OBJECTIVE: To study the underlying pathophysiology and the long-term prognosis of the syndrome of transient epileptic amnesia (STEA). BACKGROUND: STEA has been recently described as a distinct nosologic entity, in which memory impairment is the sole clinical manifestation of temporal lobe epilepsy. METHODS: Serial neuropsychologic examinations and electroencephalography (EEG) were performed on a patient with STEA, before and after treatment with antiepileptic drug for a 2-year study period. RESULTS: Initial neuropsychologic assessment revealed isolated mild-to-moderate impairment in anterograde verbal and visual memory. EEG showed intermittent sharp and spike discharges from both temporal regions, independently, consistent with an underlying seizure tendency. Treatment with extended-release carbamazepine 200 mg twice daily led to complete resolution of the memory difficulty, and the repeat neuropsychologic assessment and EEG were within normal limits. Two years after the treatment was initiated, the patient remained asymptomatic and a third neuropsychologic assessment was completely normal. CONCLUSIONS: The memory impairment in STEA does not originate from a progressive neurodegenerative mechanism, but rather from an underlying epileptic and therefore reversible etiology. When identified and treated, STEA carries no memory impairment at 2 years after diagnosis.
OBJECTIVE: To study the underlying pathophysiology and the long-term prognosis of the syndrome of transient epilepticamnesia (STEA). BACKGROUND:STEA has been recently described as a distinct nosologic entity, in which memory impairment is the sole clinical manifestation of temporal lobe epilepsy. METHODS: Serial neuropsychologic examinations and electroencephalography (EEG) were performed on a patient with STEA, before and after treatment with antiepileptic drug for a 2-year study period. RESULTS: Initial neuropsychologic assessment revealed isolated mild-to-moderate impairment in anterograde verbal and visual memory. EEG showed intermittent sharp and spike discharges from both temporal regions, independently, consistent with an underlying seizure tendency. Treatment with extended-release carbamazepine 200 mg twice daily led to complete resolution of the memory difficulty, and the repeat neuropsychologic assessment and EEG were within normal limits. Two years after the treatment was initiated, the patient remained asymptomatic and a third neuropsychologic assessment was completely normal. CONCLUSIONS: The memory impairment in STEA does not originate from a progressive neurodegenerative mechanism, but rather from an underlying epileptic and therefore reversible etiology. When identified and treated, STEA carries no memory impairment at 2 years after diagnosis.