Post-traumatic epilepsy

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Post-traumatic epilepsy
Specialty Neurology

Post-traumatic epilepsy (PTE) is a form of acquired epilepsy that results from brain damage caused by physical trauma to the brain (traumatic brain injury, abbreviated TBI). [1] A person with PTE experiences repeated post-traumatic seizures (PTS, seizures that result from TBI) more than a week after the initial injury. [2] PTE is estimated to constitute 5% of all cases of epilepsy and over 20% of cases of acquired epilepsy [3] [4] [1] (in which seizures are caused by an identifiable organic brain condition). [5]

Contents

It is not known who will develop epilepsy after TBI and who will not. [6] However, the likelihood that a person will develop PTE is influenced by the severity and type of injury; for example penetrating injuries and those that involve bleeding within the brain confer a higher risk. The onset of PTE can occur within a short time of the physical trauma that causes it, or months or years after. [3] People with head trauma may remain at a higher risk for post-traumatic seizures than the general population even decades after the injury. [7] PTE may be caused by several biochemical processes that occur in the brain after trauma, including overexcitation of brain cells and damage to brain tissues by free radicals. [8]

Diagnostic measures include electroencephalography (EEG) and brain imaging techniques such as magnetic resonance imaging, but these are not totally reliable. Antiepileptic drugs do not prevent the development of PTE after head injury, but may be used to treat the condition if it does occur. When medication does not work to control the seizures, surgery may be needed. [9] Modern surgical techniques for PTE have their roots in the 19th century, but trepanation (cutting the skull to make a hole) may have been used for the condition in ancient cultures. [10]

Classification

Seizures may occur after traumatic brain injury; these are known as post-traumatic seizures (PTS). However, not everyone who has post-traumatic seizures will continue to have post-traumatic epilepsy, because the latter is a chronic condition. However, the terms PTS and PTE are used interchangeably in medical literature. [11] [12] Seizures due to post-traumatic epilepsy are differentiated from non-epileptic post-traumatic seizures based on their cause and timing after the trauma. A person with PTE has late seizures, those occurring more than a week after the initial trauma. [13] Late seizures are considered to be unprovoked, while early seizures (those occurring within a week of trauma) are thought to result from direct effects of the injury. A provoked seizure is one that results from an exceptional, nonrecurring cause such as the immediate effects of trauma rather than a defect in the brain; it is not an indication of epilepsy. [14] Thus for a diagnosis of PTE, seizures must be unprovoked.

Disagreement exists about whether to define PTE as the occurrence of one or more late, unprovoked seizures, or whether the condition should only be diagnosed in people with two or more. [15] Medical sources usually consider PTE to be present if even one unprovoked seizure occurs, but more recently it has become accepted to restrict the definition of all types of epilepsy to include only conditions in which more than one occur. [11] Requiring more than one seizure for a diagnosis of PTE is more in line with the modern definition of epilepsy, but it eliminates people for whom seizures are controlled by medication after the first seizure. [11]

As with other forms of epilepsy, seizure types in PTE may be partial (affecting only part of one hemisphere of the brain) or generalized (affecting both hemispheres and associated with loss of consciousness). [16] In about a third of cases, people with PTE have partial seizures; these may be simple or complex. [17] In simple partial seizures, level of consciousness is not altered, while in complex partial seizures consciousness is impaired. [14] When generalized seizures occur, they may start out as partial seizures and then spread to become generalized. [17]

Causes

Cumulative incidence after 30 years of PTE in head injured individuals PTE bar graph by severity.svg
Cumulative incidence after 30 years of PTE in head injured individuals

It is not clear why some patients develop PTE while others with very similar injuries do not. [11] However, possible risk factors have been identified, including severity and type of injury, presence of early seizures, and genetic factors.

Genetics

Genetics may play a role in the risk that a person will develop PTE; people with the ApoE-ε4 allele may be at higher risk for PTE. [7] The haptoglobin Hp2-2 allele may be another genetic risk factor, possibly because it binds hemoglobin poorly and thus allows more iron to escape and damage tissues. [7] However, most studies have found that having family members with epilepsy does not significantly increase the risk of PTS, [11] suggesting that genetics are not a strong risk factor.

Severity of trauma

The more severe the brain trauma is, the more likely a person is to have late PTE. [19] Evidence suggests that mild head injuries do not confer an increased risk of developing PTE, while more severe types do. [20] In simple mild TBI, the risk for PTE is about 1.5 times that of the uninjured population. [18] By some estimates, as many as half of individuals with severe brain trauma experience PTE; [19] other estimates place the risk at 5% for all TBI patients and 15–20% for severe TBI. [21] One study found that the 30-year risk of developing PTE was 2.1% for mild TBI, 4.2% for moderate, and 16.7% for severe injuries, as shown in the chart at right. [18] [22]

