Observations
Transient Global Amnesia in Migraine Bent de Fine Olivarius and Troels Staehelin Jensen The University Department of Neurology, Aarhus Kommunehospital, Aarhus, Denmark. Parts of this paper were presented at the Scandinavian Migraine Society, Annual Meeting, Scanticon, Aarhus, Denmark, Sept. 1978. Reprint requests to: Bent de Fine Olivarius, M.D., The University Department of Neurology, Aarhus Kommune-hospital, DK-8000 Aarhus C Denmark. Accepted for Publication: June 7, 1979 SYNOPSIS The clinical features of five migraine patients, suffering one to several episodes of transient global amnesia (TGA), were evaluated. All patients were women, with an age range of 34 to 67 years. One patient had common, and four, classical migraine. Two patients had typical vertebro-basilar migraine; two others had previously experienced transitory neurological symptoms compatible with transitory circulatory disturbances in the vertebro-basilar arterial system. On the basis of these data and available literature, the pathophysiological mechanisms are discussed. It is suggested that in our patients, TGA was due to transitory ischemia in the mamillo-hippocampal formation, secondary to shortlasting vasospasms in the arteries supplying mesial and basal parts of the temporal lobes. It was concluded that TGA in migraine is a benign condition, and does not usually require extensive neuroradiological investigations. (Headache 19:335-338, 1979) Transient global amnesia (TGA) is a suddenly occurring amnesic syndrome clinically characterized by a profound disturbance of short-term memory with preservation of immediate recall and of long-term memory. The amnesic episodes, often affecting elderly persons is usually shortlasting, and apart from a slight confusion is rarely accompanied by other neurological or intellectual disturbances.1,2 After the attack there is usually some retrograde amnesia, rarely of more than a few hours duration.3,4 Since the original description of Bender5 and Fisher and Adams6 TGA has been mentioned in connexion with various pathological conditions. An unequivocal etiology or specific pathogenesis has not been delimited, although several authors have regarded a vascular pathology most probable.7,8 We find it of some interest to report on 5 patients having a combination of TGA and migraine, since the syndrome has been reported rarely in association with migraine. The simultaneous occurrence of TGA and migraine may point to a distinct pathogenesis for the syndrome in such patients. CASE HISTORIES Patient No. 1. 59-year-old woman without a family history of migraine. Since childhood attacks of diffuse pinching headache associated with pronounced photo-and phonophobia, nausea, more rarely vomiting. Attacks have occurred with intervals of weeks to months and last for up to 24 hours. For the last three years she has experienced 3 attacks of spontaneously occurring fortification lines and coloured spots before both eyes, but without headache. 10 days before admission she experienced sudden loss of memory for 6 hours. She moved quite naturally around in her home but several times told the family, that "everything felt strange". The following day her memory was intact but she felt tired and indisposed with loss of initiative, which continued for some days. On admission, neurological examination was normal. BP: 170/110-150/80 mm Hg. Special investigations are summarized in Table 1. Patient No. 2. 58-year-old woman without a family history of migraine. Since the age of 25 she had suffered from attacks of unilateral, shooting headache on either side, and accompanied by nausea, vomiting, photo- and phonophobia. Previously attacks occurred on weekends, for the past three years every 2 or 3 weeks. Some years ago she had consumed considerable amounts of ergotamine (GynergenÒ comp.). 14 days before admission she awakened in the morning with headache which had subsided following the administration of one suppository of Gynergen.Ò She has full memory of the following 10 to 12 hours. Then 15 to 20 minutes following the intake of another suppository, sudden and total amnesia occurred and continued for the following 12 hours. Her husband found her disoriented, and asking the same questions repeatedly. She was initially admitted to the local hospital and was found oriented with regard to personal data, but not to time and place. She had no memory of the events that day. The following day her behavior was
Table 1 Summary of Clinical Data in Five Migraine Patients with Transient Global Amnesia Case Neurological Other Laboratory No. Examination EEG Data 1. Normal Mild diffuse nonspecif. abn. 2. Normal Left temporal theta Brainscan normal with scattered sharp-waves 3. Normal Normal Brainscan and CT-scan both normal 4. Normal Left temporal theta Brainscan normal activity with scattered sharp-waves 5. Slight Irregular left CT-scan: central and right-sided temp. delta focus cortical atrophy. Infarction hemiparesis in left thalamus.
