Seizure

Last updated

Epileptic seizure
Other namesEpileptic fit, [1] seizure, fit, convulsions [2]
Spike-waves.png
Generalized 3 Hz spike and wave discharges in an electroencephalogram (EEG) of a patient with epilepsy
Specialty Neurology, emergency medicine
Symptoms Variable [3]
Complications Falling, drowning, car accidents, pregnancy complications, emotional health issues [4]
DurationTypically < 2 minutes [5]
TypesFocal, generalized; Provoked, unprovoked [6]
CausesProvoked: Low blood sugar, alcohol withdrawal, low blood sodium, fever, brain infection, traumatic brain injury [3] [6]
Unprovoked: Unknown, brain injury, brain tumor, previous stroke [5] [3] [6] [7]
Diagnostic method Based on symptoms, blood tests, medical imaging, electroencephalography [7]
Differential diagnosis Syncope, psychogenic non-epileptic seizure, migraine aura, transient ischemic attack [3] [5]
TreatmentLess than 5 min: Place person on their side, remove nearby dangerous objects [8]
More than 5 min: Treat as per status epilepticus [8]
Frequency~10% of people (overall worldwide lifetime risk) [5] [9]

A seizure is a period of symptoms due to abnormally excessive or synchronous neuronal activity in the brain. [6] Outward effects vary from uncontrolled shaking movements involving much of the body with loss of consciousness (tonic-clonic seizure), to shaking movements involving only part of the body with variable levels of consciousness (focal seizure), to a subtle momentary loss of awareness (absence seizure). [3] These episodes usually last less than two minutes and it takes some time to return to normal. [5] [8] Loss of bladder control may occur. [3]

Contents

Seizures may be provoked and unprovoked. [6] Provoked seizures are due to a temporary event such as low blood sugar, alcohol withdrawal, abusing alcohol together with prescription medication, low blood sodium, fever, brain infection, flashing images or concussion. [3] [6] Unprovoked seizures occur without a known or fixable cause such that ongoing seizures are likely. [5] [3] [6] [7] Unprovoked seizures may be exacerbated by stress or sleep deprivation. [3] Epilepsy describes a brain disease in which there has been at least one unprovoked seizure and where there is a high risk of additional seizures in the future. [6] Conditions that look like epileptic seizures but are not include: fainting, nonepileptic psychogenic seizure and tremor. [3]

A seizure that lasts for more than a brief period is a medical emergency. [10] Any seizure lasting longer than five minutes should be treated as status epilepticus. [8] A first seizure generally does not require long-term treatment with anti-seizure medications unless a specific problem is found on electroencephalogram (EEG) or brain imaging. [7] Typically it is safe to complete the work-up following a single seizure as an outpatient. [3] In many, with what appears to be a first seizure, other minor seizures have previously occurred. [11]

Up to 10% of people have had at least one epileptic seizure in their lifetime. [5] [9] Provoked seizures occur in about 3.5 per 10,000 people a year while unprovoked seizures occur in about 4.2 per 10,000 people a year. [5] After one seizure, the chance of experiencing a second one is about 40%. [12] [13] Epilepsy affects about 1% of the population at any given time. [9]

Signs and symptoms

The signs and symptoms of seizures vary depending on the type. [14] The most common and stereotypical type of seizure is convulsive (60%), typically called a tonic-clonic seizure. [15] Two-thirds of these begin as focal seizures prior to developing into tonic-clonic seizures. [15] The remaining 40% of seizures are non-convulsive, an example of which is absence seizure. [16] When EEG monitoring shows evidence of a seizure, but no symptoms are present, it is referred to as a subclinical seizure. [17]

Focal seizures

Focal seizures often begin with certain experiences, known as an aura. [14] These may include sensory (including visual, auditory, etc.), cognitive, autonomic, olfactory or motor phenomena. [18]

In a complex partial seizure, a person may appear confused or dazed and cannot respond to questions or direction. [18]

Jerking activity may start in a specific muscle group and spread to surrounding muscle groups—known as a Jacksonian march . [19] Unusual activities that are not consciously created may occur. [19] These are known as automatisms and include simple activities like smacking of the lips or more complex activities such as attempts to pick something up. [19]

Generalized seizures

There are six main types of generalized seizures: tonic-clonic, tonic, clonic, myoclonic, absence, and atonic seizures. [20] They all involve a loss of consciousness and typically happen without warning. [21]

Duration

A seizure can last from a few seconds to more than five minutes, at which point it is known as status epilepticus. [22] Most tonic-clonic seizures last less than two or three minutes. [22] Absence seizures are usually around 10 seconds in duration. [16]

Postictal

After the active portion of a seizure, there is typically a period of confusion called the postictal period, before a normal level of consciousness returns. [14] This period usually lasts 3 to 15 minutes, [23] but may last for hours. [24] Other symptoms during this period include: tiredness, headache, difficulty speaking, and abnormal behavior. [24] Psychosis after a seizure occurs in 6–10% of people. [25] [24]

Causes

Seizures have a number of causes. Of those who have a seizure, about 25% have epilepsy. [26] A number of conditions are associated with seizures but are not epilepsy including: most febrile seizures and those that occur around an acute infection, stroke, or toxicity. [27] These seizures are known as "acute symptomatic" or "provoked" seizures and are part of the seizure-related disorders. [27] In many the cause is unknown.

Different causes of seizures are common in certain age groups.

Metabolic

Dehydration can trigger epileptic seizures if it is severe enough. [31] A number of disorders including: low blood sugar, low blood sodium, hyperosmolar nonketotic hyperglycemia, high blood sodium, low blood calcium and high blood urea levels may cause seizures. [21] As may hepatic encephalopathy and the genetic disorder porphyria. [21]

Structural

Medications

Both medication and drug overdoses can result in seizures, [21] as may certain medication and drug withdrawal. [21] Common drugs involved include: antidepressants, antipsychotics, cocaine, insulin, and the local anaesthetic lidocaine. [21] Difficulties with withdrawal seizures commonly occur after prolonged alcohol or sedative use, a condition known as delirium tremens. [21] In people who are at risk of developing epileptic seizures, common herbal medicines such as ephedra, ginkgo biloba and wormwood can provoke seizures. [33]

Infections

Stress

Stress can induce seizures in people with epilepsy, and is a risk factor for developing epilepsy. Severity, duration, and time at which stress occurs during development all contribute to frequency and susceptibility to developing epilepsy. It is one of the most frequently self-reported triggers in patients with epilepsy. [37] [38]

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. [39]

Other

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. [21] Very high body temperatures may also be a cause. [21] Typically this requires a temperature greater than 42 °C (107.6 °F). [21]