Nature of trauma

The nature of the head trauma also influences the risk of PTE. People who have depressed skull fractures, penetrating head trauma, early PTS, and intracerebral and subdural haematomas due to the TBI are especially likely to have PTE, which occurs in more than 30% of people with any one of these findings. [19] About 50% of patients with penetrating head trauma develop PTE, [8] [20] and missile injuries and loss of brain volume are associated with an especially high likelihood of developing the condition. [23] Injuries that occur in military settings carry higher-than-usual risk for PTE, probably because they more commonly involve penetrating brain injury and brain damage over a more widespread area. [7] Intracranial hematomas, in which blood accumulates inside the skull, are one of the most important risk factors for PTE. [24] Subdural hematoma confers a higher risk of PTE than does epidural hematoma, possibly because it causes more damage to brain tissue. [8] Repeated intracranial surgery confers a high risk for late PTE, possibly because people who need more surgery are more likely to have factors associated with worse brain trauma such as large hematomas or cerebral swelling. [8] In addition, the chances of developing PTE differ by the location of the brain lesion: brain contusion that occurs on in one or the other of the frontal lobes has been found to carry a 20% PTE risk, while a contusion in one of the parietal lobes carries a 19% risk and one in a temporal lobe carries a 16% chance. [22] When contusions occur in both hemispheres, the risk is 26% for the frontal lobes, 66% for the parietal, and 31% for the temporal. [22]

Post-traumatic seizures

The risk that a person will develop PTE is heightened but not 100% if PTS occur. [20] Because many of the risk factors for both PTE and early PTS are the same, it is unknown whether the occurrence of PTS is a risk factor in and of itself. [7] However, even independent of other common risk factors, early PTS have been found to increase the risk of PTE to over 25% in most studies. [4] A person who has one late seizure is at even greater risk for having another than one who has early PTS; epilepsy occurs in 80% of people who have a late seizure. [25] Status epilepticus, a continuous seizure or multiple seizures in rapid succession, is especially strongly correlated with the development of PTE; status seizures occur in 6% of all TBIs but are associated with PTE 42% of the time, and quickly halting a status seizure reduces chances of PTE development. [22]

Pathophysiology

For unknown reasons, trauma can cause changes in the brain that lead to epilepsy. [3] [26] There are a number of proposed mechanisms by which TBI causes PTE, more than one of which may be present in a given person. [8] In the period between a brain injury and onset of epilepsy, brain cells may form new synapses and axons, undergo apoptosis or necrosis, and experience altered gene expression. [25] In addition, damage to particularly vulnerable areas of the cortex such as the hippocampus may give rise to PTE. [4]

Blood that gathers in the brain after an injury may damage brain tissue and thereby cause epilepsy. [8] Products that result from the breakdown of hemoglobin from blood may be toxic to brain tissue. [8] The "iron hypothesis" holds that PTE is due to damage by oxygen free radicals, the formation of which is catalyzed by iron from blood. [19] Animal experiments using rats have shown that epileptic seizures can be produced by injecting iron into the brain. [8] Iron catalyzes the formation of hydroxyl radicals by the Haber–Weiss reaction; [8] such free radicals damage brain cells by peroxidizing lipids in their membranes. [27] The iron from blood also reduces the activity of an enzyme called nitric oxide synthase, another factor thought to contribute to PTE. [19]

After TBI, abnormalities exist in the release of neurotransmitters, chemicals used by brain cells to communicate with each other; these abnormalities may play a role in the development of PTE. [8] TBI may lead to the excessive release of glutamate and other excitatory neurotransmitters (those that stimulate brain cells and increase the likelihood that they will fire). This excessive glutamate release can lead to excitotoxicity, damage to brain cells through overactivation of the biochemical receptors that bind and respond to excitatory neurotransmitters. Overactivation of glutamate receptors damages neurons; for example it leads to the formation of free radicals. [8] Excitotoxicity is a possible factor in the development of PTE; [13] it may lead to the formation of a chronic epileptogenic focus. [8] An epileptic focus is the part of the brain from which epileptic discharges originate. [28]

In addition to chemical changes in cells, structural changes that lead to epilepsy may occur in the brain. [3] Seizures that occur shortly after TBI can reorganize neural networks and cause seizures to occur repeatedly and spontaneously later on. [4] The kindling hypothesis suggests that new neural connections are formed in the brain and cause an increase in excitability. [19] The word kindling is a metaphor: the way the brain's response to stimuli increases over repeated exposures is similar to the way small burning twigs can produce a large fire. [29] This reorganization of neural networks may make them more excitable. [4] Neurons that are in a hyperexcitable state due to trauma may create an epileptic focus in the brain that leads to seizures. [12] In addition, an increase in neurons' excitability may accompany loss of inhibitory neurons that normally serve to reduce the likelihood that other neurons will fire; these changes may also produce PTE. [4]

Diagnosis

EEG shows abnormal activity in some types of seizure disorder, but may or may not display abnormal findings in PTE. Spike-waves.png
EEG shows abnormal activity in some types of seizure disorder, but may or may not display abnormal findings in PTE.

