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In a fraction of a second, head trauma can dramatically change a person’s life. Traumatic brain injury (TBI) is associated with an increased risk of developing epilepsy. The more severe the head trauma, the higher the risk of having seizures. For severe head injuries (for example, a patient with shrapnel piercing their brain), the chance of developing epilepsy can be as high as 50%! In addition to seizures, head trauma can result in significant neurologic impairment:
The purpose of this article is to provide information on TBI and epilepsy. In a future article, information on the short-term and long-term cognitive issues related to concussion will be provided.
A 68 year-old male was involved in a serious motor vehicle accident. He was “T-boned” by a truck that did not stop at a stop-light. The patient was wearing a seat-belt. The airbag deployed. He was knocked unconscious due to head trauma. He was transferred to the local hospital. Because of his unconscious state and fluctuating blood pressure, he was admitted to the neuro ICU. CT of the brain demonstrated a right frontal region skull fracture and a small right frontal lobe contusion (this is like a bruise on the surface of the brain).
Approximately 5 hours after the accident, the patient began to regain consciousness. Initially, he was confused, and was slightly combative. He required sedation for the first 24 hours. Within 48 hours of the trauma, the patient was awake, following commands, and speaking. He had mild weakness to his left hand, which resolved by the time he was discharged from the hospital.
Upon admission to the ICU, the patient was placed on a seizure medication (levetiracetam = Keppra). He was started on the seizure medication to prevent early seizures—these are seizures that can occur shortly after head trauma. Seizure activity can worsen brain swelling. Given that the patient already had some brain swelling related to the contusion, preventing seizures was very important. Increases in brain swelling can produce high pressure on the brain- and result in shifting of brain tissue and possible permanent damage. The patient had no seizures while in the hospital. His seizure medication was stopped after 1 week of treatment.
The patient was discharged from the hospital after a 10 day admission. His neurologic recovery was considered excellent. Three months after the motor vehicle accident, the patient experienced his first seizure. The seizure started with minor jerking in his left arm. He then lost contact, collapsed, and had a full-body convulsion. The seizure lasted for 1 minute. The patient was started on a seizure medication (levetiracetam = keppra). His seizures have been completely controlled for > 1 year.
A wide variety of definitions for head trauma are used in the literature. The table below summarizes definitions in current use by many investigators.
IMPORTANT CLINICAL ISSUES
Head trauma is one of the most commonly identified reasons that patients develop epilepsy. Studies suggest that approximately 6% of patients with epilepsy have TBI as the cause.
TBI causes epilepsy most commonly in the following age groups:
Males are at higher risk than females to have TBI. Approximately 15-25% of soldiers in the Iraq and Afghanistan wars report TBI. These soldiers are at increased risk to develop epilepsy. As noted, the more severe the head trauma, the higher the risk that a patient will develop posttraumatic epilepsy. For example, patients with penetrating brain injury have a 53% chance of developing epilepsy. The following table describes the percent chance of developing epilepsy- 5 years and 30 years after the head trauma (Arnold, Atlas of Epilepsies, 2010).
|5 year||30 year (%)|
Epilepsy does not typically develop immediately after head trauma. Typically, there are a few months, or even longer, before recurrent seizure activity is noted. Approximately one-third of patients who develop posttraumatic epilepsy have their first unprovoked seizure within 4 months of the trauma. Two-thirds have their first unprovoked seizure within 24 months of the head trauma (Temkin, Epilepsia, 2009). Some patients may go several years before epilepsy finally develops.
MECHANISM (= how trauma can result in seizure activity)(Arnold, Atlas of Epilepsies, 2010)
TBI results in damage to the neurons on the surface of the brain. Over time, this damage results in the potential for abnormal flow of electricity. The abnormal flow can lead to surges of electrical activity from regions of the brain—resulting in seizure activity.
The neurons are damaged by several possible mechanisms. Direct damage can be due to bone fragments, bullets, shrapnel or a wide range of insults. Arterial or venous bleeding can place high pressure on the brain, resulting in damage. The twisting and stretching forces on the brain tissue can result in shearing damage. Blood products, such as hemoglobin and iron, can have a toxic effect on brain tissue. Normal blood flow to brain tissue can be disrupted- causing oxygen deprivation and neuronal death. Trauma to the brain can result in swelling of brain tissue (brain contusion—like an expanding bruise)—resulting in high pressure to brain tissue and damage to neurons.
The damaged areas of the brain, over time, may change their chemical composition and their wiring patterns. These changes are associated with having an increased potential to produce abnormal electricity- the electrical power surges that produce seizures.
