Transient Global Amnesia Precipitated by Emotion in an Adolescent Phillip J. Tirman, MD; Robert C. Woody, MD Abstract Transient global amnesia has been reported to be precipitated by intense emotion in adult patients. Transient global amnesia is uncommon in the pediatric age group. We report the unusual occurrence of this syndrome, apparently precipitated on two occasions by emotion, in an adolescent who had earlier in life suffered a left temporal and occipital lobe embolic infarction from congenital heart disease. Transient global amnesia following intense emotion may be a cause of some confusional states in children and adolescents. ( J Child Neurol 1988;3:185-188). Transient global amnesia is rare in the pediatric age group. This syndrome, which usually affects middle-aged and elderly persons, was first redescribed in ported by Bender in 19561 and further 2 1964.2 and Adams in detail by Fisher Transient global amnesia consists of a sudden anterograde amnesia (inability to acquire new information), an associated retrograde amnesia (inability to remember recent events), and unaffected immediate and remote memory.2,3,4 The amnesia lasts less than 24 hours and recurrences are infrequent.5,6 Many attacks of transient global amnesia are accompanied by anxiety about the amnesia, but other neurologic signs are conspicuously absent. Transient global amnesia has been identified in which antecedent events &dquo;triggered&dquo; the amnesia. Some of the precipitants have included immersion in cold water, sexual intercourse, physical pain or exertion, and disturbing emotional events 2,4,5,6,7 Recently the clinical characteristics and prognosis of 277 adult patients with transient global amnesia were extensively re8 portend. We present a 17-year-old patient who experienced Received June 19, 1987. Received revised July 17 and Sept 4, 1987. Accepted for publication Sept 9, 1987. From the Departments of Pediatrics, Neurology and Psychiatry, University of Arkansas for Medical Sciences and Arkansas Children’s Hospital, Little Rock, AR. Address correspondence to Dr Robert C. Woody, University of Arkansas for Medical Sciences, Little Rock, AR 72205. transient global amnesia on two occasions following psychologically stressful events. Case Report A 17-year-old left-handed male was evaluated following two episodes of behavioral and memory disturbances. The first episode occurred at 15 years of age when he was admitted to a local hospital with acute appendicitis. Two hours before surgery, while resting comfortably in the hospital room, before premedication had been given, the patient suddenly appeared frightened and confused. He began to question his mother &dquo;What am I doing here?&dquo; &dquo;What is happening to me?&dquo; &dquo;How did I get here?&dquo; After seeing an speaking to his grandmother, who then stepped out of the room, he asked when his grandmother was arriving. After these questions were answered and the patient was reassured by his mother he would repeat the same questions. During this episode the patient retained recognition of self and of his family. The episode lasted until surgery. Postoperatively the patient appeared normal with complete resolution of symptoms except for a retrograde amnesia for the two- to three-hour period prior to surgery. The second episode of transient global amnesia occurred six months later on the day of the Space Shuttle Challenger’s explosion on January 28, 1986. The patient was eating in the den at home and watching the television coverage of the explosion, when he suddenly appeared frightened and unaware of what he had been doing. He asked how and when he had gotten to the chair in which he was sitting, if he had already eaten dinner, what time it was, and what he had been doing within the last hour. Some questions were repeatedly asked every five to ten minutes. The entire amnestic episode lasted approximately three hours with gradual resolution except for amnesia of the event itself. During both episodes he had no headaches, dizziness, visual disturbance, speech or language distur- 185 Downloaded from jcn.sagepub.com at OAKLAND UNIV on June 6, 2015 bance, pallor, or other complaints. No other signs or symptoms of complex partial seizures or migraine occurred. His past medical history was significant for congenital aortic valvular stenosis. At age 6 years he had an embolus from aortic valvular endocarditis leading to infarction of the left occipital and mesial temporal lobe. That stroke was manifested by weakness of the right leg and tremor of the right arm, but no identifiable disturbances of language or of visual or mental status. His aortic valve was replaced at 7 years of age. He had no further transient ischemic attacks, headaches, seizures, trauma, or meningitis. The patient was maintained on warfarin therapy to prevent recurrent emboli from his aortic valve. His family history included no members of the family with migraines, cardiovascular disease, or neuropsychiatric disturbances. The physical examination at the time of neurologic evaluation was significant for a grade II/Vl systolic murmur best heard at the right second intercostal space, radiating