Mechanism

Normally, brain electrical activity is non-synchronous. [18] In epileptic seizures, due to problems within the brain, [44] a group of neurons begin firing in an abnormal, excessive, [15] and synchronized manner. [18] This results in a wave of depolarization known as a paroxysmal depolarizing shift. [45]

Normally after an excitatory neuron fires it becomes more resistant to firing for a period of time. [18] This is due in part from the effect of inhibitory neurons, electrical changes within the excitatory neuron, and the negative effects of adenosine. [18] In epilepsy the resistance of excitatory neurons to fire during this period is decreased. [18] This may occur due to changes in ion channels or inhibitory neurons not functioning properly. [18] Forty-one ion-channel genes and over 1,600 ion-channel mutations have been implicated in the development of epileptic seizure. [46] These ion channel mutations tend to confer a depolarized resting state to neurons resulting in pathological hyper-excitability. [47] 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. [48] The following hyperpolarization is facilitated by γ-aminobutyric acid (GABA) receptors or potassium (K+) channels, depending on the type of cell. [48] 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. [49] Neuronal hyper-excitability results in a specific area from which seizures may develop, known as a "seizure focus". [18] Following an injury to the brain, another mechanism of epilepsy may be the up regulation of excitatory circuits or down regulation of inhibitory circuits. [18] [50] These secondary epilepsies occur through processes known as epileptogenesis. [18] [50] Failure of the blood–brain barrier may also be a causal mechanism. [51] While blood-brain barrier disruption alone does appear to cause epileptogenesis, it has been correlated to increased seizure activity. [52] Furthermore, it has been implicated in chronic epileptic conditions through experiments inducing barrier permeability with chemical compounds. [52] Disruption may lead to fluid leaking out of the blood vessels into the area between cells and driving epileptic seizures. [53] Preliminary findings of blood proteins in the brain after a seizure support this theory. [52]

Focal seizures begin in one hemisphere of the brain while generalized seizures begin in both hemispheres. [20] Some types of seizures may change brain structure, while others appear to have little effect. [54] 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. [54]

Seizure activity may be propagated through the brain's endogenous electrical fields. [55] Proposed mechanisms that may cause the spread and recruitment of neurons include an increase in K+ from outside the cell, [56] [ unreliable medical source ] and increase of Ca2+ in the presynaptic terminals. [48] These mechanisms blunt hyperpolarization and depolarizes nearby neurons, as well as increasing neurotransmitter release. [48]

Diagnosis

The 2017 ILAE classification of seizure types and the epilepsies (click to read full text) The 2017 ILAE classification of seizure types and the epilepsies what do people with epilepsy and their caregivers need to know%3F.pdf
The 2017 ILAE classification of seizure types and the epilepsies (click to read full text)

Seizures may be divided into provoked and unprovoked. [6] Provoked seizures may also be known as "acute symptomatic seizures" or "reactive seizures". [6] Unprovoked seizures may also be known as "reflex seizures". [6] Depending on the presumed cause blood tests and lumbar puncture may be useful. [7] 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. [7] [57]

Classification

Seizure types are organized by whether the source of the seizure is localized (focal seizures) or distributed (generalized seizures) within the brain. [20] 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. [20] [58] Some seizures such as epileptic spasms are of an unknown type. [20]

Focal seizures (previously called partial seizures) [15] are divided into simple partial or complex partial seizure. [20] Current practice no longer recommends this, and instead prefers to describe what occurs during a seizure. [20]

The classification of seizures can also be made according to dynamical criteria, observable in electrophysiological measurements. It is a classification according to their type of onset and offset. [59] [60]

Physical examination

An individual who has bitten the tip of their tongue while having a seizure Bittentongue.JPG
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. [61] When present in people thought to have had a seizure, this physical sign tentatively increases the likelihood that a seizure was the cause. [62]

Tests

An EEG can aid in locating the focus of the epileptic seizure. EEG Recording Cap.jpg
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. [63]

Diagnostic imaging by CT scan and MRI is recommended after a first non-febrile seizure to detect structural problems inside the brain. [63] MRI is generally a better imaging test except when intracranial bleeding is suspected. [7] Imaging may be done at a later point in time in those who return to their normal selves while in the emergency room. [7] If a person has a previous diagnosis of epilepsy with previous imaging repeat imaging is not usually needed with subsequent seizures. [63]

In adults, testing electrolytes, blood glucose and calcium levels is important to rule these out as causes, as is an electrocardiogram. [63] A lumbar puncture may be useful to diagnose a central nervous system infection but is not routinely needed. [7] Routine antiseizure medical levels in the blood are not required in adults or children. [63] In children additional tests may be required. [63]

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. [64] [65] Serum prolactin level is less useful for detecting partial seizures. [66] If it is normal an epileptic seizure is still possible [65] and a serum prolactin does not separate epileptic seizures from syncope. [67] It is not recommended as a routine part of diagnosis epilepsy. [63]

Differential diagnosis

Differentiating an epileptic seizure from other conditions such as syncope can be difficult. [14] Other possible conditions that can mimic a seizure include: decerebrate posturing, psychogenic seizures, tetanus, dystonia, migraine headaches, and strychnine poisoning. [14] In addition, 5% of people with a positive tilt table test may have seizure-like activity that seems due to cerebral hypoxia. [68] 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

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. [69]

In those with a history of febrile seizures, some medications (both antipyretics and anticonvulsants) have been found effective for reducing reoccurrence, however due to the frequency of adverse effects and the benign nature of febrile seizures the decision to use medication should be weighted carefully against potential negative effects. [70]

There is no clear evidence that antiepileptic drugs are effective or not effective at preventing seizures following a craniotomy, [71] following subdural hematoma, [72] after a stroke, [73] [74] or after subarachnoid haemorrhage, [75] for both people who have had a previous seizure, and those who have not.