normal. On admission to our department, neurological examination was normal: BP: 160/90 mm Hg.; fasting plasma glucose, normal. The results of special investigations are summarized in Table 1. Patient No. 3. 45-year-old woman without a family history of migraine. Within the last 8 years she had experienced 5 attacks of headache - each preceded by photopsia in the total visual fields, lasting one hour, followed by diffuse throbbing headache, nausea and vomiting. Some years ago, for a 3 month period, intermittent paraesthesias were experienced in both legs and left half of the face. 5 years and 11/2 years before admission, obtundation of consciousness had occurred, lasting a few hours, during which the patient had difficulty distinguishing between fantasy and reality and could not think clearly. She continuously asked a friend if she had talked nonsense. Both episodes were followed by headache and nausea, but no permanent amnesia. Two weeks before admission she had suddenly lost memory for a 12 hour period. Immediately after a hot shower she felt uncomfortable and asked the same questions repeatedly; the family answered patiently each time. She complained of headache, nausea and polyuria during the amnesic period. The following day she was completely normal. On admission, she was found to be a little sensitive psychologically but neurological examination was normal. Special investigations are summarized in Table 1. Patient No. 4. 34-year-old woman having a mother and one sister with migraine. She has had a tendency to vasomotor rhinitis since puberty and from school-age, attacks of migraine with intervals of weeks to months. The attacks may be provoked by tiredness or alcohol ingestion. They started with an indisposed feeling, flickering before the eyes and was followed by half-sided stabbing headache, nausea, diarrhoea and vomiting. The attacks usually last for 1 or 2 days and are occasionally accompanied by paraesthesias in both hands. Over a period of several years she would experience rare fainting, often preceded by blackening of her vision but with no associated epileptic stigmata. During the later years she has had episodes of sudden, total amnesia occurring 4 to 5 times a year, each lasting for several hours. Four months before admission amnesia occurred suddenly following the consumption of 6 to 8 drinks. The amnesia lasted until admission to the local hospital, two hours later. She was found to be awake and alert, but her blood alcohol level was elevated. The neurological examination was found to be normal, on admission. The BP was 120/80 mm Hg. For special investigations see Table 1. Patient No. 5. 67-year-old woman having mother and two children with migraine. For 4 years she was treated for diabetes mellitus and myxoedema. Both conditions were well-regulated on glibenclamide (DaonilÒ) and L-thyroxin sodium (EltroxinÒ). From age 8 years, having intervals of days to months, she suffered from left-sided throbbing headaches, preceded by 15 to 20 minute episodes of photopsia, gyratory vertigo and nausea and sometimes vomiting. Twelve years previously, she was admitted to the department because of severe attacks. Vertebral angiography was normal. Five years ago she had experienced sudden right-sided hemiplegia, which cleared in a couple of days. A slight residual clumsiness of the right arm was noted. Three weeks before admission she had a severe attack of migraine. One half hour later, amnesia occurred and lasted for 16 to 18 hours. During this period, the family found her confused, but the following day she was again alert and mentally clear, although she still complained of some impairment of memory for the next 14 days. On admission, a slight right-sided central facial
weakness and right-sided dysdiadochokinesia was found. No other abnormal neurological findings were noted. BP: 180/80 mm Hg. Fasting blood glucose: 212-272 mg%. Further investigations are summarized in the table. DISCUSSION In TGA as in some amnesic syndromes there seems to exist a transient, specific disturbance of short-term memory with loss of the ability to learn. It is generally believed that a dominating role is played by the corpora mamillaria and the hippocampus in the incorporation of new memory traces in the brain.9,10 Thus, destruction of both hippocampal regions leads to a profound defect in short-term memory and a long retrograde amnesia. These structures, however, do not seem to play any essential role for the preservation of memory traces when first established.9 TGA is not an etiological entity. In recent years most authors have disagreed with the