to the axilla and back. On physical examination, there was no evidence of embolic or vasculitic disease. Formal neurologic examination revealed a dense right homonymous hemianopsia, but no other abnormalities. The mental status examination was normal including immediate, recent, and remote memory, speech and language, affect and mood, and judgment and cognition. Cerebral arteriography revealed an abrupt cutoff of the left posterior cerebral artery. No posterior communicating arteries were visualized. Computed tomography (CT) with contrast injection revealed porencephaly of the left FIGURE 1 CT scan demonstrating left mesial occipital lobe porencephaly and ex vacuo enlargement of the occipital horn. mesial occipital lobe and enlargement of the left lateral ventricular occipital horn. The left mesial temporal lobe appeared atrophic (Figure 1). Magnetic resonance imaging revealed decreased signal intensity in the left mesial occipital lobe using Ti-weighted images which became increased using T,-weighted images (Figure 2). An awake and asleep electroencephalogram (EEG) demonstrated no evidence of epileptiform activity or significant slowing. A 24-hour, four-lead ambulatory EEG was performed, which revealed no epileptiform activity. The patient was discharged on warfarin. In the last 12 months he has had no further episodes of seizures, transient ischemic attacks, transient global amnesia, or other ictal events. Discussion Neuroradiographic studies in this adolescent demonstrated that he had pre-existing congenital and acquired anatomical cerebrovascular defects that might have predisposed him to the development of transient global amnesia. Arteriography revealed the absence of the posterior communicating arteries, a congenital vascular anomaly in the Circle of Willis. Such anomalies are common, with only 50% of the population having a &dquo;normal&dquo; configuration.9 Anom- FIGURE 2 MRI with T,-weighted images demonstrating left mesial occipital and temporal lobe porencephaly. 186 Downloaded from jcn.sagepub.com at OAKLAND UNIV on June 6, 2015 alies of the Circle of Willis such as this are associated with a higher incidence of cerebrovascular accidents, since collateral flow cannot rapidly be established in the case of sudden obstruction of another vessel. This anomaly would become clinically significant if an additional acquired insult to the Circle of Willis occurred. In this patient, presumably emboli from his damaged aortic valve lodged in the left posterior cerebral artery, infarcting the tissue supplied by this artery. Since an intact Circle of Willis was not present, collateral flow was not possible and tissue infarction of the occipital and mesial temporal lobes occurred. We could not prove that recurrent emboli precipitated the transient global amnesia episodes. The patient was appropriately anticoagulated prior to the transient global amnesia episodes, and it would seem unlikely that recurrent emboli entered the posterior cerebral artery circulation on two more occasions, since hemodynamic factors generally favor left ventricular or aortic emboli preferentially flowing to the anterior circulation, in particular, the middle cerebral vessels. Transient global amnesia associated with posterior cerebral artery infarction in adults appears particularly unusual; transient global amnesia did not occur in one series of 350 posterior cerebral artery stroke cases (C Miller Fisher, personal communication, 1987). The fact that the patient had pre-existing left mesial temporal lobe pathology is significant. Recent memory is carried out in the mesial temporal lobes, in particular in the hippocampal formations. Unilateral injury to the right hippocampal formation will not result in loss of recent memory. Amnesia can occur transiently following unilateral left hippocampal lesions. Transient or lasting injury to either mesial temporal lobe when the contralateral mesial temporal lobe has already been damaged will often cause recent memory loss. Transient global amnesia is a recent memory disturbance, which generally occurs in adults and only rarely in the pediatric age group. The pathophysiologic basis of transient global amnesia is unclear. Since it usually occurs in a patient population prone to arteriosclerotic cerebrovascular disease, bilateral arterial insufficiency to the mesial temporal lobes produced by either extracranial (for example, vertebral arteriosclerotic plaques or left ventricular or aortic valvular emboli) or intracranial arteriosclerotic disease is a possible Migrainous changes in vessels supplying the mesial temporal lobes might also cause transient global amnesia.3,5,13,14 The mesialI temporal lobes are particularly prone to epileptiform activity. Epileptiform activity in the hippocampal formation has been implicated as a possible cause of explanation.3,4,10-12 transient global amnesia and has prompted the use of anticonvulsant therapy in some patients. 5, 13,15-17 EEG recordings during episodes of transient global amnesia have failed to document epileptiform activity, and only mild or moderate and nonfocal abnormalities have been observed in a minority of patients following transient global amnesia. 