Management

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. [22] [76] Contrary to a common misconception, bystanders should not attempt to force objects into the mouth of the person having a seizure, as doing so may cause injury to the teeth and gums. [77]

Treatments of a person that is actively seizing follows a progression from initial response, through first line, second line, and third line treatments. [78] The initial response involves ensuring the person is protected from potential harms (such as nearby objects) and managing their airway, breathing, and circulation. [78] Airway management should include placing the person on their side, known as the recovery position, to prevent them from choking. [78] If they are unable to breathe because something is blocking their airway, they may require treatments to open their airway. [78]

Medication

The first line medication for an actively seizing person is a benzodiazepine, with most guidelines recommending lorazepam. [57] [79] Diazepam and midazolam are alternatives. This may be repeated if there is no effect after 10 minutes. [57] If there is no effect after two doses, barbiturates or propofol may be used. [57]

Second-line therapy for adults is phenytoin or fosphenytoin and phenobarbital for children. [80] [ page needed ] Third-line medications include phenytoin for children and phenobarbital for adults. [80] [ page needed ]

Ongoing anti-epileptic medications are not typically recommended after a first seizure except in those with structural lesions in the brain. [57] They are generally recommended after a second one has occurred. [57] Approximately 70% of people can obtain full control with continuous use of medication. [44] 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. [81]

In seizures related to toxins, up to two doses of benzodiazepines should be used. [82] If this is not effective pyridoxine is recommended. [82] Phenytoin should generally not be used. [82]

There is a lack of evidence for preventive anti-epileptic medications in the management of seizures related to intracranial venous thrombosis. [74]

Other

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. [83] Evidence for this, however, is poor. [83] 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. [84] [85] 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. [86]

Prognosis

Following a first seizure, the risk of more seizures in the next two years is around 40%. [12] [13] The greatest predictors of more seizures are problems either on the electroencephalogram or on imaging of the brain. [7] 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. [87] Up to 7% of seizures that present to the emergency department (ER) are in status epilepticus. [57] In those with a status epilepticus, mortality is between 10% and 40%. [14] 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. [88]

Epidemiology

Approximately 8–10% of people will experience an epileptic seizure during their lifetime. [89] 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. [89] 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. [90] 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. [89] The exact incidence of epileptic seizures in low-income and middle-income countries is unknown, however it probably exceeds that in high-income countries. [91] This may be due to increased risks of traffic accidents, birth injuries, and malaria and other parasitic infections. [91]

History

Epileptic seizures were first described in an Akkadian text from 2000 B.C. [92] Early reports of epilepsy often saw seizures and convulsions as the work of "evil spirits". [93] 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". [92] 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. [93]

Early surgical treatment of epilepsy was primitive in Ancient Greek, Roman and Egyptian medicine. [94] 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. [93] 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. [93]

Society and culture

Economics

Seizures result in direct economic costs of about one billion dollars in the United States. [7] Epilepsy results in economic costs in Europe of around €15.5 billion in 2004. [15] In India, epilepsy is estimated to result in costs of US$1.7 billion or 0.5% of the GDP. [44] They make up about 1% of emergency department visits (2% for emergency departments for children) in the United States. [29]

Driving

Many areas of the world require a minimum of six months from the last seizure before people can drive a vehicle. [7]

Research

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. [95]

Two promising areas include gene therapy, [96] and seizure detection and seizure prediction. [97]

Gene therapy for epilepsy consists of employing vectors to deliver pieces of genetic material to areas of the brain involved in seizure onset. [96]

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. [95] [97]

Computational neuroscience has been able to bring a new point of view on the seizures by considering the dynamical aspects. [60]

Related Research Articles

<span class="mw-page-title-main">Epilepsy</span> Group of neurological disorders causing seizures

Epilepsy is a group of non-communicable neurological disorders characterized by recurrent epileptic seizures. An epileptic seizure is the clinical manifestation of an abnormal, excessive, and synchronized electrical discharge in the brain cells called neurons. The occurrence of two or more unprovoked seizures defines epilepsy. The occurrence of just one seizure may warrant the definition in a more clinical usage where recurrence may be able to be prejudged. Epileptic seizures can vary from brief and nearly undetectable periods to long periods of vigorous shaking due to abnormal electrical activity in the brain. These episodes can result in physical injuries, either directly such as broken bones or through causing accidents. In epilepsy, seizures tend to recur and may have no detectable underlying cause. Isolated seizures that are provoked by a specific cause such as poisoning are not deemed to represent epilepsy. People with epilepsy may be treated differently in various areas of the world and experience varying degrees of social stigma due to the alarming nature of their symptoms.

A convulsion is a medical condition where the body muscles contract and relax rapidly and repeatedly, resulting in uncontrolled shaking. Because epileptic seizures typically include convulsions, the term convulsion is often used as a synonym for seizure. However, not all epileptic seizures result in convulsions, and not all convulsions are caused by epileptic seizures. Non-epileptic convulsions have no relation with epilepsy, and are caused by non-epileptic seizures.

<span class="mw-page-title-main">Febrile seizure</span> Seizure associated with high body temperature

A febrile seizure, also known as a fever fit or febrile convulsion, is a seizure associated with a high body temperature but without any serious underlying health issue. They most commonly occur in children between the ages of 6 months and 5 years. Most seizures are less than five minutes in duration, and the child is completely back to normal within an hour of the event. There are two types: simple febrile seizures and complex febrile seizures. Simple febrile seizures involve an otherwise healthy child who has at most one tonic-clonic seizure lasting less than 15 minutes in a 24-hour period. Complex febrile seizures have focal symptoms, last longer than 15 minutes, or occur more than once within 24 hours. About 80% are classified as simple febrile seizures.

Anticonvulsants are a diverse group of pharmacological agents used in the treatment of epileptic seizures. Anticonvulsants are also increasingly being used in the treatment of bipolar disorder and borderline personality disorder, since many seem to act as mood stabilizers, and for the treatment of neuropathic pain. Anticonvulsants suppress the excessive rapid firing of neurons during seizures. Anticonvulsants also prevent the spread of the seizure within the brain.

<span class="mw-page-title-main">Lamotrigine</span> Medication used for bipolar disorder, epilepsy, & many seizure disorders

Lamotrigine, sold under the brand name Lamictal among others, is a medication used to treat epilepsy and stabilize mood in bipolar disorder. For epilepsy, this includes focal seizures, tonic-clonic seizures, and seizures in Lennox-Gastaut syndrome. In bipolar disorder, lamotrigine has not been shown to reliably treat acute depression for all groups except in the severely depressed; but for patients with bipolar disorder who are not currently symptomatic, it appears to reduce the risk of future episodes of depression.

Absence seizures are one of several kinds of generalized seizures. In the past, absence epilepsy was referred to as "pyknolepsy," a term derived from the Greek word "pyknos," signifying "extremely frequent" or "grouped". These seizures are sometimes referred to as petit mal seizures ; however, usage of this terminology is no longer recommended. Absence seizures are characterized by a brief loss and return of consciousness, generally not followed by a period of lethargy. Absence seizures are most common in children. They affect both sides of the brain.

<span class="mw-page-title-main">Levetiracetam</span> Medication

Levetiracetam, sold under the brand name Keppra among others, is a medication used to treat epilepsy. It is used for partial-onset, myoclonic, or tonic–clonic seizures and is taken either by mouth as an immediate or extended release formulation or by injection into a vein.

