Psychonomic Bulletin & Review 1998,5 (3), 401-427

Transient global amnesia

ALANS. BROWN Southern Methodist University, DaUas, Texas

Transient global amnesia (TGA) is a memory dysfunction characterized by a sudden onset of dense anterograde amnesia (AA)that gradually resolves across several hours. TGAis typically accompanied by repeated questions (concerning present circumstances) with retrograde amnesia for events pre­ ceding the attack, and it usually strikes individuals in their late 50s and early 60s. The etiology of TGA remains unclear, although it probably reflects a temporary disruption of the blood supply to the tem­ porallobe. The physical and psychological events preceding the attack are diverse, but they often in­ clude acute emotional and physical stressors. TGAappears to be benign, with low risk for recurrence or residual complications. While systematic memory research on TGApatients is rare, these individu­ als present a unique opportunity to study amnestic behaviors in otherwise normal individuals. A guide to conducting future research is provided.

Over the last 4 decades, a considerable literature has ac­ psychologists to participate in the problem-solving pro­ cumulated concerning transient global amnesia (TGA). cess. The literature will be cited in detail to allow inter­ Originally described by Hague (1954; see Haas, 1983), the ested readers to pursue specific issues with the aid of a term TGA was coined by Fisher and Adams (1958) to de­ complete reference base. However, to enhance the read­ scribe a reversible, short-term (several hour) inability to ability ofthe manuscript, extensive blocks ofreferences store and/or retrieve new information most commonly ob­ will be placed in the notes at the end ofthe article. served in older adults (50-70 years old). Its onset is sud­ The literature on TGA consists ofboth empirical (de­ den, and its resolution is gradual. A period ofretrograde scribing specific TGA episodes) and interpretive (focus­ amnesia (RA) is usually observed, the duration ofwhich ing on a possible etiology; summarizing some dimension is highly variable (hours to years) across individuals and ofthe phenomenon) articles. Empirical articles are com­ shrinks during the recovery period. TGA victims often posed ofcase studies, detailing the TGA episode in one ask the same question(s) repeatedly and are generally con­ or more patients, and group summaries, in which only fused regarding time, place, and circumstances. Despite summary data from a number of TGA patients are pre­ the inability to retain new information, general intellectual sented. (Note that, in the References, case studies are indi­ function (reading, writing, speaking, calculation) and self­ cated by an asterisk [*], and group summary studies identity are preserved, and obvious neurological abnor­ are indicated by a diamond [• ]. Articles that include a malities are absent. Oddly, most TGA victims experience group summary and description ofthe TGA episode for only one episode in a lifetime. TGA appears to be unas­ a subsample of patients are tagged with both symbols. sociated with any obvious physical or psychological dis­ Some of these articles are not specifically cited in the ease process or residual disability, contrasting with other text.) The 150 case-study articles describe a total of488 memory maladies, such as Alzheimer's dementia, Korsa­ individual cases, with the majority ofthese articles (59%) koff's disease, drug addiction, or hysterical fugue states describing only one case. The 51 group articles summa­ (Markowitsch, 1995). rize a total of 2,585 TGA patients, with a mean of 51 pa­ The primary purpose ofthe present review is to acquaint tients per article. behavioral researchers with a common malady that is rel­ atively unknown among psychology professionals. De­ DEFINING TGA spite a large literature on TGA, the phenomenon is poorly understood, and no consensus has emerged on its psycho­ Since the literature on TGA has evolved slowly from logical or physiological cause. The present literature sum­ diverse areas ofmedicine (anesthesiology, neurology, and mary will hopefully allow cognitive, clinical, and health radiology), a methodological anarchy exists in the way TGA is defined and reported. For the most part, research­ ers adhere to the definitional criteria provided by Caplan The author wishes to extend special thanks to Billie Stovall in the In­ (1986b): terlibrary Loan Office of Southern Methodist University for her her­ (I) The attack onset should have been witnessed. (2) Dys­ culean efforts in procuring hundreds ofarticles from medical journals at other universities. The author would also like to thank Michael R. Best, function during the attack should have been limited to repet­ David B. Mitchell, and Leonard R. Gasney for their helpful comments on itive queries and amnesia. (3) There should have been no the manuscript. Correspondence should be sent to A. S. Brown, Depart­ other major neurological signs or symptoms. (4) The mem­ ment ofPsychology, Southern Methodist University, Dallas, TX 75275 ory loss should be transient, usually lasting hours or up to (e-mail: [email protected]). I day.

401 Copyright 1998 Psychonomic Society, Inc. 402 BROWN

Such a definition is designed to rule out other neuro­ for several years, and toward the end of his visit the pa­ logical dysfunctions or traumatic events that can cause tient's memory began to return. The period of permanent amnesia (e.g., stroke). However, some claim that this cri­ amnesia was about two hours. (Heathfield, Croft, & Swash, terion is too strict or premature in this nascent stage of 1973,p.730) research on TGA (Hodges & Warlow, 1990b; Meador, Adams, & Flanigin, 1986; Shuaib, 1986), and the fine DEMOGRAPHY OF TGA points ofthe definitional criteria debate can be found in a series of letters and replies.' As Shuaib (1986) points Incidence out, although restrictions are needed on the definition of The estimate of the incidence of TGA in the general the phenomenon, such exclusionary criteria may work at population is 5.3 per 100,000 people across six studies cross-purposes to ultimately identifying the cause of from four countries (United States, England, Spain, and TGA, given the current state of uncertainty in the field Finlandj.? Among older adults (~50 years), the incidences (see Jain et aI., 1989). In short, no general paradigm or are much higher at 32 (Koski & Marttila, 1990) and 23.5 format has evolved on reporting TGA, as illustrated by (Miller, Petersen, Metter, Millikan, & Yanagihara, 1987) these contrasting case reports: per 100,000. Thus, it appears that the likelihood ofexpe­ riencing a TGA in any given year is roughly 0.005% (1 Case 1 in 20,000 people) in the general population and 0.028% A 60-year-old civil engineer had no family history of (1 in 3,000) among older adults. nervous or mental disease ... On February 21, 1965, he These numbers probably underestimate the actual in­ had spent the day much as usual. In the morning he had cidence of TGA. Because there is minimal physical ab­ been in the garden and had eaten a normal lunch at mid­ normality during the TGA episode and recovery is gener­ day. After lunch he had gone out in his car and spent the ally complete, there may be little motivation to receive next two hours cleaning it ... He then came indoors and his behaviour was perfectly normal in every way and he medical assistance or even report the incident (Bender, went to have a bath and change. He normally took his 1956, 1960; Rollinson, 1978). As Bolwig (1968) cogently baths exceptionally hot and would soak in them for an points out, TGA "is probably more common than would hour or more. On this afternoon he emerged from the bath­ be assumed by the relatively few reports, as many pa­ room after half an hour, correctly dressed in ordinary tients would hesitate to consult a physician for symptoms clothes, but he looked puzzled and upset. His first words that are likely to impress the relatives more than the pa­ were "Am I going mad? I can't remember anything." He tients themselves" (p. 105) (cf. Dinsdale, 1971). Under­ then repeatedly asked a number of questions such as reporting may also be motivated by relatives who inter­ "What day is it? What has happened? What have I been pret the symptoms as reflecting dementia or mental doing? How did this start?" instability (Santoro, Casadei, & Venco, 1988). When a His wife replied to all these questions and he appeared to understand what she said, but he would ask the same wife ofa TGA victim heard him discussing a relative who question a few minutes later. From his behaviour he rec­ had died a year ago as if she were alive, she "grabbed the ognized his wife and knew his way around the house. He telephone and hung it up in an effort to conceal the in­ was brought a cup oftea which he drank normally, but then sanity from the rest ofthe world" (Patten, 1971, p. 690). accused his wife ofdrinking his tea, apparently forgetting Rollinson (1978) further notes that patients tend to be "the that he had himselfdrunk it. At this stage he was reminded more prominent members ofthe community, e.g. physi­ that the car was still outside the garage, so he went out and cians and relatives ofphysicians, perhaps suggesting that put it into the garage without mishap. He spent the rest of the occurrence ofTGA in such a person is less likely to the evening watching television and subsequently went to pass unnoticed" (p. 547) (cf. Hodges & Warlow, 1990b).3 bed, sleeping well. During this time his speech was coher­ The likelihood ofdifferent members in the same fam­ ent, he knew where he was working and he knew all about his friends. At first he was bewildered and wept on two oc­ ily experiencing a TGA is addressed in several reports casions, but later he became quiet and subdued. (Corston & Godwin-Austen, 1982; Dupuis, Pierre, & Gon­ On the following morning he awoke and said "What am sette, 1987; Munro, 1982; Stracciari & Rebucci, 1986). I doing in bed at this time ofday?" His wife tried to explain In group studies, Ciucci, Stracciari, and Bianchedi (1988) what had happened and then he said that he thought it was found that 7% of their patients had other family mem­ Sunday morning. Later on during the morning...his mem­ bers who had also experienced a TGA, whereas Hodges ory for previous events returned as far as lunch time on the and Warlow (1990b) noted this rate to be 2% oftheir pa­ previous day. (Evans, 1966, pp. 542-543) tients. While these familial reports flag a possible genetic component of TGA, it is also possible that families are Case 2 more alerted to the phenomenon after TGA has occurred The principal ofa Technical College was seen five days after to one member. an episode of amnesia which had occurred on his 60th birthday. He had been chopping wood for two hours on a warm day when he suddenly lost his memory. He kept ask­ Age ing the same questions and repeatedly asked his wife where The distribution ofpatients' age during the TGA epi­ he was and what he was doing. His speech and behavior sode from case-study reports is presented in Figure I, were otherwise normal. His wife called their family physi­ separately for males and females. Overall, the range is cian who confirmed the memory loss, which extended back 6-84 years (interquartile range = 51-64 years), with a TRANSIENT GLOBAL AMNESIA 403

Number of Patients 70 r------,

1 -- Males -+- Females In 60

50

40

20

10

11-16 21-26 31-36 41-46 61-66 61-66 71-76 81-86 16-20 26-30 36-40 46-60 66-60 66-70 76-80 Age During TGA

Figure 1. Frequency distribution of patients' age during the TGA attack. mean of 55.3 years (SD = 13.9 years), a median of 59 from a chance (50/50) split [X2(I) = 3.98,p < .05]. While years, and a mode of 60 years (7% of the patients were female outnumber male patients, this may be due to an 60). In the set of25 group studies reporting mean age for overrepresentation offemales in the older age range where their sample, the mean of the means is 61.0 years (me­ TGA is most common. Comparing the genders on mean dian = 60.8, range = 55-67, SD = 2.3). age during the TGA episode (see Figure 1), females were To compare this age distribution with the population significantly older than males both in case studies (males in general, statistics from the U.S. Bureau ofthe Census = 53.1 years; females = 58.1 years) [t(486) = 3.72,p < (1994 resident population) were used to compute the .01] and in the eight group studies reporting such data percent ofindividuals in each age category presented in (males = 58.7 years; females = 61.7 years) [t(7) = Figure 1 (using only individuals between the ages of 11 4.00,P < .01]. This significant age difference may simply and 85 to compose a 100% baseline). When the overall reflect that females live longer than males. population percentages are subtracted from the percent In summary, the likelihood ofexperiencing TGA in a ofTGA patients in each age category (see Figure 2), in­ given year is about 1 in 20,000 in the general population dividuals under 50 are underrepresented as TGA pa­ and 1 in 3,000 in older adults. The actual incidence ofTGA tients, whereas people between 50 and 65 are overrepre­ is probably higher, with many cases unreported. Upper­ sented as TGA patients. More importantly, the sharp class or well-educated individuals tend to be overrepre­ drop in TGA incidence after age 65 does not simply re­ sented among patients. Typical TGA patients are in their flect a natural decline in the number of older adults. In mid to late 50s or early 60s, with a slightly higher prob­ short, the ages of50-70 represent an elevated risk period ability of being female than male. Females who experi­ for experiencing TGA. ence TGA are also older than their male counterparts.

Gender THE TGA EPISODE: Patients' gender is reported in all case studies (males = GENERAL FRAMEWORK 280; females = 208) and in 37 group studies (males = 812; females = 976). Combined across both case and The following section summarizes dimensions related group studies, there were 1,092 males (48%) and 1,184 to the onset and duration ofthe TGA experience, includ­ females (52%), and these percentages differ significantly ing events preceding the attack, when an attack is likely 404 BROWN

Population % minus TGA % 20,------,

15

10

5

Ot------,f------'l,.....------j

-5

- 10 '----'---'---'----'----'--~---'---'---~---'---'---~---'---'---~--' 11-15 21-25 31-35 41-45 51-55 61-65 71-75 81-85 16-20 26-30 36-40 46-50 56-60 66-70 76-80 Age During TGA Figure 2. Difference between population and TGA age distributions, with respect to the percent of individuals in each age grouping. to occur, and the duration ofthe episode. Following this, ber of cases (8%), as does mild head injury (5%) unac­ the patient's experience during the attack is addressed, companied by concussion or loss ofconsciousness. including physical and psychological symptoms, orien­ In an effort to give coherence to this diversity of"pre­ tation, and RA. cipitating events," Caplan (1990) suggests that an abrupt change in physical activity, temperature, environmental Precipitating Events conditions, or emotions may precipitate an attack (see One ofthe most enigmatic dimensions concerning TGA Dinsmore & Callender, 1983;Frederiks, 1993), and Fisher is its cause. In this predominantly medical literature, many and Adams (1964) note that nearly a third of their pa­ investigators have searched for a specific biological trig­ tients' attacks are immediately preceded by emotionally ger, an effort that has not proved successful. Most ofthe or physically stressful events (or both). Frederiks (1990) literature focuses on events that immediately precede the evaluated the consistency in the antecedent activities for attack, and these proximal causes are reviewed first. A 19recurrent episodes experiencedby 15patients. He found few reports also include experiences preceding the attack that 11 preceding events were the same and 8 were dif­ by days, weeks, or months, and these distal factors will be ferent, suggesting an equal likelihood that multiple TGA considered second. attacks will be preceded by the same or different events. Proximal factors. A wide variety of circumstances For a more thorough description and analysis of proxi­ have been found to precede a TGA attack, and this infor­ mal precipitating events, see Fisher (1982). mation is provided in about a third (32%) ofreports. The Distal factors. Physical and psychological stressors in various preceding events are listed in the Appendix, along the weeks prior to TGA may also precipitate an attack. with the frequency and percent of cases for each. This Although such events are rarely reported (less than 10% information is presented in detail in the hopes that some ofcase reports), they include (frequency in parenthesis): readers may detect patterns that have previously gone un­ a trip for business or pleasure (17), a death or illness in the noticed. TGA attacks are most frequentlypreceded by light family (10), the end-of-year holiday season (10), hosting to moderate physical exertion (about a third ofthe time), an upcoming party (5), impending or completed surgery with the most notable activities being sexual intercourse (4), stress at work (4), severedepression (2), pregnancy (1), (8%), driving (5%), and bathing (5%). TGA also follows and financial difficulties (1). Laurent, Trillet, and Croi­ heavy physical exertion, with farm work (7%) topping the sile (1990) discovered that a third to halfoftheir patients list. General emotional stress also accounts for a fair num- had a profile of"psychological pressure" preceding the TRANSIENT GLOBAL AMNESIA 405 attack, and about a third of the patients in other studies given generally as morning (61%), afternoon (25%), or were under considerable stress prior to TGA (Miller, Pe­ evening (14%). These percentages parallel those in Fig­ tersen, Metter, et aI., 1987; see also Guyotat & Courjan, ure 3, as well as others' reports of60% (Mazzucchi, 1988) 1956, cited in Laurent et aI., 1990). Markowitsch (1983) and 62% (Zinelli, Nasuto, & Miari, 1988) of TGAs oc­ further observed that a number ofTGA patients appear to curring in the morning hours. The month ofthe TGA at­ be currently (or previously) in responsible, high-stress tack is identified in 85 cases (see Figure 4), and most positions (see Fisher, 1982). (59%) occur during the colder autumn and winter months As an example ofthe type ofemotional stress that may (October through March), with the heaviest preponder­ precipitate TGA, Merriam, Wyszynski, and Betzler (1992) ance in December (18%). This supports Mazzucchi's describe a woman who had a strong need to reunite with (1988) finding that 70% of TGA episodes occur in the her family over Christmas because it was the first time autumn and winter months. While this trend may be re­ they could get together since the recent death of her lated to cold weather, it may also be related to the prepon­ mother. Her supervisor would not allow sufficient time derance ofholidays (Thanksgiving, Christmas, and New off, causing her to agonize over the prospect ofbeing alone Years) during this period and the stress accompanying for the holidays. On the evening prior to her TGA, she re­ such events (see earlier section on Precipitating Events). ceived a note from her son pleading with her to join them, which she felt placed her in an "unbearable situation." Duration Also, Stevens and Ammerman (1974) point out that their Most case studies (95%) report TGA duration, and patient had been "agonizing over a complicated estimate these data are summarized in Figure 5, with half-hour in­ on an extensive landscape project" (p. 594) prior to TGA. crements rounded down (e.g., 2\12 h is treated as 2 h). The At any rate, as with the proximal factors, a more thor­ mean TGA duration is 8.2 h (SD = 11.1, range = 4-96), ough exploration ofthe patient's personal stressors could with a mode of 2 h and a median of 5 h. The period of help to shed light on the cause(s) ofTGA. 2-4 h accounts for more than a third (37%) of the at­ tacks. In 10 group studies (619 patients) reporting mean Time ofOnset TGA duration, the mean ofthe means is 7.2 h (SD = 3.6, TGA is more likely to occur in the morning and in colder range = 4.1-17), with a median of6.5 h. months. In the 78 cases where a starting hour was given Several cautions are in order in evaluating these data. (see Figure 3), TGA most often occurs between 7 a.m. First, the precise time of onset is often ambiguous. Al­ and 12 noon (59%). In 72 other cases, the start time is though TGA onset is believed to be sudden, the relatively

Number of TGAs 12 r------_

10

8

6

4

2

1 2 3 4 5 6 7 8 9 10 11 12 1 2 3 4 5 6 7 8 9 10 11 12 AM PM Time of Day Figure 3. Frequency distribution of times ofthe day when TGA started. 406 BROWN

Number of TGAs 16,------,

14

12

10

8

6

2

o'--_'--_'--_'--_'--_'--_.L--_.L-_.L--_.L--_-'---_-'---_-'------' Jan Feb Mar Apr May Jun Jul Aug Sep Oct Nov Dec Month Figure 4. Frequency distribution ofmonths of the year when TGA occurred.

