Epilepsy
Epilepsy | |
---|---|
Other names | Seizure disorder Neurological disability |
![]() | |
Generalized 3 Hz spike-and-wave discharges on an electroencephalogram | |
Specialty | Neurology |
Symptoms | Periods of loss of consciousness, abnormal shaking, staring, change in vision, mood changes and/or other cognitive disturbances [1] |
Duration | Long term[1] |
Causes | Unknown, brain injury, stroke, brain tumors, infections of the brain, birth defects[1][2][3] |
Diagnostic method | Electroencephalogram, ruling out other possible causes[4] |
Differential diagnosis | Fainting, alcohol withdrawal, electrolyte problems[4] |
Treatment | Medication, surgery, neurostimulation, dietary changes[5][6] |
Prognosis | Controllable in 69%[7] |
Frequency | 51.7 million/0.68% (2021)[8] |
Deaths | 140,000 (2021)[9] |
Epilepsy is a group of non-communicable neurological disorders characterized by a tendency for recurrent, unprovoked seizures.[10] A seizure is a sudden burst of abnormal electrical activity in the brain that can cause a variety of symptoms, ranging from brief lapses of awareness or muscle jerks to prolonged convulsions.[1] These episodes can result in physical injuries, either directly, such as broken bones, or through causing accidents. The diagnosis of epilepsy typically requires at least two unprovoked seizures occurring more than 24 hours apart.[11] In some cases, however, it may be diagnosed after a single unprovoked seizure if clinical evidence suggests a high risk of recurrence.[10] Isolated seizures that occur without recurrence risk or are provoked by identifiable causes are not considered indicative of epilepsy.[12]
The underlying cause is often unknown,[11] but epilepsy can result from brain injury, stroke, infections, tumors, genetic conditions, or developmental abnormalities.[13][2][3] Epilepsy that occurs as a result of other issues may be preventable.[1] Diagnosis involves ruling out other conditions that can resemble seizures, and may include neuroimaging, blood tests, and electroencephalography (EEG).[4]
Most cases of epilepsy — approximately 69% — can be effectively controlled with anti-seizure medications,[7] and inexpensive treatment options are widely available. For those whose seizures do not respond to drugs, other approaches such as surgery, neurostimulation or dietary changes may be considered.[5][6] Not all cases of epilepsy are lifelong, and many people improve to the point that treatment is no longer needed.[1]
As of 2021[update], approximately 51 million people worldwide have epilepsy, with nearly 80% of cases occurring in low- and middle-income countries.[1] The burden of epilepsy in low-income countries is more than twice that in high-income countries, likely due to higher exposure to risk factors such as perinatal injury, infections, and traumatic brain injury, combined with limited access to healthcare.[14] In 2021, epilepsy was responsible for an estimated 140,000 deaths, an increase from 125,000 in 1990.[9]
Epilepsy is more common in both children and older adults.[15][16] About 5–10% of people will have an unprovoked seizure by the age of 80.[17] The chance of experiencing a second seizure within two years after the first is around 40%.[18][19]
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.[11][20] In many countries, people with epilepsy face driving restrictions and must be seizure-free for a set period before regaining eligibility to drive.[21] The word epilepsy is from Ancient Greek ἐπιλαμβάνειν, 'to seize, possess, or afflict'.[22]
Signs and symptoms
[edit]
Epilepsy is characterized by a long-term tendency to experience recurrent, unprovoked seizures.[23] They may vary widely in their presentation depending on the affected brain regions, age of onset, and type of epilepsy.[23][24]
Seizures
[edit]According to the 2025 classification by the International League Against Epilepsy (ILAE), seizures are grouped into four main classes: focal, generalized, unknown (whether focal or generalized), and unclassified.[25]
Focal seizures
[edit]Focal seizures originate in one hemisphere of the brain and may involve localized or distributed networks.[26] For a given seizure type, the site of onset tends to be consistent across episodes. Once initiated, the seizure may remain localized or spread to adjacent areas, and in some cases, may propagate to the opposite hemisphere (contralateral spread).[25]
They are further classified based on the state of consciousness during the episode:[25]
- Focal preserved consciousness seizure: the person remains aware and responsive.
- Focal impaired consciousness seizure: awareness and/or responsiveness are affected.
Certain experiences, known as auras often precede focal seizures.[27] The seizures can include sensory (visual, hearing, or smell), psychic, autonomic, and motor phenomena depending on which part of the brain is involved.[2] Muscle jerks may start in a specific muscle group and spread to surrounding muscle groups in which case it is known as a Jacksonian march.[28]Automatisms may occur, which are non-consciously generated activities and mostly simple repetitive movements like smacking the lips or more complex activities such as attempts to pick up something.[28] Some focal seizures can evolve into focal-to-bilateral tonic-clonic seizures, where abnormal brain activity spreads to both hemispheres.[25]
Generalized seizures
[edit]Generalized seizures originate at a single point within the brain and quickly spread to involve networks across both hemispheres. Although the spread is rapid, the onset may appear asymmetric in some cases. These seizures typically impair consciousness from the outset and can take several forms, including:[25]
- Generalized tonic–clonic seizures, often with an initial tonic phase followed by clonic jerking;
- Absence seizures, which may present with eye blinking or automatisms;
- Other generalized seizures, a category that includes tonic, clonic, myoclonic, atonic seizures and epileptic spasms.[29]
Tonic–clonic seizures are among the most recognizable seizure types, typically involving sudden loss of consciousness, stiffening (tonic phase), and rhythmic jerking (clonic phase) of the limbs.[30] This form of seizure — whether focal to bilateral, generalized, or of unknown onset — is given particular emphasis due to their clinical severity; they are associated with the highest risk of injury, medical complications, and sudden unexpected death in epilepsy (SUDEP).[25]
Myoclonic seizures involve sudden, brief muscle jerks, which may affect specific muscle groups or the whole body.[31][32] They can cause falls and injury.[31] Absence seizures are characterized by brief lapses in awareness, sometimes accompanied by subtle movements such as blinking or slight head turning.[2] The person typically recovers immediately afterward without confusion. Atonic seizures involve a sudden loss of muscle tone, often resulting in falls.[28]
Triggers and reflex seizures
[edit]Triggers are external or internal factors that increase the likelihood of a seizure in someone who already has epilepsy. Common triggers include sleep deprivation, stress, illness, or alcohol. These do not cause seizures by themselves, but lower the threshold in people who are already susceptible.
About 6% of those with epilepsy have seizures that are often triggered by specific events and are known as reflex seizures.[33][34] Those with reflex epilepsy have seizures that are only triggered by specific stimuli.[33] Common triggers include flashing lights and sudden noises.[34] In certain types of epilepsy, seizures happen more often during sleep,[35] and in other types they occur almost only when sleeping.[36]
Seizure clusters
[edit]People with epilepsy may also experience seizure clusters, defined as a rapid succession of seizures over a short period without full recovery between episodes.[37] The prevalence of seizure clusters is uncertain given that studies have used different definitions to define them..[38] However, estimates suggest that the prevalence may range from 5% to 50% of people with epilepsy.[39] People with refractory epilepsy who have a high seizure frequency are at the greatest risk for having seizure clusters.[40][41][42] Seizure clusters are associated with increased healthcare use, worse quality of life, impaired psychosocial functioning, and possibly increased mortality.[38][43] Benzodiazepines are used as an acute treatment for seizure clusters.[44]
Postictal state
[edit]After the active portion of a seizure (the ictal state) there is typically a period of recovery during which there is confusion, referred to as the postictal state, before a normal level of consciousness returns,[27] lasting minutes to days.[45][46] This period is marked by confusion, headache, fatigue, or speech and motor disturbances. Some may experience Todd's paralysis, a transient focal weakness.[47] Psychosis after a seizure can also happen, occuring in 2% of people.[48][49]
Psychosocial
[edit]Epilepsy can have adverse effects on social and psychological well-being.[24] These effects may include social isolation, stigmatization, or disability.[24] They may result in lower educational achievement and worse employment outcomes.[24] Learning disabilities are common in those with the condition, and especially among children with epilepsy.[24] The stigma of epilepsy can also affect the families of those with the disorder.[20]
Certain disorders occur more often in people with epilepsy, depending partly on the epilepsy syndrome present. These include depression, anxiety, obsessive–compulsive disorder (OCD),[50] and migraine.[51] Attention deficit hyperactivity disorder (ADHD) affects three to five times more children with epilepsy than children without the condition.[52] ADHD and epilepsy have significant consequences on a child's behavioral, learning, and social development.[53] Epilepsy is also more common in children with autism.[54]
Approximately, one-in-three people with epilepsy have a lifetime history of a psychiatric disorder.[55] There are believed to be multiple causes for this including pathophysiological changes related to the epilepsy itself as well as adverse experiences related to living with epilepsy (e.g., stigma, discrimination).[56] In addition, it is thought that the relationship between epilepsy and psychiatric disorders is not unilateral but rather bidirectional. For example, people with depression have an increased risk for developing new-onset epilepsy.[57]
The presence of comorbid depression or anxiety in people with epilepsy is associated with a poorer quality of life, increased mortality, increased healthcare use and a worse response to treatment (including surgical).[58][59][60][61] Anxiety disorders and depression may explain more variability in quality of life than seizure type or frequency.[62] There is evidence that both depression and anxiety disorders are underdiagnosed and undertreated in people with epilepsy.[63]
Causes
[edit]Epilepsy can result from a wide range of genetic and acquired factors, and in many cases, both play a role.[64][65] Acquired causes include serious traumatic brain injury, stroke, brain tumors, and central nervous system infections.[64] Despite advances in diagnostic tools, no clear cause is identified in approximately 60% of cases.[24][20] The distribution of causes often varies with age. Epilepsies associated with genetic, congenital, or developmental conditions are more common in children, while epilepsy related to stroke or tumors is more frequently seen in older adults.[24]
Seizures may also occur as a direct response to acute health conditions such as stroke, head trauma, metabolic disturbances, or toxic exposures.[66] These are known as acute symptomatic seizures and are distinct from epilepsy, which involves a recurrent tendency to have unprovoked seizures over time.[67][68]
The International League Against Epilepsy (ILAE) classifies the causes of epilepsy into six broad categories: structural, genetic, infectious, metabolic, immune, and unknown. These categories are not mutually exclusive, and more than one may apply in an individual case.[69]
Structural
[edit]Structural causes of epilepsy refer to abnormalities in the anatomy of the brain that increase the risk of seizures. These may be acquired — such as from a stroke, traumatic brain injury, brain tumor, or central nervous system infection — or developmental and genetic in origin, as seen in conditions like focal cortical dysplasia or certain congenital brain malformations. A major example is mesial temporal sclerosis (MTS), a common cause of temporal lobe epilepsy.[70][69]
Of those with brain tumors, almost 30% have epilepsy, making them the cause of about 4% of cases.[71] The risk is greatest for tumors in the temporal lobe and those that grow slowly.[71] Other mass lesions such as cerebral cavernous malformations and arteriovenous malformations have risks as high as 40–60%.[71] Of those who have had a stroke, 6–10% develop epilepsy.[72][73] Risk factors for post-stroke epilepsy include stroke severity, cortical involvement, hemorrhage and early seizures.[74][75] Between 6 and 20% of epilepsy is believed to be due to head trauma.[71] Mild brain injury increases the risk about two-fold while severe brain injury increases the risk seven-fold.[71] In those who have experienced a high-powered gunshot wound to the head, the risk is about 50%.
In clinical practice, a structural cause is typically identified through neuroimaging (such as MRI), which reveals an abnormality that plausibly accounts for the individual's seizure semiology and EEG findings. The lesion must be epileptogenic, meaning that it is capable of generating seizures. Infections like encephalitis or brain abscess may lead to permanent structural damage, increasing the risk of epilepsy even after the infection resolves.[69]
Structural damage can also result from perinatal brain injury, such as hypoxic-ischemic encephalopathy, especially in low- and middle-income countries where access to prenatal and neonatal care may be limited. When seizures are linked to a clearly defined structural lesion, epilepsy surgery may be considered — particularly in individuals whose seizures do not respond to medication.[69]
Genetics
[edit]Genetic causes of epilepsy are those in which a person’s genes directly contribute to the development of seizures. This includes cases where a specific mutation has been identified, as well as situations where the family history and clinical features strongly suggest a genetic basis, even if no known mutation is found. In the updated classification by the ILAE, the term genetic replaces the older term idiopathic, to highlight that these epilepsies arise from inherited or spontaneous changes in a person’s biology — not from injury or infection.[69]
Genetic factors are believed to contribute to many cases of epilepsy, either directly or by increasing vulnerability to other causes.[76] Some forms are caused by a single gene defect, which account for around 1–2% of cases. However, most are due to a combination of multiple genes and environmental influences.[13] Many of the genes known to play a role in epilepsy affect how brain cells send electrical signals, especially those involved in ion channels, receptors, or signaling proteins.[31]
Genetics is believed to play an important role in epilepsies by a number of mechanisms. Simple and complex modes of inheritance have been identified for some of them. However, extensive screening have failed to identify many single gene variants of large effect.[77] More recent exome and genome sequencing studies have begun to reveal a number of de novo gene mutations that are responsible for some epileptic encephalopathies, including CHD2 and SYNGAP1[78][79][80] and DNM1, GABBR2, FASN and RYR3.[81]
Some genetic disorders, including phakomatoses such as tuberous sclerosis complex and Sturge–Weber syndrome, are strongly associated with epilepsy.[82] These conditions are often discussed separately due to their multisystem involvement and high epilepsy burden.
Infectious
[edit]Infectious causes include infections of the central nervous systemthat directly affect brain tissue and lead to long-term seizure susceptibility.[71] Examples include herpes simplex encephalitis, which carries a high risk of developing epilepsy, and neurocysticercosis, a major preventable cause of epilepsy in endemic regions. Other infections such as cerebral malaria, toxoplasmosis, and toxocariasis.[71] Some infections cause seizures during the acute illness, but only a subset result in chronic epilepsy.
