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The causes of epilepsy in childhood vary. In about ⅔ of cases, it is unknown.
- Unknown 67.6%
- Congenital 20%
- Trauma 4.7%
- Infection 4%
- Stroke 1.5%
- Tumor 1.5%
- Degenerative .7%
Seizures in cats are caused by various onsets. Cats can have reactive, primary (idiopathic) or secondary seizures. Idiopathic seizures are not as common in cats as in dogs however a recent study conducted showed that of 91 feline seizures, 25% were suspected to have idiopathic epilepsy. In the same group of 91 cats, 50% were secondary seizures and 20% reactive.
Onset is between 3 and 15 years of age with a mean of around 8. Both sexes are equally affected. The disorder accounts for about 2–7% of benign childhood focal seizures.
The prognosis for Rolandic seizures is invariably excellent, with probably less than 2% risk of developing absence seizures and less often GTCS in adult life.
Remission usually occurs within 2–4 years from onset and before the age of 16 years. The total number of seizures is low, the majority of patients having fewer than 10 seizures; 10–20% have just a single seizure. About 10–20% may have frequent seizures, but these also remit with age.
Children with Rolandic seizures may develop usually mild and reversible linguistic, cognitive and behavioural abnormalities during the active phase of the disease. These may be worse in children with onset of seizures before 8 years of age, high rate of occurrence and multifocal EEG spikes.
The development, social adaptation and occupations of adults with a previous history of Rolandic seizures were found normal.
The mortality rate ranges from 3–7% in a mean follow up period of 8.5 to 9.7 years. Death is often related to accidents.
Like many other types of seizures, gelastic seizures are hard to control for an extended period of time. The best outlook is for children suffering the seizures due to a benign tumor in their hypothalamus. The removal of these tumors can be effective not only for the frequency of the seizures, but also the behavioral and cognitive symptoms that come along with the syndrome. Cases have also been described where that antiepileptic drugs have stopped seizures fully.
Idiopathic epilepsy does not have a classification due to the fact there are no known causes of these seizures, however both reactive and symptomatic secondary epilepsy can be placed into classifications.
Consistent risk factors include:
- Severity of seizures, increased refractoriness of epilepsy and presence of generalized tonic-clonic seizures: the most consistent risk factor is an increased frequency of tonic–clonic seizures.
- Poor compliance. Lack of therapeutic levels of anti-epileptic drugs, non-adherence to treatment regimens, and frequent changes in regimens are risk factors for sudden death.
- Young age, and early age of seizures onset.
- Male gender
- Poly-therapy of epilepsy. It remains unclear whether this is an independent risk factor or a surrogate marker for severity of epilepsy.
- Being asleep during a seizure is likely to favour SUDEP occurrence.
People with epilepsy are at an increased risk of death. This increase is between 1.6 and 4.1 fold greater than that of the general population and is often related to: the underlying cause of the seizures, status epilepticus, suicide, trauma, and sudden unexpected death in epilepsy (SUDEP). Death from status epilepticus is primarily due to an underlying problem rather than missing doses of medications. The risk of suicide is increased between two and six times in those with epilepsy. The cause of this is unclear. SUDEP appears to be partly related to the frequency of generalized tonic-clonic seizures and accounts for about 15% of epilepsy related deaths. It is unclear how to decrease its risk. The greatest increase in mortality from epilepsy is among the elderly. Those with epilepsy due to an unknown cause have little increased risk. In the United Kingdom, it is estimated that 40–60% of deaths are possibly preventable. In the developing world, many deaths are due to untreated epilepsy leading to falls or status epilepticus.
The prognosis of ICOE-G is unclear, although available data indicate that remission occurs in 50–60% of patients within 2–4 years of onset. Seizures show a dramatically good response to carbamazepine in more than 90% of patients. However, 40–50% of patients may continue to have visual seizures and infrequent secondarily generalized convulsions, particularly if they have not been appropriately treated with antiepileptic drugs.