Number of TGAs 70,------,

60

50~-········· ./ -\ _ - -.. -_ .

40

30

20

10

'1 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 2436+ TGA Duration (hours)

Figure 5. Frequency distribution of TGA duration. TRANSIENT GLOBAL AMNESIA 407 subtle change in the patient's behavior (disorientation, ofreports (16%). Ofthe 253 reported physical symptoms, inability to encode new information) may not be imme­ headache accounts for nearly half (48%) (Laurent et al., diately apparent ifthe victim is engaged in routine (work, 1990), followed by nausea/vomiting (14%) and dizziness/ hobby) or isolated (watching television) activities. An­ unsteadiness (14%), paleness (5%), tearfulness (4%), other difficulty in evaluating the temporal extent of the and neck pain (2%). As with the psychological symptoms, TGA episode is that recovery is usually gradual making physical symptoms may be either a direct result ofTGA a precise termination point difficult to establish. A fur­ or the patients' reaction to the episode. ther complication is that some individuals wake up in the morning with TGA or go to bed prior to recovery (Fisher, ANTEROGRADE MEMORY PERFORMANCE 1982), and reported TGA duration mayor may not in­ clude the sleep period. This distribution may also be trun­ The primary defining feature ofTGA is temporary an­ cated at each end because researchers sometimes ex­ terograde amnesia (AA), or inability to encode new in­ clude TGA episodes that are very short « 1h) and/or very formation. Direct measurements ofAA are covered under long (> 24 h) (Laurent et al., 1990). the topics of working memory (less than 1 min) and ep­ With respect to gender, the mean TGA duration is iden­ isodic memory (2 min or longer). Indirect indications of tical (8.2 h) for males and females. With respect to age, memory dysfunction are reflected in repeated questions there is no significant correlation (p > .05) between age and behaviors, answers to physicians' orienting ques­ and TGA length either overall (r == +.09) or when the ex­ tions, and patients' self-reflections on their present cir­ tremes ofage (patients younger than 40) and TGA length cumstances. (episodes longer than 20 h) are excluded from the analy­ A major difficulty in assessing anterograde memory sis (r == +.07). Comparing older (~60 years) with younger dysfunction is that the TGA episode is transient with «59 years) patients, there is a nonsignificant trend for gradual resolution. Thus, as an evaluation is being per­ longer TGA episodes with older patients (8.9 h) than with formed, the episode is usually clearing up. This problem younger patients (7.5 h) [F(1,418) == 1.63,p > .05]. is illustrated by Kritchevsky, Squire, and Zouzounis In summary, the typical TGA episode lasts 2-4 hand (1988): occurs in the morning hours and during colder weather Patients were examined and tested between 2 and II hours (winter). The length of attack does not differ as a func­ after the onset of the TGA. All patients were amnestic at tion ofage or gender ofthe patient. A wide variety ofevents this time, although in three cases ... family members stated may precede the TGA, although most appear to involve that the memory problems had begun to improve by the some emotional and/or physical stressor. time of testing. A fourth patient ... recovered noticeably during the testing session. The fifth patient ... developed Nonmemory Symptoms memory problems in the hospital, was examined and tested Although the memory-related symptoms are at the heart beginning 2 h later, and did not exhibit signs ofimprovement until several hours after the completion oftesting. (p. 213) ofthe TGA experience, TGA patients do exhibit a vari­ ety of physical and psychological symptoms during the Thus, evaluations conducted during the episode provide attack, which are usually described by physicians, rela­ a conservative account ofthe full extent ofcognitive and tives, and friends. Of the psychological symptoms de­ memory impairment resulting from TGA (also see Kri­ scribed, 50% involve confusion (confused, bewildered, tchevsky & Squire, 1989). disoriented, dazed, puzzled, perplexed), 36% involve arousal (anxious, agitated, restless, astonished, euphoric, Working Memory disturbed), and 14% involve lethargy (tired, quiet, strange, With respect to working memory, the most commonly vegetative, apathetic). It is often reported that complex used test is digit span. The forward digit span is consis­ behaviors are carried out in a bland or blunted manner. tently in the normal range of 5-9 digits, with a mode For example, a man who insisted on playing with his band across studies of7.4 For backward digit span, performance during TGA was reported (by his wife) as playing in a is within the normal range (4~6 digits) in most (10 of 15) detached manner, as ifsimply going through the motions cases.> Also consistently in the normal range are forward (Palmer, 1986). Laurent et al. (1990) suggest that this typ­ word span (Gordon & Marin, 1979) and serial subtrac­ ical passive or quiet personality might reflect the patient's tions (generally by 7S).6 Immediate recall of short (sub­ desire to keep others from discovering their temporary span) lists ofwords is also normal (Cafarra, Moretti, Maz­ dysfunction. Some patients report feeling psychologi­ zucchi, & Parma, 1981; Wilson, Koller, & Kelly, 1980), cally distant, like being a "long way off" (Munro, 1982) as is kinesthetic working memory (Cafarra et al., 1981; or "looking through the wrong end ofa telescope" (Mea­ Gallassi, Lorusso, & Stracciari, 1986; Hodges & Ward, dor, Adams, & Flanigin, 1985). Any ofthese symptoms 1989). may reflect either the patients' reaction to their cognitive Several dimensions ofworking memory do reflect de­ dysfunction or a changed physical state during TGA. ficiencies, or mixed performance. When the task becomes The physical symptoms experienced during TGA are more complex or demanding, performance appears to more diverse and are reported in only a small percentage suffer. Paired-associate learning appears to be impaired, 408 BROWN with the 17 TGA patients tested performing (on the aver­ should be viewed skeptically for several reasons. Pa­ age) at about 30% ofthe level ofcontrol subjects (Hodges tients who hear witness' descriptions of their episodes & Ward, 1989; Kritchevsky & Squire, 1989; Kritchevsky may later mistakenly identify these "recollections" as et aI., 1988). A more serious deficiency involves spatial their own (Brown & Murphy, 1989). Also, these experi­ ability. All 4 patients tested for immediate spatial recall ences may have occurred when the episodes were close showed very poor (or no) ability to reproduce a spatial to resolution. In any case, these recollections appear to be arrangement (Cafarra et aI., 1981; Hodges & Ward, 1989; rare exceptions, and the general rule is that the patient re­ Ponsford & Donnan, 1980). Auditory verbal processing calls nothing from the episode. (oral presentation ofwords) is also markedly impaired in the 3 patients evaluated (Berthier & Starkstein, 1990; Repeated Questions Gallassi et aI., 1986; Stracciari, Rebucci, & Gallassi, Aside from direct empirical measurement of antero­ 1987). Finally, patients' ability to process visual (non­ grade memory during TGA, there are several indirect in­ verbal) information is also mixed. When evaluating vi­ dications ofimpaired memory function-the most obvi­ sual retention (Benton test), 2 of 3 patients were in the ous ofwhich is repeated questioning. normal range (Araga, Fukada, Kagimoto, Inagawa, & The patient would ask, in a very polite but stereotyped Takahashi, 1989; Berthier & Starkstein, 1990; Cafarra manner as ifit were a new event, "Excuse me, I know that et aI., 1981). With figure copying (Rey complex figure this is a silly question, but what am I doing here?" The ex­ test), some have found that TGA patients perform com­ aminer made exactly the same reply each time. "You are in parably to controls, whereas others have found impaired this place because of some trouble with memory which performance relative to controls." you seem to have. Youwill be well very soon." This same In summary, while working memory is generally in­ conversation took place 15 to 20 times, with the same de­ tact, there may be some problem with complex material gree of surprise on the part ofthe patient. No recollection (story recall, paired associate learning), as well as spatial ofit was ever noticed. (Goldenberg, Podreka, Pfaffelmeyer, ability and visual memory. However, the limited number Wessely, & Deecke, 1991, p. 573) ofpatients evaluated on these dimensions limit the gener­ Repeated questions are asked by 40% ofcase-study pa­ ality ofsuch conclusions, and further research is strongly tients and between 50% and 92% of patients in group indicated. summaries (50%, Kushner & Hauser, 1985; 61%, Cap­ lan, 1985; 90%, Fisher, 1982; 92%, Hodges & Warlow, Episodic Memory 1990b). Most patients ask the same question(s) 10-20 The evidence for severe impairment ofretention 2 min times, with the same stereotyped vocal pattern each time after input is absolutely monolithic, with most patients (Bender, 1956; Fisher, 1982), "as ifa fragment ofsound unable to recall even experiencing the earlier input task. track is being repeatedly re-run" (Frederiks, 1993, p. 266). Dismal levels ofepisodic memory have been confirmed If several questions are asked, they are usually in the with word lists in visual or auditory format, numbers same order each time (Hodges & Ward, 1989). In 125 case and letters, faces, visual figures, objects, stories, paired­ reports where specific questions are described, 46% ofthe associate lists, and spatial location.f Shuttleworth and patients repeated one, 30% repeated two, 16% repeated Wise (1973) compared a variety of different materials three, and 8% repeated four through six questions. (proprioceptive/kinesthetic, olfactory, auditory nonverbal, The specific questions mainly concern present situa­ auditory verbal, visual verbal, and tactile) and failed to tion (51%), with the most typical being "what am I doing find evidence ofmemory in any dimension. Even provid­ here?" (15%), "why am I here?" (6%), and "how did I get ing associative and rehearsal strategies at input (Gordon here?" (4%). The temporal dimension is the focus of & Marin, 1979) or cuing at recall (Caplan, 1985; Gordon 27% of questions ("what time/day/month/year is it?"), & Marin, 1979; Patten, 1971; Stillhard, Landis, Schiess, with spatial disorientation ("where am I?") involved in Regard, & Sialer, 1990) fails to help. 19% ofthe queries. Finally, questions relating to person­ Post-TGA memory gap. Following recovery from nel are relatively rare (2%). TGA patients, almost with­ TGA, most patients do not recall any experiences from out exception, retain an awareness of who they are. Ad­ the period ofAA, even though they are aware ofthe mem­ ditional speculation on the neurological significance of ory gap. Although concerned during the episode, pa­ repeated questioning can be found in Fisher (1982). tients are typically unconcerned after TGA about the A few case reports (5%) describe repeated behaviors, memory gap and what it may portend (Frederiks, 1993). such as wandering through the rooms ofa familiar house, Patients occasionally recall fragments ofexperiences that pacing back and forth, repeatedly calling someone, vis­ had occurred during the amnesic period." although such iting a friend over and over, turning the TV on and off, memories usually have a dreamlike quality (Evans, 1966). getting in and out of a chair, and walking up and down These memory pockets may also be a result of rare oc­ stairs. Also noted are repeated "checking" behaviors in­ casions where AA is less "dense" (Okada, Ito, & Tsuka­ volving such things as a dishwasher, car trunk, or closet. moto, 1987) or the TGA onset is gradual or "stuttering" Similar to repeated questions, repeated behaviors prob­ (Laurent et aI., 1990). However, such occasional reports ably reflect the patient's inability to keep track ofrecent TRANSIENT GLOBAL AMNESIA 409 experiences. Interestingly, prospective memory may be ofhis employees, "it was like I knew them years ago but more intact than retrospective memory, in that the patient there was not a vivid present thing." ... To his wife he can keep track ofthe goal but not whether they have ac­ stated "Helen, you seem to be a million years away." He then complished it. A precise record ofthe nature and timing states he felt he was in a setting "like I just returned from ofsuch behaviors would be ofconsiderable value in eval­ a long interval, like I had to get reacquainted again." uating the distinction between prospective and retro­ (pp. 594-595) spective memory function. This feeling ofbeing distant or far away is similar to other patients' descriptions ofbeing disoriented, dream­ Physician's Exam ing, in a haze, in a fog, and everything being strange and In addition to repeated questions and behaviors, dis­ far away. It could be ofconsiderable value to systemati­ orientation during TGA also may be inferred from a cally gather these metamemory and metacognitive eval­ physician's standard neurological examination (Amit, uations through a structured questionnaire. To date, no Shapira, Flusser, & Aker, 1986). None of74 patients was case study has done this. correctly oriented to the present event or situation, and only 15% were correctly oriented for time (0% for time RETROGRADE MEMORY PERFORMANCE ofday, 7% for day ofweek, 17% for date, 25% for month, and 18% for year). Patients are more aware ofplace, with Researchers with considerable experience evaluating 30% able to identify where they were. Orientation to per­ TGA claim that all patients have some RA during TGA son is the most successful. Patients always know who (Caplan, 1990; Markowitsch, 1983), and many research­ they are, and they recognize familiar others 63% of the ers use it as a defining criterion. Although frequently de­ time. Interestingly, recognition is higher for relatives scribed, haphazard reporting makes it difficult to deter­ (64%) than for acquaintances (30%), which may reflect mine how often RA actually accompanies TGA and the the level of prior familiarity with the person. In a large exact nature and duration ofthe dysfunction. While a few group study, Hodges and Warlow (1990a) found percent­ studies have attempted a formal, structured assessment ages roughly similar to the present ones: 13% ofpatients ofthe duration ofRA, many more have evaluated its ex­ were oriented to time, and 42% were oriented to place. istence in a more informal manner. In summary, orientation improves across the domains of situation (0%), time (9%), place (30%), and person Formal Quantitative Assessment (57%). The relative degree of orientation parallels that A few investigations have utilized standardized tech­ found with repeated questions, with most questions about niques to evaluate the existence, and extent, of remote situation and fewest about personnel. memory during the TGA episode. With the Famous Faces Test (Albert, Butters, & Levin, 1979; Sanders & War­ Self-Awareness rington, 1971), Hodges and Ward (1989) found that dur­ During TGA, some patients (18% of case reports) ex­ ing TGA there is a "graded" RA, with name identifica­ press concern over their dysfunction (Bender, 1956; Evans, tion ability more impaired for the most recent decade. 1966). While 5% ofreports simply note that the patient is However, with the Famous Events Test, Hodges and aware ofa disability, the remainder provide quotes that re­ Ward found that recognition is normal for all patients for flect the patient's reflective position: 8% note a general all decades. Despite adequate recognition, dating these functional problem ("what has happened to me?" "there's events is problematic. While 3 patients showed selec­ something wrong with me"), 3% comment on a general tively poor performance for events from the most recent cognitive difficulty ("have I lost my mind?" "I'm disori­ 2 decades (graded RA), 2 others performed more poorly ented"), and 3% mention a specific memory dysfunction on all decades (flat RA). Using a similar test of public ("I can't remember anything," "I have amnesia"). Ofspe­ events, Kritchevsky and Squire (1989) found degraded cial note is the patient who commented that "my memory recall performance for the period of 25 years preceding is a tape that is being erased as it is made." Memory com­ the episode, along with a recognition deficit extending ments are occasionally repeated (similar to questions), as back 5 years. In contrast, a recognition test for single­ illustrated by Fisher and Adams's (1964) patient who re­ season TV shows showed no diminished remote mem­ peated "I can't remember today" about 30 times. ory (Kritchevsky et aI., 1988). Patients' diverse comments on their present, amnestic The Crovitz Test of Remote Autobiographical Mem­ situation have the potential to yield valuable information ory (Crovitz & Schiffman, 1974) requires individuals to concerning the subjective experience of TGA, but they generate (free associate) personal events to common noun remain largely untapped by researchers. An exception is cue words (birds, tree, car). While control individuals Stevens and Ammerman's (1974) description of an un­ produce 25% of their personal events from the most re­ usually reflective patient: cent 5-year period, Hodges and Ward (1989) found that He states "everything evaporated into the distance. I knew TGA patients produced only 4% of responses from this what I had to do but knew that I couldn't think how to do period during the episode. Incontrast, Kritchevsky et al. it, I was conscious through the whole thing." He vainly (1988) failed to find any difference between pre- and post­ struggled to reconstruct the events of the day, tried to think TGA performance at any time period on this test. Using 410 BROWN a test constructed from the patients' own areas ofinterests Informal Quantitative Assessment and experiences, Kritchevsky and Squire (1989) found that Most of the information on the extent ofRA has been the most severe performance decrement during TGA derived from physicians' queries, errors in the patient's (compared with post-TGA recall) is for the year and a voluntary verbal reports, or comments by friends or rela­ halfpreceding TGA. tives concerning patients' behaviors. For example, while In summary, although the amount of research is lim­ nearly all patients remember their birth date, most are un­ ited, there is a consistent evidence of a graded remote able to recall their current age, 10 or they claim to be several memory deficit during TGA, with remote memory dif­ years younger than they actually are-a discrepancy that ficulties more pronounced for recent events than for older logically reflects RA. With voluntary reports, a particularly events. Although there are some exceptions, this has been striking example ofRA is the patient who asked what hap­ found across a variety of materials (famous faces, pub­ pened to the fingers on his left hand, not remembering that lic events, personal experiences) and tests (recall, recog­ they had been traumatically amputated in a farm machin­ nition, free association). The existence ofgraded RA has ery accident 4 months earlier (Logan & Sherman, 1983). important implications for the question concerning the The extent of RA has been assessed both during and significance of flat versus graded RA in amnesics (Al­ after TGA, and these data are presented separately. A bert et al., 1979; Beatty, Salmon, Butters, Heindel, & range oftimes is often given, such as Evans's (1966) pa­ Granholm, 1988; Kopelman, 1989; Squire, Haist, & Shi­ tient whose RA "was judged to be several days, if not a mamura, 1989). Prior evidence for graded RA has been few weeks" (p. 540). In such instances, the more conser­ found mainly in amnestic patients with neurodegenera­ vative estimate (2 days) is used in the data summary. tive diseases (Alzheimer, Korsakoff), making the inter­ During TGA. RA during TGA is reported in 39% of pretation ofsuch selective impairment problematic: Did case reports, with 7% simply noting its existence and a gradual onset ofthe dysfunction result in progressively 32% providing a specific time period. In group summar­ degraded encoding prior to the amnesia? Thus, the exis­ ies, RA is found in the majority ofpatients (66%, Hinge, tence ofgraded RA in TGA patients suggests that graded Jensen, Kjaer, Marquardsen, & Olivarius, 1986; 78%, RA is not a result ofprogressive encoding inadequacies Hodges & Warlow, 1990b). Data from 160 case-study pa­ but rather can be considered a retrieval phenomenon. tients, summarized in Figure 6, reveal considerable vari-

