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
Abstract
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
structures.
(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
Unit
A Z J Zeman
J R Hodges
Department of Clinical
Neurophysiology,
Addenbrooke’s
Hospital, Hills Road,
Cambridge, UK
S J Boniface
MRC Applied
Psychology Unit, 15
Chaucer Rd,
Cambridge, UK
J R Hodges
Correspondence to:
Professor J R Hodges, MRC
Applied Psychology Unit, 15
Chaucer Rd,Cambridge CB2
2QQ, UK. Telephone 0044
1223 245151; fax: 0044
1223 336941.
Received 30 April 1997 and
in revised form 21 July 1997
Accepted 29 July 1997
disturbance of retrograde memory? If so, what
mechanism is responsible?
Methods
PATIENTS AND DIAGNOSTIC CRITERIA
Patients had initially been referred to the
Memory and Cognitive Disorders Clinic at
Addenbrooke’s Hospital, Cambridge (four) or
seen in general neurology clinics in East Anglia
by the authors (four) or their colleagues (two).
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 and/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.
STUDY PROTOCOL
History and examination
We reviewed the history of attacks in detail with
the patient and with a witness (who was a
spouse in every case) independently, and
enquired whether any other memory problems
had been noticed by either patient or spouse,
following the methods described by Hodges.15
Other information regarding handedness, education
and work history, risk factors for
epilepsy (for example, birth history, febrile
convulsions, head injury, CNS infections, alcohol
use, family history), other medical history,
psychiatric history, and drug history was
collected using a proforma designed for the
study. The patients underwent a standard
neurological examination.
Investigations
All EEGs (16 channel digital and/or analogue
with a 10/20 montage) were assessed by one of
us (SB). If a sleep EEG (sleep deprived or drug
induced) had not already been performed, one
was arranged. Sleep deprived EEGs were
performed after three to four hours of sleep
deprivation on the preceding night. Drug
induced sleep EEGs were performed after the
administration of 300 mg amylobarbitone by
mouth. Interictal EEG features were classified
as follows:16 (1) epileptiform, with reproducible
examples (>2) of unequivocal focal epileptiform
complexes; (2) non-reproducible, with
two or less unequivocal epileptiform focal
abnormalities of comparable waveform in 30
minutes; (3) polyrhythmic, with brief polyrhythmic
abnormalities of no diagnostic relevance;
(4) normal, with none of the above
abnormalities. Normal small sharp spikes and
regional slow wave rhythms or complexes
attributable to the effects of aging or vascular
lesions were all excluded. Neuroimaging was
reviewed.
Neuropsychology
A battery of tests designed to assess verbal and
non-verbal anterograde recall and recognition
memory, and retrograde memory for public
and personal events, was administered to each
patient. These were the national adult reading
test,17 immediate and delayed story recall from
the Wechsler memory scale revised,18 reproduction
and delayed recall of the Rey-
Osterrieth complex figure,19 the recognition
memory test for words and faces,20 famous
faces and famous names tests,21 and the
autobiographical memory interview.22 the patients’
results were compared with those from
25 normal controls from the MRC Applied
Psychology Unit’s panel matched for age, years
of education, and NART score using one tailed
tests (see below). To examine the performance
of individual patients, we also identified
instances in which the patients’ scores fell
below 2 SD of the controls’ mean on any test.
Results
DEMOGRAPHY
Table 1 shows that nine of our 10 patients were
men. Their ages ranged from 49–73 with a
mean of 65. The aetiology of their epilepsy was
uncertain, but preceding vascular events were
common: three patients (cases 3, 5, and 7) had
a history of myocardial infarction, one patient
(case 6) had recently undergone aortic valve
replacement, and another (case 9) coronary
artery bypass grafting. Two patients (cases 1
and 8) reported significant head injuries with
loss of consciousness in early adulthood: the
post-traumatic amnesia had been negligible in
the first case and had lasted two hours in the
second.