<span class="mw-page-title-main">Clonazepam</span> Benzodiazepine medication

Clonazepam, sold under the brand names Klonopin and Rivotril, is a medication used to prevent and treat anxiety disorders, seizures, bipolar mania, agitation associated with psychosis, OCD and akathisia. It is a long-acting tranquilizer of the benzodiazepine class. It possesses anxiolytic, anticonvulsant, sedative, hypnotic, and skeletal muscle relaxant properties. It is typically taken by mouth but is also used intravenously. Effects begin within one hour and last between eight and twelve hours in adults.

Epilepsia partialis continua is a rare type of brain disorder in which a patient experiences recurrent motor epileptic seizures that are focal, and recur every few seconds or minutes for extended periods. It is sometimes called Kozhevnikov's epilepsia named after Russian psychiatrist Aleksei Yakovlevich Kozhevnikov who first described this type of epilepsy.

<span class="mw-page-title-main">Status epilepticus</span> Medical condition

Status epilepticus (SE), or status seizure, is a medical condition consisting of a single seizure lasting more than 5 minutes, or 2 or more seizures within a 5-minute period without the person returning to normal between them. Previous definitions used a 30-minute time limit. The seizures can be of the tonic–clonic type, with a regular pattern of contraction and extension of the arms and legs, or of types that do not involve contractions, such as absence seizures or complex partial seizures. Status epilepticus is a life-threatening medical emergency, particularly if treatment is delayed.

<span class="mw-page-title-main">Temporal lobe epilepsy</span> Chronic focal seizure disorder

In the field of neurology, temporal lobe epilepsy is an enduring brain disorder that causes unprovoked seizures from the temporal lobe. Temporal lobe epilepsy is the most common type of focal onset epilepsy among adults. Seizure symptoms and behavior distinguish seizures arising from the medial temporal lobe from seizures arising from the lateral (neocortical) temporal lobe. Memory and psychiatric comorbidities may occur. Diagnosis relies on electroencephalographic (EEG) and neuroimaging studies. Anticonvulsant medications, epilepsy surgery and dietary treatments may improve seizure control.

Sudden unexpected death in epilepsy (SUDEP) is a fatal complication of epilepsy. It is defined as the sudden and unexpected, non-traumatic and non-drowning death of a person with epilepsy, without a toxicological or anatomical cause of death detected during the post-mortem examination.

<span class="mw-page-title-main">Generalized tonic–clonic seizure</span> Type of generalized seizure that affects the entire brain

A generalized tonic–clonic seizure, commonly known as a grand mal seizure or GTCS, is a type of generalized seizure that produces bilateral, convulsive tonic and clonic muscle contractions. Tonic–clonic seizures are the seizure type most commonly associated with epilepsy and seizures in general and the most common seizure associated with metabolic imbalances. It is a misconception that they are the sole type of seizure, as they are the main seizure type in approximately 10% of those with epilepsy.

Post-traumatic epilepsy (PTE) is a form of acquired epilepsy that results from brain damage caused by physical trauma to the brain. A person with PTE experiences repeated post-traumatic seizures more than a week after the initial injury. PTE is estimated to constitute 5% of all cases of epilepsy and over 20% of cases of acquired epilepsy.

<span class="mw-page-title-main">Spike-and-wave</span>

Spike-and-wave is a pattern of the electroencephalogram (EEG) typically observed during epileptic seizures. A spike-and-wave discharge is a regular, symmetrical, generalized EEG pattern seen particularly during absence epilepsy, also known as ‘petit mal’ epilepsy. The basic mechanisms underlying these patterns are complex and involve part of the cerebral cortex, the thalamocortical network, and intrinsic neuronal mechanisms.

<span class="mw-page-title-main">Rolandic epilepsy</span> Most common epilepsy syndrome in childhood, usually subsiding with age

Benign Rolandic epilepsy or self-limited epilepsy with centrotemporal spikes is the most common epilepsy syndrome in childhood. Most children will outgrow the syndrome, hence the label benign. The seizures, sometimes referred to as sylvian seizures, start around the central sulcus of the brain.

Generally, seizures are observed in patients who do not have epilepsy. There are many causes of seizures. Organ failure, medication and medication withdrawal, cancer, imbalance of electrolytes, hypertensive encephalopathy, may be some of its potential causes. The factors that lead to a seizure are often complex and it may not be possible to determine what causes a particular seizure, what causes it to happen at a particular time, or how often seizures occur.

<span class="mw-page-title-main">Epilepsy in children</span>

Epilepsy is a neurological condition of recurrent episodes of unprovoked epileptic seizures. A seizure is an abnormal neuronal brain activity that can cause intellectual, emotional, and social consequences. Epilepsy affects children and adults of all ages and races, it is one of the most common neurological disorders of the nervous system. As well as, this condition is more common among children than adults affecting about 6 out of 1000 US children that are between the age of 0 to 5 years old. The epileptic seizures can be of different types depending on the part of the brain that was affected, seizures are classified in 2 main types partial seizure or genralized seizure.

People with epilepsy may be classified into different syndromes based on specific clinical features. These features include the age at which seizures begin, the seizure types, and EEG findings, among others. Identifying an epilepsy syndrome is useful as it helps determine the underlying causes as well as deciding what anti-seizure medication should be tried. Epilepsy syndromes are more commonly diagnosed in infants and children. Some examples of epilepsy syndromes include benign rolandic epilepsy, childhood absence epilepsy and juvenile myoclonic epilepsy. Severe syndromes with diffuse brain dysfunction caused, at least partly, by some aspect of epilepsy, are also referred to as epileptic encephalopathies. These are associated with frequent seizures that are resistant to treatment and severe cognitive dysfunction, for instance Lennox-Gastaut syndrome and West syndrome.

A neonatal seizure is a seizure in a baby younger than age 4-weeks that is identifiable by an electrical recording of the brain. It is an occurrence of abnormal, paroxysmal, and persistent ictal rhythm with an amplitude of 2 microvolts in the electroencephalogram,. These may be manifested in form of stiffening or jerking of limbs or trunk. Sometimes random eye movements, cycling movements of legs, tonic eyeball movements, and lip-smacking movements may be observed. Alteration in heart rate, blood pressure, respiration, salivation, pupillary dilation, and other associated paroxysmal changes in the autonomic nervous system of infants may be caused due to these seizures. Often these changes are observed along with the observance of other clinical symptoms. A neonatal seizure may or may not be epileptic. Some of them may be provoked. Most neonatal seizures are due to secondary causes. With hypoxic ischemic encephalopathy being the most common cause in full term infants and intraventricular hemorrhage as the most common cause in preterm infants.

