Posts Tagged Epilepsy

[WEB SITE] Canceling Is Kindness: Keeping Safe From COVID-19 With Epilepsy

Those of us living with pre-existing health conditions like epilepsy have likely felt the impact of COVID-19. Medical appointments may have been rescheduled or switched to virtual, work and school may be closed, and we may worry about how the illness will impact ourselves and our loved ones.

Fortunately, social distancing is a powerful tool to slow or prevent the spread of infection. Social distancing only works when everyone stays home and limits their contact with others.

When Friends or Family Aren’t Worried

Some of us have family members or friends who think the threat of the virus is being blown out of proportion. They may pressure you to join in activities as usual or become upset when you cancel plans to help keep yourself and your community safe during this high-risk time.

Here are some tactics that may help you talk to them about why health — yours, theirs, and the community’s — should be everyone’s first priority right now.

Have a Heart-to-Heart

Ask them to walk in your shoes. Ask them to imagine what you must be going through. Maybe your loved one thinks they will be fine, but you may be more vulnerable to being severely impacted by it. Individuals with neurological conditions like epilepsy may be at increased risk for COVID-19 complications. Speak with your doctor to understand your particular risk.

If your doctors have canceled or modified your appointments, share how your medical care is being affected. If your health care provider has recommended any additional precautions you should take, share that as well.

Show Them the Numbers

According to research on COVID-19 in China, people who had one additional disease — from diabetes to cardiovascular disease to cancer — had a 79 percent higher risk of requiring intensive care, needing a respirator, or dying as a result of the coronavirus infection.

Six in 10 adults in America have at least one chronic illness.

Put It Into Perspective

The threat of COVID-19 was deemed serious enough to affect major institutions:

  • Walt Disney World and Disneyland are closed. These attractions have previously only closed for disasters such as the assassination of President John F. Kennedy or the terrorist attacks on September 11, 2001.
  • Las Vegas Strip casinos including Bellagio, MGM Grand, The Mirage, Wynn Las Vegas, and Wynn Encore are closing.
  • The NBA has suspended the professional basketball season.
  • MLB has ended its training season and pushed back the start of baseball season at least two weeks.
  • The 2020 Summer Olympics may be canceled or postponed.

These organizations are prioritizing public health over the hundreds of millions of dollars (or more) they will lose by closing. If we can stay home, we should stay home.

Use Peer Pressure

If you have any other friends or family who are taking the coronavirus threat seriously, ask them to talk to that loved one on your behalf. Social distancing only works if everyone is on board.

Distance Doesn’t Mean Isolation

As our families, communities, and countries make it through this pandemic together, it’s more important than ever to find ways to stay connected. Here are a few suggestions for ways to socialize from a safe distance.

  • Phone calls. Being stuck at home is a great time to call people and catch up.
  • Video gatherings. FaceTime and apps like Zoom or Skype can allow you to see and hear each other, no matter how distant, on mobile phone, tablet, or computer. You can even have a party with dozens of people on screen.
  • Gaming apps. Many mobile gaming apps allow you to connect and play with friends remotely.
  • Movie night. Cue up the same movie or show (whether on a streaming service or a DVD you both have) and stay on the phone or on video chat the whole time. You can even plan to eat the same snack while you watch and talk.
  • Listening party. Music apps, such as Spotify, allow people to share music playlists and even collaborate to create lists of songs.

MyEpilepsyTeam is another way our community of 81,000 members living with seizures stays strong together. Here are a few conversations about how members of MyEpilepsyTeam are getting through this difficult time:

Have you found ways to talk to your loved ones about COVID-19 safety measures? What are you doing to stay connected to others during this time of heightened concern and social distancing? Share in the comments below or post on MyEpilepsyTeam.

via Canceling Is Kindness: Keeping Safe From COVID-19 With Epilepsy | MyEpilepsyTeam

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[WEB SITE] You’ve Just Been Diagnosed With Epilepsy. Now What?


We all respond differently to information about our health. After learning you have epilepsy, you might be stunned, scared, or even relieved to have a diagnosis that explains your seizures. No matter what you’re feeling, you’re not alone. On MyEpilepsyTeam, there are thousands of others who have been in your shoes.

You can’t figure out everything about epilepsy at once, and you don’t need to. Taking small steps to adjust to your new reality can be empowering in a time of major change. According to the American Psychological Association, active coping strategies like getting organized and making a plan for managing your health can improve mental and emotional well-being.

Create Space for Epilepsy
It’s normal to feel out of control when you first learn you have epilepsy. You may have a pile of pamphlets crowding your kitchen table and a head full of questions that you forget the moment you set foot in a doctor’s office. You can begin to tame the chaos by implementing very simple organizational techniques that will help you create space for this new aspect of your life.

Put Everything in One Place
Storing all of your printed doctor’s visit summaries, pamphlets about epilepsy, and other resources in a designated spot can help create some order and help you find information when you need it. You don’t need a fancy filing system – a kitchen drawer, an old binder, or simply an orderly stack on your bedside table can make a big difference. In addition to helping you keep track of important papers, there is evidence that controlling clutter is associated with better moods.

Remember Your Questions
Keep a list of questions about epilepsy for your healthcare provider in a dedicated notebook or on your smartphone. Jot down your questions as you think of them and bring your list to your appointments so you can remember your questions and write down the answers.

Manage Your Appointments
If you already rely on a digital calendar or paper planner to manage work and family obligations, stick with that method for managing your new doctor’s visits. If keeping a calendar is new to you, consider using what you’ve already got at home, such as a grocery list notepad or a piece of paper and a magnet on the fridge. You can also ask your doctor’s office about phone call or text message reminders that can help you keep on top of appointments.

Track Your Medications
Using an old-fashioned pill organizer is a great way to keep track of oral medications. You can also use a paper medication tracker. If you’re comfortable using a smartphone, consider downloading a medication tracking app.

Reach Out for Support
It can feel overwhelming to reach out after receiving an epilepsy diagnosis, but you don’t have to face your diagnosis alone. Support from loved ones, your medical team, and other people with epilepsy is crucial as you embark on treatment and adjust to your new normal. There are a few basic steps you can take to start building your network of support.

Epilepsy Communities
You may not be ready to talk about your diagnosis with your loved ones right away. You may also not have time or be comfortable joining an in-person support group. That’s ok. Connecting with members on MyEpilepsyTeam can be a first step towards finding support. Your community on MyEpilepsyTeam can provide an ongoing emotional boost whenever you feel worried or overwhelmed about life with epilepsy or want to celebrate a victory.

Healthcare Providers
Many hospitals and medical practices offer resources that extend beyond your medical appointments. These may include chaplaincy services, health education classes, patient liaisons or nurse navigators, on-site support groups, and referrals to other services.

Friends and Family
Sharing your epilepsy diagnosis with friends and family can be hard. They may be afraid and struggle to react in a helpful way. Try to remember that everyone is doing their best with difficult news. If you’re able, let your loved ones know how they can be most helpful to you during this time, whether that’s helping with household chores or offering a listening ear.

Learn More About Epilepsy
You might not have known much about epilepsy before your diagnosis, but now you probably want to learn more. Your healthcare provider is a great resource for information, but you may also want to do your own research. Remember to be cautious of what you read online, especially if someone is offering a quick fix or selling a cure. You can always reach out to your healthcare provider or patient liaison if you have questions about something you’ve read.

Here are a few resources to get you started:

You never have to feel alone when you’re living with epilepsy. Members on MyEpilepsyTeam are always available to answer questions and offer encouragement when things get rough.

Here are some conversations from MyEpilepsyTeam members about facing a new diagnosis:

If you have a pressing question, you can go straight to the Q+A section.
You can also read more about how to get started on MyEpilepsyTeam.

