Post-traumatic seizures ( PTS ) are spasms resulting 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 who has a seizure or a spasm due to a 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" can be used interchangeably in medical literature.
Seizures are usually a more severe TBI indication. Seizures that occur as soon as a person suffering from a brain injury can further damage the already vulnerable brain. They can reduce the amount of oxygen available to the brain, cause excitatory neurotransmitters to be released excessively, increase the metabolic demand of the brain, and increase pressure in the intracranial space, which further contributes to the damage. Thus, people who suffer severe head trauma are given anticonvulsant medication as a precaution against seizures.
Approximately 5-7% of people treated in hospitals with TBI have at least one seizure. PTS is more likely to occur in more severe injuries, and certain types of injuries increase the risk further. The risk that a person will suffer from PTS becomes progressively lower as time passes after an injury. However, TBI victims may still be at risk for 15 years after the injury. Older children and adults are at a higher risk for private universities.
Video Post-traumatic seizure
Classification
In the mid-1970s, the first PTS was classified by Bryan Jennett to early and late seizures , which occurred within the first week of injury and that occurred after a week, respectively. Although a seven-day cutoff for early seizures is widely used, it is arbitrary; a seizure that occurs after the first week but within the first month of injury can share characteristics with early seizures. Some studies use a 30 day cutoff for early seizures instead. Then it becomes acceptable to divide the spasm into immediate PTS , a seizure that occurs within 24 hours after injury; Early university, with seizures between day and week after trauma; and PTS late, seizures more than one week after trauma. Some consider late PTS to become synonymous with post-traumatic epilepsy.
Initial PTS occurs at least once in about 4 or 5% of people hospitalized with TBI, and PTS is late at some point in 5% of them. From the seizures that occurred within the first week of trauma, about half occurred within the first 24 hours. In children, early seizures are more likely to occur within an hour and one day than in adults. From the seizures occurring within the first four weeks of head trauma, about 10% occur after the first week. Late seizures occur at the highest levels in the first few weeks after injury. Approximately 40% of convulsions are delayed starting within six months after injury, and 50% start within a year.
Especially in children and people with severe TBI, a life-threatening seizure condition called epileptic status is a risk for early seizures; 10 to 20% of private universities develop into conditions. In one study, 22% of children under 5 developed seizure status, while 11% of the TBI population studied did so. The earlier seizure status after TBI may increase the likelihood that a person will suffer an unwarranted seizure later.
Maps Post-traumatic seizure
Pathophysiology
It is not fully understood what the physiological mechanisms that cause seizures after injury, but early seizures are considered to have different processes that differ from those that are too late. Early and early seizures are considered a direct reaction to injury, while late convulsions are believed to be caused by damage to the cerebral cortex by mechanisms such as excitotoxicity and iron from the blood. Immediate seizures that occur within two seconds of injury may occur because the power of the injury stimulates the brain tissue that has a low threshold for seizures when stimulated. Initial PTS is considered a provocated provocation, as they are derived from the direct effects of head trauma and thus are not considered to be true epilepsy, while late seizures are thought to exhibit permanent changes in brain structure and imply epilepsy. Early seizures can be caused by factors such as cerebral edema, intracranial hemorrhage, cerebral contusions or lacerations. Factors that can cause seizures that occur within two weeks of humiliation include the presence of blood in the brain; changes in blood brain barrier; excessive release of excitatory neurotransmitters such as glutamate; tissue damage caused by free radicals; and changes in the way cells generate energy. Late convulsions are thought to be the result of epileptogenesis, in which neural networks are restructured in a way that increases the likelihood that they will become excited, leading to seizures.
Prevention
Shortly after TBI, people were given anticonvulsant medications, since seizures that occur early after trauma can increase brain damage through hypoxia, excessive excitatory neurotransmitters, increased metabolic demand, and increased pressure in intracranial space. Drugs used to prevent seizures include valproate, phenytoin, and phenobarbital. It is recommended that treatment with anti-seizure drugs begin as soon as possible after TBI. Prevention of early seizures differs from convulsions late, since the purpose of the first is to prevent damage caused by seizures, while the latter goal is to prevent epileptogenesis. Strong evidence from clinical trials suggests that antiepileptic drugs given within one day of injury prevent seizures within the first week of injury, but not after. For example, a 2003 medical literature review found phenytoin as an early prevention, but may not be a late PTS. In children, anticonvulsants may not be effective for early and advanced seizures. For unknown reasons, prophylactic use of antiepileptic drugs over a long period is associated with an increased risk for seizures. For this reason, antiepileptic drugs are widely recommended for a short time after head trauma to prevent immediate and early, but not late, seizures. There is no widely accepted treatment to prevent the development of epilepsy. However, drugs may be given to suppress more seizures if a seizure is delayed.
Assessment and care
Medics aim to determine whether a seizure is caused by a patient's biochemical changes, such as hyponatremia. Neurologic examinations and tests to measure serum electrolyte levels were performed.
Not all convulsions after trauma are PTS; they may be due to an already existing seizure disorder, which may even have caused trauma. In addition, post-traumatic seizures should not be confused with conusive convulsions, which may soon follow a concussion but are not actually a seizure and not a predictive factor for epilepsy.
Neuroimaging is used to guide treatment. Often, MRI is performed on every patient with a PTS, but a less sensitive but more accessible CT scan may also be used.