Seizure medications can control a significant proportion of patients with posttraumatic epilepsy. Treatment of epilepsy due to TBI is similar to the treatment of focal seizures due to other causes. Thus, at this time, there is no specialized/specific medication for posttraumatic epilepsy (unfortunately!). Standard seizure medications, such as phenytoin (=Dilantin), carbamazepine (=Tegretol) or levetiracetam (=Keppra) are commonly utilized. These three medications are listed as examples—a patient’s doctor will analyze the patient’s clinical features to pick the best medication. Factors to consider: side effect profile issues, drug interactions, age, gender, weight, and seizure types. By taking a careful history, performing a neurological exam, and performing testing, such as EEG and MRI, the best antiepileptic drug can be chosen.
Selected patients with posttraumatic epilepsy can undergo successful epilepsy surgery. The key is to find a relatively small area of the brain where the seizures are coming from. Once this area is identified, testing is performed to make sure that removing this part of the brain is safe. This area of the brain should not overlap with critical function- such as areas important for speech, memory or movement. If it is determined to be safe, this small area of the brain is removed by the surgeon. Ideally, the patient can become seizure free and have no neurological deficits related to the surgery.
Good results can be achieved with surgery. It appears to be important to remove the entire area of abnormal brain tissue that can be seen on MRI-if possible. For patients with a clearly identified seizure onset area in a single region of the brain that is safe to remove, > 70% of patients can become seizure free (Kazemi, Epilepsia, 1997). It should be noted that TBI can often times result in multiple areas where seizures can start—and thus some patients are not candidates for surgery or can only hope for a reduction in seizures if they undergo epilepsy surgery.
Another option to consider, for a significant percentage of patients, is Vagus Nerve Stimulation therapy. This is a device that stimulates a nerve in the neck. This stimulation is then transmitted to the brainstem and the cerebral cortex. This electrical stimulation is typically programmed to stimulate for 30 seconds, and then be off for 5 minutes. This stimulation pattern continues throughout the day. The stimulation is associated with a reduction in seizures in a significant number of patients.
HOPE FOR THE FUTURE: USING A WINDOW IN TIME TO PREVENT EPILEPSY
Question: If a person has head trauma, can I place the patient on a seizure medication and prevent the patient from developing epilepsy?
Answer: No (not at this time!).
As noted above, there is a time lag between the head trauma and when epilepsy eventually could develop. This “window in time” allows investigators to study if medications can prevent the development of epilepsy before it starts- very exciting stuff! This is studied by giving a medication immediately after the head trauma. So far, the prevention of epilepsy has not been proven. Studies have been performed that show that starting a seizure medication immediately after head trauma will reduce the frequency of seizures in the first week after the trauma. Unfortunately, over the long-term, seizure medications do not prevent the development of epilepsy. Thus, the current literature does not support the use of seizure medications as preventative therapy for late seizures. In general, seizure medications should not be used long-term in TBI patients, unless they have had seizures.
The exciting hope for the future is that therapy to prevent epilepsy can be developed. Consider this possible futuristic approach: We know that patients with severe head trauma are at high risk to develop epilepsy. Perhaps this group of patients could be treated with a medication that prevents the process that leads to seizure activity (stops epileptogenesis). This would be a wonderful advance over just waiting for the first seizure! Experts in the field are studying how to accomplish this important goal.
Head trauma is a frequent and important cause of epilepsy. Medication and surgical treatment can effectively control seizures in many patients. The hope for the future is to develop treatments that will stop the development of epilepsy before it starts!
Arnold FJL, McEvoy AW. Traumatic brain injury and epileptic seizures. In: Panayiotopoulos CP, ed. Atlas of epilepsies. New York: Springer-Verlag London Limited 2010;p. 129-135.
Hauser WA, Amnegers JF, Kurland LT. Incidence of epilepsy and unprovoked seizures in Rochester, Minnesota:1935-1984. Epilepsia 1993;34:453-468.
Kazemi NJ, Elson LS, Mosewich RK, et al. Resection of frontal encephalomalacias for intractable epilepsy: outcome and prognostic factors. Epilepsia 1997;38:670-677.
Lowenstein DH. Epilepsy after head inury: An overview. Epilepsia 2009; 50 (suppl 2):4-9.
Ropper AH, Gorson KC. Concussion. New England Journal of Medicine 2007;356:166-72.
Temkin N. Preventing and treating posttraumatic seizures: The human experience. Epilepsia 2009; 50 (suppl 2):10-13.
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