For the newly diagnosed, what information are you seeking?
For the epilepsy veterans, what do you wish you knew when you were first diagnosed?
Share in the comments below or directly on MyEpilepsyTeam.


via You’ve Just Been Diagnosed With Epilepsy. Now What? | MyEpilepsyTeam

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[BLOG POST]What is epilepsy? A neurological disorder that causes seizures. – NARIC

According to the Mayo Clinicepilepsy is a “central nervous system (neurological) disorder in which brain activity becomes abnormal causing seizures or periods of unusual behavior, sensations, and sometimes loss of awareness.” Anyone can develop epilepsy and it affects all genders, races, ethnic backgrounds, and ages. Symptoms can vary widely, from staring blankly for a few seconds during a seizure to twitching of arms or legs, and may include temporary confusion, loss of consciousness or awareness, and psychiatric symptoms such as fear or anxiety. Epilepsy has no identifiable cause in about half the people with the condition. For the other half of the population with epilepsy, the condition may be traced to various factors, including genetic influence, head trauma, brain conditions, infectious diseases, prenatal injury, or developmental disorders. There are certain risk factors that may increase a person’s risk of epilepsy, which include age, family history, head injuries, dementia, and stroke and other vascular diseases.

To diagnose a person with epilepsy, a doctor will review their symptoms and medical history, along with ordering a neurological exam and blood tests. They may also suggest other tests to detect brain abnormalities, such as electroencephalograms (EEG), computerized tomography (CT) scans, a magnetic resonance imaging (MRI) scan, and/or a functional MRI. An accurate diagnosis of a person’s seizure type and where seizures begin gives the best chance for finding an effective treatment. Doctors may begin treatment of epilepsy with medications, which may help people become seizure-free. For some people, medications may not treat their epilepsy and their doctor may suggest surgery or different types of therapies, such as vagus nerve stimulation, a ketogenic diet, or deep brain stimulation.

Researchers continue to study epilepsy and are studying many potential new interventions for epilepsy, including responsive neurostimulation and minimally invasive surgery. During the last 28 years, NIDILRR has funded several projects to study the impact of epilepsy and develop and test interventions, including a currently funded project that is studying a home-based self-management and cognitive training program to improve the quality of life for people with refractory epilepsy.  NARIC’s information specialists searched REHABDATA and found over 1,500 research articles, book chapters, and factsheets related to epilepsy from the NIDILRR community and beyond. If you have any questions about epilepsy or would like assistance in conducting your own search in NARIC’s databases, contact NARIC’s information specialists for more information.

Please note: This article provides basic information and is not intended to diagnose or recommend interventions for epilepsy. If you believe you have experienced a seizure, seek medical advice from a qualified primary care provider or specialist.

via What is epilepsy? A neurological disorder that causes seizures. | Collection Spotlight from the National Rehabilitation Information Center

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[ARTICLE] Basic and clinical role of vitamins in epilepsy – Full Text PDF


Background & Aims: Epilepsy is a brain disorder which affects about 50 million people worldwide. Good diet is an essential measure to controlling seizure attacks. Since some combination therapy can reduce epileptogenesis, therefore this review summarizes the available evidences about the application of vitamins in animal models and humans for understanding what specific combinations of antiepileptic drugs and vitamins are likely to be effective for epilepsy therapy.

Material and methods: In this review, electronic databases including PubMed and Google Scholar were searched for monotherapy and polytherapy by vitamins.

Results: Administration of vit A inhibits development of seizures and lethality in animal models. Also vitamins B1, B6 and B12 pretreatment might lead to a protective effect against degenerative cellular in mice. In addition use of low dose of sodium valproate with vitamins C or E increase the anticonvulsant activity of the drug in mice. Moreover, Vitamin D enhances antiepileptic effects of lamotrigine, phenytoin and valproate in animal’s models. Vitamin E has an anticonvulsant effect in ferrous chloride seizures, hyperbaric oxygen seizures as well as penicillin-induced seizures in contrast kindling, maximal electroshock and kainite models. Some researches demonstrated that vitamins D and B as adjunctive therapy in epileptic patient can relieve seizures. A clinical data have shown beneficial effects of vitamin E in raising total antioxidant capacity, catalase, and glutathione in patients with uncontrolled epilepsy. Only few clinical studies exist to support the efficacy of the vitamin A and K in epilepsy.

Conclusion: However vitamin therapy is not a substitute for antiepileptic drugs but add on therapy by them may relieve drugs-induced deficiencies as well as more researches are needed to evaluate the effectiveness of vitamins in epileptic humans.


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[WEB PAGE] Types of Epilepsy | MyEpilepsyTeam


Article written by Kelly Crumrin

Epilepsy is a spectrum of neurological disorders that involve recurring seizures caused by abnormal electrical activity in the brain. Diagnosing the specific type of epilepsy helps you and your doctor better know what to expect regarding seizure progression, any challenges in learning and physical development, and which treatments will be most effective.

Each type of epilepsy involves specific types of seizures and other symptoms.

Localized epilepsies and syndromes

Some types of epilepsy are referred to as localized, which means they are known by the location in the brain where seizures originate. A related term is focal epilepsy, which indicates seizures that have abnormal electrical activity focused in one area of the brain. Other types of epilepsy are known as syndromes, or collections of specific signs and symptoms that point to a certain medical condition. Each type of epilepsy has unique characteristics. Some syndromes are considered benign, meaning children will eventually become seizure-free with age, while other types of epilepsy are lifelong conditions.

Temporal lobe epilepsy (TLE)

Approximately 60 percent of people with epilepsy have temporal lobe epilepsy (TLE), or seizures that originate in the temporal lobe of the brain. The temporal lobe is located on the sides of the brain, near the ears, and is responsible for processing sound and language as well as memories relating to sound and vision. About one-third of TLE or other cases of focal epilepsy are resistant to anti-epileptic drugs (AEDs). Surgery may be recommended, and vagus nerve stimulation may also be therapeutic.

TLE usually develops between late adolescence and early adulthood, often after a head injury or febrile (fever-induced) seizure. For women with TLE, hormonal changes during the menstrual cycle can increase seizure activity. Focal onset seizures are most common for people with TLE, though some people may experience prolonged seizures or, in rare circumstances, status epilepticus. Read more about seizure types and symptoms.

Frontal lobe epilepsy (FLE)

Frontal lobe epilepsy is the second most common form of focal epilepsy after TLE. FLE may be inherited, or it may be caused by a structural problem such as a birth defect, an abnormal blood vessel, trauma, or scaring caused by infection. In about 50 percent of FLE cases, no cause is ever determined.

The frontal lobes of the brain are large, and some of its functions include reasoning, paying attention, regulating emotion, organizing, and solving problems. Researchers have not discovered the functions of many areas. It is possible for a seizure to begin in the frontal lobe and proceed without symptoms before spreading to other parts of the brain, leading to a tonic-clonic seizure. FLE seizure symptoms can vary widely, depending on the function of the affected part of the lobe. Learn more about seizure symptoms and types.

FLE is usually responsive to medications, but in cases where AEDs are ineffective, surgery or vagus nerve stimulation may help.

Occipital lobe epilepsy and parietal lobe epilepsy

Epilepsy that originates in the occipital and parietal lobes is much less common than TLE and FLE. Seizures that begin in these lobes are usually idiopathic – of unknown cause. The occipital lobe is in the back of the brain and is primarily responsible for vision. The parietal lobe is located on the top and upper sides of the head and is known as the “association cortex” because it is where perception becomes reality. Sounds are recognized as words, visual images are created, and touch becomes associated with an object.

In both types of epilepsy, AEDs are the first treatment option. If medication fails, surgery may be recommended.

Panayiotopoulos syndrome (PS)

Also known as early onset occipital epilepsy, PS commonly begins in early childhood. Typically, onset is between the ages of 3 and 10. PS affects boys and girls equally, and it is idiopathic (cause unknown). As many as 6 percent of children who have nonfebrile (not caused by fever) seizures have PS. PS frequently stops two to three years after the first seizure.

Children with PS will have focal seizures that can spread to a generalized seizure. Seizures in PS often last 20 to 60 minutes, and more than half occur during sleep. Pale skin, a sick feeling, and vomiting are typical symptoms during a PS seizure. Some children may also have tonic-clonic movements. Read more about types of seizures.

