Sports and Epilepsy

Terminology and Classification

Diagnosis and Evaluation

The diagnosis of epilepsy is based on clinical history. A single seizure can be provoked by electrolyte imbalances, dehydration, infection, or trauma. Other conditions should also be considered in persons presenting with a paroxysmal event, including cardiac arrhythmias, prolonged QT syndrome, syncope, complicated migraine, paroxysmal movement disorders, and psychogenic events. Although an outpatient EEG is an indispensable tool in clinical diagnosis, clinical history is the most critical determinant. Of all persons with epilepsy, 17% have normal interictal EEG findings (when they are not having an overt seizure). In addition, abnormal EEG findings do not guarantee that a seizure has occurred. Lastly, following the diagnosis of epilepsy, a head imaging study—preferably a magnetic resonance imaging scan of the head—should be obtained. Exceptions to this rule may include a child or an adult diagnosed with childhood absence epilepsy, juvenile absence epilepsy, or juvenile myoclonic epilepsy.

Treatment

Therapy with an antiepileptic drug (AED) is not typical after a single seizure because recurrence risk after a first unprovoked seizure is only 30% to 40%. Risk for additional seizures increases to approximately 75% after a second unprovoked seizure. After this second seizure, an AED is usually prescribed. Occasionally, an AED is started after a first unprovoked seizure if the EEG demonstrates epileptiform discharges (spike or sharp waves) in the temporal region or generalized spike and slow wave discharges. The chance of recurrence in these situations may be closer to 90%.

Approximately 30 AEDs are used to treat epilepsy. The choice of AED is based on seizure type and epilepsy syndrome. The following general principles relate to the choice of AED:

• 1.

  Monotherapy is effective and avoids unpleasant drug interactions. About 60% of patients will experience control of their epilepsy with an appropriate first AED. An additional 10% will respond to a second AED. Unfortunately, chances of a subsequent medication trial succeeding when the first two AEDs have failed are less than 5%. Thus 30% of patients will most likely be refractory to therapy. For these patients, alternative therapies including vagus nerve stimulation, diet therapies (e.g., a ketogenic diet), and epilepsy surgery need to be considered.

• 2.

  If possible, AEDs should be titrated slowly and only to the point of seizure control.

• 3.

  Seizure control should not be achieved at the expense of adverse effects. An alternative medication should be chosen if a person experiences adverse effects.

• 4.

  Drug compliance is enhanced when medication is administered once or twice daily. When available, a sustained-release medication should be considered.

• 5.

  Therapeutic blood levels are not absolute; they are formulated based on trough levels and represent a statistical range of efficacy.

Persons caring for patients with epilepsy should be cognizant of AED adverse effects that may impair sports participation. For example, some AEDs at high doses can produce cognitive or behavioral changes, diplopia, dizziness, and general fatigue. Phenytoin, carbamazepine, valproate, and lamotrigine can induce tremors or dyskinesias. Topiramate and zonisamide can cause oligohydrosis. Thus patients should be advised to maintain hydration, carry a spray bottle of cool water, and monitor for overheating when participating in sports. Carba­mazepine and oxcarbazepine can cause hyponatremia. Additionally, valproate can cause weight gain and topiramate can induce weight loss.

Several AEDs can affect bone health by decreasing bone mineral density in adults and children. One study demonstrated that as a group, people with epilepsy had lower overall bone density than did the general population. Furthermore, the bone density of persons for whom an enzyme-inducing AED was prescribed was lower than that of persons for whom a nonenzyme-inducing agent was prescribed. Therefore monitoring bone health is critical in patients with epilepsy, especially those using phenytoin, phenobarbital, or carbamazepine. Both the patient and health care provider should be aware of the risk of bone fractures as a result of sports participation.

Exercise and Seizures

In 1960, Dr. William G. Lennox, an early leader of pediatric epileptology, wrote: “Epilepsy prefers to attack when the person is off guard, sleeping, resting, idling. This is easily demonstrable in persons who experience very frequent petits [absence seizures], which may be almost absent during skating, swimming, or running, and abundant while sewing, eating, or just sitting. Parents picture their child as stopping or falling in a seizure and being run over while attempting to cross a busy street. I have never known this to happen, and I can remember only a few instances of a person having an attack while running or swimming.” Based on these observations, Lennox labeled activity as an antagonist of seizures .

Most human and translational animal studies completed in the interim support Dr. Lennox's empirical conclusion that exercise may, in fact, be protective against seizures and that it is rare for seizures to occur during activity. However, it is reasonable to expect that physical activity may induce seizures because strenuous exercise can result in hyperventilation, and in the EEG laboratory, hyperventilation is used to provoke seizures. However, the net effects of hyperventilation at rest and during exercise are different. At rest, hyperventilation triggers a decrease in carbon dioxide (respiratory alkalosis). The ensuing drop in cerebral blood flow and hypoxia results in network excitability and seizures. During exercise, however, hyperventilation is a compensatory mechanism that avoids hypercapnia and meets increased oxygen demands, thus the respiratory alkalosis required to induce a seizure does not occur.