To be diagnosed with PTE, a person must have a history of head trauma and no history of seizures prior to the injury. [30] Witnessing a seizure is the most effective way to diagnose PTE. [12] Electroencephalography (EEG) is a tool used to diagnose a seizure disorder, but a large portion of people with PTE may not have the abnormal "epileptiform" EEG findings indicative of epilepsy. [12] In one study, about a fifth of people who had normal EEGs three months after an injury later developed PTE. However, while EEG is not useful for predicting who will develop PTE, it can be useful to localize the epileptic focus, to determine severity, and to predict whether a person will have more seizures if they stop taking antiepileptic medications. [8]

Magnetic resonance imaging (MRI) is performed in people with PTE, and CT scanning can be used to detect brain lesions if MRI is unavailable. [8] However, it is frequently not possible to detect the epileptic focus using neuroimaging. [31]

For a diagnosis of PTE, seizures must not be attributable to another obvious cause. [4] Seizures that occur after head injury are not necessarily due to epilepsy or even to the head trauma. [11] Like anyone else, TBI survivors may have seizures due to factors including imbalances of fluid or electrolytes, epilepsy from other causes, hypoxia (insufficient oxygen), and ischemia (insufficient blood flow to the brain). [11] Withdrawal from alcohol is another potential cause of seizures. [32] Thus these factors must be ruled out as causes of seizures in people with head injury before a diagnosis of PTE can be made.

Prevention

Prevention of PTE involves preventing brain trauma in general; protective measures include bicycle helmets and child safety seats. [8] No specific treatment exists to prevent the development of epilepsy after TBI occurs. [3] In the past, antiepileptic drugs were used with the intent of preventing the development of PTE. [3] However, while antiepileptic drugs can prevent early PTS, clinical studies have failed to show that prophylactic use of antiepileptic drugs prevents the development of PTE. [2] [3] [7] [33] Why antiepileptic drugs in clinical trials have failed to stop PTE from developing is not clear, but several explanations have been offered. [7] The drugs may simply not be capable of preventing epilepsy, or the drug trials may have been set up in a way that did not allow a benefit of the drugs to be found (e.g. drugs may have been given too late or in inadequate doses). [7] Animal studies have similarly failed to show much protective effect of the most commonly used seizure medications in PTE trials, such as phenytoin and carbamazepine. [7] Antiepileptic drugs are recommended to prevent late seizures only for people in whom PTE has already been diagnosed, not as a preventative measure. [34] On the basis of the aforementioned studies, no treatment is widely accepted to prevent the development of epilepsy. [19] However, it has been proposed that a narrow window of about one hour after TBI may exist during which administration of antiepileptics could prevent epileptogenesis (the development of epilepsy). [9] There is no evidence to support or went against the usage of antiepileptic drugs for prophylaxis of late PTE. [35]

Corticosteroids have also been investigated for the prevention of PTE, but clinical trials revealed that the drugs did not reduce late PTS and were actually linked to an increase in the number of early PTS. [3]

Treatment

Carbamazepine, commonly used to treat PTE Carbamazepine 3D.png
Carbamazepine, commonly used to treat PTE

Antiepileptic drugs may be given to prevent further seizures; these drugs eliminate seizures for about 35% of people with PTE. [22] However, antiepileptics only prevent seizures while they are being taken; they do not reduce the occurrence once the patient stops taking the drugs. [2] Medication may be stopped after seizures have been controlled for two years. [4] PTE is commonly difficult to treat with drug therapy, [3] [36] and antiepileptic drugs may be associated with side effects. [34] The antiepileptics carbamazepine and valproate are the most common drugs used to treat PTE; phenytoin may also be used but may increase risk of cognitive side effects such as impaired thinking. [9] Other drugs commonly used to treat PTE include clonazepam, phenobarbitol, primidone, gabapentin, and ethosuximide. [12] Among antiepileptic drugs tested for seizure prevention after TBI (phenytoin, valproic acid, carbamazepine, phenobarbital), no evidence from randomized controlled trials has shown superiority of one over another. [8]

People whose PTE does not respond to medication may undergo surgery to remove the epileptogenic focus, the part of the brain that is causing the seizures. [9] However surgery for PTE may be more difficult than it is for epilepsy due to other causes, [9] and is less likely to be helpful in PTE than in other forms of epilepsy. [8] It can be particularly difficult in PTE to localize the epileptic focus, in part because TBI may affect diffuse areas of the brain. [31] Difficulty locating the seizure focus is seen as a deterrent to surgery. [4] However, for people with sclerosis in the mesial temporal lobe (in the inner aspect of the temporal lobe), who comprise about one third of people with intractable PTE, surgery is likely to have good outcome. [4] When there are multiple epileptic foci or the focus cannot be localized, and drug therapy is not effective, vagus nerve stimulation is another option for treating PTE. [31]

People with PTE have follow-up visits, in which health care providers monitor neurological and neuropsychological function and assess the efficacy and side effects of medications. [8] As with other types of epilepsy, individuals with PTE are advised to exercise caution when performing activities for which seizures could be particularly risky, such as rock climbing. [9]