If seizures are infrequent, medication may not be needed. However, if they are needed, AEDs are usually effective at controlling PS seizures. Neurologists often teach parents how to initiate rescue therapy and create an emergency plan for children with PS.

Benign rolandic epilepsy (BRE)

Also known as benign epilepsy with centrotemporal spikes (BECTS), BRE usually begins around ages 6 to 8. Boys are slightly more likely to have BRE than girls. BRE accounts for approximately 15 percent of all epilepsies in children.

Benign rolandic epilepsy is characterized by numbness, twitching, or tingling of the face or tongue. Seizures may inhibit speech and cause drooling. The child remains conscious during the seizure. Seizures are not frequent and occur mostly at night. AEDs may be prescribed if the seizures happen during the day or disrupt sleep, but many children do not need medication. Seizures stop by early adolescence in almost all children with BRE.

Generalized epilepsies and syndromes

In contrast to localized types of epilepsy discussed above, generalized types of epilepsy feature seizures that do not originate, or do not remain confined, in one lobe or area of the brain. Generalized epileptic syndromes tend to be idiopathic – of unknown cause. Idiopathic generalized epilepsies account for one-third of epilepsy cases.

Juvenile myoclonic epilepsy (JME)

JME, also known as Janz syndrome, begins between the ages of 8 and 26, but most commonly between the ages of 12 and 16. Absence seizures may be the first type of seizure most people with JME experience, although this type happens less often. Mild myoclonic seizures, generalized tonic-clonic (GTC), or clonic-tonic-clonic seizures (GTC seizures that begin with a clonic phase) seizures are the most common types. Myoclonic seizures tend to occur immediately upon waking in the morning. Photosensitivity – seizures triggered by flashing or flickering light – affects 40 percent of people with JME. Photosensitive seizures usually show on an electroencephalography (EEG) test. Read more about seizure types.

Most cases of juvenile myoclonic epilepsy are treatable with AEDs. Most people with JME need to remain on medication for life.

Childhood absence epilepsy (CAE)

CAE accounts for 2 to 8 percent of childhood epilepsy. Childhood absence epilepsy typically begins between the ages of 3 and 11, most frequently between ages 5 and 8. One-third of children with CAE have a family history of seizures, suggesting that the cause may be genetic. Siblings of children with CAE have a 1-in-10 chance of developing epilepsy.

Children with CAE experience absence seizures (formerly known as petit mal seizures). The child is not aware or responsive during seizures, and may stare, blink, or roll their eyes up. You may notice a chewing motion or other repetitive movements. Seizures last about 10 seconds, after which the child immediately returns to normal. The child is usually not aware they have had a seizure. Seizures may be infrequent or happen as often as 100 times a day. One-third of children with CAE have concentration and memory problems before seizures start; these issues often improve after AEDs are started. Rarely, children who have very frequent seizures may develop learning difficulties.

If AEDs are not effective, the ketogenic diet may help children with CAE. At least two-thirds of children with CAE respond to treatment, and their seizures will cease by mid-adolescence. However, 10 to 15 percent of children with CAE will develop other seizure types during adolescence – typically myoclonic seizures, generalized tonic-clonic seizures, or both. Read more about seizure types.

Juvenile absence epilepsy (JAE)

JAE is similar to childhood absence epilepsy; however, it starts later in childhood (generally between ages 9 and 13) and is usually a lifelong condition. Two percent of people with epilepsy have juvenile absence epilepsy (JAE). Although it is rare to have a family history of seizures, the cause of JAE is thought to be genetic.

People with JAE experience absence seizures lasting from 10 to 45 seconds. Seizures may happen infrequently or 100 times a day. Seizures often happen during exercise. Seventy-five percent of those with JAE will also have tonic-clonic seizures. The risk of absence status epilepticus (also known as nonconvulsive status epilepticus), in which seizures can last minutes or even hours, is higher in people with JAE.

Children with JAE generally develop normally, though they may experience learning difficulties if they have frequent seizures. One-third of children with JAE have concentration and memory problems before seizures start; these issues often improve after AEDs are started. AEDs work well to treat JAE and must be taken for life.

Lennox-Gastaut syndrome (LGS)

LGS is an uncommon epilepsy syndrome; between 2 and 5 percent of children with epilepsy have LGS. Lennox-Gastaut syndrome often starts between the ages of 3 and 5. Atonic seizures, also known as drop attacks, are most common in children with Lennox-Gastaut syndrome (LGS). Seizures may happen multiple times a day and cause the child to suddenly drop to the ground. Drop attacks may be perceived as a trip or the result of poor balance. Injuries are common, making the seizures very upsetting for the child. Atypical absence seizures and tonic seizures are also common, especially at night, but children with LGS may experience other types of seizures as well.

LGS is very difficult to treat and is often referred to as intractable or refractory. Some AEDs can be effective, and the ketogenic diet may help. Surgery may be recommended if diet and medication do not work, though surgical treatment will not stop the seizures altogether.

Children with LGS have moderate to severe learning difficulties, with some children exhibiting developmental delays before their first seizure. Twenty percent of children who have West syndrome (infantile spasms) will develop LGS.

Progressive myoclonic epilepsies

The progressive myoclonic epilepsies are a group of rare syndromes characterized by a combination of tonic-clonic and myoclonic seizures. Disorders that fall under this category include Lafora disease, mitochondrial encephalopathies, severe myoclonic epilepsy of infancy (also referred to as Dravet syndrome), and Unverricht-Lundborg disease (also known as Baltic myoclonus). The cause is often hereditary but may be unknown. Progressive myoclonic epilepsies affect males and females equally and start at different ages, depending on the specific condition. Read more about seizure types.

In progressive myoclonic epilepsies, seizures are difficult to control. As the condition progresses, people with PME accumulate cognitive (relating to thinking and memory) and motor (relating to movement) disabilities.

Medications may be successful at first, but effectiveness declines over months or years as the disease progresses.

Other epilepsy syndromes

Epilepsy is a broad spectrum involving dozens of neurological disorders. While those described above are the most commonly diagnosed, there are many other syndromes that cause epilepsy. Examples include Angelman syndrome, Doose syndrome (myoclonic astatic epilepsy), Dravet syndrome, neurocutaneous syndromes (such as Sturge-Weber syndrome), Rasmussen’s syndrome, and Rett syndrome.


External resources

MyEpilepsyTeam resources

via Types of Epilepsy | MyEpilepsyTeam

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[ARTICLE] Epilepsy Benchmarks Area I: Understanding the Causes of the Epilepsies and Epilepsy-Related Neurologic, Psychiatric, and Somatic Conditions – Full Text


The 2014 NINDS Benchmarks for Epilepsy Research included area I: Understand the causes of the epilepsies and epilepsy-related neurologic, psychiatric, and somatic conditions. In preparation for the 2020 Curing Epilepsies Conference, where the Benchmarks will be revised, this review will cover scientific progress toward that Benchmark, with emphasize on studies since 2016.

Introductory Vignette by Lizbeth Carmichael. Epilepsy, Depression, and SUDEP—A Parent’s Perspective

My son John developed epilepsy in his late teens, and despite medications, his seizures remained severe and uncontrolled. John was a talented and creative musician and a caring and thoughtful brother and son. He had many friends, and he desperately wanted an independent life. As John’s epilepsy progressed, he also experienced declining mental health. John, who was normally a very peaceful individual, had periods of severe irritability and rage. He also became very anxious at times, and this was a sign of an impending seizure. John heard voices and developed paranoia, hallucinations, and depression. Our family was told to see specialists, but we found that the communication and coordination of care between epileptologists and mental health professionals was impossible, even when he was hospitalized and referrals were made. Ultimately, his mental health issues were not understood or addressed and contributed significantly to his decline. John died of sudden unexpected death in epilepsy (SUDEP) in 2012. Our family’s wish is that those around John had been more attuned to the mental health comorbidities that he was experiencing, and that his medical issues were jointly managed as the outcome for him might have been different.

