495201

research-article2013
EEGXXX10.1177/1550059413495201Clinical EEG and NeuroscienceLapenta et al

Article
Clinical EEG and Neuroscience

Transient Epileptic Amnesia: Clinical

2014, Vol. 45(3) 179183
EEG and Clinical Neuroscience
Society (ECNS) 2013
Report of a Cohort of Patients Reprints and permissions:
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DOI: 10.1177/1550059413495201
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Leonardo Lapenta1, Valerio Brunetti1, Anna Losurdo1, Elisa Testani1,

Nadia Mariagrazia Giannantoni1, Davide Quaranta1,
Vincenzo Di Lazzaro2, and Giacomo Della Marca1

Abstract
Transient epileptic amnesia is a seizure disorder, usually with onset in the middle-elderly and good response to low dosages
of antiepileptic drugs. We describe the clinical, electroencephalography (EEG), and neuroimaging features of 11 patients with
a temporal lobe epilepsy characterized by amnesic seizures as the sole or the main symptom. We outline the relevance of a
detailed clinical history to recognize amnesic seizures and to avoid the more frequent misdiagnoses. Moreover, the response to
monotherapy was usually good, although the epileptic disorder was symptomatic of acquired lesions in the majority of patients.

Keywords
epilepsy, transient amnesia, temporal lobe epilepsy, symptomatic epilepsy, differential diagnosis
Received April 3, 2013; revised May 3, 2013; accepted June 3, 2013

Introduction
Episodes of transient amnesia may be a seizure disorder, mainly
originating from temporal lobes.1
Despite the wide range of differential diagnoses (such as
transient global amnesia [TGA], closed head injury, psycho-
genic amnesia, transient ischemic attack [TIA], migraine, and
drug effects)2 that frequently lead to an underdetection of these
phenomena, recurrent acute episodes of memory dysfunction
may be the sole or the main feature of epileptic seizures.
Recently, transient epileptic amnesia (TEA) has been proposed
as a distinctive epileptic syndrome with defined diagnostic cri-
teria.2 However, the definition and the classification of this epi-
leptic disorder are still debated; different studies2-4 have
reported the clinical and neurophysiological features of these
patients to outline the clinical syndrome.
On the basis of the reported features, we describe the clini-
cal, EEG, and neuroimaging characteristics of 11 patients with
TEA and their response to antiepileptic treatment.
Methods and Subjects
We enrolled 11 patients (7 men and 4 women, age range =
35-79 years; mean age = 59.7 years) with episodes of TEA.
These were defined as witnessed epileptic seizures, characterized
by brief, recurrent episodes of amnesia (anterograde, retro-
grade, or both) with sparing of other cognitive functions.2-4 The
evidence of a diagnosis of epilepsy was provided by (1) wake
or sleep EEG, (2) co-occurrence of other clinical features of
epilepsy, and (3) a clear-cut response to antiepileptic therapy.
For each patient, EEG and ambulatory 24-hour EEG (A-EEG),
magnetic resonance imaging (MRI), and pharmacological
treatment were analyzed; moreover, detailed clinical and epi-
leptological history regarding ictal, interictal, and peri-ictal
features were collected (for details see Tables 1 and 2). All
patients underwent a structured psychiatric interview. Standard
neuropsychological tests were used to assess anterograde and
short memory (copy and 30-minute delayed recall of the Rey
Osterreith complex figure, the Rey 15-Item Memory Test, the
Rey Word Recognition Test, constructive praxis (figures copy),
general intelligence (Ravens progressive matrices), selective
attention (the Stroop test), and language (semantic and phono-
logical word production).
Characteristics of the Population
Four patients satisfied all the 3 proposed criteria, 7 patients sat-
isfied criteria 1 and 3. The age at onset of amnesic seizures
ranged from 35 to 78 years (mean = 54.9 years). Eight patients
referred to our Neurological Department for amnesic epi-
sodes or memory disturbances, whereas 3 patients presented
1
Institute of Neurology, Catholic University, Rome, Italy
2
Institute of Neurology, Campus Biomedico University, Rome, Italy
Corresponding Author:
Leonardo Lapenta, Department of Neurosciences, Catholic University,
Policlinico Universitario A. Gemelli L.go A. Gemelli, 8, 00168 Rome, Italy.
Email: leonardo.lapenta@gmail.com
Full-color figures are available online at http://eeg.sagepub.com

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180 Clinical EEG and Neuroscience 45(3)

Table 1. General characteristics of the patients and EEG, MRI and memory tests findings.

