Epilepsy is a common chronic neurological disorder that is characterized by recurrent unprovoked seizures. These seizures are transient signs and/or symptoms due to abnormal, excessive or synchronous neuronal activity in the brain. About 50 million people worldwide have epilepsy at any one time. Epilepsy is usually controlled, but not cured, with medication, although surgery may be considered in difficult cases. Not all epilepsy syndromes are lifelong – some forms are confined to particular stages of childhood. Epilepsy should not be understood as a single disorder, but rather as a group of syndromes with vastly divergent symptoms but all involving episodic abnormal electrical activity in the brain.

The word epilepsy is derived from the Greek epilepsia, which in turn can be broken in to epi- (upon) and lepsis (to take hold of, or seizure). In the past, epilepsy was associated with religious experiences and even demonic possession. Claudius Galen was the first person who described epilepsy as a brain disease. Boerhaave was the first person who differentiate petit mal epilepsy, grand mal epilepsy and hysteria. Marshall Hall described reflex theory in which paroxysmal nervous discharges are responsible for epilepsy seizures. The very first evidence of epilepsy treatment goes back to 10,000 years ago when making holes in skull bones was done in order to treat epilepsy. In the past three decades anti-epileptic drugs are used widely for symptomatic control of epileptic patients.

Epilepsy may be classified according to type of onset into focal, generalized and unknown. Each of these groups can be further divided into motor and non-motor subgroups.

It is understood that epileptic seizure is the result of uncontrolled unusual synchronized, localized or widely distributed neuronal electrical discharges. The underlying event in all types of seizures is the paroxysmal depolarization shift (PDS) which also causes the EEG changes. In a normal circumstance we have a refractory period after every action potential, but in PDS, the absence of refractory period causes a prolonged membrane depolarization. In order to cause a seizure, so many PDSs most happen in the same time. Any alternation in a synaptic characteristics such as amount of neurotransmitters, function of inhibitory neurons, function of excitatory neurons, synaptic structure and ion channels involved in neurotransmitter release and conduction of action potential can prone a person to epilepsy. In focal epilepsy, epileptiform activity starts in a specific area of brain. It can further spread and cause secondary generalized seizure. In generalized epilepsy seizures occur in both cerebral hemispheres simultaneously or spread so fast from one to another that in EEG, we can see bilateral epileptiform activity from the start.

Common causes of epilepsy include head trauma, brain tumor, brain hemorrhage, encephalitis, hypoglycemia, hypoxic encephalopathy, stroke, cerebral palsy, electrolyte disturbances, epileptic encephalopathy – Lennox-Gastaut type, febrile seizures, Huntington’s disease, intoxication and uremia.

Epilepsy must be differentiated from psychogenic nonepileptic attacks (PNEAs), syncope, hypoglycemia, panic attacks, acute dystonic reactions, hemifacial spasm, nonepileptic myoclonus, parasomnias, cataplexy, hypnic jerks, transient ischemic attacks, migraines and transient global amnesia.

Epilepsy’s approximate annual incidence rate is 40–70 per 100,000 in industrialized countries and 100–190 per 100,000 in resource-poor countries; socioeconomically deprived people are at higher risk. The prevalence of active epilepsy is roughly in the range 5–10 per 1000 people. Many studies have demonstrated that mortality rate is higher in people with epilepsy. The most common causes of death in these patients are trauma, pneumonia, suicide, status epilepticus and sudden unexpected death. Epilepsy is one of the most common of the serious neurological disorders. Genetic, congenital, and developmental conditions are mostly associated with it among younger patients; tumors are more likely over age 40; head trauma and central nervous system infections may occur at any age. There is no evidence of race differences in incidence and prevalence of epilepsy. It was demonstrated that nonsymptomatic epilepsy such as cryptogenic localization-related and idiopathic generalized epilepsy are more common in women while symptomatic localization-related epilepsy is more common in men.

Common triggers of seizure include sleep deprivation, fever, light flashing, hyperventilation, alcohol, physical stress such as physical exercise or illness, psychological stress, depression.

There is insufficient evidence to recommend routine screening for epilepsy.

If left untreated, 23% to 71% of patients with a single unprovoked seizure may experience it again within 2 years. After the second unprovoked seizure, the chance of having another seizure increase to 73%. Recurrent seizures with no underlying illness emphasis on epilepsy diagnosis. Common complications of epilepsy include status epilepticus, sudden unexpected death, submersion Injury, dental injury, burns, fractures, head injury, soft tissue injury and motor vehicle accidents.