References

  1. Shorvon S (2009). Epilepsy. OUP Oxford. p. 1. ISBN   9780199560042.
  2. "Epileptic Seizures - National Library of Medicine". PubMed Health. Retrieved 16 October 2018.
  3. 1 2 3 4 5 6 7 8 9 10 11 Misulis KE, Murray EL (2017). Essentials of Hospital Neurology. Oxford University Press. p. Chapter 19. ISBN   9780190259433.
  4. Mayo Clinic Staff. "Seizures – Symptoms and causes". Mayo Clinic .
  5. 1 2 3 4 5 6 7 8 Ferri FF (2018). Ferri's Clinical Advisor 2019 E-Book: 5 Books in 1. Elsevier Health Sciences. p. 959. ISBN   9780323550765.
  6. 1 2 3 4 5 6 7 8 9 10 11 Fisher RS, Acevedo C, Arzimanoglou A, Bogacz A, Cross JH, Elger CE, et al. (April 2014). "ILAE official report: a practical clinical definition of epilepsy". Epilepsia. 55 (4): 475–482. doi: 10.1111/epi.12550 . PMID   24730690. S2CID   35958237.
  7. 1 2 3 4 5 6 7 8 9 10 11 12 Wilden JA, Cohen-Gadol AA (August 2012). "Evaluation of first nonfebrile seizures". American Family Physician. 86 (4): 334–340. PMID   22963022.
  8. 1 2 3 4 "The Epilepsies and Seizures: Hope Through Research". National Institute of Neurological Disorders and Stroke. Retrieved 16 October 2018.
  9. 1 2 3 "Epilepsy". World Health Organization. 9 February 2023. Retrieved 4 June 2023.
  10. Schachter SC, Shafer PL, Sirven JI (5 November 2013). "What Is A Seizure Emergency". epilepsy.com.
  11. Angus-Leppan H (April 2014). "First seizures in adults". BMJ. 348: g2470. doi:10.1136/bmj.g2470. PMID   24736280. S2CID   31709502.
  12. 1 2 Neligan, Aidan; Adan, Guleed; Nevitt, Sarah J; Pullen, Angie; Sander, Josemir W; Bonnett, Laura; Marson, Anthony G (23 January 2023). Cochrane Epilepsy Group (ed.). "Prognosis of adults and children following a first unprovoked seizure". Cochrane Database of Systematic Reviews. 2023 (1): CD013847. doi:10.1002/14651858.CD013847.pub2. PMC   9869434 . PMID   36688481.
  13. 1 2 "Epilepsy: what are the chances of having a second seizure?". NIHR Evidence. National Institute for Health and Care Research. 2023. doi:10.3310/nihrevidence_59456. S2CID   260965684.
  14. 1 2 3 4 5 6 Shearer P. "Seizures and Status Epilepticus: Diagnosis and Management in the Emergency Department". Emergency Medicine Practice. Archived from the original on 30 December 2010.
  15. 1 2 3 4 5 National Institute for Health and Clinical Excellence (January 2012). "Chapter 1: Introduction" (PDF). The Epilepsies: The diagnosis and management of the epilepsies in adults and children in primary and secondary care. National Clinical Guideline Centre. pp. 21–28. Archived (PDF) from the original on 16 December 2013.
  16. 1 2 Hughes JR (August 2009). "Absence seizures: a review of recent reports with new concepts". Epilepsy & Behavior. 15 (4): 404–412. doi:10.1016/j.yebeh.2009.06.007. PMID   19632158. S2CID   22023692.
  17. Sokol DK, Markand ON, Daly EC, Luerssen TG, Malkoff MD (July 2000). "Near infrared spectroscopy (NIRS) distinguishes seizure types". Seizure. 9 (5): 323–327. doi: 10.1053/seiz.2000.0406 . PMID   10933986.
  18. 1 2 3 4 5 6 7 8 9 10 11 12 13 McPhee SJ, Hammer GD, eds. (2010). "7". Pathophysiology of disease : an introduction to clinical medicine (6th ed.). New York: McGraw-Hill Medical. ISBN   978-0-07-162167-0.
  19. 1 2 3 4 5 Bradley WG (2012). "67". Bradley's neurology in clinical practice (6th ed.). Philadelphia, PA: Elsevier/Saunders. ISBN   978-1-4377-0434-1.
  20. 1 2 3 4 5 6 7 National Institute for Health and Clinical Excellence (January 2012). "Chapter 9: Classification of seizures and epilepsy syndromes" (PDF). The Epilepsies: The diagnosis and management of the epilepsies in adults and children in primary and secondary care. National Clinical Guideline Centre. pp. 119–129. Archived (PDF) from the original on 16 December 2013.
  21. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 Greenberg DA, Aminoff MJ, Simon RP (2012). "12". Clinical neurology (8th ed.). New York: McGraw-Hill Medical. ISBN   978-0-07-175905-2.
  22. 1 2 3 Trinka E, Höfler J, Zerbs A (September 2012). "Causes of status epilepticus". Epilepsia. 53 (Suppl 4): 127–138. doi:10.1111/j.1528-1167.2012.03622.x. PMID   22946730. S2CID   5294771.
  23. Holmes TR (2008). Handbook of epilepsy (4th ed.). Philadelphia: Lippincott Williams & Wilkins. p. 34. ISBN   978-0-7817-7397-3.
  24. 1 2 3 Panayiotopoulos CP (2010). A clinical guide to epileptic syndromes and their treatment based on the ILAE classifications and practice parameter guidelines (Rev. 2nd ed.). [London]: Springer. p. 445. ISBN   978-1-84628-644-5.
  25. James W. Wheless, ed. (2009). Advanced therapy in epilepsy. Shelton, Conn.: People's Medical Pub. House. p. 443. ISBN   978-1-60795-004-2.
  26. Stasiukyniene V, Pilvinis V, Reingardiene D, Janauskaite L (2009). "[Epileptic seizures in critically ill patients]". Medicina. 45 (6): 501–507. doi: 10.3390/medicina45060066 . PMID   19605972.
  27. 1 2 Thurman DJ, Beghi E, Begley CE, Berg AT, Buchhalter JR, Ding D, et al. (September 2011). "Standards for epidemiologic studies and surveillance of epilepsy". Epilepsia. 52 (Suppl 7): 2–26. doi: 10.1111/j.1528-1167.2011.03121.x . PMID   21899536. S2CID   8505004.
  28. Graves RC, Oehler K, Tingle LE (January 2012). "Febrile seizures: risks, evaluation, and prognosis". American Family Physician. 85 (2): 149–153. PMID   22335215.