Significant comorbidities often accompany epilepsy and can be more debilitating than the seizures themselves. A better understanding of the underlying mechanisms of epilepsy-associated comorbidities and appropriate clinical care is critical for increased quality of life for those impacted by epilepsy and their families.

Lizbeth Carmichael. Forever John’s Mom. Citizens United for Research in Epilepsy (CURE).


In this review, we provide an update on preclinical and clinical advances into our understanding of the many etiologies of the epilepsies, as well as progress in assigning etiology to epilepsy-related neuropsychiatric and somatic comorbidities. Since the most recent summary in this area,1 expansion in our knowledge of epilepsy genetics and autoimmune epilepsies has continued to result in fewer individuals being labeled with epilepsy of unknown etiology. With the advent of next-generation sequencing technologies, the number of “epilepsy genes” continues to expand. Assigning a causative role to such genes requires verification in not only larger cohorts with statistical rigor but also a number of criteria that take into account normal variation, determination of how a genetic change leads to altered molecular function, and the demonstration of an epilepsy or epilepsy-related phenotype in genetically manipulated model organisms.2 Similar considerations apply for autoimmune epilepsies, for which the relative epileptogenic effects of T-cell infiltration and circulating antibodies continue to be clarified.

Preclinical models of genetic, autoimmune, and brain injury-related epilepsies have been essential to advance our knowledge into upstream and downstream cellular and neurophysiological perturbations that may promote hypersynchrony and the transition to the ictal state. It is only with this type of knowledge that we will be able to better inform treatment of epilepsy related to these types of epilepsy. Incomplete penetrance and variable phenotypes in both humans and animal models strongly implicate genetic modifiers of susceptibility, which need to be identified and validated so as to appreciate mechanisms by which epilepsy may be therapeutically modulated.

In parallel with efforts to address the causes of epilepsy and epileptogenesis, there has been an expansion in efforts designed to unravel the genesis of epilepsy’s various psychiatric comorbidities. Generally, these are etiologically related to broad network dysfunction that may be secondary to the underlying epileptogenic lesion (genetic, structural, or unknown) and actively modulated by the burden of ongoing seizures (if present) and antiseizure medications. Animal models of monogenic epilepsies provide the most tractable route to assigning etiology to epilepsy-associated comorbidities, albeit with some limitations in the ability to assess psychiatric comorbidities in various models. Incorporating optogenetic and chemogenetic strategies in these models affords the ability to definitively test whether specific network abnormalities affect seizure risk or impact limbic function or cognitive function or both.

We conclude our review with a set of general recommendations for future research into the causes of epilepsy spectrum disorders that will guide our understanding into epilepsy prevention (area II), treatment options (area III), and the adverse consequences of seizures themselves (area IV).

Key Advances in Area I

Epilepsy Genetics

Advances in our understanding of the genetics of the epilepsies have continued to accrue since the last Benchmarks update and have been reviewed in several excellent publications.36 Many new variants associated with epilepsy are identified as “de novo dominant,” meaning that they are present in the heterozygous state in sporadically affected individuals. At a cellular level, these genes encode proteins that display a broad range of functions that extend well beyond ion channels, including cell adhesion (eg, PCDH19), DNA binding and chromatin remodeling (eg, CHD2), and neurotransmitter release (eg, STXBP1).7 The importance of genetic etiologies in focal epilepsy in particular has become even more clear, with the involvement of DEPDC5 and associated GATOR1-complex mTOR repressors in epileptogenic cortical malformations being notable examples.8

De novo postzygotic (somatic) mutation has been increasingly recognized to play a role in focal epilepsy, largely involving the mTOR pathway in the pathogenesis of lesional epilepsies such as focal cortical dysplasia and hemimegalencephaly, with a majority of cases explained by this mechanism.911 Extending the discovery of somatic mutation to a new pathway and, interestingly, to both focal cortical dysplasia (type I) and nonlesional focal epilepsy was a report on mosaic variants in the gene SLC35A2, which encodes an UDP-galactose transporter previously associated in nonmosaic form with developmental and epileptic encephalopathy.12 The discovery of these 2 distinct pathways may point to very different targeted therapies after further study, which is promising but also demands attention to precision in classifying individuals with focal epilepsy and establishing a molecular diagnosis before pursuing experimental therapy.

Although most newly discovered pathogenic variants each seem to be causative in only a small number of individuals, taken together their combined impact is substantial. From the perspective of practicing epileptologists, we now benefit from a relatively high rate of identifiable genetic causes in neonatal and early childhood epilepsies, particularly in those individuals with comorbid intellectual disability, so that more routine usage of next-generation sequencing methods in this population may be warranted.13,14 Much more research is needed, however, to separate out the effects of seizures, genetic changes, and treatments on the intellectual impairments that are found in the epileptic encephalopathies.15

Animal models have permitted important insights into the specific mechanisms by which genetic aberrations may promote hyperexcitability. In additional to conventional “knockout” mice, mutants with conditional gene deletions (permitted via Cre-LoxP technology) have helped dissect the individual contributions of specific neuronal populations to seizure generation. For example, mice with a conditional deletion of Lgi1 in parvalbumin-positive interneurons alone are devoid of spontaneous seizures, while conditional deletions of Lgi1 in forebrain glutamatergic neurons result in frequent early-life seizures and premature death,16 just as in Lgi1 knockout mice.17 These results not only provide guidance to future gene replacement strategies but also show that while Lgi1 is an extracellularly secreted protein that is expressed in both GABAergic and glutamatergic neurons, restoring Lgi1 expression in glutamatergic neurons may be more likely to ameliorate seizures. The lack of spontaneous seizures in mice with heterozygous deletions of Lgi1 (recapitulating the haploinsufficiency of LGI1 mutation-related lateral temporal lobe epilepsy [TLE]) illustrates an important point with regard to gene dosage in animal models. Similar findings exist with other epilepsy genes, including KCNQ2,18 CDKL5,19 and DEPDC5. 20 Heterozygous DEPDC5 variants are found in cases of familial focal epilepsy as well as focal cortical dysplasia–associated epilepsy.20,21 Mice or rats with homozygous germ line deletions of Depdc5 had embryonic lethality,2224 which is itself etiologically nonspecific and may even reflect placental pathology.25 In contrast, rats with heterozygous deletions of Depdc5 do not display spontaneous seizures.24 Mice with a conditional brain-specific homozygous deletion of Depdc5 display extremely rare seizures, together with macrocephaly, impaired survival, and biochemical evidence of mTOR1 complex activation.22 Thus, it appears that for certain genetic variants strongly associated with epilepsy in humans, mice with corresponding gene deletions or transgenic “knock-ins” of variants seen in individuals with the specific epilepsy syndrome may not display spontaneous seizures or even reflex audiogenic seizures, a common expression of epilepsy in mice. This phenomenon may reflect the influences of variations in genetic background or fundamental differences in mechanisms of genetic epileptogenesis between mice and humans.

Confirming the epilepsy-inducing or epilepsy-modifying effects of specific variants may be greatly aided through the use of other vertebrate models, such as zebrafish (Danio rerio). Classically employed as a model to study embryology and development, zebrafish has now been adopted to study a variety of neurological disorders, including epilepsy. This species is amenable to exon deletion via homologous recombination, and specific single-nucleotide variants can be introduced via CRISPR-Cas9 technology.2628 As with mice, stereotyped spontaneous or induced seizures can be identified by video tracking and/or electroencephalography. The small size and rapid development of zebrafish also permit high-throughput drug screening29 that may be individualized to identify a treatment for a specific variant.30

Despite the impressive array of genetic advances, the translation of these findings into gene-related or pathway-based clinical treatments has had mixed results.31 There are genetic diagnoses for which specific antiepileptic therapies are either indicated or relatively contraindicated (eg, GLUT1 deficiency, pyridoxine dependency, SCN1A-related epilepsy), and mTOR inhibitors are now known to be at least partially effective for tuberous sclerosis complex–associated epilepsy.32 By contrast, the use of quinidine for KCNT1-related epilepsy, initially thought to be promising following the report of a single case,33 has not been shown to reduce seizure frequency in subsequent studies.34 Overall, these and other findings suggest that simply modulating a causative pathway featuring a rational drug target can lead to variable responses. More work is clearly necessary to bring genetic discoveries from the bench successfully to therapeutic application at the bedside.