Cause of
Patient Age Age (Years) First Medical Memory Tests
No. Gender (Years) at Onset Consultation EEG Findings MRI Findings (Abnormal Scores)
1 Male 75 62 Brief loss of Left temporal spikes and Posttraumatic left Verbal and spatial span,
consciousness 4-5 Hz slow waves temporal horn recency effect, Stroop
meningoencephalocele test
2 Female 64 62 TGA-like Asynchronous bitemporal Bilateral mesial temporal none
sharp waves lobe gliosis
3 Male 46 35 Nocturnal 5-6 Hz bilateral posttraumatic bilateral Verbal and spatial span,
generalized frontotemporal slow basalfrontal gliosis, recency effect
seizure and sharp waves right hippocampal
sclerosis
4 M 60 58 TGA-like Right frontotemporal Posttraumatic right Verbal and spatial span,
sharp waves and spikes frontal horn gliosis recency effect
5 Female 47 40 Generalized Right frontotemporal Right temporalpolar None
seizure sharp waves and spikes low grade glioma
6 Male 60 58 TGA-like Asynchronous Normal None
bitemporal sharp
waves and spikes
7 Male 42 36 TGA-like Normal Normal None
8 Male 35 29 TGA-like Normal Normal None
9 Female 79 78 TGA-like Right frontotemporal Posttraumatic right basal/ None
spikes orbital frontal gliosis
10 Female 75 73 TGA-like Asynchronous Right cerebellar and basal None
bitemporal spikes and ganglia postischemic
sharp waves gliosis
11 Male 74 73 TGA-like Left frontotemporal Postsurgical right None
sharp waves and spikes occipital gliosis (AVM)

Abbreviations: EEG, electeoencephalogram; MRI, magnetic resonance imaging; AVM, arteriovenous malformation; TGA, transient global amnesia.

Table 2. Clinical characteristics, semiology and treatment of the amnesic seizures.

Time From
No. of The Last
Patient Amnesic Episode
No. Seizures Duration Ictal Semiology of Amnesia Peri-ictal Features Treatment Episodes (Months)
1 3 min up to 2 h Anterograderetrograde Slight abdominal discomfort CBZ 800 mg/d >30 37
2 2 min up to 3 h Anterograde None CBZ 800 mg/d 7 39
3 4 min Anterograde None OXC 600 mg/d, CLZ 4 mg/d 48 2
4 2-10 min Anterograderetrograde None VPA 600 mg/d 3 33
5 5-10 min Anterograderetrograde None LEV 1000 mg/d 9 25
6 10 min Anterograde Olfactory hallucinations LEV 1000 mg/d 3 20
7 3-5 min Anterograderetrograde None LEV 750 mg/d 11 6
8 2-3 min Anterograderetrograde None LEV 1000 mg/d 9 9
9 5-30 min Anterograderetrograde None LEV 1000 mg/d 8 24
10 2 min up to 48 h Anterograderetrograde Slight confusion CBZ 200 mg/d 9 11
11 5 min up to 3 h Anterograderetrograde Oral automatisms LEV 1000 mg/d 15 8

Abbreviations: CBZ, carbamazepine; CLZ, clobazam; LEV, levetiracetam; OXC, oxcarbazepine; VPA, valproate.

episodes of loss of consciousness or generalized tonicclonic
seizures, in one case during sleep. Amnesic attacks lasted from
2 minutes to 48 hours. Except for the first episode, which was
prolonged in 3 patients (up to 48 hours in one case), the dura-
tion ranged between 2 and 10 minutes (mean 4.4 minutes). In 4
of 11 patients the amnesic seizures were accompanied by other
peri-ictal signs or symptoms, in particular olfactory hallucina-
tions and/or epigastric rising, oral automatisms, abdominal dis-
comfort, and slight confusion. In the remaining 7 patients,
seizures were only characterized by anterograde amnesia or