original proposal of Fisher and Adams,2 that it could be a special form of epilepsy. Many are now of the opinion, that TGA may be the result of transitory cerebral ischemia in the posterior circulation of the brain, especially in the hippocampal regions, that are supplied by the posterior cerebral artery.7.8,10 TGA has previously been mentioned in the context of migraine, occurring either as part of the aura of "classical" migraine or as a migraine equivalent.11,12 Among Fischer and Adams2 17 patients with TGA, a 62-year-old man with "classic" migraine, had experienced several isolated attacks of transient homonymous hemianopsia preceding amnesic episodes, for several years. Similar cases have been described by others.1,13 Recently Caplan et al14 in a short congress report have briefly mentioned 7 patients with TGA, 6 of whom had "classic" and one "common" migraine. In four patients transient global amnesia occurred in the preheadache phase, while in one patient it occurred simultaneously with the headache. The data of our patients are summarized in Table 2. Four patients had "classic" and one, "common" migraine. Two patients (Nos. 4 and 5) had a typical vertebro-basilar migraine, while two patients had previously experienced transitory neurological symptoms compatible with transitory circulatory disturbances in the vertebro-basilar arterial systems (Nos. 1 and 3). In two cases, the amnesic episodes were not related to typical attacks of headache. In one it occurred after an attack of headache, and in two, during migraine attacks. Basilar artery migraine is a well-known syndrome, first described by Bickerstaff.15 Besides headache, the dominant symptoms are vertigo, bilateral fortification spectra, paraesthesia in the hands and/or around the mouth, dysarthria and sometimes drop-attacks. The same combination of symptoms may be seen in vertebro-basilar arterial insufficiency, either of arterio-sclerotic origin or occurring as a complication to vertebral angiography. Dynamic studies of cerebral blood flow in migraine patients have shown that there is a reduction of regional cerebral blood flow in the prodromal phase, while the headache phase is accompanied by a marked increase of cerebral blood flow.16 It is reasonable to believe that similar flow changes occur in the vertebro-basilar arterial system in some patients, especially in those with clinical symptoms pointing to transitory disturbances of function in the brain stem and occipital lobes (regions not accessible to measurements of regional blood flow). This hypothesis is further strengthened by indirect evidence from the studies of Hauge,17 on complications of vertebral angiography. He found that many patients developed unilateral headache during the procedure that was clinically indistinguishable from migraine.
Case No. 1.
2. 3.
4. 5.
Table 2 Summary of Clinical Data in Five Migraine Patients with Transient Global Amnesia Amnesia Migraine Previous Vascular Precipitating Age and Sex Type Cerebral Symptoms Duration Factors Headache 59, F Common Shortlasting forti6 hrs. None fication spectra last 3 years 58, F Classic 12 hrs. Ergotamin? During 45, F Classic 7 years ago: 12 hrs. Hot shower After paraesthesia in legs and face for 3 months 34, F Classic Some attacks 2 hrs. Alcohol? None (v-b) of fainting 67, F Classic 4 years ago: 16-18 hrs. During (v-b) right-sided hemiparesis
v-b:vertebro-basilar migraine
Previous Attacks
2 (partial)
Several
Other transitory disturbances were vertigo, disturbances of vision, dysarthria, varying paraesthesia and various mental changes, inter alia amnesia. The arteriographic picture often suggested vasospasm. We have had similar experiences in patients undergoing vertebral angiography, including amnesic periods of hours duration and cortical blindness lasting for 24 to 48 hours. These investigations thus imply that the pathogenesis of the migrainous attacks in this connection is vasospasm in the vertebro-basilar arterial system, including transitory ischemic lesions in the distribution of the posterior cerebral arteries. Considering the clinical and other indirect evidence, we find that TGA in our patients was probably due to transitory ischemia in the mamillo-hippocampal regions, secondary to shortlasting vasospasm in the vertebro-basilar arterial system, especially affecting the arteries supplying mesial and basal parts of the temporal regions. TGA in migraine is a benign condition, which does not usually require extensive neuroradiological investigations. REFERENCES 1.
Evans JH: Transient loss of memory, an organic mental syndrome, Brain 89:539-548, 1966.