  29. 1 2 Martindale JL, Goldstein JN, Pallin DJ (February 2011). "Emergency department seizure epidemiology". Emergency Medicine Clinics of North America. 29 (1): 15–27. doi:10.1016/j.emc.2010.08.002. PMID   21109099.
  30. Harrison's Principles of Medicine. 15th edition
  31. "diet and nutrition". 8 May 2013. Archived from the original on 29 June 2015.
  32. Hildebrand J (July 2004). "Management of epileptic seizures". Current Opinion in Oncology. 16 (4): 314–317. doi:10.1097/01.cco.0000127720.17558.38. PMID   15187884. S2CID   12828909.
  33. Bauer, Derek; Quigg, Mark (April 2019). "Optimizing Management of Medically Responsive Epilepsy". CONTINUUM: Lifelong Learning in Neurology. 25 (2): 343–361. doi:10.1212/CON.0000000000000709. ISSN   1080-2371. PMID   30921013. S2CID   85563793.
  34. Bhalla D, Godet B, Druet-Cabanac M, Preux PM (June 2011). "Etiologies of epilepsy: a comprehensive review". Expert Review of Neurotherapeutics. 11 (6): 861–876. doi:10.1586/ern.11.51. PMID   21651333. S2CID   21190601.
  35. "Management of Convulsion in Children, a Health concern in Nigeria". Public Health Nigeria. October 2018. Archived from the original on 18 October 2018. Retrieved 18 October 2018.
  36. Carlson N (22 January 2012). Physiology of Behavior. Neurological Disorders. Vol. 11th edition. Pearson. p. 550. ISBN   978-0-205-23939-9.
  37. Nakken KO, Solaas MH, Kjeldsen MJ, Friis ML, Pellock JM, Corey LA (February 2005). "Which seizure-precipitating factors do patients with epilepsy most frequently report?". Epilepsy & Behavior. 6 (1): 85–89. doi:10.1016/j.yebeh.2004.11.003. PMID   15652738. S2CID   36696690.
  38. Haut SR, Hall CB, Masur J, Lipton RB (November 2007). "Seizure occurrence: precipitants and prediction". Neurology. 69 (20): 1905–1910. doi:10.1212/01.wnl.0000278112.48285.84. PMID   17998482. S2CID   27433395.
  39. Gunn BG, Baram TZ (November 2017). "Stress and Seizures: Space, Time and Hippocampal Circuits". Trends in Neurosciences. 40 (11): 667–679. doi:10.1016/j.tins.2017.08.004. PMC   5660662 . PMID   28916130.
  40. Bushara KO (April 2005). "Neurologic presentation of celiac disease". Gastroenterology. 128 (4 Suppl 1): S92–S97. doi: 10.1053/j.gastro.2005.02.018 . PMID   15825133.
  41. "Photosensitive epilepsy | Epilepsy Society". epilepsysociety.org.uk. 23 February 2020. Retrieved 8 June 2023.
  42. "Photosensitivity and Seizures". Epilepsy Foundation. Retrieved 8 June 2023.
  43. Burlo, F.; Barbi, E.; Carrozzi, M.; Zanus, C. (16 November 2022). "Case report: A relevant misdiagnosis: Photosensitive epilepsy mimicking a blinking tic". Frontiers in Pediatrics. 10: 918420. doi: 10.3389/fped.2022.918420 . PMC   9709211 . PMID   36467468.
  44. 1 2 3 "Epilepsy". Fact Sheets. World Health Organization. October 2012. Archived from the original on 11 March 2016. Retrieved 24 January 2013.
  45. Somjen GG (2004). Ions in the Brain Normal Function, Seizures, and Stroke. New York: Oxford University Press. p. 167. ISBN   978-0-19-803459-9.
  46. Wei F, Yan LM, Su T, He N, Lin ZJ, Wang J, et al. (August 2017). "Ion Channel Genes and Epilepsy: Functional Alteration, Pathogenic Potential, and Mechanism of Epilepsy". Neuroscience Bulletin. 33 (4): 455–477. doi:10.1007/s12264-017-0134-1. PMC   5567559 . PMID   28488083.
  47. Ropper A (2014). Adams and Victor's Principles of Neurology (10th ed., p. Chapter 16. Epilepsy and Other Seizure Disorders). New York: McGraw-Hill.
  48. 1 2 3 4 Lowenstein DH. Seizures and Epilepsy. In: Jameson J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. eds. (2018) Harrison's Principles of Internal Medicine, 20e New York, NY: McGraw-Hill.
  49. Liu YQ, Yu F, Liu WH, He XH, Peng BW (December 2014). "Dysfunction of hippocampal interneurons in epilepsy". Neuroscience Bulletin. 30 (6): 985–998. doi:10.1007/s12264-014-1478-4. PMC   5562563 . PMID   25370443.
  50. 1 2 Goldberg EM, Coulter DA (May 2013). "Mechanisms of epileptogenesis: a convergence on neural circuit dysfunction". Nature Reviews. Neuroscience. 14 (5): 337–349. doi:10.1038/nrn3482. PMC   3982383 . PMID   23595016.
  51. Oby E, Janigro D (November 2006). "The blood-brain barrier and epilepsy". Epilepsia. 47 (11): 1761–1774. doi: 10.1111/j.1528-1167.2006.00817.x . PMID   17116015. S2CID   15074513.
  52. 1 2 3 van Vliet EA, Aronica E, Gorter JA (February 2015). "Blood-brain barrier dysfunction, seizures and epilepsy". Seminars in Cell & Developmental Biology. 38: 26–34. doi:10.1016/j.semcdb.2014.10.003. PMID   25444846.
  53. Marchi N, Banjara M, Janigro D (February 2016). "Blood-brain barrier, bulk flow, and interstitial clearance in epilepsy". Journal of Neuroscience Methods. 260: 118–124. doi:10.1016/j.jneumeth.2015.06.011. PMC   4835226 . PMID   26093166.
  54. 1 2 Jerome Engel Jr.; Timothy A. Pedley, eds. (2008). Epilepsy : a comprehensive textbook (2nd ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 483. ISBN   978-0-7817-5777-5.
  55. Qiu C, Shivacharan RS, Zhang M, Durand DM (December 2015). "Can Neural Activity Propagate by Endogenous Electrical Field?". The Journal of Neuroscience. 35 (48): 15800–15811. doi:10.1523/JNEUROSCI.1045-15.2015. PMC   4666910 . PMID   26631463. electric fields can be solely responsible for spike propagation at ... This phenomenon could be important to explain the slow propagation of epileptic activity and other normal propagations at similar speeds.
