Can the syndrome of transient epileptic amnesia be the first feature of Alzheimer's disease?

Transient epileptic amnesia (TEA) is a specific type of temporal lobe seizure involving the hippocampus and the parahippocampal gyrus, which can be recognized with now published criteria. The etiology of TEA is still under debate and probably not unique. Apart from rare patients showing structural lesions on brain MRI, microvascular brain load and/or immune-mediated neuronal aggression have been proposed as alternative causes. A neurodegenerative process is also possible, as suggested by decreased hippocampal volume and ongoing memory complaints despite seizure freedom in many treated subjects. Thus, late onset Alzheimer’s disease (LOAD) logically appears as a potential cause of TEA. Indeed, we present a case of TEA that secondarily evolved into AD 16 years after seizures onset. The patient was right-handed and had 9 years of education. She had no remarkable medical history. Her mother had been diagnosed with LOAD at the age of 70. The patient was 64 when she came in 2009 to our Memory Clinic for cognitive complaints developing since her first transient antero-retrograde amnesia (in 1994) that lasted about 10 h and started with a preceding aura (ascending thoraco-abdominal pain with diffuse heat sensation and nausea) while witnesses described contact loss for 2 min, bilateral arm dystonia and oral automatisms (tongue smacking). Transient global amnesia (TGA) was diagnosed because screening blood tests, brain CT scan and EEG were all within the normal range. In 1994, her MMSE score was 30/30, even though she was complaining of abnormal long term forgetting and autobiographical difficulties (she did not remember her wedding or several vacations during the previous 10 years). Another antero-retrograde amnesia occurred 5 years later (1999), which lasted 2 h and was preceded by the same aura and a sudden fall. Witnesses again described partial contact loss during amnesia. CT-scan and EEG were still normal as was the cardiovascular work-up. Thereafter, the patient became depressed and the subjective cognitive