CRITERIA FOR DIAGNOSIS
Table 1 shows that four patients had unequivocal
reproducible abnormalities referable to the
temporal lobes on wake or sleep EEG (see
below). Of the remaining six patients, five had
other seizure types which lent support to the
diagnosis of epilepsy (see below), and in the
remaining case anticonvulsant treatment abolished
the amnesic episodes. In six of the 10
patients more than one factor supported the
diagnosis of epilepsy.
CHARACTERISTICS OF THE AMNESIC EPISODES
Table 1 shows that at the time of the diagnosis
of TEA, the history of amnesic episodes ranged
in duration from four months to 14 years, with
a mean of three years. The number of episodes
ranged from three to 20 with a mean of nine. In
six patients all episodes had lasted for one hour
or less, in two patients some but not all attacks
had lasted for an hour or less, whereas in the
remaining two patients attacks had always
lasted hours, and sometimes days. Anterograde
and retrograde memory were both disturbed in
typical episodes, but five patients had partial
recall for at least some attacks, suggesting that
the anterograde amnesia was incomplete. Nine
of the 10 patients had questioned their
companions repetitively during episodes. The
retrograde amnesia during attacks was sometimes
brief, but all patients had experienced
436 Zeman, Boniface, Hodges
attacks in which it extended over several
months. It is noteworthy that in six of the 10
the retrograde amnesia sometimes extended
over many years. In every case at least one episode
had occurred on waking. Nine patients
were treated with anticonvulsant drugs and one
declined treatment; in seven there was clear cut
benefit, with abolition of overt attacks in six
and pronounced reduction of frequency in the
seventh. In the remaining two patients the
effects of treatment are uncertain, in one
patient because of a short period of follow up,
in the other because attacks had occurred only
at long intervals before the initiation of
treatment.
OTHER SEIZURE TYPES
Table 1 shows that seven of the 10 patients
reported other types of epileptic phenomena.
These comprised olfactory hallucinations in
two patients (cases 1 and 3), frequent episodes
of déjà vu in one patient (case 6), episodes of
vertigo in one patient (case 2), complex partial
seizures in three (cases 3, 9, and 10), and
tonic-clonic seizures in two patients (cases 8
and 10). In four patients (cases 1, 2, 6, and 9)
these phenomena sometimes preceded amnesic
episodes. In all cases the other seizure types
had first occurred at around the same time as
the amnesic episodes with the exception of
patient 6 who recalled a brief flurry of episodes
of déjà vu occurring about 45 years ago. In
three patients (cases 4, 5, and 7) there was no
history from either patient or spouse to suggest
the occurrence of any epileptic phenomena
apart from the amnesic episodes themselves.
RETROGRADE AMNESIA AND OTHER MEMORY
COMPLAINTS
Table 1 shows that seven of the 10 patients
complained spontaneously of an unusual and
persistent impairment of remote memory. In
every case this included an inability to recall
some salient episodes from their personal lives.
This was often first noted when the patients
encountered photographs of episodes from
recent holidays and realised that they had no
recollection of them. In all cases, the patients
and their spouses thought that this impairment
was “patchy”, with preservation of recall for
some, but loss of recall for other, episodes. The
impairment was more severe for episodes from
recent years than for the distant past, but in five
of the seven cases the impairment affected
recall for episodes which predated the clinical
onset of TEA. In these five patients, the retrograde
memory disorder extended from a minimum
of 18 months to a maximum of about 30
years (case 3). Six patients gave a history
suggestive of topographical amnesia, with
failure to recognise familiar landmarks and to
recall familiar routes. Three complained of difficulty
in recalling the names of longstanding
friends and acquaintances, and two complained
that they had lost their grasp of
techniques which they had used professionally
for many years. Patients were asked to assess
their day to day anterograde memory as well as
their recall for more remote events: only one of
the seven patients who complained of an
impairment of retrograde memory (case 10)
thought that he had a comparable disturbance
of day to day memory.
PSYCHIATRIC BACKGROUND
Two patients gave a history of mood disorder.
