Concussion, traumatic brain injury and seizures

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ARTICLE HIGHLIGHTS

  • Head trauma is one of the most commonly identified reasons that patients develop epilepsy. Most studies suggest that approximately 6% of patients with epilepsy have TBI as the cause.
  • The more severe the head trauma, the higher the risk of developing epilepsy. For example, patients with penetrating brain injury have a 53% chance of developing epilepsy.
  • Epilepsy does not typically develop immediately after head trauma. Often, there are a few months, or even longer, before recurrent seizure activity is noted.
  • Medication or 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!

INTRODUCTION

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:

  • Paralysis, weakness
  • Coordination problems
  • Problems with sensation
  • Headaches
  • Memory problems
  • Concentration problems
  • Depression and anxiety

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.

Illustrative Case

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.

Illustrative points:

  • Seizure medications are often used to prevent early seizures.
  • Early seizures can contribute to brain swelling—this can be dangerous in patient with significant head trauma.
  • Patients with head trauma are at significant risk to develop seizures-often a few months after the head trauma.

DEFINITIONS

A wide variety of definitions for head trauma are used in the literature. The table below summarizes definitions in current use by many investigators.

  •     Concussion: Immediate and transient loss of consciousness accompaniedby a brief period of amnesia after a blow to the head (Ropper,    NEJM, 2007). Most concussions meet criteria for mild traumatic brain injury.
  •     Mild traumatic brain injury (TBI): loss of consciousness less than 30 minutes and no skull fracture.
  •     Moderate TBI: loss of consciousness greater than 30 minutes and less than 24 hours, with or without skull fracture.
  •     Severe TBI: loss of consciousness greater than 24 hours, with contusion, hematoma, or skull fracture (Lowenstein,     Epilepsia, 2009).

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.

Based on: Hauser, Epilepsia, 1993

 TBI causes epilepsy most commonly in the following age groups:

  • < 5 yo
  • 15-24 yo
  • > 65 yo

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 (%)
Mild TBI 0.5% 2.1%
Moderate TBI 1.2% 4.2%
Severe TBI 10% 16.7%

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.

TREATMENT

Medical Treatment

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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.

Surgical Treatment

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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.

CONCLUSIONS

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!

REFERENCES

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.

Credits for photos:

Dreamstime:

http://www.dreamstime.com

vichie81:
http://www.freedigitalphotos.net/images/view_photog.php?photogid=2023

Apple’s Eyes Studio:
http://www.freedigitalphotos.net/images/view_photog.php?photogid=2000

Written by James White, MD

Dr. White has been practicing as a full-time epileptologist since 1999. His practice focuses on optimizing the diagnosis and treatment of patients with seizure disorders. Dr. White’s special interests include patient education, improving the side-effect profile of seizure medications, and epilepsy surgery.

8 Responses to “Concussion, traumatic brain injury and seizures”

  1. Dr. White,

    Good stuff! Two questions for you. 1) Let’s say a patient suffers TBI in the form of an enclosed head injury with brain swelling and contusions. Five years later, a softball sized (benign) brain tumor is removed. Two years later, seizures ensue. During the 2 years prior to the first seizure, the patient suffers from auras (not knowing what they were or what they meant). If an EEG had been done during the 2 years the patient was having the auras, would that have shown up as abnormal activity on the EEG, and if so, would it still be too early to start AED therapy? 2) If scar tissue formed can be the cause of abnormal electrical flow in the brain leading to epilepsy, can the epilepsy surgery itself cause new scar tissue to form, eventually causing more seizures?

    Deb T.