Immune
[edit]Immune causes include conditions like autoimmune encephalitis, in which the immune system attacks brain tissue, often presenting with seizures. Certain autoimmune epilepsies are associated with specific autoantibodies, including those against the NMDA receptor, LGI1, and CASPR2. These cases often present with rapid-onset, difficult-to-treat seizures.[69]
Celiac disease has also been associated with epilepsy in rare syndromic forms, such as the triad of epilepsy, cerebral calcifications, and celiac disease.[83][84]
Metabolic
[edit]Metabolic causes of epilepsy include metabolic disorders that disrupt the brain’s normal function. In rare cases, epilepsy may result from inborn errors of metabolism, such as mitochondrial diseases, urea cycle disorders, or glucose transporter type 1 (GLUT1) deficiency. These often present early in life and may be associated with developmental delays, movement disorders, or other neurological symptoms.[69]
Seizures can also occur in the context of acquired metabolic disturbances, such as hypoglycemia, hyponatremia, or hypocalcemia. These seizures are often considered acute symptomatic seizures, and are not epilepsy.
Some forms of malnutrition, particularly in low- and middle-income countries, have been associated with a higher risk of epilepsy, although it remains unclear whether the relationship is causal or due to other contributing factors.[14]
Unknown
[edit]Unknown causes of epilepsy refer to cases where no clear structural, genetic, infectious, immune, or metabolic origin can be identified despite thorough evaluation. This category acknowledges the limits of current diagnostic techniques and scientific understanding. A substantial proportion of epilepsy cases still fall into this group, particularly in regions with limited access to advanced testing.[69]
Mechanism
[edit]Normally brain electrical activity is non-synchronous, as large numbers of neurons do not normally fire at the same time, but rather fire in order as signals travel throughout the brain.[2] Neuron activity is regulated by various factors both within the cell and the cellular environment. Factors within the neuron include the type, number and distribution of ion channels, changes to receptors and changes of gene expression.[85] Factors around the neuron include ion concentrations, synaptic plasticity and regulation of transmitter breakdown by glial cells.[85][86]
Epilepsy
[edit]The exact mechanism of epilepsy is unknown,[87] but a little is known about its cellular and network mechanisms. However, it is unknown under which circumstances the brain shifts into the activity of a seizure with its excessive synchronization.[88][89][90][91]
In epilepsy, the resistance of excitatory neurons to fire during this period is decreased.[2] This may occur due to changes in ion channels or inhibitory neurons not functioning properly.[2] This then results in a specific area from which seizures may develop, known as a "seizure focus".[2] Another mechanism of epilepsy may be the up-regulation of excitatory circuits or down-regulation of inhibitory circuits following an injury to the brain.[2][3] These secondary epilepsies occur through processes known as epileptogenesis.[2][3] Failure of the blood–brain barrier may also be a causal mechanism as it would allow substances in the blood to enter the brain.[92]
Seizures
[edit]There is evidence that epileptic seizures are usually not a random event. Seizures are often brought on by factors (also known as triggers) such as stress, excessive alcohol use, flickering light, or a lack of sleep, among others. The term seizure threshold is used to indicate the amount of stimulus necessary to bring about a seizure; this threshold is lowered in epilepsy.[88]
In epileptic seizures a group of neurons begin firing in an abnormal, excessive,[24] and synchronized manner.[2] This results in a wave of depolarization known as a paroxysmal depolarizing shift.[93] Normally, after an excitatory neuron fires it becomes more resistant to firing for a period of time.[2] This is due in part to the effect of inhibitory neurons, electrical changes within the excitatory neuron, and the negative effects of adenosine.[2]
Focal seizures begin in one area of the brain while generalized seizures begin in both hemispheres.[68] Some types of seizures may change brain structure, while others appear to have little effect.[94] 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.[94]
The seizures can be described on different scales, from the cellular level[95] to the whole brain.[96] These are several concomitant factor, which on different scale can "drive" the brain to pathological states and trigger a seizure.
Diagnosis
[edit]The diagnosis of epilepsy is primarily clinical, based on a thorough evaluation of the person’s history, seizure features, and risk of recurrence. While diagnostic tests such as electroencephalograms and neuroimaging can support the diagnosis, there is no single test that can confirm or exclude epilepsy.
Clinicians must also distinguish epileptic seizures from other conditions that can mimic them and determine whether the event was provoked by an acute, reversible cause or if it suggests a long-term tendency for unprovoked seizures.
Definition
[edit]According to the International League Against Epilepsy (ILAE), a diagnosis of epilepsy can be made when any one of the following criteria is met:[10]
- At least two unprovoked (or reflex) seizures occurring more than 24 hours apart
- One unprovoked (or reflex) seizure and a probability of further seizures similar to the general recurrence risk (at least 60%) after two unprovoked seizures, occurring over the next 10 years
- Diagnosis of an epilepsy syndrome
The ILAE also introduced the concept of resolved epilepsy, which applies to individuals who are past the typical age range for an age-dependent syndrome, or who have remained seizure-free for at least 10 years, including the last 5 years without medication.[10]
TThis 2014 practical definition built upon the broader 2005 conceptual framework, which defined epilepsy as a disorder involving an enduring predisposition to generate epileptic seizures. The updated criteria incorporated recurrence risk and reflected the realities of clinical decision-making. While widely adopted in clinical settings, other definitions—such as the traditional “two unprovoked seizures” rule still used by the World Health Organization — remain appropriate in epidemiology and public health contexts, provided they are clearly stated. The 2014 revision also shifted terminology, referring to epilepsy as a disease rather than a disorder, to reflect its medical seriousness and public health impact.[97][10]
Classification
[edit]
Once epilepsy is diagnosed, the ILAE recommends a three-level framework to guide further classification and management:[69]
- Identify the seizure type, based on clinical features and EEG (e.g., focal aware seizure, generalized absence)
- Determine the epilepsy type, such as focal, generalized, combined, or unknown
- Identify an epilepsy syndrome, if applicable
Not all levels can always be determined; in some cases, only the seizure type is identifiable. The etiology — whether structural, genetic, infectious, metabolic, immune, or unknown — should be considered at each stage of classification, as it often influences treatment and prognosis.[98][69]
The classification of epilepsies has evolved significantly over time.[99] Earlier systems emphasized seizure location and used terms such as “partial” or “cryptogenic,” which have been replaced in the modern framework.[100][101] The current system, introduced in 2017, reflects advances in neuroimaging, genetics, and clinical understanding, and allows for a more individualized and dynamic diagnostic approach.
Syndromes
[edit]An epilepsy syndrome is a specific diagnosis based on a combination of features, including seizure types, age of onset, EEG patterns, imaging findings, and associated symptoms or comorbidities. In many cases, a known genetic or structural cause may also support the diagnosis. Recognizing a syndrome can guide treatment decisions, inform prognosis, and provide clarity for individuals and families navigating an epilepsy diagnosis.[102][103]
Some syndromes are self-limited and age-dependent, such as childhood absence epilepsy, juvenile myoclonic epilepsy, and self-limited epilepsy with centrotemporal spikes.[67] These typically respond well to treatment or remit with age. In contrast, more severe syndromes fall under the category of developmental and epileptic encephalopathies (DEEs).[104] These include Lennox–Gastaut syndrome, West syndrome, and Dravet syndrome, which are associated with early onset, drug-resistant seizures, and significant neurodevelopmental impairments.[105]
Some epilepsy syndromes do not yet fit neatly within current etiological categories, particularly when no definitive cause has been identified. In many cases, a genetic cause is presumed based on age of onset, family history, and electroclinical features, even if no mutation has been found. As genetic and neuroimaging technologies continue to evolve, the classification of epilepsy syndromes is expected to become more precise.[98]
Tests
[edit]
The diagnostic evaluation of epilepsy begins with confirming whether the reported event was in fact a seizure. A detailed clinical history remains essential, supported by eyewitness accounts and, when possible, video recordings. The initial assessment aims to distinguish epileptic seizures from common mimics such as syncope, psychogenic non-epileptic seizures, or transient ischemic attacks.
Following clinical evaluation, selected tests may be used to rule out acute causes and seizure mimics. A 12-lead electrocardiogram (ECG) is recommended for all individuals presenting with a first seizure, to screen for cardiac arrhythmias and other cardiovascular conditions that may resemble epilepsy. Blood tests may be performed to identify metabolic disturbances such as hypoglycemia, electrolyte imbalances, or renal and hepatic dysfunction, particularly in acute settings.[106]
Once epilepsy is suspected, electroencephalography (EEG) is used to support the diagnosis, classify seizure types, and help identify specific epilepsy syndromes. A routine EEG may include activation techniques such as hyperventilation or photic stimulation. However, a normal EEG does not rule out epilepsy. When initial EEG findings are inconclusive, further studies such as sleep-deprived EEG, ambulatory EEG, or long-term video EEG monitoring may be considered.[106]
Neuroimaging, usually with magnetic resonance imaging (MRI), is recommended to detect structural causes of epilepsy. If MRI is contraindicated or unavailable, computed tomography (CT) may be considered. Imaging should be interpreted by radiologists with expertise in epilepsy.[106]
Additional tests may be guided by clinical context. Genetic testing may be considered in individuals with early-onset epilepsy, developmental delay, or features of a known genetic epilepsy syndrome. Testing for neuronal antibodies may be appropriate in suspected cases of autoimmune encephalitis, particularly when seizures are new-onset, rapidly progressive, or resistant to standard treatment. Metabolic testing may be pursued in infants or children with unexplained epilepsy, especially when developmental regression or multisystem involvement is present.[106]
Serum prolactin may occasionally be measured after a suspected seizure, particularly to help distinguish epileptic seizures from non-epileptic events. While it can be elevated following certain seizure types, the test lacks sufficient sensitivity and specificity and is not recommended for routine use.
Differential diagnosis
[edit]Diagnosing epilepsy can be challenging, as many other conditions may mimic seizures. Common seizure mimics include syncope, psychogenic non-epileptic seizures (PNES), transient ischemic attacks, migraine, narcolepsy, and various sleep or movement disorders.[107][108] For example, syncope can sometimes be accompanied by brief convulsive movements, and episodes of paroxysmal dyskinesia may resemble focal motor seizures.[109] In children, normal behaviors such as breath-holding spells, night terrors, tics, and shudder attacks are occasionally mistaken for epileptic seizures. In infants, gastroesophageal reflux can lead to posturing or arching that resembles seizure activity.[108] The cause of a drop attack can be, among many others, an atonic seizure.[108]
Among the most challenging conditions to distinguish from epilepsy is PNES, which involves seizure-like events that are psychological in origin and do not involve abnormal electrical activity in the brain. Studies suggest that approximately 20% of individuals referred to epilepsy centers are diagnosed with PNES,[17] and up to 10% of these individuals also have coexisting epilepsy.[110] Differentiating between the two can be difficult and often requires prolonged video EEG monitoring.[110]
Misdiagnosis remains a concern. Estimates of misdiagnosis rates in epilepsy vary widely, ranging from approximately 2% to as high as 71%, depending on the population studied and the criteria used for diagnosis.[111]
Misdiagnosis can also occur in the opposite direction — when epilepsy is present but attributed to another condition. Certain forms of epilepsy, particularly those with subtle or nocturnal symptoms, may be mistaken for behavioral or psychological disorders. For example, nocturnal frontal lobe epilepsy has historically been misdiagnosed as night terrors or parasomnias,[112] while focal seizures may be confused with anxiety, dissociation, or ADHD, especially in children. In infants, seizures may be misinterpreted as reflux, colic, or motor stereotypies. Delays in diagnosis can lead to prolonged morbidity and inappropriate treatment, highlighting the importance of careful clinical assessment and appropriate use of EEG and video documentation.
Prevention
[edit]Although many causes of epilepsy are not preventable, several known risk factors are modifiable. Perinatal care, including prevention of birth trauma, hypoxia, and maternal infections, can lower the risk of epilepsy in infants.[7] Vaccination programs, especially against neurotropic infections such as measles and meningitis, play a key role in preventing epilepsy caused by central nervous system infections. In low- and middle-income countries, neurocysticercosis remains a major preventable cause of epilepsy, which can be reduced through improved sanitation and food safety.[14][20] In older adults, reducing the risk of stroke, traumatic brain injury, and cardiovascular disease may also help prevent epilepsy.
Complications
[edit]Epilepsy can lead to a range of medical, psychological, and social complications, particularly when seizures are frequent or uncontrolled.[11] One of the most serious risks is injury during a seizure, including falls, burns, or accidents while driving, swimming, or operating machinery. The risk of drowning is significantly increased in people with epilepsy, especially those with poor seizure control. Aspiration pneumonia may also occur during or after seizures, particularly generalized tonic–clonic seizures.
People with epilepsy are at greater risk for mental health conditions, including depression, anxiety, and social isolation. These challenges are often compounded by stigma, employment difficulties, and driving restrictions. In children, epilepsy — especially when drug-resistant — can interfere with cognitive development and academic performance.
A rare but serious complication is sudden unexpected death in epilepsy (SUDEP), which is most often associated with uncontrolled generalized tonic–clonic seizures, particularly during sleep.
Medication side effects, including fatigue, mood changes, and cognitive slowing, may also contribute to complications in some individuals. Comprehensive management aims to reduce these risks by achieving seizure control, minimizing adverse effects, and addressing comorbid conditions.
Management
[edit]
The primary goals of epilepsy management are to control seizures, minimize treatment side effects, and optimize quality of life. Management strategies are individualized based on the type of seizures or epilepsy syndrome, the underlying cause when known, the person’s age and comorbidities, and their preferences and life circumstances.[106]
Supporting people's self-management of their condition may be useful.[113] In drug-resistant cases different management options may be considered, including special diets, the implantation of a neurostimulator, or neurosurgery.