Prognosis

The prognosis for epilepsy due to trauma is worse than that for epilepsy of undetermined cause. [20] People with PTE are thought to have shorter life expectancies than people with brain injury who do not have seizures. [12] Compared to people with similar structural brain injuries but without PTE, people with PTE take longer to recover from the injury, have more cognitive and motor problems, and perform worse at everyday tasks. [12] This finding may suggest that PTE is an indicator of a more severe brain injury, rather than a complication that itself worsens outcome. [12] PTE has also been found to be associated with worse social and functional outcomes but not to worsen patients' rehabilitation or ability to return to work. [8] However, people with PTE may have trouble finding employment if they admit to having seizures, especially if their work involves operating heavy machinery. [37]

The period of time between an injury and development of epilepsy varies, and it is not uncommon for an injury to be followed by a latent period with no recurrent seizures. [25] The longer a person goes without developing seizures, the lower the chances are that epilepsy will develop. [4] At least 80–90% of people with PTE have their first seizure within two years of the TBI. [8] People with no seizures within three years of the injury have only a 5% chance of developing epilepsy. [38] However, one study found that head trauma survivors are at an increased risk for PTE as many as 10 years after moderate TBI and over 20 years after severe TBI. [7] Since head trauma is fairly common and epilepsy can occur late after the injury, it can be difficult to determine whether a case of epilepsy resulted from head trauma in the past or whether the trauma was incidental. [31]

The question of how long a person with PTE remains at higher risk for seizures than the general population is controversial. [7] About half of PTE cases go into remission, but cases that occur later may have a smaller chance of doing so. [20]

Epidemiology

Studies have found that the incidence of PTE ranges between 1.9 and more than 30% of those with TBI, varying by severity of injury and by the amount of time after TBI for which the studies followed subjects. [7]

Brain trauma is one of the strongest predisposing factors for epilepsy development, and is an especially important factor in young adults. [22] Young adults, who are at the highest risk for head injury, also have the highest rate of PTE, [8] which is the largest cause of new-onset epilepsy cases in young people. [39] Children have a lower risk for developing epilepsy; 10% of children with severe TBI and 16–20% of similarly injured adults develop PTE. [22] Being older than 65 is also a predictive factor in the development of epilepsy after brain trauma. [25] One study found PTE to be more common in male TBI survivors than in females. [12]

History

Benjamin Winslow Dudley performed trepanation for PTE before antisepsis was available. Benjamin Winslow Dudley.jpg
Benjamin Winslow Dudley performed trepanation for PTE before antisepsis was available.

Records of PTE exist from as early as 3000 BC. [37] Trepanation, in which a hole is cut in the skull, may have been used to treat PTE in ancient cultures. [10] In the early 19th century, the surgeons Baron Larrey and WC Wells each reported having performed the operation for PTE. [10] The French-educated American surgeon Benjamin Winslow Dudley (1785–1870) performed six trepanations for PTE between the years of 1819 and 1832 in Kentucky and had good results despite the unavailability of antisepsis. [40] The surgery involved opening the skull at the site of injury, debriding injured tissue, and sometimes draining blood or fluid from under the dura mater. [40] Dudley's work was the largest series of its kind that had been done up to that point, and it encouraged other surgeons to use trepanation for post-traumatic seizures. [40] His reports on the operations came before it was accepted that surgery to relieve excess pressure within the skull was effective in treating epilepsy, but it helped set the stage for trepanation for PTE to become common practice. [40] The procedure became more accepted in the late 19th century once antisepsis was available and cerebral localization was a familiar concept. [40] However, in 1890, the prominent German physician Ernest von Bergmann criticized the procedure; he questioned its efficacy (except in particular circumstances) and suggested that operations had been declared successful too soon after the procedures to know whether they would confer a long-term benefit. [10] The late 19th century saw the advent of intracranial surgery, operating on brain lesions believed to be causing seizures, a step beyond cranial surgery which involved just the skull and meninges. [10] By 1893, at least 42 intracranial operations had been performed for PTE in the US, with limited success. [10]

Surgery was the standard treatment for PTE until the years following World War II, when the condition received more attention as soldiers who had survived head trauma developed it. [19] The increased need for drugs to treat PTE led to trials with antiepileptics; these early trials suggested that the drugs could prevent epileptogenesis (the development of epilepsy). [19] It was still thought that antiepileptic drugs could prevent epileptogeneis in the 1970s; [27] in 1973, 60% of physicians surveyed used them to prevent PTE. [33] However, the clinical trials which had supported a protective effect of antiepileptics were uncontrolled; in later, controlled trials the drugs failed to demonstrate an antiepileptogenic effect. [41] Studies did show that antiepileptics prevented seizures occurring within a week after injury, and in 1995 the task force of the Brain Trauma Foundation published a recommendation suggesting their use to protect against seizures early after trauma. [33] However, recommendations were published against the prophylactic use of antiepileptic drugs more than a week after injury by the Brain Injury Special Interest group of the American Academy of Physical Medicine and Rehabilitation in 1998 and by the American Association of Neurological Surgeons in 2000. [12]

