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    Transient epileptic amnesia:

    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 discharges
    on EEG, concurrent onset of other seizure
    types, and a response to anticonvulsant
    therapy.Of these three criteria, the first two are
    the strongest. Two of the patients in this study
    (cases 2 and 3) satisfy all three criteria; four
    others (cases 2, 8, 9, and 10) satisfy two; cases
    4, 5, 6, and 7 satisfy one criterion each.We have
    included the third group, in which the diagnosis
    is least certain, on the hypothesis that the
    clinical features of their attacks are identical to
    those in the first two groups and reflect, therefore,
    a common mechanism of transient amnesia.
    CLINICAL CHARACTERISTICS OF TEA
    Table 3 summarises these previously reported
    cases. The reports have generally applied similar
    criteria for diagnosis to those we have used,
    with some exceptions: in four of the 21
    patients,11–13 amnesic episodes always followed
    complex partial seizures; some reports do not
    mention whether a description from a witness
    was available. The onset of attacks is commonly
    in middle or old age. Only one case in
    the literature,23 and none in the present series
    had amnesic episodes below the age of 40. The
    aetiology of the epilepsy is usually obscure,
    with negative results from neuroimaging,
    although two previous cases were associated
    with tumour,24 25 and right hippocampal atrophy
    was noted in one of our patients (case 10).
    A history of cardiac disease was common
    among our patients, suggesting that cardiac
    related hypoxic damage to mesial temporal
    lobe structures may be mediating their epilepsy.
    The attacks themselves have several distinctive
    features:
    (1) they tend to be more numerous than episodes
    of TGA. In our series the mean number
    of attacks was nine, at a rate of three attacks a
    year. This compares with a recurrence rate of
    about 3% a year for episodes of TGA.7
    (2) Episodes of TEA are usually relatively
    brief: eight of 10 of our patients and 17 of 21 of
    the previously reported cases had at least some
    attacks lasting less than one hour. This
    compares with a mean duration of four to six
    hours for attacks of TGA.7
    (3) The occurrence of attacks on waking is
    characteristic. Every patient in our series
    reported at least one such attack; they were a
    typical feature in six of 10. Likewise attacks on
    waking were noted in eight of 10 previously
    reported cases for which this information is
    available. By contrast, episodes of TGA sometimes
    occur on rising in the morning, but
    probably no more often than would be
    expected by chance.26 By contrast with Kapur’s
    finding,6 that repetitive questioning is unusual
    in TEA, all but one of our patients had
    questioned a companion repetitively during at
    least one attack. One feature which may distinguish
    TEA from TGA is, however, the ability to
    recall some details about the amnesic episode:
    half of our patients had some recall for their
    attacks. In particular, they were “able to
    remember not being able to remember” recent
    events during attacks, indicating that their
    anterograde amnesia during the attack was
    sometimes incomplete. Whereas this feature
    may distinguish TEA from TGA, a careful
    standardised comparison between patients
    with the two conditions is required to reach a
    definite conclusion on this point. Retrograde
    amnesia of variable duration is undoubtedly a
    common feature during attacks of TEA. It was
    noted in all our cases, and in all those cases in
    the literature in which the issue is discussed,
    with the exception of the cases described by
    Palmini et al.9 whereas their findings show that
    inconspicuous or unnoticed anterograde amnesia
    may be the sole manifestation of temporal
    lobe epilepsy, the claim that all “amnestic
    seizures” are of this kind is not compelling:
    patients included in this study were highly
    selected, and all had a pre-existing diagnosis of
    intractable temporal lobe epilepsy.We return to
    this issue below. Isolated transient amnesia
    may, on occasions, be the sole manifestation of
    440 Zeman, Boniface, Hodges
    epilepsy. In three of our 10 patients, and in
    seven of 21 cases in the literature (32%
    overall), episodic amnesia was the only manifestation
    of epilepsy.We disagree therefore with
    Palmini et al9 who concluded that pure amnestic
    seizures “never represent the only type of
    seizures” in patients with temporal lobe
    epilepsy. Their study considered only patients
    with pre-existing temporal lobe epilepsy. Our
    findings suggest that temporal lobe epilepsy is
    an important diagnosis to consider in patients
    with brief recurrent episodes of amnesia, especially
    if they occur on waking. This is consistent
    with the results of Hodges7 who reported that
    eight of 114 patients satisfying strict criteria for
    TGA subsequently developed epilepsy; six of
    these had complex partial seizures. In this
    study patients with more than one episode of
    “TGA” and/or episodes of less than hour were
    at an increased risk of subsequent epilepsy by
    comparison with patients with single protracted
    episodes. A recent study by Melo et al27
    disputed this view on the grounds that only one
    of their five patients with brief recurrent
    episodes diagnosed as TGA proved to have
    epilepsy. We would not claim that all brief
    recurrent amnesic episodes have an epileptic
    basis. It could be relevant that Melo et al did
    not report the results of sleep EEGs.