Number of TGAs 25 r------,

20

15

10

5

o <1 2 3-6 7-9 10-14 2 3-11 2 3-4 5-6 7+ Days Months Years Retrograde Amnesia During TGA

Figure 6. Frequency distribution of retrograde amnesia period during TGA. TRANSIENT GLOBAL AMNESIA 411 ability in the temporal extent ofRA during TGA, with a manent RA is unclear. Many studies do not provide this median of 7 days and modes of 1 and 2 days (range = information, even when RA during TGA is reported. Oth­ 0.5 h to 35 years) (note that these data summarize infor­ ers (perhaps mistakenly) assume that permanent RA is a mal assessments). Since RA almost always shrinks dur­ necessary result ofTGA (Rollinson, 1978) and therefore ing TGA, with more remote events recovering first (Ba­ do not consider it necessary to comment on it. sior, Vogel,& Mitton, 1985; Benson & Geschwind, 1967; Relationship ofRAto AA. Are RA and AA related to Fisher & Adams, 1964; Hodges & Ward, 1989), the far­ each other (Kritchevsky et al., 1988; Laurent et al., 1990)? ther into the TGA episode that RA is assessed, the shorter This issue has stirred considerable interest because, if its duration. This makes the present summary ofRA length true, it implies that the same structures mediate both AA during TGA conservative. and RA (Blomert & Sisler, 1974; Russel & Nathan, 1946; AfterTGA. While RA is common during TGA, some Shimamura & Squire, 1986). Kritchevsky et al. (1988) patients also exhibit a permanent, residual RA following note that, among their 5 patients, those with less severe the attack. RA always shrinks by the end ofTGA, and it AA had shorter RA. The present data were examined for is not uncommon for RA to continue to shrink even after evidence of a relationship between the length of TGA the episode is over, as illustrated by the following exam­ and RA. Comparing short (5 h or less; 67 cases) versus ples: a 2-month RA during TGA reduced to 8 h the fol­ long (6 h or more; 63 cases) TGA episodes, RA during lowing day, 2 h a few days later, and 1 h after 3 months TGA is greater than 2 days in 51% ofshort episodes and (Jensen, 1980); a 2-month RA during TGA shrank to 1 62% of long episodes, but this difference is not statisti­ month after 9 h, 15 h after 1 day, and was gone by 2 days cally significant [X2(1) = 1.62,p> .05]. Comparing short (Regard & Landis, 1984); a 2-year RA during TGA de­ (43 cases) TGA episodes with long (41 cases) TGA epi­ creased to less than 1 h after 12 h, and was gone by 3 days sodes for RA following TGA, RA is greater than 1 h in (Stracciari, Rebucci, & Gallassi, 1987). 40% ofshort episodes and 49% oflong episodes, a differ­ A summary of the extent of final, or permanent, RA, ence that is again nonsignificant [X2(1) = 3.05,p > .05]. which is provided in 21% of cases (see Figure 7), indi­ In general, it appears that a typical RA of 1 or 2 days cates a median and mode for post-TGA RA of! h (range = during the TGA shrinks to about 1 h by the end ofthe at­ oh to 5 months) (see Fisher, 1982). Among group studies, tack (see Hodges & Ward, 1989). However, unlike the the percent of patients exhibiting permanent RA varies conservative measurements during TGA, evaluations considerably from 20% (Kritchevsky et al., 1988) to after TGA are most likely liberal because many are done 44% (Fisher, 1982) to 78% (Hodges & Warlow, 1990b). soon after recovery. Also, ifpatients are queried days or The actual percentage of patients who experience per- weeks following the attack, friends or relatives are likely

Number of TGAs 25,..------,

15

10

5

NONE .6H 1H 2H 3H 4H 6-12H 10 20 3-60 1W Retrograde Amnesia After TGA Figure 7. Frequency distribution of retrograde amnesia period after TGA. 412 BROWN to have discussed pre- TGA behaviors with the patients, General Knowledge contaminating the patient's own recollections. While there The general knowledge base ofpatients is usually un­ is a nonsignificant trend for longer (more serious?) TGA affected during TGA. Often, such confirmation is global episodes to be associated with longer RA (see Vohanka and nonspecific, such as a report that the patient has nor­ & Zouhar, 1988), this potentially important question mal reading, writing, and language comprehension abil­ warrants further investigation using more precise mea­ ities (see Stillhard et aI., 1990), left-right orientation (Amit sures ofboth the severity ofAA and the length ofRA (see et aI., 1986; Gorelick, Amico, Ganellen, & Benevento, Fisher & Adams, 1964; Whitty, 1977). 1988; Halsey, 1967; Stillhard et aI., 1990), and writing to dictation (Donaldson, 1985; Gorelick et aI., 1988). More Qualitative Assessment specific memory tests involving such things as simple In addition to measuring the duration ofRA, there are analogies, proverb interpretation, or object naming also other alterations in the quality of the remote memories reveal preserved performance. 12All patients provided their that deserve comment. For instance, dating remote events home address (17) or birth date (10) correctly, although appears to be consistently problematic during TGA (Ca­ 7 of the latter 10 underestimated their age. Remember­ farra et aI., 1981; Gallassi et aI., 1986; Hodges & Ward, ing personally relevant numbers (social security, safe 1989; Stracciari, Rebucci, & Gallassi, 1987). Wood, Me­ combination, telephone) is also problematic, with only 7 Henry, Roman-Campos, and Poser (1980) describe their of 15 patients answering such queries correctly. In sum­ patients' extensive (1O-year)retrograde "amnesia" as con­ mary, general knowledge is usually preserved during sisting ofnumerous islands ofintact memories detached TGA, with the only sign of dysfunction being with nu­ from the temporal context, resulting in considerable con­ merical information such as addresses, current age, and fusion ofevent sequence. Anecdotal reports confirm this phone numbers. dating difficulty, as illustrated by patients who could, for example, describe a car but did not know whether he cur­ Procedural Memory rently or previously owned it (Regard & Landis, 1984), While procedural memory also appears to be unaf­ remember his two daughters and their names but did not fected during TGA, this conclusion is mainly derived know who was older (Regard & Landis, 1984), not remem­ from reports of complex behaviors performed during ber whether he had retired in 1969 or 1971 (Kritchevsky TGA rather than systematic empirical evaluation. TGA et aI., 1988), remember the recent Presidents but got their episodes often occur while the patient is driving, and order confused (Bender, 1960), and recall a helicopter witnesses consistently report that this does not interfere landing but not whether it happened "a few minutes ago, in any obvious way with the control of the automobile. a few hours ago or on a previous day" (Regard & Landis, During TGA, patients are also able to complete a sporting 1984, p. 668). event (Giroud, Guard, & Dumas, 1987; Posteraro, 1988), There is also a consistent tendency during TGA for per­ taxi an airplane for takeoff(Fisher, 1982), complete a bell­ sonal recollections of remote experiences to be "curi­ ringing musical performance (Hodges & Warlow, 1990b), ously empty and lacking in colour ... as ifreduced to the and cook a meal (Evans, 1966) without any diminution bare bones ofmemory" (Hodges & Ward, 1989, p. 600). ofskill. One surgeon was in the midst ofan operation when In addition, confabulation rarely occurs during sponta­ TGA occurred, and, despite his confused comments to neous recall, the physician's interview, or standardized his nurse, he finished the surgical incision "as well as he tests. II In fact, Hodges and Ward (1989) note that their had closed up any gallbladder ... in the last dozen years. patients often begin confidently to respond to an autobi­ Technically his hands had performed their job as well as ographical inquiry, and this quickly turns to surprise and ever" (Klawans, 1988, p. 14). frustration when an "unexpected void" is encountered. Sometimes patients revert to an earlier (outdated) ver­ On occasion, recall of remote events may have scat­ sion ofa complex behavior sequence. For example, a re­ tered lacunae rather than being completely missing (see tired music professor stricken with TGA in the middle of Kritchevsky & Squire, 1989; Whitty, 1977). This "patchy" a piano recital and duet with his wife (Byer & Crowley, RA is illustrated by patients who had no memory ofeat­ 1980) completed the performance successfully, but with­ ing lunch just before the TGA and a "vague" and "in­ out recent modifications practiced many times prior to complete" memory ofthe morning events preceding lunch the recital. Similarly, a patient who was ballroom dancing (Kritchevsky & Squire, 1989), no memory for 2 days and when TGA occurred could only perform older dance rou­ poor memory for 2 weeks prior to the TGA (Meador, Lor­ tines (Hodges & Warlow, 1990b). Such cases could pro­ ing, King, & Nichols, 1988), dense amnesia for 2 weeks vide an indirect measure ofthe extent ofRA, as reflected and patchy amnesia for 2 months before TGA (Stillhard in the time span in which the recent updating occurred. et aI., 1990), and dense amnesia for 1 day and patchy for When automated behavior involves spatial directions, I week prior to the TGA (Wilson et aI., 1980). In all cases, procedural behavior is often disrupted by TGA. During the memory void (dense period) is always immediately an attack, patients often get confused in a familiar area, preceding TGA, while the period of degraded memory or lost when following a familiar route, as illustrated by (patchy period) precedes the dense period. patients who had difficulty walking to a local bus stop TRANSIENT GLOBAL AMNESIA 413

(Cuningham, 1968), got lost or were found wandering in across both case and group studies, 13 13% ofpatients re­ a familiar area close to home (Amit et aI., 1986; Bender, port one additional TGA, 2% claim two other attacks, 1956; Palmer, 1986), drove an incorrect or unusual route and 2% report three or more additional TGA episodes. home (Fisher & Adams, 1964; Hall, 1982; Martin, 1970), Thus, 17% of TGA patients will experience multiple and got lost driving to work (Okura, Maeda, & Abe, 1985). episodes. This low recurrence rate adds to the puzzle of Given the growing interest in the area of procedural TGA. As Hodges (1992) notes, "the fact that most attacks memory, it is surprising that only two studies have at­ are singular ... has been one ofthe facts most difficult to tempted an empirical evaluation. In one investigation on accommodate into any aetiological theory" (p. 238). a single patient, Goldenberg et al. (1991) found that "in These overall recurrence data are problematic for sev­ contrast to the absence ofany learning effect across five eral reasons. Since retrospective reports are usually un­ trials of verbal learning, the patient markedly improved verified, one cannot be sure whether the prior experience from the first to the second trial ofa procedural learning is TGA or another memory dysfunction. Also, the follow­ test which assessed recognition of fragmented digits" up period in prospective studies is often short, averaging (p. 1749), with performance increasing from 67% on 3 years or less in most (62%) studies. Finally, the prospec­ Trial 1 to 100% on Trial 2. Unfortunately, there are only tive follow-up period varies considerably across studies, four or five sentences concerning the materials and out­ and patient to patient within studies, as the following come, making any interpretation difficult. sample ofgroup studies illustrates: 7-210 months (M = In another study of procedural memory, Kazui et al. 67 months) in Hinge et al. (1986); 1-150 months (M = (1995) primed 3 TGA patients with word solutions to 73 months) in Jensen and Olivarius (1981); 19-51 Kanji letters and then later tested them twice, once dur­ months (M = 30 months) in Matias-Guiu, Casquero, Al­ ing and once following TGA. The mean percents ofprimed varez, and Bonaventura (1987). Kanji solutions both during (41%) and after (41%) TGA A recurrence statistic that controls for variations in were higher than the base rate in an unprimed control follow-up period is average annual rate, or the percent group (16%). Furthermore, a primed control group showed of TGA patients who can expect a recurrence in any a solution rate (42%) comparable to the TGA patients' given year. This varies from 2% to 5% across 10 studies, performance during (and after) the episode. Although with a median of3%.14Although this rate suggests that Kazui et al. provide more detail than Goldenberg et al. the chance that a TGA will recur in a given year is rela­ (1991), there is insufficient detail on materials, procedures, tively small (1 in 33), it is much greater than the inci­ or analysis to adequately assess the outcome. dence of TGA in the general population of older adults In summary, procedural, or implicit, memory appears (1 in 3,000; see the earlier section on Age). However, a to be generally preserved during TGA, as is true in other higher report rate is to be expected among TGA patients, forms ofamnesia (Graf, Squire, & Mandler, 1984; Squire, who are more sensitized to such an occurrence than are Cohen, & Zouzounis, 1984). The disruption of the spa­ individuals in the general population. tial component probably reflects an inability to monitor The interval between successive attacks in multip1e­ the current context rather than poor procedural function TGA patients (71 cases; see Figure 8) suggests that most per se (see Working Memory section). The experimental (56%) happen within 3 years, a figure close to the 24­ exploration of procedural memory is an important, un­ month (Melo, Ferro, & Paiva, 1994), 29-month (Miller, tapped dimension of TGA. Additional investigation of Petersen, Metter, et aI., 1987), 34-month (Frederiks, 1993; this topic with more patients and a more comprehensive Gandolfo et aI., 1992), and 36-month (Jacome, 1989) av­ description of the experimental methodology would be erage interattack intervals reported in other studies. Aside ofconsiderable value (Goldenberg, 1995). from the possible increased risk ofa recurrent TGA, the survival rate for TGA patients appears to be normal (Gan­ POST-TGA EFFECTS dolfo et aI., 1992).

This section addresses two important and frequently Cognitive Functioning raised questions concerning TGA. The first is the likeli­ Two common assumptions about TGA are that mem­ hood of experiencing another TGA. Is this malady be­ ory performance (1) returns to normal soon after the at­ nign, or are people who have had a TGA at risk for an­ tack and (2) is not permanently altered by the experience. other attack? The second question is whether there is any These assumptions have been challenged in a number of residual cognitive deficit after the attack, or whether re­ investigations. With respect to the first issue, 12 studies covery is complete following TGA. have traced the changes in 17patients' cognitive functions across multiple testings following TGA (see Table 1). Recurrence While some research indicates that spatial/performance Data on the likelihood ofa repeat TGA have been gath­ and verbal abilities may recover as rapidly as 1 day later, ered only sporadically, both retrospectively from patients most studies show that cognitive function usually takes and prospectively from visits to physicians or phone in­ several days to weeks to fully recover. IS This slow recov­ terviews. Combining retrospective and prospective reports ery contrasts with the impression of the patient, as well 414 BROWN

Number of Patients 16 r------.,

14

12

8

6

4

2

1 2 3 4 5 6 7 8 9 10 11+ Interval Between TGA Attacks (years)