Interneuronopathy-Related Epilepsies

Interneuronopathies can be broadly defined as those conditions in which epilepsy or neuropsychiatric comorbidities arise as a consequence of either developmental or functional changes in interneurons. Alterations in interneuron migration or numbers have been identified in multiple epilepsy mouse models, including mice with deletions of Cntnap2,35 Wwox,36 and Syngap1,37 as well as in certain models of acquired epilepsy,38,39 and after traumatic brain injury.40,41 Epilepsy that occurs in Dravet syndrome associated with pathogenic variants in SCN1A may also be classified in this category based on evidence that interneurons in Scn1a heterozygous mice display a selective decrease in excitability, and selective deletions of Scn1a in interneurons are sufficient to recapitulate the spectrum of Dravet-related phenotypes.4244 The term “interneuronopathy” was first used in the setting of a very severe genetic epilepsy syndrome (X-linked lissencephaly with ambiguous genitalia, XLAG) caused by pathogenic variants in ARX, with significant reductions in interneuron density in hippocampal and cortical regions observed in this condition.4547

A more detailed understanding of interneuron development and migration patterns will be critical for developing novel treatments for these specific genetic epilepsy syndromes and will guide our explorations into the therapeutic potential of either transplantation48,49 and/or optogenetic/chemogenetic manipulations of interneurons.

Tumor-Related Epilepsies

The incidence of epilepsy in individuals with brain tumors ranges from 70% to 80% in glioneuronal tumors (including gangliogliomas and dysembryoplastic neuroepithelial tumors) to 20% to 35% in individuals with brain metastases.50 Epileptogenesis associated with gliomas, the most common malignant primary brain tumor, has been a focus of intense research, with 2 nonmutually exclusive mechanisms explored extensively.

For some neurodevelopmental tumors such as ganglioglioma, a genetic profile has become apparent in the form of a BRAF V600E variant, suggesting the possibility of treatment with BRAF inhibitors.51 Furthermore, in some tumors, malignant glial cells release excessive amounts of glutamate through the cystine/glutamate transporter (SLC7A11), a gene whose expression is upregulated in at least half of all glial tumors.52 SLC7A11-mediated glutamate release results in hyperexcitability that spreads to adjacent tissues,53 and in preclinical studies, a currently available SLC7A11 inhibitor (sulfasalazine, utilized in the treatment of Crohn disease) resulted in improved seizure frequency and prolonged survival.54 Mutations in isocitrate dehydrogenase (IDH1) are a strong predictor of epilepsy in patients with low-grade glial tumors.55 Mutant IDH1 converts isocitrate to 2-hydroxyglutarate (instead of α-ketoglutarate), which is structurally similar to glutamate and sufficient to lengthen burst duration in cultured rat cortical neurons in an NMDA-receptor-dependent fashion.55

A second potential mechanism involves the dysregulation of chloride homeostasis in peritumoral cortical neurons through the aberrant downregulation of KCC2 (potassium chloride cotransporter) and upregulation of NKCC1 (sodium potassium chloride cotransporter) within these cells.56 Under these conditions, γ-aminobutyric acid (GABA) binding to ionotropic receptors results in depolarization, and inhibitors of NKCC1 (which reverse altered chloride gradients) in preclinical glioma models improve seizure susceptibility.57 It remains to be seen whether similar mechanisms of epileptogenesis may be involved in epilepsies related to meningiomas or metastatic lesions, for which preclinical models are less well developed. Clearly, cortically based or invading tumors seem to possess the greatest risk of epilepsy.50

Autoimmune Epilepsies

As of 2019, antibodies to at least 11 different antigens have been associated with epilepsy occurring in the context of encephalitis. Antibodies against extracellular antigens raise neuronal excitability and impose synaptic dysfunction either by disrupting specific protein interactions (eg, LGI1, NMDAR), enhancing receptor internalization (AMPAR), or by functioning as an antagonist (GABA-BR).58 In contrast, antibodies against intracellular antigens are thought to produce epilepsy as a consequence of direct cytotoxic T-cell infiltration (eg, amphiphysin, GAD-65). The clinical presentation of autoimmune encephalitides is highly variable (signs and symptoms of limbic or motor dysfunction may or may not be present), and seizures may be the presenting symptom, a late symptom, or absent entirely.59

Establishing a direct causative link between individual antibodies and their specific mechanisms of epileptogenesis has been possible through experiments in which patient-derived antibodies are infused into mouse or rat models. For example, hippocampal specimens from mice that received intracerebroventricularly infused LGI1 antibodies over 14 days displayed reduced synaptic expression of the voltage-gated potassium channel KV1.1 (KCNA1) together with increases in presynaptic-release probability and postsynaptic current amplitudes, as well as diminished long-term potentiation and impairments in learning and memory.60 These mice did not develop spontaneous seizures, suggesting that at least in mice, either longer durations of anti-LGI1 antibody exposure or higher antibody titers may be necessary for seizure generation. In contrast, similar infusions of anti-NMDAR antibodies in mice produced spontaneous seizures without impairments in memory or motor function.61

Recent genome-wide association studies have revealed that particular human leukocyte antigen (HLA) haplotypes may increase the risk of specific antibody-mediated encephalitides,59,62,63 just as with other autoimmune conditions such as type I diabetes mellitus or ankylosing spondylitis; these HLA associations provide pathophysiological insights into the genesis of these antibodies. Fortunately, only a minority of patients who display acute symptomatic seizures during active encephalitis go on to develop epilepsy.58 Early immunomodulatory therapy appears to be critical to avoid future drug resistance, while other factors, such as medical complications or hypoxia, may also contribute to long-term seizure risk.58,59

Epilepsy-Related Conditions

Adults have a median of 2 chronic medical conditions, but this number rises to 6 in individuals older than 65 years.64 Thus, “comorbidities” are a central aspect of all chronic medical conditions, and epilepsy is no exception. In epilepsy, comorbidities can be broadly divided into those which affect mental health (including sleep), general physical health (including trauma), and reproductive health.65,66 Together, these comorbidities contribute tremendously to overall disability, impairments in quality of life, and premature mortality.67,68 Outside of chance or artifactual comorbidities that may reflect various forms of bias,64 4 main mechanisms of comorbidity have been proposed69: (1) independent comorbidity (etiologically unrelated to epilepsy), (2) consequent comorbidity (a direct consequence of epilepsy), (3) iatrogenic comorbidity (treatment related), and (4) shared risk factor (in which epilepsy and its comorbidity independently arise from a single etiology). Importantly, shared risk factors may epidemiologically resemble a bidirectional association (in which each condition causes the other).

Psychiatric comorbidities in epilepsy have received the greatest emphasis. Epilepsy is associated with significantly higher rates of mood and anxiety disorders,70,71 psychosis,72 fatigue,73 and autism spectrum disorder.74 These entities are each independently associated with varying degrees of intellectual disability. Cross-sectional and/or prospective human data provide a framework for mechanistic hypotheses into their etiology; ultimately, these hypotheses require verification in animal models. Unfortunately, this schema is inherently limited since many psychiatric endophenotypes are either absent entirely (eg, suicidality) or difficult to measure (eg, depressed mood, psychosis) in animal models.

Depression, or major depressive disorder, has and will continue to be a major focus of comorbidity research. Individuals with epilepsy are twice as likely to develop depression over their lifetime,70 and either entity can occur first.75 The severity of depression is associated with the risk of epilepsy.76 Depression and suicidality tend to be more prominent in individuals with TLE compared with those who have genetic generalized epilepsies,77,78 and within TLE, depression severity correlates with pharmacoresistance but does not correlate with the side57 or the extent of hippocampal atrophy,79 if present. Improvements in depression that follow temporal lobectomy are strongly associated with improvements in seizure control.80 To date, there has been no high-quality evidence to suggest that antidepressants (in conjunction with standard anticonvulsant therapy) are sufficient to either impact epilepsy risk or reduce seizure frequency.81 On the other hand, behavioral interventions such as cognitive behavioral therapy or mindfulness training have been shown to improve both seizure control and quality of life.82 Overall, this body of evidence argues strongly for the presence of shared noniatrogenic neurobiological risk factors that simultaneously raise the risk of depression and epilepsy.

