Abstracts

Rationale: Fatigue is a strong predictor of cognitive dysfunction and quality of life in epilepsy. There are concerns regarding increased seizure risk with the use of stimulants such as modafinil. We examined whether addition of modafinil caused exacerbation of seizures in patients with epilepsy. Methods: A centralized clinical registry was queried to identify patients who had a diagnosis code of epilepsy (345) and who were taking modafinil during a 10 year period (January 1999-August 2009). The records were examined to determine the etiology of the seizure disorder, antiepileptic drug use, indication and dose for modafinil, whether there was clinical or electrographic evidence of seizure exacerbation, and reason for discontinuation of modafinil. We compared patients with epilepsy without another underlying neurological disease to patients where seizures were secondary to a brain lesion. Results: A total of 262 patients were reviewed. Of these, 106 did not have evidence of seizures or modafinil use; 156 patients were included for analysis. EEGs were available in 113 patients; epileptiform discharges were seen in 34. Sixty-eight patients had seizures while on modafinil but in all but 4, it was not felt that modafinil contributed to an exacerbation. In another 3 patients, seizures occurred only after modafinil was started, but in 2 of them, modafinil had been discontinued prior to seizure onset. The most common reasons for discontinuation included death due to reasons unrelated to modafinil use (12), no longer needed (9), psychiatric side effects (5), suspected medical complications (5), and ineffectiveness (3), though the exact reason could not be determined from medical records in a large number (43). The most common etiology for underlying seizures was brain tumor (33). Twenty-three patients had epilepsy without other symptomatic brain injury; they were younger (age 49.3 vs 53.2) and took a higher dose of modafinil (254.5 vs 202.9 mg/day), though not statistically significant. Two patients had undergone temporal lobectomy, and had recurrence of seizures. Eight patients were on monotherapy AED at the time modafinil was administered; 11 were on 2 or more AEDs, and 4 were not on AEDs because they did not have active seizures. Modafinil had been started in 9 patients because of clear medication induced fatigue, 8 because of fatigue not otherwise specified, and for other reasons (6). Eight patients experienced seizures while on modafinil (p=NS). Clinical exacerbation of seizures occurred in no patients. EEG was available after modafinil was started in 4 patients. Two patients showed less slowing as compared to EEGs obtained prior to modafinil. Conclusions: Our results demonstrate that the use of modafinil is not associated with exacerbation of seizures over a wide variety of neurological conditions. This was also seen in patients with epilepsy not secondary to an underlying lesion. Addition of modafinil did not exacerbate their seizures even in patients who were on AED polytherapy. Modafinil appears to be safe, and may potentially be used in patients with epilepsy and fatigue.