Figure 8. Frequency distribution of years between multiple TGA episodes. as their friends and family, that recovery is complete im­ WAIS; Wechsler Bellevue Intelligence Scale) supports mediately after the episode (Hodges & Ward, 1989; Re­ this speculation: Mean performance (116.8) is signifi­ gard & Landis, 1984; Stracciari, Rebucci, & Gallassi, cantly higher than mean verbal score (110.9) [t(28) = 1987). This slow recovery also parallels the continued 2.80,p < .01]. Matias-Guiu and Codina (1985) found a shrinkage in RA for days following the end ofthe episode. similar pattern among their 29 patients (mean perfor­ With respect to possible permanent cognitive dysfunc­ mance = 100.4; mean verbal = 92.8), although no sta­ tions resulting from TGA, there is considerable specula­ tistical test was performed. tion that TGA results in a permanent, albeit slight, im­ In contrast, Hodges and Oxbury (1990) found no dif­ pairment of verbal abilities (Caplan, 1985; Hodges & ference, and they, as well as others (Matias-Guiu, Bona­ Oxbury, 1990; Mazzucchi, Moretti, Caffarra, & Parma, ventura, Casquero, Calatayud, & Codina, 1987; Strac­ 1980; Posteraro, 1988). Summarizing the 29 cases where ciari, Rebucci, & Gallassi, 1987), claim that any verbal individuals' verbal and performance LQ. scores were deficit is due to testing too soon after the TGA, prior to measured after TGA (Wechsler Adult Intelligence Scale, full recovery. Comparing short « 6 months) versus long (9-35 months) TGA-to-test intervals, Gallassi et al. (1993) Table 1 found comparable performance on verbal tasks at both Retest Intervals for Cognitive Function in TGA Patients intervals, but short-delay patients performed poorer than Retest Interval did long-delay patients on spatial learning and complex Study Hours Days Weeks Months figure copying and recall. Finally, Faglioni, Scarpa, Co­ Cafarra et al. (1981) 6 lombo, Botti, and Grisanti (1992) also found no evidence Evans et al. (1993) 2 2 ofmemory impairment in TGA patients relative to con­ Gallassi et al. (1986) 1,2,3 1 trols using a variety of different materials (story, paired­ Goldenberg et al. (1991) 12 10 1 Gorelick et al. (1988) 2 associate list, 10-wordlist), and they attribute the "perma­ Hodges & Ward (1989) 1 nent" verbal deficit found in some prior studies (Mathew Meador et al. (1988) 1 & Meyer, 1974; Mazzucchi et aI., 1980; Roman-Campos, Ponsford & Donnan (1980) 1 2 Poser, & Wood, 1980; Steinmetz & Vroom, 1972) to con­ Regard & Landis (1984) 9 1,2,3 1 tamination ofthe TGA sample with individuals with other Stillhard et al. (1990) 15 1\12,5 1\12, 3 12 Stracciari, Rebucci, & 12 1\12,3 1,9 neurological pathologies. Gallassi (1987) With respect to long-term remote memory, Hodges Wilson et al. (1980) 1,2 and Oxbury (1990) compared a large number of TGA Note-All studies except Gorelick et al. (1988) include a test during TGA. patients with controls long after the TGA and found that, TRANSIENT GLOBAL AMNESIA 415 with the Famous Faces Test (Albert et al., 1979), the TGA may be partially attributed to the loose and inconsistent patients scored more poorly than did normal controls in manner in which TGA has been defined (Hodges & both naming and recognition, but not personal identifi­ Ward, 1989) or to patients' RA for the physical and psy­ cation. Thus, although impaired in name memory, TGA chological conditions immediately preceding the epi­ patients could supply ancillary information (e.g., occu­ sode (Rosenberg, 1979). pation) concerning the person. In contrast, on the Fa­ Early speculation on the etiology ofTGA included de­ mous Events Test (Hodges & Ward, 1989), TGA patients mentia (Alzheimer's or Pick's disease), toxic-metabolic performed comparably to controls on recognition but were disorders (hypoglycemia, acute alcoholism, uremia), significantly worse in dating when the events occurred. aphasia, psychogenic amnesia, and concussion (Cafarra Thus, the event-dating difficulty found during TGA may et aI., 1981), although these have now been uniformly have some permanent residual. discarded. Most current speculation centers on three Another facet ofthis question is whether patients who possibilities: epilepsy, migraine, and ischemia (tempo­ experience multiple TGA episodes have greater cogni­ rary blood flow reduction). Although evidence can be se­ tive dysfunction than those who have only one attack. lected to support each, none clearly emerges as the sole Mathew and Meyer (1974) discovered that all who showed and consistent cause ofTGA.16 Given the technical den­ permanent memory impairment were multiple-episode sity of the medical arguments and counterarguments in TGA patients, whereas all who showed no memory im­ the TGA literature, each position will be briefly summa­ pairment were single-episode patients. In addition, Gal­ rized, with the interested reader directed to more detailed lassi, Stracciari, Morreale, Lorusso, and Ciucci (1988) discussions. note greater post-TGA impairments of memory and at­ tention in multiple- compared with single-episode pa­ Epilepsy tients, but a later study by Gallassi et aI. (1993) found low­ TGA may reflect a temporary dysfunction ofthe elec­ ered performance for multiple-episode patients only for trical activity of the cortex, including the structures in­ visual, perceptual-motor, and attentional tests, but not volved in memory formation and retrieval: the verte­ verbal tests. In short, there is strong evidence that multiple­ brobasilar and posterior cerebral arterial systems that serve episode patients are at greater risk ofsome degree ofper­ the hippocampus, fornix, amygdala, mamillary bodies, manent cognitive impairment. and the mesial and basilar portions ofthe temporal lobe. Overall, the data suggest that the recovery ofmemory The most likely culprit is an epileptic seizure in the tern­ function takes at least a week, and probably longer. Thus, porallobe, which disrupts the normal consolidation and testing patients too soon after the attack may give the mis­ retrieval processes. Although the original reports on TGA impression ofa permanent cognitive deficit. Any cogni­ by Fisher and Adams (1958, 1964) suggest epilepsy, sup­ tive disability seems to be more likely with attention and port for this position has weakened as evidence has ac­ spatial abilities and with multiple-episode patients. Of cumulated. An epileptic attack can produce a period of course, without a pre-TGA memory evaluation, one can­ amnesia (Croft, Heathfield, & Swash, 1973; Gallassi & not rule out TGA as a symptom ofa preexisting subclin­ Morreale, 1990), although this is distinct from TGA by ical memory impairment (Cattaino, Pomes, Querin, & the absence ofrepetitive questioning, frequent episodes Cecotto, 1989). Although there are sufficient indications of short duration (30 min or less), partial (rather than of a permanent memory dysfunction in some TGA pa­ global) AA, and cessation of the episode following the tients (i.e., those with multiple episodes), a definitive an­ administration of antiepileptic medication (see Kapur, swer awaits further investigation. Additional discussion 1990,1993). ofpost-TGA memory function can be found in Columbo Evaluation of epilepsy as a possible cause is made and Scarpa (1990). more difficult because "epileptic features" (Hodges & Warlow, 1990b) or a history of epilepsy (Erli, Franza, ETIOLOGY OF TGA Viscardi, & Defanti, 1988; Gandolfo et aI., 1992) are sometimes used as exclusionary criteria in TGA. Inter­ Perhaps the most puzzling dimension of TGA is its estingly, Hodges and Warlow (1990b) excluded epilep­ cause. Despite an enormous amount of research, analy­ tics but found that 9% of patients developed epilepsy sis, and conjecture, no single cause has been identified. during the follow-up period. In addition, a patient was Most ofthe literature on TGA is devoted to an extensive, more likely to develop subsequent epilepsy if (1) he/she almost tedious, rehashing ofa few possible causes, a sit­ had had multiple episodes ofTGA and (2) the TGA epi­ uation probably encouraged by this ambiguity. As Cap­ sode was short « 1 h) rather than long. lan (1985) cogently commented after a review of 485 While TGA patients are routinely evaluated for epi­ patients, "Despite numerous case reports...TGA re­ lepsy (and other seizure disorders), only a miniscule mains a disorder ofuncertain cause. In fact, there may be number (less than 1%) have the disorder. While some a number ofdiverse causes which have in common only post-TGA EEG analyses have yielded evidence of epi­ transient dysfunction of structures critical for memory leptic activity."? most research finds credible evidence function" (p. 216). The difficulty in identifying a cause lacking. 18 Primavera, Novello, and Stara (1993) further 416 BROWN

caution that post-TGA irregularities in EEG may have While migraines are suggested as precipitating spe­ been created by the TGA episode. cific TGA episodes (Cochran, 1984; Dupuis et aI., 1987; A potentially stronger test ofthe epileptic hypothesis Jensen, 1980; Olivarius & Jensen, 1979; Santoro et aI., comes from recordings done during TGA. These out­ 1988; Stracciari & Rebucci, 1986), few make the claim comes, unfortunately, are as ambiguous as post-TGA that TGA is caused solely by migraine. As with support­ analyses. Among case-study reports, evidence of EEG ers of epilepsy, these researchers suggest that it is one of abnormalities have been found about as often as not, 19 al­ several possible causes. One problem with the migraine though one study did record a seizure during TGA (Tas­ hypothesis is that the malady is most prevalent between sinari et aI., 1991). Among group studies, the evidence the ages of 12 and 50, which is outside ofthe age range is overwhelmingly negative. While one study found ab­ typical of TGA patients (Frederiks, 1993). For further normal activity during TGA (Heathfield et aI., 1973), discussion ofthe migraine hypothesis, see Caplan, Chedru, most have failed to find such evidence.P Additional neg­ Lhermitte, and Mayman (1981), Crowell et al. (1984), ative evidence comes from the serendipitous EEG record­ Haas (1990), and Kushner and Gzesh (1990). ing (during routine medical tests) at the onset ofa TGA attack (Cole, Gloor, & Kaplan, 1987), which revealed no Ischemia difference in electrical activity before and after the onset Perhaps the most viable explanation ofTGA is a tem­ ofTGA. porary vascular insufficiency ofthe temporal lobe struc­ The ambiguity ofthese data may be due, in part, to mea­ tures involved in the formation and storage of new mem­ surement difficulties. Many studies supporting the epi­ ories, probably in the medial-temporal branches of the leptogenic origin lack sufficient technical detail to sup­ basilar artery. Most researchers find it sufficient to advo­ port their claims (Gallassi & Morreale, 1990) or point to cate the nonspecific disruption ofthe blood supply (tran­ "abnormalities" that are found routinely in normal re­ sient ischemic attack, or TIA) unrelated to a structural or cordings (Pedley, 1983; Tharp, 1979). Fogelholm, Kivalo, functional abnormality (tumor, lesion, concussion, etc.).22 and Bergstrom (1975) further note that EEG abnormali­ Cerebral blood flowmeasurement during TGA, through ties become progressively more common with age, es­ doppler (rCBF) or tomographic (SPECT, PET) techniques, pecially in the range typical of TGA patients (Miller, has consistently verified a reduced blood supply to the Yanagihara, Petersen, & Klass, 1987). temporal lobe.P Out of 19 patients who have been mea­ It should be emphasized that none who supports an sured in this manner, 5 showed bilateral reduction to the epileptic etiology suggests that it is the exclusive cause of temporal lobe, and 7 showed a unilateral reduction (6 on TGA, but rather it is one ofseveral possible causes that the left and 1 on the right temporal lobe). There were also accounts for only a small percentage of cases. Additional reductions to the thalamus (3 bilateral, 1 left, 1 right), discussion of epilepsy as a cause ofTGA can be found frontal lobe (1 bilateral, 2 left, I right), hippocampus (2 in Gallassi and Morreale (1990), and Stracciari, Ciucci, bilateral, 1 right), and occipital lobe (1 bilateral). Thus, Bianchedi, and Rebucci (1990) provide a detailed descrip­ the most commonly observed blood supply reduction is tion of how to differentiate TGA from transient epilep­ to the left temporal lobe, with 11 of 19 patients evaluated tic amnesia. exhibiting this pattern. A blood supply insufficiency has also been noted in most patients soon after the TGA epi­ Migraine sode (Crowell et aI., 1984; Fayad, Kain, Hoffer, Smith, & Another possible cause ofTGA is a migraine attack, Brass, 1990; Laloux, Brichant, Cauwe, & Decoster, which disturbs the electrical activity and/or blood supply 1992; Matsuda et aI., 1993), although Croisile, Trillet, (vasodilation/vasoconstriction) in the brain, resulting in and Laurent (1990) found that this slowly returns to nor­ a temporary dysfunction ofthe structures involved with mal 40 days after TGA. memory formation (Crowell, Stump, Biller, McHenry, & Others have speculated that some structural or func­ Toole, 1984; Kushner & Gzesh, 1990). Among the case tional brain pathology might underlie the temporary vas­ studies, 11 % of patients reported migraine, and, across cular insufficiency. This would suggest a higher inci­ 19 group studies, the percents ofmigraineurs varies con­ dence of stroke among TGA patients than among the siderably from 4% to 42%.21 general population, but data on this are ambiguous-' (see Some research points to spreading depression ofLeao Ghika & Bogousslavsky, 1990). Others try to document as a neurological disturbance common to both migraine the presence of cerebrovascular risk factors (hyperten­ and TGA (Hinge et aI., 1986; Hodges & Warlow, 1990a; sion, hypercholesterolemia, smoking, etc.) in TGA pa­ Nichelli & Menabue, 1988; Olesen & Jorgensen, 1986). tients, but large variations across studies in what is in­ According to Olesen and Jorgensen (1986), when a highly cluded in the set ofrisk factors make these data relatively emotional experience excites the hippocampus, glutamate uninterpretable (Frederiks, 1993). is released, which then triggers a spreading neurological On some occasions, a specific malady can be identi­ depression in the hippocampus, resulting in a temporary fied as the apparent cause ofthe temporary reduction in shutdown ofnormal memory activity. blood supply leading to TGA, and these include heart TRANSIENT GLOBAL AMNESIA 417 dysfunctions ofa structural (Crowell et al., 1984; Jack­ to alter the course of TGA (Croisile et al., 1990). Anti­ son, Boughner, Bolton, Hopkins, & Barnett, 1985; Shup­ platelet aggregation medications have been recommended ing, Toole, & Alexander, 1980) or functional (Dugan, as a precaution against vascular coagulation during the Nordgren, & O'Leary, 1981; Fisher & Adams, 1964; TGA (Jensen & Olivarius, 1980, 1981; Mathew & Meyer, Greenlee, Crampton, & Miller, 1975) nature, as well as 1974), and vasoactive drugs have been suggested as a vascular difficulties, usually involving the carotid prophylactic measure after the TGA episode (Erokhina, artery." Stakhovskaya, & Sarycheva, 1988), but the efficacy of Everyday behaviors that cause a temporary reduction either treatment has not been evaluated. ofcerebral blood supply have also been implicated in pre­ Some physicians suggest modified behavioral routines cipitating TGA: sudden neck extension or flexion (includ­ for TGA patients as a precautionary measure. Cartlidge ing whiplash) resulting in temporary arterial constriction (1991) admonishes his TGA patients to refrain from dri­ (Ardila, 1989; Fogelholm et al., 1975; Hofstad & Gjerde, ving for 6 months after the attack and reports that one 1985; Muller & Mase, 1981); hypocapnia, or reduced English licensing authority (Swansea) puts a l-year post­ oxygen supply from the lungs (Martin, 1970), from such attack restriction on vocational drivers' licenses ofTGA activities as "singing lustily" in church (Evans, 1966); a patients. Similarly, Palmer (1986) advises his TGA pa­ sudden drop in blood pressure caused by rapidly stand­ tients to refrain from complex business activities for 1 ing from a seated position (Evans, 1966) or a period of month after the attack, while Hodges and Warlow (1990b) quiescence following intense physical activity (Evans, suggest that TGA patients who have had either several 1966). TGA episodes or attacks ofvery short duration (less than Further discussion of the ischemic hypothesis can be 1 h) be advised against driving for 12 months after the found in Ghika and Bogousslavsky (1990) and Scarpa episode due to an increased risk ofdeveloping epilepsy. and Columbo (1990). Others suggest that TGA is benign except where other cerebrovascular risk factors are present, in which case Other Causes more careful follow-up and therapy are indicated (Jensen In a few instances, a TGA can be traced to damage to & Olivarius, 1981). brain structures due to stroke, cyst, tumor, hydrocephalus, neurosyphilis, and infection-s (see Brillman, 1990). Vari­ Legal Implications ous drugs have also been implicated in producing TGA, in­ Although most patients carry out routine activities cluding scopolamine (Ardila & Moreno, 1991), digitalis with little difficulty during TGA, some professionals raise (Greenlee et al., 1975), and alcohol (Hodges & Warlow, a concern that TGA patients might engage in legally 1990b). Of special interest is clioquinol, a drug used to problematic actions. Rolak (1984) describes an alterca­ treat diarrhea (Cras & Martin, 1990; Kaeser, 1984; Mu­ tion between a person experiencing a TGA and a park menthaler, Kaeser, Meyer, & Hess, 1979). Parkin (1987) owner over fees and regulations: "The arguement be­ notes that serious flooding in Japan in 1966 lead to the came so heated the owner brandished a knife and threat­ widespread distribution ofclioquinol to combat dysentery. ened the patient. The patient retrieved a rifle...and held This resulted in over 100 reports of a malady similar to the owner at bay until the police arrived.... The rifle was TGA, although Kaeser (1984) cautions that these episodes never fired and the patient was not charged with any may differ from typical TGA on several dimensions (e.g., crime." As expected, the next morning the patient had no younger patients, longer episodes, insidious onset). memory ofthe conflict. Finally, benzodiazepines have supposedly precipitated Such incidents are extremely rare, and most evidence TGA attacks (Gilbert & Benson, 1972; Morris & Estes, suggests that patients are so distracted by their mne­ 1987; Pande, 1987; Sandyk, 1985; cf. Trillet, Laurent, & monic dysfunction that they become reflective and con­ Croisile, 1990). Interestingly, Merriam (1988; Merriam fused rather than aggressive and hostile. Despite the ab­ et al., 1992) suggests that emotionally stressful events, sence of historical precedent, Stracciari, Rebucci, and which often precede TGA attacks, could release a nat­ Ciucci (1989) raise a flag concerning the medicolegal as­ ural benzodiazepine receptor ligand, which temporarily pects of TGA, and Parwatikar (1990) provides a thor­ interferes with hippocampal function. Frederiks (1993) ough overview of the possible legal implications for a cautions, however, against classifying these drug-in­ patient accused ofcommitting a crime during an episode duced amnesic episodes as TGA because the episode has (see Suranyi, 1983). At the very least, the status ofTGA a slow onset and recovery, with disturbed consciousness as a psychological dysfunction should be formally rec­ during the attack. ognized by inclusion in the Diagnostic and Statistical Manual, or DSM-IV (Caine, 1993). MANAGING THE TGA AND ITS AFTEREFFECTS LOOKING FORWARD