First aid and acute management of seizures
[edit]During a generalized tonic–clonic seizure, the primary goals are to ensure safety and prevent injury. The following steps should be taken:[114]
- Stay calm and remove any potential hazards from the area. Clear the space of sharp objects, furniture, or anything that might cause injury.
- If the person is standing, gently guide them to the ground to avoid a fall.
- Position the person on their side and into the recovery position, which helps keep the airway clear and reduces the risk of choking. If possible, place something soft (e.g., a jacket or cushion) under their head to prevent injury.
- Do not restrain their movements or attempt to hold them down. Do not put anything in their mouth, as this may cause harm.[27][114]
If the seizure lasts longer than 5 minutes or if multiple seizures occur without full recovery in between, it is important to call for emergency medical assistance immediately, as it is considered a medical emergency known as status epilepticus.[115]
Convulsive status epilepticus requires immediate medical attention to prevent serious complications. In a community setting (such as at home or in the ambulance), first-line treatment includes the administration of benzodiazepines. If the person has an individualized emergency management plan — which may have been developed with healthcare providers and outlines personalized treatment steps (such as the use of buccal midazolam or rectal diazepam) — this plan should be followed immediately.[106] In hospital, intravenous lorazepam is preferred.[106]
If seizures continue after the first dose of benzodiazepine, emergency medical services should be contacted, and further doses can be given. For ongoing seizures, levetiracetam, phenytoin, or sodium valproate may be used as second-line treatments, with levetiracetam preferred for its quicker action and fewer side effects.[106]
Most institutions have a preferred pathway or protocol to be used in a seizure emergency like status epilepticus. These protocols have been found to be effective in reducing time to delivery of treatment.[106]
Medications
[edit]
The primary treatment for epilepsy involves the use of antiseizure medications (ASMs), which aim to control seizures while minimizing side effects. Treatment plans should be individualized, taking into account the seizure type, epilepsy syndrome, patient age, sex, comorbidities, lifestyle factors, and the potential for drug interactions.[106]
First-line treatment for most individuals with epilepsy is monotherapy with a single ASM. For many people with epilepsy, seizure control is achieved with a single medication, but some may require combination therapy if seizures are not well-controlled with monotherapy.[106]
There are a number of medications available including phenytoin, carbamazepine and valproate. Evidence suggests that these drugs are similarly effective for both focal and generalized seizures, although their side-effect profiles vary.[116][117] Controlled release carbamazepine appears to work as well as immediate release carbamazepine, and may have fewer side effects.[118] In the UK, carbamazepine or lamotrigine are recommended as first-line treatments for focal seizures, with levetiracetam and valproate used as second-line treatments due to concerns about cost and side effects. Valproate is the first-line choice for generalized seizures, while lamotrigine is used as second-line. For absence seizures, ethosuximide or valproate are recommended, with valproate also being effective for myoclonic and tonic–clonic seizures.[106][119]
Controlled-release formulations of carbamazepine may be preferred in some cases, as they appear to be equally effective as immediate-release carbamazepine but may have fewer side effects. Once a person’s seizures are well-controlled on a specific treatment, it is generally not necessary to routinely check medication blood levels, unless there are concerns about side effects or toxicity.[106]
In low- and middle-income countries (LMICs), the management of epilepsy is often hindered by limited access to medications, diagnostic tools, and specialized care.[14] While phenytoin and carbamazepine are commonly used as first-line treatments due to their availability and low cost, newer drugs like levetiracetam and lamotrigine may not be accessible. Additionally, surgical options and advanced therapies, such as vagus nerve stimulation or resective surgery, are typically inaccessible due to high costs and lack of infrastructure.
The least expensive anticonvulsant is phenobarbital at around US$5 a year.[14] The World Health Organization gives it a first-line recommendation in LMICs and it is commonly used in these countries.[120][121] Access, however, may be difficult as some countries label it as a controlled drug.[14]
Adverse effects from medications are reported in 10% to 90% of people, depending on how and from whom the data is collected.[122] Most adverse effects are dose-related and mild.[122] Some examples include mood changes, sleepiness, or an unsteadiness in gait.[122] Certain medications have side effects that are not related to dose such as rashes, liver toxicity, or suppression of the bone marrow.[122] Up to a quarter of people stop treatment due to adverse effects.[122] Some medications are associated with birth defects when used in pregnancy.[123] Many of the common used medications, such as valproate, phenytoin, carbamazepine, phenobarbital, and gabapentin have been reported to cause increased risk of birth defects,[124] especially when used during the first trimester.[125] Despite this, treatment is often continued once effective, because the risk of untreated epilepsy is believed to be greater than the risk of the medications.[125] Among the antiepileptic medications, levetiracetam and lamotrigine seem to carry the lowest risk of causing birth defects.[124]
Slowly stopping medications may be reasonable in some people who do not have a seizure for two to four years; however, around a third of people have a recurrence, most often during the first six months.[123][126] Stopping is possible in about 70% of children and 60% of adults.[20] Measuring medication levels is not generally needed in those whose seizures are well controlled.[127]
Surgery
[edit]Epilepsy surgery should be considered for any person with epilepsy who is medically refractory.[15] People with epilepsy are evaluated on a case-by-case basis in centres that are familiar with and have expertise in epilepsy surgery.[15] Results from a 2023 systematic review found that surgical interventions for children aged 1–36 months with drug-resistant epilepsy can lead to significant seizure reduction or freedom, especially when other treatments have failed.[128] Epilepsy surgery may be an option for people with focal seizures that remain a problem despite other treatments.[129][130] These other treatments include at least a trial of two or three medications.[131] The goal of surgery has been total control of seizures.[132] However, most physicians believe that even palliative surgery where the burden of seizures is reduced significantly can help in achieving developmental progress or reversal of developmental stagnation in children with drug-resistant epilepsy and this may be achieved in 60–70% of cases.[131] Common procedures include cutting out the hippocampus via an anterior temporal lobe resection, removal of tumors, and removing parts of the neocortex.[131] Some procedures such as a corpus callosotomy are attempted in an effort to decrease the number of seizures rather than cure the condition.[131] Following surgery, medications may be slowly withdrawn in many cases.[131][129]
Neurostimulation
[edit]Neurostimulation via neuro-cybernetic prosthesis implantation may be another option in those who are not candidates for surgery, providing chronic, pulsatile electrical stimulation of specific nerve or brain regions, alongside standard care.[123] Three types of neurotherapy have been used in those who do not respond to medications: vagus nerve stimulation (VNS), anterior thalamic stimulation, and closed-loop responsive stimulation (RNS).[5][133][134]
Vagus nerve stimulation
[edit]Non-pharmacological modulation of neurotransmitters via high-level VNS (h-VNS) may reduce seizure frequency in children and adults who do not respond to medical and/or surgical therapy, when compared with low-level VNS (l-VNS).[134] In a 2022 Cochrane review of four randomized controlled trials, with moderate certainty of evidence, people receiving h-VNS treatment were 73% more likely (13% more likely to 164% more likely) to experience a reduction in seizure frequency by at least 50% (the minimum threshold defined for individual clinical response).[134] Potentially 249 (163 to 380) per 1000 people with drug-resistant epilepsy may achieve a 50% reduction in seizures following h-VNS, benefiting an additional 105 per 1000 people compared with l-VNS.[134]
This outcome was limited by the number of studies available, and the quality of one trial in particular, wherein three people received l-VNS in error. A sensitivity analysis suggested that the best case scenario was that the likelihood of clinical response to h-VNS may be 91% (27% to 189%) higher than those receiving l-VNS. In the worst-case scenario, the likelihood of clinical response to h-VNS was still 61% higher (7% higher to 143% higher) than l-VNS.[134]
Despite the potential benefit for h-VNS treatment, the Cochrane review also found that the risk of several adverse-effects was greater than those receiving l-VNS. There was moderate certainty of evidence that voice alteration or hoarseness risk may be 2.17(1.49 to 3.17) fold higher than people receiving l-VNS. Dyspnoea risk was also 2.45 (1.07 to 5.60) times that of l-VNS recipients, although the low number of events and studies meant that the certainty of evidence was low. The risk of rebound-withdrawal symptoms, coughing, pain and paraesthesia was unclear.[134]
Diet
[edit]There is promising evidence that a ketogenic diet (high-fat, low-carbohydrate, adequate-protein) decreases the number of seizures and eliminates seizures in some; however, further research is necessary.[6] A 2022 systematic review of the literature has found some evidence to support that a ketogenic diet or modified Atkins diet can be helpful in the treatment of epilepsy in some infants.[135] These types of diets may be beneficial for children with drug-resistant epilepsy; the use for adults remains uncertain.[6] The most commonly reported adverse effects were vomiting, constipation and diarrhoea.[6] It is unclear why this diet works.[136] In people with coeliac disease or non-celiac gluten sensitivity and occipital calcifications, a gluten-free diet may decrease the frequency of seizures.[83]
Other
[edit]Avoidance therapy consists of minimizing or eliminating triggers. For example, those who are sensitive to light may have success with using a small television, avoiding video games, or wearing dark glasses.[137] Operant-based biofeedback based on the EEG waves has some support in those who do not respond to medications.[138] Psychological methods should not, however, be used to replace medications.[123]
Exercise has been proposed as possibly useful for preventing seizures,[139] with some data to support this claim.[140] Some dogs, commonly referred to as seizure dogs, may help during or after a seizure.[141][142] It is not clear if dogs have the ability to predict seizures before they occur.[143]
There is moderate-quality evidence supporting the use of psychological interventions along with other treatments in epilepsy.[144] This can improve quality of life, enhance emotional wellbeing, and reduce fatigue in adults and adolescents.[144] Psychological interventions may also improve seizure control for some individuals by promoting self-management and adherence.[144]
As an add-on therapy in those who are not well controlled with other medications, cannabidiol appears to be useful in some children.[145][146] In 2018 the FDA approved this product for Lennox–Gastaut syndrome and Dravet syndrome.[147]
There are a few studies on the use of dexamethasone for the successful treatment of drug-resistant seizures in both adults and children.[148]
Alternative medicine
[edit]Alternative medicine, including acupuncture,[149] routine vitamins,[150] and yoga,[151] have no reliable evidence to support their use in epilepsy. Melatonin, as of 2016[update], is insufficiently supported by evidence.[152] The trials were of poor methodological quality and it was not possible to draw any definitive conclusions.[152]
Several supplements (with varied reliabilities of evidence) have been reported to be helpful for drug-resistant epilepsy. These include high-dose Omega-3, berberine, Manuka honey, reishi and lion's mane mushrooms, curcumin,[153] vitamin E, coenzyme Q-10, and resveratrol. The reason these can work (in theory) is that they reduce inflammation or oxidative stress, two of the major mechanism contributing to epilepsy.[154]
Contraception and pregnancy
[edit]Women of child-bearing age, including those with epilepsy, are at risk of unintended pregnancies if they are not using an effective form of contraception.[155] Women with epilepsy may experience a temporary increase in seizure frequency when they begin hormonal contraception.[155]
Some anti-seizure medications interact with enzymes in the liver and cause the drugs in hormonal contraception to be broken down more quickly. These enzyme inducing drugs make hormonal contraception less effective, and this is particularly hazardous if the anti-seizure medication is associated with birth defects.[156] Potent enzyme-inducing anti-seizure medications include carbamazepine, eslicarbazepine acetate, oxcarbazepine, phenobarbital, phenytoin, primidone, and rufinamide. The drugs perampanel and topiramate can be enzyme-inducing at higher doses.[157] Conversely, hormonal contraception can lower the amount of the anti-seizure medication lamotrigine circulating in the body, making it less effective.[155] The failure rate of oral contraceptives, when used correctly, is 1%, but this increases to between 3–6% in women with epilepsy.[156] Overall, intrauterine devices (IUDs) are preferred for women with epilepsy who are not intending to become pregnant.[155]
Women with epilepsy, especially if they have other medical conditions, may have a slightly lower, but still high, chance of becoming pregnant.[155] Women with infertility have about the same chance of success with in vitro fertilisation or other forms of assisted reproductive technology as women without epilepsy.[155] There may be a higher risk of pregnancy loss.[155]
Once pregnant, there are two main concerns related to pregnancy. The first concern is about the risk of seizures during pregnancy, and the second concern is that the anti-seizure medications may result in birth defects.[124] Most women with epilepsy must continue treatment with anti-seizure drugs, and the treatment goal is to balance the need to prevent seizures with the need to prevent drug-induced birth defects.[155][158]
Pregnancy does not seem to change seizure frequency very much.[155] When seizures happen, however, they can cause some pregnancy complications, such as pre-term births or the babies being smaller than usual when they are born.[155]
All pregnancies have a risk of birth defects, e.g., due to smoking during pregnancy.[155] In addition to this typical level of risk, some anti-seizure drugs significantly increase the risk of birth defects and intrauterine growth restriction, as well as developmental, neurocognitive, and behavioral disorders.[158] Most women with epilepsy receive safe and effective treatment and have typical, healthy children.[158] The highest risks are associated with specific anti-seizure drugs, such as valproic acid and carbamazepine, and with higher doses.[124][155] Folic acid supplementation, such as through prenatal vitamins, reduced the risk.[155] Planning pregnancies in advance gives women with epilepsy an opportunity to switch to a lower-risk treatment program and reduced drug doses.[155]
Although anti-seizure drugs can be found in breast milk, women with epilepsy can breastfeed their babies, and the benefits usually outweigh the risks.[155]
Prognosis
[edit]
Epilepsy cannot usually be cured, but medication can control seizures effectively in about 70% of cases.[7] Of those with generalized seizures, more than 80% can be well controlled with medications while this is true in only 50% of people with focal seizures.[5] One predictor of long-term outcome is the number of seizures that occur in the first six months.[24] Other factors increasing the risk of a poor outcome include little response to the initial treatment, generalized seizures, a family history of epilepsy, psychiatric problems, and waves on the EEG representing generalized epileptiform activity.[159] According to the ILAE epilepsy is considered to be resolved if an individual with epilepsy is seizure free for 10 years and off anticonvulsant for 5 years.[160]
In the developing world, 75% of people are either untreated or not appropriately treated.[20] In Africa, 90% do not get treatment.[20] This is partly related to appropriate medications not being available or being too expensive.[20]
Mortality