Research

How epilepsy develops after an injury to the brain is not fully understood, and gaining such understanding may help researchers find ways to prevent it, or make it less severe or easier to treat. [22] Researchers hope to identify biomarkers, biological indications that epileptogenesis is occurring, as a means to find drugs that can target pathways by which epilepsy develops. [25] For example, drugs could be developed to interfere with secondary brain injury (injury that does not occur at the moment of trauma but results from processes initiated by it), by blocking pathways such as free radical damage to brain tissue. [31] An increase in understanding of age differences in epilepsy development after trauma may also help researchers find biomarkers of epileptogenesis. [25] There is also interest in finding more antiepileptic drugs, with the potential to interfere with epileptogenesis. [42] Some new antiepileptic drugs such as topiramate, gabapentin, and lamotrigine have already been developed and have shown promise in treatment of PTE. [8] No animal model has all the characteristics of epileptogenesis in humans, so research efforts aim to identify one. [22] [25] Such a model may help researchers find new treatments and identify the processes involved in epileptogenesis. [7] However, the most common mechanical models of traumatic brain injury such as fluid percussion injury, controlled cortical impact, and weight-drop injury models exhibit epileptogenesis at chronic time points with documented remote electroencephalographic and behavioral seizures, and increased seizure susceptibility. [43] It has been reported that PTE can also occur in zebrafish, resulting in similar pathophysiological responses to human TBI. [44]

See also

Related Research Articles

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

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

<span class="mw-page-title-main">Seizure</span> Period of symptoms due to excessive or synchronous neuronal brain activity

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

<span class="mw-page-title-main">Convulsion</span> Medical condition where body muscles contract and relax rapidly and repeatedly

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

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

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

A concussion, also known as a mild traumatic brain injury (mTBI), is a head injury that temporarily affects brain functioning. Symptoms may include loss of consciousness; memory loss; headaches; difficulty with thinking, concentration, or balance; nausea; blurred vision; dizziness; sleep disturbances, and mood changes. Any of these symptoms may begin immediately, or appear days after the injury. Concussion should be suspected if a person indirectly or directly hits their head and experiences any of the symptoms of concussion. Symptoms of a concussion may be delayed by 1–2 days after the accident. It is not unusual for symptoms to last 2 weeks in adults and 4 weeks in children. Fewer than 10% of sports-related concussions among children are associated with loss of consciousness.

<span class="mw-page-title-main">Traumatic brain injury</span> Injury of the brain from an external source

A traumatic brain injury (TBI), also known as an intracranial injury, is an injury to the brain caused by an external force. TBI can be classified based on severity ranging from mild traumatic brain injury (mTBI/concussion) to severe traumatic brain injury. TBI can also be characterized based on mechanism or other features. Head injury is a broader category that may involve damage to other structures such as the scalp and skull. TBI can result in physical, cognitive, social, emotional and behavioral symptoms, and outcomes can range from complete recovery to permanent disability or death.

<span class="mw-page-title-main">Primidone</span> Barbiturate medication used to treat seizures and tremors

Primidone, sold under various brand names, is a barbiturate medication that is used to treat partial and generalized seizures and essential tremors. It is taken by mouth.

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

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

Frontal lobe epilepsy (FLE) is a neurological disorder that is characterized by brief, recurring seizures arising in the frontal lobes of the brain, that often occur during sleep. It is the second most common type of epilepsy after temporal lobe epilepsy (TLE), and is related to the temporal form in that both forms are characterized by partial (focal) seizures.

Epilepsy in animals is a group of neurological disorders characterized by seizures, caused by uncontrolled, abnormal bursts of electrical activity in the brain. They can start and stop very abruptly and last any amount of time from a few seconds to a few minutes. Canine epilepsy is often genetic but epilepsy in cats and other pets is rarer, likely because there is no hereditary component to epilepsy in these animals.

Post-concussion syndrome (PCS), also known as persisting symptoms after concussion, is a set of symptoms that may continue for weeks, months, or years after a concussion. PCS is medically classified as a mild traumatic brain injury (TBI). About 35% of people with concussion experience persistent or prolonged symptoms 3 to 6 months after injury. Prolonged concussion is defined as having concussion symptoms for over four weeks following the first accident in youth and for weeks or months in adults.

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

Racine stages are a categorization of rodent epileptic seizures proposed by Ronald J. Racine in 1972. Prior to Racine's research in animal epilepsy models, a quantifiable means to describe seizure intensities and their causes was not readily available. Racine's work allowed for studies among different laboratories to be compared and understood more clearly.

Post-traumatic seizures (PTS) are seizures that result from traumatic brain injury (TBI), brain damage caused by physical trauma. PTS may be a risk factor for post-traumatic epilepsy (PTE), but a person having a seizure or seizures due to traumatic brain injury does not necessarily have PTE, which is a form of epilepsy, a chronic condition in which seizures occur repeatedly. However, "PTS" and "PTE" may be used interchangeably in medical literature.