What are these risk factors? Genetic or epigenetic factors may play only a modulatory role since major depression and epilepsy display little to no evidence of genetic overlap (unlike autism and epilepsy).78 The roots of epilepsy–depression comorbidity may be related to changes in network functional connectivity. In major depression, such functional rearrangements are broad, bilateral, and vary by depression subtype.83,84 At least within TLE circuits,85 hyperexcitability within the anterior hippocampus (corresponding to the ventral hippocampus in rodents) may be one such anatomical substrate for comorbidity. In mice, ventral hippocampal injections of kainic acid produce epileptic seizures together with memory impairments and anhedonic behavior; these behavioral comorbidities were not observed in mice that received dorsal kainic acid injections.86 Hypersynchrony in the anterior/ventral hippocampus region may contribute to depressive symptoms by compromising functional connectivity to ipsilateral frontal regions.87

Testing these hypotheses in preclinical models is now possible with optogenetics, in which an anatomically or molecularly defined neuronal population is genetically or virally transduced to express an excitatory or inhibitory ion channel that is activated by light of a specific wavelength. Bilateral optogenetic activations of ventral hippocampal afferent pathways in nonepileptic mice are sufficient to produce depression and anxiety-like symptoms.88,89 Similarly, the optogenetic inhibition of mossy cells within the dentate gyrus (simulating mossy fiber loss) is sufficient to produce impairments in object memory in mice.90 Aside from these focal network derangements, aberrations in a variety of other neuromolecular axes have been proposed as substrates that may raise seizure risk and compromise mood, including disturbances in neurotransmitter signaling (glutamate, GABA, serotonin), dysfunctional hypothalamo–pituitary–adrenal axis signaling, and a host of cellular and secreted mediators of neuroinflammation.57,91

Looking Forward: Opportunities and Challenges

Given the progress over the past several years and the remaining gaps in knowledge in the field, we have identified some ambitious but feasible future priorities in epilepsy research that we believe should guide our scientific efforts in this area over the next decade. First, it is notable that a large portion of this update has been devoted to genetic advances, given the substantial work in this area. We also recognize that many patients worldwide have epilepsy primarily caused by infection, head injury, birth trauma, hypoxic–ischemic insult, or any of a number of other perturbations of nervous system function. We support an increased focus on investigating the underlying causes and mechanisms of all forms of epilepsy, including these acquired forms of epilepsy, in order to improve our ability to prevent and treat these conditions successfully.

We also support further work on the cognitive and behavioral deficits that accompany epilepsy through experimental animal models, including further use of chemogenetic and optogenetic strategies to study specific cellular populations in the pathogenesis of epilepsy and related conditions. An important question with direct clinical relevance centers on the transition to the ictal state: Since seizures occur only in discrete episodes in most instances, we need a better understanding of what allows them to arise at any particular time and what limits transition to an ictal state at other times.92

We support continued attention on interneuron pathology, central neuronal signaling pathways, and autoimmune factors as underlying mechanistic factors in both genetic and acquired epilepsy syndromes. Further, invoking another less well-studied cell type in the nervous system, we support evaluation of the role of glia in epileptogenesis and seizure propagation. The pathogenesis of infection-related epilepsy, including virus-induced epilepsy and parasite-induced epilepsy, the latter of which is a leading cause of epilepsy worldwide but lacks a relevant animal model, needs further exploration. In general, the links between the brain and immune system and the relationship between inflammation and neural excitability should be critical targets of investigation. Despite the large volume of new advances in epilepsy genetics, we believe there needs to be further characterization of genes associated with the most prevalent early-life syndromes and further research on the use of “rational” therapy design to modulate known pathogenic pathways.

Although some work has been devoted to understanding the causality behind some of the most common epilepsy-related comorbidities, much more is required. We would support further research aimed at disentangling the effects of seizures, genetic changes, and antiseizure medication in contributing to the intellectual impairments that are present in patients with epileptic encephalopathies. In addition, we believe that further timely study of epilepsy etiologies in elderly individuals, who represent a second peak of epilepsy incidence after early childhood, could be highly impactful. Recent findings related to hippocampal hyperexcitability in individuals with Alzheimer disease93 and the discovery of associations between lifestyle risk factors and late-onset epilepsy94 provide tantalizing suggestions of important etiological connections in older adults who had multiple medical conditions.

“Doctor, what is causing my seizures?” At the current time, in a significant majority of individuals, including those without a definite brain lesion, an encephalitic prodrome, evidence for a familial epilepsy syndrome, or a comorbid neurodevelopmental syndrome, the answer to this question remains unknown. Fortunately, 65% of individuals will experience seizure freedom with 1 or more currently available antiseizure medications.95 To improve the lives of all individuals affected by epilepsy, however, we must address the fundamental causes of epilepsy and its associated conditions. As demonstrated in the introductory vignette, we also have a responsibility to translate our scientific advances toward the treatment of epilepsy and fcognitive and psychiatric comorbidities in a coordinated fashion.


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[WEB PAGE] Epilepsy – Symptoms and causes – Mayo Clinic


Epilepsy is a central nervous system (neurological) disorder in which brain activity becomes abnormal, causing seizures or periods of unusual behavior, sensations, and sometimes loss of awareness.

Anyone can develop epilepsy. Epilepsy affects both males and females of all races, ethnic backgrounds and ages.

Seizure symptoms can vary widely. Some people with epilepsy simply stare blankly for a few seconds during a seizure, while others repeatedly twitch their arms or legs. Having a single seizure doesn’t mean you have epilepsy. At least two unprovoked seizures are generally required for an epilepsy diagnosis.

Treatment with medications or sometimes surgery can control seizures for the majority of people with epilepsy. Some people require lifelong treatment to control seizures, but for others, the seizures eventually go away. Some children with epilepsy may outgrow the condition with age.

Epilepsy care at Mayo Clinic


Because epilepsy is caused by abnormal activity in the brain, seizures can affect any process your brain coordinates. Seizure signs and symptoms may include:

  • Temporary confusion
  • A staring spell
  • Uncontrollable jerking movements of the arms and legs
  • Loss of consciousness or awareness
  • Psychic symptoms such as fear, anxiety or deja vu

Symptoms vary depending on the type of seizure. In most cases, a person with epilepsy will tend to have the same type of seizure each time, so the symptoms will be similar from episode to episode.

Doctors generally classify seizures as either focal or generalized, based on how the abnormal brain activity begins.

Focal seizures

When seizures appear to result from abnormal activity in just one area of your brain, they’re called focal (partial) seizures. These seizures fall into two categories:

  • Focal seizures without loss of consciousness. Once called simple partial seizures, these seizures don’t cause a loss of consciousness. They may alter emotions or change the way things look, smell, feel, taste or sound. They may also result in involuntary jerking of a body part, such as an arm or leg, and spontaneous sensory symptoms such as tingling, dizziness and flashing lights.
  • Focal seizures with impaired awareness. Once called complex partial seizures, these seizures involve a change or loss of consciousness or awareness. During a complex partial seizure, you may stare into space and not respond normally to your environment or perform repetitive movements, such as hand rubbing, chewing, swallowing or walking in circles.

Symptoms of focal seizures may be confused with other neurological disorders, such as migraine, narcolepsy or mental illness. A thorough examination and testing are needed to distinguish epilepsy from other disorders.

Generalized seizures

Seizures that appear to involve all areas of the brain are called generalized seizures. Six types of generalized seizures exist.