  56. Depannemaecker D, Ivanov A, Lillo D, Spek L, Bernard C, Jirsa V (17 February 2021). "A unified physiological framework of transitions between seizures, sustained ictal activity and depolarization block at the single neuron level": 2020.10.23.352021. doi: 10.1101/2020.10.23.352021 . S2CID   225962412.{{cite journal}}: Cite journal requires |journal= (help)
  57. 1 2 3 4 5 6 7 "Current Guidelines For Management of Seizures in the Emergency Department" (PDF). Archived from the original on 30 December 2010.
  58. Simon D. Shorvon (2004). The treatment of epilepsy (2nd ed.). Malden, Mass.: Blackwell Pub. ISBN   978-0-632-06046-7.
  59. Saggio ML, Crisp D, Scott JM, Karoly P, Kuhlmann L, Nakatani M, et al. (July 2020). "A taxonomy of seizure dynamotypes". eLife. 9: e55632. doi: 10.7554/eLife.55632 . PMC   7375810 . PMID   32691734.
  60. 1 2 Depannemaecker D, Destexhe A, Jirsa V, Bernard C (August 2021). "Modeling seizures: From single neurons to networks". Seizure. 90: 4–8. doi: 10.1016/j.seizure.2021.06.015 . PMID   34219016. S2CID   235468072.
  61. Peeters SY, Hoek AE, Mollink SM, Huff JS (April 2014). "Syncope: risk stratification and clinical decision making". Emergency Medicine Practice. 16 (4): 1–22, quiz 22–3. PMID   25105200.
  62. Brigo F, Nardone R, Bongiovanni LG (October 2012). "Value of tongue biting in the differential diagnosis between epileptic seizures and syncope". Seizure. 21 (8): 568–572. doi: 10.1016/j.seizure.2012.06.005 . PMID   22770819.
  63. 1 2 3 4 5 6 7 National Institute for Health and Clinical Excellence (January 2012). "4" (PDF). The Epilepsies: The diagnosis and management of the epilepsies in adults and children in primary and secondary care. National Clinical Guideline Centre. pp. 57–83.
  64. Luef G (October 2010). "Hormonal alterations following seizures". Epilepsy & Behavior. 19 (2): 131–133. doi:10.1016/j.yebeh.2010.06.026. PMID   20696621. S2CID   945952.
  65. 1 2 Ahmad S, Beckett MW (March 2004). "Value of serum prolactin in the management of syncope". Emergency Medicine Journal. 21 (2): 3e–3. doi:10.1136/emj.2003.008870. PMC   1726305 . PMID   14988379.
  66. Shukla G, Bhatia M, Vivekanandhan S, Gupta N, Tripathi M, Srivastava A, et al. (August 2004). "Serum prolactin levels for differentiation of nonepileptic versus true seizures: limited utility". Epilepsy & Behavior. 5 (4): 517–521. doi:10.1016/j.yebeh.2004.03.004. PMID   15256189. S2CID   2381873.
  67. Chen DK, So YT, Fisher RS (September 2005). "Use of serum prolactin in diagnosing epileptic seizures: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology". Neurology. 65 (5): 668–675. doi: 10.1212/01.wnl.0000178391.96957.d0 . PMID   16157897.
  68. Passman R, Horvath G, Thomas J, Kruse J, Shah A, Goldberger J, Kadish A (September 2003). "Clinical spectrum and prevalence of neurologic events provoked by tilt table testing". Archives of Internal Medicine. 163 (16): 1945–1948. doi: 10.1001/archinte.163.16.1945 . PMID   12963568.
  69. Greenhalgh J, Weston J, Dundar Y, Nevitt SJ, Marson AG (April 2020). "Antiepileptic drugs as prophylaxis for postcraniotomy seizures". The Cochrane Database of Systematic Reviews. 4 (4): CD007286. doi:10.1002/14651858.CD007286.pub5. PMC   7195181 . PMID   32343399.
  70. Offringa M, Newton R, Nevitt SJ, Vraka K (June 2021). "Prophylactic drug management for febrile seizures in children". The Cochrane Database of Systematic Reviews. 2021 (6): CD003031. doi:10.1002/14651858.CD003031.pub4. PMC   8207248 . PMID   34131913.
  71. Greenhalgh, Janette; Weston, Jennifer; Dundar, Yenal; Nevitt, Sarah; Marson, Anthony (28 April 2020). "Antiepileptic drugs as prophylaxis for postcraniotomy seizures". The Cochrane Database of Systematic Reviews. 4 (4): CD007286. doi:10.1002/14651858.CD007286.pub5. ISSN   1469-493X. PMC   7195181 . PMID   32343399.
  72. Ratilal BO, Pappamikail L, Costa J, Sampaio C (June 2013). "Anticonvulsants for preventing seizures in patients with chronic subdural haematoma". The Cochrane Database of Systematic Reviews. 6 (6): CD004893. doi:10.1002/14651858.CD004893.pub3. PMC   7388908 . PMID   23744552.
  73. Chang, Richard S.; Leung, William Cy; Vassallo, Michael; Sykes, Lucy; Battersby Wood, Emma; Kwan, Joseph (7 February 2022). "Antiepileptic drugs for the primary and secondary prevention of seizures after stroke". The Cochrane Database of Systematic Reviews. 2022 (2): CD005398. doi:10.1002/14651858.CD005398.pub4. ISSN   1469-493X. PMC   8819727 . PMID   35129214.
  74. 1 2 Price M, Günther A, Kwan JS (April 2016). "Antiepileptic drugs for the primary and secondary prevention of seizures after intracranial venous thrombosis". The Cochrane Database of Systematic Reviews. 2016 (4): CD005501. doi:10.1002/14651858.CD005501.pub4. hdl: 10722/226344 . PMC   7265129 . PMID   27098266.
  75. Marigold R, Günther A, Tiwari D, Kwan J (June 2013). "Antiepileptic drugs for the primary and secondary prevention of seizures after subarachnoid haemorrhage". The Cochrane Database of Systematic Reviews. 6 (6): CD008710. doi:10.1002/14651858.CD008710.pub2. hdl:10722/194540. PMC   6885058 . PMID   23740537.