[edit]People with epilepsy may have a higher risk of premature death compared to those without the condition.[161] This risk is estimated to be between 1.6 and 4.1 times greater than that of the general population.[162] The greatest increase in mortality from epilepsy is among the elderly.[162] Those with epilepsy due to an unknown cause have a relatively low increase in risk.[162]
Mortality is often related to the underlying cause of the seizures, status epilepticus, suicide, trauma, and sudden unexpected death in epilepsy (SUDEP).[161] Death from status epilepticus is primarily due to an underlying problem rather than missing doses of medications.[161] The risk of suicide is between two and six times higher in those with epilepsy;[163][164] the cause of this is unclear.[163] SUDEP appears to be partly related to the frequency of generalized tonic-clonic seizures[165] and accounts for about 15% of epilepsy-related deaths;[159] it is unclear how to decrease its risk.[165] Risk factors for SUDEP include nocturnal generalized tonic-clonic seizures, seizures, sleeping alone and medically intractable epilepsy.[166]
In the United Kingdom, it is estimated that 40–60% of deaths are possibly preventable.[24] In the developing world, many deaths are due to untreated epilepsy leading to falls or status epilepticus.[14]
Epidemiology
[edit]Epilepsy is one of the most common serious neurological disorders[167] affecting about 50 million people as of 2021[update].[8][168] It affects 1% of the population by age 20 and 3% of the population by age 75.[16] It is more common in males than females with the overall difference being small.[14][67] Most of those with the disorder (80%) are in low income populations[169] or the developing world.[20]
The estimated prevalence of active epilepsy (as of 2012[update]) is in the range 3–10 per 1,000, with active epilepsy defined as someone with epilepsy who has had at least one unprovoked seizure in the last five years.[67][170] Epilepsy begins each year in 40–70 per 100,000 in developed countries and 80–140 per 100,000 in developing countries.[20] Poverty is a risk and includes both being from a poor country and being poor relative to others within one's country.[14] In the developed world epilepsy most commonly starts either in the young or in the old.[14] In the developing world its onset is more common in older children and young adults due to the higher rates of trauma and infectious diseases.[14] In developed countries the number of cases a year has decreased in children and increased among the elderly between the 1970s and 2003.[170] This has been attributed partly to better survival following strokes in the elderly.[67]
History
[edit]
The oldest medical records show that epilepsy has been affecting people at least since the beginning of recorded history.[171] Throughout ancient history, the condition was thought to be of a spiritual cause.[171] The world's oldest description of an epileptic seizure comes from a text in Akkadian (a language used in ancient Mesopotamia) and was written around 2000 BC.[22] The person described in the text was diagnosed as being under the influence of a moon god, and underwent an exorcism.[22] Epileptic seizures are listed in the Code of Hammurabi (c. 1790 BC) as reason for which a purchased slave may be returned for a refund,[22] and the Edwin Smith Papyrus (c. 1700 BC) describes cases of individuals with epileptic convulsions.[22]
The oldest known detailed record of the condition itself is in the Sakikku, a Babylonian cuneiform medical text from 1067–1046 BC.[171] This text gives signs and symptoms, details treatment and likely outcomes,[22] and describes many features of the different seizure types.[171] As the Babylonians had no biomedical understanding of the nature of epilepsy, they attributed the seizures to possession by evil spirits and called for treating the condition through spiritual means.[171] Around 900 BC, Punarvasu Atreya described epilepsy as loss of consciousness;[172] this definition was carried forward into the Ayurvedic text of Charaka Samhita (c. 400 BC).[173]
The ancient Greeks had contradictory views of the condition. They thought of epilepsy as a form of spiritual possession, but also associated the condition with genius and the divine. One of the names they gave to it was the sacred disease (Ancient Greek: ἠ ἱερὰ νόσος).[22][174] Epilepsy appears within Greek mythology: it is associated with the Moon goddesses Selene and Artemis, who afflicted those who upset them. The Greeks thought that important figures such as Julius Caesar and Hercules had the condition.[22] The notable exception to this divine and spiritual view was that of the school of Hippocrates. In the fifth century BC, Hippocrates rejected the idea that the condition was caused by spirits. In his landmark work On the Sacred Disease, he proposed that epilepsy was not divine in origin and instead was a medically treatable problem originating in the brain.[22][171] He accused those of attributing a sacred cause to the condition of spreading ignorance through a belief in superstitious magic.[22] Hippocrates proposed that heredity was important as a cause, described worse outcomes if the condition presents at an early age, and made note of the physical characteristics as well as the social shame associated with it.[22] Instead of referring to it as the sacred disease, he used the term great disease, giving rise to the modern term grand mal, used for tonic–clonic seizures.[22] Despite his work detailing the physical origins of the condition, his view was not accepted at the time.[171] Evil spirits continued to be blamed until at least the 17th century.[171]
In Ancient Rome people did not eat or drink with the same pottery as that used by someone who was affected.[175] People of the time would spit on their chest believing that this would keep the problem from affecting them.[175] According to Apuleius and other ancient physicians, to detect epilepsy, it was common to light a piece of gagates, whose smoke would trigger the seizure.[176] Occasionally a spinning potter's wheel was used, perhaps a reference to photosensitive epilepsy.[177]
In most cultures, persons with epilepsy have been stigmatized, shunned, or even imprisoned. As late as in the second half of the 20th century, in Tanzania and other parts of Africa epilepsy was associated with possession by evil spirits, witchcraft, or poisoning and was believed by many to be contagious.[178] In the Salpêtrière, the birthplace of modern neurology, Jean-Martin Charcot found people with epilepsy side by side with the mentally ill, those with chronic syphilis, and the criminally insane.[179] In Ancient Rome, epilepsy was known as the morbus comitialis or 'disease of the assembly hall' and was seen as a curse from the gods. In northern Italy, epilepsy was traditionally known as Saint Valentine's malady.[180] In at least the 1840s in the United States of America, epilepsy was known as the falling sickness or the falling fits, and was considered a form of medical insanity.[181] Around the same time period, epilepsy was known in France as the haut-mal lit. 'high evil', mal-de terre lit. 'earthen sickness', mal de Saint Jean lit. 'Saint John's sickness', mal des enfans lit. 'child sickness', and mal-caduc lit. 'falling sickness'.[181] People of epilepsy in France were also known as tombeurs lit. 'people who fall', due to the seizures and loss of consciousness in an epileptic episode.[181]
In the mid-19th century, the first effective anti-seizure medication, bromide, was introduced.[122] The first modern treatment, phenobarbital, was developed in 1912, with phenytoin coming into use in 1938.[182]
Society and culture
[edit]Stigma
[edit]Social stigma is commonly experienced, around the world, by those with epilepsy.[11][183] It can affect people economically, socially and culturally.[183] In India and China, epilepsy may be used as justification to deny marriage.[20] People in some areas still believe those with epilepsy to be cursed.[14] In parts of Africa, such as Tanzania and Uganda, epilepsy is claimed to be associated with possession by evil spirits, witchcraft, or poisoning and is incorrectly believed by many to be contagious.[178][14] Before 1971 in the United Kingdom, epilepsy was considered grounds for the annulment of marriage.[20] The stigma may result in some people with epilepsy denying that they have ever had seizures.[67] A 2024 cross-sectional study revealed that 64.8% of relatives of epilepsy patients experienced moderate stigma and held moderately positive attitudes toward epilepsy. The study found that higher levels of stigma among participants were associated with more negative attitudes toward the condition. Additionally, relatives of patients who experienced frequent seizures (one or more per month) faced greater stigma, while those of patients who did not adhere to their medication regimen exhibited more negative attitudes toward epilepsy.[184]
Economics
[edit]Seizures result in direct economic costs of about one billion dollars in the United States.[17] Epilepsy resulted in economic costs in Europe of around 15.5 billion euros in 2004.[24] In India epilepsy is estimated to result in costs of US$1.7 billion or 0.5% of the GDP.[20] It is the cause of about 1% of emergency department visits (2% for emergency departments for children) in the United States.[185]
Vehicles
[edit]Those with epilepsy are at about twice the risk of being involved in a motor vehicular collision and thus in many areas of the world are not allowed to drive or only able to drive if certain conditions are met.[21] Diagnostic delay has been suggested to be a cause of some potentially avoidable motor vehicle collisions since at least one study showed that most motor vehicle accidents occurred in those with undiagnosed non-motor seizures as opposed to those with motor seizures at epilepsy onset.[186] In some places physicians are required by law to report if a person has had a seizure to the licensing body while in others the requirement is only that they encourage the person in question to report it themselves.[21] Countries that require physician reporting include Sweden, Austria, Denmark and Spain.[21] Countries that require the individual to report include the UK and New Zealand, and physicians may report if they believe the individual has not already.[21] In Canada, the United States and Australia the requirements around reporting vary by province or state.[21] If seizures are well controlled most feel allowing driving is reasonable.[187] The amount of time a person must be free from seizures before they can drive varies by country.[187] Many countries require one to three years without seizures.[187] In the United States the time needed without a seizure is determined by each state and is between three months and one year.[187]
Those with epilepsy or seizures are typically denied a pilot license.[188]
- In Canada if an individual has had no more than one seizure, they may be considered after five years for a limited license if all other testing is normal.[189] Those with febrile seizures and drug related seizures may also be considered.[189]
- In the United States, the Federal Aviation Administration does not allow those with epilepsy to get a commercial pilot license.[190] Rarely, exceptions can be made for persons who have had an isolated seizure or febrile seizures and have remained free of seizures into adulthood without medication.[191]
- In the United Kingdom, a full national private pilot license requires the same standards as a professional driver's license.[192] This requires a period of ten years without seizures while off medications.[193] Those who do not meet this requirement may acquire a restricted license if free from seizures for five years.[192]
Support organizations
[edit]There are organizations that provide support for people and families affected by epilepsy. The Out of the Shadows campaign, a joint effort by the World Health Organization, the ILAE and the International Bureau for Epilepsy, provides help internationally.[20] In the United States, the Epilepsy Foundation is a national organization that works to increase the acceptance of those with the disorder, their ability to function in society and to promote research for a cure.[194] The Epilepsy Foundation, some hospitals, and some individuals also run support groups in the United States.[195] In Australia, the Epilepsy Foundation provides support, delivers education and training and funds research for people living with epilepsy.
International Epilepsy Day (World Epilepsy Day) began in 2015 and occurs on the second Monday in February.[196][197]
Purple Day, a different world-wide epilepsy awareness day for epilepsy, was initiated by a nine-year-old Canadian named Cassidy Megan in 2008, and is every year on 26 March.[198]
Research
[edit]Seizure prediction and modeling
[edit]Seizure prediction refers to attempts to forecast epileptic seizures based on the EEG before they occur.[199] As of 2011[update], no effective mechanism to predict seizures has been developed.[199] Although no effective device that can predict seizures is available, the science behind seizure prediction and ability to deliver such a tool has made progress.
Kindling, where repeated exposures to events that could cause seizures eventually causes seizures more easily, has been used to create animal models of epilepsy.[200] Different animal models of epilepsy have been characterized in rodents that recapitulate the EEG and behavioral concomitants of different forms of epilepsy, in particular the occurrence of recurrent spontaneous seizures.[201] Because epileptic seizures of different kinds are observed naturally in some of these animals, strains of mice and rats have been selected to be used as genetic models of epilepsy. In particular, several lines of mice and rats display spike-and-wave discharges when EEG recorded and have been studied to understand absence epilepsy.[202] Among these models, the strain of GAERS (Genetic Absence Epilepsy Rats from Strasbourg) was characterized in the 1980s and has helped to understand the mechanisms underlying childhood absence epilepsy.[203]
Rat brain slices serve as a valuable model for assessing the potential of compounds in reducing epileptiform activity. By evaluating the frequency of epileptiform bursting in hippocampal networks, researchers can identify promising candidates for novel anti-seizure drugs.[204]
Reductionist views on the mechanisms of epileptiform discharges are often expressed through mathematical models. The simplest of these models are based on a few ordinary differential equations, such as the Epileptor model.[205] The more physiologically explicit Epileptor-2 model[206] replicates brief interictal discharges—observed as clusters of action potential spikes in the activity of individual neurons—and longer ictal discharges, represented as clusters of these shorter discharges. According to this model, brief interictal discharges are characterized as stochastic oscillations of the membrane potential and synaptic resources, while ictal discharges emerge as oscillations in the extracellular concentration of potassium ions and the intracellular concentration of sodium ions. These models demonstrate [207] that ionic dynamics play a decisive role in the generation of pathological activity.
One of the hypotheses present in the literature is based on inflammatory pathways. Studies supporting this mechanism revealed that inflammatory, glycolipid, and oxidative factors are higher in people with epilepsy, especially those with generalized epilepsy.[208]
Potential future therapies
[edit]Gene therapy is being studied in some types of epilepsy.[209] Medications that alter immune function, such as intravenous immunoglobulins, may reduce the frequency of seizures when including in normal care as an add-on therapy; however, further research is required to determine whether these medications are very well tolerated in children and in adults with epilepsy.[210] Noninvasive stereotactic radiosurgery is, as of 2012[update], being compared to standard surgery for certain types of epilepsy.[211]
Other animals
[edit]Epilepsy occurs in a number of other animals, including dogs and cats; it is in fact the most common brain disorder in dogs.[212] It is typically treated with anticonvulsants, such as levetiracetam, phenobarbital, or bromide, in dogs, and phenobarbital in cats.[212] Imepitoin is also used in dogs.[213] While generalized seizures in horses are fairly easy to diagnose, it may be more difficult in non-generalized seizures and EEGs may be useful.[214] Juvenile idiopathic epilepsy (JIE) in foals is a condition with varying outcomes, depending on the severity and management of the condition. Some foals eventually outgrow the condition without significant long-term effects, while others may face severe consequences, including death or lifelong complications, if left untreated. This variability highlights the importance of timely intervention and care. Earlier research has pointed to a significant genetic influence in the development of JIE, suggesting that the condition may follow the inheritance pattern of a single-gene trait. These findings underscore the need for further genetic studies to confirm this hypothesis and explore potential breeding strategies to reduce the prevalence of JIE.[215]
See also
[edit]References
[edit]- ^ a b c d e f g "Epilepsy Fact sheet". WHO. February 2016. Archived from the original on 11 March 2016. Retrieved 4 March 2016.