Epileptogenesis is the gradual process by which a typical brain develops epilepsy. Epilepsy is a chronic condition in which seizures occur. These changes to the brain occasionally cause neurons to fire in an abnormal, hypersynchronous manner, known as a seizure.

Primary and secondary brain injury are ways to classify the injury processes that occur in brain injury. In traumatic brain injury (TBI), primary brain injury occurs during the initial insult, and results from displacement of the physical structures of the brain. Secondary brain injury occurs gradually and may involve an array of cellular processes. Secondary injury, which is not caused by mechanical damage, can result from the primary injury or be independent of it. The fact that people sometimes deteriorate after brain injury was originally taken to mean that secondary injury was occurring. It is not well understood how much of a contribution primary and secondary injuries respectively have to the clinical manifestations of TBI.

Traumatic brain injury can cause a variety of complications, health effects that are not TBI themselves but that result from it. The risk of complications increases with the severity of the trauma; however even mild traumatic brain injury can result in disabilities that interfere with social interactions, employment, and everyday living. TBI can cause a variety of problems including physical, cognitive, emotional, and behavioral complications.

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

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

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

An epilepsy syndrome is defined as "a characteristic cluster of clinical and Electroencephalography (EEG) features, often supported by specific etiological findings ."

References

  1. 1 2 Brady RD, Casillas-Espinosa PM, Agoston DV, Bertram EH, Kamnaksh A, Semple BD, Shultz SR (March 2019). "Modelling traumatic brain injury and posttraumatic epilepsy in rodents". Neurobiology of Disease. 123: 8–19. doi:10.1016/j.nbd.2018.08.007. PMC   6348144 . PMID   30121231.
  2. 1 2 3 Pagni CA, Zenga F (2005). "Posttraumatic epilepsy with special emphasis on prophylaxis and prevention". Acta Neurochirurgica. Acta Neurochirurgica Supplementum. 93: 27–34. doi:10.1007/3-211-27577-0_3. ISBN   978-3-211-24150-9. PMID   15986723.
  3. 1 2 3 4 5 6 7 8 9 Garga N, Lowenstein DH (2006). "Posttraumatic Epilepsy: A Major Problem in Desperate Need of Major Advances". Epilepsy Currents. 6 (1): 1–5. doi:10.1111/j.1535-7511.2005.00083.x. PMC   1363374 . PMID   16477313.
  4. 1 2 3 4 5 6 7 8 9 10 11 Mani J, Barry E (2006). "Posttraumatic epilepsy". In Wyllie E, Gupta A, Lachhwani DK (eds.). The Treatment of Epilepsy: Principles and Practice. Hagerstown, MD: Lippincott Williams & Wilkins. pp. 521–524. ISBN   0-7817-4995-6.
  5. ↑ Scheffer IE, Berkovic S, Capovilla G, Connolly MB, French J, Guilhoto L, Hirsch E, Jain S, Mathern GW (April 2017). "ILAE classification of the epilepsies: Position paper of the ILAE Commission for Classification and Terminology". Epilepsia. 58 (4): 512–521. doi:10.1111/epi.13709. PMC   5386840 . PMID   28276062.
  6. ↑ Pitkänen A, Kharatishvili I, Karhunen H, et al. (2007). "Epileptogenesis in experimental models". Epilepsia. 48 (Supplement 2): 13–20. doi: 10.1111/j.1528-1167.2007.01063.x . PMID   17571349. S2CID   23523719.
  7. 1 2 3 4 5 6 7 8 9 10 11 12 13 D'Ambrosio R, Perucca E (2004). "Epilepsy after head injury". Current Opinion in Neurology. 17 (6): 731–735. doi:10.1097/00019052-200412000-00014. PMC   2672045 . PMID   15542983.
  8. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 Agrawal A, Timothy J, Pandit L, Manju M (2006). "Post-traumatic epilepsy: An overview". Clinical Neurology and Neurosurgery. 108 (5): 433–439. doi:10.1016/j.clineuro.2005.09.001. PMID   16225987. S2CID   2650670.
  9. 1 2 3 4 5 6 Posner E, Lorenzo N (October 11, 2006). "Posttraumatic epilepsy". Emedicine.com. Retrieved on 2008-07-30.