14,18 Transient global amnesia has also been reported to be associated with a variety of other conditions or procedures including polycythemia, &dquo;,’3 migraine, 19 tumors of the mesial diazepam toxitemporal lobes, 20,21 digitalis cardiac cerebral and arteriography,24 arterial City,23 subtraction angiography,25 myxomatous dedigital mitral of the valve,lo and arterial embogeneration lism.26 Of the rare reported cases of transient global amnesia in childhood, a 16-year-old male developed transient global amnesia lasting nine hours during an all-night hike during which he became cold and drenched in the rain.6 Dinsmore and Callender suggested that exposure to the cold precipitated transient global amnesia in the boy. Acute confusional migraine, a condition relatively more common in the pediatric age group than in adults, exhibits similarities with transient global amnesia. In acute confusional migraine, the child develops an agitated confusion, with or without other signs or symptoms of migraine. The spells may be associated with amnesia for the episode .27-29 Although the neuroanatomic basis for acute confusional migraine is not known, it is reasonable that bilateral posterior cerebral artery migrainous activity could present with both agitated confusion and amnesia. Fisher described 78 patients, 48 to 84 years of age, who developed a total of 85 episodes of transient global amnesia.’ Of these 85 episodes, 26 were associated with an unusual precipitating event. These toxicity,22 events were usually emotionally or physically painful, related to sexual intercourse (7 of 26), or followed diving into the cold waters off the north Atlantic Ocean coast (3 of 26). Examples cited by Fisher of emotionally painful precipitants included a man robbed and handcuffed by thieves, a woman tearfully reconciled with her daughter who had run away, a woman whose husband died before her eyes, a man forced to resign his long-held job, a woman having a bitter fight with her husband, and others. All of Fisher’s patients developed transient global amnesia in close proximity to the emotionally stressful event. Fisher speculated that this association of pain, emotion, and temperature precipitating transient global amnesia might have a common anatomic explanation. Both emotion and memory share a similar neuroanatomic territory. Since both emotion and 187 Downloaded from jcn.sagepub.com at OAKLAND UNIV on June 6, 2015 memory share these structures anatomically and, presumably, physiologically, intense afferent input might reasonably be expected to alter the orderly processing of recent memory. 13. Crowell F, Stump DA, Biller J, et al: The transient global amnesia-migraine connection. Arch Neurol 1984;41:75-79. 14. Jaffe R, Bender MB: EEG studies in the syndrome of isolated episodes of confusion with amnesia ’transient global amnesia. J Neurol Neurosurg Psychiatry 1966;29:472-474. 15. Cantor F: Transient global amnesia and temporal lobe seizures. Nevrology 1985;31:430-431. 16. Deisenhammer E: Transient global amnesia Acknowledgment The authors thank Dr C. Miller Fisher for his valuable suggestions used in the preparation of this manuscript. as an epileptic manifestation.J Neurol 1981;225:289-292. 17. Pritchard PB, Holmstrom VL, Roltzsch JC, et al: Epileptic amnesia attacks: Benefits from antiepileptic drugs. Neurology 1985;35:1185-1189. 3. Scand 1964;40(Suppl 19):7-82. Jensen TR: Transient global amnesia in childhood. Dev Med 18. Miller JW, Yanagihara T, Petersen RC, et al: Transient global amnesia and epilepsy: Electroencephalographic distinction. Arch Neurol 1987;44:629-633. 19. Caplan L, Chedru F, Chermitte F: Transient global amnesia and migraine. Neurology 1981;31:1167-1170. 20. Hartley TC, Hellman KM, Garci-Bengochea F: A case of transient global amnesia due to a pituitary tumor. Neurology 4. Child Neurol 1980;22:654-657. Logan W, Sherman G: Transient 21. Lisak RP, Zimmerman RA: Transient global amnesia due to a References 1. Bender MD: Syndrome of isolated episode of confusion with amnesia.J Hillside Hosp 1956;5:212-215. 2. Fisher CM, Adams RD: Transient global amnesia. Acta Neurol 1974;24:998-1000. global amnesia. Stroke 1983;14:1005-1006. 5. Fisher CM: Transient global amnesia: Precipitating activities and other observations. Arch Neurol 1982;39:605-608. 6. Dinsmore WW, Callender ME: Juvenile transient global amnesia.J Neurol Neurosurg Psychiatry 1983;46:876-877. Mayeux R: Sexual intercourse and transient global amnesia. N EnglJ Med 1979;300:864. 8. 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Reichter RE, Belt TG: Transient global amnesia: Complication of arterial DSA. AJNR 1986;7:179-180. 26. Shuttleworth EC, Wise GR: Transient global amnesia due to arterial embolism. Arch Neurol 1973;29:340-342. 27. Ehyai A, Fenichel GM: The natural history of acute confusional migraine. Arch Neurol 1978;35:368-369. 28. Emery ES: Acute confusional state in children with migraine. Pediatrics 1977; 60:539-548. 29. Gascon G, Barlow C: Juvenile migraine presenting as an acute confusional state. Pediatrics 1970;45:628-635. 188 Downloaded from jcn.sagepub.com at OAKLAND UNIV on June 6, 2015