- ^ a b c d e f g h i j k l m Hammer GD, McPhee SJ, eds. (2010). "7". Pathophysiology of disease: an introduction to clinical medicine (6th ed.). New York: McGraw-Hill Medical. ISBN 978-0-07-162167-0.
- ^ a b c d 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.
- ^ a b c Longo DL (2012). "369 Seizures and Epilepsy". Harrison's principles of internal medicine (18th ed.). McGraw-Hill. p. 3258. ISBN 978-0-07-174887-2.
- ^ a b c d Bergey GK (June 2013). "Neurostimulation in the treatment of epilepsy". Experimental Neurology. 244: 87–95. doi:10.1016/j.expneurol.2013.04.004. PMID 23583414.
- ^ a b c d e Martin-McGill KJ, Bresnahan R, Levy RG, Cooper PN (June 2020). "Ketogenic diets for drug-resistant epilepsy". The Cochrane Database of Systematic Reviews. 2020 (6): CD001903. doi:10.1002/14651858.CD001903.pub5. PMC 7387249. PMID 32588435.
- ^ a b c d Eadie MJ (December 2012). "Shortcomings in the current treatment of epilepsy". Expert Review of Neurotherapeutics. 12 (12): 1419–1427. doi:10.1586/ern.12.129. PMID 23237349.
- ^ a b "GBD 2021 Cause and Risk Summary: EPILEPSY". Institute for Health Metrics and Evaluation (IHME). Seattle, USA: University of Washington. 2021. Archived (PDF) from the original on 19 July 2024. Retrieved 19 July 2024.
- ^ a b Sinmetz JD, Seeher KM, Schiess N, Nichols E, Cao B, Servili C, et al. (1 April 2024). "Global, regional, and national burden of disorders affecting the nervous system, 1990–2021: a systematic analysis for the Global Burden of Disease Study 2021". The Lancet Neurology. 23 (4). Elsevier: 344–381. doi:10.1016/S1474-4422(24)00038-3. hdl:1959.4/102176. PMC 10949203. PMID 38493795.
- ^ a b c d e 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.
- ^ a b c d e "Epilepsy". World Health Organization. Retrieved 1 April 2023.
- ^ Fisher RS, van Emde Boas W, Blume W, Elger C, Genton P, Lee P, et al. (April 2005). "Epileptic seizures and epilepsy: definitions proposed by the International League Against Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE)". Epilepsia. 46 (4): 470–472. doi:10.1111/j.0013-9580.2005.66104.x. PMID 15816939.
- ^ a b Pandolfo M (November 2011). "Genetics of epilepsy". Seminars in Neurology. 31 (5): 506–518. doi:10.1055/s-0031-1299789. PMID 22266888.
- ^ a b c d e f g h i j k l m Newton CR, Garcia HH (September 2012). "Epilepsy in poor regions of the world". Lancet. 380 (9848): 1193–1201. doi:10.1016/S0140-6736(12)61381-6. PMID 23021288.
- ^ a b c Brodie MJ, Elder AT, Kwan P (November 2009). "Epilepsy in later life". The Lancet. Neurology. 8 (11): 1019–1030. doi:10.1016/S1474-4422(09)70240-6. PMID 19800848.
- ^ a b Holmes TR, Browne GL (2008). Handbook of epilepsy (4th ed.). Philadelphia: Lippincott Williams & Wilkins. p. 7. ISBN 978-0-7817-7397-3.
- ^ a b c Wilden JA, Cohen-Gadol AA (August 2012). "Evaluation of first nonfebrile seizures". American Family Physician. 86 (4): 334–340. PMID 22963022.
- ^ Neligan A, Adan G, Nevitt SJ, Pullen A, Sander JW, Bonnett L, et al. (Cochrane Epilepsy Group) (January 2023). "Prognosis of adults and children following a first unprovoked seizure". The Cochrane Database of Systematic Reviews. 1 (1): CD013847. doi:10.1002/14651858.CD013847.pub2. PMC 9869434. PMID 36688481.
- ^ Epilepsy: what are the chances of having a second seizure? (Report). 16 August 2023. doi:10.3310/nihrevidence_59456.
- ^ a b c d e f g h i j k l m n "Epilepsy". Fact Sheets. World Health Organization. October 2012. Retrieved 24 January 2013.
- ^ a b c d e f L Devlin A, Odell M, L Charlton J, Koppel S (December 2012). "Epilepsy and driving: current status of research". Epilepsy Research. 102 (3): 135–152. doi:10.1016/j.eplepsyres.2012.08.003. PMID 22981339.
- ^ a b c d e f g h i j k l 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.
- ^ a b Duncan JS, Sander JW, Sisodiya SM, Walker MC (April 2006). "Adult epilepsy". Lancet. 367 (9516): 1087–1100. doi:10.1016/S0140-6736(06)68477-8. PMID 16581409.
- ^ a b c d e f g h i j k National Clinical Guideline Centre (January 2012). The Epilepsies: The diagnosis and management of the epilepsies in adults and children in primary and secondary care (PDF). National Institute for Health and Clinical Excellence. pp. 21–28. Archived (PDF) from the original on 16 December 2013.
- ^ a b c d e f Beniczky S, Trinka E, Wirrell E, Abdulla F, Al Baradie R, Alonso Vanegas M, et al. (23 April 2025). "Updated classification of epileptic seizures: Position paper of the International League Against Epilepsy". Epilepsia. doi:10.1111/epi.18338. ISSN 0013-9580. PMID 40264351.
- ^ Berg AT, Berkovic SF, Brodie MJ, Buchhalter J, Cross JH, Van Emde Boas W, et al. (2010). "Revised terminology and concepts for organization of seizures and epilepsies: Report of the ILAE Commission on Classification and Terminology, 2005–2009". Epilepsia. 51 (4): 676–685. doi:10.1111/j.1528-1167.2010.02522.x. ISSN 1528-1167. PMID 20196795.
- ^ a b c Shearer P. "Seizures and Status Epilepticus: Diagnosis and Management in the Emergency Department". Emergency Medicine Practice. Archived from the original on 30 December 2010.
- ^ a b c Bradley WG (2012). "67". Bradley's neurology in clinical practice (6th ed.). Philadelphia, PA: Elsevier/Saunders. ISBN 978-1-4377-0434-1.
- ^ National Clinical Guideline Centre (January 2012). The Epilepsies: The diagnosis and management of the epilepsies in adults and children in primary and secondary care (PDF). National Institute for Health and Clinical Excellence. pp. 119–129. Archived (PDF) from the original on 16 December 2013.
- ^ Engel J (2008). Epilepsy: a comprehensive textbook (2nd ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 2797. ISBN 978-0-7817-5777-5. Archived from the original on 20 May 2016.
- ^ a b c Simon DA, Greenberg MJ, Aminoff RP (2012). "12". Clinical neurology (8th ed.). New York: McGraw-Hill Medical. ISBN 978-0-07-175905-2.
- ^ Stephenson JB (1990). Fits and faints. London: Mac Keith Press. ISBN 0-632-02811-4. OCLC 25711319.
- ^ a b Xue LY, Ritaccio AL (March 2006). "Reflex seizures and reflex epilepsy". American Journal of Electroneurodiagnostic Technology. 46 (1): 39–48. doi:10.1080/1086508X.2006.11079556. PMID 16605171.
- ^ a b Steven C. Schachter, ed. (2008). Behavioral aspects of epilepsy: principles and practice ([Online-Ausg.]. ed.). New York: Demos. p. 125. ISBN 978-1-933864-04-4.
- ^ Malow BA (November 2005). "Sleep and epilepsy". Neurologic Clinics. 23 (4): 1127–1147. doi:10.1016/j.ncl.2005.07.002. PMID 16243619.
- ^ Tinuper P, Provini F, Bisulli F, Vignatelli L, Plazzi G, Vetrugno R, et al. (August 2007). "Movement disorders in sleep: guidelines for differentiating epileptic from non-epileptic motor phenomena arising from sleep". Sleep Medicine Reviews. 11 (4): 255–267. doi:10.1016/j.smrv.2007.01.001. PMID 17379548.
- ^ Mitchell WG (1996). "Status epilepticus and acute repetitive seizures in children, adolescents, and young adults: etiology, outcome, and treatment". Epilepsia. 37 (s1): S74 – S80. doi:10.1111/j.1528-1157.1996.tb06025.x. PMID 8647055.
- ^ a b Jafarpour S, Hirsch LJ, Gaínza-Lein M, Kellinghaus C, Detyniecki K (May 2019). "Seizure cluster: Definition, prevalence, consequences, and management". Seizure. 68: 9–15. doi:10.1016/j.seizure.2018.05.013. PMID 29871784.
- ^ Faught E (September 2022). "Economic aspects of treating seizure clusters". Epilepsia. 63 (Suppl 1): S45 – S54. doi:10.1111/epi.17340. PMID 35999172.
- ^ Haut SR, Shinnar S, Moshé SL (January 2005). "Seizure clustering: risks and outcomes". Epilepsia. 46 (1): 146–149. doi:10.1111/j.0013-9580.2005.29004.x. PMID 15660781.
- ^ Chen B, Choi H, Hirsch LJ, Katz A, Legge A, Wong RA, et al. (July 2017). "Prevalence and risk factors of seizure clusters in adult patients with epilepsy". Epilepsy Research. 133: 98–102. doi:10.1016/j.eplepsyres.2017.04.016. PMID 28475999.
- ^ Komaragiri A, Detyniecki K, Hirsch LJ (June 2016). "Seizure clusters: A common, understudied and undertreated phenomenon in refractory epilepsy". Epilepsy & Behavior. 59: 83–86. doi:10.1016/j.yebeh.2016.02.030. PMID 27116535.
- ^ Chung S, Szaflarski JP, Choi EJ, Wilson JC, Kharawala S, Kaur G, et al. (November 2021). "A systematic review of seizure clusters: Prevalence, risk factors, burden of disease and treatment patterns". Epilepsy Research. 177: 106748. doi:10.1016/j.eplepsyres.2021.106748. PMID 34521043.
- ^ Gidal B, Detyniecki K (September 2022). "Rescue therapies for seizure clusters: Pharmacology and target of treatments". Epilepsia. 63 (Suppl 1): S34 – S44. doi:10.1111/epi.17341. PMC 9543841. PMID 35999174.
- ^ Pottkämper JC, Hofmeijer J, van Waarde JA, van Putten MJ (2020). "The postictal state-What do we know?". Epilepsia. 61 (6): 1045–1061. doi:10.1111/epi.16519. ISSN 1528-1167. PMC 7317965. PMID 32396219.
- ^ 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.
- ^ Larner AJ (2010). A dictionary of neurological signs (3rd ed.). New York: Springer. p. 348. ISBN 978-1-4419-7095-4.
- ^ Clancy MJ, Clarke MC, Connor DJ, Cannon M, Cotter DR (13 March 2014). "The prevalence of psychosis in epilepsy; a systematic review and meta-analysis". BMC Psychiatry. 14 (1): 75. doi:10.1186/1471-244X-14-75. ISSN 1471-244X. PMC 3995617. PMID 24625201.
- ^ 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.
- ^ Kaplan PW (November 2011). "Obsessive-compulsive disorder in chronic epilepsy". Epilepsy & Behavior. 22 (3): 428–432. doi:10.1016/j.yebeh.2011.07.029. PMID 21889913.
- ^ Stefan H (2012). Epilepsy Part I: Basic Principles and Diagnosis E-Book: Handbook of Clinical Neurology (Volume 107 of Handbook of Clinical Neurology ed.). Newnes. p. 471. ISBN 978-0-444-53505-4.
- ^ Plioplys S, Dunn DW, Caplan R (November 2007). "10-year research update review: psychiatric problems in children with epilepsy". Journal of the American Academy of Child and Adolescent Psychiatry. 46 (11): 1389–1402. doi:10.1097/chi.0b013e31815597fc. PMID 18049289.
- ^ Reilly CJ (May–June 2011). "Attention deficit hyperactivity disorder (ADHD) in childhood epilepsy". Research in Developmental Disabilities. 32 (3): 883–893. doi:10.1016/j.ridd.2011.01.019. PMID 21310586.
- ^ Levisohn PM (2007). "The autism-epilepsy connection". Epilepsia. 48 (Suppl 9): 33–35. doi:10.1111/j.1528-1167.2007.01399.x. PMID 18047599.
- ^ Lin JJ, Mula M, Hermann BP (September 2012). "Uncovering the neurobehavioural comorbidities of epilepsy over the lifespan". Lancet. 380 (9848): 1180–1192. doi:10.1016/s0140-6736(12)61455-x. PMC 3838617. PMID 23021287.
- ^ Kanner AM, Schachter SC, Barry JJ, Hesdorffer DC, Mula M, Trimble M, et al. (June 2012). "Depression and epilepsy: epidemiologic and neurobiologic perspectives that may explain their high comorbid occurrence". Epilepsy & Behavior. 24 (2): 156–168. doi:10.1016/j.yebeh.2012.01.007. PMID 22632406.