    PATHOPHYSIOLOGY OF TEA
    Interictal temporal lobe epileptiform abnormalities
    are sometimes non-localising because
    of either neurophysiological propagation or
    volume conduction. In combination with the
    clinical features of associated seizures, however,
    these features imply that TEA is a pathophysiological
    phenomenon of the temporal
    lobe.
    Does TEA result from mesial temporal
    dysfunction?
    The critical role of the mesial temporal lobes
    (hippocampus subiculum, parahippocampal
    gyrus, and entorhinal cortex) in the acquisition
    of new memories and the retrieval of recent
    ones is well established.28 29 It is plausible,
    therefore, that dysfunction of these structures
    is responsible for TEA. The preponderance of
    anterior and mid-temporal abnormalities in
    our series is consistent with a mesial temporal
    origin, but these may have been propagated
    rather than volume conducted. Surface EEGs
    do not permit precise localisation of the underlying
    electrical focus, as three dimensional
    localisation of the epileptogenic region from
    digital surface EEG is model dependent and
    independent bitemporal interictal abnormalities
    do not necessarily imply bilateral pathology.
    Information from a few in depth studies
    supports the view that epileptic amnesia results
    from current or recent paroxysmal activity in
    the mesial temporal lobes.9 30–32
    IS TEA AN ICTAL OR A POST-ICTAL STATE?
    Several reports bear on the question of whether
    TEA is likely to be an ictal or a postictal state.
    Palmini et al9 describe a brief episode of
    bilateral mesial temporal epileptiform activity
    associated with disruption of anterograde
    memory. The patient successfully conducted a
    telephone conversation during this episode for
    which she later had no recall. She had been
    unaware at the time that anything was wrong.
    This case shows that a period of pure
    anterograde amnesia can be the manifestation
    of a mesial temporal seizure. On the other
    hand, it has also been shown that recently
    acquired memories are vulnerable to transient
    temporal lobe seizures. Bridgman et al30
    reported that a subclinical unilateral hippocampal
    seizure, without spread to the temporal
    neocortex, disrupted recall of a previously
    learned word list. Similarly, Halgren et al33
    showed that brief bilateral stimulation of mesial
    temporal structures at either the time of
    memory acquisition, or the time of memory
    retrieval, could disrupt performance without
    any other effect on behaviour. Taken together,
    these findings suggest that ictal activity in
    mesial temporal structures is capable of
    disrupting both anterograde and retrograde
    memory, and that this disruption may go
    unnoticed by the subject. Can longer periods of
    amnesia occur as an ictal phenomenon or are
    these always postictal? Lee et al32 describe the
    remarkable case of a previously well 38 year old
    woman in whom a 12 day period of continuous
    anterograde amnesia, with additional retrograde
    amnesia for events of the past four
    months, occurred as a manifestation of partial
    status epilepticus: nasopharyngeal electrodes
    showed frequent bilateral spikes and runs of
    ictal activity arising independently in both
    mesiotemporal lobes. Thus ictal amnesia
    closely resembling TGA can occur as a
    manifestation of semicontinuous temporal lobe
    discharges. Similarly, Vuilleumier et al34 have
    recently described a 41 year old woman with a
    history of numerous episodes of profound retrograde
    and apparent retrograde amnesia,
    occurring since adolescence, which had been
    regarded as hysterical. Attacks often started on
    waking, and were preceded by an epigastric
    aura. An EEG during a severe attack disclosed
    generalised epileptiform spikes with spike and
    wave activity at a frequency of 3.5–4 Hz,
    involving occasional frontotemporal phase reversal.
