menos que se encuentre un problema específico en el electroencefalograma (EEG) o las imágenes cerebrales. [6] Por lo general, es seguro completar el estudio después de una sola convulsión como paciente ambulatorio . [3] En muchos, con lo que parece ser una primera convulsión, han ocurrido previamente otras convulsiones menores. [10]

Hasta el 10% de las personas tienen al menos un ataque epiléptico. [4] [8] Las convulsiones provocadas ocurren en aproximadamente 3.5 de cada 10,000 personas por año, mientras que las convulsiones no provocadas ocurren en aproximadamente 4.2 de cada 10,000 personas por año. [4] Después de una convulsión, la probabilidad de experimentar una segunda es aproximadamente del 50%. [11] La epilepsia afecta aproximadamente al 1% de la población en un momento dado [8] con aproximadamente el 4% de la población afectada en algún momento. [6] Casi el 80% de las personas con epilepsia viven en países en desarrollo . [8] Muchos lugares requieren que las personas dejen de conducir hasta que no hayan tenido una convulsión durante un período específico. [4]

Signos y síntomas [ editar ]

Ver también: tipos de convulsiones

Los signos y síntomas de las convulsiones varían según el tipo. [12] El tipo de ataque más común y estereotipado es el convulsivo (60%). [13] Dos tercios de estos comienzan como convulsiones focales y se generalizan, mientras que un tercio comienzan como convulsiones generalizadas. [13] El 40% restante de las convulsiones no son convulsivas, un ejemplo de las cuales es la convulsión de ausencia . [14]

Convulsiones focales [ editar ]

Las convulsiones focales a menudo comienzan con ciertas experiencias, conocidas como aura . [12] Estos pueden incluir fenómenos sensoriales, visuales, psíquicos, autónomos, olfativos o motores. [15]

En una convulsión parcial compleja, una persona puede parecer confundida o aturdida y no puede responder a preguntas o instrucciones. La convulsión focal puede generalizarse. [15]

La actividad de sacudidas puede comenzar en un grupo de músculos específico y extenderse a los grupos de músculos circundantes, lo que se conoce como marcha de Jackson . [16] Pueden ocurrir actividades inusuales que no se crean conscientemente. [16] Estos se conocen como automatismos e incluyen actividades simples como chasquear los labios o actividades más complejas como intentar levantar algo. [dieciséis]

Convulsiones generalizadas [ editar ]

Hay seis tipos principales de convulsiones generalizadas: convulsiones tónico-clónicas, tónicas, clónicas, mioclónicas, de ausencia y atónicas. [17] Todos implican una pérdida del conocimiento y generalmente ocurren sin previo aviso. [18]

  • Las convulsiones tónico-clónicas se presentan con una contracción de las extremidades seguida de su extensión, junto con un arqueamiento de la espalda durante 10 a 30 segundos. [18] Se puede escuchar un llanto debido a la contracción de los músculos del pecho. [18] Las extremidades comienzan a temblar al unísono. [18] Una vez que ha cesado el temblor, la persona puede tardar entre 10 y 30 minutos en volver a la normalidad. [18]
  • Las convulsiones tónicas producen contracciones constantes de los músculos. [18] La persona puede ponerse azul si tiene problemas para respirar. [18]
  • Las convulsiones clónicas implican sacudir las extremidades al unísono. [18]
  • Las convulsiones mioclónicas involucran espasmos de músculos en algunas áreas o generalizados en todo el cuerpo. [18]
  • Las convulsiones de ausencia pueden ser sutiles, con solo un ligero giro de la cabeza o un parpadeo de los ojos. [15] La persona a menudo no se cae y puede volver a la normalidad inmediatamente después de que termina la convulsión, aunque también puede haber un período de desorientación posictal. [15]
  • Las convulsiones atónicas implican la pérdida de actividad muscular durante más de un segundo. [16] Esto suele ocurrir de forma bilateral (en ambos lados del cuerpo). [dieciséis]

Duración [ editar ]

Una convulsión puede durar desde unos pocos segundos hasta más de cinco minutos, momento en el que se conoce como estado epiléptico . [19] La mayoría de las convulsiones tónico-clónicas duran menos de dos o tres minutos. [19] Las convulsiones de ausencia suelen durar alrededor de 10 segundos. [14]