- ^ Adelöw C, Andersson T, Ahlbom A, Tomson T (February 2012). "Hospitalization for psychiatric disorders before and after onset of unprovoked seizures/epilepsy". Neurology. 78 (6): 396–401. doi:10.1212/wnl.0b013e318245f461. PMID 22282649.
- ^ Taylor RS, Sander JW, Taylor RJ, Baker GA (December 2011). "Predictors of health-related quality of life and costs in adults with epilepsy: a systematic review". Epilepsia. 52 (12): 2168–2180. doi:10.1111/j.1528-1167.2011.03213.x. PMID 21883177.
- ^ Lacey CJ, Salzberg MR, Roberts H, Trauer T, D'Souza WJ (August 2009). "Psychiatric comorbidity and impact on health service utilization in a community sample of patients with epilepsy". Epilepsia. 50 (8): 1991–1994. doi:10.1111/j.1528-1167.2009.02165.x. PMID 19490049.
- ^ Nogueira MH, Yasuda CL, Coan AC, Kanner AM, Cendes F (July 2017). "Concurrent mood and anxiety disorders are associated with pharmacoresistant seizures in patients with MTLE". Epilepsia. 58 (7): 1268–1276. doi:10.1111/epi.13781. PMID 28555776.
- ^ Kanner AM, Byrne R, Chicharro A, Wuu J, Frey M (March 2009). "A lifetime psychiatric history predicts a worse seizure outcome following temporal lobectomy". Neurology. 72 (9): 793–799. doi:10.1212/01.wnl.0000343850.85763.9c. PMID 19255406.
- ^ Boylan LS, Flint LA, Labovitz DL, Jackson SC, Starner K, Devinsky O (January 2004). "Depression but not seizure frequency predicts quality of life in treatment-resistant epilepsy". Neurology. 62 (2): 258–261. doi:10.1212/01.wnl.0000103282.62353.85. PMID 14745064.
- ^ Munger Clary HM, Croxton RD, Allan J, Lovato J, Brenes G, Snively BM, et al. (March 2020). "Who is willing to participate in research? A screening model for an anxiety and depression trial in the epilepsy clinic". Epilepsy & Behavior. 104 (Pt A): 106907. doi:10.1016/j.yebeh.2020.106907. PMC 7282472. PMID 32000099.
- ^ a b Berkovic SF, Mulley JC, Scheffer IE, Petrou S (July 2006). "Human epilepsies: interaction of genetic and acquired factors". Trends in Neurosciences. 29 (7): 391–397. doi:10.1016/j.tins.2006.05.009. PMID 16769131.
- ^ Balestrini S, Arzimanoglou A, Blümcke I, Scheffer IE, Wiebe S, Zelano J, et al. (February 2021). "The aetiologies of epilepsy". Epileptic Disorders. 23 (1): 1–16. doi:10.1684/epd.2021.1255. hdl:2158/1262349. PMID 33720020.
- ^ 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.
- ^ a b c d e f 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 978-0-444-52898-8. PMID 22938966.
- ^ a b National Clinical Guideline Centre (January 2012). The Epilepsies: The diagnosis and management of the epilepsies in adults and children in primary and secondary care (PDF). National Institute for Health and Clinical Excellence. pp. 119–129. Archived (PDF) from the original on 16 December 2013.
- ^ a b c d e f g h i j Scheffer IE, Berkovic S, Capovilla G, Connolly MB, French J, Guilhoto L, et al. (2017). "ILAE classification of the epilepsies: Position paper of the ILAE Commission for Classification and Terminology". Epilepsia. 58 (4): 512–521. doi:10.1111/epi.13709. ISSN 0013-9580. PMC 5386840. PMID 28276062.
- ^ Thom M (2014). "Review: Hippocampal sclerosis in epilepsy: a neuropathology review". Neuropathology and Applied Neurobiology. 40 (5): 520–543. doi:10.1111/nan.12150. ISSN 1365-2990. PMC 4265206. PMID 24762203.
- ^ a b c d e f g 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.
- ^ Galovic M, Döhler N, Erdélyi-Canavese B, Felbecker A, Siebel P, Conrad J, et al. (February 2018). "Prediction of late seizures after ischaemic stroke with a novel prognostic model (the SeLECT score): a multivariable prediction model development and validation study". The Lancet. Neurology. 17 (2): 143–152. doi:10.1016/S1474-4422(17)30404-0. PMID 29413315.
- ^ Ren Z, Wen Q, Yan X, Wang Y, Zhang Y (September 2022). "Post-stroke epilepsy and risk of all-cause mortality: A systematic review and meta-analysis of cohort studies". Clinical Neurology and Neurosurgery. 220: 107362. doi:10.1016/j.clineuro.2022.107362. PMID 35839716.
- ^ Zelano J, Holtkamp M, Agarwal N, Lattanzi S, Trinka E, Brigo F (June 2020). "How to diagnose and treat post-stroke seizures and epilepsy". Epileptic Disorders. 22 (3): 252–263. doi:10.1684/epd.2020.1159. PMID 32597766.
- ^ Zöllner JP, Schmitt FC, Rosenow F, Kohlhase K, Seiler A, Strzelczyk A, et al. (December 2021). "Seizures and epilepsy in patients with ischaemic stroke". Neurological Research and Practice. 3 (1): 63. doi:10.1186/s42466-021-00161-w. PMC 8647498. PMID 34865660.
- ^ Steinlein OK (31 March 2008). "Genetics and epilepsy". Dialogues in Clinical Neuroscience. 10 (1): 29–38. doi:10.31887/DCNS.2008.10.1/oksteinlein. PMC 3181863. PMID 18472482.
- ^ Heinzen EL, Depondt C, Cavalleri GL, Ruzzo EK, Walley NM, Need AC, et al. (August 2012). "Exome sequencing followed by large-scale genotyping fails to identify single rare variants of large effect in idiopathic generalized epilepsy". American Journal of Human Genetics. 91 (2): 293–302. doi:10.1016/j.ajhg.2012.06.016. PMC 3415540. PMID 22863189.
- ^ Carvill GL, Heavin SB, Yendle SC, McMahon JM, O'Roak BJ, Cook J, et al. (July 2013). "Targeted resequencing in epileptic encephalopathies identifies de novo mutations in CHD2 and SYNGAP1". Nature Genetics. 45 (7): 825–830. doi:10.1038/ng.2646. PMC 3704157. PMID 23708187.
- ^ Chénier S, Yoon G, Argiropoulos B, Lauzon J, Laframboise R, Ahn JW, et al. (2014). "CHD2 haploinsufficiency is associated with developmental delay, intellectual disability, epilepsy and neurobehavioural problems". Journal of Neurodevelopmental Disorders. 6 (1): 9. doi:10.1186/1866-1955-6-9. PMC 4022362. PMID 24834135.
- ^ Suls A, Jaehn JA, Kecskés A, Weber Y, Weckhuysen S, Craiu DC, et al. (November 2013). "De novo loss-of-function mutations in CHD2 cause a fever-sensitive myoclonic epileptic encephalopathy sharing features with Dravet syndrome". American Journal of Human Genetics. 93 (5): 967–975. doi:10.1016/j.ajhg.2013.09.017. PMC 3824114. PMID 24207121.
- ^ EuroEPINOMICS-RES Consortium (October 2014). "De novo mutations in synaptic transmission genes including DNM1 cause epileptic encephalopathies". American Journal of Human Genetics. 95 (4): 360–370. doi:10.1016/j.ajhg.2014.08.013. PMC 4185114. PMID 25262651.
- ^ Stafstrom CE, Staedtke V, Comi AM (2017). "Epilepsy Mechanisms in Neurocutaneous Disorders: Tuberous Sclerosis Complex, Neurofibromatosis Type 1, and Sturge-Weber Syndrome". Frontiers in Neurology. 8: 87. doi:10.3389/fneur.2017.00087. PMC 5355446. PMID 28367137.
- ^ a b Jackson JR, Eaton WW, Cascella NG, Fasano A, Kelly DL (March 2012). "Neurologic and psychiatric manifestations of celiac disease and gluten sensitivity". The Psychiatric Quarterly. 83 (1): 91–102. doi:10.1007/s11126-011-9186-y. PMC 3641836. PMID 21877216.
- ^ Grossman G (April 2008). "Neurological complications of coeliac disease: what is the evidence?". Practical Neurology. 8 (2): 77–89. doi:10.1136/jnnp.2007.139717. PMID 18344378.
- ^ a b Bromfield EB (2006). "Basic Mechanisms Underlying Seizures and Epilepsy". An Introduction to Epilepsy. American Epilepsy Society.
- ^ Blumenfeld H (2005). "Cellular and network mechanisms of spike-wave seizures". Epilepsia. 46 (Suppl.9): 21–33. doi:10.1111/j.1528-1167.2005.00311.x. PMID 16302873.
- ^ Noebels JL, Avoli M (29 June 2012). Jasper's Basic Mechanisms of the Epilepsies. Oxford University Press. pp. 466, 470. ISBN 978-0-19-974654-5. Retrieved 16 October 2014.
- ^ a b Le Van Quyen M, Navarro V, Martinerie J, Baulac M, Varela FJ (2003). "Toward a neurodynamical understanding of ictogenesis". Epilepsia. 44 (Suppl.12): 30–43. doi:10.1111/j.0013-9580.2003.12007.x. PMID 14641559.
- ^ Lopes da Silva F, Blanes W, Kalitzin SN, Parra J, Suffczynski P, Velis DN (2003). "Epilepsies as dynamical diseases of brain systems: basic models of the transition between normal and epileptic activity". Epilepsia. 44 (Suppl.12): 72–83. doi:10.1111/j.0013-9580.2003.12005.x. PMID 14641563.
- ^ Henshall DC, Hamer HM, Pasterkamp RJ, Goldstein DB, Kjems J, Prehn JH, et al. (December 2016). "MicroRNAs in epilepsy: pathophysiology and clinical utility". The Lancet. Neurology. 15 (13): 1368–1376. doi:10.1016/S1474-4422(16)30246-0. PMID 27839653.
- ^ Henshall DC (April 2014). "MicroRNA and epilepsy: profiling, functions and potential clinical applications". Current Opinion in Neurology. 27 (2): 199–205. doi:10.1097/WCO.0000000000000079. PMC 4127484. PMID 24553459.
- ^ 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.
- ^ 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.
- ^ a b Engel J, Pedley TA, eds. (2008). Epilepsy: a comprehensive textbook (2nd ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 483. ISBN 978-0-7817-5777-5.
- ^ Depannemaecker D, Ivanov A, Lillo D, Spek L, Bernard C, Jirsa V (February 2022). "A unified physiological framework of transitions between seizures, sustained ictal activity and depolarization block at the single neuron level". Journal of Computational Neuroscience. 50 (1): 33–49. doi:10.1007/s10827-022-00811-1. PMC 8818009. PMID 35031915.
- ^ 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.
- ^ Panayiotopoulos CP (December 2011). "The new ILAE report on terminology and concepts for organization of epileptic seizures: a clinician's critical view and contribution". Epilepsia. 52 (12): 2155–2160. doi:10.1111/j.1528-1167.2011.03288.x. PMID 22004554.
- ^ a b Shorvon SD (June 2011). "The etiologic classification of epilepsy". Epilepsia. 52 (6): 1052–1057. doi:10.1111/j.1528-1167.2011.03041.x. PMID 21449936.
- ^ "Proposal for revised classification of epilepsies and epileptic syndromes. Commission on Classification and Terminology of the International League Against Epilepsy". Epilepsia. 30 (4): 389–399. 1989. doi:10.1111/j.1528-1157.1989.tb05316.x. PMID 2502382.
- ^ Engel J (August 2006). "ILAE classification of epilepsy syndromes". Epilepsy Research. 70 (Suppl 1): S5-10. doi:10.1016/j.eplepsyres.2005.11.014. PMID 16822650.
- ^ Berg AT, Berkovic SF, Brodie MJ, Buchhalter J, Cross JH, van Emde Boas W, et al. (April 2010). "Revised terminology and concepts for organization of seizures and epilepsies: report of the ILAE Commission on Classification and Terminology, 2005-2009". Epilepsia. 51 (4): 676–685. doi:10.1111/j.1528-1167.2010.02522.x. PMID 20196795.
- ^ "Epilepsy syndromes". International league against epilepsy. Archived from the original on 6 October 2014. Retrieved 6 October 2014.
- ^ Wirrell EC, Nabbout R, Scheffer IE, Alsaadi T, Bogacz A, French JA, et al. (2022). "Methodology for classification and definition of epilepsy syndromes with list of syndromes: Report of the ILAE Task Force on Nosology and Definitions". Epilepsia. 63 (6): 1333–1348. doi:10.1111/epi.17237. ISSN 1528-1167.
- ^ Raga S, Specchio N, Rheims S, Wilmshurst JM (1 February 2021). "Developmental and epileptic encephalopathies: recognition and approaches to care". Epileptic Disorders: International Epilepsy Journal with Videotape. 23 (1): 40–52. doi:10.1684/epd.2021.1244. ISSN 1950-6945. PMID 33632673.
- ^ Nordli DR (October 2012). "Epileptic encephalopathies in infants and children". Journal of Clinical Neurophysiology. 29 (5): 420–424. doi:10.1097/WNP.0b013e31826bd961. PMID 23027099.
- ^ a b c d e f g h i j k l m Epilepsies in children, young people and adults. National Institute for Health and Care Excellence: Guidelines. London: National Institute for Health and Care Excellence (NICE). 2022. ISBN 978-1-4731-4513-9. PMID 35700280.
- ^ Brodtkorb E (2013). "Common imitators of epilepsy". Acta Neurologica Scandinavica. Supplementum. 127 (196): 5–10. doi:10.1111/ane.12043. PMID 23190285.
- ^ a b c Marx JA, ed. (2010). Rosen's emergency medicine: concepts and clinical practice (7th ed.). Philadelphia: Mosby/Elsevier. p. 2228. ISBN 978-0-323-05472-0.