There is no single diagnostic study of choice for the diagnosis of epilepsy, but epilepsy can be diagnosed based on history, symptoms and physical examination of a patient with seizure complain. Among the patients who present with clinical signs of seizure, the EEG is the most efficient test for diagnosis. Video-EEG monitoring is a combination of recording EEG and clinical behavior of the patient. Although it’s more expensive, it is more effective in differentiating different type if seizures. With the first seizure, we should perform laboratory study ( electrolytes, glucose, calcium, magnesium, complete blood count, renal function tests, liver function tests, urinalysis, toxicology screens), imaging study ( MRI, CT Scan), EEG, video-EEG monitoring and lumbar puncture.

A positive history of family member with epilepsy, brain traumatic injuries, meningitis and encephalitis, febrile seizure in the childhood, enuresis, drug abuse and previous episod of seizure is suggestive of epilepsy. The most common symptoms of epileptic seizure include paroxysmal manner, similarity to each other in a patient in the aspect of duration and general characteristics, presenting with a motor phenomena which can be accompanied with sensory and autonomic manifestation, impaied consciousness, aura (sensory, autonomic, or psychic symptoms), starting with a triggers, post-ictal drowsiness, tongue biting and urine and fecal incontinence.

Common physical examination findings of epileptic seizure include Automatic behaviors, upward eye rolling, unconsciousness, drooling, cyanosis, post-ictal drowsiness, fever, tachycardia, hypertension, mydriasis, nystagmus, urine and fecal incontinence, disorientation to persons, place, and time, altered mental status, automatic behaviors (repetitive muscle movement), Muscle rigidity and hyper-reflexia.

Laboratory findings consistent with the diagnosis of epilepsy include elevated creatine phosphokinase (CPK), elevated cortisol, elevated white blood cell count, elevated lactate dehydrogenase and elevated neuron-specific enolase.

An ECG may be helpful in the diagnosis of epilepsy. Findings on an EEG suggestive of epilepsy include synchronous generalized spikes and waves in all leads in tonic-clonic seizures, spike and wave activity at a frequency of approximately 3 HZ in absence seizures, localized epileptic activity over the seizure focus in focal seizures with intact consciousness and temporal slow waves or spikes in focal seizures with impaired consciousness.

There are no x-ray findings associated with epilepsy.

In one case report, a 65-year-old woman presented with seizure. Echocardiography was performed and revealed a left atrium tumor.

CT Scan is mostly used in patients who are contraindicated for MRI or in the cases with skull fracture suspicious.

MRI may be helpful in the diagnosis of epilepsy. Findings on MRI suggestive epileptic seizure include mesial temporal sclerosis, sequelae of head injury, congenital anomalies, brain tumors, cysticercosis, vascular lesions, strokes, cerebral degeneration and neoplasms.

There are no other imaging findings associated with epilepsy.

Lumbar puncture may be helpful in differentiating epilepsy from infectious etiology of seizures.

Supportive therapy for Guillain-Barre syndrome include respiratory assistance, Heart rate and blood pressure monitoring, prevention of thromboembolic complications by heparin, minimal sedation in intensive care units, pain control and early passive movements. Immunomodulating therapy for Guillain-Barre syndrome include plasma exchange, high dose immunoglobulin and Corticosteroids.

Surgery is not the first-line treatment option for patients with epilepsy. Surgery is usually reserved for patients who their seizure continues to happen despite using maximum dosage of anti-seizure drugs.

Effective measures for the primary prevention of epilepsy include reducing the chance of possible epilepsy causes to happen (Head trauma, Hypoglycemia, Cerebral palsy, Electrolyte disturbances, fever, drug abuse and Vitamin deficiency) and reduce the seizure triggers (sleep deprivation, fever, light flashing, hyperventilation, alcohol, physical stress such as physical exercise or illness, psychological stress and depression).

Effective measures for the secondary prevention of epilepsy include early diagnosis and effective treatment.

