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Abstract Details

Tiagabine-Induced Encephalpathy
Epilepsy/Clinical Neurophysiology (EEG)
P9 - Poster Session 9 (12:00 PM-1:00 PM)
12-001
Introduction: High doses and dose escalation of tiagabine may precipitate encephalopathy and non-convulsive status epilepticus (NCSE). We present a case of a 22 year-old woman with confusional episodes consistent with tiagabine-induced toxic encephalopathy recorded on prolonged video EEG monitoring.
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Case Report: A 22 year-old woman with a BMI of 22.4 kilograms/meter2 was initiated on tiagabine for pain secondary to Chronic Regional Pain Syndrome. Two years later, confusional spells began after dose escalation to 32 milligrams (mg) per day and continued despite decreasing the dose to 28 mg per day in three divided doses. Spells began gradually with poor concentration and a hot sensation, followed by one to 10 hours of confusion with impaired awareness. She could complete complex tasks but displayed atypical behavior, such as undressing. Approximately forty-percent of spells occurred one hour after ingesting tiagabine.

Prolonged video EEG monitoring for one day revealed intermittent generalized theta and delta slowing. Within one hour of challenging the patient with an escalated dose of tiagabine 12 mg, a typical six-hour spell of slowed responsiveness and word finding difficulty was recorded. EEG during the event demonstrated continuous, high amplitude, rhythmic, generalized monomorphic delta slowing. Following resolution of symptoms, EEG showed generalized, frontally dominant, atypical spike and wave and polyspike and wave discharges, which completely resolved in the final hours of the EEG recording.

The patient tapered tiagabine by four mg per week until off. Spells had not recurred at eight months follow-up, which supports the hypothesis of tiagabine-induced encephalopathy.
Conclusion: Based on reproduction of clinical symptoms with tiagabine administration and non-epileptiform EEG findings during the clinical event, this case is most consistent with tiagabine-induced episodic toxic encephalopathy. Low BMI, as in this patient, has previously been identified as a risk factor for this complication.
Authors/Disclosures
Kiran M. Kanth, MD (UC Davis Medical Center Department of Neurology)
PRESENTER
Dr. Kanth has nothing to disclose.
Nicholas M. Gregg, MD (Mayo Clinic) The institution of Dr. Gregg has received research support from NIH. The institution of Dr. Gregg has received research support from Medtronic Plc.
Kate W. Hocquard, MD (Olmsted Medical Center) No disclosure on file
Cheolsu Shin, MD (Mayo Clinic) No disclosure on file
Jeffrey W. Britton, MD, FÂé¶¹´«Ã½Ó³»­ (Mayo Graduate School of Medicine) Dr. Britton has received personal compensation in the range of $0-$499 for serving as a Online course with American Clinical Neurophysiology Society.