In addition, the most common provoking factors for seizures include stress, mental strain, and physical fatigue, all of which can occur with intense physical exercise and competition. Stress may activate seizures through sympathetic stimulation, and fatigue may cause seizures because of a chronically drowsy state. Metabolic disturbances during prolonged, strenuous exercise, such as hyponatremia, dehydration, and overhydration, can theoretically aggravate an underlying propensity for seizures. However, the literature includes only a few cases of clear exertion-induced seizures, and larger studies have not documented exercise-induced seizures, even during contact sports.

Several studies and observations bear mention. In a single-center study of more than 15,000 patients with epilepsy, not a single case of exercise-induced seizures was reported. In a second observational study of 400 patients, only two patients reported seizures during exercise. Nakken has reported that 10% of 204 patients with epilepsy had minor injuries during exercise because of a seizure. Additionally, 36% reported injuries during exercise that were unrelated to seizures and 36% reported that seizure frequency was reduced as the result of exercise. Conversely, Ablah and colleagues reported a higher frequency of seizures related to exercise. However, only 53% of the 18% who reported seizures around the time of exercise had a seizure while exercising.

Experimental intervention studies have found that exercise either leads to fewer seizures or does not change seizure frequency. A study examining physical activity in women with intractable epilepsy found that average seizure frequency decreased from 2.9 to 1.7 per week with exercise. In contrast, Nakken and colleagues demonstrated that a 4-week training program did not alter seizure frequency. In addition, a longer 12-week study found no significant impact on seizure frequency, but did demonstrate improved vigor, as well as decreased anxiety and depression. Although these studies do not provide evidence for exercise as a prophylaxis for seizures, the data do not demonstrate that exercise triggers seizures.

The mechanism by which exercise may serve as an antagonist to seizures is not known. Studies that have found a decrease in the frequency of epileptiform discharges on EEGs during exercise suggest that exercise affects the cerebral mechanisms responsible for generating these discharges. During exercise, persons are typically more vigilant, alert, and attentive. Epileptiform discharges can be activated with drowsiness, and studies have documented a decrease in epileptiform discharges when patients with epilepsy are engaged in an interesting task or activity. Exercise can also reduce stress and increase endorphin levels. Stress is a known precipitant for seizures in persons with epilepsy, and β-endorphins have been shown to reduce epileptiform discharges.

Lastly, studies using animal models of epilepsy to investigate the effects of exercise on seizure threshold have suggested other protective effects through mechanisms such as insulin growth factor 1 pathways or the prevention of oxidative free radical mechanisms.

Although seizure risk with exercise appears to be low, AED compliance is critical because a decrease in serum drug levels increases the risk for seizures in any setting. Variations in drug metabolism could theoretically increase seizure risk (increased metabolism) or increase adverse effects (decreased metabolism). However, changes in drug metabolism have not been observed in studies that have evaluated drug levels during exercise.

Acute Management of Seizures

Persons with well-controlled epilepsy may have a seizure during exercise. The first tenet of acute seizure management is to stay calm, because a seizure is almost always a self-limited event that requires minimal intervention. It is important to protect the person from self-injury. Objects close to the person, particularly during a convulsive seizure, should be removed. Restricting equipment or uniforms should be loosened. A tongue blade or other object should never be inserted between the teeth because a person will not swallow his or her tongue. Instead, the person may bite and break the object or injure the care provider. If a mouthpiece is present, it should be removed only if removal can be accomplished safely.

If the seizure does not terminate within 5 minutes, emergency medical services should be activated. Rectal diazepam is often prescribed for persons prone to prolonged seizures. The person administering diazepam should be aware of the potential for decreased respiratory drive. However, the benefit of stopping the seizure generally outweighs the risk of respiratory suppression.

When the seizure is over, the person may be tired and confused. He or she may be allowed to lie down, but because vomiting may occur during the postictal period, he or she should be turned sideways to prevent aspiration. This position is not imperative if the seizure was nonconvulsive (e.g., a focal seizure with alteration of awareness with stereotypic or bizarre behaviors).

After acute management of a seizure, it is important to consider the person's emotional needs. The embarrassment that may be felt should be acknowledged, and it is important to recognize that although some persons may wish to speak about their experience, others may not. A simple “How are you feeling?” is often appreciated. The same approach applies to persons who witness the seizure. Given the many misperceptions about epilepsy, the witnesses need to know that self-limited seizures are often not harmful, that these persons usually recover, and that most persons lead fulfilling lives with only rare or zero breakthrough seizures.

Return-to-Activity Guidelines

No clear guidelines exist for safe return to activity after a seizure. Activity should be restricted if the person is either lethargic or confused. However, not all seizures result in a prolonged period of postictal symptoms (e.g., absence seizures), and thus return-to-activity decisions should be made on an individual basis.

Although a single self-limited seizure is not harmful, seizures can potentially result in injuries. The most common seizure-related injuries include fractures of the humeral neck, femur, clavicle, and ankle; chipped teeth; and shoulder and hip dislocations. However, in a study that spanned more than 16 years, Aisenson et al. documented that the accident rate in patients with epilepsy was similar to that of their control patients without epilepsy. In a more recent study by Fischer and Daute, it also was found that during exercise, no difference in accident rates existed in children with or without epilepsy.