- ^ Zaidi A, Clough P, Cooper P, Scheepers B, Fitzpatrick AP (July 2000). "Misdiagnosis of epilepsy: many seizure-like attacks have a cardiovascular cause". Journal of the American College of Cardiology. 36 (1): 181–184. doi:10.1016/S0735-1097(00)00700-2. PMID 10898432.
- ^ a b Jerome E (2013). Seizures and epilepsy (2nd ed.). New York: Oxford University Press. p. 462. ISBN 978-0-19-532854-7.
- ^ Xu Y, Nguyen D, Mohamed A, Carcel C, Li Q, Kutlubaev MA, et al. (1 October 2016). "Frequency of a false positive diagnosis of epilepsy: A systematic review of observational studies". Seizure - European Journal of Epilepsy. 41: 167–174. doi:10.1016/j.seizure.2016.08.005. ISSN 1059-1311. PMID 27592470.
- ^ Miano S, Peraita-Adrados R (1 March 2013). "[Nocturnal frontal lobe epilepsy is often misdiagnosed as sleep disorders in children: a case series]". Revista De Neurologia. 56 (5): 257–267. ISSN 1576-6578. PMID 23440753.
- ^ Helmers SL, Kobau R, Sajatovic M, Jobst BC, Privitera M, Devinsky O, et al. (March 2017). "Self-management in epilepsy: Why and how you should incorporate self-management in your practice". Epilepsy & Behavior. 68: 220–224. doi:10.1016/j.yebeh.2016.11.015. PMC 5381244. PMID 28202408.
- ^ a b Michael GE, O'Connor RE (February 2011). "The diagnosis and management of seizures and status epilepticus in the prehospital setting". Emergency Medicine Clinics of North America. 29 (1): 29–39. doi:10.1016/j.emc.2010.08.003. PMID 21109100.
- ^ Wheless JW, Willmore J, Brumback RA (2009). Advanced therapy in epilepsy. Shelton, Conn.: People's Medical Pub. House. p. 144. ISBN 978-1-60795-004-2.
- ^ Nevitt SJ, Marson AG, Tudur Smith C (July 2019). "Carbamazepine versus phenytoin monotherapy for epilepsy: an individual participant data review". The Cochrane Database of Systematic Reviews. 2019 (7): CD001911. doi:10.1002/14651858.CD001911.pub4. PMC 6637502. PMID 31318037.
- ^ Nevitt SJ, Marson AG, Weston J, Tudur Smith C (August 2018). "Sodium valproate versus phenytoin monotherapy for epilepsy: an individual participant data review". The Cochrane Database of Systematic Reviews. 2018 (8): CD001769. doi:10.1002/14651858.CD001769.pub4. PMC 6513104. PMID 30091458.
- ^ Powell G, Saunders M, Rigby A, Marson AG (9 December 2016). "Immediate-release versus controlled-release carbamazepine in the treatment of epilepsy". Cochrane Database of Systematic Reviews. 2017 (4): CD007124. doi:10.1002/14651858.CD007124.pub5. PMC 6463840. PMID 27933615.
- ^ Nevitt SJ, Sudell M, Cividini S, Marson AG, Tudur Smith C (April 2022). "Antiepileptic drug monotherapy for epilepsy: a network meta-analysis of individual participant data". The Cochrane Database of Systematic Reviews. 2022 (4): CD011412. doi:10.1002/14651858.CD011412.pub4. PMC 8974892. PMID 35363878.
- ^ Ilangaratne NB, Mannakkara NN, Bell GS, Sander JW (December 2012). "Phenobarbital: missing in action". Bulletin of the World Health Organization. 90 (12): 871–871A. doi:10.2471/BLT.12.113183. PMC 3524964. PMID 23284189.
- ^ Shorvon S, Perucca E, Engel Jr J, eds. (2009). The treatment of epilepsy (3rd ed.). Chichester, UK: Wiley-Blackwell. p. 587. ISBN 978-1-4443-1667-4. Archived from the original on 21 May 2016.
- ^ a b c d e f Perucca P, Gilliam FG (September 2012). "Adverse effects of antiepileptic drugs". The Lancet. Neurology. 11 (9): 792–802. doi:10.1016/S1474-4422(12)70153-9. PMID 22832500.
- ^ a b c d National Clinical Guideline Centre (January 2012). The Epilepsies: The diagnosis and management of the epilepsies in adults and children in primary and secondary care (PDF). National Institute for Health and Clinical Excellence. pp. 57–83. Archived (PDF) from the original on 16 December 2013.
- ^ a b c d Bromley R, Adab N, Bluett-Duncan M, Clayton-Smith J, Christensen J, Edwards K, et al. (August 2023). "Monotherapy treatment of epilepsy in pregnancy: congenital malformation outcomes in the child". The Cochrane Database of Systematic Reviews. 2023 (8): CD010224. doi:10.1002/14651858.CD010224.pub3. PMC 10463554. PMID 37647086.
- ^ a b Kamyar M, Varner M (June 2013). "Epilepsy in pregnancy". Clinical Obstetrics and Gynecology. 56 (2): 330–341. doi:10.1097/GRF.0b013e31828f2436. PMID 23563876.
- ^ Lawrence S. Neinstein, ed. (2008). Adolescent health care: a practical guide (5th ed.). Philadelphia: Lippincott Williams & Wilkins. p. 335. ISBN 978-0-7817-9256-1.
- ^ "American Epilepsy Society Choosing Wisely". www.choosingwisely.org. 14 August 2018. Retrieved 30 August 2018.
- ^ Tsou AY, Kessler SK, Wu M, Abend NS, Massey SL, Treadwell JR (3 January 2023). "Surgical Treatments for Epilepsies in Children Aged 1–36 Months: A Systematic Review". Neurology. 100 (1): e1 – e15. doi:10.1212/WNL.0000000000201012. PMC 9827129. PMID 36270898.
- ^ a b Krucoff MO, Chan AY, Harward SC, Rahimpour S, Rolston JD, Muh C, et al. (December 2017). "Rates and predictors of success and failure in repeat epilepsy surgery: A meta-analysis and systematic review". Epilepsia. 58 (12): 2133–2142. doi:10.1111/epi.13920. PMC 5716856. PMID 28994113.
- ^ Benoit PW, Yagiela A, Fort NF (February 1980). "Pharmacologic correlation between local anesthetic-induced myotoxicity and disturbances of intracellular calcium distribution". Toxicology and Applied Pharmacology. 52 (2): 187–198. Bibcode:1980ToxAP..52..187B. doi:10.1016/0041-008x(80)90105-2. PMID 7361318.
- ^ a b c d e Duncan JS (April 2007). "Epilepsy surgery". Clinical Medicine. 7 (2): 137–142. doi:10.7861/clinmedicine.7-2-137. PMC 4951827. PMID 17491501.
- ^ Birbeck GL, Hays RD, Cui X, Vickrey BG (May 2002). "Seizure reduction and quality of life improvements in people with epilepsy". Epilepsia. 43 (5): 535–538. doi:10.1046/j.1528-1157.2002.32201.x. PMID 12027916.
- ^ Edwards CA, Kouzani A, Lee KH, Ross EK (September 2017). "Neurostimulation Devices for the Treatment of Neurologic Disorders". Mayo Clinic Proceedings. 92 (9): 1427–1444. doi:10.1016/j.mayocp.2017.05.005. PMID 28870357.
- ^ a b c d e f Panebianco M, Rigby A, Marson AG (July 2022). "Vagus nerve stimulation for focal seizures". The Cochrane Database of Systematic Reviews. 2022 (7): CD002896. doi:10.1002/14651858.CD002896.pub3. PMC 9281624. PMID 35833911.
- ^ Treadwell JR, Wu M, Tsou AY (2022). Management of Infantile Epilepsies: A Systematic Review (Report). doi:10.23970/AHRQEPCCER252. PMID 36383706.
- ^ Maria BL, ed. (2009). Current management in child neurology (4th ed.). Hamilton, Ont.: BC Decker. p. 180. ISBN 978-1-60795-000-4. Archived from the original on 24 June 2016.
- ^ Verrotti A, Tocco AM, Salladini C, Latini G, Chiarelli F (November 2005). "Human photosensitivity: from pathophysiology to treatment". European Journal of Neurology. 12 (11): 828–841. doi:10.1111/j.1468-1331.2005.01085.x. PMID 16241971.
- ^ Tan G, Thornby J, Hammond DC, Strehl U, Canady B, Arnemann K, et al. (July 2009). "Meta-analysis of EEG biofeedback in treating epilepsy". Clinical EEG and Neuroscience. 40 (3): 173–179. doi:10.1177/155005940904000310. PMID 19715180.
- ^ Arida RM, Scorza FA, Scorza CA, Cavalheiro EA (March 2009). "Is physical activity beneficial for recovery in temporal lobe epilepsy? Evidences from animal studies". Neuroscience and Biobehavioral Reviews. 33 (3): 422–431. doi:10.1016/j.neubiorev.2008.11.002. PMID 19059282.
- ^ Arida RM, Cavalheiro EA, da Silva AC, Scorza FA (2008). "Physical activity and epilepsy: proven and predicted benefits". Sports Medicine. 38 (7): 607–615. doi:10.2165/00007256-200838070-00006. PMID 18557661.
- ^ Di Vito L, Naldi I, Mostacci B, Licchetta L, Bisulli F, Tinuper P (June 2010). "A seizure response dog: video recording of reacting behaviour during repetitive prolonged seizures". Epileptic Disorders. 12 (2): 142–145. doi:10.1684/epd.2010.0313. PMID 20472528.
- ^ Kirton A, Winter A, Wirrell E, Snead OC (October 2008). "Seizure response dogs: evaluation of a formal training program". Epilepsy & Behavior. 13 (3): 499–504. doi:10.1016/j.yebeh.2008.05.011. PMID 18595778.
- ^ Doherty MJ, Haltiner AM (January 2007). "Wag the dog: skepticism on seizure alert canines". Neurology. 68 (4): 309. doi:10.1212/01.wnl.0000252369.82956.a3. PMID 17242343.
- ^ a b c Michaelis R, Tang V, Wagner JL, Modi AC, LaFrance WC, Goldstein LH, et al. (October 2017). "Psychological treatments for people with epilepsy". The Cochrane Database of Systematic Reviews. 10 (10): CD012081. doi:10.1002/14651858.CD012081.pub2. PMC 6485515. PMID 29078005.
- ^ Stockings E, Zagic D, Campbell G, Weier M, Hall WD, Nielsen S, et al. (July 2018). "Evidence for cannabis and cannabinoids for epilepsy: a systematic review of controlled and observational evidence". Journal of Neurology, Neurosurgery, and Psychiatry. 89 (7): 741–753. doi:10.1136/jnnp-2017-317168. hdl:1959.4/unsworks_50076. PMID 29511052.
- ^ Cannabis derivative may reduce seizures in some severe drug-resistant epilepsies, but adverse events increase (Report). 26 June 2018. doi:10.3310/signal-000606.
- ^ "Press Announcements - FDA approves first drug comprised of an active ingredient derived from marijuana to treat rare, severe forms of epilepsy". www.fda.gov. 25 June 2018. Retrieved 4 October 2018.
- ^ "Archive of "Journal of Investigative Medicine High Impact Case Reports". – PMC". www.ncbi.nlm.nih.gov.
- ^ Cheuk DK, Wong V (May 2014). "Acupuncture for epilepsy". The Cochrane Database of Systematic Reviews. 2014 (5): CD005062. doi:10.1002/14651858.CD005062.pub4. PMC 10105317. PMID 24801225.
- ^ Ranganathan LN, Ramaratnam S (April 2005). "Vitamins for epilepsy". The Cochrane Database of Systematic Reviews (2): CD004304. doi:10.1002/14651858.CD004304.pub2. PMID 15846704.
- ^ Panebianco M, Sridharan K, Ramaratnam S (October 2017). "Yoga for epilepsy". The Cochrane Database of Systematic Reviews. 2017 (10): CD001524. doi:10.1002/14651858.CD001524.pub3. PMC 6485327. PMID 28982217.
- ^ a b Brigo F, Igwe SC, Del Felice A (August 2016). "Melatonin as add-on treatment for epilepsy". The Cochrane Database of Systematic Reviews. 2016 (8): CD006967. doi:10.1002/14651858.CD006967.pub4. PMC 7386917. PMID 27513702.
- ^ He LY, Hu MB, Li RL, Zhao R, Fan LH, He L, et al. (2021). "Natural Medicines for the Treatment of Epilepsy: Bioactive Components, Pharmacology and Mechanism". Frontiers in Pharmacology. 12: 604040. doi:10.3389/fphar.2021.604040. PMC 7969896. PMID 33746751.
- ^ Aguiar CC, Almeida AB, Araújo PV, de Abreu RN, Chaves EM, do Vale OC, et al. (2012). "Oxidative stress and epilepsy: literature review". Oxidative Medicine and Cellular Longevity. 2012: 795259. doi:10.1155/2012/795259. PMC 3403512. PMID 22848783.
- ^ a b c d e f g h i j k l m n o King A, Gerard EE (April 2022). "Contraception, fecundity, and pregnancy in women with epilepsy: an update on recent literature". Current Opinion in Neurology. 35 (2): 161–168. doi:10.1097/WCO.0000000000001039. PMC 9230745. PMID 35191408.
- ^ a b Reimers A, Brodtkorb E, Sabers A (May 2015). "Interactions between hormonal contraception and antiepileptic drugs: Clinical and mechanistic considerations". Seizure. 28: 66–70. doi:10.1016/j.seizure.2015.03.006. PMID 25843765.
- ^ "Enzyme-inducing antiepileptic drugs". NICE. May 2023. Retrieved 2 November 2023.