Seizures caused by TBI are often difficult to treat. Antiepileptic drugs that can be administered intravenously immediately after injury include phenytoin, sodium valproate, carbamazepine, and phenobarbital. Antiepileptic drugs do not prevent all seizures in everyone, but phenytoin and sodium valproate usually stop the ongoing seizures.
Prognosis
PTS is associated with a generally good prognosis. It is not known exactly how long after a person's TBI is at a higher risk for seizures than the rest of the population, but estimates have suggested a length of 10 to over 15 years. For most people with TBI, seizures do not occur after three months, and only 20-25% of people who have TBI have PTS more than two years after the injury. However, moderate and severe TBI still presents a high risk for PTS to five years after injury.
Research has reported that 25-40% of PTS patients have remissions; Subsequent studies were conducted after the development of more effective seizure drugs reported higher overall remission rates. In a quarter of people with seizures due to head trauma, the drug controls it well. However, some patients experience seizures despite aggressive antiepileptic drug therapy. It is likely that the PTS will go into lower remissions for people with frequent seizures in the first year after injury.
Risk of developing PTE
It is not known whether PTS increases the likelihood of developing PTE. Initial PTS, although not always epilepsy, is associated with higher PTE risk. However, PTS does not suggest that epilepsy develops inevitably occur, and it is difficult to isolate the PTS from the severity of injury as a factor in the development of PTE. Approximately 3% of patients without early seizures develop late PTE; this amount is 25% in those who have an initial PTS, and the difference is greater if other risk factors for developing PTE are excluded. The seizures that occur immediately after the defamation are generally believed to not give an increased risk of recurrent seizures, but evidence from at least one study has shown that both immediate and early seizures may be a risk factor for late seizures. Early seizures may be less predictors for PTE in children; while as many as one-third of adults with early seizures developed PTE, the share of children with early PTSs who had late seizures was less than a fifth in children and may be as low as one-tenth. The incidence of advanced seizures is about half in adults with comparable injuries.
Epidemiology
Studies have found that PTS incidence varies greatly according to the population studied; may be as low as 4.4% or as high as 53%. Of all TBI patients admitted to hospital, 5 to 7% have private universities. PTS occurs in about 3.1% of traumatic brain injury, but the severity of the injury affects the likelihood of occurrence.
The most important factor in whether a person will develop early and late seizures is the extent of damage to the brain. More severe brain injury also poses a risk for developing PTS for a longer time after the event. One study found that the probability that a seizure would occur within 5 years of injury was 0.5% of mild traumatic brain injury (defined as no skull fracture and less than 30 minutes post-traumatic amnesia, abbreviated PTA, or loss of consciousness, abbreviated LOC) ; 1.2% moderate injury (skull fracture or PTA or LOC lasting between 30 minutes and 24 hours); and 10.0% of severe injury (cerebral contusions, intracranial hematoma, or LOC or PTA for more than 24 hours). Another study found that the risk of seizures 5 years after TBI was 1.5% in mild (defined as PTA or LOC for less than 30 min), 2.9% in moderate (LOC lasting between 30 min and 1 day), and 17, 2% on TBI weight (cerebral contusions, subdural hematoma, or LOC for more than a day; images on the right).
Seizures soon have an incidence of 1 to 4%, initial seizures are 4 to 25%, and late seizures are 9 to 42%.
Age affects PTS risk. With age, the risk of early and late seizures decreases; one study found that the initial PTS occurred in 30.8% of children aged 7 or under, 20% of children between the ages of 8 and 16, and 8.4% of those over the age of 16 at the time they were injured (graph in right). Early seizures occur up to twice as often in brain-injured children as is the case with their adult counterparts. In one study, children under five with trivial brain injury (those without LOC, no PTA, no fractured skull fractures, and no bleeding) suffered an initial spasm of 17% of the time, while people in over the age of 5 doing so so only 2% of the time. Children under the age of five also experience seizures in an hour more often than adults. One study found the incidence of early seizures was highest among infants younger than one year and very high among those with perinatal injury. However, adults are at higher risk than children for late seizures. People over the age of 65 are also at greater risk of developing PTS after the injury, with PTS risks 2.5 times higher than their younger counterparts.
Risk factors
The likelihood that a person will have PTS is affected by factors involving the injury and the person. The greatest risk for private universities is to have a changing level of consciousness for a long time after injury, severe injury with focal lesions, and fractures. The greatest risk for PTS is the penetrating head trauma, which carries a 35-50% risk of seizures within 15 years. If the metal fragments remain inside the skull after injury, the risk of early and late PTSs may increase. Head trauma victims who abuse alcohol before injury are also at high risk for developing seizures.
Occurrence of seizures varies greatly even among people with similar injuries. It is not known whether genetics plays a role in PTS risk. Studies have had conflicting results with regard to the question of whether people with private universities are more likely to have family members with seizures, which would indicate a genetic role in the PTS. Most studies have found that epilepsy in family members does not significantly increase PTS risk. People with ApoE-4 alleles are also at higher risk for late PTSs.
Risks for late PTS include hydrocephalus, reduced blood flow to the temporal lobe of the brain, brain contusions, subdural hematoma, tear dura mater, and focal neurological deficits. PTA that lasts for more than 24 hours after injury is a risk factor for early and late PTSs. Up to 86% of people who experience post-traumatic seizures are late to have another within two years.
See also
- Complications of traumatic brain injury
References
Source of the article : Wikipedia
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