Postictal [ editar ]

Después de la parte activa de una convulsión, generalmente hay un período de confusión llamado período postictal antes de que regrese un nivel normal de conciencia . [12] Esto suele durar de 3 a 15 minutos [20] pero puede durar horas. [21] Otros síntomas comunes incluyen: cansancio, dolor de cabeza , dificultad para hablar y comportamiento anormal. [21] La psicosis después de una convulsión es relativamente común y ocurre entre el 6 y el 10% de las personas. [22] A menudo, la gente no recuerda lo que ocurrió durante este tiempo. [21]

Causas [ editar ]

Artículo principal: Causas de las convulsiones.

Las convulsiones tienen varias causas. De los que tienen convulsiones, alrededor del 25% padece epilepsia . [23] Varias afecciones están asociadas con convulsiones, pero no son epilepsia, entre ellas: la mayoría de las convulsiones febriles y las que ocurren alrededor de una infección aguda, accidente cerebrovascular o toxicidad. [24] Estas convulsiones se conocen como convulsiones "sintomáticas agudas" o "provocadas" y son parte de los trastornos relacionados con las convulsiones. [24] En muchos casos se desconoce la causa.

Las diferentes causas de convulsiones son comunes en ciertos grupos de edad.

  • Las convulsiones en los bebés son causadas con mayor frecuencia por encefalopatía isquémica hipóxica , infecciones del sistema nervioso central (SNC), traumatismos, anomalías congénitas del SNC y trastornos metabólicos .
  • La causa más frecuente de convulsiones en los niños son las convulsiones febriles, que ocurren en el 2 al 5% de los niños entre las edades de seis meses y cinco años. [25]
  • Durante la infancia, generalmente se observan síndromes epilépticos bien definidos.
  • En la adolescencia y la edad adulta joven, el incumplimiento del régimen de medicación y la falta de sueño son posibles desencadenantes.
  • El embarazo y el trabajo de parto y el parto, y el período posparto o posparto (después del nacimiento) pueden ser momentos de riesgo, especialmente si existen ciertas complicaciones como la preeclampsia .
  • Durante la edad adulta, las causas probables son las relacionadas con el alcohol, los accidentes cerebrovasculares, los traumatismos, las infecciones del SNC y los tumores cerebrales. [26]
  • En los adultos mayores, la enfermedad cerebrovascular es una causa muy común. Otras causas son los tumores del SNC, los traumatismos craneoencefálicos y otras enfermedades degenerativas que son comunes en el grupo de mayor edad, como la demencia . [27]

Metabólico [ editar ]

La deshidratación puede desencadenar ataques epilépticos si es lo suficientemente grave. [28] Una serie de trastornos que incluyen: niveles bajos de azúcar en sangre , niveles bajos de sodio en sangre , hiperglucemia hiperosmolar no cetósica , niveles altos de sodio en sangre , niveles bajos de calcio en sangre y niveles altos de urea en sangre pueden causar convulsiones. [18] Al igual que la encefalopatía hepática y el trastorno genético porfiria . [18]

Estructural [ editar ]

  • El cavernoma o malformación cavernosa es una afección médica tratable que puede causar convulsiones, dolores de cabeza y hemorragias cerebrales.
  • La malformación arteriovenosa (MAV) es una afección médica tratable que puede causar convulsiones, dolores de cabeza y hemorragias cerebrales.
  • Lesiones que ocupan espacio en el cerebro ( abscesos , tumores ). En personas con tumores cerebrales , la frecuencia de la epilepsia depende de la ubicación del tumor en la región cortical . [29]

Medicamentos [ editar ]

Tanto la medicación como la sobredosis de drogas pueden provocar convulsiones [18], al igual que ciertos medicamentos y la abstinencia de drogas . [18] Los fármacos habituales implicados incluyen: antidepresivos , antipsicóticos , cocaína , insulina y el anestésico local lidocaína . [18] Las dificultades con las convulsiones por abstinencia ocurren comúnmente después del uso prolongado de alcohol o sedantes , una condición conocida como delirium tremens . [18]