  76. Al-Mufti F, Claassen J (October 2014). "Neurocritical care: status epilepticus review". Critical Care Clinics. 30 (4): 751–764. doi:10.1016/j.ccc.2014.06.006. PMID   25257739.
  77. O'connor A (22 April 2008). "The Claim: During a Seizure, You Can Swallow Your Tongue". The New York Times. Archived from the original on 6 March 2017.
  78. 1 2 3 4 Betjemann JP (December 2015). "Current Trends in Treatment of Status Epilepticus and Refractory Status Epilepticus". Seminars in Neurology. 35 (6): 621–628. doi: 10.1055/s-0035-1564304 . PMID   26595862.
  79. De Waele L, Boon P, Ceulemans B, Dan B, Jansen A, Legros B, et al. (December 2013). "First line management of prolonged convulsive seizures in children and adults: good practice points". Acta Neurologica Belgica. 113 (4): 375–380. doi:10.1007/s13760-013-0247-x. hdl: 1854/LU-4182539 . PMID   24019121. S2CID   17641491.
  80. 1 2 Marx, J. A., Hockberger, R. S., Walls, R. M., Adams, J., & Rosen, P. (Eds.). (2013). Rosen's emergency medicine: concepts and clinical practice (8th ed). Philadelphia: Mosby/Elsevier.
  81. Leone MA, Giussani G, Nevitt SJ, Marson AG, Beghi E (May 2021). "Immediate antiepileptic drug treatment, versus placebo, deferred, or no treatment for first unprovoked seizure". The Cochrane Database of Systematic Reviews. 2021 (5): CD007144. doi:10.1002/14651858.CD007144.pub3. PMC   8094016 . PMID   33942281.
  82. 1 2 3 Sharma AN, Hoffman RJ (February 2011). "Toxin-related seizures". Emergency Medicine Clinics of North America. 29 (1): 125–139. doi:10.1016/j.emc.2010.08.011. PMID   21109109.
  83. 1 2 Doherty MJ, Haltiner AM (January 2007). "Wag the dog: skepticism on seizure alert canines". Neurology. 68 (4): 309. CiteSeerX   10.1.1.1003.1543 . doi:10.1212/01.wnl.0000252369.82956.a3. PMID   17242343. S2CID   33328776.
  84. Gloss D, Vickrey B (March 2014). "Cannabinoids for epilepsy". The Cochrane Database of Systematic Reviews. 2014 (3): CD009270. doi:10.1002/14651858.CD009270.pub3. PMC   7120304 . PMID   24595491.
  85. Belendiuk KA, Baldini LL, Bonn-Miller MO (April 2015). "Narrative review of the safety and efficacy of marijuana for the treatment of commonly state-approved medical and psychiatric disorders". Addiction Science & Clinical Practice. 10 (1): 10. doi: 10.1186/s13722-015-0032-7 . PMC   4636852 . PMID   25896576.
  86. Martin-McGill, Kirsty J.; Bresnahan, Rebecca; Levy, Robert G.; Cooper, Paul N. (24 June 2020). "Ketogenic diets for drug-resistant epilepsy". The Cochrane Database of Systematic Reviews. 2020 (6): CD001903. doi:10.1002/14651858.CD001903.pub5. ISSN   1469-493X. PMC   7387249 . PMID   32588435.
  87. Bonnett LJ, Tudur-Smith C, Williamson PR, Marson AG (December 2010). "Risk of recurrence after a first seizure and implications for driving: further analysis of the Multicentre study of early Epilepsy and Single Seizures". BMJ. 341: c6477. doi:10.1136/bmj.c6477. PMC   2998675 . PMID   21147743.
  88. Neligan A, Hauser WA, Sander JW (2012). "The epidemiology of the epilepsies". Epilepsy. Handbook of Clinical Neurology. Vol. 107. pp. 113–33. doi:10.1016/B978-0-444-52898-8.00006-9. ISBN   9780444528988. PMID   22938966.; Sander JW, Shorvon SD (November 1996). "Epidemiology of the epilepsies". Journal of Neurology, Neurosurgery, and Psychiatry. 61 (5): 433–443. doi:10.1136/jnnp.61.5.433. PMC   1074036 . PMID   8965090.
  89. 1 2 3 Gavvala JR, Schuele SU (December 2016). "New-Onset Seizure in Adults and Adolescents: A Review". JAMA. 316 (24): 2657–2668. doi:10.1001/jama.2016.18625. PMID   28027373.
  90. Camfield P, Camfield C (June 2015). "Incidence, prevalence and aetiology of seizures and epilepsy in children". Epileptic Disorders. 17 (2): 117–123. doi: 10.1684/epd.2015.0736 . PMID   25895502. S2CID   20719640.
  91. 1 2 Ba-Diop A, Marin B, Druet-Cabanac M, Ngoungou EB, Newton CR, Preux PM (October 2014). "Epidemiology, causes, and treatment of epilepsy in sub-Saharan Africa". The Lancet. Neurology. 13 (10): 1029–1044. doi:10.1016/S1474-4422(14)70114-0. PMC   5497080 . PMID   25231525.
  92. 1 2 Magiorkinis E, Sidiropoulou K, Diamantis A (January 2010). "Hallmarks in the history of epilepsy: epilepsy in antiquity". Epilepsy & Behavior. 17 (1): 103–108. doi:10.1016/j.yebeh.2009.10.023. PMID   19963440. S2CID   26340115.
  93. 1 2 3 4 Ali R, Connolly ID, Feroze AH, Awad AJ, Choudhri OA, Grant GA (June 2016). "Epilepsy: A Disruptive Force in History". World Neurosurgery. 90: 685–690. doi:10.1016/j.wneu.2015.11.060. PMID   26709155.
  94. Meador KJ, Loring DW, Flanigin HF (January 1989). "History of epilepsy surgery". Journal of Epilepsy. 2 (1): 21–25. doi:10.1016/0896-6974(89)90054-6. ISSN   0896-6974.
  95. 1 2 Litt B, Echauz J (May 2002). "Prediction of epileptic seizures". The Lancet. Neurology. 1 (1): 22–30. doi:10.1016/S1474-4422(02)00003-0. PMID   12849542. S2CID   10109539.
  96. 1 2 Walker MC, Schorge S, Kullmann DM, Wykes RC, Heeroma JH, Mantoan L (September 2013). "Gene therapy in status epilepticus". Epilepsia. 54 (Suppl 6): 43–45. doi: 10.1111/epi.12275 . PMID   24001071. S2CID   13942394.
  97. 1 2 Mormann F, Andrzejak RG, Elger CE, Lehnertz K (February 2007). "Seizure prediction: the long and winding road". Brain. 130 (Pt 2): 314–333. doi: 10.1093/brain/awl241 . PMID   17008335.