Medical assistance during a TGA episode is rare, and TGA has considerable potential as a crucible within drugs designed to enhance memory function (physostig­ which to examine various dimensions ofmemory in tem­ mine, vasopressin, and naloxone) have consistently failed porarily dysfunctional individuals. Particularly exciting 418 BROWN is the prospect ofusing amnestic individuals as their own tives or close friends of the patient should also be given controls to examine both the loss and the subsequent re­ a questionnaire addressing the behavior and circum­ covery of various memory functions. A similar line of stances ofthe patient prior to TGA: Has the patient been research involves the pharmacological induction of a under unusual stress? Have you noticed any recent changes temporary amnestic state by the use ofdrugs in the ben­ in the patient's behavior? Did anything unusual happen zodiazepine family (Danion, Zimmerman, Willard­ to the patientjust prior to TGA? Both the patient and the Schroeder, Grange, & Singer, 1989; Fang, Hinrichs, & relative/friend questionnaires should have two sections, Ghoneim, 1987; Polster, 1993; Polster, McCarthy, covering both distal (previous 3 months) and proximal O'Sullivan, Gray, & Park, 1993). However, participants (prior day) periods preceding the attack. in such a drugged state are encumbered by a general Exclusionary criteria. The exclusionary criteria for diminution of cognitive skills, whereas patients experi­ identifying TGA episodes (Caplan, 1985) usually in­ encing TGA appear to be fully functional with the ex­ volve such things as episode length restrictions, presence ception ofthe mnemonic deficit. ofRA and repeated questions, and witnesses being pre­ For this unique research opportunity to be fully real­ sent. Even these simple inclusion/exclusion criteria are ized, changes must be made in the way TGA episodes often adhered to in a selective or haphazard manner. For are recorded and evaluated. There is a serious lack ofcon­ instance, in 29 studies that explicitly state their selection sistency in reporting TGA episodes with respect to de­ criteria (rather than simply indicating that they follow mographic information, inclusion and exclusion criteria, Caplan, 1985), there is only moderate compliance: 62% re­ physical and psychological precursors of the TGA epi­ quire that the attack be witnessed, 52% have the dysfunc­ sode, repeated questions during TGA, assessment ofmem­ tion limited to repeated questions and amnesia, and 69% ory dysfunction, and the post-TGA follow-up. This in­ require that the amnesia last between several hours to 1 consistency stems primarily from the nascent stage of day. In the future, these criteria should be noted but not research, with much of the data collected indirectly (by used to eliminate cases from the database. Given our cur­ relatives) and after the attack (retrospectively) and guided rent lack ofunderstanding about TGA, a better approach by a medical focus on the biological etiology ofthe dys­ would be to loosen the restrictions but list the exceptions. function. Researchers are often interested in a specific issue related to TGA (does it happen in children? is it re­ Documenting the Episode lated to migraine attacks? is it likely to recur?) and ig­ A thorough record of the attack should be made, in­ nore a rich variety of behavioral and psychological data cluding when it started (day ofthe week, time ofday, date, not relevant to their research question. Since most arti­ month), where the patient was when the attack began and cles emanate from the medical domain with a focus on a for the short period prior to it, who was with the patient, possible etiology ofTGA, there is relatively little atten­ and what the patient was doing at the onset ofTGA, no tion to documenting the variety ofbehaviors preceding, matter how ordinary. In the absence ofunusual or dramatic during, and following the attack. Perhaps the most strik­ events prior to TGA, researchers frequently conclude ing lacuna in the TGA literature is the paucity of detail that there were no special circumstances (Vohanka & Zou­ on memory function, given that the disability is primar­ har, 1988). In fact, less than a third ofcase studies report ily mnemonic. such information for just this reason. However, the key In short, there needs to be a paradigm shift away from to understanding TGA may lie in a careful analysis ofthe an explanatory and toward a descriptive approach to collage ofthese preceding events and behaviors. Where TGA. A more complete and standardized set of guide­ possible, an audiotape or videotape recording ofthe epi­ lines for data collection, presented below, could help re­ sode would be useful to document the patient's affective, frame this research within a psychological perspective. verbal, and physical behaviors. Ifthe patient is examined by a physician/researcher, the time from the beginning Background History ofthe attack to the beginning ofthe examination/testing More extensive background information is needed on should be noted, as well as the duration ofthe evaluation. each patient, including age, gender, occupation, socio­ Anterograde amnesia. A standardized set of verbal economic status, educational background, ethnicity, and and nonverbal instruments should be developed to eval­ race. Does the patient have a history ofhypertension, mi­ uate the encoding/retrieval difficulties during the TGA. graine, epilepsy, or head trauma, and was he/she taking To document the time course ofthe gradual improvement any medication(s) at the time of the attack? A thorough in the amnestic state, a short battery ofcognitive tests (e.g., record ofboth mundane (e.g., hot bath) and unusual (e.g., forward and backward digit span; l O-word list tested death of a friend) preceding events should be made. after 1 min) should be readministered at regular (half­ After recovery, the TGA patient should receive a ques­ hour) intervals during the attack. tionnaire regarding current life stressors that existed pre­ A complete log should be made ofthe frequency, tim­ ceding the attack, including physical health problems, ing, and content of repeated questions and behaviors. emotional difficulties, family relationships, professional The cycle ofrepeated questions could provide a natural­ activities, sexual problems, and financial issues. Rela- istic avenue to evaluate the temporal extent ofshort-term TRANSIENT GLOBAL AMNESIA 419

memory, with the time interval between cycles ofrepeated or answer(s), it is impressive that patients repeatedly du­ questions as an index. Furthermore, given that there is a plicate the same query. A thorough analysis ofthis unique gradual clearing ofthe period ofAA, is there an increase form of "self-priming" could provide a valuable tool to in the interval between repeated questions over the course evaluate procedural memory function. ofTGA to reflect this gradual resolution? What point in Metamemory. A rich, untapped, source of informa­ the episode do the repeated questions (behaviors) cease? tion concerning the psychological dimensions ofTGA is The existence ofrepeated questions should not be used the patients' perception oftheir current circumstances. A as an exclusionary criterion (Caplan, 1986b), because structured query concerning the patients' impressions of some patients may not vocalize their confusion. Also, their cognitive functioning should be administered dur­ while there are very few reports ofrepeated behaviors dur­ ing TGA, including their perception of the present cir­ ing TGA (5% ofcase studies), it is unclear whether such cumstances (what are you thinking about?), emotional data are not recorded because oftheir apparently periph­ reaction to their encoding failure (what are you feeling?), eral nature or whether such behaviors are actually this subjective impression ofhow their learning and retrieval rare. In any case, such information could provide a bet­ are impaired (are you confused? does there appear to be ter understanding ofprospective behavior. a memory void? how familiar are your surroundings?), Retrograde amnesia. In the vast majority ofthe case reactions to the typical time and space distortions, and studies, the extent ofRA is determined informally through impression ofthe quality oftheir remote memory (hazy? lacunae in the patients' recollections (i.e., they do not re­ patchy? missing?). As illustrated by the rich detail pro­ member a wedding, death ofa relative, birth ofa grand­ vided by Stevens and Ammerman's (1974) patient (cited child, purchase of a car). To evaluate dense RA during earlier), a considerable amount ofuntapped information TGA, standardized instruments should be routinely in­ may be available concerning the metacognitions ofTGA cluded (personal and cultural; Presidents test), as well as patients. the question, "What was the last thing you remember prior to the attack?" This should be readministered at GENERAL SUMMARY regular (half-hour) intervals during TGA to document the course of shrinking RA. While it is often reported TGA is a mnemonic dysfunction characterized by the that there was no residual RA after TGA, this is usually sudden onset of a temporary inability to retain new in­ done through an informal query of the patient. Relative formation. From information on 3,037 patients described to the inordinately large period ofRA during TGA (months in 201 articles, this disability strikes individuals mainly to years), a shrinkage to an hour or less might be inter­ in their 50s and 60s, and it affects women slightly more preted as a "complete" resolution by contrast. The eval­ often than men. The modal TGA attack is 2 h, and it is uation offinal RA should be delayed until at least 1week most likely to occur during the morning hours and in win­ following TGA, given that RA may continue to shrink ter (holiday) months. RA is typically experienced with following the episode. Finally, precautions should be TGA, extending back 1-2 days during the episode and taken to evaluate the extent to which the patient's pre­ back 1 h when the episode resolves. The patient retains TGA memories have been implanted by others after the self-orientation but is disoriented to space, time, and pre­ episode. Such an evaluation of RA and its posttrauma sent situation, and he/she asks repeated questions that re­ shrinkage with TGA patients could be especially en­ flect this disorientation. Physical symptoms are rare and lightening, given that the cognitive confusions typical of are usually restricted to headache, dizziness, and nausea. head-trauma patients are not present in TGA patients. Psychological symptoms include confusion and arousal, Procedural memory. TGA presents a unique oppor­ along with lethargy. While retention ofinformation past tunity to evaluate implicit memory function in "amnestic" several minutes is universally absent during the attack, patients who will soon recover. While a few researchers working memory is generally preserved, except for some have attempted such an evaluation (Ghidoni, Pattacini, & difficulties with visual/spatial information. Both proce­ Previdi, 1988; Goldenberg et aI., 1991), these have been dural and semantic memory are also preserved during neither extensive nor systematic. During the episode, pa­ TGA, although there is a problem with spatial orientation tients should be administered a set ofverbal (words, trivia (getting lost) and temporal dating (confusing event order) information) or pictorial material. Following input, ex­ preceding TGA. plicit (recognition) and implicit (fragment completion) Recovery from the period ofAA is gradual, extending tests should be given at regular intervals during and fol­ over several hours. About 1 in 6 patients experience an­ lowing the episode, with each test consisting ofa mix of other TGA episode. Complete recovery ofcognitive func­ repeated and new items. tion usually takes weeks, even though patients feel fully Procedural memory could also be studied through an recovered immediately after the episode. There may be a analysis ofthe repeated questions asked during TGA. It slight, permanent erosion of verbal and spatial memory is often reported that the patient repeats the same ques­ abilities following the TGA, although further research is tion(s) with the same inflection and in the same order (if needed. A diverse set of circumstances precedes TGA, more than one). With no memory ofthe prior question(s) but a common thread appears to be a moderate emotional 420 BROWN

or physical stressor or an abrupt change in the psycho­ BLOMERT, D. M., & SISLER, G. C. (1974). The measurement of retro­ logical or physical environment. Although migraine and grade post-traumatic amnesia.Canadian Psychiatric Association Jour­ epilepsy have been cited as causes ofTGA, the most likely nal, 19,185-192. BOGOUSSLAVSKY, J., & REGLI, E (1988). Transient global amnesia and explanation is a transient disruption in the posterior stroke. European Neurology, 28,106-110.* cerebral blood supply, probably in the medial-temporal BOKURA, H., YAMAGUCHI, S., TSUCHIYA, H., YAMASHITA, K., & KOBA­ branches ofthe basilar artery. YASHI, S. (1994). Reduction of visual P300 during transient global In the broad sense, TGA provides a natural laboratory amnesia. Electroencephalography & Clinical Neurophysiology, 92, 422-425.* to compare implicit and explicit memory in temporary BOLWIG, T.G. (1968). Transientglobal amnesia. Acta Neurologica Scan­ amnesics (see Wilson et al., 1980). Martin (1970) has dinavica,44,IOI-106.* even suggested that, since the consequences ofTGA are BRILLMAN, J. (1990). Transient global amnesia in cases with space­ apparently benign, the phenomenon could be studied by occupying lesions. In H. J. Markowitsch (Ed.), Transient global having the patient duplicate the triggering event (a cold amnesia and related disorders (pp. 48-57). Toronto: Hogrefe & Huber. swim in the ocean) to see if a similar attack is elicited. BROWN, A. S., & MURPHY, D. (1989). Cryptomnesia: Delineating inad­ Although this approach is ethically questionable, indi­ vertent plagiarism. Journal ofExperimental Psychology: Learning, viduals have experienced a repeat TGA under similar Memory, & Cognition, 15, 432-442. conditions. For instance, Frederiks (1990) reports a man BYER, J. A., & CROWLEY, W. J. (1980). Musical performance during transient global amnesia. Neurology, 30, 80-82.* who experienced TGA on three separate occasions during CAFARRA, P.,MORETTI, G., MAZZUCCHI, A.,& PARMA, M. (1981).Neuro­ exciting card games. In any case, TGA has the potential psychological testing during a transient global amnesia episode and to provide unique insights in the areas ofpsychosomatics, its follow-up. Acta Neurologica Scandinavica, 63, 44-50." emotion, cognition, geriatrics, neuropsychology,and mem­ CAINE, E. D. (1993). Amnesic disorders. Journal ofNeuropsychiatry, 5, ory. As Mazzucci (1988) cogently remarked, "the study 6-8. CANTOR, E K. (1971). Transient global amnesia and temporal lobe ofa so pure form ofamnesia, which exhibits all the char­ seizures. Neurology, 21,430-431.. acteristics of an experiment conducted by nature, could CAPLAN, L. R. (1983). Transient global amnesia and migraine: Reply. provide a greater number ofanswers to general questions Neurology, 33,1107. about memory" (p. 14). CAPLAN, L. R. (1985). Transient global amnesia. In P.1. Vinken, G. W. Bruyn, & H. L. Klawans (Eds.), Handbook ofclinical neurology (Vol. I, pp. 205-218). Amsterdam: Elsevier. REFERENCES CAPLAN, L. R. (1986a). TGA criteria: What's in a name? Reply. Neu­ rology,36, 1625. ACCURTI, 1., & PROLl, E (1988). Transient global amnesia: A personal CAPLAN, L. R.(I986b). Transientglobal amnesia: Criteria and classifica­ seriesof idiopathic and post-traumatic cases. Italian Journal ofNeuro­ tion. Neurology, 36, 441. logical Sciences, 9, 25-28.* CAPLAN, L. R. (1990). Transient global amnesia: Characteristic features AHMED, I. (1978). Transient global amnesia. Journal ofthe Kansas and overview. In H. 1. Markowitsch (Ed.), Transient global amnesia Medical Society, 79, 670-672.* and related disorders (pp. 15-27). Toronto: Hogrefe & Huber. ALBERT, M. S., BUTTERS, N., & LEVIN, J. (1979). Temporal gradients in CAPLAN, L., CHEDRU, E, LHERMITTE, E, & MAYMAN, C. (1981). Tran­ the retrograde amnesia of patients with alcoholic Korsakoff's disease. sient global amnesia and migraine. Neurology, 31, 1167-1170.* Archives ofNeurology, 36, 211-216. CARTLIDGE, N. E. E (1991). Transient global amnesia. British Medical AMIT, R., SHAPIRA, Y, FLUSSER, H., & AKER, M. (1986). Basilar mi­ Journal, 302, 62-63. graine manifesting as transient global amnesia in a 9-year-old child. CATTAINO, G. (1988). Transient global amnesia: A personal series of Headache, 26,17-18.* 60 cases. Italian Journal ofNeurological Sciences, 9, 21-22.• ARAGA, S., FUKADA, M., KAGIMOTO, H., INAGAWA, T.,& TAKAHASHI, K. CATTAINO, G., POMES, A., QUERIN, E, & CECOTTO, C. (1989). Eth­ (1989). Transient global amnesia and falcotentorial meningioma: A moidal meningioma revealedby transient global amnesia. Italian Jour­ casereport.Japanese Journal ofPsychiatry & Neurology,43, 201-203.* nal ofNeurological Sciences, 10,187-191.* ARD!LA, A. (1989). Transient global amnesia resulting from mild trauma. CATTAINO, G., QUERIN, E, POMES, A., & PIAZZA, P. (1984). Transient Neuropsychology, 3, 23-27.* global amnesia. Acta Neurologica Scandinavica, 70, 385-390.• ARD!LA, A., & MORENO, C. (1991). Scopolamine intoxication as a CHATHAM, P.,& BRILLMAN, J. (1985). Transient global amnesia associ­ model of transient global amnesia. Brain & Cognition, 15,236-245. ated with bilateral subdural hematomas. Neurosurgery, 17,971-973. * BARON, J. C., PETIT-TABOUE, M. C; LE DOZE, E, DESGRANGES, B., CIUCCI, G., STRACCIARI, A., & BlANCHED!, G. (1988). Transient global RAVENEL, N., & MARCHAL, G. (1994).Right frontalcortex hypometab­ amnesia: Analysis of 42 consecutive cases. Italian Journal ofNeuro­ olism in transient global amnesia: A PET study.Brain, 117, 545-552.* logical Sciences, 9, 23-24.• BASIOR, J., VOGEL, S., & MITTON, J. (1985). Transient global amnesia: COCHRAN, J. W. (1983). Transient global amnesia after cerebral angiog­ Diagnosis in the emergency department. American Journal ofEmer­ raphy: In reply. Archives ofNeurology, 40, 259. gency Medicine, 3, 352-357. * COCHRAN, J. W. (1984). Transient global amnesia. Archives ofNeurol­ BEATTY, W. W., SALMON, D. P., BUTTERS, N., HEINDEL, W. C., & ogy, 41, 585.* GRANHOLM, E. L. (1988). Retrograde amnesia in patients with Alz­ COCHRAN, J. W., MORRELL, E, HUCKMAN, M. S., & COCHRAN, E. J. heimer's disease or Huntington's disease. Neurobiology ofAging, 9, (1982). Transient global amnesia after cerebral angiography.Archives 181-186. ofNeurology, 39, 593-594.* BENDER, M. B. (1956). Syndrome of isolated episode ofconfusion with COLE, A. J., GLOOR, P.,& KAPLAN, R. (1987). Transient global amnesia: amnesia. Journal ofthe Hillside Hospital.S, 212-215. The electroencephalogramat onset.Annals ofNeurology, 22, 771-772.* BENDER, M. B. (1960). Single episode of confusion with amnesia. Bul­ COLLINS, M. P., & FREEMAN, J. W. (1986). Meningioma and transient letin ofthe New YorkAcademy ofMedicine, 36, 197-207.* global amnesia: Another report. Neurology, 36, 594.* BENSON, D. E, & GESCHWIND, N. (1967). Shrinking retrograde amnesia. COLUMBO, A, & SCARPA, M. (1988). Transient global amnesia: Patho­ Journal ofNeurology, Neurosurgery, & Psychiatry, 30, 539-544. genesis and prognosis. European Neurology, 28, 111-114.• BERTHIER, M. L., & STARKSTEIN, S. E. (1990). Transientpartial amnesia. COLOMBO, A., & SCARPA, M. (1990). The neuropsychological follow­ Journal ofNeuropsychiatry, 2, 465-466.* up of ischemic transient global amnesia. In H. 1. Markowitsch (Ed.), TRANSIENT GLOBAL AMNESIA 421

