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Transient epileptic amnesia: A concise review
YEBEH-03649; No. of pages: 3; 4C: Epilepsy & Behavior xxx (2013) xxx–xxx
Contents lists available at ScienceDirect
Epilepsy & Behavior journal homepage: www.elsevier.com/locate/yebeh
Review
Transient epileptic amnesia: A concise review Ali A. Asadi-Pooya ⁎ Neurosciences Research Center, Shiraz Medical School, Shiraz University of Medical Sciences, Shiraz, Iran Jefferson Comprehensive Epilepsy Center, Department of Neurology, Thomas Jefferson University, Philadelphia, USA
a r t i c l e
i n f o
Article history: Received 28 August 2013 Revised 13 October 2013 Accepted 14 October 2013 Available online xxxx Keywords: Transient epileptic amnesia Criteria EEG Treatment
a b s t r a c t Transient epileptic amnesia (TEA) is a distinctive syndrome and comprises episodic transient amnesia with an epileptic basis, without impairment of other aspects of cognitive function. Additional interictal memory deficits are common in TEA. An epileptic origin, after other etiologies have been excluded, should be considered and carefully investigated in patients complaining of isolated memory disturbances, particularly with recurrent short-lasting amnesic attacks. In all suspected cases of epilepsy, a detailed clinical history is of paramount importance, but ancillary tests including EEG and MRI could be very helpful. Transient epileptic amnesia is typically a benign and treatable condition. Future studies should investigate the exact mechanism(s) of this unique syndrome. © 2013 Elsevier Inc. All rights reserved.
1. Introduction Transient epileptic amnesia (TEA) is a syndrome of epilepsy in which the principle manifestation of seizures is recurrent episodes of isolated memory loss. It represents an underdiagnosed type of temporal lobe epilepsy. Transient amnesia is sometimes the only manifestation of a temporal lobe seizure, and indeed, it may be the only seizure type to occur in some patients [1,2]. Various terms have been used to describe these attacks including pure amnestic seizures, epileptic amnesia, epileptic amnesic attacks, epileptic transient amnesia, and transient epileptic amnesia or TEA. The onset of the attacks in TEA is commonly in late–middle or old age [1–3]. It is more common among men [3]. 2. Clinical characteristics During an attack of TEA, there are often no obvious classical signs of a seizure to an observer. The patient's behavior is often appropriate. Approximately one-third of the affected patients have TEA as their unique seizure type. Other clinical features include the following: (1) attacks, which are less than 1 h in duration, often occur on waking; (2) coexistence of other seizure types, including olfactory hallucinations (in two-thirds of the patients); (3) electroencephalographic (EEG) abnormalities; and finally, (4) favorable response to antiepileptic drugs (AEDs). Proposed diagnostic criteria for TEA comprise the following: (1) a history of recurrent witnessed episodes of transient amnesia; (2) cognitive functions other than memory are intact during ⁎ Corresponding author at: M.D. Associate Professor of Epileptology, Neurosciences Research Center,Shiraz Medical School, Shiraz University of Medical Sciences, Shiraz, Iran. Tel.: +98 9352274990. E-mail address: [email protected].
typical episodes as observed by a reliable witness; and (3) other evidence for a diagnosis of epilepsy. This evidence could be either (a) epileptiform abnormalities in EEG, (b) the concurrent onset of other clinical features of an epileptic seizure (e.g., lip-smacking and olfactory hallucinations), or (c) a clear-cut response to antiepileptic drugs, or by a combination of these three [1–6]. However, not all patients meet all these criteria. 3. Memory dysfunctions Acute and transient memory dysfunctions in patients with TEA have typical characteristics: a repetitive, acute transient impairment of memory, lasting minutes (typically, less than an hour), which follows a seizure or may be the sole evident manifestation of a seizure in a patient with or without other kinds of seizures. Amnesia is anterograde, retrograde, or anteroretrograde, in a state of normal vigilance, and absent or with only mild behavioral abnormalities (perplexity, excessive quietness, or repetitive questions in some cases) with partial or complete amnesia for the episodes [7]. The extent of the retrograde amnesia during attacks varies from days to years [1]. The most important pointers to the epileptic origin of acute memory impairment are the relatively frequent repetition and the short duration of the attacks [8]. Seizures other than the attacks of transient amnesia may not be evident, but the patient may have more clinically obvious seizures (e.g., convulsions or olfactory hallucinations). Interictal memory disturbances can be conspicuous, leading the patient to medical consultation. Transient epileptic amnesia is associated with two unusual forms of interictal memory impairment: accelerated long-term forgetting [the rapid loss of newly acquired memories over days to weeks despite normal retention at standard (~30 min) intervals] and autobiographical amnesia [9,10].