Infecciones [ editar ]

  • La infección por la tenia del cerdo , que puede causar neurocisticercosis , es la causa de hasta la mitad de los casos de epilepsia en áreas del mundo donde el parásito es común. [30]
  • Infecciones parasitarias como malaria cerebral . En Nigeria, esta es una de las causas más comunes de convulsiones entre los niños menores de 5 años. [31]
  • Infección , como encefalitis o meningitis [32]

Estrés [ editar ]

El estrés puede provocar convulsiones en personas con  epilepsia y es un factor de riesgo para desarrollar epilepsia. La gravedad, la duración y el momento en que se produce el estrés durante el desarrollo contribuyen a la frecuencia y la susceptibilidad de desarrollar la epilepsia. Es uno de los desencadenantes autoinformados con más frecuencia en pacientes con epilepsia. [33] [34]

Stress exposure results in hormone release that mediates its effects in the brain. These hormones act on both excitatory and inhibitory neural synapses, resulting in hyper-excitability of neurons in the brain. The hippocampus is known to be a region that is highly sensitive to stress and prone to seizures. This is where mediators of stress interact with their target receptors to produce effects.[35]

Other[edit]

Seizures may occur as a result of high blood pressure, known as hypertensive encephalopathy, or in pregnancy as eclampsia when accompanied by either seizures or a decreased level of consciousness.[18] Very high body temperatures may also be a cause.[18] Typically this requires a temperature greater than 42 °C (107.6 °F).[18]

  • Head injury may cause non-epileptic post-traumatic seizures or post-traumatic epilepsy
  • About 3.5 to 5.5% of people with celiac disease also have seizures.[36]
  • Seizures in a person with a shunt may indicate failure
  • Hemorrhagic stroke can occasionally present with seizures, embolic strokes generally do not (though epilepsy is a common later complication); cerebral venous sinus thrombosis, a rare type of stroke, is more likely to be accompanied by seizures than other types of stroke
  • Multiple sclerosis may cause seizures
  • Electroconvulsive therapy (ECT) deliberately sets out to induce a seizure for the treatment of major depression.

Mechanism[edit]

Normally, brain electrical activity is non-synchronous.[15] In epileptic seizures, due to problems within the brain,[37] a group of neurons begin firing in an abnormal, excessive,[13] and synchronized manner.[15] This results in a wave of depolarization known as a paroxysmal depolarizing shift.[38]

Normally after an excitatory neuron fires it becomes more resistant to firing for a period of time.[15] This is due in part from the effect of inhibitory neurons, electrical changes within the excitatory neuron, and the negative effects of adenosine.[15] In epilepsy the resistance of excitatory neurons to fire during this period is decreased.[15] This may occur due to changes in ion channels or inhibitory neurons not functioning properly.[15] Forty-one ion-channel genes and over 1,600 ion-channel mutations have been implicated in the development of epileptic seizure.[39] These ion channel mutations tend to confer a depolarized resting state to neurons resulting in pathological hyper-excitability.[40] This long-lasting depolarization in individual neurons is due to an influx of Ca2+ from outside of the cell and leads to extended opening of Na+ channels and repetitive action potentials.[41] The following hyperpolarization is facilitated by γ-aminobutyric acid (GABA) receptors or potassium (K+) channels, depending on the type of cell.[41] Equally important in epileptic neuronal hyper-excitability, is the reduction in the activity of inhibitory GABAergic neurons, an effect known as disinhibition. Disinhibition may result from inhibitory neuron loss, dysregulation of axonal sprouting from the inhibitory neurons in regions of neuronal damage, or abnormal GABAergic signaling within the inhibitory neuron.[42] Neuronal hyper-excitability results in a specific area from which seizures may develop, known as a "seizure focus".[15] Following an injury to the brain, another mechanism of epilepsy may be the up regulation of excitatory circuits or down regulation of inhibitory circuits.[15][43] These secondary epilepsies occur through processes known as epileptogenesis.[15][43] Failure of the blood–brain barrier may also be a causal mechanism.[44] While blood-brain barrier disruption alone does appear to cause epileptogenesis, it has been correlated to increased seizure activity.[45] Furthermore, it has been implicated in chronic epileptic conditions through experiments inducing barrier permeability with chemical compounds.[45] Disruption may lead to fluid leaking out of the blood vessels into the area between cells and driving epileptic seizures.[46] Preliminary findings of blood proteins in the brain after a seizure support this theory.[45]