  10. 1 2 3 4 5 6 Eadie MJ, Bladin PF (2001). A Disease Once Sacred: A History of the Medical Understanding of Epilepsy. London: John Libbey. pp. 215–216. ISBN   0-86196-607-4.
  11. 1 2 3 4 5 6 7 Frey LC (2003). "Epidemiology of posttraumatic epilepsy: A critical review". Epilepsia. 44 (Supplement 10): 11–17. doi: 10.1046/j.1528-1157.44.s10.4.x . PMID   14511389. S2CID   34749005.
  12. 1 2 3 4 5 6 7 8 9 10 Tucker GJ (2005). "Seizures". In Silver JM, McAllister TW, Yudofsky SC (eds.). Textbook Of Traumatic Brain Injury. American Psychiatric Pub., Inc. pp. 309–321. ISBN   1-58562-105-6.
  13. 1 2 Gupta YK, Gupta M (2006). "Post traumatic epilepsy: A review of scientific evidence" (PDF). Indian Journal of Physiology and Pharmacology. 50 (1): 7–16. PMID   16850898. Archived from the original (PDF) on 2011-07-13. Retrieved 2008-07-31.
  14. 1 2 Ayd FJ (2000). Lexicon of Psychiatry, Neurology, and the Neurosciences. Philadelphia, Pa: Lippincott-Williams & Wilkins. pp. 888–890. ISBN   0-7817-2468-6.
  15. ↑ Statler KD (2006). "Pediatric posttraumatic seizures: Epidemiology, putative mechanisms of epileptogenesis and promising investigational progress". Dev. Neurosci. 28 (4–5): 354–363. doi:10.1159/000094162. PMID   16943659. S2CID   24833791.
  16. ↑ Cuccurullo S (2004). Physical Medicine and Rehabilitation Board Review. Demos Medical Publishing. pp. 68–71. ISBN   1-888799-45-5.
  17. 1 2 Parent JM, Aminoff MJ (2004). "Treatment of epilepsy in general medical conditions". In Dodson WE, Avanzini G, Shorvon SD, Fish DR, Perucca E (eds.). The Treatment of Epilepsy. Oxford: Blackwell Science. p. 244. ISBN   0-632-06046-8.
  18. 1 2 3 Annegers JF, Hauser WA, Coan SP, Rocca WA (January 1998). "A population-based study of seizures after traumatic brain injuries". New England Journal of Medicine. 338 (1): 20–4. doi: 10.1056/NEJM199801013380104 . PMID   9414327.
  19. 1 2 3 4 5 6 7 8 9 Iudice A, Murri L (2000). "Pharmacological prophylaxis of post-traumatic epilepsy". Drugs. 59 (5): 1091–9. doi:10.2165/00003495-200059050-00005. PMID   10852641. S2CID   28616181.
  20. 1 2 3 4 5 JW Sander, MC Walker and JE Smalls (2007). "Chapter 12: Adult onset epilepsies, DW Chadwick" (PDF). Epilepsy: From Cell to Community – A Practical Guide to Epilepsy (PDF). National Society for Epilepsy. pp. 127–132. ISBN   978-0-9519552-4-6 . Retrieved 2008-07-26.
  21. ↑ Oliveros-Juste A, Bertol V, Oliveros-Cid A (2002). "Preventive prophylactic treatment in posttraumatic epilepsy". Revista de Neurología (in Spanish). 34 (5): 448–459. doi:10.33588/rn.3405.2001439. PMID   12040514.
  22. 1 2 3 4 5 6 7 8 9 Pitkänen A, McIntosh TK (2006). "Animal models of post-traumatic epilepsy". Journal of Neurotrauma. 23 (2): 241–261. doi:10.1089/neu.2006.23.241. PMID   16503807.
  23. ↑ Beghi E (2004). "Aetiology of epilepsy". In Dodson WE, Avanzini G, Shorvon SD, Fish DR, Perucca E (eds.). The Treatment of Epilepsy. Oxford: Blackwell Science. p. 61. ISBN   0-632-06046-8.
  24. ↑ de la Peña P, Porta-Etessam J (1998). "Post-traumatic epilepsy". Revista de Neurología (in Spanish). 26 (150): 256–261. doi:10.33588/rn.26150.981066. PMID   9580443.
  25. 1 2 3 4 5 6 7 Herman ST (2002). "Epilepsy after brain insult: Targeting epileptogenesis". Neurology. 59 (9 Suppl 5): S21–S26. doi:10.1212/wnl.59.9_suppl_5.s21. PMID   12428028. S2CID   6978609.
  26. ↑ Mazarati A (2006). "Is Posttraumatic Epilepsy the Best Model of Posttraumatic Epilepsy?". Epilepsy Currents. 6 (6): 213–214. doi:10.1111/j.1535-7511.2006.00149.x. PMC   1783489 . PMID   17260063.
  27. 1 2 Willmore LJ (1990). "Post-traumatic epilepsy: Cellular mechanisms and implications for treatment". Epilepsia. 31 (Supplement 3): S67–73. doi:10.1111/j.1528-1157.1990.tb05861.x. PMID   2226373. S2CID   34342615.
  28. ↑ Morimoto K, Fahnestock M, Racine RJ (May 2004). "Kindling and status epilepticus models of epilepsy: Rewiring the brain". Prog. Neurobiol. 73 (1): 1–60. doi:10.1016/j.pneurobio.2004.03.009. PMID   15193778. S2CID   36849482.