2.
Fisher CM and Adams RD: Transient global amnesia. Acta Neurol Scand Suppl 9, 40:7-83, 1964.
3.
Symonds C: Disorders of memory. Brain 89:625-644, 1966.
4.
Bolwig TG: Transient global amnesia. Acta Neurol Scand 44:127-135, 1968.
5.
Bender MB: Single episode of confusion with amnesia. Bull NY Acad Med 36:197-207, 1960.
6.
Fisher CM and Adams RD: Transient global amnesia. Trans Amer Neurol Ass 83:143-146, 1958.
7.
Heathfield KWG, Croft PB and Swash M: The syndrome of transient global amnesia. Brain 96:729-736, 1973.
8.
Steinmetz EF and Vroom FQ: Transient global amnesia. Neurology 22:1193-1200, 1972.
9.
Barbizet J: Defect of memorizing of hippocampal-mamillary origin: A review. J Neurol Neurosurg Psychiat 26:127-135, 1963.
10.
Whitty CWM and Lishman WA: Amnesia in cerebral disease, in Whitty CWM and Zangwill OL (ed.): Amnesia, London, Butterworth, 1966, pp 36-76.
11.
Moersch FP: Psychic manifestations in migraine. Amer J Psychiatry 80:697-716, 1924.
12.
Nielsen JM: Migraine equivalent. Amer J Psychiatry 9:637-641, 1930.
13.
Gilbert JJ and Benson DF: Transient global amnesia: Report of two cases with definite etiologies. J Nerv Ment Dis 154:461-464, 1972.
14.
Caplan LR, Chedru F and Lhermitte F: Transient global amnesia and migraine. Neurology. (Abstract), 387, 1978.
15.
Bickerstaff ER: Basilar artery migraine. Lancet 2:15, 1961.
16.
Skinhøj E: Hemodynamic studies within the brain during migraine. Arch Neurol 29:95-98, 1973.
17.
Hauge T: Catheter vertebral angiography. Acta Radiol (Stockholm), (Suppl) 109:1-219, 1954.
Transient Global Amnesia in Migraine Bent de Fine Olivarius and Troels Staehelin Jensen The University Department of Neurology, Aarhus Kommunehospital, Aarhus, Denmark. Parts of this paper were presented at the Scandinavian Migraine Society, Annual Meeting, Scanticon, Aarhus, Denmark, Sept. 1978. Reprint requests to: Bent de Fine Olivarius, M.D., The University Department of Neurology, Aarhus Kommune-hospital, DK-8000 Aarhus C Denmark. Accepted for Publication: June 7, 1979 SYNOPSIS The clinical features of five migraine patients, suffering one to several episodes of transient global amnesia (TGA), were evaluated. All patients were women, with an age range of 34 to 67 years. One patient had common, and four, classical migraine. Two patients had typical vertebro-basilar migraine; two others had previously experienced transitory neurological symptoms compatible with transitory circulatory disturbances in the vertebro-basilar arterial system. On the basis of these data and available literature, the pathophysiological mechanisms are discussed. It is suggested that in our patients, TGA was due to transitory ischemia in the mamillo-hippocampal formation, secondary to shortlasting vasospasms in the arteries supplying mesial and basal parts of the temporal lobes. It was concluded that TGA in migraine is a benign condition, and does not usually require extensive neuroradiological investigations. (Headache 19:335-338, 1979) Transient global amnesia (TGA) is a suddenly occurring amnesic syndrome clinically characterized by a profound disturbance of short-term memory with preservation of immediate recall and of long-term memory. The amnesic episodes, often affecting elderly persons is usually shortlasting, and apart from a slight confusion is rarely accompanied by other neurological or intellectual disturbances.1,2 After the attack there is usually some retrograde amnesia, rarely of more than a few hours duration.3,4 Since the original description of Bender5 and Fisher and Adams6 TGA has been mentioned in connexion with various pathological conditions. An unequivocal etiology or specific pathogenesis has not been delimited, although several authors have regarded a vascular pathology most probable.7,8 We find it of some interest to report on 5 patients having a combination of TGA and migraine, since the syndrome has been reported rarely in association with migraine. The simultaneous occurrence of TGA and migraine may point to a distinct pathogenesis for the syndrome in such patients. CASE HISTORIES Patient No. 1. 59-year-old woman without a family history of migraine. Since childhood attacks of diffuse pinching headache associated with pronounced photo-and phonophobia, nausea, more rarely vomiting. Attacks have occurred with intervals of weeks to months and last for up to 24 hours. For the last three years she has experienced 3 attacks of spontaneously occurring fortification lines and coloured spots before both eyes, but without headache. 