    Intravenous clonazepam abolished both
    the EEG discharges and the amnesia, disclosing
    unexpectedly clear recall for events occurring
    during the seizure. Tassinari et al35 and
    Morrell31 describe somewhat similar cases, but
    these authors emphasise the persistence of the
    amnesic state at times when no epileptiform
    activity was apparent on the EEG, comparing it
    to a “Todd’s paralysis” of memory. Palmini et
    al9 cite the case of a patient with a postictal
    period of combined anterograde and retrograde
    amnesia lasting more than a month after
    a flurry of temporal lobe seizures over a 24
    hour period. In conclusion, both brief and prolonged
    episodes of amnesia, affecting anterograde
    and/or retrograde memory, can occur as
    ictal phenomena, but prolonged amnesic states
    can also occur in the aftermath of ictal activity.
    It is uncertain, therefore, whether the recurrent
    episodes of amnesia experienced by our
    patients represent ictal or postictal phenomena.
    Ictal EEG studies of patients during
    Transient epileptic amnesia 441
    amnesic episodes might help to clarify these
    issues. Such studies may also help to disclose
    the factors which determine whether or not a
    period of amnesia comes to the patient’s
    notice.
    INTERICTAL RETROGRADE MEMORY IMPAIRMENT
    IN TEA
    Some previous case reports mention “difficulty
    with memory” occurring between attacks of
    TEA.13 36 The occurrence of a pronounced
    persisting impairment of retrograde memory in
    association with TEA has been highlighted
    recently by Kapur,37 and by Kopelman et al.8
    Despite the striking complaints of retrograde
    memory impairment in our patients, performance
    on objective tests of both anterograde and
    retrograde memory was largely within normal
    limits. The principal exceptions were tests of
    retrograde memory, on which five patients had
    a defective score (greater than 2 SD below the
    controls’ mean) on at least one test, although
    the degree of impairment was modest except in
    one patient (case 2). Kapur, likewise, found
    that tests of anterograde memory were normal
    in his patient with striking complaints of retrograde
    memory impairment37; scores on tests of
    retrograde memory were depressed. Kopelman’s
    patient8 obtained borderline scores on
    tests of retrograde memory with somewhat
    poor anterograde memory in relation to his
    high IQ. Interestingly, a similar combination of
    impaired retrograde memory with symptoms
    of poor autobiographical memory but good
    performance on anterograde memory tests has
    been reported in a patient with paraneoplastic
    limbic encephalitis.38 Our failure to demonstrate
    consistent deficits on objective tests of
    retrograde memory may reflect the patchy
    nature of the impairment. Several of the
    patients report lacunes in their autobiographical
    memory, extending back over a decade or
    more. Preliminary results of detailed testing of
    one patient (patient 3), using tailor-made tests
    of the type used in other similar single case
    studies,37 39 40 suggest a profound impoverishment
    of autobiographical memory for events of
    the past 30 years. Islands of preserved recall
    permitted a misleadingly normal score on the
    AMI in this patient.
    What is the explanation for this patchy
    impairment of remote memory? There are
    three possibilities: failure to encode episodes
    into long term memory, failure to consolidate
    and maintain memories, and failure to retrieve
    memories which have been successfully acquired.
    Some factors could potentially impair
    memory acquisition in such patients including
    impairment of consciousness in the course of
    complex partial seizures, anterograde amnesia
    in the immediate postictal phase, unnoticed
    episodes of TEA giving rise to anterograde
    amnesia, or a generalised impairment of
    anterograde memory. These all seem unlikely
    explanations for our patients’ subjective complaints
    of retrograde amnesia given that
    autobiographical memories which predate the
    clinical onset of their epilepsy—sometimes by a
    number of years—are affected, and the lack of
    evidence for impairment of anterograde
    memory on standard tests. It is clearly difficult
    to exclude the possibility that patients may
    have had subclinical seizures for some time
    before the onset of their TEA attacks, but this
    seems an unlikely explanation as in one patient
    (case 3) the retrograde amnesia extended back
    over 30 years.