Focal seizures begin in one hemisphere of the brain while generalized seizures begin in both hemispheres.[17] Some types of seizures may change brain structure, while others appear to have little effect.[47] Gliosis, neuronal loss, and atrophy of specific areas of the brain are linked to epilepsy but it is unclear if epilepsy causes these changes or if these changes result in epilepsy.[47]

Seizure activity may be propagated through the brain's endogenous electrical fields.[48] Proposed mechanisms that may cause the spread and recruitment of neurons include an increase in K+ from outside the cell, and increase of Ca2+ in the presynaptic terminals.[41] These mechanisms blunt hyperpolarization and depolarizes nearby neurons, as well as increasing neurotransmitter release.[41]

Diagnosis[edit]

The 2017 ILAE classification of seizure types and the epilepsies (click to read full text)

Seizures may be divided into provoked and unprovoked.[5] Provoked seizures may also be known as "acute symptomatic seizures" or "reactive seizures".[5] Unprovoked seizures may also be known as "reflex seizures".[5] Depending on the presumed cause blood tests and lumbar puncture may be useful.[6] Hypoglycemia may cause seizures and should be ruled out. An electroencephalogram and brain imaging with CT scan or MRI scan is recommended in the work-up of seizures not associated with a fever.[6][49]

Classification[edit]

Seizure types are organized by whether the source of the seizure is localized (focal seizures) or distributed (generalized seizures) within the brain.[17] Generalized seizures are divided according to the effect on the body and include tonic-clonic (grand mal), absence (petit mal), myoclonic, clonic, tonic, and atonic seizures.[17][50] Some seizures such as epileptic spasms are of an unknown type.[17]

Focal seizures (previously called partial seizures[13]) are divided into simple partial or complex partial seizure.[17] Current practice no longer recommends this, and instead prefers to describe what occurs during a seizure.[17]

Physical examination[edit]

An individual who has bitten the tip of their tongue while having a seizure

Most people are in a postictal state (drowsy or confused) following a seizure. They may show signs of other injuries. A bite mark on the side of the tongue helps confirm a seizure when present, but only a third of people who have had a seizure have such a bite.[51] When present in people thought to have had a seizure, this physical sign tentatively increases the likelihood that a seizure was the cause.[52]

Tests[edit]

An EEG can aid in locating the focus of the epileptic seizure.

An electroencephalography is only recommended in those who likely had an epileptic seizure and may help determine the type of seizure or syndrome present. In children it is typically only needed after a second seizure. It cannot be used to rule out the diagnosis and may be falsely positive in those without the disease. In certain situations it may be useful to prefer the EEG while sleeping or sleep deprived.[53]

Diagnostic imaging by CT scan and MRI is recommended after a first non-febrile seizure to detect structural problems inside the brain.[53] MRI is generally a better imaging test except when intracranial bleeding is suspected.[6] Imaging may be done at a later point in time in those who return to their normal selves while in the emergency room.[6] If a person has a previous diagnosis of epilepsy with previous imaging repeat imaging is not usually needed with subsequent seizures.[53]

In adults, testing electrolytes, blood glucose and calcium levels is important to rule these out as causes, as is an electrocardiogram.[53] A lumbar puncture may be useful to diagnose a central nervous system infection but is not routinely needed.[6] Routine antiseizure medical levels in the blood are not required in adults or children.[53] In children additional tests may be required.[53]

A high blood prolactin level within the first 20 minutes following a seizure may be useful to confirm an epileptic seizure as opposed to psychogenic non-epileptic seizure.[54][55] Serum prolactin level is less useful for detecting partial seizures.[56] If it is normal an epileptic seizure is still possible[55] and a serum prolactin does not separate epileptic seizures from syncope.[57] It is not recommended as a routine part of diagnosis epilepsy.[53]

Differential diagnosis[edit]

Differentiating an epileptic seizure from other conditions such as syncope can be difficult.[12] Other possible conditions that can mimic a seizure include: decerebrate posturing, psychogenic seizures, tetanus, dystonia, migraine headaches, and strychnine poisoning.[12] In addition, 5% of people with a positive tilt table test may have seizure-like activity that seems due to cerebral hypoxia.[58] Convulsions may occur due to psychological reasons and this is known as a psychogenic non-epileptic seizure. Non-epileptic seizures may also occur due to a number of other reasons.

