What Is the Best Management Strategy for Benign Epilepsy With Centrotemporal Spikes?

Michael R. Sperling, MD

Disclosures

September 05, 2000

Question

A 6-year-old boy presented with simple partial seizures in July 1999. The initial seizure was focal, involving the (L) angle of mouth, with drooling lasting for approximately 1 minute. A similar seizure occurred 1 week later. The EEG showed mildly abnormal bilateral parietal seizure activity pattern. The child was prescribed carbamazepine (CBZ).

He was asymptomatic for 6 months, but had a seizure in January 2000, lasting a few seconds. We increased his CBZ dose to 20 mg/kg. In February 2000, serum CBZ levels were 7 mcg/mL.

In July 2000, the boy again experienced a seizure lasting approximately 30 seconds. An EEG showed (R) frontotemporal spikes. CT with contrast was negative. We have increased the CBZ dose again and will get drug levels in another 2 weeks.

The child has always been totally conscious during the episodes. They occur at 10:15 to 10:20 PM, soon after he is fast asleep. He wakes up to inform his parents, and soon returns to a sound sleep. There is no reported aura or postictal morbidity. He can demonstrate the episode. The child is doing very well at school, sports, and generally at home.

He has a history of generalized tonic clonic febrile seizures at the age of 2 years, no intranatal/postnatal trauma, normal developmental milestones, and scores high on IQ testing. He is very sensitive.

What would be the best management strategy at this point?

Response from Michael R. Sperling, MD

This child has a history that typifies the syndrome known as benign epilepsy with centrotemporal spikes, or rolandic epilepsy. This is an autosomally dominant inherited trait that usually begins at age 5 or 6 and remits by the onset of puberty. Children with this condition typically have focal motor seizures involving the face or hand, and, on occasion, may experience secondarily generalized tonic-clonic seizures as well. The children are of normal intellect, have normal examinations, have a characteristic EEG abnormality, and an excellent prognosis.

Management of this condition depends on the severity of the seizures and the patient's and his or her family's ability to tolerate them. Because the seizures are benign and brief, many authorities do not even treat short simple partial seizures to avoid drug side effects. However, if seizures are disturbing or if convulsive seizures appear, treatment is usually offered to minimize medical risks and to allay family concerns. Carbamazepine is an effective agent for this condition, and often all that is required is to raise the dose to achieve slightly higher serum levels if the current regimen is unsatisfactory. This child will probably be controlled with serum carbamazepine levels approaching 9 or 10 mcg/mL. Should that level not prove effective, and lacking side effects, the dose could still be increased.

However, before raising the dose further, the dosing schedule could be changed to try to provide maximal protection for the time during which he is most vulnerable to seizures. Therefore, I would recommend splitting the dose so that the evening dose is 60% to 66% of the daily dose, and the morning dose comprises the remainder. Also, by giving the evening dose 1.0-1.5 hours before bedtime, one achieves higher serum levels at sleep onset than if waiting until bedtime to give the evening dose. The regular preparation of carbamazepine is preferable to the extended-release form, so that rapid absorption can occur before bedtime. If carbamazepine is ineffective, phenytoin or valproate could be used, again adjusting dosages to achieve maximal levels at bedtime when seizures are most likely to occur.

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