Abstracts

RATIONALE: Confusion in association with non-convulsive (spike-slow wave) status epilepticus has been a well-described but rare phenomenon in patients taking tiagabine. We encountered three patients who developed severe episodic confusion while taking tiagabine, but whose video-EEG monitoring did not show status epilepticus.
METHODS: Over a two-year period, three epilepsy patients were evaluated with prolonged video-EEG monitoring for episodes of severe confusion while taking tiagabine. We reviewed their histories and laboratory tests including the video-EEG recordings of their episodes of confusion. The information was assessed for factors that may explain the development of the episodic confusion in these patients.
RESULTS: Case 1: A 46-year old man presented with a nine-month history of weekly spells of confusion, feeling [dsquote]dazed[dsquote] and disoriented, for 30 minutes to 2 hours each spell. During video-EEG monitoring, the patient did not have a spell when his anticonvulsants were discontinued. Upon re-challenging with tiagabine (56mg/day), the patient had a prolonged spell of confusion, agitation, and disorientation. Accompanying EEG showed generalized, frontally predominant delta frequency slowing.
Case 2: A 63 year-old woman developed spells of ascending paresthesia and subsequent confusion and amnesia, when her tiagabine was increased to 48mg/day. The spells usually occurred in the evening, and they lasted one to three hours each time. EEG showed frontal intermittent rhythmic delta activity (FIRDA) and occasional triphasic waves.
Case 3: A 38 year-old woman underwent a right anterior temporal lobectomy for intractable partial epilepsy. Pre-operative medications included tiagabine (28mg/day), though the patient[ssquote]s dosing schedule was irregular on the day prior to surgery. She did well immediately after surgery, but she soon became confused and agitated on the first post-operative day. EEG monitoring revealed frequent bursts of generalized slowing. No change in the EEG was seen after the administration of IV lorazepam.
The EEG in all three patients did not show any generalized spike-wave discharges or any other type of seizure activity. None was concomitantly taking another gabaergic drug. Comprehensive evaluation revealed no other potential cause for the encephalopathy. Mental confusion and EEG abnormality resolved in all three patients when tiagabine was either reduced or discontinued.
CONCLUSIONS: Evidence in our three patients indicates that they developed encephalopathy in association with tiagabine therapy. Patients who develop mental confusion while taking tiagabine should not be presumed to have non-convulsive status epilepticus. Video-EEG recording may be needed to distinguish between the two conditions.