    The second possibility, that an impairment
    of long term consolidation underlies this
    persistent retrograde amnesia, merits further
    consideration. Some patients in our series have
    told us that their memories for recent personal
    events seem to be intact initially but may then
    disappear without trace, suggesting that acquisition
    is normal but consolidation is impaired.
    This is in keeping with their normal performance
    on standard tests of anterograde memory
    which typically test recall over 30 minutes or so
    rather than over long periods. Current computational
    neural network models of long term
    memory processing, based on human neuropsychological
    and animal data,41–43 suggest
    that the medial temporal lobe complex plays a
    critical, but temporally limited, part in the
    encoding and storage of new episodic memories.
    Over time a process of long term consolidation
    or information transfer occurs whereby
    memories become independent of the hippocampus
    by the development of direct corticocortico
    links. Ictal activity in the mesial temporal
    lobes or involving the temporal neocortex
    might be capable of disrupting recent memories
    during this vulnerable stage of consolidation.
    In this context, it is of interest that TEA
    often occurs in relation to sleep, as there is
    accumulating evidence that processes of
    memory consolidation may be particularly
    active in sleep.44 45 The fact that many patients
    have early morning TEA attacks and show
    abnormal sleep EEGs suggests that disturbed
    consolidation during sleep may be a critical
    factor. In keeping with this hypothesis is the
    finding of impaired memory at long, but not
    short, retention intervals in patients with temporal
    lobe epilepsy.46 It is, however, open to
    question whether disruption of consolidation is
    an adequate explanation for the impaired recall
    of very remote episodic and more semantic
    type memories seen in some of our patients.
    The occurrence of topographical amnesia for
    extremely familiar places, impaired recognition
    of familiar faces, and degradation of established
    professional abilities points to pathology
    in the more lateral temporal neocortex in addition
    to mesial temporal structures. The neural
    basis of very long term autobiographical and
    semantic memory remains unclear. Current
    evidence points to a critical role for the left
    inferolateral temporal neocortex in the storage
    of general semantic knowledge46–48; the equivalent
    right sided structure may be specialised for
    person based knowledge.49 It is possible that
    pathology in these regions which have, for
    example, a hypoxic basis, could give rise both
    to epilepsy and to retrograde amnesia. In the
    absence of more detailed neuroimaging such as
    volumetric MRI or PET we cannot exclude the
    possibility of subtle medial or temporal lobe
    pathology in our cases. Failure of retrieval may
    be difficult to distinguish from failure of
    442 Zeman, Boniface, Hodges
    storage. Preliminary work with a patient with
    particularly severe retrograde amnesia (case 3)
    indicates that his retrograde memory gaps are
    consistent over time and little improved by
    cueing: these features argue for a primary failure
    of consolidation or storage rather than a
    retrieval deficit.
    In conclusion, a persistent impairment of
    retrograde memory is a common accompaniment
    of TEA. There is circumstantial evidence
    that this may be the result of disruption of
    memory consolidation, related to recurrent
    ictal activity in mesial temporal structures.
    Detailed neuropsychological study of individual
    cases, particularly including analysis of
    long term forgetting rates, combined with
    ambulatory EEG recording in patients with
    ongoing memory disturbance, will be of value
    in testing this hypothesis.
    We thank Dr Peter Harvey, Dr David Dick, Dr Colin Brown,
    and Dr Iain Wilkinson who referred patients included in this
    series; Dr Kristen Breen and Dr German Berrios who contributed
    to the assessment of patients in the Cambridge Memory
    Clinic; Naida Graham and Dr John Greene for providing
    neuropsychological control data, and Nick Carvill for his technical
    assistance with the EEGs.
    1 Hughlings-Jackson J. On a particular variety of epilepsy
    (intellectual aura), one case with symptoms of organic brain
    disease. Brain 1989;11:179–207.