Patient 9 experienced lowering of his mood
after retirement and was being treated with
sertraline at the onset of his episodes of
transient amnesia; patient 10 had a long history
of intermittent depression, preceding the onset
of his episodic amnesia. He had received treatment
with paroxetine for an exacerbation of
depression some months after the onset of
amnesic episodes. A history of possible past
psychiatric disorder was obtained in two other
patients: patient 1 had been seen by a neurologist
on two occasions, seven and 24 years
before the onset of his current illness, with
symptoms which were attributed to stress.
Patient 6 had a history of excessive alcohol but
his episodes of amnesia had not occurred in the
context of alcohol misuse.
NEUROPHYSIOLOGY
Table 1 shows that all patients had sleep EEGs;
in eight of the 10 cases these were preceded by
wake records. Amylobarbitone was used to
induce sleep in five patients, and five patients
were sleep deprived. Four patients had clear
cut epileptiform EEG abnormalities as defined
above. In one of these (case 4) the wake EEG
was normal, in two (cases 2 and 3) the wake
EEGs showed non-reproducible epileptifom
abnormalities. The remaining patient (case 5)
did not have a wake EEG: epileptiform
discharges were detected in both the wake and
sleep portions of his sleep deprived EEG.
Table 1 Current series: clinical, EEG, and neuropsychological features
Case Age Sex
History
(duration) Attacks
Attack
(duration)
Repetitive
questioning
Sleep
related EEG findings Rx response
Other
epilepsy
TEA
aura
Focal retrograde
amnesia
1 63 M 3 y 20 1 h + + – + CBZ sps +/- +
2 49 M 4 months 12 <1 h + + +Bilateral + CBZ sps +/- +
3 68 M 8 months 5 h-days + + +Bilateral + SVP sps,cps – +
4 66 F 14 5 <1 h>1 h + + +L E CBZ – – –
5 79 M 15 months 3 h-days + + +Bilateral E CBZ – – +
6 70 M 2 y 13 <1 h + + Polyr no Rx sps +/- –
7 73 M 6 months 5 1-2 h – + Polyr + P – – –
8 60 M 6 months 3 <1 h>1 h + + – + SVP tcl – +
9 69 M 4 months 3 <1 h + + – + CBZ cps +/- +
10 56 M 9 months 20 <1 h + + – + CBZ cps, tcl – +
Polyr = polyrhythmic abnormalities present; Rx response = treatment response (+ = abolition or substantial reduction of episodes, E = equivocal reduction, CBZ =
carbamazepine; P = phenytoin, SVP = sodium valproate); sps = simple partial seizures; cps = complex partial seizures; tcl = tonic-clonic seizures; TEA aura = occurrence
of co-occurring seizure type as prodrome of amesic episode (+ = co-occurring seizure type always precedes TEA, +/- = co-occurring seizure type sometimes
precedes TEA, – = no co-occurring seizure type).
Transient epileptic amnesia 437
Patients 3 and 4 had drug induced sleep EEGs;
patients 2 and 5 were sleep deprived. In all
cases the discharges were referable to the anterior
or mid-temporal lobe. They were bilateral
and independent in three of the four patients
(cases 2, 3, and 5). Two of the six remaining
records (cases 6 and 7) showed sparse focal
polyrhythmic abnormalities on sleep EEG.
NEUROIMAGING
All patients had CT except for patient 1. These
were within normal limits. Four patients had
MRI; these were normal in patients 1 and 2; in
patient 5 there was evidence of focal infarction
in the posterior corpus callosum and in patient
10 there was focal atrophy of the anterior and
mid-hippocampus on the right. HMPAOSPECT
was performed in patients 1 and 3;
both showed a minor degree of frontal lobe
hypoperfusion.
NEUROPSYCHOLOGY
Table 2 shows that although there were no significant
differences between the group data for
patients and controls on any of the demographic
or neuropsychological variables, analysis
of individual patient’s scores disclosed that
seven had impaired performance on at least
one test (as judged by obtaining a score more
than 2 SD below the control group mean).
Interestingly, all but one of these tests examined
retrograde memory: the famous faces test
(two patients), the famous names test (four
patients), the autobiographical memory interview
(three patients), and the recognition
memory test (one patient). In total, five
patients showed impairment of one or more
tests of remote memory but in most cases, their
scores were only just below the 2 SD cut off.