10 days before admission she experienced sudden loss of memory for 6 hours. She moved quite naturally around in her home but several times told the family, that "everything felt strange". The following day her memory was intact but she felt tired and indisposed with loss of initiative, which continued for some days. On admission, neurological examination was normal. BP: 170/110-150/80 mm Hg. Special investigations are summarized in Table 1. Patient No. 2. 58-year-old woman without a family history of migraine. Since the age of 25 she had suffered from attacks of unilateral, shooting headache on either side, and accompanied by nausea, vomiting, photo- and phonophobia. Previously attacks occurred on weekends, for the past three years every 2 or 3 weeks. Some years ago she had consumed considerable amounts of ergotamine (GynergenÒ comp.). 14 days before admission she awakened in the morning with headache which had subsided following the administration of one suppository of Gynergen.Ò She has full memory of the following 10 to 12 hours. Then 15 to 20 minutes following the intake of another suppository, sudden and total amnesia occurred and continued for the following 12 hours. Her husband found her disoriented, and asking the same questions repeatedly. She was initially admitted to the local hospital and was found oriented with regard to personal data, but not to time and place. She had no memory of the events that day. The following day her behavior was
Table 1 Summary of Clinical Data in Five Migraine Patients with Transient Global Amnesia Case Neurological Other Laboratory No. Examination EEG Data 1. Normal Mild diffuse nonspecif. abn. 2. Normal Left temporal theta Brainscan normal with scattered sharp-waves 3. Normal Normal Brainscan and CT-scan both normal 4. Normal Left temporal theta Brainscan normal activity with scattered sharp-waves 5. Slight Irregular left CT-scan: central and right-sided temp. delta focus cortical atrophy. Infarction hemiparesis in left thalamus.
normal. On admission to our department, neurological examination was normal: BP: 160/90 mm Hg.; fasting plasma glucose, normal. The results of special investigations are summarized in Table 1. Patient No. 3. 45-year-old woman without a family history of migraine. Within the last 8 years she had experienced 5 attacks of headache - each preceded by photopsia in the total visual fields, lasting one hour, followed by diffuse throbbing headache, nausea and vomiting. Some years ago, for a 3 month period, intermittent paraesthesias were experienced in both legs and left half of the face. 5 years and 11/2 years before admission, obtundation of consciousness had occurred, lasting a few hours, during which the patient had difficulty distinguishing between fantasy and reality and could not think clearly. She continuously asked a friend if she had talked nonsense. Both episodes were followed by headache and nausea, but no permanent amnesia. Two weeks before admission she had suddenly lost memory for a 12 hour period. Immediately after a hot shower she felt uncomfortable and asked the same questions repeatedly; the family answered patiently each time. She complained of headache, nausea and polyuria during the amnesic period. The following day she was completely normal. On admission, she was found to be a little sensitive psychologically but neurological examination was normal. Special investigations are summarized in Table 1. Patient No. 4. 34-year-old woman having a mother and one sister with migraine. She has had a tendency to vasomotor rhinitis since puberty and from school-age, attacks of migraine with intervals of weeks to months. The attacks may be provoked by tiredness or alcohol ingestion. They started with an indisposed feeling, flickering before the eyes and was followed by half-sided stabbing headache, nausea, diarrhoea and vomiting. The attacks usually last for 1 or 2 days and are occasionally accompanied by paraesthesias in both hands. Over a period of several years she would experience rare fainting, often preceded by blackening of her vision but with no associated epileptic stigmata. During the later years she has had episodes of sudden, total amnesia occurring 4 to 5 times a year, each lasting for several hours. Four months before admission amnesia occurred suddenly following the consumption of 6 to 8 drinks. The amnesia lasted until admission to the local hospital, two hours later. She was found to be awake and alert, but her blood alcohol level was elevated. The neurological examination was found to be normal, on admission. The BP was 120/80 mm Hg. For special investigations see Table 1. Patient No. 5. 