The word epilepsy is derived from the Greek epilepsia, which in turn can be broken in to epi- (upon) and lepsis (to take hold of, or seizure). In the past, epilepsy was associated with religious experiences and even demonic possession. Claudius Galen was the first person who described epilepsy as a brain disease. Boerhaave was the first person who differentiate petit mal epilepsy, grand mal epilepsy and hysteria. Marshall Hall described reflex theory in which paroxysmal nervous discharges are responsible for epilepsy seizures. The very first evidence of epilepsy treatment goes back to 10,000 years ago when making holes in skull bones was done in order to treat epilepsy. In the past three decades anti-epileptic drugs are used widely for symptomatic control of epileptic patients.

• The word epilepsy is derived from the Greek epilepsia, which in turn can be broken in to epi- (upon) and lepsis (to take hold of, or seizure)^[1]
• In the past, epilepsy was associated with religious experiences and even demonic possession.
• In ancient times, epilepsy was known as the “Sacred Disease” because people thought that epileptic seizures were a form of attack by demons, or that the visions experienced by persons with epilepsy were sent by the Gods.
• Among animist Hmong families, for example, epilepsy was understood as an attack by an evil spirit, but the affected person could become revered as a shaman through these otherworldly experiences.[3]

• However, in most cultures, persons with epilepsy have been stigmatized, shunned, or even imprisoned.
• In the Salpêtrière, the birthplace of modern neurology, Jean-Martin Charcot found people with epilepsy side-by-side with the mentally retarded, those with chronic syphilis, and the criminally insane.
• In Tanzania to this day, as with other parts of Africa, epilepsy is associated with possession by evil spirits, witchcraft, or poisoning and is believed by many to be contagious.^[2]
• In ancient Rome, epilepsy was known as the Morbus Comitialis (‘disease of the assembly hall’) and was seen as a curse from the gods.

• Stigma continues to this day, in both the public and private spheres, but polls suggest it is generally decreasing with time, at least in the developed world.
• Hippocrates remarked that epilepsy would cease to be considered divine the day it was understood.^[3]

• Claudius Galen was the first person who described epilepsy as a brain disease.

• Boerhaave was the first person who differentiate petit mal epilepsy, grand mal epilepsy and hysteria.
• Marshall Hall described reflex theory in which paroxysmal nervous discharges are responsible for epilepsy seizures.^[4]

• Important Investigators of Epilepsy:
  • Jean-Martin Charcot
  • John Hughlings Jackson
  • Hans Berger
  • Herbert Jasper
  • Wilder Penfield
  • H. Houston Merritt
  • William G. Lennox^[4]

• The very first evidence of epilepsy treatment goes back to 10,000 years ago when making holes in skull bones was done in order to treat epilepsy.^[4]
• In the past three decades anti-epileptic drugs are used widely for symptomatic control of epileptic patients.^[5][6]

The following are a few famous cases who are said to have had epilepsy:^[7]

• Pythagoras (582–500 BC)
• Aristotle (384–322 BC)
• Hannibal (Barca) (247–183 BC)
• Alfred the Great (849–899)
• Dante Alighieri (1265–1321)
• Johanne la Pucelle (Joan of Arc) (1412–1431)
• Leonardo da Vinci (1452–1519)
• Michelangelo Buonarroti (1475–1564)
• Armand-Jean du Plessis (Cardinal Richelieu) (1585–1642)
• King Louis XIII of France (1601–1643)
• Jean-Baptiste Poquelin-Molie´re (1622–1673)
• Blaise Pascal (1623–1662)
• Sir Isaac Newton (1642–1727)
• William of Orange (1650–1702)
• Jonathan Swift (1667–1745)
• George Frideric Handel (1685–1759)
• William Pitt, Earl of Chatham (1708–1778)
• Samuel Johnson (1709–1784)
• Jean Jacques Rousseau (1712–1778)
• James Madison (1751–1836)
• Ludwig von Beethoven (1770–1827)
• Sir Walter Scott (1771–1832)
• Niccolo Paganini (1784–1840)
• George Gordon, Lord Byron (1788–1824)
• Percy Bysshe Shelley (1792–1822)
• Louis Hector Berlioz (1803–1869)
• Edgar Allan Poe (1809–1849)
• Alfred Lord Tennyson (1809–1892)
• Robert Schumann (1810–1856)
• Charles Dickens (1812–1870)
• Søren Aabye Kierkegaard (1813–1855)
• Hermann Ludwig Ferdinand Von Helmholtz (1821–1894)
• Gustave Flaubert (1821–1880)
• Leo Tolstoy (1828–1910)
• Charles Lutwidge Dodgson, Lewis Carroll (1832–1898)
• Alfred Nobel (1833–1896)
• William Morris (1834–1896)
• Algernon Charles Swinburne (1837–1909)
• Henri-Rene´-Albert Guy de Maupassant (1850–1893)
• Agatha (Miller) Christie (1890–1976)
• Truman (Streckfus Persons) Capote (1924–1984)
• Richard Burton (1925–1984)

Many studies demonstrated that there are doubts about diagnosis of epilepsy in these patients.