Prevention[edit]

A number of measures have been attempted to prevent seizures in those at risk. Following traumatic brain injury anticonvulsants decrease the risk of early seizures but not late seizures.[59]

In those with a history of febrile seizures, medications (both antipyretics and anticonvulsants) have not been found effective for prevention. Some, in fact, may cause harm.[60]

There is no clear evidence that antiepileptic drugs are effective or not effective at preventing seizures following a craniotomy,[61][needs update] following subdural hematoma,[62] after a stroke,[63][64] or after subarachnoid haemorrhage,[65] for both people who have had a previous seizure, and those who have not.

Management[edit]

Potentially sharp or dangerous objects should be moved from the area around a person experiencing a seizure so that the individual is not hurt. After the seizure, if the person is not fully conscious and alert, they should be placed in the recovery position. A seizure longer than five minutes, or two or more seizures occurring within the time of five minutes is a medical emergency known as status epilepticus.[19][66] Contrary to a common misconception, bystanders should not attempt to force objects into the mouth of the person suffering a seizure, as doing so may cause injury to the teeth and gums.[67]

Treatments of a person that is actively seizing follows a progression from initial response, through first line, second line, and third line treatments.[68] The initial response involves ensuring the person is protected from potential harms (such as nearby objects) and managing their airway, breathing, and circulation.[68] Airway management should include placing the person on their side, known as the recovery position, to prevent them from choking.[68] If they are unable to breathe because something is blocking their airway, they may require treatments to open their airway.[68]

Medication[edit]

The first line medication for an actively seizing person is a benzodiazepine, with most guidelines recommending lorazepam.[49][69] Diazepam and midazolam are alternatives. This may be repeated if there is no effect after 10 minutes.[49] If there is no effect after two doses, barbiturates or propofol may be used.[49] Benzodiazepines given by a non-intravenous route appear better than those given by intravenous, as the intravenous takes longer to have an effect.[70]

Second-line therapy for adults is phenytoin or fosphenytoin and phenobarbital for children.[71][page needed] Third-line medications include phenytoin for children and phenobarbital for adults.[71][page needed]

Ongoing anti-epileptic medications are not typically recommended after a first seizure except in those with structural lesions in the brain.[49] They are generally recommended after a second one has occurred.[49] Approximately 70% of people can obtain full control with continuous use of medication.[37] Typically one type of anticonvulsant is preferred. Following a first seizure, while immediate treatment with an anti-seizure drug lowers the probability of seizure recurrence up to five years it does not change the risk of death and there are potential side effects.[72]

In seizures related to toxins, up to two doses of benzodiazepines should be used.[73] If this is not effective pyridoxine is recommended.[73] Phenytoin should generally not be used.[73]

There is a lack of evidence for preventive anti-epileptic medications in the management of seizures related to intracranial venous thrombosis.[64]

Other[edit]

Helmets may be used to provide protection to the head during a seizure. Some claim that seizure response dogs, a form of service dog, can predict seizures.[74] Evidence for this, however, is poor.[74] At present there is not enough evidence to support the use of cannabis for the management of seizures, although this is an ongoing area of research.[75][76] There is low quality evidence that a ketogenic diet may help in those who have epilepsy and is reasonable in those who do not improve following typical treatments.[77]

Prognosis[edit]