The age of onset ranges from 1 to 14 years with 75% starting between 7–10 years. There is a 1.5 male predominance, prevalence is around 15% in children aged 1–15 years with non-febrile seizures and incidence is 10–20/100,000 of children aged 0–15 years
Following a first seizure, the risk of more seizures in the next two years is 40%–50%. The greatest predictors of more seizures are problems either on the electroencephalogram or on imaging of the brain. In adults, after 6 months of being seizure-free after a first seizure, the risk of a subsequent seizure in the next year is less than 20% regardless of treatment. Up to 7% of seizures that present to the emergency department (ER) are in status epilepticus. In those with a status epilepticus, mortality is between 10% and 40%. Those who have a seizure that is provoked (occurring close in time to an acute brain event or toxic exposure) have a low risk of re-occurrence, but have a higher risk of death compared to those with epilepsy.
Both medication and drug overdoses can result in seizures, as may certain medication and drug withdrawal. Common drugs involved include: antidepressants, antipsychotics, cocaine, insulin, and the local anaesthetic lidocaine. Difficulties with withdrawal seizures commonly occurs after prolonged alcohol or sedative use, a condition known as delirium tremens.
It is unknown as to what causes abdominal epilepsy. While a causal relationship between seizure activity and the GI symptoms has not been proven, the GI symptoms cannot be explained by other pathophysiological mechanisms, and are seen to improve upon anticonvulsant treatment. Because the condition is so rare, no high-quality studies exist. There have been too few reported cases to identify risk factors, genetic factors, or other potential causes.
Epilepsy is a relatively common disorder, affecting between 0.5-1% of the population, and frontal lobe epilepsy accounts for about 1-2% of all epilepsies. The most common subdivision of epilepsy is symptomatic partial epilepsy, which causes simple partial seizures, and can be further divided into temporal and frontal lobe epilepsy. Although the exact number of cases of frontal lobe epilepsy is not currently known, it is known that FLE is the less common type of partial epilepsy, accounting for 20-30% of operative procedures involving intractable epilepsy. The disorder also has no gender or age bias, affecting males and females of all ages. In a recent study, the mean subject age with frontal lobe epilepsy was 28.5 years old, and the average age of epilepsy onset for left frontal epilepsy was 9.3 years old whereas for right frontal epilepsy it was 11.1 years old.
The lack of generally recognized clinical recommendations available are a reflection of the dearth of data on the effectiveness of any particular clinical strategy, but on the basis of present evidence, the following may be relevant:
- Epileptic seizure control with the appropriate use of medication and lifestyle counseling is the focus of prevention.
- Reduction of stress, participation in physical exercises, and night supervision might minimize the risk of SUDEP.
- Knowledge of how to perform the appropriate first-aid responses to seizure by persons who live with epileptic people may prevent death.
- People associated with arrhythmias during seizures should be submitted to extensive cardiac investigation with a view to determining the indication for on-demand cardiac pacing.
- Successful epilepsy surgery may reduce the risk of SUDEP, but this depends on the outcome in terms of seizure control.
- The use of anti suffocation pillows have been advocated by some practitioners to improve respiration while sleeping, but their effectiveness remain unproven because experimental studies are lacking.
- Providing information to individuals and relatives about SUDEP is beneficial.
Possible causes include:
- Syncope (fainting)
- Reflex anoxic seizures
- Breath-holding spells of childhood
- Hypoglycaemia
- Cataplexy
- Hyperekplexia, also called startle syndrome
- Migraine
- Narcolepsy
- Non-epileptic myoclonus
- Opsoclonus
- Parasomnias, including night terrors
- Paroxysmal kinesigenic dyskinesia
- Repetitive or ritualistic behaviours
- Tics
- AADC Deficiency
Epilepsy with myoclonic-astatic seizures has a variable course and outcome. Spontaneous remission with normal development has been observed in a few untreated cases. Complete seizure control can be achieved in about half of the cases with antiepileptic drug treatment (Doose and Baier 1987b; Dulac et al. 1990). In the remainder of cases, the level of intelligence deteriorates and the children become severely intellectually disabled. Other neurologic abnormalities such as ataxia, poor motor function, dysarthria, and poor language development may emerge (Doose 1992b). However, this proportion may not be representative because in this series the data were collected in an institution for children with severe epilepsy.