    2 Penfield W, Mathieson G. Memory: autopsy findings and
    comments on the role of hippocampus in experiential
    recall. Arch Neurol 1974;31:145–54.
    3 Dugan TM, Nordgren RE, O’Leary P. Transient global
    amnesia associated with bradycardia and temporal lobe
    spikes. Cortex 1981;17:633–8.
    4 Pritchard PB, Holmstrom VL, Roitzsch JC, et al. Epileptic
    amnesic attacks: benefit from antiepileptic drugs. Neurology
    1985;35:1188–9.
    5 Miller JW, Yanagihara T, Petersen RC, et al.Transient global
    amnesia and epilepsy: electroencephalographic distinction.
    Arch Neurol 1987;44:629–33.
    6 Kapur N. Transient epileptic amnesia—a clinical update
    and a reformulation. J Neurol Neurosurg Psychiatry
    1993;56:1184–90.
    7 Hodges JR. Transient global amnesia. London:WB Saunders,
    1991.
    8 Kopelman MD, Panayiotopoulos CP, Lewis P. Transient
    epileptic amnesia differentiated from psychogenic “fugue”:
    neuropsychological, EEG and PET findings. J Neurol Neurosurg
    Psychiatry 1994;57:1002–4.
    9 Palmini AL, Gloor P, Jones-Gotman M. Pure amnestic seizures
    in temporal lobe epilepsy. Brain 1992;115:749–69.
    10 Rowan AJ. Ictal amnesia and fugue states. In: Smith D,
    Treiman D, Trimble M, eds. Neurobehavioural problems in
    epilepsy. New York: Raven Press, 1991:357–67.
    11 Gallassi R, Morreale A. Transient global amnesia and
    epilepsy. In: Markowitsch HJ, ed. Transient global amnesia
    and related disorders.Toronto: Hogrefe and Huber, 1990.
    12 Gallassi R, Pazzaglia P, Lorusso S, et al. Neuropsychological
    findings in epileptic amnesic attacks. Eur Neurol 1986;25:
    299–303.
    13 Stracciari A,Ciucci G, Bianchedi G, et al. Epileptic transient
    amnesia. Eur Neurol 1990;30:176–9.
    14 Kapur N. Transient epileptic amnesia: a clinically distinct
    form of neurological memory disorder. In: Markowitsch H,
    ed. Transient global amnesia and related disorders. New York:
    Hogrefe and Huber, 1990:140–51.
    15 Hodges JR. Cognitive assessment for clinicians. Oxford:Oxford
    University Press, 1994.
    16 Blume WT, Kaibara M. Atlas of adult encephalography. New
    York: Raven Press, 1995.
    17 Nelson HE, O’Connell A. Dementia: the estimation of levels
    of premorbid intelligence using the new adult reading
    test. Cortex 1978;14:234–44.
    18 Wechsler DA. Wechsler memory scale-revised. New York: The
    Psychological Corporation, 1987.
    19 Osterrieth P, Rey A. Le test de copie d’une figure complexe.
    Arch Psychol 1944;30:205–20.
    20 Warrington EK. The recognition memory test. Windsor:
    NFER, 1984.
    21 Greene JDW, Hodges JR. Identification of famous faces and
    famous names in early Alzheimer’s disease. Brain 1996;19:
    111–28.
    22 Kopelman MD, Wilson BA, Baddeley AD. The autobiographical
    memory interview. Bury St Edmunds: Thames
    Valley Test Company, 1990.
    23 Deisenhammer E. Transient global amnesia as an epileptic
    manifestation. Neurology 1981;225:289–92.
    24 Shuping JR. Transient global amnesia due to glioma in the
    dominant hemisphere. Neurology 1980;30:88–90.
    25 Meador KJ, Adams RJ, Flanigin HF. Transient global
    amnesia and meningioma. Neurology 1985;35:769–71.
    26 Fisher CM. Transient global amnesia: precipitating activities
    and other observations. Arch Neurol 1982;39:605–8.
    27 Melo TP. Are brief or recurrent transient global amnesias of
    epileptic origin? J Neurol Neurosurg Psychiatry 1994;57:
    622–5.