Only one score (for the autobiographical
memory interview in patient 2, described
below) fell more than 3 SD below the control
mean.
The cases are briefly summarised below:
Case 1
A 63 year old engineer had experienced about
20 episodes of transient amnesia lasting for
around one hour each over the past three years.
Most had occurred on waking. He would characteristically
say “I’m not sure where I am” at
the onset; his conversation would then disclose
a retrograde amnesia extending back for about
10 years. He has no recall for events during the
attacks. In other respects, he converses and
behaves normally during attacks. Over the year
before presenting to us he had complained to
his wife of a “strange smell or taste” which he
noticed at the onset of attacks. He had been
knocked out by a fly press in 1966. MRI and
wake and sleep EEG were normal. Treatment
with carbamazepine abolished the attacks.
Case 2
A 49 year old businessman presented with a
four month history of brief episodes of vertigo
accompanied by “ringing in the ears”, which
usually woke him from sleep and which was
often followed by a period of amnesia lasting
for less than one hour. Amnesia on waking
sometimes occurred without the prodrome of
vertigo. The amnesic episodes involved retrograde
amnesia for up to 30 years accompanied
by incomplete anterograde amnesia. Apart
from repetitive questioning to his wife, behaviour
during attacks was normal. During this
period he has developed a patchy persistent
amnesia for recent events. Brain MRI was normal
but sleep and wake EEG showed independent
unequivocal bitemporal epileptiform
abnormalities. Treatment with carbamazepine
has abolished the amnesic episodes.
Case 3
A 68 year old retired engineer gave an eight
month history of episodes of amnesia which
usually occurred on waking, and involved
extensive retrograde amnesia with incomplete
anterograde amnesia for the episodes themselves.
Apart from occasional repetitive questioning
his behaviour was normal during the
initial attacks. He sometimes complained of an
odd taste or smell. Seven months after the first
attack he had an episode of amnesia during
which he was clearly confused and unable to
dress himself; after this, his wife described episodes
in which he became inaccessible for a few
minutes, with no subsequent recall of events
during the episodes. During this period it
became clear that he had developed an
extensive patchy retrograde amnesia for events
of the past 30 years. He had a history of myocardial
infarctions seven and nine years ago.
Brain CT was normal and SPECT showed
minor reduction in uptake frontally.Wake EEG
showed sharpened theta activity in both
temporal lobes; sleep deprived EEG showed
independent bitemporal unequivocal epileptiform
abnormalities. Treatment with sodium
valproate abolished the episodes of overt
amnesia.
Table 2 Neuropsychological test results
TEA
mean (SD)
Controls
mean (SD)
Anterograde memory tests (maximum score in parenthesis):
Age 65 (9) 70 (8)
Education (y) 12 (2) 11 (2)
NART 115 (6) 119 (7)
Story recall WMS:
Immediate (21) 13 (4) 12 (4)
Delayed (21) 10 (3) 9 (3)
Rey-Ostereith figure:
Copy (36) 35 (1) 34 (3)
Delayed recall (36) 20 (4) 15 (8)
Recognition memory test:
Words (50) 46 (3) 47 (3)
Faces (50) 43 (4) 44 (4)
Retrograde memory tests (maximum scores in parenthesis):
Famous faces test
Recognition (50) 47 (2) 43 (7)
Identification (50) 38 (5) 39 (9)
Naming (50) 26 (10) 31 (4)
Famous names test
Recognition (50) 49 (1) 50 (1)
Identification (50) 46 (2) 49 (1)
Autobiographical memory interview:
Personal semantic:
Childhood (21) 19 (2) 20 (2)
Early adulthood (21) 18 (2) 20 (2)
Late adulthood (21) 20 (2) 20 (1)
Personal incident:
Childhood (9) 8 (2) 7 (2)
Early adulthood (9) 7 (2) 8 (2)
Late adulthood (9) 7 (3) 7 (2)
438 Zeman, Boniface, Hodges
Case 4
A 67 year old housewife experienced four episodes
of transient amnesia, lasting from a few
minutes to several hours, over the course of 15
years. Anterograde amnesia was incomplete in
the first two episodes but the third and fourth
were clinically indistinguishable from transient
global amnesia. Behaviour was normal during
the episodes apart from repetitive questioning.