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Lapenta et al 181
Figure 1. Brain magnetic resonance images: (A) posttraumatic
bilateral basalfrontal gliosis in a patient with drug-resistant
amnesic seizures; (B) posttraumatic left temporal horn
meningoencephalocele; (C) right hippocampal sclerosis; and (D)
posttraumatic right frontal horn gliosis.
both anterograde and retrograde amnesia. MRI findings were
normal in 3 patients; 5 patients had mesial temporal lobe signal
abnormalities (Table 1, Figure 1). Seven patients underwent an
MRI study within 4 days from an amnesic episode; none of
them showed diffusion weighted image abnormalities indicat-
ing acute focal cytotoxic edema. EEG and A-EEG demon-
strated epileptic abnormalities over the frontotemporal regions
in 7 patients (2 left-sided, 2 right-sided, and 3 bilateral asyn-
chronous), whereas 2 patients presented focal sharp waves over
the same regions (Figure 2); 2 of 9 patients had normal EEG.
Ten patients were successfully treated with relatively low dos-
ages of antiepileptic drugs, whereas 1 patient had a drug-resis-
tant epilepsy (Table 2). One patient was described in a previous
article.5 Neuropsychological assessments demonstrated altera-
tions in memory in 3 patients, in particular in recognition mem-
ory and recall with slight decrease of the recency effect;
moreover, these patients showed a similar subtle delay in the
Stroop test. The remaining 8 patients showed no alterations
(Table 1).
Discussion
Few recent studies2-4 have reported that transient amnesic epi-
sodes may represent the main or the sole feature of epileptic
seizures, especially of temporal lobe origin, probably because
of the involvement of the mesial regions by the seizure
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Figure 2. Ambulatory EEG (upper panel): low-voltage spikes over
the left temporal region during the nonrapid eye movement sleep
(N2 phase); right temporal sharp waves and spikes with spreading
over the frontocentral regions (lower panel).
activity.1 On the basis of the increasing number of reports of
patients with similar clinical features, TEA has been proposed
as a distinctive epileptic entity.2-4 In this study, we collected
and analyzed the clinical, neuroradiological, and EEG charac-
teristics of 11 consecutive patients with TEA and their response
to pharmacological treatment. As previously stated,4 the major-
ity of these patients (8/11) referred to our department for acute
memory impairment, sometimes of prolonged duration. Most
of these patients were misdiagnosed at the first medical consul-
tation as affected by TGA. Usually, the diagnosis of epilepsy as
the cause of amnesic episodes is not considered by clinicians.2,3
TGA, TIA, and psychogenic amnesia are the conditions most
often requiring differentiation from TEA.1,4 Moreover, other
possible causes of transient amnesia (such as closed head
injury, migraine, and drug effects)2,3,6 should be considered. On
a clinical ground, the evaluation of the patients during the
amnesic episodes may help in the diagnosis, but the short dura-
tion does not often allow medical examination in the acute
phase. However, although the clinical core of the ictal manifes-
tation in our patients (ie, anterograde/retrograde amnesia) was
not easily recognizable as of epileptic origin, a targeted inter-
view with patients relatives and/or with medical staff may pro-
vide a diagnostic clue. Indeed, the possible occurrence of
additional slight clinical signs or symptoms (in our cases olfac-
tory hallucinations, abdominal discomfort, oral automatisms,
and confusional features) may indicate an epileptic origin of
the episodes.
Interestingly, the cause of the first medical consultation was
a prolonged amnesic episode in 3 patients (from 3 hours up to
48 hours). From a speculative point of view, these episodes
could be retrospectively considered as a nonconvulsive status
epilepticus because they showed the same semiological fea-
tures of the shorter attacks; alternatively, the prolonged amne-
sia may represent a postictal state. Indeed, it is well known that
182 Clinical EEG and Neuroscience 45(3)
both seizures and postictal dysfunction can be prolonged, espe-
cially in older patients.2 However, in the previous history of
these patients no amnesic episodes were reported nor brief epi-
sodes of impairment of consciousness.
As concerns the anamnestic interview with the patients or the
relatives, it is possible that episodes of transient epileptic amne-
sia may be underestimated because of the amnesic nature of
the disorder, especially if characterized by both anterograde/
retrograde amnesia. However, for the same reasons, it can be
difficult to distinguish when the amnesic episode represents the
ictal clinical phenomenon or, by contrast, when it represents the
postictal state of a seizure not recognized by the relatives or
forgotten by the patients. In our view, the amnesic postictal
states, if identified, should not be considered as episodes of
transient epileptic amnesia, especially when associated with
impairment of consciousness although they represent the pre-
dominant clinical core of the episodes. Indeed, it is well known
that seizures, especially of temporal lobe origin, are followed by
amnesic or dysmnesic postictal states. A clear distinction
between ictal and postictal clinical symptoms, especially in
association with the EEG findings, may help to define these
patients as affected by a syndrome rather than by epilepsy.
The concurrent onset of other features of epilepsy may represent
another confounding factor; however, on the basis of the pro-
posed diagnostic criteria, we considered these patients as
affected by amnesic seizures when the episodes, although asso-
ciated with other features of epilepsy, were clearly characterized