    28 Squire LR. Memory and the hippocampus: a synthesis from
    findings with rats, monkeys, and humans. Physiol Rev
    1962;99:195–231.
    29 Squire LR, Alvarez P. Retrograde amnesia and memory
    consolidation: a neurobiological perspective. Curr Opin
    Neurobiol 1995;5:178–83.
    30 Bridgman PA, Malamut BL, Sperling MR, et al. Memory
    during subclinical hippocampal seizures.Neurology 1989;
    39:853–6.
    31 Morrell F. Memory loss as a Todd’s paralysis. Epilepsia
    1980;21:185.
    32 Lee BI, Lee BC, Hwang YM, et al. Prolonged ictal amnesia
    with transient focal abnormlaities on magnetic resonance
    imaging. Epilepsia 1992;33:1042–6.
    33 Halgren E, Wilson CL, Stapleton JM. Human medial temporal
    lobe stimulation disrupts both formation and
    retrieval of human memories. Brain Cogn 1985;4:287–95.
    34 Vuilleumier P, Desplane PA, Regli F. Failure to recall (but
    not to remember): pure transient amnesia during nonconvulsive
    status epilepticus. Neurology 1996;46:1036–9.
    35 Tassinari CA, Ciarmatori C, Alesi C, et al. Transient global
    amnesia as a postictal state from recurrent partial seizures.
    Epilepsia 1991;32:882–5.
    36 Gallassi R, Morreale A, Lorusso S, et al. Epilepsy presenting
    as memory disturbances. Epilepsia 1988;29:624–9.
    37 Kapur N. Focal retrograde amnesia: a long term clinical and
    neuropsychological follow up. Cortex 1989;25:387–402.
    38 Ahern GL,O’Connor M, Dalmau J, et al. Paraneoplastic
    temporal lobe epilepsy with testicular neoplasm and atypical
    amnesia. Neurology 1994;44:1270–4.
    39 Hodges JR, McCarthy R. Autobiographical amnesia resulting
    from bilateral paramedian thalamic infarction. Brain
    1993;116:921–40.
    40 Evans JJ, Breen EK, Antoun N, et al. Focal retrograde
    amnesia for autobiographical events following cerebral
    vasculitis: a connectionist account. Neurocase 1996;2:1–12.
    41 Alvarez P, Squire LR. Memory consolidation and the medial
    temporal lobe: a simple network model. Proc Natl Acad Sci
    USA 1994;91:7041–5.
    42 McClelland JL, McNaughton BL, O’Reilly RC. Why are
    there complementary learning systems in the hippocampus
    and neocortex: insights from the successes and failures of
    connectionist models of learning and memory. Psychol Rev
    1995;102:419–37.
    43 Murre JMJ. Implicit and explicit memory in amnesia: some
    explanations and predictions by the tracelink model.
    Memory 1997;5:213–32.
    44 Karni A. Dependence on REM sleep of overnight improvement
    of a perceptual skill. Science 1994;265:679–82.
    45 Wilson MA. Reactivation of hippocampal ensemble memories
    during sleep. Science 1994;265:676–9.
    46 Martin RC, Loring DW, Meador KJ, et al. Impaired
    long-term retention despite normal verbal learning in
    patients with temporal lobe dysfunction.Neuropsychology
    1991;5:3–12.
    47 Patterson K, Hodges JR.Disorders of semantic memory. In:
    Baddeley AD, Wilson BA, Watts FN, eds. Handbook of
    memory disorders: John Wiley, 1995:167–86.
    48 Garrard P, Perry R, Hodges JR. Disorders of semantic
    memory. J Neurol Neurosurg Psychiatry 1997;62:431–5
    49 Evans JJ, Heggs AJ, Antoun N, et al. Progressive prosopagnosia
    associated with selective right temporal lobe atrophy:
    a new syndrome? Brain 1995;118:1–13.
    50 Lou HOC. Repeated episodes of transient global amnesia.
    Acta Neurol Scand 1968;44:612–7.
    Transient epileptic amnesia 443

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