Transient global amnesia and related disorders (pp. 168-171). FISHER, C. M. (1982). Transient global amnesia: Precipitating activities Toronto: Hogrefe & Huber. and other observations. Archives ofNeurology, 39, 605-608.• CORSTON, R. N., & GODWIN-AuSTEN, R. B. (1982). Transient global FISHER, C. M., & ADAMS, R D. (1958). Transient global amnesia. Trans­ amnesia in four brothers. Journal ofNeurology, Neurosurgery, & Psy­ actions ofthe American Neurological Association, 83, 143-146.* chiatry, 45,375-377.* FISHER, C. M., & ADAMS, R. D. (1964). Transient global amnesia. Acta CRAS, P., & MARTIN, J. (1990). Transient global amnesia following in­ Neurologica Scandinavica, 40, 1-83.* gestion of chloroquine. Journal ofNeurology, Neurosurgery, & Psy­ FOGELHOLM, R, KJVALO, E., & BERGSTROM, L. (1975). The transient chiatry, 53, 926.* global amnesia syndrome: An analysis of 35 cases. European Neu­ CROFT, P.B., HEATHFIELD, K. W. G., & SWASH, M. (1973). Differential rology, 13, 72-84.*. diagnosis of transient amnesia. British Medical Journal, 4, 593-596.* FRANK, G. (1981). Amnestische Episoden [Amnesic episodes]. Berlin: CROISILE, B., TRILLET, M., & LAURENT, B. (1990). Cerebral blood flow Springer. and pharmacological tests during transient global amnesia. In H. 1. FREDERIKS, J. A. M. (1990). Transient global amnesia: An amnesic TlA. Markowitsch (Ed.), Transient global amnesia and related disorders In H. 1.Markowitsch (Ed.), Transientglobal amnesia and related dis­ (pp. 121-130). Toronto: Hogrefe & Huber.* orders (pp. 28-47). Toronto: Hogrefe & Huber.• CROVITZ, H. E, & SCHIFFMAN, H. (1974). Frequency ofepisodic mem­ FREDERIKS, J. A. M. (1993). Transient global amnesia. Clinical Neurol­ ories as a function oftheir age. Bulletin ofthe Psychonomic Society, ogy & Neurosurgery, 95, 265-283. 4,517-518. FUJII, K., SADOSHIMA, S., & FUJISHIMA, M. (1990). Positron emission CROWELL, G. E, STUMP, D. A, BILLER, 1., MCHENRY, L. c. & TOOLE, tomographic study in patients with transient global amnesia. In H. 1. J. E (1984). The transient global amnesia-migraine connection. Markowitsch (Ed.), Transient global amnesia and related disorders Archives ofNeurology, 41,75-79.* (pp, 131-139). Toronto: Hogrefe & Huber. CUNINGHAM, 1. A. K. (1968). Transient global amnesia. New Zealand FUJII, K., SADOSHIMA, S., ISHITSUKA, T., KUSUDA, K., KUWABARA, Y, Medical Journal, 67, 531-532.* IcHIYA, Y., & FUJISHIMA, M. (1989). Regional cerebral blood flow DANION, J., ZIMMERMAN, M., WILLARD-SCHROEDER, D., GRANGE, D., and metabolism in patients with transient global amnesia: A positron & SINGER, L. (1989). Diazepam induces a dissociation between ex­ emission tomography study. Journal ofNeurology. Neurosurgery. & plicit and implicit memory. Psychopharmacology, 99, 238-243. Psychiatry, 52, 622-630. * DEISENHAMMER, E. (1981). Transientglobal amnesia as an epileptic mani­ GALLASSI, R., LORUSSO, S., & STRACCIARI, A. (1986). Neuropsycho­ festation. Journal ofNeurology, 225, 289-292.* logical findings during a transient global amnesia attack and its DINSDALE, H. B. (1971). Transient global amnesia. Annual Review of follow-up. Italian Journal ofNeurological Sciences, 7, 45-49.* the College ofPhysicians & Surgeons ofCanada, 3, 41.. GALLASSI, R., & MORREALE, A. (1990). Transient global amnesia and DINSMORE, W.w., & CALLENDER, M. E. (1983). Juvenile transient global epilepsy. In H. 1. Markowitsch (Ed.), Transient global amnesia and amnesia. Journal ofNeurology, Neurosurgery, & Psychiatry, 46, 876­ related disorders (pp, 58-65). Toronto: Hogrefe & Huber. 877.* GALLASSI, R, STRACCIARI, A., MORREALE, A., LORUSSO, S., & DONALDSON, I. M. (1985). "Psychometric" assessment during transient CIUCCI, G. (1988). Transientglobal amnesia follow-up:A neuropsycho­ global amnesia. Cortex, 21,149-152.* logical investigation. Italian Journal ofNeurological Sciences, 9, DUGAN, T.M., NORDGREN, R E., & O'LEARY, P.(1981). Transient global 33-34.• amnesia associated with bradycardia and temporal lobe spikes. Cor­ GALLASSI, R., STRACCIARI, A., MORREALE, A., LORUSSO, S., RE­ tex, 17, 633-638.* BUCCI, G. G., & LUGARESI, E. (1993). Transient global amnesia: Neuro­ DUPUIS, M. J. M., PiERRE, P. H., & GONSETTE, R. E. (1987). Transient logical findings after single and multiple attacks. European Neurol­ global amnesia and migraine in twin sisters. Journal ofNeurology, ogy,33,294-298.• Neurosurgery, & Psychiatry, 50, 816-817.* GANDOLFO, C, CAPONNETTO, C., CONTI, M., DAGNINO, N., DEL DYKES, M. H. M., SEARS, B. R, & CAPLAN, L. R. (1972). Transient global SETTE, M., & PRIMAVERA, A (1992). Prognosis of transient global am­ amnesia following spinal anesthesia. Anesthesiology, 36, 615-617.* nesia: A long-term follow-up study. European Neurology, 32, 52-57.• ERLI, L. c, FRANZA, A, VISCARDI, M., & DEFANTI, C. A. (1988). Tran­ GHIDONI, E., PATTACINI, E, & PREVIDI, P.(1988). Transient global am­ sient global amnesia: A clinical and EEG study. Italian Journal of nesia: A large series with neuropsychological examination and a Neurological Sciences, 9, 29-30.• case-control study Italian Journal ofNeurological Sciences, 9, 31-32.• EROKHINA, L. G., STAKHOVSKAYA, L. v.. & SARYCHEVA, T. V. (1988). GHIKA, J., & BOGOUSSLAVSKY, J. (1990). Transient global amnesia and Syndrome of transient global amnesia. Neuroscience & Behavioral stroke. In H. 1. Markowitsch (Ed.), Transient global amnesia and re­ Physiology, 18, 354-357 .• lated disorders (pp. 66-78). Toronto: Hogrefe & Huber. EVANS, J. H. (1966). Transient loss of memory, an organic mental syn­ GIANG, D. W., & KIDO, D. K. (1989). Transient global amnesia associ­ drome. Brain, 89, 539-548. * ated with cerebral angiography performed with use of iopamidol. EVANS, J., H. WILSON, B., WRAIGHT, E. P., & HODGES, J. R (1993). Radiology, 172, 195-196.* Neuropsychological and SPECT scan findings during and after tran­ GILBERT, G. J. (1978). Transient global amnesia: Manifestation of medial sient global amnesia: Evidence for the differential impairment of re­ temporal lobe epilepsy. Clinical Electroencephalography, 9, 45-49.* mote episodic memory. Journal ofNeurology, Neurosurgery, & Psy­ GILBERT, J. J., & BENSON, D. E (1972). Transient global amnesia: Re­ chiatry, 56, 1227-1230.* port oftwo cases with definite etiologies. Journal ofNervous & Men­ FAGLIONI, P., SCARPA, M., COLOMBO, A, BOTTI, C., & GRISANTI, A. tal Disease, 154,461-464.* (1992). A model-based study oflearning and memory following tran­ GIROUD, M., GUARD, 0., & DUMAS, R (1987). Transient global amnesia sient global amnesia attacks. Cortex, 28, 9-22. associated with hydrocephalus: Report oftwo cases. Journal ofNeu­ FANG, J., HINRICHS, J., & GHONEIM, M. (1987). Diazepam and memory: rology, 235,118-119.* Evidence for spared memory function. Pharmacology, Biochemistry GOLDENBERG, G. (1995). Transient global amnesia. In A. D. Baddeley, & Behavior, 28, 347-352. B. A. Wilson, & F.N. Watts (Eds.), Handbook ofmemory disorders FAYAD, P., KAIN, T., HOFFER, P., SMITH, E., & BRASS, L. M. (1990). (pp. 109-133). Chichester, U.K.: Wiley.*. SPECT findings in transient global amnesia. Neurology, 40, 171. GOLDENBERG, G., PODREKA, I., PFAFFELMEYER, N., WESSELY, P., & FEUER, D., & WEINBERGER, J. (1987). Extracranial carotid artery in pa­ DEECKE, L. (1991). Thalamic ischemia in transient global amnesia: tients with transient global amnesia: Evaluation by real-time B-mode A SPECT study. Neurology, 41, 1748-1752.* ultrasonography with duplex doppler flow. Stroke, 18,951-953.• GORDON, B., & MARIN, O. S. M. (1979). Transient global amnesia: An FINDLER, G., FEINSOD, M., LIJOVETZKY, G., & HADANI, M. (1983). extensive case report. Journal ofNeurology, Neurosurgery, & P5Y­ Transient global amnesia associated with a single metastasis in the chiatry, 42,572-575.* non-dominant hemisphere. Journal ofNeurosurgery, 58, 303-305.* GORELICK, P. B., AMICO, L. L., GANELLEN. R.. & BENEVENTO, L. A 422 BROWN

(1988). Transient global amnesia and thalamic infarction. Neurology, effects. In P. P. Roy-Byrne & D. S. Cowley (Eds.). Benzodiazepines 38,496-499.* in clinical practice: Risks and benefits (pp. 113-130). Washington, GRAF, P., SQUIRE, L. R., & MANDLER, G. (1984). The information that DC: American Psychiatric Press. amnesic patients do not forget. Journal ofExperimental Psychology: HOWARD, R. S., FESTENSTEIN, R., MELLERS, J., KARTSOUNIS, L. D., & Learning, Memory. & Cognition, 10, 164-178. RON, M. (1992). Transient amnesia heralding brain stem infarction. GREENE, H. H., & BENNETT, D. R. (1974). Transient global amnesia Journal ofNeurology, Neurosurgery, & Psychiatry, 55, 977.* with a previously unreported EEG abnormality. Electroencephalog­ JACKSON, A. c, BOUGHNER, D. R., BOLTON, C. F.,HOPKINS, M., & BAR­ raphy & Clinical Neurophysiology, 36, 409-413.* NETT, H. 1. M. (1985). Transient global amnesia associated with mi­ GREENLEE, J. E., CRAMPTON, R. S., & MILLER, J. Q. (1975). Transient tral valve prolapse. Neurology, 35, 215. global amnesia associated with cardiac arrhythmia and digitalis intox­ JACOME, D. E. (1989). EEG features in transient global amnesia. Clini­ ication. Stroke, 6, 513-516.* cal Electroencephalography, 20, 183-192.• GUIDOTTI, M., ANZALONE, N., MORABITO, A., & LANDI, G. (1989). A JACOME, D. E. (1990). Transient global amnesia: Clinical and EEG con­ case-control study oftransient global amnesia. Journal ofNeurology, siderations. American Journal ofEEG Technology, 30, 195-209.• Neurosurgery, & Psychiatry, 52, 320-323.• JACOME, D. E., & YANEZ, G. F.(1988). Transient global amnesia and left GUYOTAT, 1., & COURJAN, J. (1956). Les ictus amnesiques [Amnesic frontal haemorrhage. Postgraduate Medical Journal, 64, 137-139.* episodes]. Journal de Medecine de Lyon, 37, 697-701. JAFFE, R., & BENDER, M. B. (1966). E.E.G. studies in the syndrome of HAAS, D. C. (1983). Transient global amnesia after cerebral angiogra­ isolated episodes ofconfusion with amnesia "transient global amne­ phy. Archives ofNeurology, 40, 258-259. sia."Journal ofNeurology. Neurosurgery. & Psychiatry, 29, 472-474. HAAS, D. C. (1990). Transient global amnesia triggered by mild head JAIN, S., MOONIS, M., PRASAD, K., MISHRA, N. K., GOULATlA, R. K., & trauma: A form of traumatic migraine. In H. 1. Markowitsch (Ed.), MAHESHWARI, M. C. (1989). The problem oftransient global amne­ Transient global amnesia andrelated disorders (pp. 79-88). Toronto: sia definition: Reply. Acta Neurologica Scandinavica, 79, 78. Hogrefe & Huber.* JENSEN, T. S. (1980). Transient global amnesia in childhood. Develop­ HAAS, D. C., & Ross, G. S. (1986). Transient global amnesia triggered mental Medicine & Child Neurology, 22, 654-658.* by mild head trauma. Brain, 109,251-257.* JENSEN, T. S., & OUVARIUS, B. DE F.(1980). Transient global amnesia HAGUE, T. (1954), Catheter vertebral angiography. Acta Radiologica, as a manifestation oftransient cerebral ischemia. Acta Neurologica 109, 1-219. Scandinavica, 61,115-124.* HAHN, A. L. (1983). Transient global amnesia and migraine. Neurology, JENSEN, T. S., & OUVARIUS, B. DE F. (1981). Transient global amne­ 33,1106-1107.* sia-Its clinical and pathophysiological basis and prognosis. Acta HALL, 1. A. S. (1982). Transient global amnesia in neurolues. The Prac­ Neurologica Scandinavica, 63, 220-230.• tioner, 226, 953-955.* JOYNT, R. 1., SATRAN, R., & CHARLTON, M. (1973). Transient global HALSEY, J. H. (1967). Cerebral infarction with transient global amnesia. amnesia and psychomotor epilepsy. Epilepsia, 14, 99. Alabama Journal ofMedical Science, 4, 436-438.* JUNI, J., MORERA, J., LAINEZ, J. M., ESCUDERO, J., FERRER, C., & SAN­ HARTLEY, T. C., HEILMAN, K. M., & GARCIA-BENGOCHEA, F.(1974). A CHO, J. (1992). Transient global amnesia after cerebral angiography case of a transient global amnesia due to a pituitary tumor. Neurol­ with iohexol. Neuroradiology, 34,141-142.* ogy,58,998-IOOO.* KADOTA, E., IRINO, T., NISHIDE, M., KANEDA, H., & HASHIMOTO, S. HEATHFIELD, K. W.G., CROFT, P.B., & SWASH, M. (1973). The syndrome (1981). Pathological findings in an autopsied case of transient global of transient global amnesia. Brain, 96, 729-736.* amnesia. No To Shinkei [Brain and Nerve], 33, 399-406.* HINGE, H., & JENSEN, T. S. (1990). The prognosis of transient global KAESER, H. E. (1984). Transient global amnesia due to clioquinol. Acta amnesia. In H. 1. Markowitsch (Ed.), Transient global amnesia and Neurologica Scandinavica, 70,175-179. related disorders (pp. 172-180). Toronto: Hogrefe & Huber.* KANE, C. A. (1983). Transient global amnesia: A common, benign con­ HINGE, H., JENSEN, T. S., KJAER, M., MARQUARDSEN, J., & OUVARJUS, dition. Western Journal ofMedicine, 138, 725-727. * B. DE F. (1986). The prognosis oftransient global amnesia: Results KApUR, N. (1990). Transient epileptic amnesia: A clinically distinct form ofa multicenter study. Archives ofNeurology, 43, 673-676.• ofneurological memory disorder. In H. 1. Markowitsch (Ed.), Tran­ HODGES, J. R. (1992). Transient global amnesia. In R. Campbell (Ed.), sient global amnesia and related disorders (pp. 140-151). Toronto: Mental lives: Case studies in cognition (pp. 237-254). Oxford: Black­ Hogrefe & Huber. well.* KAPUR, N. (1993). Transient epileptic amnesia-A clinical update and HODGES, J. R. (1994). Semantic memory and frontal executive function a reformulation. Journal ofNeurology. Neurosurgery. & Psychiatry, during transient global amnesia. Journal ofNeurology, Neurosurgery, 56,1184-1190. & Psychiatry, 57, 605-608.* KAZUI, H., TANABE, H., IKEDA, M., HASHIMOTO, M., & YAMADA, N. HODGES, J. R., & OXBURY, S. M. (1990). Persistent memory impairment (1994). Retrograde amnesia during transient global amnesia. Japa­ followingtransient global amnesia. Journal ofClinical & Experimen­ neseJournalofNeuropsychology, 10,122-130.* tal Neuropsychology, 12, 904-920. KAZUI, H., TANABE, H., IKEDA, M., NAKAGAWA, Y., SHIRAISHI, J., & HODGES, J. R., & WARD, C. D. (1989). Observations during transient HASHIKAWA, K. (1995). Memory and cerebral blood flow in cases of global amnesia: A behavioural and neuropsychological study offive transient global amnesia during and after the attack. Behavioural cases. Brain, 112, 595-620.* Neurology, 8, 93-101.* HODGES, 1. [R.], & WARLOW, C. P.(1985). Is transient global amnesia a KENNEDY, R. M., RATNAM, D., FREEMAN, J. W., & ZIEGLER, D. K. form of cerebral ischaemic attack? Journal ofNeurology, Neuro­ (1979). Transient global amnesia. Journal ofthe American Medical surgery, and Psychiatry, 48, 604-605.• Association, 241, 2703.* HODGES, J. R., & WARLOW, C. P. (l990a). The etiology of transient KLAWANS, H. L. (1988). Toscanini Sfumble and other tales ofclinical global amnesia: A case-control study of 114 cases with prospective neurology. New York:Bantam.* follow-up. Brain, 113, 639-657.• KOPELMAN, M. D. (1989). Remote and autobiographical memory, tem­ HODGES, J. R., & WARLOW, C. P. (I990b). Syndromes oftransient am­ poral context memory and frontal atrophy in Korsakoff and Alzheimer nesia: Towardsa classification. A study of153 cases. Journal ofNeu­ patients. Neuropsychologia, 27, 437-460. rology, Neurosurgery, & Psychiatry, 53, 834-843.• KOSKI, K. J., & MARTTlLA, R. J. (1990). Transient global amnesia: In­ HOFSTAD, H., & GJERDE, I. O. (1985). Transient global amnesia after cidence in an urban population. Acta Neurologica Scandinavica, 81, whiplash trauma. Journal ofNeurology, Neurosurgery, & Psychiatry, 358-360.• 48,956-957.* KRITCHEVSKY, M. (1992). Transient global amnesia. In L. R. Squire & HOGG, M., & HULL, P.(1980). Transient global amnesia and temporary N. Butters (Eds.), Neuropsychology ofmemory (pp. 147-155). New memory loss. Medical Journal ofAustralia, 31, 558.*. York: Guilford. HOMMER, D. W.(1991). Benzodiazepines: Cognitive and psychomotor KRtTCHEVSKY, M., & SQUIRE, L. R. (1989).Transientglobal amnesia:Evi- TRANSIENT GLOBAL AMNESIA 423