Brain CT and wake EEG were normal, but a
sleep record showed unequivocal left temporal
epileptiform abnormalities. On treatment with
carbamazepine she had had one further
episode lasting 20 minutes.
Case 5
A 79 year old retired manager experienced several
episodes of amnesia lasting hours or days.
At least one episode occurred on wakening. He
asked questions repetitively during the episodes.
Over the same period he developed a
patchy amnesia for recent events. Two and a
half years before presentation he had had a
myocardial infarct. Brain MRI disclosed an
area of infarction in the posterior corpus callosum.
EEG showed independent bitemporal
unequivocal independent epileptiform abnormalities.
Follow up after starting treatment
with carbamazepine has been too brief to judge
the response.
Case 6
A 70 year old retired surveyor had experienced
unusually frequent episodes of déjà vu in his
mid-20s. He presented to us with a two year
history of numerous episodes of dense anterograde
amnesia lasting minutes, with some
retrograde amnesia, sometimes occurring on
waking and often preceded by a sense of déjà
vu. He questioned his wife repetitively during
these episodes, but could perform complex
tasks—for example, playing cards. He was
drinking up to 10 units of alcohol a day at the
onset of these episodes and required an aortic
valve replacement during this period. An EEG
showed right temporal polyrhythmic abnormalities;
brain CT was normal. He declined
treatment.
Case 7
A 73 year old retired electrician presented with
a history of five attacks of amnesia lasting one
to two hours over the preceding six months.He
typically complained of feeling odd at the
onset, and sometimes of a strange feeling over
the left side of his face. He would then ask
“What are we doing here?”, and question his
wife repetitively. His questions sometimes
betrayed amnesia for recent events. One attack
occurred on waking in the early hours. Brain
CT was normal; EEG showed right temporal
polyrhythmic abnormalities. Treatment with
phenytoin abolished the attacks.
Case 8
A 60 year old printer presented after three episodes
of amnesia in the last six months. The
first occurred on waking and involved repetitive
questioning, lasting for at least one hour.
Shortly after this he had a tonic-clonic seizure
in sleep. The third amnesic episode culminated
in a series of brief generalised convulsions. He
developed a patchy retrograde amnesia for
recent events, familiar faces, and places. He
had a history of head injury with loss of
consciousness in a motorbike accident at the
age of 18. Brain CT and wake and sleep EEGs
were normal. There have been no more attacks
since treatment with sodium valproate was
started.
Case 9
A 69 year old retired civil engineer had experienced
three episodes of amnesia in four
Table 3 Previously reported cases: clinical, EEG, and neuropsychological features
Reference Age Sex
History
(duration) Attacks (n)
Attack
(duration)
Repetitive
questioning
Sleep
related
EEG
findings
Rx
response
Other
epilepsy
TEA
aura
Focal
retrograde
amnesia
Memory
tests
Lou50 61 M ? 9 15 min>h + + +R +OXZ – – – Ant
Shuping24 60 M ? 3 <1 h ? ? – – tcl – – ND
Deisenhammer23 11 F 1 month 4 <1 h + + +R + CBZ – – – ND
Dugan et al3 82 M 2 months 3 3–4 h + ? +Bilateral + P – – – ND
Pritchard et al4:
i 65 M 4 y 10 <15 min – ? +Bilateral + P – – ? ND
ii 64 M 6 months 3 1–24 h – ? +Bilateral + CBZ – – ? ND
Meador et al25 47 F 10 months 2 <1 h – – +Bilateral + P/surg cps – Normal
Galassi et al12 67 M 2 y 25 <1 h + + ThetaR E P sps/cps + Imp mem Verb
Gallassi et al36:
i 70 F 3 y 2-3/weeks <1 h + ? +R + CBZ cps + Imp mem Vis/verb
ii 66 M 2 y 1/m <1 h + ? ThetaL + CBZ cps + Imp mem Verb
Miller et al5:
i 62 M 14 months 8 <30 mins + + +Bilateral + P – – – ND
ii 22 ? Weeks Several <1 h ? ? +L + ? cps +/- ? ND
Stracciari et al13 70 F 8 months 8 10 min–7 h + – +L + CBZ cps +/- Imp mem Vis/verb
Kapur37 74 M 5 y 20 30 min>h ? + +Bilateral ? cps +/- + Retro
Kapur6:
i 63 F 3 y 35 Mins>h – ? ThetaL + SVP cps +/- Imp mem Vis/retro
ii 67 F 4 months 6 30 min–1 h – ? ThetaL + P – – – Normal
iii 28 M ? 20 1–2 day + + +Bilateral + CBZ/P cps +/- ? Vis/verb
iv 61 F ? 2 Min ? + +L + CBZ cps +/- Imp mem ?