67-year-old woman having mother and two children with migraine. For 4 years she was treated for diabetes mellitus and myxoedema. Both conditions were well-regulated on glibenclamide (DaonilÒ) and L-thyroxin sodium (EltroxinÒ). From age 8 years, having intervals of days to months, she suffered from left-sided throbbing headaches, preceded by 15 to 20 minute episodes of photopsia, gyratory vertigo and nausea and sometimes vomiting. Twelve years previously, she was admitted to the department because of severe attacks. Vertebral angiography was normal. Five years ago she had experienced sudden right-sided hemiplegia, which cleared in a couple of days. A slight residual clumsiness of the right arm was noted. Three weeks before admission she had a severe attack of migraine. One half hour later, amnesia occurred and lasted for 16 to 18 hours. During this period, the family found her confused, but the following day she was again alert and mentally clear, although she still complained of some impairment of memory for the next 14 days. On admission, a slight right-sided central facial
weakness and right-sided dysdiadochokinesia was found. No other abnormal neurological findings were noted. BP: 180/80 mm Hg. Fasting blood glucose: 212-272 mg%. Further investigations are summarized in the table. DISCUSSION In TGA as in some amnesic syndromes there seems to exist a transient, specific disturbance of short-term memory with loss of the ability to learn. It is generally believed that a dominating role is played by the corpora mamillaria and the hippocampus in the incorporation of new memory traces in the brain.9,10 Thus, destruction of both hippocampal regions leads to a profound defect in short-term memory and a long retrograde amnesia. These structures, however, do not seem to play any essential role for the preservation of memory traces when first established.9 TGA is not an etiological entity. In recent years most authors have disagreed with the original proposal of Fisher and Adams,2 that it could be a special form of epilepsy. Many are now of the opinion, that TGA may be the result of transitory cerebral ischemia in the posterior circulation of the brain, especially in the hippocampal regions, that are supplied by the posterior cerebral artery.7.8,10 TGA has previously been mentioned in the context of migraine, occurring either as part of the aura of "classical" migraine or as a migraine equivalent.11,12 Among Fischer and Adams2 17 patients with TGA, a 62-year-old man with "classic" migraine, had experienced several isolated attacks of transient homonymous hemianopsia preceding amnesic episodes, for several years. Similar cases have been described by others.1,13 Recently Caplan et al14 in a short congress report have briefly mentioned 7 patients with TGA, 6 of whom had "classic" and one "common" migraine. In four patients transient global amnesia occurred in the preheadache phase, while in one patient it occurred simultaneously with the headache. The data of our patients are summarized in Table 2. Four patients had "classic" and one, "common" migraine. Two patients (Nos. 4 and 5) had a typical vertebro-basilar migraine, while two patients had previously experienced transitory neurological symptoms compatible with transitory circulatory disturbances in the vertebro-basilar arterial systems (Nos. 1 and 3). In two cases, the amnesic episodes were not related to typical attacks of headache. In one it occurred after an attack of headache, and in two, during migraine attacks. Basilar artery migraine is a well-known syndrome, first described by Bickerstaff.15 Besides headache, the dominant symptoms are vertigo, bilateral fortification spectra, paraesthesia in the hands and/or around the mouth, dysarthria and sometimes drop-attacks. The same combination of symptoms may be seen in vertebro-basilar arterial insufficiency, either of arterio-sclerotic origin or occurring as a complication to vertebral angiography. Dynamic studies of cerebral blood flow in migraine patients have shown that there is a reduction of regional cerebral blood flow in the prodromal phase, while the headache phase is accompanied by a marked increase of cerebral blood flow.16 It is reasonable to believe that similar flow changes occur in the vertebro-basilar arterial system in some patients, especially in those with clinical symptoms pointing to transitory disturbances of function in the brain stem and occipital lobes (regions not accessible to measurements of regional blood flow). This hypothesis is further strengthened by indirect evidence from the studies of Hauge,17 on complications of vertebral angiography. He found that many patients developed unilateral headache during the procedure that was clinically indistinguishable from migraine.