dence for extensive,temporallygraded retrogradeamnesia. Neurology, MATIAs-Gum, J., DAVALOS, A., ANTEM, M., & CODINA, A. (1984). High 39,213-218* density lipoprotein cholesterol in transient global amnesia. Journal of KRITCHEVSKY, M., SQUIRE, L. R., & ZOUZOUNIS, 1. A. (1988). Transient Neurology. Neurosurgery, & Psychiatry, 47,1139-1140.• global amnesia: Characterization ofanterograde and retrograde am­ MATIAs-Gum, J., GARCIA, C, GALDOS, L., & CODINA, A. (1985). Pro­ nesia. Neurology, 38, 213-219.* lactin concentration in serum unchanged in transient global amnesia. KUSHNER, M. J., & GZESH, D. J. (1990). Migrainous influences and Clinical Chemistry, 31, 1764.* transient global amnesia. In H. 1. Markowitsch(Ed.), Transientglobal MATIAs-Gum, J., MASAGUE, L, & CODINA, A. (1985). Transient global amnesia and related disorders (pp. 89-95). Toronto:Hogrefe & Huber. amnesia and high haematocritlevels. Journal ofNeurology, 232, 383­ KUSHNER, M. J., & HAUSER, W.A. (1985). Transient global amnesia: A 384. case-control study. Annals ofNeurology, 18, 684-691.• MATIAs-Gum, J., Prco, M., BONAVENTURA, I., MARTIN, R., & MONAS­ LADURNER, G., SKVARC, A., & SAGER, W.D. (1982). Computed tomog­ TERIO, J. (1989). Platelet aggregation in transient global amnesia. raphy in transient global amnesia. European Neurology, 21, 34-40.* Italian Journal ofNeurological Sciences, 10, 171-174.• LAINE, M., PORTIN, R., & KOSKI, K. (1984). Cognitive changes in tran­ MATSUDA, H., HIGASHI, S., TSUJI, S., SUMIYA, H., MIYAUCHI, T., sient global amnesia. Acta Neurologica Scandinavica, 69, 287-288.• HISADA, K., & YAMASHITA, 1. (1993).High resolutionTc-99m HMPAO LALOUX, P., BRICHANT, C, CAUWE, F., & DECOSTER, P. (1992). SPECT in a patient with transient global amnesia. Clinical Nuclear Technetium-99m HM-PAOsingle photon emission computed tomog­ Medicine, 18,46-49.* raphy imaging in transient global amnesia. Archives ofNeurology, MAYEUX, R. (1979). Sexual intercourse and transient global amnesia. 49,543-546.* New England Journal ofMedicine, 300, 864.* LANDI, G., GIUSTI, M. C, & GUIDOTTI, M. (1982). Transient global am­ MAZZUCCHI, A. (1988). Transient global amnesia: Definition and nesia due to left temporal haemorrhage. Journal ofNeurology, Neuro­ clinical phenomenology. Italian Journal ofNeurological Sciences, 9, surgery, & Psychiatry, 45, 1062-1063.* 11-16. LATERRA, J., GEBARSKI, S., & SACKELLARES, J. C (1988). Transient am­ MAZZUCCHI, A., MORETTI, G., CAFFARRA, P., & PARMA, M. (1980). nesia resulting from vertebral artery dissection. Stroke, 19, 98-101.* Neuropsychological functions in the follow-up of transient global LAURENT, B., TRILLET, M., & CROISILE, B. (1990). Atypical semiology amnesia. Brain, 103, 161-178.* in transient global amnesia. In H. 1. Markowitsch (Ed.), Transient MAZZUCCHI, A., & PARMA, M. (1990). Neuropsychological testing of global amnesia and related disorders (pp. 112-120).Toronto: Hogrefe transient global amnesia during attack and during follow-up. In H. 1. & Huber.• Markowitsch (Ed.), Transient global amnesia and related disorders LiN,K., LIU, R., YEH, T.,WANG, S., & LIU, H. (1993). Posterior ischemia (pp. 152-167). Toronto: Hogrefe & Huber. during an attack oftransient global amnesia. Stroke, 24, 1093-1095.* MEADOR, K. J., ADAMS, R. J., & FLANIGIN, H. F. (1985). Transient LISAK, R. P.,& ZIMMERMAN, R. A. (1977). Transient global amnesia due global amnesia and meningioma. Neurology, 35, 769-771. to a dominant hemisphere tumor.Archives ofNeurology, 34, 317-318.* MEADOR, K. J., ADAMS, R. J., & FLANIGIN, H. F. (1986). Transient LoGAN, w., & SHERMAN, D. G. (1983). Transientglobal amnesia. Stroke, global amnesia: Criteria and classification: Reply.Neurology, 36, 441. 14,1005-1007.* MEADOR, K. J., LORING, D. w., KING, D. W., & NICHOLS, F. T. (1988). LONGRIDGE, N. S., HACHINSKI, v.. & BARBER, H. O. (1979). Brain stem The P3 evoked potential and transient global amnesia. Archives of dysfunction in transient global amnesia. Stroke, 10,473-474.* Neurology, 45, 465-467.* Lou, H. O. C (1968). Repeated episodes of transient global amnesia. MELO, T. P., FERRO, J. M., & FERRO, H. (1992). Transient global amne­ Acta Neurologica Scandinavica, 44, 612-618.* sia: A case control study. Brain, 115, 261-270 .• MAN-SON-HING, C T. (1968). An uncommon type oftransient loss of MELO, T. P., FERRO, J. M., & PAIVA, T. (1994). Are brief or recurrent memory: A report of three cases. Canadian Medical Association transient global amnesias ofepileptic origin? Journal ofNeurology. Journal, 98, 594-599.* Neurosurgery, & Psychiatry, 57, 622-625.• MARKOWITSCH, H. J. (1983). Transient global amnesia. Neuroscience MERRIAM, A. E. (1988). Emotional arousal-induced transient global and Biobehavioral Reviews, 7, 35-43. amnesia: Case report, differentiation from hysterical amnesia, and an MARKOWITSCH, H. J. (1995). Anatomical basis ofmemory disorders. In etiologic hypothesis. Neuropsychiatry, Neuropsychology, & Behav­ M. S. Gazzaniga (Ed.), The cognitive neurosciences (pp. 765-779). ioral Neurology, 1,73-78. * Cambridge, MA: MIT Press. MERRIAM, A. E., WYSZYNSKI, B., & BETZLER, T. (1992). Emotional MARTIN, E. A. (1970). Transientglobal amnesia: A report of elevencases, arousal-induced transient global amnesia: A clue to the neuraltran­ including five ofamnesia at the seaside. Irish Journal ofMedical Sci­ scription ofemotion? Psychosomatics, 33, 109-113.* ence, 3, 331-335.* MILANDRE, L., DON NET, A., RUMEAU, C, ALICHERIF, A., & KHALIL, R. MATHEW, N. T., & MEYER, 1. S. (1974). Pathogenesis and natural his­ (1990). Transient global amnesia followed by vertebrobasilar is­ tory oftransient global amnesia. Stroke, 5, 303-311.• chemia in a case of dolichoectatic basilar artery. Acta Neurologica MATIAS-GUIU, J., BLANQUER, J., FALIP, R., OLTRA, A., & MARTIN, M. Belgica, 90, 248-253* (1992). Incidence oftransient global amnesia in Alcoi (Spain). Acta MILLER, J. W., PETERSEN, R. C., METTER, E. J., MILLIKAN, C. H., & Neurologica Scandinavica, 86, 221. YANAGIHARA, T. (1984). Transient global amnesia: Clinical charac­ MATIAS-GuIU, J., BONAVENTURA, L, CASQUERO, P., CALATAYUD, E., & teristics. Neurology, 34, 244.• CODINA, A. (1987). Transient global amnesia and transient ischaemic MILLER, J. W., PETERSEN, R. C, METTER, E. J., MILLIKAN, C. H., & attacks: Controversy concerning the neuropsychological assessment YANAGIHARA, T. (1987). Transient global amnesia: Clinical charac­ in the follow-up. Journal ofNeurology, 235,125-127. teristics and prognosis. Neurology, 37, 733-737.• MATIAS-GuIU, J.,BONAVENTURA, L,CERVERA, C., & CODINA, A. (1985). MILLER, J. W., PETERSEN, R. C, & YANAGIHARA, T. (1987). Transient Whiplash amnesia. Neurology, 35,1259.* global amnesia: Reply. Neurology, 37, 1890. MATIAS-GUIU, J., CASQUERO, P, ALVAREZ, J., & BONAVENTURA, L(1987). MILLER, J. W., YANAGIHARA, T., & KLAUS, D. W. (1986). Electro­ The prognosis of transient global amnesia. Cephalalgia, 7, 202-203.• encephalographic findings in transient global amnesia. Neurology, MATIAS-GUIU, J., & CODINA, A. (1985). Neuropsychological functions 36,170. in the follow-up of transient global amnesia. Journal ofNeurology, MILLER, J. W., YANAGIHARA, T., PETERSEN, R. C., & KLASS, D. W. Neurosurgery, & Psychiatry, 48, 713.• (1987). Transient global amnesia and epilepsy. Archives ofNeurol­ MATIAS-GUIU, J., & CODINA, A. (1986). Transient global amnesia: Cri­ ogy, 44, 629-633.* teria and classification: Comment. Neurology, 36, 441-442. MINUK, J., MELANCON, D., TAMPIERI, D., & ETHIER, R. (1990). Tran­ MATIAS-GUIU, J., COLOMER, R., SEGURA, A., & CODINA, A. (1986). sient global amnesia associated with cerebral angiography performed Cranial CT scan in transient global amnesia. Acta Neurologica Scan­ with use ofiopamidol. Radiology, 174,285-286.* dinavica, 73, 298-30 I. *. MONTALBAN, J., ARBOIX, A., STAUB, H., BARQUINERO, J., MARTI- 424 BROWN

VILALTA, J., CODINA, A., & HUGHES, G. R. V. (1989). Transient neuropsychological investigations of memory. Psychological Bul­ global amnesia and anti phospholipid antibodies. Clinical & Experi­ letin, 114,477-493. mental Rheumatology, 7,85-87.* POLSTER, M., MCCARTHY, R., O'SULLIVAN, G., GRAY, P., & PARK, G. MOONIS, M., JAIN,S., PRASAD, K., MISHRA, N. K., GOULATIA, R. K., & (1993). Midazolam-induced amnesia: Implications for the implicit/ MAHESHWARI, M. C. (1988). Left thalamic hypertensive haemorrhage explicit memory distinction. Brain & Cognition, 22, 244-265. presenting as transient global amnesia. Acta Neurologica Scandi­ POMMER, B., PILz, P., & HARRER, G. (1983). Transient global amnesia navica, 77, 331-334.* as a manifestation ofEpstein-Barr virus encephalitis. Journal ofNeu­ MORIOKA, H., NOMAGUCHI, M., SHIKAI, H., NAGATOMO, I., TOMI­ rology, 229,125-127'* NAGA, H., & MATSUMOTO, K. (1988). A case oftransient global am­ PONSFORD, J. L., & DONNAN, G. A. (1980). Transient global amnesia­ nesia following psychogenic stress. Kyushu Neuro-Psychiatry, 34, A hippocampal phenomenon? Journal ofNeurology, Neurosurgery, 278-28\.* & Psychiatry, 43, 285-287'* MORRIS, H. H., & ESTES, M. L. (1987). Traveler's amnesia: Transient POSER, C. M., & ZIEGLER, D. K. (1960). Temporary amnesia as a man­ global amnesia secondary to triazolam. Journal of the American ifestation ofcerebrovascular insufficiency. Transactions ofthe Amer­ Medical Association, 258, 945-946. ican Neurological Association, 85, 221-223.* MULLER, H. R. (1990). Recurrences in transient global amnesia. Jour­ POSTERARO, L. (1988). Post-traumatic transient amnesias. Italian Jour­ nal ofNeurology, 237,140.• nal ofNeurological Sciences, 9, 45-47.* MULLER, H. R., & MASE, R. (1981). Pathogenesis and prognosis oftran­ PRIMAVERA, A., NOVELLO, P., & STARA, S. (1993). Transient global am­ sient global amnesia. Gerontology, 27, llO-II\.. nesia: A quantified electroencephalographic study. Acta Neurolog­ MUMENTHALER, M., KAESER, H. E., MEYER, A., & HESS, T (1979). ica Scandinavica, 87, 115-117.• Transient global amnesia after clioquinol: Five personal observations RAFFAELE, R., TORNALI, C; GENAZZANI, A. A., VECCHIO, I., & RAM­ from outside Japan. Journal ofNeurology, Neurosurgery, & Psychi­ PELLO, L. (1995). Transient global amnesia and cerebral infarct: A atry, 42, 1084-1090'* case report. Brain Injury, 9, 815-818.* MUNRO, J. M. (1982). Transient global amnesia-familial incidence. REGARD, M., & LANDIS, T (1984). Transient global amnesia: Neuropsy­ Journal ofNeurology, Neurosurgery, & Psychiatry, 45,1070.* chological dysfunction during attack and recovery in two "pure" cases. NAUSIEDA, P. A. (1979). Transient global amnesia: In reply. Journal of Journal ofNeurology, Neurosurgery, & Psychiatry, 47, 668-672.* the American Medical Association, 25, 2703. REICHTER, R. E., BELT,T G., & STEVENS, J. (1986). Transient global NAUSIEDA, P. A., & SHERMAN, I. C. (1979). Long-term prognosis in tran­ amnesia: Complication ofarterial DSA. American Journal ofNeuro­ sient global amnesia. Journal ofthe American Medical Association, radiology, 7,179-180.* 241,392-393.• ROBINSON, B. W., & LONG, W. D. (1972). Transient global amnesia and NICHELLI, P., & MENABUE, R. (1988). Can association between tran­ carotid lesions. Neurology, 22, 405 .• sient global amnesia and migraine tell us something about the patho­ ROLAK, L. A. (1984). Transient global amnesia. Archives ofNeurology, physiology oftransient global amnesia? Italian Journal ofNeurolog­ 41, 1130.* ical Sciences, 9, 41-43. ROLLINSON, R. D. (1978). Transient global amnesia-A review of213 NISHIDA, A., KAIYA, H., UEMATSU, M., MAEDA, M., MORI, S., & cases from the literature. Australian & New Zealand Journal ofMed­ WAKABAYASHI, S. (1990). Transient global amnesia and Raynaud's icine, 8, 547-549. phenomenon in scleroderma. Acta Neurologica Scandinavica, 81, ROMAN-CAMPOS, G., POSER, C. M., & WOOD, E B. (1980). Persistent 550-552'* retrograde memory deficit after transient global amnesia. Cortex, 16, OKADA, E, ITo, N., & TSUKAMOTO, R. (1987). Two cases of transient 509-518.* partial amnesia in the course oftransient global amnesia. Journal of ROSENBERG, G. A. (1979). Transient global amnesia with a dissecting Clinical Psychiatry, 48, 449-450.* aortic aneurysm. Archives ofNeurology, 36, 255.* OKURA, M., MAEDA, M., & ABE, A. (1985). A case oftransient global ROWAN, A. J., & PROTASS, L. M. (1974). Transient global amnesia: Clin­ amnesia with detailed course of recovery from amnesia. Kyushu ical and electroencephalographic findings in eight cases. Neurology, Neuro-Psychiatry, 31, 225-231.* 24,350.• OLESEN, J., & JORGENSEN, M. B. (1986). Leao's spreading depression ROWAN, A. J., & PROTASS, L. M. (1979). Transient global amnesia: Clin­ in the hippocampus explains transient global amnesia. Acta Neuro­ ical and electroencephalographic findings in 10 cases. Neurology, 29, logica Scandinavica, 73, 219-220. 869-872.. OLIVARlUS, B. DEE, & JENSEN, T S. (1979). Transient global amnesia RUMPL, E., & RUMPL, H. (1979). Recurrent transient global amnesia in in migraine. Headache, 19,335-338.* a case with cerebrovascular lesions and livedo reticularis (Sneddon OTA,T, TAKAMATSU, S., & YAMADA, M. (1978). Transient global am­ syndrome). Journal ofNeurology, 221, 127-13\.* nesia. Bulletin ofYamaguchi Medical School, 25,101-106.* RUSSEL, W. R., & NATHAN, P. W.(1946). Traumatic amnesia. Brain, 69, PACKARD, R. C. (1976). Transient global amnesia: Case report. Military 280-300. Medicine, 141, 182.* SACQUEGNA, T, CORTELLI, P., BALDRATI, A., DECAROLIS, P., & TINU­ PALMER, E. P. (1986). Transient global amnesia and the amnestic syn­ PER, P. (1987). Impairment of consciousness and memory in mi­ drome. Medical Clinics ofNorth America, 70, 1361-1374.* graine: A review. Headache, 27, 30-33'* PANDE, A. C. (1987). Sublinguallorazepam use. Canadian Journal of SAKASHITA, Y, SUGIMOTO, T., TAKI, S., & MATSUDA, H. (1993). Ab­ Psychiatry, 32, 228.* normal cerebral blood flow following transient global amnesia. Jour­ PARKIN, A. J. (1987). Memory andamnesia. New York: Basil Blackwell. nalofNeurology, Neurosurgery, & Psychiatry, 56,1327.* PARWATIKAR, S. D. (1990). Medicolegal aspects ofTGA.ln H. 1.Marko­ SANDERS, H. I., & WARRINGTON, E. K. (1971). Memory for remote witsch (Ed.), Transient global amnesia and relateddisorders (pp. 191­ events in amnesic patients. Brain, 94, 661-668. 205). Toronto: Hogrefe & Huber. SANDYK, R. (1984). Transient global amnesia: A presentation of sub­ PATTEN, B. M. (1971). Transient global amnesia syndrome. Journal of arachnoid haemorrhage. Journal ofNeurology, 231, 283-284.* the American Medical Association, 217, 690-69\.* SANDYK, R. (1985). Transient global amnesia induced by lorzapam. Clin­ PAULSON, G. W.(1981). Transient global amnesia: Perplexing to patient ical Neurology, 8, 3. and physician alike. Postgraduate Medicine, 69, 171-178.• SANTORO, G., CASADEI, B., & VENCO, A. (1988). The transient global PEDLEY, T A. (1983). Differential diagnosis of episodic symptoms. amnesia-migraine connection: Case report. Functional Neurology, Epilepsia, 24, 31-44. 3,353-360'* PEXMAN, J. H., & COATES, R. K. (1983). Amnesia after femorocerebral SCARPA, M., & COLOMBO, A. (1990). Transient global amnesia and is­ angiography. American Journal ofNeuroradiology, 4, 979-983. chemia. In H. 1.Markowitsch (Ed.), Transient global amnesia and re­ POLSTER, M. (1993). Drug-induced amnesia: Implications for cognitive lated disorders (pp. 96-99). Toronto: Hogrefe & Huber. TRANSIENT GLOBAL AMNESIA 425