Epilepsy may be classified according to type of onset into focal, generalized and unknown. Each of these groups can be further divided into motor and non-motor subgroups.

• Epilepsy may be classified according to type of onset into:^[1]

It is understood that epileptic seizure is the result of uncontrolled unusual synchronized, localized or widely distributed neuronal electrical discharges. The underlying event in all types of seizures is the paroxysmal depolarization shift (PDS) which also causes the EEG changes. In a normal circumstance we have a refractory period after every action potential, but in PDS, the absence of refractory period causes a prolonged membrane depolarization. In order to cause a seizure, so many PDSs most happen in the same time. Any alternation in a synaptic characteristics such as amount of neurotransmitters, function of inhibitory neurons, function of excitatory neurons, synaptic structure and ion channels involved in neurotransmitter release and conduction of action potential can prone a person to epilepsy. In focal epilepsy, epileptiform activity starts in a specific area of brain. It can further spread and cause secondary generalized seizure. In generalized epilepsy seizures occur in both cerebral hemispheres simultaneously or spread so fast from one to another that in EEG, we can see bilateral epileptiform activity from the start.

• The normal physiology of neuronal action potential can be understood as follows:

• When an action potential reaches the plasma membrane of a neuron cell, voltage gated Na+ channels will open and Na+ flows into the cell and makes it depolarized.
• When plasma membrane potential reaches a specific level, K+ channel opening will hyperpolarize the neuronal membrane.^[1]

• It is understood that epileptic seizure is the result of uncontrolled unusual synchronized, localized or widely distributed neuronal electrical discharges.^[2]
• The underlying event in all types of seizures is the paroxysmal depolarization shift (PDS) which also causes the EEG changes.^[3]
• In a normal circumstance we have a refractory period after every action potential, but in PDS, the absence of refractory period causes a prolonged membrane depolarization.^[4]
• The likelihood of PDS happening depends on so many factors such as intrinsic neuronal characteristic (channelopathies) and extrinsic characteristics (excess excitatory or inadequate inhibitory neurotransmitters).
• In order to cause a seizure, so many PDSs most happen in the same time.^[5]
• Any alternation in a synaptic characteristics can prone a person to epilepsy. They include:
  • Amount of neurotransmitters
  • Function of inhibitory neurons
  • Function of excitatory neurons
  • Synaptic structure
  • Ion channels involved in neurotransmitter release and conduction of action potential.^[6]
• The underlying pathophysiology of focal epilepsy is different than generalized epilepsy.
  • Focal epilepsy:
    • In these kind of seizures, epileptiform activity starts in a specific area of brain. It can further spread and cause secondary generalized seizure.
  • Generalized epilepsy:
    • These seizures occur in both cerebral hemispheres simultaneously or spread so fast from one to another that in EEG, we can see bilateral epileptiform activity from the start.^[7]

• There are many genes involved in ion channels and neurotransmitter receptors. The polymorphism of these genes determine a person’s susceptibility for developing epilepsy after an offending injury.^[8]

• Mutations in several genes have been linked to some types of epilepsy. Several genes that code for protein subunits of voltage-gated and ligand-gated ion channels have been associated with forms of generalized epilepsy and infantile seizure syndromes.^[9]
• there are some forms of Mendelian syndromes which are the result of mutation in SCN1A gene (Dravet syndrome) or GABR1 gene (autosomal dominant nocturnal frontal lobe epilepsy, juvenile myoclonic epilepsy).^[8]

• On gross pathology, slight opacity and thickening of the meninges, signs of meningitis, vascular disturbances, ecchymoses on the surface of various organs and fatty changes in the heart and striated muscles can be seen in epilepsy.^[10]

• On microscopic pathology histopathological analysis:
  • In the hippocampus of patients with temporal lobe epilepsy there is evidence of cell loss mainly in CA1 and CA4 sectors, CA1 neuron loss and gliosis and CA4 neuronal cell loss and gliosis.
  • In dentate gyrus there is evidence of Substantial granule cell loss and Cell dispersion.^[11]

Common causes of epilepsy include Head trauma, Brain tumor, Brain hemorrhage, Encephalitis, Hypoglycemia, Hypoxic encephalopathy, Stroke, Cerebral palsy, Electrolyte disturbances, febrile seizures, Intoxication and uremia.

