In one case, a man with untreated TEA experienced ongoing seizures (~12 over the 5‐year period), but maintained average performance on standard memory measures, with no evidence of general cognitive decline, and no further medical conditions reported. With only one case to date reporting recovery of some remote episodic memories that had been inaccessible.įollow‐up information at 5 years or beyond is extremely limited, with mixed results. The patchy loss of memory for personal life events, however, appears to persist, (although in some cases ongoing memory difficulty is reported despite seizure cessation). Short‐term follow‐up studies over a 6‐ to 18‐month period suggest ongoing seizure control and the potential for improvements in some aspects of memory once seizures have ceased Other neuropsychological domains tend to remain intact.Īlthough these characteristics of TEA are now well documented, the long‐term prognosis, with regard to seizure control, dementia risk, medical comorbidity, and seizure control has not yet been well studied. Standard neuropsychological tests of anterograde memory tend not to reveal severe impairments, with reductions either in the mild to moderate range Treatment for TEA typically involves a low‐dose anti‐seizure medication, resulting in a high rate of seizure cessation.Īlthough this addresses the ictal memory disturbance, many group studies comparing patients on treatment with matched healthy controls suggest ongoing cognitive sequelae in the form of patchy retrograde amnesia for salient life events,Īccelerated forgetting of recently acquired memories, Other comorbidities reported in TEA cohort studies include autoimmune conditions and depression,Īlthough how these rates compare with population norms has yet to be established. Comorbidity with certain cardiovascular conditions (cardiac arrhythmia, cardiac valve disease, arterial aneurysm) may occur at a higher rate than in age‐matched controls. however, in many cases the genesis remains unknown. Mechanisms leading to the onset of TEA appear variable, including reports of limbic encephalitis, Or brief spells of unresponsiveness, are commonly experienced immediately preceding or in conjunction with these amnestic attacks. Additional epileptic phenomenon, such as olfactory hallucinations, Onset in mid‐late adult life (on average 57–63 years), monthly frequency of attacks, These studies have been important in identifying characteristic features, including male predominance, Where typically only one, longer (eg, 4–6 h) amnesic episode occurs without evidence of epilepsy Īnd the more broadly defined epileptic amnesic syndrome, where pronounced interictal memory deficits may arise in the context of subtle, nonamnestic temporal lobe seizures.įollowing publication of the diagnostic criteria in 1998, ~250 cases of TEA have been reported. Using these criteria, TEA may be distinguished from other similar conditions: transient global amnesia, To meet diagnostic criteria, amnesic episodes must be witnessed, and there must be supporting evidence of epilepsy via other clinical features (eg, lip‐smacking, presence of an aura), epileptiform abnormalities on electroencephalography (EEG), or through response to antiseizure medication. Transient epileptic amnesia (TEA) is a form of adult‐onset epilepsy in which brief episodes of amnesia recur in the absence of disruption to other cognitive functions.
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