Transient epileptic amnesia: a description of the clinical and neuropsychological features in 10 cases and a review of the literature.

Transient epileptic amnesia: a description of the
clinical and neuropsychological features in 10
cases and a review of the literature
Adam Z J Zeman, Simon J Boniface, John R Hodges
Objectives—To clarify the clinical and
neuropsychological aspects of transient
epileptic amnesia (TEA) based on 10 personally
studied cases as well as review of
21 previously published cases; and to propose
tentative diagnostic criteria for the
diagnosis of TEA.
Methods—All 10 patients and informants
underwent a standardised clinical interview.
The radiological and neurophysiological
(EEG) data were also reviewed in
all cases. The diagnosis of transient epileptic
amnesia was made on the basis of
the following criteria: (1) there was a history
of recurrent witnessed episodes of
transient amnesia; (2) cognitive functions
other than memory were judged to be
intact during typical episodes by a reliable
witness; (3) there was evidence for a diagnosis
of epilepsy. This evidence was provided
by either (a) wake or sleep EEG, or
(b) the co-occurrence of other seizure
types (if their roughly concurrent onset or
close association with episodes of transient
amnesia suggested a connection), or
(c) a clear cut response to anticonvulsant
therapy, or by a combination of these
three factors. In addition all patients were
administered a comprehensive neuropsychological
test battery designed to assess
verbal and non-verbal anterograde
memory and retrograde memory for
famous personalities and personal events.
Their results were compared with those of
25 age and IQ matched normal controls.
Results—TEA usually begins in later life,
with a mean age of 65 years in this series.
Episodes are typically brief, lasting less
than one hour, and recurrent, with amean
frequency of three a year. Attacks on waking
are characteristic. Repetitive questioning
occurs commonly during attacks.
The anterograde amnesia during episodes
is, however, often incomplete so that
patients may later be able to “remember
not being able to remember”. The extent
of the retrograde amnesia during attacks
varies from days to years. Most patients
experience other seizure types compatible
with an origin in the temporal lobes, but
transient amnesia is the only manifestation
of epilepsy in about one third of
patients. Epileptiform abnormalities arising
from the temporal lobes are most
often detected on interictal sleep EEG.
Despite normal performance on tests of
anterograde memory,many patients complain
of persistent interictal disturbance
of autobiographical memory, involving a
significant but variable loss of recall for
salient personal episodes. The epochs
affected may predate the onset of epilepsy
by many years.
Conclusions—TEA is an identifiable syndrome
and comprises episodic transient
amnesia with an epileptic basis, without
impairment of other aspects of cognitive
function. Future studies should consider
the question of whether TEA reflects ictal
activity or a postictal state, and the mechanism
of the persistent autobiographical
amnesia. It is hypothesised that the latter
may result in part from impairment of
very long term memory consolidation as a
result of epileptic activity in mesial temporal
(J Neurol Neurosurg Psychiatry 1998;64:435–443)
Keywords:Transient epileptic amnesia; electroencephalography
It has been recognised for over 100 years that
amnesia for episodes of complex and well integrated
behaviour can occur in association with
temporal lobe epilepsy.1 2 More recent reports
have suggested that transient amnesia is sometimes
the only manifestation of a temporal lobe
seizure, and indeed that it may be the only seizure
type to occur in some patients.3–6 Seizures
causing prominent amnesia are easily mistaken
for episodes of transient global amnesia
(TGA)7 or of psychogenic amnesia.8 Various
terms has been used to describe these attacks
including pure amnestic seizures,9 ictal
amnesia,10 epileptic amnesia,11 epileptic amnesic
attacks,4 12 epileptic transient amnesia,13 and
transient epileptic amnesia or TEA.6 14 We have
adopted the last of these terms to highlight the
similarity of this syndrome to, but also its
distinction from, TGA.Our aims were to clarify
the clinical and neuropsychological features of
this disorder in the light of 10 cases of TEA
studied prospectively, and to compare these
with the features suggested by 15 previously
published reports of 21 cases. The largest previous
series describes four cases.6 We focus on
the following questions: (1) Is transient amnesia
a distinctive presentation of temporal lobe
epilepsy? If so, what are its characteristic
features? (2) What is the pathophysiology of
TEA, and in particular is it an ictal or postictal
phenomenon? (3) Is TEA associated, as Kapur
has suggested,6 with a persistent interictal
J Neurol Neurosurg Psychiatry 1998;64:435–443 435
University of
Cambridge Neurology
A Z J Zeman
J R Hodges
Department of Clinical