- ^ a b c Tomson T, Battino D, Bromley R, Kochen S, Meador K, Pennell P, et al. (December 2019). "Management of epilepsy in pregnancy: a report from the International League Against Epilepsy Task Force on Women and Pregnancy". Epileptic Disorders. 21 (6): 497–517. doi:10.1684/epd.2019.1105. hdl:11336/119061. PMID 31782407.
- ^ a b Kwan P (2012). Fast facts: epilepsy (5th ed.). Abingdon, Oxford, UK: Health Press. p. 10. ISBN 978-1-908541-12-3.
- ^ 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.
- ^ a b c Hitiris N, Mohanraj R, Norrie J, Brodie MJ (May 2007). "Mortality in epilepsy". Epilepsy & Behavior. 10 (3): 363–376. doi:10.1016/j.yebeh.2007.01.005. PMID 17337248.
- ^ a b c Shorvon S, Perucca E, Engel J, eds. (2009). The treatment of epilepsy (3rd ed.). Chichester, UK: Wiley-Blackwell. p. 28. ISBN 978-1-4443-1667-4. Archived from the original on 10 June 2016.
- ^ a b Bagary M (April 2011). "Epilepsy, antiepileptic drugs and suicidality". Current Opinion in Neurology. 24 (2): 177–182. doi:10.1097/WCO.0b013e328344533e. PMID 21293270.
- ^ Mula M, Sander JW (August 2013). "Suicide risk in people with epilepsy taking antiepileptic drugs". Bipolar Disorders. 15 (5): 622–627. doi:10.1111/bdi.12091. PMID 23755740.
- ^ a b Ryvlin P, Nashef L, Tomson T (May 2013). "Prevention of sudden unexpected death in epilepsy: a realistic goal?". Epilepsia. 54 (Suppl 2): 23–28. doi:10.1111/epi.12180. PMID 23646967.
- ^ Kløvgaard M, Sabers A, Ryvlin P (November 2022). "Update on Sudden Unexpected Death in Epilepsy". Neurologic Clinics. 40 (4): 741–754. doi:10.1016/j.ncl.2022.06.001. PMID 36270688.
- ^ Hirtz D, Thurman DJ, Gwinn-Hardy K, Mohamed M, Chaudhuri AR, Zalutsky R (January 2007). "How common are the "common" neurologic disorders?". Neurology. 68 (5): 326–337. doi:10.1212/01.wnl.0000252807.38124.a3. PMID 17261678.
- ^ Vos T, Allen C, Arora M, Barber RM, Bhutta ZA, Brown A, et al. (October 2016). "Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015". Lancet. 388 (10053): 1545–1602. doi:10.1016/S0140-6736(16)31678-6. PMC 5055577. PMID 27733282.
- ^ Espinosa-Jovel C, Toledano R, Aledo-Serrano Á, García-Morales I, Gil-Nagel A (March 2018). "Epidemiological profile of epilepsy in low income populations". Seizure. 56: 67–72. doi:10.1016/j.seizure.2018.02.002. PMID 29453113.
- ^ a b Sander JW (April 2003). "The epidemiology of epilepsy revisited". Current Opinion in Neurology. 16 (2): 165–170. doi:10.1097/00019052-200304000-00008. PMID 12644744.
- ^ a b c d e f g h Saraceno B, Avanzini G, Lee P, eds. (2005). Atlas: Epilepsy Care in the World. World Health Organization. ISBN 978-92-4-156303-1. Retrieved 21 October 2023.
- ^ Eadie MJ, Bladin PF (2001). A Disease Once Sacred: A History of the Medical Understanding of Epilepsy. John Libbey Eurotext. ISBN 978-0-86196-607-3.
- ^ "Epilepsy: An historical overview". World Health Organization. February 2001. Archived from the original on 30 October 2013. Retrieved 27 December 2013.
- ^ "Epilepsy: historical overview". World Health Organization. Archived from the original on 20 January 2011. Retrieved 20 March 2011.
- ^ a b Temkin O (1 March 1994). The Falling Sickness: A History of Epilepsy from the Greeks to the Beginnings of Modern Neurology. JHU Press. p. Section 1. ISBN 978-1-4214-0053-2.
- ^ Stol M (1993). Epilepsy in Babylonia. BRILL. p. 143. ISBN 978-90-72371-63-8.
- ^ Harding GF, Jeavons PM (1994). Photosensitive Epilepsy. Cambridge University Press. p. 2. ISBN 978-1-898683-02-5.
- ^ a b Jilek-Aall L (March 1999). "Morbus sacer in Africa: some religious aspects of epilepsy in traditional cultures". Epilepsia. 40 (3): 382–386. doi:10.1111/j.1528-1157.1999.tb00723.x. PMID 10080524.
- ^ "Epilepsy and its Management: A Review". ResearchGate. January 2012. Retrieved 22 February 2022.
- ^ Illes J (2011). Encyclopedia of Mystics, Saints & Sages. HarperCollins. p. 1238. ISBN 978-0-06-209854-2. Archived from the original on 11 January 2014.
Saint Valentine is invoked for healing as well as love. He protects against fainting and is requested to heal epilepsy and other seizure disorders. In northern Italy, epilepsy was once traditionally known as Saint Valentine's Malady.
- ^ a b c Lewis E (17 February 2012). Report of The Trial and Conviction of John Haggerty, for The Murder of Melchoir Fordney, Late of The City of Lancaster, Pennsylvania. Gale, Making of Modern Law. p. 62. ISBN 978-1-275-31136-7.
- ^ Caravati EM (2004). Medical toxicology (3rd ed.). Philadelphia [u.a.]: Lippincott Williams & Wilkins. p. 789. ISBN 978-0-7817-2845-4.
- ^ a b de Boer HM (December 2010). "Epilepsy stigma: moving from a global problem to global solutions". Seizure. 19 (10): 630–636. doi:10.1016/j.seizure.2010.10.017. PMID 21075013.
- ^ Erkal E, Kiyak E, Uren Y, Milanlioglu A (October 2024). "Determination of stigma and attitude in relatives of patients with epilepsy". Seizure: European Journal of Epilepsy. 121: 64–69. doi:10.1016/j.seizure.2024.07.022. PMID 39089140.
- ^ 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.
- ^ Pellinen J, Tafuro E, Yang A, Price D, Friedman D, Holmes M, et al. (December 2020). "Focal nonmotor versus motor seizures: The impact on diagnostic delay in focal epilepsy". Epilepsia. 61 (12): 2643–2652. doi:10.1111/epi.16707. PMID 33078409.
- ^ a b c d Engel J, Pedley TA, eds. (2008). Epilepsy: a comprehensive textbook (2nd ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 2279. ISBN 978-0-7817-5777-5.
- ^ Bor R (2012). Aviation Mental Health: Psychological Implications for Air Transportation. Ashgate Publishing. p. 148. ISBN 978-1-4094-8491-2.
- ^ a b "Seizure Disorders". Transport Canada. Government of Canada. Archived from the original on 30 December 2013. Retrieved 29 December 2013.
- ^ Wilner AN (2008). Epilepsy 199 answers: a doctor responds to his patients' questions (3rd ed.). New York: Demos Health. p. 52. ISBN 978-1-934559-96-3. Archived from the original on 17 May 2016.
- ^ "Guide for Aviation Medical Examiners". Federal Aviation Administration. Archived from the original on 17 October 2013. Retrieved 29 December 2013.
- ^ a b "National PPL (NPPL) Medical Requirements". Civil Aviation Authority. Archived from the original on 16 October 2013. Retrieved 29 December 2013.
- ^ Drivers Medical Group (2013). "For Medical Practitioners: At a glance Guide to the current Medical Standards of Fitness to Drive" (PDF). p. 8. Archived (PDF) from the original on 30 December 2013. Retrieved 29 December 2013.
- ^ "Epilepsy Foundation of America – EFA". Healthfinder.gov. US Department of Health and Human Services. 28 April 2011. Archived from the original on 16 July 2014. Retrieved 28 July 2014.
- ^ Engel J, Pedley TA, eds. (2008). Epilepsy: a comprehensive textbook (2nd ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 2245. ISBN 978-0-7817-5777-5.
- ^ Aleem MA (February 2015). "World epilepsy day". Epilepsia. 56 (2): 168. doi:10.1111/epi.12814. PMID 25404065.
- ^ Perucca E (February 2015). "Commentary: why an international epilepsy day?". Epilepsia. 56 (2): 170–171. doi:10.1111/epi.12813. PMID 25403985.
- ^ Carr F (26 March 2018). "People Are Wearing Purple Today for Epilepsy Awareness Day. Here's What That Is". Time. Retrieved 18 April 2018.
- ^ a b Carney PR, Myers S, Geyer JD (December 2011). "Seizure prediction: methods". Epilepsy & Behavior. 22 (Suppl 1): S94-101. doi:10.1016/j.yebeh.2011.09.001. PMC 3233702. PMID 22078526.
- ^ Engel J, ed. (2008). Epilepsy: a comprehensive textbook (2nd ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 426. ISBN 978-0-7817-5777-5.
- ^ Guillemain, I., Kahane, P. & Depaulis, A. Animal models to study aetiopathology of epilepsy: what are the features to model? Epileptic Disord 14, 217–225 (2012).
- ^ Jarre, G., Guillemain, I., and, C. D. M. of S. & 2017. Genetic Models of Absence Epilepsy in Rats and Mice. Elsevier 455–471 (2017)
- ^ Depaulis, A. & Charpier, S. Pathophysiology of absence epilepsy: Insights from genetic models. Neurosci Lett 667, 53–65 (2018)
- ^ Morris G, Heiland M, Lamottke K, Guan H, Hill T, Zhou Y, et al. (January 2022). "BICS01 Mediates Reversible Anti-seizure Effects in Brain Slice Models of Epilepsy". Frontiers in Neurology. 12: 791608. doi:10.3389/fneur.2021.791608. PMC 8770400. PMID 35069421.
- ^ Jirsa VK, Stacey WC, Quilichini PP, Ivanov AI, Bernard C (August 2014). "On the nature of seizure dynamics". Brain. 137 (8): 2210–2230. doi:10.1093/brain/awu133. ISSN 1460-2156. PMC 4107736. PMID 24919973.
- ^ Chizhov AV, Zefirov AV, Amakhin DV, Smirnova EY, Zaitsev AV (31 May 2018). "Minimal model of interictal and ictal discharges "Epileptor-2"". PLOS Computational Biology. 14 (5): e1006186. Bibcode:2018PLSCB..14E6186C. doi:10.1371/journal.pcbi.1006186. ISSN 1553-7358. PMC 6005638. PMID 29851959.
- ^ "Epileptor-2 model".
- ^ Kegler A, Pascotini ET, Caprara AL, Arend J, Gabbi P, Duarte MM, et al. (February 2021). "Relationship between seizure type, metabolic profile, and inflammatory markers in blood samples of patients with epilepsy". Epileptic Disorders. 23 (1): 74–84. doi:10.1684/epd.2021.1236. PMID 33602662.
- ^ 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.
- ^ Panebianco M, Walker L, Marson AG, et al. (Cochrane Epilepsy Group) (October 2023). "Immunomodulatory interventions for focal epilepsy". The Cochrane Database of Systematic Reviews. 2023 (10): CD009945. doi:10.1002/14651858.CD009945.pub3. PMC 10577807. PMID 37842826.
- ^ Quigg M, Rolston J, Barbaro NM (January 2012). "Radiosurgery for epilepsy: clinical experience and potential antiepileptic mechanisms". Epilepsia. 53 (1): 7–15. doi:10.1111/j.1528-1167.2011.03339.x. PMC 3519388. PMID 22191545.
- ^ a b Thomas WB (January 2010). "Idiopathic epilepsy in dogs and cats". The Veterinary Clinics of North America. Small Animal Practice. 40 (1): 161–179. doi:10.1016/j.cvsm.2009.09.004. PMID 19942062.
- ^ Rundfeldt C, Löscher W (January 2014). "The pharmacology of imepitoin: the first partial benzodiazepine receptor agonist developed for the treatment of epilepsy". CNS Drugs. 28 (1): 29–43. doi:10.1007/s40263-013-0129-z. PMID 24357084.
- ^ van der Ree M, Wijnberg I (2012). "A review on epilepsy in the horse and the potential of Ambulatory EEG as a diagnostic tool". The Veterinary Quarterly. 32 (3–4): 159–167. doi:10.1080/01652176.2012.744496. PMID 23163553.
- ^ Ciosek J, Kimes A, Vinardell T, Miller DC, Antczak DF, Brooks S (23 August 2023). "Juvenile idiopathic epilepsy in Arabian horses is not a single-gene disorder". Journal of Heredity. 114 (5): 488–491. doi:10.1093/jhered/esad029. PMID 37145017.
Further reading
[edit]- Scheffer IE, Berkovic S, Capovilla G, Connolly MB, French J, Guilhoto L, et al. (April 2017). "ILAE classification of the epilepsies: Position paper of the ILAE Commission for Classification and Terminology". Epilepsia. 58 (4): 512–521. doi:10.1111/epi.13709. PMC 5386840. PMID 28276062.
- Programme for Neurological Diseases and Neuroscience (2005). Atlas, epilepsy care in the world, 2005. Global Campaign against Epilepsy; International League against Epilepsy. Geneva: Department of Mental Health and Substance Abuse, World Health Organization. ISBN 978-92-4-156303-1.
- Wilson JV, Reynolds EH (April 1990). "Texts and documents. Translation and analysis of a cuneiform text forming part of a Babylonian treatise on epilepsy". Medical History. 34 (2): 185–198. doi:10.1017/s0025727300050651. PMC 1036070. PMID 2187129.
External links
[edit]- "Epilepsy Basics: An Overview for Behavioral Health Providers". YouTube. Epilepsy Foundation. 30 May 2019. Archived from the original on 11 December 2021.
- "What To Do If Someone Has A Seizure – First Aid Training – St John Ambulance". YouTube. St John Ambulance. 1 February 2017. Archived from the original on 11 December 2021.
- World Health Organization fact sheet