1525-5050/$ – see front matter © 2013 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.yebeh.2013.10.021
Please cite this article as: Asadi-Pooya AA, Transient epileptic amnesia: A concise review, Epilepsy Behav (2013), http://dx.doi.org/10.1016/ j.yebeh.2013.10.021
2
A.A. Asadi-Pooya / Epilepsy & Behavior xxx (2013) xxx–xxx
4. Electroencephalography (EEG) Electroencephalographic abnormalities can contribute to the diagnosis of TEA [7]. Electroencephalographic findings may include epileptiform abnormalities (Fig. 1) in more than 1/3 of the patients, nonspecific focal slow waves in 1/3, and normal EEG in about 1/3 [3]. For these reasons, a normal EEG or a nonspecific EEG abnormality does not necessarily exclude the diagnosis of TEA [7]. Bilateral deep abnormal brain discharges involving the hippocampal–mesial temporal lobe regions probably explain the acute and transient disturbance of episodic memory of epileptic amnestic attacks in some cases; in others, the amnestic attacks are probably a postictal phenomenon. The evidence supports these changes [7,11]. The purposeful behavior during the amnesic period with scarcity of consciousness impairment could be explained by temporal lobe dysfunction, with or without minimal involvement of other cortical regions, the thalamus, or the brainstem nuclei [7]. 5. Imaging studies In a recent study, magnetic resonance volumetry confirmed the presence of subtle, bilateral hippocampal atrophy. Additional atrophy was revealed in perirhinal and orbitofrontal cortices. The volumes of these regions correlated with anterograde memory performance [12]. In a related study, manual volumetry identified subtle hippocampal volume loss in patients with TEA [13]. Functional magnetic resonance imaging has been used to examine retrieval of memories from across the lifespan in patients with TEA and healthy controls. Both groups engaged the autobiographical memory network, but activation in patients was less extensive than in controls. Direct comparison revealed hypoactivation of regions in the right hemisphere in patients. Specifically, patients showed reduced activation of the posterior parahippocampal gyrus, with decreased engagement of the right temporoparietal junction and the cerebellum [10]. The results of these studies support the hypothesis that TEA is a focal medial temporal lobe epilepsy syndrome [10,12,13]. In an illustrative study, a 71-year-old man with TEA had a meningoencephalocele in his magnetic
resonance imaging (MRI) in the middle cranial fossa with expansion ahead of the temporal ventricular horn. In the coronal scan, left-sided focal hippocampal atrophy was evident. His EEG showed left temporal spikes [14]. 6. Treatment Once TEA has been diagnosed, an antiepileptic drug appropriate for this condition may be prescribed. The goal of treatment is to prevent future seizures from recurring. Treatment is typically started with one of the first-line AEDs for localization-related epilepsy (partial onset seizures); these drugs (considering the age of the patients) include lamotrigine and levetiracetam among others [15–18]. In patients with TEA, the seizures (episodic transient amnesia) usually respond promptly to treatment with antiepileptic drugs, whereas the interictal impairments might persist [1–8]. If a first-line drug controls seizures and does not cause side effects, therapeutic adjustments are not needed. If seizures persist, the medication regimen should be adjusted [16]. Despite appropriate medical treatment, individuals with TEA occasionally have persistent seizures [19]. Epilepsy surgery might alleviate seizures and memory complaints in some patients with TEA and medically refractory seizures [19]. 7. Prognosis of interictal memory problems In a longitudinal study in one patient, when identified and treated, No memory impairment occurred at two years after diagnosis [20]. However, in another case study, the authors described a patient with TEA and found that an antiepileptic drug prevented accelerated forgetting but not dense retrograde amnesia. They suggested that accelerated forgetting in TEA was treatable, but retrograde amnesia was an irreversible process [21]. In an illustrative study, the patient underwent right anterior amygdalohippocampectomy for symptoms resembling refractory TEA with additional complex partial seizures. The patient remained seizure-free during the 15-month follow-up, and memory complaints remitted [19].
Fig. 1. T4 (right midtemporal) sharp wave in a 59-year-old woman with transient epileptic amnesia. EEG is an important element in making the diagnosis of TEA.
Please cite this article as: Asadi-Pooya AA, Transient epileptic amnesia: A concise review, Epilepsy Behav (2013), http://dx.doi.org/10.1016/ j.yebeh.2013.10.021
A.A. Asadi-Pooya / Epilepsy & Behavior xxx (2013) xxx–xxx
3
Table 1 Transient epileptic amnesia (TEA) versus transient global amnesia (TGA) and psychogenic amnesia.a Clinical feature
TEA
TGA
Psychogenic amnesia
Precipitating factor Aura Amnesia during the attack Impaired cognition during the attack Automatism during the attack Coexistence of other seizure types Duration of attack Recurrence rate EEG abnormalities Favorable response to antiepileptic drugs Interictal memory problems
Often occurs on waking Probable Yes No Possible Possible Typically b1 h High Probable Yes Yes
Emotional stress or physical exertion No Yes No No No b24 h Low No No No
Stressful experiences or psychological trauma No Yes Possible No No Variable ? No No Possible
a
References [21,23,24].
8. Conclusion Transient epileptic amnesia is a distinctive syndrome and comprises episodic transient amnesia with an epileptic basis, without impairment of other aspects of cognitive function. An epileptic origin, after other etiologies (e.g., transient global amnesia, psychogenic amnesia, transient ischemic amnesia, dementia, and migraine) have been excluded [22–26], should be considered and carefully investigated in patients complaining of isolated memory disturbances, particularly with recurrent shortlasting amnesic attacks (Table 1). In all suspected cases of epilepsy, a detailed clinical history is of paramount importance, but ancillary tests including EEG and MRI can be very helpful [27,28]. Transient epileptic amnesia is typically a benign and treatable condition, yet the associated decline in autobiographical and remote memory despite antiepileptic therapy poses challenges to elucidate through further research [29].
Conflict of interest statement The author serves on a scientific advisory board for Cobel Darou.
References [1] Zeman AZJ, Boniface SJ, Hodges JR. Transient epileptic amnesia: a description of the clinical and neuropsychological features in 10 cases and a review of the literature. J Neurol Neurosurg Psychiatry 1998;64:435–43. [2] Pritchard III PB, Holmstrom VL, Roitzsch JC, Giacinto J. Epileptic amnesic attacks: benefit from antiepileptic drugs. Neurology 1985;35:1188–9. [3] Butler CR, Graham KS, Hodges JR, Kapur N, Wardlaw JM, Zeman AZ. The syndrome of transient epileptic amnesia. Ann Neurol 2007;61:587–98. [4] Mendes MH. Transient epileptic amnesia: an under-diagnosed phenomenon? Three more cases. Seizure 2002;11(4):238–42. [5] Kapur N. Transient epileptic amnesia—a clinical update and reformulation. J Neurol Neurosurg Psychiatry 1993;56:1184–90. [6] Palmini AL, Gloor P, Jones-Gotman M. Pure amnestic seizures in temporal lobe epilepsy. Brain 1992;115:749–69. [7] Gallassi R. Epileptic amnesic syndrome: an update and further considerations. Epilepsia 2006;47(Suppl. 2):103–5. [8] Hodges JR, Warlow CP. Syndromes of transient amnesia: towards a classification. A study of 153 cases. J Neurol Neurosurg Psychiatry 1990;53(10):834–43. [9] Hoefeijzers S, Dewar M, Della Sala S, Zeman A, Butler C. Accelerated long-term forgetting in transient epileptic amnesia: an acquisition or consolidation deficit? Neuropsychologia 2013;51(8):1549–55.
[10] Milton F, Butler CR, Benattayallah A, Zeman AZ. The neural basis of autobiographical memory deficits in transient epileptic amnesia. Neuropsychologia 2012;50(14): 3528–41. [11] Walsh RD, Wharen Jr RE, Tatum IV WO. Complex transient epileptic amnesia. Epilepsy Behav 2011;20(2):410–3. [12] Butler C, van Erp W, Bhaduri A, Hammers A, Heckemann R, Zeman A. Magnetic resonance volumetry reveals focal brain atrophy in transient epileptic amnesia. Epilepsy Behav 2013;28(3):363–9. [13] Butler CR, Bhaduri A, Acosta-Cabronero J, Nestor PJ, Kapur N, Graham KS, et al. Transient epileptic amnesia: regional brain atrophy and its relationship to memory deficits. Brain 2009;132(Pt 2):357–68. [14] Della Marca G, Dittoni S, Pilato F, Profice P, Losurdo A, Testani E, et al. Teaching NeuroImages: transient epileptic amnesia. Neurology 2010;75(10):e47–8. [15] Marson AG, Al-Kharusi AM, Alwaidh M. The SANAD study of effectiveness of carbamazepine, gabapentin, lamotrigine, oxcarbazepine, or topiramate for treatment of partial epilepsy: an unblinded randomized controlled trial. Lancet 2007;369: 1000–15. [16] Asadi-Pooya AA, Sperling MR. Antiepileptic drugs: a clinician's manual. Oxford University Press; 2009 [264 pages, ISBN13: 978-0-19-536821-5; ISBN10: 0-19536821-5]. [17] Consoli D, Bosco D, Postorino P, Galati F, Plastino M, Perticoni GF, et al. Levetiracetam versus carbamazepine in patients with late poststroke seizures: a multicenter prospective randomized open-label study (EpIC Project). Cerebrovasc Dis 2012;34(4):282–9. [18] Villanueva V, Sánchez-Álvarez JC, Peña P, Puig JS, Caballero-Martínez F, Gil-Nagel A. Treatment initiation in epilepsy: an expert consensus in Spain. Epilepsy Behav 2010;19(3):332–42. [19] Soper AC, Wagner MT, Edwards JC, Pritchard PB. Transient epileptic amnesia: a neurosurgical case report. Epilepsy Behav 2011;20(4):709–13. [20] Razavi M, Barrash J, Paradiso S. A longitudinal study of transient epileptic amnesia. Cogn Behav Neurol 2010;23(2):142–5. [21] Midorikawa A, Kawamura M. Recovery of long-term anterograde amnesia, but not retrograde amnesia, after initiation of an anti-epileptic drug in a case of transient epileptic amnesia. Neurocase 2007;13(5):385–9. [22] Butler CR, Zeman A. A case of transient epileptic amnesia with radiological localization. Nat Clin Pract Neurol 2008;4(9):516–21. [23] Ung KY, Larner AJ. Transient amnesia: epileptic or global? A differential diagnosis with significant implications for management. QJM 2012. [24] Schipper S, Riederer F, Sándor PS, Gantenbein AR. Acute confusional migraine: our knowledge to date. Expert Rev Neurother 2012;12(3):307–14. [25] Kopelman MD. Amnesia: organic and psychogenic. Brit J Psychiatry 1987;150:428–42. [26] Staniloiu A, Markowitsch HJ, Brand M. Psychogenic amnesia — a malady of the constricted self. Conscious Cogn 2010;19(3):778–801. [27] Asadi-Pooya AA, Emami M, Ashjazadeh N, Nikseresht A, Shariat A, Petramfar P, et al. Reasons for uncontrolled seizures in adults; the impact of pseudointractability. Seizure 2013;22(4):271–4. [28] Asadi-Pooya AA, Emami M, Sperling MR. A clinical study of syndromes of idiopathic (genetic) generalized epilepsy. J Neurol Sci 2013;324(1–2):113–7. [29] Ioannidis P, Balamoutsos G, Karabela O, Kosmidis MH, Karacostas D. Transient epileptic amnesia in a memory clinic setting: a report of three cases. Epilepsy Behav 2011;20(2):414–7.
Please cite this article as: Asadi-Pooya AA, Transient epileptic amnesia: A concise review, Epilepsy Behav (2013), http://dx.doi.org/10.1016/ j.yebeh.2013.10.021
Contents lists available at ScienceDirect
Epilepsy & Behavior journal homepage: www.elsevier.com/locate/yebeh
Review
Transient epileptic amnesia: A concise review Ali A. Asadi-Pooya ⁎ Neurosciences Research Center, Shiraz Medical School, Shiraz University of Medical Sciences, Shiraz, Iran Jefferson Comprehensive Epilepsy Center, Department of Neurology, Thomas Jefferson University, Philadelphia, USA
a r t i c l e
i n f o
Article history: Received 28 August 2013 Revised 13 October 2013 Accepted 14 October 2013 Available online xxxx Keywords: Transient epileptic amnesia Criteria EEG Treatment
a b s t r a c t Transient epileptic amnesia (TEA) is a distinctive syndrome and comprises episodic transient amnesia with an epileptic basis, without impairment of other aspects of cognitive function. Additional interictal memory deficits are common in TEA. An epileptic origin, after other etiologies have been excluded, should be considered and carefully investigated in patients complaining of isolated memory disturbances, particularly with recurrent short-lasting amnesic attacks. In all suspected cases of epilepsy, a detailed clinical history is of paramount importance, but ancillary tests including EEG and MRI could be very helpful. Transient epileptic amnesia is typically a benign and treatable condition. Future studies should investigate the exact mechanism(s) of this unique syndrome. © 2013 Elsevier Inc. All rights reserved.
1. Introduction Transient epileptic amnesia (TEA) is a syndrome of epilepsy in which the principle manifestation of seizures is recurrent episodes of isolated memory loss. It represents an underdiagnosed type of temporal lobe epilepsy. Transient amnesia is sometimes the only manifestation of a temporal lobe seizure, and indeed, it may be the only seizure type to occur in some patients [1,2]. Various terms have been used to describe these attacks including pure amnestic seizures, epileptic amnesia, epileptic amnesic attacks, epileptic transient amnesia, and transient epileptic amnesia or TEA. The onset of the attacks in TEA is commonly in late–middle or old age [1–3]. It is more common among men [3]. 2. Clinical characteristics During an attack of TEA, there are often no obvious classical signs of a seizure to an observer. The patient's behavior is often appropriate. Approximately one-third of the affected patients have TEA as their unique seizure type. Other clinical features include the following: (1) attacks, which are less than 1 h in duration, often occur on waking; (2) coexistence of other seizure types, including olfactory hallucinations (in two-thirds of the patients); (3) electroencephalographic (EEG) abnormalities; and finally, (4) favorable response to antiepileptic drugs (AEDs). Proposed diagnostic criteria for TEA comprise the following: (1) a history of recurrent witnessed episodes of transient amnesia; (2) cognitive functions other than memory are intact during ⁎ Corresponding author at: M.D. Associate Professor of Epileptology, Neurosciences Research Center,Shiraz Medical School, Shiraz University of Medical Sciences, Shiraz, Iran. Tel.: +98 9352274990. E-mail address: [email protected].
typical episodes as observed by a reliable witness; and (3) other evidence for a diagnosis of epilepsy. This evidence could be either (a) epileptiform abnormalities in EEG, (b) the concurrent onset of other clinical features of an epileptic seizure (e.g., lip-smacking and olfactory hallucinations), or (c) a clear-cut response to antiepileptic drugs, or by a combination of these three [1–6]. However, not all patients meet all these criteria. 3. Memory dysfunctions Acute and transient memory dysfunctions in patients with TEA have typical characteristics: a repetitive, acute transient impairment of memory, lasting minutes (typically, less than an hour), which follows a seizure or may be the sole evident manifestation of a seizure in a patient with or without other kinds of seizures. Amnesia is anterograde, retrograde, or anteroretrograde, in a state of normal vigilance, and absent or with only mild behavioral abnormalities (perplexity, excessive quietness, or repetitive questions in some cases) with partial or complete amnesia for the episodes [7]. The extent of the retrograde amnesia during attacks varies from days to years [1]. The most important pointers to the epileptic origin of acute memory impairment are the relatively frequent repetition and the short duration of the attacks [8]. Seizures other than the attacks of transient amnesia may not be evident, but the patient may have more clinically obvious seizures (e.g., convulsions or olfactory hallucinations). Interictal memory disturbances can be conspicuous, leading the patient to medical consultation. Transient epileptic amnesia is associated with two unusual forms of interictal memory impairment: accelerated long-term forgetting [the rapid loss of newly acquired memories over days to weeks despite normal retention at standard (~30 min) intervals] and autobiographical amnesia [9,10].
1525-5050/$ – see front matter © 2013 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.yebeh.2013.10.021
Please cite this article as: Asadi-Pooya AA, Transient epileptic amnesia: A concise review, Epilepsy Behav (2013), http://dx.doi.org/10.1016/ j.yebeh.2013.10.021
2
A.A. Asadi-Pooya / Epilepsy & Behavior xxx (2013) xxx–xxx
4. Electroencephalography (EEG) Electroencephalographic abnormalities can contribute to the diagnosis of TEA [7]. Electroencephalographic findings may include epileptiform abnormalities (Fig. 1) in more than 1/3 of the patients, nonspecific focal slow waves in 1/3, and normal EEG in about 1/3 [3]. For these reasons, a normal EEG or a nonspecific EEG abnormality does not necessarily exclude the diagnosis of TEA [7]. Bilateral deep abnormal brain discharges involving the hippocampal–mesial temporal lobe regions probably explain the acute and transient disturbance of episodic memory of epileptic amnestic attacks in some cases; in others, the amnestic attacks are probably a postictal phenomenon. The evidence supports these changes [7,11]. The purposeful behavior during the amnesic period with scarcity of consciousness impairment could be explained by temporal lobe dysfunction, with or without minimal involvement of other cortical regions, the thalamus, or the brainstem nuclei [7]. 5. Imaging studies In a recent study, magnetic resonance volumetry confirmed the presence of subtle, bilateral hippocampal atrophy. Additional atrophy was revealed in perirhinal and orbitofrontal cortices. The volumes of these regions correlated with anterograde memory performance [12]. In a related study, manual volumetry identified subtle hippocampal volume loss in patients with TEA [13]. Functional magnetic resonance imaging has been used to examine retrieval of memories from across the lifespan in patients with TEA and healthy controls. Both groups engaged the autobiographical memory network, but activation in patients was less extensive than in controls. Direct comparison revealed hypoactivation of regions in the right hemisphere in patients. Specifically, patients showed reduced activation of the posterior parahippocampal gyrus, with decreased engagement of the right temporoparietal junction and the cerebellum [10]. The results of these studies support the hypothesis that TEA is a focal medial temporal lobe epilepsy syndrome [10,12,13]. In an illustrative study, a 71-year-old man with TEA had a meningoencephalocele in his magnetic
resonance imaging (MRI) in the middle cranial fossa with expansion ahead of the temporal ventricular horn. In the coronal scan, left-sided focal hippocampal atrophy was evident. His EEG showed left temporal spikes [14]. 6. Treatment Once TEA has been diagnosed, an antiepileptic drug appropriate for this condition may be prescribed. The goal of treatment is to prevent future seizures from recurring. Treatment is typically started with one of the first-line AEDs for localization-related epilepsy (partial onset seizures); these drugs (considering the age of the patients) include lamotrigine and levetiracetam among others [15–18]. In patients with TEA, the seizures (episodic transient amnesia) usually respond promptly to treatment with antiepileptic drugs, whereas the interictal impairments might persist [1–8]. If a first-line drug controls seizures and does not cause side effects, therapeutic adjustments are not needed. If seizures persist, the medication regimen should be adjusted [16]. Despite appropriate medical treatment, individuals with TEA occasionally have persistent seizures [19]. Epilepsy surgery might alleviate seizures and memory complaints in some patients with TEA and medically refractory seizures [19]. 7. Prognosis of interictal memory problems In a longitudinal study in one patient, when identified and treated, No memory impairment occurred at two years after diagnosis [20]. However, in another case study, the authors described a patient with TEA and found that an antiepileptic drug prevented accelerated forgetting but not dense retrograde amnesia. They suggested that accelerated forgetting in TEA was treatable, but retrograde amnesia was an irreversible process [21]. In an illustrative study, the patient underwent right anterior amygdalohippocampectomy for symptoms resembling refractory TEA with additional complex partial seizures. The patient remained seizure-free during the 15-month follow-up, and memory complaints remitted [19].
Fig. 1. T4 (right midtemporal) sharp wave in a 59-year-old woman with transient epileptic amnesia. EEG is an important element in making the diagnosis of TEA.
Please cite this article as: Asadi-Pooya AA, Transient epileptic amnesia: A concise review, Epilepsy Behav (2013), http://dx.doi.org/10.1016/ j.yebeh.2013.10.021
A.A. Asadi-Pooya / Epilepsy & Behavior xxx (2013) xxx–xxx
3
Table 1 Transient epileptic amnesia (TEA) versus transient global amnesia (TGA) and psychogenic amnesia.a Clinical feature
TEA
TGA
Psychogenic amnesia
Precipitating factor Aura Amnesia during the attack Impaired cognition during the attack Automatism during the attack Coexistence of other seizure types Duration of attack Recurrence rate EEG abnormalities Favorable response to antiepileptic drugs Interictal memory problems
Often occurs on waking Probable Yes No Possible Possible Typically b1 h High Probable Yes Yes
Emotional stress or physical exertion No Yes No No No b24 h Low No No No
Stressful experiences or psychological trauma No Yes Possible No No Variable ? No No Possible
a
References [21,23,24].
8. Conclusion Transient epileptic amnesia is a distinctive syndrome and comprises episodic transient amnesia with an epileptic basis, without impairment of other aspects of cognitive function. An epileptic origin, after other etiologies (e.g., transient global amnesia, psychogenic amnesia, transient ischemic amnesia, dementia, and migraine) have been excluded [22–26], should be considered and carefully investigated in patients complaining of isolated memory disturbances, particularly with recurrent shortlasting amnesic attacks (Table 1). In all suspected cases of epilepsy, a detailed clinical history is of paramount importance, but ancillary tests including EEG and MRI can be very helpful [27,28]. Transient epileptic amnesia is typically a benign and treatable condition, yet the associated decline in autobiographical and remote memory despite antiepileptic therapy poses challenges to elucidate through further research [29].
Conflict of interest statement The author serves on a scientific advisory board for Cobel Darou.
References [1] Zeman AZJ, Boniface SJ, Hodges JR. Transient epileptic amnesia: a description of the clinical and neuropsychological features in 10 cases and a review of the literature. J Neurol Neurosurg Psychiatry 1998;64:435–43. [2] Pritchard III PB, Holmstrom VL, Roitzsch JC, Giacinto J. Epileptic amnesic attacks: benefit from antiepileptic drugs. Neurology 1985;35:1188–9. [3] Butler CR, Graham KS, Hodges JR, Kapur N, Wardlaw JM, Zeman AZ. The syndrome of transient epileptic amnesia. Ann Neurol 2007;61:587–98. [4] Mendes MH. Transient epileptic amnesia: an under-diagnosed phenomenon? Three more cases. Seizure 2002;11(4):238–42. [5] Kapur N. Transient epileptic amnesia—a clinical update and reformulation. J Neurol Neurosurg Psychiatry 1993;56:1184–90. [6] Palmini AL, Gloor P, Jones-Gotman M. Pure amnestic seizures in temporal lobe epilepsy. Brain 1992;115:749–69. [7] Gallassi R. Epileptic amnesic syndrome: an update and further considerations. Epilepsia 2006;47(Suppl. 2):103–5. [8] Hodges JR, Warlow CP. Syndromes of transient amnesia: towards a classification. A study of 153 cases. J Neurol Neurosurg Psychiatry 1990;53(10):834–43. [9] Hoefeijzers S, Dewar M, Della Sala S, Zeman A, Butler C. Accelerated long-term forgetting in transient epileptic amnesia: an acquisition or consolidation deficit? Neuropsychologia 2013;51(8):1549–55.
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Please cite this article as: Asadi-Pooya AA, Transient epileptic amnesia: A concise review, Epilepsy Behav (2013), http://dx.doi.org/10.1016/ j.yebeh.2013.10.021