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 who has 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.
Seizures are usually an indication of a more severe TBI. Seizures that occur shortly after a person suffers a brain injury may further damage the already vulnerable brain.They may reduce the amount of oxygen available to the brain,cause excitatory neurotransmitters to be released in excess, increase the brain”s metabolic need, and raise the pressure within the intracranial space, further contributing to damage.Thus, people who suffer severe head trauma are given anticonvulsant medications as a precaution against seizures.
Around 5–7% of people hospitalized with TBI have at least one seizure.PTS are more likely to occur in more severe injuries, and certain types of injuries increase the risk further. The risk that a person will suffer PTS becomes progressively lower as time passes after the injury. However, TBI survivors may still be at risk over 15 years after the injury. Children and older adults are at a higher risk for PTS.
It is not completely understood what physiological mechanisms cause seizures after injury, but early seizures are thought to have different underlying processes than late ones.Immediate and early seizures are thought to be a direct reaction to the injury, while late seizures are believed to result from damage to the cerebral cortex by mechanisms such as excitotoxicity and iron from blood. Immediate seizures occurring within two seconds of injury probably occur because the force from the injury stimulates brain tissue that has a low threshold for seizures when stimulated. Early PTS are considered to be provoked seizure, because they result from the direct effects of the head trauma and are thus not considered to be actual epilepsy, while late seizures are thought to indicate permanent changes in the brain”s structure and to imply epilepsy. Early seizures can be caused by factors such as cerebral edema, intracranial hemorrhage, cerebral contusion or laceration. Factors that may result in seizures that occur within two weeks of an insult include the presence of blood within the brain; alterations in the blood brain barrier; excessive release of excitatory neurotransmitters such as glutamate; damage to tissues caused by free radicals; and changes in the way cells produce energy. Late seizures 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.
Shortly after TBI, people are given anticonvulsant medication, because seizures that occur early after trauma can increase brain damage through hypoxia, excessive release of excitatory neurotransmitters, increased metabolic demands, and increased pressure within the intracranial space. Medications used to prevent seizures include valproate, phenytoin, and phenobarbital. It is recommended that treatment with anti-seizure medication be initiated as soon as possible after TBI. Prevention of early seizures differs from that of late seizures, because the aim of the former is to prevent damage caused by the seizures, whereas the aim of the latter is to prevent epileptogenesis. Strong evidence from clinical trials suggests that antiepileptic drugs given within a day of injury prevent seizures within the first week of injury, but not after. For example, a 2003 review of medical literature found phenytoin to be preventative of early, but probably not late PTS. In children, anticonvulsants may be ineffective for both early and late seizures. For unknown reasons, prophylactic use of antiepileptic drugs over a long period is associated with an increased risk for seizures. For these reasons, antiepileptic drugs are widely recommended for a short time after head trauma to prevent immediate and early, but not late, seizures. No treatment is widely accepted to prevent the development of epilepsy. However, medications may be given to repress more seizures if late seizures do occur.
Assessment and treatment
Medical personnel aim to determine whether a seizure is caused by a change in the patient”s biochemistry, such as hyponatremia. Neurological examinations and tests to measure levels of serum electrolytes are performed.
Not all seizures that occur after trauma are PTS; they may be due to a seizure disorder that already existed, which may even have caused the trauma. In addition, post-traumatic seizures are not to be confused with concussive convulsions, which may immediately follow a concussion but which are not actually seizures and are not a predictive factor for epilepsy.
Neuroimaging is used to guide treatment. Often, MRI is performed in any patient with PTS, but the less sensitive but more easily accessed CT scan may also be used.
Seizures that result from TBI are often difficult to treat. Antiepileptic drugs that may be given intravenously shortly after injury include phenytoin, sodium valproate, carbamazepine, and phenobarbital. Antiepileptic drugs do not prevent all seizures in all people, but phenytoin and sodium valproate usually stop seizures that are in progress.
The chances that a person will suffer PTS are influenced by factors involving the injury and the person. The largest risks for PTS are having an altered level of consciousness for a protracted time after the injury, severe injuries with focal lesions, and fractures. The single largest risk for PTS is penetrating head trauma, which carries a 35 to 50% risk of seizures within 15 years. If a fragment of metal remains within the skull after injury, the risk of both early and late PTS may be increased. Head trauma survivors who abused alcohol before the injury are also at higher risk for developing seizures.
Occurrence of seizures varies widely even among people with similar injuries. It is not known whether genetics play a role in PTS risk. Studies have had conflicting results with regard to the question of whether people with PTS are more likely to have family members with seizures, which would suggest a genetic role in PTS. Most studies have found that epilepsy in family members does not significantly increase the risk of PTS. People with the ApoE-ε4 allele may also be at higher risk for late PTS.
Risks for late PTS include hydrocephalus, reduced blood flow to the temporal lobes of the brain, brain contusions, subdural hematomas, a torn dura mater, and focal neurological deficits. PTA that lasts for longer than 24 hours after the injury is a risk factor for both early and late PTS. Up to 86% of people who have one late post-traumatic seizure have another within two years.