Following a first seizure, the risk of more seizures in the next two years is 40%–50%.[6] The greatest predictors of more seizures are problems either on the electroencephalogram or on imaging of the brain.[6] In adults, after 6 months of being seizure-free after a first seizure, the risk of a subsequent seizure in the next year is less than 20% regardless of treatment.[78] Up to 7% of seizures that present to the emergency department (ER) are in status epilepticus.[49] In those with a status epilepticus, mortality is between 10% and 40%.[12] Those who have a seizure that is provoked (occurring close in time to an acute brain event or toxic exposure) have a low risk of re-occurrence, but have a higher risk of death compared to those with epilepsy.[79]

Epidemiology[edit]

Approximately 8–10% of people will experience an epileptic seizure during their lifetime.[80] In adults, the risk of seizure recurrence within the five years following a new-onset seizure is 35%; the risk rises to 75% in persons who have had a second seizure.[80] In children, the risk of seizure recurrence within the five years following a single unprovoked seizure is about 50%; the risk rises to about 80% after two unprovoked seizures.[81] In the United States in 2011, seizures resulted in an estimated 1.6 million emergency department visits; approximately 400,000 of these visits were for new-onset seizures.[80] The exact incidence of epileptic seizures in low-income and middle-income countries is unknown, however it probably exceeds that in high-income countries.[82] This may be due to increased risks of traffic accidents, birth injuries, and malaria and other parasitic infections.[82]

History[edit]

Epileptic seizures were first described in an Akkadian text from 2000 B.C.[83] Early reports of epilepsy often saw seizures and convulsions as the work of “evil spirits”.[84] The perception of epilepsy, however, began to change in the time of Ancient Greek medicine. The term "epilepsy" itself is a Greek word, which is derived from the verb "epilambanein", meaning "to seize, possess, or afflict".[83] Although the Ancient Greeks referred to epilepsy as the “sacred disease”, this perception of epilepsy as a "spiritual" disease was challenged by Hippocrates in his work “On the Sacred Disease", who proposed that the source of epilepsy was from natural causes rather than supernatural ones.[84]

Early surgical treatment of epilepsy was primitive in Ancient Greek, Roman and Egyptian medicine.[85] The 19th century saw the rise of targeted surgery for the treatment of epileptic seizures, beginning in 1886 with localized resections performed by Sir Victor Horsley, a neurosurgeon in London.[84]  Another advancement was that of the development by the Montreal procedure by Canadian neurosurgeon Wilder Penfield, which involved use of electrical stimulation among conscious patients to more accurately identify and resect the epileptic areas in the brain.[84]

Society and culture[edit]

Economics[edit]

Seizures result in direct economic costs of about one billion dollars in the United States.[6] Epilepsy results in economic costs in Europe of around €15.5 billion in 2004.[13] In India, epilepsy is estimated to result in costs of US$1.7 billion or 0.5% of the GDP.[37] They make up about 1% of emergency department visits (2% for emergency departments for children) in the United States.[26]

Driving[edit]

Many areas of the world require a minimum of six months from the last seizure before people can drive a vehicle.[6]

Research[edit]

Scientific work into the prediction of epileptic seizures began in the 1970s. Several techniques and methods have been proposed, but evidence regarding their usefulness is still lacking.[86]

Two promising areas include gene therapy,[87] and seizure detection and seizure prediction.[88]

Gene therapy for epilepsy consists of employing vectors to deliver pieces of genetic material to areas of the brain involved in seizure onset.[87]

Seizure prediction is a special case of seizure detection in which the developed systems is able to issue a warning before the clinical onset of the epileptic seizure.[86][88]

References[edit]

  1. ^ Shorvon, Simon (2009). Epilepsy. OUP Oxford. p. 1. ISBN 9780199560042.
  2. ^ "Seizures - National Library of Medicine". PubMed Health. Retrieved 16 October 2018.
  3. ^ a b c d e f g h i j k Misulis, Karl E.; Murray, E. Lee (2017). Essentials of Hospital Neurology. Oxford University Press. p. Chapter 19. ISBN 9780190259433.
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External links[edit]

Classification
D
  • ICD-10: G40
  • ICD-9-CM: 345.9, 780.3
  • MeSH: D012640
  • DiseasesDB: 19011
External resources
  • MedlinePlus: 003200
  • eMedicine: neuro/415 neuro/694
  • Seizure at Curlie