by the sparing of other cognitive functions except the memory.
In partial contrast to other reports,2-4 3 patients had their first
medical consultation for episodes of loss of consciousness of
probable epileptic origin (generalized tonicclonic seizures
and recurrent brief episodes of unresponsiveness sometimes
associated with slight abdominal discomfort); also in these
cases, the collection of the past history has allowed us to iden-
tify previous brief episodes with a pure amnesic core. In these
patients, no medical evaluation was performed before the onset
of the episodes of loss of consciousness.
To corroborate the diagnosis of amnesic seizures, it is worth
noting the key role of neurophysiological assessment (EEG and
A-EEG). In our patients, epileptic abnormalities were consis-
tently over the frontotemporal regions, in 3 cases were bilateral
and asynchronous; except for 1 patient in whom epileptic dis-
charges were evident in routine examination, in all other
cases A-EEG revealed epileptic abnormalities in nonrapid eye
movement sleep (mainly stage N2) whereas the routine EEG
was unremarkable (Figure 2). Although isolated, this report
outlined the importance of studying sleep EEG in patients with
episodes of transient amnesia of unknown origin. A significant
point may be EEG examination in the acute phase; however,
these patients are generally referred to the emergency department
after symptoms and it is often not possible to perform these
assessments. Moreover, as with most of our patients, the misdi-
agnosis of TGA did not lead to EEG examination, and focused
diagnostic workup on cerebrovascular diseases. Difficulties in
the diagnosis of epileptic amnesia are reflected in the relatively
rare EEG-documented cases in the literature.7
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In previous reports, a symptomatic etiology was a rare find-
ing2-4,8 in patients with epileptic amnesia, whereas it represents
the majority in our cases (8 of 11). Brain MRI showed acquired
lesions localized in the frontotemporal lobes or, in one case, in
the occipital lobe close to medial temporal structures (for
details, see Figure 1). One patient had postischemic right cere-
bellar and basal ganglia gliosis in the context of a chronic cere-
brovascular disease. MRI performed within a few days from an
amnesic episode did not show signal abnormalities; in particu-
lar, the hippocampal diffusion weighted image hyperintensity,
which is considered a hallmark of TGA,9 was never detected in
our population. MRI lesions associated with localized EEG
abnormalities and with the seizures semiology indirectly sug-
gest the correlation between the lesions and the epilepsy.
However, as previously stated by other authors,1-3 despite the
symptomatic etiology, our patients were easily and success-
fully treated with relatively low dosages of antiepileptic drugs,
except for one patient with a drug-resistant epilepsy. These fea-
tures seem to confirm reported findings in the literature2,3,9 and
lead to considering TEA as a typical elderly epilepsy, charac-
terized by a favorable response to treatment with low dosages
of monotherapy.
No patient had psychiatric disturbances. The neuropsycho-
logical assessment demonstrated subtle deficits in memory of
three patients, in particular in recognition and recall, and addi-
tional slight deficits were reported in the selective attention by
the Stroop test. Of these, 3 patients, 2 (patients 1 and 3) had
hippocampal MRI abnormalities, and 1 (patient 4) had a post-
traumatic right frontal horn gliosis. Two of them (patients 1 and
3) reported the highest number of events in our population. The
remaining patients showed no abnormalities in memory nor in
the other tested fields, as previously stated in other works.2 The
relatively low prevalence of persistent memory impairment in
our cohort, as compared with literature,6 could be because of
the early diagnosis and treatment and, consequently, to the low
number of reported seizures. There is an emerging literature
focused on 2 novel memory complaints (ie, accelerated long-
term forgetting and remote memory impairment) described by
patients with TEA.10-12 Unfortunately, we have not used these
specific tests to assess our patients. Although recent works pro-
vide evidence of accelerated long-term forgetting in patients
with extratemporal epilepsy,12 further studies are required to
clarify if remote memory impairment may represent a feature
of patients with TEA or, more widely, with temporal lobe
epilepsy.
In conclusion, TEA represents a form of temporal lobe epi-
lepsy, usually with onset in the middle-elderly age, with good
response to relatively low dosages of antiepileptic drugs.
Although the reported TEA patients were mainly affected by
probable cryptogenic, symptomatic, temporal lobe epilepsy,2,3,8
the majority of our patients (8/11) showed symptomatic etiol-
ogy. Moreover, we outlined the relevance of clinical history to
recognize TEA, especially if ictal EEG was not available. Since
TEA carries a risk of persistent memory impairment that can be
mistaken for dementia, early diagnosis and treatment are
strongly required.6 Further work is warranted to clarify if ictal
Lapenta et al 183
and postictal amnesic states are actually part of the same condi-
tion and to understand if these features may represent a distinc-
tive epileptic syndrome.
Acknowledgments
The authors convey their special thanks to Catello Vollono, Valentina
Gnoni, Chiara Di Blasi, Salvatore Mazza for their invaluable
assistance.
Declaration of Conflicting Interests
The author(s) declared no conflicts of interest with respect to the
research, authorship, and/or publication of this article.
Funding
The author(s) received no financial support for the research, author-
ship, and/or publication of this article.
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