Life-threatening causes of epilepsy include:^{[1][2][3][4][5][6]}

• Head trauma
• Brain tumor
• Brain hemorrhage
• Encephalitis
• Hypoglycemia
• Hypoxic encephalopathy
• Stroke

Common causes of epilepsy may include:^{[7][8][9][10][11][12]}

• Cerebral palsy
• Electrolyte disturbances
• Epileptic encephalopathy – Lennox-Gastaut type
• Febrile seizures
• Huntington’s disease
• Intoxication
• Uremia

Less common causes of epilepsy include:^[13]

• Vitamin deficiency

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Epilepsy must be differentiated from: Psychogenic nonepileptic attacks (PNEAs), syncope, hypoglycemia, panic attacks, acute dystonic reactions, hemifacial spasm, nonepileptic myoclonus, parasomnias, cataplexy, hypnic jerks, transient ischemic attacks, migraines and transient global amnesia.

Epilepsy must be differentiated from:

• Psychogenic nonepileptic attacks (PNEAs):
  • Psychogenic non epileptic attacks most commonly happens in young women and is the most common disease misdiagnosed with epilepsy.^[1][2][3]
  • There are some features which can help us differentiate PNEAs from epilepsy:
    • These patients are resistance to anti-epileptic drugs.^[4]
    • PNEAs rarely happens in sleep and mostly happens in the present of an audience.^[5]
    • In physical examination of PNEAs patients we can observe histrionic features.^[6]
    • Tongue biting, urine incontinence and postictal confusion are in favor of epilepsy.^[6]
    • In PNEAs we have normal EEGs.^[7]

• Syncope:
  • Syncope is another misdiagnosed disease with epilepsy. The reason for this misdiagnosis is that syncope attacks happens in a convulsive manner and patients may have body jerks and clonic movement.^[8]
  • Syncope also cause EEG changes and make it more difficult to differentiate it from epilepsy.^[9]
  • There are some presyncope symptoms such as sweating, dizziness, nausea and malaise which helps us differentiate it from epilepsy.^[10]
• Hypoglycemia
• Panic attacks: Panic attacks mostly resemble PNEAs rather than epilepsy.^[11][12] In mesiotemporal epilepsy the patient experience fear as an aura and it can be mistaken with panic attack specially if the typical seizure doesn’t happen after aura.^[13]
• Acute dystonic reactions: Drugs such as anti-dopaminergic, anti-emetics, carbamazepine, lithium and trazodone can cause twisting movements of craniopharyngeal and cervical muscles for seconds to hours. This condition response very well to anticholinergic treatment.^[14]

• Hemifacial spasm: Hemifacial spasm (HFS) can be mistaken with simple partial seizure or facial clonic seizure. There are some features which helps us to differentiate it from epilepsy:
  • HFS is a progressive and chronic condition and it’s not a paroxysmal phenomenon.
  • In partial epilepsy we have involvement of perioral muscle but HFS mostly involves periorbital muscles.^[15]
• Nonepileptic myoclonus
• Parasomnias: Non-REM parasomnias such as night terrors and sleepwalking can misdiagnosed with epilepsy specially because they are paroxysmal and can cause amnesia and unresponsiveness. These patients have normal EEG and their attacks mostly starts in a specific stage of sleep.^[16][17]
• Cataplexy: Cataplexy commonly misdiagnosed with atonic seizures (drop attacks) These attacks mostly trigger by emotion such as laughter.^[18][19]
• Hypnic jerks: Hypanic jerk is a very common condition which happens at the beginning of sleep resembles myoclonic seizures.^[20]
• Transient ischemic attacks: The key difference between TIA and seizure is TIA attacks have negative symptoms instead of positive symptoms we observe in seizures.^[21]
• Migraines
• Transient global amnesia: Patients with this condition experience periods of anterograde amnesia for few hours which resolves on its own.^[22]

A quick algorithm to differentiate epilepsy from other causes of altered mental status is demonstrated below:

Abbreviations: SCD: Sudden cardiac death;T-LOC: Transient-Loss of consciousness.

