Abstracts

Rationale: Ictal hypersalivation is due to increased saliva production from salivary gland stimulation or to decreased saliva clearance from oropharyngeal muscle contraction. It is a prominent feature of childhood Rolandic epilepsy, but it can also occur in Panayiotopoulos and other childhood epilepsy syndromes. Drooling during a seizure is not uncommon in adults, but hypersalivation as the dominant ictal semiology has been reported in only a few cases of acquired temporal, parietal, and frontal lobe epilepsies. None of the published reports of ictal salivation mentioned parotid gland hypertrophy as a complication. Methods: We describe the case of a 33-year-old man with type 1 diabetes mellitus and frontal lobe epilepsy. The latter is a sequela of a hemorrhagic stroke which occurred 3 years ago due to rupture of a right anterior communicating artery aneurysm. His first seizure, which occurred a year ago, was a convulsion in the setting of diabetic ketoacidosis. He was discharged on levetiracetam and remained seizure-free until 3 months ago when he started convulsing again due to diabetic ketoacidosis. Further convulsions were prevented by uptitrating levetiracetam, but a new type of seizure has emerged. The seizures consisted of left hand posturing or movements (scratching of the left face), pronounced hypersalivation, staring, and speech arrest. Each episode lasted about 2 minutes. He has no recollection of these events in between seizures. The seizures gradually increased in frequency over a two-month period—from 3 per day to 60 per day. During the past two weeks prior to admission, his parotid glands have increased in size leading his family to suspect mumps. Results: Head CT showed encephalomalacia in the right frontal lobe that is unchanged when compared to old images. Extensive otolaryngology evaluation did not find any reason for the parotid gland enlargement. Ictal electroencephalogram showed seizure onset in the right frontocentral area, first as rhythmic alpha then as rhythmic theta, followed by recruitment of temporal cortex and emergence of rhythmic delta, first on the right then in both hemispheres. When the seizures were successfully controlled with levetiracetam 1500 milligrams (mg) twice a day and lacosamide 100 mg twice a day, the patient’s parotid glands started to decrease in size. Conclusions: As in childhood Rolandic epilepsy, the mechanism of ictal hypersalivation in our patient is most likely epileptic activation of the frontal operculum. The parotid gland hypertrophy is most likely a physiological response to frequent ictal activation. Since Rolandic seizures occur infrequently in childhood Rolandic epilepsy, children with this epilepsy syndrome are unlikely to manifest parotid gland hypertrophy. Funding: None