  29. ↑ Abel MS, McCandless DW (1992). "The kindling model of epilepsy". In Adams RN, Baker GB, Baker JM, Bateson AN, Boisvert DP, Boulton AA, et al. (eds.). Neuromethods: Animal Models of Neurological Disease. Totowa, NJ: Humana Press. pp. 153–155. ISBN   0-89603-211-6.
  30. ↑ Menkes JH, Sarnat HB, Maria BL (2005). Child Neurology. Hagerstown, MD: Lippincott Williams & Wilkins. pp. 683–684. ISBN   0-7817-5104-7.
  31. 1 2 3 4 5 Firlik KS, Spencer DD (2004). "Surgery of post-traumatic epilepsy". In Dodson WE, Avanzini G, Shorvon SD, Fish DR, Perucca E (eds.). The Treatment of Epilepsy. Oxford: Blackwell Science. pp. 775–778. ISBN   0-632-06046-8.
  32. ↑ Barry E, Bergey GK, Krumholz A, et al. (1997). "Posttraumatic seizure types vary with the interval after head injury". Epilepsia. 38 (Supplement 8): 49S–50S. doi: 10.1111/j.1528-1157.1997.tb01495.x . S2CID   221735326.
  33. 1 2 3 Schierhout G, Roberts I (2008) [2001]. Schierhout G (ed.). "Anti-epileptic drugs for preventing seizures following acute traumatic brain injury". Cochrane Database of Systematic Reviews (4): CD000173. doi:10.1002/14651858.CD000173. PMID   11687070. (Retracted, see doi:10.1002/14651858.CD000173.pub2, PMID   22696316 . If this is an intentional citation to a retracted paper, please replace {{ retracted |...}} with {{ retracted |...|intentional=yes}}.)
  34. 1 2 Beghi E (2003). "Overview of studies to prevent posttraumatic epilepsy". Epilepsia. 44 (Supplement 10): 21–26. doi: 10.1046/j.1528-1157.44.s10.1.x . PMID   14511391. S2CID   25635858.
  35. ↑ Szaflarski JP, Nazzal Y, Dreer LE (2014). "Post-traumatic epilepsy: current and emerging treatment options". Neuropsychiatric Disease and Treatment. 10: 1469–77. doi: 10.2147/NDT.S50421 . PMC   4136984 . PMID   25143737.
  36. ↑ Aroniadou-Anderjaska V, Fritsch B, Qashu F, Braga MF (February 2008). "Pathology and Pathophysiology of the Amygdala in Epileptogenesis and Epilepsy". Epilepsy Res. 78 (2–3): 102–16. doi:10.1016/j.eplepsyres.2007.11.011. PMC   2272535 . PMID   18226499.
  37. 1 2 Young B (1992). "Post-traumatic epilepsy". In Barrow DL (ed.). Complications and Sequelae of Head Injury. Park Ridge, Ill: American Association of Neurological Surgeons. pp. 127–132. ISBN   1-879284-00-6.
  38. ↑ Swash M (1998). Outcomes in Neurological and Neurosurgical Disorders. Cambridge, UK: Cambridge University Press. pp. 172–173. ISBN   0-521-44327-X.
  39. ↑ Diaz-Arrastia R, Agostini MA, Frol AB, et al. (November 2000). "Neurophysiologic and neuroradiologic features of intractable epilepsy after traumatic brain injury in adults". Archives of Neurology. 57 (11): 1611–1616. doi: 10.1001/archneur.57.11.1611 . PMID   11074793.
  40. 1 2 3 4 5 Jensen RL, Stone JL (1997). "Benjamin Winslow Dudley and early American trephination for posttraumatic epilepsy". Neurosurgery. 41 (1): 263–268. doi:10.1097/00006123-199707000-00045. PMID   9218316.
  41. ↑ Willmore LJ (December 2005). "Antiepileptic drugs and neuroprotection: Current status and future roles". Epilepsy & Behavior. 7 (Supplement 3): S25–S28. doi:10.1016/j.yebeh.2005.08.006. PMID   16239127. S2CID   40670766.
  42. ↑ Chang BS, Lowenstein DH (2003). "Practice parameter: Antiepileptic drug prophylaxis in severe traumatic brain injury: Report of the Quality Standards Subcommittee of the American Academy of Neurology". Neurology. 60 (1): 10–16. doi: 10.1212/01.wnl.0000031432.05543.14 . PMID   12525711.
  43. ↑ Glushakov AV, Glushakova OY, Doré S, Carney PR, Hayes RL (2016). "Animal Models of Posttraumatic Seizures and Epilepsy". Injury Models of the Central Nervous System. Methods in Molecular Biology. Vol. 1462. pp. 481–519. doi:10.1007/978-1-4939-3816-2_27. ISBN   978-1-4939-3814-8. ISSN   1940-6029. PMC   6036905 . PMID   27604735.
  44. ↑ Cho SJ, Park E, Telliyan T, Baker A, Reid AY (August 2020). "Zebrafish model of posttraumatic epilepsy". Epilepsia. 61 (8): 1774–1785. doi:10.1111/epi.16589. ISSN   0013-9580. PMID   32592416. S2CID   220120920.

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