v 60 M 3 y Many 10–15 min + ? +Bilateral + CBZ sps, cps + ? Verb
vi 54 M 21 months 8 30 min–1 h + ? +Bilateral + P cps +/- + Ant
Vuilleumier et al34 41 F >20 y Many Hours – + +Bilateral + CBZ sps + – Normal
Rx response = treatment response (+ = abolition or substantial reduction of episodes, E = equivocal reduction, CBZ = carbamazepine, P = phenytoin, SVP = sodium
valproate, OXZ = oxazepam, surg = surgery); other epilepsy = other co-occurring seizure types, (sps = simple partial seizures, cps = complex partial seizures, tcl =
tonic-clonic seizures); TEA aura = occurrence of co-occurring seizure type as prodrome of amesic episode, (+ = co-occurring seizure type always precedes TEA, +/-
= co-occurring seizure type sometimes precedes TEA, – = no co-occurring seizure type); Imp mem = complaint of impaired memory not further specified; vis/verb
= deficits on tests of anterograde visual/verbal memory; ant = anterograde memory impairment not further specified; retro = deficits on tests of retrograde memory.
Transient epileptic amnesia 439
months. Two of these occurred on waking and
involved anterograde amnesia, with repetitive
questioning, and retrograde amnesia for recent
events. Several subsequent episodes of amnesia
followed brief spells of loss of consciousness
which were sometimes preceded by lip smacking
and sometimes associated with scanty convulsive
movements. Over the same period he
developed a patchy amnesia for events of the
past three years. He had had triple coronary
artery bypass surgery two years before. Shortly
before the onset of these episodes sertraline
had been prescribed for depression. Brain CT
and wake and sleep EEGs were normal. There
have been no further attacks since starting
treatment with carbamazepine.
Case 10
A 56 year old lecturer reported numerous episodes
of anterograde amnesia, accompanied by
retrograde amnesia for recent events, lasting for
less than one hour, over a nine month period.
These commonly occurred on waking from
naps.On other occasions, however, his wife saw
him “drift off into a trance and make choking
noises for a second or two”, after which he
would be amnesic. He went on to have three
witnessed tonic-clonic convulsions, shortly
after starting paroxetine for depression. He
complained of poor memory for day to day
events and for familiar places, and of abnormal
forgetting over time. Brain MRI showed focal
atrophy of the right hippocampus. Sleep EEG
was normal. Since starting treatment with carbamazepine
there have been no further episodes
of amnesia or overt seizures.
Discussion
VALIDATION OF TEA AS A DISTINCT
NEUROLOGICAL ENTITY
Table 3 shows several previous reports that
have suggested that episodes of transient
amnesia, often closely resembling the syndrome
of transient global amnesia, can have an
epileptic basis, but this fact has not received
wide acceptance. Our 10 cases provide further
evidence for the existence of TEA which we
argue is a distinctive manifestation of temporal
lobe epilepsy.The evidence is most persuasive
in those patients with support from all three
criteria adopted in this study: epileptiform discha