Epilepsy’s approximate annual incidence rate is 40–70 per 100,000 in industrialized countries and 100–190 per 100,000 in resource-poor countries; socioeconomically deprived people are at higher risk. The prevalence of active epilepsy is roughly in the range 5–10 per 1000 people. Many studies have demonstrated that mortality rate is higher in people with epilepsy. The most common causes of death in these patients are trauma, pneumonia, suicide, status epilepticus and sudden unexpected death. Epilepsy is one of the most common of the serious neurological disorders. Genetic, congenital, and developmental conditions are mostly associated with it among younger patients; tumors are more likely over age 40; head trauma and central nervous system infections may occur at any age. There is no evidence of race differences in incidence and prevalence of epilepsy. It was demonstrated that nonsymptomatic epilepsy such as cryptogenic localization-related and idiopathic generalized epilepsy are more common in women while symptomatic localization-related epilepsy is more common in men.

• Epilepsy’s approximate annual incidence rate is 40–70 per 100,000 in industrialized countries and 100–190 per 100,000 in resource-poor countries; socioeconomically deprived people are at higher risk. In industrialized countries the incidence rate decreased in children but increased among the elderly during the three decades prior to 2003, for reasons not fully understood.^[1]

• The prevalence of active epilepsy is roughly in the range 5–10 per 1000 people. Up to 50 per 1000 people experience nonfebrile seizures at some point in life; epilepsy’s lifetime prevalence is relatively high because most patients either stop having seizures or (less commonly) die. ^[1]

• Many studies have demonstrated that mortality rate is higher in people with epilepsy.^[2][3] The most common causes of death in these patients are trauma, pneumonia, suicide, status epilepticus and sudden unexpected death.^[4][5][6][7]

• Epilepsy is one of the most common of the serious neurological disorders.^[8] Genetic, congenital, and developmental conditions are mostly associated with it among younger patients; tumors are more likely over age 40; head trauma and central nervous system infections may occur at any age.^[1]

• There is no evidence of race differences in incidence and prevalence of epilepsy.^[9][10]

• It was demonstrated that nonsymptomatic epilepsy such as cryptogenic localization-related and idiopathic generalized epilepsy are more common in women while symptomatic localization-related epilepsy is more common in men.^[11]

Common triggers of seizure include: Sleep deprivation, fever, light flashing, hyperventilation, alcohol, physical stress such as physical exercise or illness, psychological stress, depression.

Common risk factors of seizure include:^[1][2][3]

• Sleep deprivation
• Fever
• Light flashing
• Hyperventilation
• Alcohol
• Physical stress such as physical exercise or illness
• Psychological stress
• Depression

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There is insufficient evidence to recommend routine screening for epilepsy.

There is insufficient evidence to recommend routine screening for epilepsy.

If left untreated, 23% to 71% of patients with a single unprovoked seizure may experience it again within 2 years. After the second unprovoked seizure, the chance of having another seizure increase to 73%. Recurrent seizures with no underlying illness emphasis on epilepsy diagnosis. Common complications of epilepsy include: Status epilepticus, sudden unexpected death, submersion Injury, dental injury, burns, fractures, head injury, soft tissue injury and motor vehicle accidents.

• If left untreated, 23% to 71% of patients with a single unprovoked seizure may experience it again within 2 years.
• After the second unprovoked seizure, the chance of having another seizure increase to 73%.
• Recurrent seizures with no underlying illness emphasis on epilepsy diagnosis.

• In contrast to adolescent onset epilepsy syndromes most of the childhood onset epilepsy such as benign childhood epilepsy with centrotemporal spikes will go to remission.
• There is no evidence demonstrating the effect of medical therapy on natural history of epilepsy.^[1]

• Common complications of epilepsy include:
  • Status epilepticus^[2]
  • Sudden unexpected death^[3]
  • Submersion Injury
  • Dental injury^[4]
  • Burns^[5]
  • Fractures^[6]
  • Head injury
  • Soft tissue injury^[7]
  • Motor vehicle accidents^[8]
  • Epileptic heart^[9]
  • Sudden cardiac death