  • Absence seizures. Absence seizures, previously known as petit mal seizures, often occur in children and are characterized by staring into space or subtle body movements such as eye blinking or lip smacking. These seizures may occur in clusters and cause a brief loss of awareness.
  • Tonic seizures. Tonic seizures cause stiffening of your muscles. These seizures usually affect muscles in your back, arms and legs and may cause you to fall to the ground.
  • Atonic seizures. Atonic seizures, also known as drop seizures, cause a loss of muscle control, which may cause you to suddenly collapse or fall down.
  • Clonic seizures. Clonic seizures are associated with repeated or rhythmic, jerking muscle movements. These seizures usually affect the neck, face and arms.
  • Myoclonic seizures. Myoclonic seizures usually appear as sudden brief jerks or twitches of your arms and legs.
  • Tonic-clonic seizures. Tonic-clonic seizures, previously known as grand mal seizures, are the most dramatic type of epileptic seizure and can cause an abrupt loss of consciousness, body stiffening and shaking, and sometimes loss of bladder control or biting your tongue.

When to see a doctor

Seek immediate medical help if any of the following occurs:

  • The seizure lasts more than five minutes.
  • Breathing or consciousness doesn’t return after the seizure stops.
  • A second seizure follows immediately.
  • You have a high fever.
  • You’re experiencing heat exhaustion.
  • You’re pregnant.
  • You have diabetes.
  • You’ve injured yourself during the seizure.

If you experience a seizure for the first time, seek medical advice.


Epilepsy has no identifiable cause in about half the people with the condition. In the other half, the condition may be traced to various factors, including:

  • Genetic influence. Some types of epilepsy, which are categorized by the type of seizure you experience or the part of the brain that is affected, run in families. In these cases, it’s likely that there’s a genetic influence.

    Researchers have linked some types of epilepsy to specific genes, but for most people, genes are only part of the cause of epilepsy. Certain genes may make a person more sensitive to environmental conditions that trigger seizures.

  • Head trauma. Head trauma as a result of a car accident or other traumatic injury can cause epilepsy.
  • Brain conditions. Brain conditions that cause damage to the brain, such as brain tumors or strokes, can cause epilepsy. Stroke is a leading cause of epilepsy in adults older than age 35.
  • Infectious diseases. Infectious diseases, such as meningitis, AIDS and viral encephalitis, can cause epilepsy.
  • Prenatal injury. Before birth, babies are sensitive to brain damage that could be caused by several factors, such as an infection in the mother, poor nutrition or oxygen deficiencies. This brain damage can result in epilepsy or cerebral palsy.
  • Developmental disorders. Epilepsy can sometimes be associated with developmental disorders, such as autism and neurofibromatosis.

Risk factors

Certain factors may increase your risk of epilepsy:

  • Age. The onset of epilepsy is most common in children and older adults, but the condition can occur at any age.
  • Family history. If you have a family history of epilepsy, you may be at an increased risk of developing a seizure disorder.
  • Head injuries. Head injuries are responsible for some cases of epilepsy. You can reduce your risk by wearing a seat belt while riding in a car and by wearing a helmet while bicycling, skiing, riding a motorcycle or engaging in other activities with a high risk of head injury.
  • Stroke and other vascular diseases. Stroke and other blood vessel (vascular) diseases can lead to brain damage that may trigger epilepsy. You can take a number of steps to reduce your risk of these diseases, including limiting your intake of alcohol and avoiding cigarettes, eating a healthy diet, and exercising regularly.
  • Dementia. Dementia can increase the risk of epilepsy in older adults.
  • Brain infections. Infections such as meningitis, which causes inflammation in your brain or spinal cord, can increase your risk.
  • Seizures in childhood. High fevers in childhood can sometimes be associated with seizures. Children who have seizures due to high fevers generally won’t develop epilepsy. The risk of epilepsy increases if a child has a long seizure, another nervous system condition or a family history of epilepsy.


Having a seizure at certain times can lead to circumstances that are dangerous to yourself or others.

  • Falling. If you fall during a seizure, you can injure your head or break a bone.
  • Drowning. If you have epilepsy, you’re 15 to 19 times more likely to drown while swimming or bathing than the rest of the population because of the possibility of having a seizure while in the water.
  • Car accidents. A seizure that causes either loss of awareness or control can be dangerous if you’re driving a car or operating other equipment.

    Many states have driver’s license restrictions related to a driver’s ability to control seizures and impose a minimum amount of time that a driver be seizure-free, ranging from months to years, before being allowed to drive.

  • Pregnancy complications. Seizures during pregnancy pose dangers to both mother and baby, and certain anti-epileptic medications increase the risk of birth defects. If you have epilepsy and you’re considering becoming pregnant, talk to your doctor as you plan your pregnancy.

    Most women with epilepsy can become pregnant and have healthy babies. You’ll need to be carefully monitored throughout pregnancy, and medications may need to be adjusted. It’s very important that you work with your doctor to plan your pregnancy.

  • Emotional health issues. People with epilepsy are more likely to have psychological problems, especially depression, anxiety and suicidal thoughts and behaviors. Problems may be a result of difficulties dealing with the condition itself as well as medication side effects.

Other life-threatening complications of epilepsy are uncommon, but may happen, such as:

  • Status epilepticus. This condition occurs if you’re in a state of continuous seizure activity lasting more than five minutes or if you have frequent recurrent seizures without regaining full consciousness in between them. People with status epilepticus have an increased risk of permanent brain damage and death.
  • Sudden unexpected death in epilepsy (SUDEP). People with epilepsy also have a small risk of sudden unexpected death. The cause is unknown, but some research shows it may occur due to heart or respiratory conditions.

    People with frequent tonic-clonic seizures or people whose seizures aren’t controlled by medications may be at higher risk of SUDEP. Overall, about 1 percent of people with epilepsy die of SUDEP.


via Epilepsy – Symptoms and causes – Mayo Clinic

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[NEWS] Novel artificial intelligence algorithm helps detect brain tumor


A brain tumor is a mass of abnormal cells that grow in the brain. In 2016 alone, there were 330,000 incident cases of brain cancer and 227,000 related-deaths worldwide. Early detection is crucial to improve patient prognosis, and thanks to a team of researchers, they developed a new imaging technique and artificial intelligence algorithm that can help doctors accurately identify brain tumors.


Image Credit: create jobs 51 /

Image Credit: create jobs 51 /

Published in the journal Nature Medicine, the study reveals a new method that combines modern optical imaging and an artificial intelligence algorithm. The researchers at New York University studied the accuracy of machine learning in producing precise and real-time intraoperative diagnosis of brain tumors.

In the past, the only way to diagnose brain tumors is through hematoxylin and eosin staining of processed tissue in time. Plus, interpretation of the findings relies on pathologists who examine the specimen. The researchers hope the new method will provide a better and more accurate diagnosis, which can help initiate effective treatments right away.

In cancer treatment, the earlier cancer has been diagnosed, the earlier the oncologists can start the treatment. In most cases, early detection improves health outcomes. The researchers have found that their novel method of detection yielded a 94.6 percent accuracy, compared to 93.9 percent for pathology-based interpretation.

The imaging technique

The researchers used a new imaging technique called stimulated Raman histology (SRH), which can reveal tumor infiltration in human tissue. The technique collects scattered laser light and emphasizes features that are not usually seen in many body tissue images.

With the new images, the scientists processed and studied using an artificial intelligence algorithm. Within just two minutes and thirty seconds, the researchers came up with a brain tumor diagnosis. The fast detection of brain cancer can help not only in diagnosing the disease early but also in implementing a fast and effective treatment plan. With cancer caught early, treatments may be more effective in killing cancer cells.

The team also utilized the same technology to accurately identify and remove undetectable tumors that cannot be detected by conventional methods.

“As surgeons, we’re limited to acting on what we can see; this technology allows us to see what would otherwise be invisible, to improve speed and accuracy in the OR, and reduce the risk of misdiagnosis. With this imaging technology, cancer operations are safer and more effective than ever before,” Dr. Daniel A. Orringer, associate professor of Neurosurgery at NYU Grossman School of Medicine, said.

Study results

The study is a walkthrough of various ideas and efforts by the research team. First off, they built the artificial intelligence algorithm by training a deep convolutional neural network (CNN), containing more than 2.5 million samples from 415 patients. The method helped them group and classify tissue samples into 13 categories, representing the most common types of brain tumors, such as meningioma, metastatic tumors, malignant glioma, and lymphoma.