SHIMAMURA, A P., & SQUIRE, L. R (1986). Korsakoff's syndrome: A TOLOSA, E., & GUMNIT, R. J. (1973). Isolated recent memory loss in tran­ study of the relation between anterograde and remote memory im­ sient global amnesia. Neurology, 23, 399-400.• pairment. Behavioral Neuroscience, 100, 165-170. TRILLET, M., LAURENT, B., & CROISILE, B. (1990). Transient memory SHUAIB, A. (1986). TGA criteria: What's in a name? Neurology, 36, 1625. disturbances after administration of benzodiazepines or anticholin­ SHUPING, 1. R., ROLLINSON, R. D., & TOOLE, J. E (1980). Transient ergic drugs. In H. 1. Markowitsch (Ed.), Transient global amnesia global amnesia. Annals ofNeurology, 7, 281-285.*+ and related disorders (pp. 100-111). Toronto: Hogrefe & Huber. SHUPING, J. R., TOOLE, J. E, & ALEXANDER, E. (1980). Transient global TuKEL,K (1977). Cases oftransient global amnesia. Medical Bulletin amnesia due to glioma in the dominant hemisphere. Neurology, 30, ofIstanbul, 10, 184-192.* 88-90.* VAN CREVEL, H. (1969). Transient global amnesia. Psychiatrica. Neuro­ SHUTTLEWORTH, E. c., & MORRIS, C. E. (1966). The transient global logia. Neurochirurgia, 72, 319-324.* amnesia syndrome. Archives ofNeurology, 15, 515-520.* VINCENT, F. M. (1974). Transient global amnesia in a middle-aged SHUTTLEWORTH, E. C; & WISE, G. R. (1973). Transient global amne­ woman. Postgraduate Medicine, 56, 219-220.* sia due to arterial embolism. Archives 0/Neurology, 29, 340-342.* VINCENT, EM., & HAMATI, Y 1.(1974). Transient global amnesia. Min­ SMITH, D. L., & BIRKMANN, L. W. (1982). Transient global amnesia. nesota Medicine, 9,710-712.* Nebraska Medical Journal, 67, 178-181.* VOHANKA, S., & ZOUHAR, A. (1988). Transient global amnesia after SQUIRE, L. R, COHEN, N. J., & ZOUZOUNIS, J. A. (1984). Preserved mild head injury in childhood. Activitas Nervosa Superior, 30, 68­ memory in retrograde amnesia: Sparing ofa recently acquired skill. 74.* Neuropsychologia, 22,145-152. VOLPE, B. T., HERSCOVITCH, P., RAICHLE, M. E., HIRST, W., & GAZ­ SQUIRE, L. R, HAIST, E, & SHIMAMURA, A. P.(1989). The neurology of ZANIGA, M. S. (1983). Cerebral blood flow and metabolism in human memory: Quantitative assessment ofretrograde amnesia in two groups amnesia. Journal ofCerebral Blood Flow & Metabolism, 3, S5-S6. ofamnesic patients. Journal 0/Neuroscience, 9, 828-839. VROOM, E Q. (1973). Electroencephalographic findings in transient STEIN, M. J. (1975). Transient global amnesia. Journal ofthe American global amnesia. Electroencephalography & Clinical Neurophysiol­ Osteopathic Association, 74, 716-722* ogy, 34, 734-735.• STEINMETZ, E. E, & VROOM, E Q. (1972). Transient global amnesia. WALES, L. R., & Nov, A. A (1981). Transient global amnesia: Compli­ Neurology, 22, 1193-1200.* cation ofcerebral angiography. American Journal ofNeuroradiology, STEVENS, H., & AMMERMAN, B. J. (1974). Transient global amnesia. 2,275-277.* Medical Annals ofthe District ofColumbia, 43, 593-596* WHITTY, C. W M. (1977). Transient global amnesia. In C. W.M. Whitty STILLHARD, G., LANDIS, T, SCHIESS, R, REGARD, M., & SIALER, G. & O. L. Zangwill (Eds.), Amnesia (pp. 93-103). London: Butterworths.* (1990). Bitemporal hypoperfusion in transient global amnesia: 99m­ WILSON, R S., KOLLER, W, & KELLY, M. P. (1980). The amnesia of Tc-HM-PAO SPECT and neuropsychological findings during and transient global amnesia. Journal 0/Clinical Neuropsychology, 2, after an attack. Journal 0/Neurology, Neurosurgery, & Psychiatry, 259-266.* 53, 339-342.* WOOD, E, McHENRY, L., ROMAN-CAMPOS, G., & POSER, C. M. (1980). STRACCIARI, A, CIUCCI, G., BIANCHEDI, G., & REBUCCI, G. G. (1990). Regional cerebral blood flow response in a patient with remitted Epileptic transient amnesia. European Neurology, 30, 176-179. global amnesia. Brain & Language, 9,123-128.* STRACCIARI, A, CIUCCI, G., & BISSI, G. (1987). Transient global amne­ ZINELLI, P., NASUTO, S., & MIARI, A (1988). Transient global amnesia: sia associated with a large arachnoid cyst ofthe middle cranial fossa Case-reports. Italian Journal ofNeurological Sciences, 9, 19-20.• ofthe non-dominant hemisphere. Italian Journal ofNeurological Sci­ ences, 8, 609-611.* NOTES STRACCIARI, A., & REBUCCI, G. G. (1986). Transient global amnesia and migraine: Familial incidence. Journal 0/Neurology, Neurosurgery, I. Caplan (1983, 1986a, 1986b); Jain et al. (1989); Matias-Guiu and & Psychiatry, 49, 716.* Codina (1986); Mazzucchi (1988); Meador et al. (1986); Stracciari et al. STRACCIARI, A, REBUCCI, G. G., & CIUCCI, G. (1989). The problem of (1989). transient global amnesia definition. Acta Neurologica Scandinavica, 2. 2.8 (Miller, Petersen, Metter, Millikan, & Yanagihara, 1984); 3.0 79,77. (Matias-Guiu, Blanquer, Falip, Oltra, & Martin, 1992); 3.4 (Hodges & STRACCIARI, A., REBUCCI, G. G., & GALLASSI, R. (1987). Transient Warlow, 1990a); 5.2 (Miller, Petersen, Metter, et al., 1987); 7.5 (Hodges global amnesia: Neuropsychological study ofa "pure" case. Journal & Warlow, 1990b); and 10 (Koski & Marttila, 1990). 0/Neurology,234,126-127.* 3. TGA patient is a physician (Donaldson, 1985; Fisher & Adams, SURANYI, L. (1983). Transient global amnesia and the law. Archives 0/ 1964; Klawans, 1988; Mazzucchi et aI., 1980; Morris & Estes, 1987), Neurology, 40, 393. or the physician was the son (Nishida et aI., 1990; Tanabe et al., 1991), TANABE, H., HASHIKAWA, K., NAKAGAWA, Y, IKEDA, M., YAMA­ daughter (Bender, 1960; Gorelick et aI., 1988), husband (Fisher & MOTO, H., HARADA, K, TSUMOTO, T, NISHIMURA, T, SHIRAISHI, J., Adams, 1958; Mumenthaler et aI., 1979), father (Mumenthaler et al., & KIMURA, K (1991). Memory loss due to transient hypoperfusion 1979), or other relative (Fisher & Adams, 1964; Whitty, 1977) of the in the medial temporal lobes including hippocampus. Acta Neuro­ TGApatient. logica Scandinavica, 84, 22-27.* 4. Cafarra et al. (1981); Donaldson (1985); Evans, Wilson, Wraight, TASSINARI, C. A., CIARMATORI, c., ALESI, c., CARDINALETTI, L., & Hodges (1993); Fisher and Adams (1964); Gallassi et al. (1986); SALVI, E, RUBBOLl, G., PLASMATI, R, FORTI, A, & MICHELUCCI, R. Goldenberg et al. (1991); Gordon and Marin (1979); Halsey (1967); (1991). Transient global amnesia as a postictal state from recurrent Hodges and Ward (1989); Lin, Liu, Yeh, Wang, and Liu (1993); Meador partial seizures. Epilepsia, 32, 882-885. * et al. (1988); Merriam et al. (1992); Patten (1971); Ponsford and Don­ THARP, B. R. (1969). The electroencephalogram in transient global nan (1980); Regard and Landis (1984); Roman-Campos et al. (1980); amnesia. Electroencephalography & Clinical Neurophysiology, 26, Stracciari, Rebucci, & Gallassi (1987); Wilson et al. (1980). 96-99.* 5. Normal range (Cafarra et aI., 1981; Donaldson, 1985; Evans et al., THARP, B. R (1979). Correspondence. Clinical Electroencephalogra­ 1993; Fisher & Adams, 1964; Goldenberg et aI., 1991; Hodges & Ward, phy, 10,54. 1989; Meador et aI., 1988; Regard & Landis, 1984; Roman-Campos 'fIRMAN, P. J., & WOODY, R. C. (1988). Transient global amnesia pre­ et aI., 1980); below normal range (Gallassi et al., 1986; Halsey, 1967; cipitated by emotion in an adolescent. Journal ofChild Neurology, 3, Hodges & Ward, 1989; Patten, 1971; Stracciari, Rebucci, & Gallassi, 185-188* 1987). TORUN, S., KUTLu, C; DUMAN, T, & OZDEMIR, G. (1990). The role of 6. Cafarra et al. (1981); Dinsmore and Callender (1983); Fisher and cerebral vascular and other factors in transient global amnesia. Jour­ Adams (1964); Gordon and Marin (1979); Gorelick et al. (1988); Roman­ nal 0/Neurology, 237, 133.• Campos et al. (1980). 426 BROWN

7. Comparable to controls (Berthier & Starkstein, 1990; Goldenberg and Meyer (1974); Primavera et a!. (1993); Rowan and Protass (1974); et a!., 1991; Hodges & Ward, 1989; Meador et a!., 1988; Regard & Lan­ Steinmetz and Vroom (1972). dis, 1984; Stracciari, Rebucci, & Gallassi, 1987); impaired relative to 18. Case studies (Araga et al., 1989; Collins & Freeman, 1986; Croft controls (Kritchevsky & Squire, 1989; Kritchevsky et a!., 1988). et a!., 1973; Shuttleworth & Morris, 1966); group studies (Cattaino 8. Word lists (Cafarra et a!., 1981; Gallassi et a!., 1986; Goldenberg et a!., 1984; Ciucci et a!., 1988; Fogelholm et a!., 1975; Frederiks, 1990, et a!., 1991; Gordon & Marin, 1979; Regard & Landis, 1984; Stillhard 1993; Jacome, 1989, 1990; Jaffe & Bender, 1966; Jensen & Olivarius, et al., 1990; Stracciari, Rebucci, & Gallassi, 1987; Wilson et al., 1980); 1981; Kushner & Hauser, 1985; Laloux et al., 1992; Lou, 1968; Man­ numbers and letters (Gordon & Marin, 1979); faces (Gorelick et al., Son-Hing, 1968; Mathew & Meyer, 1974; Miller, Yanagihara, & Klaus, 1988); visual figures (Goldenberg et al., 1991; Hodges & Ward, 1989; 1986; Miller, Yanagihara, Petersen, & Klass, 1987; Nausieda, 1979; Kritchevsky & Squire, 1989; Kritchevsky et a!., 1988; Meador et a!., Shuping, Rollinson, & Toole, 1980). 1988; Regard & Landis, 1984; Stracciari, Rebucci, & Gallassi, 1987); 19. EEG abnormalities found (Dugan et al., 1981; Tassinari et a!., objects (Gordon & Marin, 1979; Gorelick et al., 1988; Hodges & Ward, 1991, Tharp, 1969); EEG abnormalities not found (Bender, 1960; Cole 1989; Roman-Campos et al., 1980; Shuttleworth & Wise, 1973); stories et a!., 1987; Collins & Freeman, 1986; Hodges & Ward, 1989). (Gallassi et a!., 1986; Hodges & Ward, 1989; Kritchevsky & Squire, 20. Guidotti et a!. (1989); Jaffe and Bender (1966); Man-Son-Hing 1989; Kritchevsky et al., 1988); paired-associate lists (Hodges & Ward, (1968); Melo et al. (1992); Miller et al. (1986); Miller, Yanagihara, et a!. 1989); spatial location (Gorelick et al., 1988). (1987). 9. Fisher and Adams (1964); Kritchevsky and Squire (1989); 21. 4% (Columbo & Scarpa, 1988; Jacome, 1989; Zinelli et a!., Kritchevsky et al. (1988); Man-Son-Hing (1968); Okada et al, (1987); 1988); 6% (Kushner & Hauser, 1985); 8% (Accurti & Proli, 1988); 13% Patten (1971); Paulson (1981); Shuttleworth and Morris (1966); Tanabe (Guidotti et a!., 1989); 14% (Miller, Petersen, Metter, et al., 1987); 19% et al. (1991). (Ciucci et a!., 1988); 20% (Hinge et a!., 1986; Matias-Guiu, Pico, Bona­ 10. Cafarra et al., 1981; Cole et a!. (1987); Cuningham (1968); Fisher ventura, Martin, & Monasterio, 1989); 23% (Matias-Guiu, Colomer, and Adams (1964); Giang and Kido (1989); Patten (1971); Stracciari, Segura, & Codina, 1986); 25% (Melo et al., 1992); 30% (Hodges & War­ Rebucci, & Gallassi (1987). low, 1990b); 32% (Laine et a!., 1984); 39% (Jensen & Olivarius, 1981); 11. Bolwig (1968); Donaldson (1985); Gallassi et al. (1986); Hodges 42% (Crowell et a!., 1984). and Ward (1989); Markowitsch (1983); Patten (1971); Ponsford and 22. Ahmed (1978); Bender (1956, 1960); Bogousslavsky and Regli Donnan (1980); Regard and Landis (1984); Stillhard et a!. (1990); Tan­ (1988); Bolwig (1968); Caplan (1985); Cattaino et a!. (1984); Evans abe et a!. (1991). (1966); Fisher and Adams (1964); Fogelholm et a!. (1975); Frederiks 12. Simple analogies (Gallassi et a!., 1986; Stracciari, Rebucci, & (1990,1993); Fujii et a!. (1990); Heathfield et a!. (1973); Jensen and Gallassi, 1987); proverb interpretation (Gordon & Marin, 1979; Gore­ Olivarius (1980); Kushner and Hauser (1985); Ladurner, Skvarc, and lick et al., 1988); object naming (Amit et al., 1986; Donaldson, 1985; Sager (1982); Longridge, Hachinski, and Barber (1979); Man-Son­ Gorelick et a!., 1988; Kritchevsky & Squire, 1989; Regard & Landis, Hing (1968); Markowitsch (1983); Martin (1970); Mathew and Meyer 1984); Stroop color-word naming (Regard & Landis, 1984); providing (1974); Matias-Guiu et a!. (1986); Mazzucchi (1988); Mi1andre, Don­ the rules ofcontract bridge (Gordon & Marin, 1979); WAIS subscales net, Rumeau, Ali Cherif, and Khalil (1990); Olivarius and Jensen (1979); (Berthier & Starkstein, 1990; Ponsford & Donnan, 1980); successive Ponsford and Donnan (1980); Poser and Ziegler (1960); Rowan and category generation (Cafarra et al., 1981; Gordon & Marin, 1979; Wil­ Protass (1979); Shuping, Rollinson, and Toole (1980); Shuping, Toole, son et a!., 1980). and Alexander (1980); Stevens and Ammerman (1974); Tharp (1969). 13. 3% (Muller, 1990); 4% (Hinge & Jensen, 1990); 5% (Columbo 23. Baron et a!. (1994); Croisi1e et a!. (1990); Evans et a!. (1993); & Scarpa, 1988; Hinge et al., 1986); 6% (Fisher & Adams, 1964); 7% Goldenberg (1995); Goldenberg et a!. (1991); Hodges (1994); Kazui (Kushner & Hauser, 1985); 8% (Hodges & Warlow, 1990b); 10% et a!. (1995); