Epilepsin, 33(6): 1042-1046, 1992 Raven Press, Ltd., New York 0 International League Against Epilepsy
Prolonged Ictal Amnesia with Transient Focal Abnormalities on Magnetic Resonance Imaging B. I. Lee, B. C. Lee, Y. M. Hwang, Y. H. Sohn, J. W. Jung, S. C. Park, and *M. H. Han Department of Neurology, Yonsei University College of Medicine; and *Depurtment of Rudiology, Seoul National University, College of Medicine, Seoul, Korea
Summary: A previously healthy woman had a prolonged amnestic state caused by complex partial status epilepticus with bilateral mesiotemporal lobe involvement confirmed by EEG with nasopharyngeal electrodes. A magnetic resonance imaging (MRI) scan obtained shortly af-
ter recovery from the amnesia showed reversible focal abnormalities consisting of increased signal intensity on T,-weighted scan in the mesiotemporal lobe. Key Words: Status epilepticus-Complex partial seizures-Transient global amnesia-Magnetic resonance imaging.
Mesiotemporal lobe including hippocampus is critical for formation and recall of short-term memory (Brierley, 1966). Transient ischemia (Rowan and Protass, 1979) or abnormal electrical activity (Bickford et al., 1958) in mesiotemporal lobe may cause transient global amnesia (TGA) (Fisher and Adams, 1964). A clear demonstration of ictal events as the cause of TGA has not been reported. Morrel (1980), using implanted electrodes, reported a case of chronic temporal lobe epilepsy (TLE) with a brief TGA in the immediate postictal stage and suggested that TGA could be a postictal phenomenon consistent with Todd’s paralysis. On the other hand, Rowan and Protass (1979) suggested that interictal epileptiform discharges observed in TGA patients resulted from transient ischemia of the deep temporal structures rather than being an epileptic manifestation. We report a case of prolonged amnestic state caused by complex partial status epilepticus of mesiotemporal lobe origin.
amnesia. She was a married, college graduate, highschool teacher. She had been healthy until the morning before admission when she received an overseas telephone call from her husband who was on a business trip abroad. She could not remember his trip and kept asking why and when he left home. Shortly afterward, her mother noted that she was amnesic for any events that had occurred in the previous 4 months, specifically, her husband’s trip, her niece’s wedding, her daughter’s violin lessons, or a field trip with her students. In the ER, she was alert, pleasant, and had stable vital signs. She was aware of her memory impairment and expressed concern. She denied fever, headache, or other symptoms. Past family medical histories were significant for an uncomplicated febrile convulsion at age 3 years and febrile convulsions in her sister and son. General physical examination was normal. Mental status examination showed that she was oriented to person, place, year, and month, but not to date. Digits span was normal. Serial sevens and calculations were intact. Fund of knowledge, judgment, and proverb interpretation were normal. Memory examination showed intact immediate recall, recall of the telephone call from the husband, and what she had had for breakfast. The amnesia for events of the previous 4 months was persistent. Memory for events before the previous 4 months was intact. The remainder of the neurologic examination was negative.
CASE REPORT
A 38-year-old, right-handed woman was brought to the emergency room (ER) for abrupt onset of Received November 1991; revision accepted February 1992. Presented at the 19th International Epilepsy Congress, in Rio de Janeiro, Brazil, October 1991, and published in abstract form in Epilepsia 1991;32 (suppl 1):41. Address correspondence and reprint requests to Dr. B. I. Lee at Department of Neurology, Yonsei University College of Medicine, 134, Shinchon-dong Sudaemoon-ku, Seoul, Korea.
1042
TGA IN STATUS EPILEPTICUS
Admission laboratory studies included complete blood count (CBC), SMA12, electrolytes, electrocardiogram, chest roentgenogram, and computed tomography (CT) scan before and after contrast; all were normal. On hospital day 1, global amnesia persisted. She could not recognize her physician’s name and face. She realized that she was in a hospital but did not remember how and when she was admitted. She could not recall any of three words and three hidden objects after 5 min. In the afternoon, she was found wandering on a different hospital floor. Routine scalp 16-channel EEG was normal. Psychiatric consultation suggested an organic nature rather than a fugue state. On hospital day 4, an EEG with nasopharyngeal electrodes after overnight sleep deprivation showed very active sharp waves and two episodes of ictal discharges arising independently from the left and right nasopharyngeal electrodes (Fig. I). Distribution of electrical ictal discharges was restricted to a unilateral nasopharyngeal electrode, with only volume-conducted activities recorded on the contralateral side. When the EEG findings were explained to her family, they became furious about the diagnosis of “seizures” and removed her from the hospital against medical advice and sought help from an herb doctor. Eight
1043
days later, she returned because of lack of improvement. She looked tired and again failed to recognize her physician or previous hospitalization. Mental status and neurologic examination were essentially unchanged from the previous hospitalization. During 4-h closed-circuit (CC)TV-EEG recording with nasopharyngeal electrodes, 22 episodes of ictal discharges lasting 60-120 s were recorded. All episodes arose from and remained localized to the left nasopharyngeal electrode without subsequent spread to contralateral electrodes (Fig. 2). During electrical ictal discharges, she could count normally and was able to carry on a conversation with no cognitive or other behavioral changes of complex partial seizures. Persistent amnestic state was the only clinical manifestation during CCTV-EEG recording. Valium (10 mg) and phenytoin (18 mg/kg) were administered intravenously (i.v .), with complete cessation of ictal discharges. Carbamazepine (CBZ) (400 mg/day) was prescribed, with subsequent full recovery of memory except for the events of the 12 days from the morning of admission to the day of antiepileptic drug (AED) treatment. MRI on the fifth day of CBZ therapy, when memory was improved, showed increased signal in both mesiotem-
FIG. 1. Onset (arrow) of electrical ictal discharges arising from the right nasopharyngeal electrode. lctal discharges were localized to that electrode, with only volume-conducted electrical activities being recorded from the contralateral nasopharyngeal electrode. *Interictal epileptiform discharges localized to the left nasopharygeal electrode. Epilepsia, Vol. 33, No. 6, 1992
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B . I . LEE ET AL.
poral regions, with higher intensity on the left but with no mass effect on T,-weighted imaging. Coronal slices through the body of the hippocampus on T,-weighted imaging showed an atrophic change in the left hippocampus. One year later, MRI showed resolution of all but the left mesiotemporal atrophy (Fig. 3). Two and a half years later, she had had no recurrent amnestic spells, but had had several episodes of brief dizziness with no impairment of consciousness. EEG at 2 years showed occasional sharp waves in the left nasopharyngeal electrode. DISCUSSION We report a case of TGA with retrograde and anterograde global amnesia but intact behavior and other cognitive functions, which recovered completely after AED treatment. The prolonged duration of amnesia and lack of prior episodes were unusual for an epileptic amnestic attack (Gallassi et al., 1988). Throughout hospitalization and 4-h CCTV-EEG recording, no other clinical manifestations of complex partial seizures were observed despite occurrence of numerous episodes of electrical ictal discharges. The electroclinical findings were clearly indicative of complex partial status epilepticus, with amnesia as the sole clinical manifestion. Epilepsia, Vol. 33, No. 6 , 1992
Penfield and Milner (1958) reported catastrophic effects on memory of bilateral temporal lobe resection and postulated that short-term memory impairment occurred only with bilateral temporal lobe lesions. Bridgman et al. (1989) reported minimal recall impairment with subclinical ictal events confined to unilateral hippocampus. Overt clinical manifestation of TGA may require bilateral mesiotemporal structure dysfunction as in our patient. The persistence of left hippocampal atrophy on MRI and focal left mesiotemporal EEG sharp waves strongly suggest the left mesiotemporal lobe as the epileptic focus in our patient, although we could not exclude the possibility of an independent right mesiotemporal lobe focus. We speculate that our patient had an underlying structural substrate, left hippocampal atrophy, probably caused by the febrile convulsion, which resulted in the complex partial status epilepticus precipitated by an unknown mechanism. We speculate that recruitment of the right mesiotemporal lobe might have occurred during status epilepticus to cause bilateral mesiotemporal lobe dysfunction, resulting in the clinical picture of TGA. The unilateral distribution of ictal EEG discharges during episodes may explain the lack of behavioral and cognitive changes ordinarily observed with complex partial seizures.
TCA IN STATUS EPILEPTICUS
1045
A
T
%
Ac
LT
FIG. 3. Spin-echo magnetic resonance imaging (MRI) T,-weighted (TR/TE = 3,000/80) axial (AA) and coronal (A,) showing abnormally high intensity in mesiotemporal regions (arrows) bilaterally with higher intensity on the left. T,-weighted (TR/TE = 500/30) coronal image (A,) showed widening of the hippocampal fissure and a smaller hippocampus on the left. Abnormal signal intensity was no longer evident in the temporal region on SE T,-weighted (TR/TE = 2,500/80) axial image (B) obtained 1 year after initial MRI. Left mesiotemporal lobe was smaller than right mesiotemporal lobe (by a 25% reduction in diameter), which was consistent with the left hippocampal atrophy evident in A., H, hippocampus; P, parahippocampal gyrus; TH, temporal horn; HF, hippocampal fissure; CV, circummesencephalic vessel.
Reversible focal CT or MRI abnormalities have been reported in patients with partial status epilepticus. The most likely pathogenesis of reversible focal abnormalities would be cerebral edema resulting from increased energy demand caused by recurrent ictal activities, increased regional cerebral blood flow, or regional blood-brain barrier breakdown (Kramer et al., 1987). As described by other investigators (Jayakumar et al., 1985; Kramer et al., 1987), lack of mass effect in the focal lesions were demonstrated in our patient, showing clear atrophic change in the left hippocampus on TI-weighted image despite prominent signal intensity on T,weighted image. Recurrent ictal activities generating transient focal abnormalities consisting of increased signal intensity on T,-weighted image in the mesiotemporal lobe raises the question of the nature of this specific abnormality in TLE. Space-occupying lesions or foreign tissue abnormalities are readily detected by
MRI. Whether the increased MRI T,-weighted signal intensity in the mesiotemporal region indicates mesiotemporal sclerosis, the most common pathology of TLE observed in 60-70% of surgical specimens, is controversial. Kuzniecky et al. (1987) reported this feature as characteristic of mesiotemporal sclerosis, and Jackson et al. (1990) demonstrated that the combined features of focal hippocampal atrophy and increased T,-weighted signal intensity predicted the presence of mesiotemporal sclerosis in all of their TLE series. On the other hand, Sperling et al. (1986) and Ormson et al. (1986) failed to find correlations between mesiotemporal sclerosis and increased T,-weighted signal intensity in the mesiotemporal region. Brooks et al. (1990) reported that increased T,weighted signal intensity was observed in only 8% of patients with pathologically proven mesiotemporal sclerosis and Jack et al. (1990) reported that volumetric measurement of hippocampal atrophy was Epilepsiu, Vol. 33, N o . 6 , 1992
B. I . LEE ET AL.
I046
a much more reliable predictor of mesiotemporal sclerosis than was increased T,-weighted signal intensity. Therefore, the significance of this abnormality for mesiotemporal sclerosis remains unclear. MRI findings in our patient suggest that the increased T,-weighted signal intensity in the mesiotemporal lobe may not necessarily be specific for mesiotemporal sclerosis but instead simply reflects increased water content either caused by severe glosis or repetitive electrical discharges. Acknowledgment: We thank Dr. G. D. Jackson, Queen Square, London, for helpful comments and Ms. Yoon for secretarial assistance.
REFERENCES Bickford RG, Mulder DW, Dodge HW, et al. Changes in memory function produced by electrical stimulation of the temporal lobe in man. Res Publ Assoc Res Nerv Men{ Dis 1958;36: 227-43. Brierley JB. The neuropathology of amnesia states. In: Whitty CW, Zangwill OL, eds. Amnesiu. London: Butterworths, 1966:15@-80. Bridgman PA, Malamut BL, Sperling MR, et al. Memory during subclinical hippocampal seizures. Neurdogy 1989;39:853-6. Brooks BS, King DW, Gamma1 TE, et al. MR imaging in patients with intractable complex partial seizures. AJNR 1990;ll: 93-9. Falconer MA. Mesial temporal (Ammorn’s horn) sclerosis as a common cause of epilepsy: aetiology , treatment and prevention. Lancet 1974;2:767-70. Fisher CM, Adams RD. Transient global amnesia syndrome. Acta Neurol Scund 1964;40(suppl 9):7-82. Gallassi R, Morreale A, Lomsso S,et al. Epilepsy presenting as memory disturbances. Epilepsia 1988;19:624-9. Jack CR, Sharbrough FW, Twomey CK, et al. Temporal lobe seizures: lateralization with MR volume measurements of the hippocampal formation. Rudiology 1990;175:423-9. Jackson GD, Berkovic SF, Tress BM, et al. Hippocampal sclerosis can be reliably detected by magnetic resonance imaging. Neurology 1990;40:1869-75. Jayakumar PN, Taly AB, Mohan PK. Transient computerized tomographic abnormalities following partial seizures. Actu Neurol Scand 1985;72:2&9. Krdmer RE, Luders H, Lesser RP, et al. Transient focal abnormalities of neuroimaging studies during focal status epilepticus. Epiiepiu 1987;28:528-32. Kuzniecky R, de la Sayette V, Ethier K, et al. Magnetic reso-
Epilepsiu, Vol. 33, N o . 6 , 1992
nance imaging in temporal lobe epilepsy: pathological correlation. Ann Neurol 1987;22:341-7. Morrell F. Memory loss as a Todd’s paralysis (Abstract]. Epilepsia 1980;21:185. Ormson MJ, Kispert DB, Sharbrough FW, et al. Cryptic struCtural lesions in refractory partial epilepsy: MR imaging and CT studies. Radiology 1986;160:215-9. Penfield W, Milner B. Memory deficits produced by bilateral lesions in the hippocampal zone. Arch Neurol Psychiutty 1Y58;7Y:475-97. Rowan AJ, Protass LM. Transient global amnesia: clinical and electroencephalographic findings in 10 cases. Neurology 1979;29:868-72. Sperling MR, Wilson G, Engel J Jr, et al. Magnetic resonance imaging in intractable, partial epilepsy: correlative studies. Ann Nrurol 1986:20:5762.
RESUME Une patiente sans antecedent a ete vue dans un etat amnesique prolong6 dont I’origine etait un etat de ma1 Cpileptique partiel complexe, impliquant les structures temporo-mtsiales bilat&ales, cornme I’a confirme I’EEG employant des electrodes nasopharyngees. L’IRM obtenue peu de temps apres gutrison de I’amntsie a mis en evidence des anomalies focales representees par une augmentation de I’intensite du signal en T2 au niveau de la partie mtdiane du lobe temporal.
(P. Genton, Marseille)
RESUMEN Una mujer sana present6 un estado amnesico prolongado causado por un status epileptico de crisis parciales complejas con afectaci6n temporal medial bilateral confirmada en el EEG utihando electrodos nasofaringeos. La Resonancia MagnCtica obtenida poco tiempo despues de la recuperacibn de la amnesia mostro anomalias focales reversibles que consistian en un incremento de la intensidad de la sefial en 10s estudios T2 en la regidn medial del lobulo temporal. (A. Portera-SAnchez, Madrid)
ZUSAMMENFASSUNG Eine bislang gesunde Frau zeigte einen verlingerten amnestischen Zustand, der durch einen komplex-partiellen Status epilepticus unter Einbeziehung der bilateralen medialen Temporallappen, nachgewiesen durch EEG mit nasopharyngealen Elektroden, verursacht war. Ein MRT kurz nach Erholung von der Amnesie zeigte reversible, fokale Abnormalitaten mit erhohter T2-Signalintensitit im medialen Temporallappen. ( C . K. Benninger, Heidelberg)
Prolonged Ictal Amnesia with Transient Focal Abnormalities on Magnetic Resonance Imaging B. I. Lee, B. C. Lee, Y. M. Hwang, Y. H. Sohn, J. W. Jung, S. C. Park, and *M. H. Han Department of Neurology, Yonsei University College of Medicine; and *Depurtment of Rudiology, Seoul National University, College of Medicine, Seoul, Korea
Summary: A previously healthy woman had a prolonged amnestic state caused by complex partial status epilepticus with bilateral mesiotemporal lobe involvement confirmed by EEG with nasopharyngeal electrodes. A magnetic resonance imaging (MRI) scan obtained shortly af-
ter recovery from the amnesia showed reversible focal abnormalities consisting of increased signal intensity on T,-weighted scan in the mesiotemporal lobe. Key Words: Status epilepticus-Complex partial seizures-Transient global amnesia-Magnetic resonance imaging.
Mesiotemporal lobe including hippocampus is critical for formation and recall of short-term memory (Brierley, 1966). Transient ischemia (Rowan and Protass, 1979) or abnormal electrical activity (Bickford et al., 1958) in mesiotemporal lobe may cause transient global amnesia (TGA) (Fisher and Adams, 1964). A clear demonstration of ictal events as the cause of TGA has not been reported. Morrel (1980), using implanted electrodes, reported a case of chronic temporal lobe epilepsy (TLE) with a brief TGA in the immediate postictal stage and suggested that TGA could be a postictal phenomenon consistent with Todd’s paralysis. On the other hand, Rowan and Protass (1979) suggested that interictal epileptiform discharges observed in TGA patients resulted from transient ischemia of the deep temporal structures rather than being an epileptic manifestation. We report a case of prolonged amnestic state caused by complex partial status epilepticus of mesiotemporal lobe origin.
amnesia. She was a married, college graduate, highschool teacher. She had been healthy until the morning before admission when she received an overseas telephone call from her husband who was on a business trip abroad. She could not remember his trip and kept asking why and when he left home. Shortly afterward, her mother noted that she was amnesic for any events that had occurred in the previous 4 months, specifically, her husband’s trip, her niece’s wedding, her daughter’s violin lessons, or a field trip with her students. In the ER, she was alert, pleasant, and had stable vital signs. She was aware of her memory impairment and expressed concern. She denied fever, headache, or other symptoms. Past family medical histories were significant for an uncomplicated febrile convulsion at age 3 years and febrile convulsions in her sister and son. General physical examination was normal. Mental status examination showed that she was oriented to person, place, year, and month, but not to date. Digits span was normal. Serial sevens and calculations were intact. Fund of knowledge, judgment, and proverb interpretation were normal. Memory examination showed intact immediate recall, recall of the telephone call from the husband, and what she had had for breakfast. The amnesia for events of the previous 4 months was persistent. Memory for events before the previous 4 months was intact. The remainder of the neurologic examination was negative.
CASE REPORT
A 38-year-old, right-handed woman was brought to the emergency room (ER) for abrupt onset of Received November 1991; revision accepted February 1992. Presented at the 19th International Epilepsy Congress, in Rio de Janeiro, Brazil, October 1991, and published in abstract form in Epilepsia 1991;32 (suppl 1):41. Address correspondence and reprint requests to Dr. B. I. Lee at Department of Neurology, Yonsei University College of Medicine, 134, Shinchon-dong Sudaemoon-ku, Seoul, Korea.
1042
TGA IN STATUS EPILEPTICUS
Admission laboratory studies included complete blood count (CBC), SMA12, electrolytes, electrocardiogram, chest roentgenogram, and computed tomography (CT) scan before and after contrast; all were normal. On hospital day 1, global amnesia persisted. She could not recognize her physician’s name and face. She realized that she was in a hospital but did not remember how and when she was admitted. She could not recall any of three words and three hidden objects after 5 min. In the afternoon, she was found wandering on a different hospital floor. Routine scalp 16-channel EEG was normal. Psychiatric consultation suggested an organic nature rather than a fugue state. On hospital day 4, an EEG with nasopharyngeal electrodes after overnight sleep deprivation showed very active sharp waves and two episodes of ictal discharges arising independently from the left and right nasopharyngeal electrodes (Fig. I). Distribution of electrical ictal discharges was restricted to a unilateral nasopharyngeal electrode, with only volume-conducted activities recorded on the contralateral side. When the EEG findings were explained to her family, they became furious about the diagnosis of “seizures” and removed her from the hospital against medical advice and sought help from an herb doctor. Eight
1043
days later, she returned because of lack of improvement. She looked tired and again failed to recognize her physician or previous hospitalization. Mental status and neurologic examination were essentially unchanged from the previous hospitalization. During 4-h closed-circuit (CC)TV-EEG recording with nasopharyngeal electrodes, 22 episodes of ictal discharges lasting 60-120 s were recorded. All episodes arose from and remained localized to the left nasopharyngeal electrode without subsequent spread to contralateral electrodes (Fig. 2). During electrical ictal discharges, she could count normally and was able to carry on a conversation with no cognitive or other behavioral changes of complex partial seizures. Persistent amnestic state was the only clinical manifestation during CCTV-EEG recording. Valium (10 mg) and phenytoin (18 mg/kg) were administered intravenously (i.v .), with complete cessation of ictal discharges. Carbamazepine (CBZ) (400 mg/day) was prescribed, with subsequent full recovery of memory except for the events of the 12 days from the morning of admission to the day of antiepileptic drug (AED) treatment. MRI on the fifth day of CBZ therapy, when memory was improved, showed increased signal in both mesiotem-
FIG. 1. Onset (arrow) of electrical ictal discharges arising from the right nasopharyngeal electrode. lctal discharges were localized to that electrode, with only volume-conducted electrical activities being recorded from the contralateral nasopharyngeal electrode. *Interictal epileptiform discharges localized to the left nasopharygeal electrode. Epilepsia, Vol. 33, No. 6, 1992
1044
B . I . LEE ET AL.
poral regions, with higher intensity on the left but with no mass effect on T,-weighted imaging. Coronal slices through the body of the hippocampus on T,-weighted imaging showed an atrophic change in the left hippocampus. One year later, MRI showed resolution of all but the left mesiotemporal atrophy (Fig. 3). Two and a half years later, she had had no recurrent amnestic spells, but had had several episodes of brief dizziness with no impairment of consciousness. EEG at 2 years showed occasional sharp waves in the left nasopharyngeal electrode. DISCUSSION We report a case of TGA with retrograde and anterograde global amnesia but intact behavior and other cognitive functions, which recovered completely after AED treatment. The prolonged duration of amnesia and lack of prior episodes were unusual for an epileptic amnestic attack (Gallassi et al., 1988). Throughout hospitalization and 4-h CCTV-EEG recording, no other clinical manifestations of complex partial seizures were observed despite occurrence of numerous episodes of electrical ictal discharges. The electroclinical findings were clearly indicative of complex partial status epilepticus, with amnesia as the sole clinical manifestion. Epilepsia, Vol. 33, No. 6 , 1992
Penfield and Milner (1958) reported catastrophic effects on memory of bilateral temporal lobe resection and postulated that short-term memory impairment occurred only with bilateral temporal lobe lesions. Bridgman et al. (1989) reported minimal recall impairment with subclinical ictal events confined to unilateral hippocampus. Overt clinical manifestation of TGA may require bilateral mesiotemporal structure dysfunction as in our patient. The persistence of left hippocampal atrophy on MRI and focal left mesiotemporal EEG sharp waves strongly suggest the left mesiotemporal lobe as the epileptic focus in our patient, although we could not exclude the possibility of an independent right mesiotemporal lobe focus. We speculate that our patient had an underlying structural substrate, left hippocampal atrophy, probably caused by the febrile convulsion, which resulted in the complex partial status epilepticus precipitated by an unknown mechanism. We speculate that recruitment of the right mesiotemporal lobe might have occurred during status epilepticus to cause bilateral mesiotemporal lobe dysfunction, resulting in the clinical picture of TGA. The unilateral distribution of ictal EEG discharges during episodes may explain the lack of behavioral and cognitive changes ordinarily observed with complex partial seizures.
TCA IN STATUS EPILEPTICUS
1045
A
T
%
Ac
LT
FIG. 3. Spin-echo magnetic resonance imaging (MRI) T,-weighted (TR/TE = 3,000/80) axial (AA) and coronal (A,) showing abnormally high intensity in mesiotemporal regions (arrows) bilaterally with higher intensity on the left. T,-weighted (TR/TE = 500/30) coronal image (A,) showed widening of the hippocampal fissure and a smaller hippocampus on the left. Abnormal signal intensity was no longer evident in the temporal region on SE T,-weighted (TR/TE = 2,500/80) axial image (B) obtained 1 year after initial MRI. Left mesiotemporal lobe was smaller than right mesiotemporal lobe (by a 25% reduction in diameter), which was consistent with the left hippocampal atrophy evident in A., H, hippocampus; P, parahippocampal gyrus; TH, temporal horn; HF, hippocampal fissure; CV, circummesencephalic vessel.
Reversible focal CT or MRI abnormalities have been reported in patients with partial status epilepticus. The most likely pathogenesis of reversible focal abnormalities would be cerebral edema resulting from increased energy demand caused by recurrent ictal activities, increased regional cerebral blood flow, or regional blood-brain barrier breakdown (Kramer et al., 1987). As described by other investigators (Jayakumar et al., 1985; Kramer et al., 1987), lack of mass effect in the focal lesions were demonstrated in our patient, showing clear atrophic change in the left hippocampus on TI-weighted image despite prominent signal intensity on T,weighted image. Recurrent ictal activities generating transient focal abnormalities consisting of increased signal intensity on T,-weighted image in the mesiotemporal lobe raises the question of the nature of this specific abnormality in TLE. Space-occupying lesions or foreign tissue abnormalities are readily detected by
MRI. Whether the increased MRI T,-weighted signal intensity in the mesiotemporal region indicates mesiotemporal sclerosis, the most common pathology of TLE observed in 60-70% of surgical specimens, is controversial. Kuzniecky et al. (1987) reported this feature as characteristic of mesiotemporal sclerosis, and Jackson et al. (1990) demonstrated that the combined features of focal hippocampal atrophy and increased T,-weighted signal intensity predicted the presence of mesiotemporal sclerosis in all of their TLE series. On the other hand, Sperling et al. (1986) and Ormson et al. (1986) failed to find correlations between mesiotemporal sclerosis and increased T,-weighted signal intensity in the mesiotemporal region. Brooks et al. (1990) reported that increased T,weighted signal intensity was observed in only 8% of patients with pathologically proven mesiotemporal sclerosis and Jack et al. (1990) reported that volumetric measurement of hippocampal atrophy was Epilepsiu, Vol. 33, N o . 6 , 1992
B. I . LEE ET AL.
I046
a much more reliable predictor of mesiotemporal sclerosis than was increased T,-weighted signal intensity. Therefore, the significance of this abnormality for mesiotemporal sclerosis remains unclear. MRI findings in our patient suggest that the increased T,-weighted signal intensity in the mesiotemporal lobe may not necessarily be specific for mesiotemporal sclerosis but instead simply reflects increased water content either caused by severe glosis or repetitive electrical discharges. Acknowledgment: We thank Dr. G. D. Jackson, Queen Square, London, for helpful comments and Ms. Yoon for secretarial assistance.
REFERENCES Bickford RG, Mulder DW, Dodge HW, et al. Changes in memory function produced by electrical stimulation of the temporal lobe in man. Res Publ Assoc Res Nerv Men{ Dis 1958;36: 227-43. Brierley JB. The neuropathology of amnesia states. In: Whitty CW, Zangwill OL, eds. Amnesiu. London: Butterworths, 1966:15@-80. Bridgman PA, Malamut BL, Sperling MR, et al. Memory during subclinical hippocampal seizures. Neurdogy 1989;39:853-6. Brooks BS, King DW, Gamma1 TE, et al. MR imaging in patients with intractable complex partial seizures. AJNR 1990;ll: 93-9. Falconer MA. Mesial temporal (Ammorn’s horn) sclerosis as a common cause of epilepsy: aetiology , treatment and prevention. Lancet 1974;2:767-70. Fisher CM, Adams RD. Transient global amnesia syndrome. Acta Neurol Scund 1964;40(suppl 9):7-82. Gallassi R, Morreale A, Lomsso S,et al. Epilepsy presenting as memory disturbances. Epilepsia 1988;19:624-9. Jack CR, Sharbrough FW, Twomey CK, et al. Temporal lobe seizures: lateralization with MR volume measurements of the hippocampal formation. Rudiology 1990;175:423-9. Jackson GD, Berkovic SF, Tress BM, et al. Hippocampal sclerosis can be reliably detected by magnetic resonance imaging. Neurology 1990;40:1869-75. Jayakumar PN, Taly AB, Mohan PK. Transient computerized tomographic abnormalities following partial seizures. Actu Neurol Scand 1985;72:2&9. Krdmer RE, Luders H, Lesser RP, et al. Transient focal abnormalities of neuroimaging studies during focal status epilepticus. Epiiepiu 1987;28:528-32. Kuzniecky R, de la Sayette V, Ethier K, et al. Magnetic reso-
Epilepsiu, Vol. 33, N o . 6 , 1992
nance imaging in temporal lobe epilepsy: pathological correlation. Ann Neurol 1987;22:341-7. Morrell F. Memory loss as a Todd’s paralysis (Abstract]. Epilepsia 1980;21:185. Ormson MJ, Kispert DB, Sharbrough FW, et al. Cryptic struCtural lesions in refractory partial epilepsy: MR imaging and CT studies. Radiology 1986;160:215-9. Penfield W, Milner B. Memory deficits produced by bilateral lesions in the hippocampal zone. Arch Neurol Psychiutty 1Y58;7Y:475-97. Rowan AJ, Protass LM. Transient global amnesia: clinical and electroencephalographic findings in 10 cases. Neurology 1979;29:868-72. Sperling MR, Wilson G, Engel J Jr, et al. Magnetic resonance imaging in intractable, partial epilepsy: correlative studies. Ann Nrurol 1986:20:5762.
RESUME Une patiente sans antecedent a ete vue dans un etat amnesique prolong6 dont I’origine etait un etat de ma1 Cpileptique partiel complexe, impliquant les structures temporo-mtsiales bilat&ales, cornme I’a confirme I’EEG employant des electrodes nasopharyngees. L’IRM obtenue peu de temps apres gutrison de I’amntsie a mis en evidence des anomalies focales representees par une augmentation de I’intensite du signal en T2 au niveau de la partie mtdiane du lobe temporal.
(P. Genton, Marseille)
RESUMEN Una mujer sana present6 un estado amnesico prolongado causado por un status epileptico de crisis parciales complejas con afectaci6n temporal medial bilateral confirmada en el EEG utihando electrodos nasofaringeos. La Resonancia MagnCtica obtenida poco tiempo despues de la recuperacibn de la amnesia mostro anomalias focales reversibles que consistian en un incremento de la intensidad de la sefial en 10s estudios T2 en la regidn medial del lobulo temporal. (A. Portera-SAnchez, Madrid)
ZUSAMMENFASSUNG Eine bislang gesunde Frau zeigte einen verlingerten amnestischen Zustand, der durch einen komplex-partiellen Status epilepticus unter Einbeziehung der bilateralen medialen Temporallappen, nachgewiesen durch EEG mit nasopharyngealen Elektroden, verursacht war. Ein MRT kurz nach Erholung von der Amnesie zeigte reversible, fokale Abnormalitaten mit erhohter T2-Signalintensitit im medialen Temporallappen. ( C . K. Benninger, Heidelberg)