  2. Great questions Deb. I want to start with a reminder (mainly for other readers–I realize you are very aware of this): it is, of course, not good medical care to give specific medical advice on-line. Providing general education on epilepsy related topics is our goal. Deb, your questions bring up several very important issues. I will make general comments on these questions. Not specific to a given patient, but rather as general education.
    1) Auras are seizures.At one time, it was debated whether the feelings that people get before seizures (= auras) were seizures or not. For example, some people get a nauseated feeling as their aura. They sometimes will only get the nausea- no other seizure activity. Sometimes they will get the nausea feeling before losing awareness, falling to the ground and convulsing. Auras are known to be seizures, in part, because of EEG data. If a patient is hooked-up to the EEG and has the nausea, the eeg may show spikes–which is proof that the feeling is due to abnormal electrical activity in the brain–this is what a seizure is. Please note- auras do not always show up on the EEG. There is a certain amount of electrical activity required to show EEG changes. Some auras, that are seizures, may have such a small amount of charge, that they do not show up on the EEG. When a patient is having an aura that is thought to be a seizure- the patient is usually started on a seizure medication. The reason for this is that an aura can progress to a more intense seizure- including a full convulsive seizure.
    2) In general, the scar that is made during surgery–from the surgeon’s knife removing brain tissue–does not typically result in producing a seizure focus. The evidence for this: the thousands of patients who have become seizure free after epilepsy surgery (the surgeon removes brain tissue where the seizures are coming from) .

    Let me know if the above answers your questions. Again, thank you for your interest and the great questions.

  3. My apologies. My comments/questions weren’t intended to discuss a specific patient online, but rather as an example to set up a scenario. However, upon reading it today, it certainly does come across different than intended. In my excitement to ask the questions, along with the time crunch I was in yesterday I forgot to edit my own comments for content. Your response does answer my questions. Thanks for taking the time to do so.

    Deb T.

  4. Thanks Deb. I really want to say that I did not think you were trying to discuss specifics on a case. The reminder (about not providing specific medical advice on-line) is something you are going to see from me alot. It is a reminder to me and to all who read the information. I very much want to provide high quality education. This is, of course, a good thing. The concern is that if I get too close to even sounding like I am giving specific medical advice on-line–that of course will cause all sorts of problems! I certainly know you understand these issues, but I thought an explanation would help. Again, thank you for your interest. As you can probably tell, I greatly enjoy writing these articles!

  5. Can a number of concussions lead to photosensitive seizures when exposed to flourescent lighting and generalized nocturnal seizures in a person who already has simple partical seizures? Can a number of concussions worsen an already existing seizure disorder?

  6. I have some questions, A metal antique desk fell about 4 and half feet and hit my husband in the head. He did have to lay down and he saw black for a few minutes. He had sinus problems at the time so wasnt sure if headache was from that or sinus. It did not split head open and it did make a small area swollen on his head. As he continued to suffer headaches after concussion 2 weeks later he was doing work out in yard and came in not feeling well, I noticed his whole left side was tremoring, pale, speech was getting very slow, eyes were real glassy as he was having problems seeing, then started sweating perfusly even after sitting down for a bit. I took his BPand it was fine, then his pulse and it was 130. Then a massive headache come on and he couldn’t take it, with his pulse rate climbing I rushed him to ER. By then his heart rate was 150. They got him back there and started working on him and finally it took about 45 min while they started doing all their tests and ct scan everything came back normal. I am taking him in next week for a mri. That was his second episode in a week like that but pulse rate didnt go as high the 1st time and it seems it happens only when he does something to raise his heart rate like more than just resting. ER says concussion and would be fine to go right back to work. I disagreed. His work is physical labor. Any suggesstions?

  7. I have a general question on seizures and epilepsy. I started having convulsive seizures back in 2002 and have continued since. but my question goes back to when I was in grade school and Jr. High School.

    at the time i was 12 or 13 I was diagnosed as being ADHD and placed on Ritalin. I used it through Jr. High but stopped before starting High School. after my seizures were discovered I started doing research on Epilepsy, general seizures and what might have caused them in me.

    the ADHD meds really never helped me and ended up as more of a problem than a help hence why I stopped taking them. I was diagnosed as ADHD because I was having troubles focusing, keeping my awareness on school work and they thought that it was.

    could they have missed diagnosed me back then? and istead have been suffering from Petit mal seizures.?

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