For validation, the researchers recruited 278 patients who are having brain tumor resection or epilepsy surgery at three university medical centers. The tumor samples from the brain were examined and biopsied. The researchers grouped the samples into two groups – control and experimental.

The team assigned the control group to be processed traditionally in a pathology laboratory. The process spans 20 to 30 minutes. On the other hand, the experimental group had been tested and studied intraoperatively, from getting images and processing the examination through CNN.

There were noted errors in both the experimental and control groups but were unique from each other. The new tool can help centers detect and diagnose brain tumors, particularly those without expert neuropathologists.

“SRH will revolutionize the field of neuropathology by improving decision-making during surgery and providing expert-level assessment in the hospitals where trained neuropathologists are not available,” Dr. Matija Snuderl, associate professor in the Department of Pathology at NYU Grossman School of Medicine, explained.

Journal references:

Patel, A., Fisher, J, Nichols, E., et al. (2019). Global, regional, and national burden of brain and other CNS cancer, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016. The Lancet Neurology.

Hollon, T., Pandian, B, Orringer, D. (2019). Near real-time intraoperative brain tumor diagnosis using stimulated Raman histology and deep neural networks. Nature Medicine.


via Novel artificial intelligence algorithm helps detect brain tumor

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[Abstract] Effects of Seizure Frequency, Depression and Generalized Anxiety on Suicidal Tendency in People with Epilepsy


  • Seizure frequency was positively associated with suicidal tendency.
  • Depression mediated the relationship between seizure frequency and suicidal tendency.
  • Generalized anxiety moderated the effect of seizure frequency on suicidal tendency.



The highest risk of suicide was identified among patients diagnosed with both epilepsy and comorbid psychiatric disease. The most common comorbid psychiatric conditions of epilepsy are anxiety and depression. This study examines whether and how seizure frequency, depression and generalized anxiety interact to influence suicidal tendency.


A consecutive cohort of PWE was recruited from the First Affiliated Hospital of Chongqing Medical University. Each patient completed the Neurological Disorders Depression Inventory for Epilepsy scale[NDDI-E], the Generalized Anxiety Disorder-7 (GAD-7), and the suicidality module of Mini-International Neuropsychiatric Interview(MINI) v.5.0.0. Spearman’s correlation and moderated mediation analysis were used to examine the associations among seizure frequency, depression, generalized anxiety and suicidal tendency.


Seizure frequency was positively associated with suicidal tendency. Depression severity partially mediated the relationship between seizure frequency and suicidal tendency. The indirect effect of seizure frequency on suicidal tendency was positive, and accounted for 50.2% of the total effect of seizure frequency on suicidal tendency. The indirect effect of seizure frequency on suicidal tendency through depression severity was positively moderated by generalized anxiety severity.


Reducing seizure frequency may be the basis of suicide prevention in PWE. At the same time, the effect of seizure frequency on suicidal tendency can be partially explained by the mediation of depression severity, and the magnitude of the indirect effect of seizure frequency on suicidal tendency was contingent upon generalized anxiety severity. In addition to depression severity, generalized anxiety severity also exerts an important effect on suicidal tendency in PWE.

via Effects of Seizure Frequency, Depression and Generalized Anxiety on Suicidal Tendency in People with Epilepsy – ScienceDirect

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[WEB SITE] What Happens During a Sexual Seizure? – Psychology Today

Orgasms and Epilepsy

By Amee Baird Ph.D. Posted Jan 11, 2020

Of all neurological diseases, epilepsy is the one that has been most frequently linked to sex. “Coitus brevis epilepsia est” (“Sex is a brief seizure”) is an ancient proverb attributed to Galen, the famous physician of the Roman Empire. In the 18th and 19th centuries, some doctors, including Samuel-Auguste Tissot and Edward Sieveking, argued that excessive masturbation could cause epilepsy. At the time, castration and clitoridectomy (removal of the clitoris) were reportedly performed on people with severe epilepsy.

Renowned neurologists John Hughlings Jackson and William Gowers did not consider sex to be the origin of epilepsy. Rather, they identified neurophysiological (brain-based) causes and laid the foundations for current views of the origins of epilepsy.

The notion that sex causes epilepsy has been well and truly debunked, but in rare cases, an association between sex and seizures does exist. Temporal lobe seizures can be triggered by an orgasm, or even cause orgasms. Orgasm-induced seizures occur much more commonly in women than in men and are usually associated with a right temporal lobe seizure focus.

Andrew Baird

Source: Andrew Baird

These seizures can be frightening for partners and have a significant impact on a person’s sex life. They can lead to a life spent avoiding sex and fear of orgasm, which can have a devastating effect on relationships. In one case, the husband of a woman who experienced orgasm-induced seizures was so frustrated by their sex life that he threatened divorce if neurosurgery to cure her seizures was not successful. 

In contrast to orgasm-induced seizures, seizures that result in orgasms may be savoured by those who experience them. Orgasmic “auras” (a feeling or warning sign that a seizure is about to happen) linked to seizures are also more common in women and typically arise from the right temporal lobe.

Case studies of women who experience these pleasurable seizures have found that they often keep them a secret from their doctors – for decades in some cases – even when they are undergoing investigations for epilepsy and know that orgasmic auras are part of their seizures. Some people have refused to have neurosurgery to cure their seizures out of fear of losing these unexpected orgasms.

Spontaneous orgasms might sound like fun, but these sexual seizures can occur suddenly and in unexpected situations. Imagine travelling on a bus during peak hour on your way to work, standing in the aisle jammed in between other passengers, and suddenly feeling a wave of tingling. You know what is coming, and you know that you are about to experience it in front of an audience of strangers.

Brain imaging studies of healthy men and women have found that orgasm, and its lead-up, is predominantly associated with activation (and, in some earlier studies, deactivation) in the temporal and frontal brain regions, including the amygdala and orbitofrontal cortex; other regions involved in sensory, motor and reward processes are also implicated. It appears that if the neurons (the nerve cells) in those very brain regions are highly sensitive, perhaps due to scar tissue or other causes of seizures, such as hippocampal sclerosis, then a seizure can be triggered by the activation or stimulation of those exact regions that occurs during orgasm.

Apart from orgasm, there are other sexual behaviours that can occur during a seizure. Sexual automatisms (automatic behaviours that the person later has no memory of) include writhing, thrusting, rhythmic movement of the pelvis and legs, and rhythmic handling of genitals or masturbation. These are rare and occur relatively equally in men and women who experience frontal lobe seizures.

Sexual “ictal” manifestations (that is, those that occur during a seizure) have also been reported, such as erotic feelings, genital sensations and sexual desire; these have been found to occur most commonly in women with right temporal lobe seizures.

So although sex does not cause epilepsy, sexual behaviours can be associated with certain types of seizures that arise from the temporal (typically right-sided) or frontal lobes, brain regions that are critical parts of our sexual neural network.

This is an adapted excerpt from Sex in the Brain: How Your Brain Controls Your Sex Life (NewSouth Publishing, 2019; and forthcoming Columbia University Press, 2020).


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Rémillard, G.M., Andermann, F., Testa, G.F., Gloor, P., Aube, M., Martin, J.B., …  Simpson, C. (1983). Sexual ictal manifestations predominate in women with temporal lobe epilepsy: A finding suggesting sexual dimorphism in the human brain. Neurology, 33(3), 323–330.


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Spencer, S.S., Spencer, D.D., Williamson, P.D., & Mattson, R.H. (1983). Sexual automatisms in complex partial seizures. Neurology, 33(5), 527–533.


Stoléru, S., Fonteille, V., Cornélis, C., Joyal, C., & Moulier, V. (2012). Functional neuroimaging studies of sexual arousal and orgasm in healthy men and women: A review and meta-analysis. Neuroscience & Biobehavioral Reviews, 36(6), 1481–1509.


via What Happens During a Sexual Seizure? | Psychology Today

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