Case No. 1.
2. 3.
4. 5.
Table 2 Summary of Clinical Data in Five Migraine Patients with Transient Global Amnesia Amnesia Migraine Previous Vascular Precipitating Age and Sex Type Cerebral Symptoms Duration Factors Headache 59, F Common Shortlasting forti6 hrs. None fication spectra last 3 years 58, F Classic 12 hrs. Ergotamin? During 45, F Classic 7 years ago: 12 hrs. Hot shower After paraesthesia in legs and face for 3 months 34, F Classic Some attacks 2 hrs. Alcohol? None (v-b) of fainting 67, F Classic 4 years ago: 16-18 hrs. During (v-b) right-sided hemiparesis
v-b:vertebro-basilar migraine
Previous Attacks
2 (partial)
Several
Other transitory disturbances were vertigo, disturbances of vision, dysarthria, varying paraesthesia and various mental changes, inter alia amnesia. The arteriographic picture often suggested vasospasm. We have had similar experiences in patients undergoing vertebral angiography, including amnesic periods of hours duration and cortical blindness lasting for 24 to 48 hours. These investigations thus imply that the pathogenesis of the migrainous attacks in this connection is vasospasm in the vertebro-basilar arterial system, including transitory ischemic lesions in the distribution of the posterior cerebral arteries. Considering the clinical and other indirect evidence, we find that TGA in our patients was probably due to transitory ischemia in the mamillo-hippocampal regions, secondary to shortlasting vasospasm in the vertebro-basilar arterial system, especially affecting the arteries supplying mesial and basal parts of the temporal regions. TGA in migraine is a benign condition, which does not usually require extensive neuroradiological investigations. REFERENCES 1.
Evans JH: Transient loss of memory, an organic mental syndrome, Brain 89:539-548, 1966.
2.
Fisher CM and Adams RD: Transient global amnesia. Acta Neurol Scand Suppl 9, 40:7-83, 1964.
3.
Symonds C: Disorders of memory. Brain 89:625-644, 1966.
4.
Bolwig TG: Transient global amnesia. Acta Neurol Scand 44:127-135, 1968.
5.
Bender MB: Single episode of confusion with amnesia. Bull NY Acad Med 36:197-207, 1960.
6.
Fisher CM and Adams RD: Transient global amnesia. Trans Amer Neurol Ass 83:143-146, 1958.
7.
Heathfield KWG, Croft PB and Swash M: The syndrome of transient global amnesia. Brain 96:729-736, 1973.
8.
Steinmetz EF and Vroom FQ: Transient global amnesia. Neurology 22:1193-1200, 1972.
9.
Barbizet J: Defect of memorizing of hippocampal-mamillary origin: A review. J Neurol Neurosurg Psychiat 26:127-135, 1963.
10.
Whitty CWM and Lishman WA: Amnesia in cerebral disease, in Whitty CWM and Zangwill OL (ed.): Amnesia, London, Butterworth, 1966, pp 36-76.
11.
Moersch FP: Psychic manifestations in migraine. Amer J Psychiatry 80:697-716, 1924.
12.
Nielsen JM: Migraine equivalent. Amer J Psychiatry 9:637-641, 1930.
13.
Gilbert JJ and Benson DF: Transient global amnesia: Report of two cases with definite etiologies. J Nerv Ment Dis 154:461-464, 1972.
14.
Caplan LR, Chedru F and Lhermitte F: Transient global amnesia and migraine. Neurology. (Abstract), 387, 1978.
15.
Bickerstaff ER: Basilar artery migraine. Lancet 2:15, 1961.
16.
Skinhøj E: Hemodynamic studies within the brain during migraine. Arch Neurol 29:95-98, 1973.
17.
Hauge T: Catheter vertebral angiography. Acta Radiol (Stockholm), (Suppl) 109:1-219, 1954.