The outcome is unfavorable if generalized tonic-clonic, tonic, or clonic seizures appear at the onset or occur frequently during the course. Generalized tonic-clonic seizures usually occur during the daytime in this disorder, at least in the early stages. Nocturnal generalized tonic-clonic seizures, which may develop later, are another unfavorable sign. If tonic seizures appear, prognosis is poor.
Status epilepticus with myoclonic, astatic, myoclonic-astatic, or absence seizures is another ominous sign, especially when prolonged or appearing early.
Failure to suppress the EEG abnormalities (4- to 7-Hz rhythms and spike-wave discharges) during therapy and absence of occipital alpha-rhythm with therapy also suggest a poor prognosis (Doose 1992a).
LGS is seen in approximately 4% of children with epilepsy, and is more common in males than in females. Usual onset is between the ages of three and five. Children can have no neurological problems prior diagnosis, or have other forms of epilepsy. West syndrome is diagnosed in 20% of patients before it evolves into LGS at about 2 years old.
Childhood absence epilepsy is a fairly common disorder with a prevalence of 1 in 1000 people. Few of these people will likely have mutations in CACNA1H or GABRG2 as the prevalence of those in the studies presented is 10% or less.
Though there is limited evidence, outcomes appear to be relatively poor with a review of outcome studies finding that two thirds of PNES patients continue to experience episodes and more than half are dependent on social security at three-year followup. This outcome data was obtained in a referral-based academic epilepsy center and loss to follow-up was considerable; the authors point out ways in which this may have biased their outcome data. Outcome was shown to be better in patients with higher IQ, social status, greater educational attainments, younger age of onset and diagnosis, attacks with less dramatic features, and fewer additional somatoform complaints.
Most people with PNES (75%) are women, with onset in the late teens to early twenties being typical.
Some studies have reported an elevated frequency of childhood abuse in people with PNES. However, others that have controlled for other demographic factors have failed to find a higher rate of reported childhood abuse than in a comparable groups with organic disease (usually epilepsy).
A number of studies have also reported a high incidence of abnormal personality traits or personality disorders in people with PNES such as borderline personality. However, again, when an appropriate control group is used, the incidence of such characteristics it not always higher in PNES than in similar illnesses arising due to organic disease (e.g., epilepsy).
Other risk factors for PNES include having a diagnosis of epilepsy, having recently had a head injury or recently undergone neurosurgery.
Dravet syndrome is a severe form of epilepsy. It is a rare genetic disorder that affects an estimated 1 in every 20,000–40,000 births.
Epilepsy can have both genetic and acquired causes, with interaction of these factors in many cases. Established acquired causes include serious brain trauma, stroke, tumours and problems in the brain as a result of a previous infection. In about 60% of cases the cause is unknown. Epilepsies caused by genetic, congenital, or developmental conditions are more common among younger people, while brain tumors and strokes are more likely in older people.
Seizures may also occur as a consequence of other health problems; if they occur right around a specific cause, such as a stroke, head injury, toxic ingestion or metabolic problem, they are known as acute symptomatic seizures and are in the broader classification of seizure-related disorders rather than epilepsy itself.
The main sign of a gelastic seizure is a sudden outburst of laughter or crying with no apparent cause. The laughter may sound unpleasant and sardonic rather than joyful. The outburst usually lasts for less than a minute. During or shortly after a seizure, an individual might display some twitching, strange eye movements, lip smacking, fidgeting or mumbling. If a person who suffers from the seizures is hooked up to an electroencephalogram it will reveal interictal epileptic discharges. This syndrome usually manifests itself before the individual reaches the age of three or four. The temporal lobes, and the hypothalamus are the areas of the brain with the most involvement with these seizures. This may cause learning disabilities, and faulted cognitive function as well. It is not uncommon for children to have tonic-clonic seizures, and atonic seizures directly following the seizure. Those that are associated with hypothalamic hamartomas may occur as often as several times hourly and typically begin during infancy. Seizures that occur in infancy may include bursts of cooing, respirations, giggling, and smiling. Due to early hypothalamic-pituitary-gonadal axis activation in girls who suffer from the seizures, it is not uncommon for them to display secondary sex characteristics before the age of eight.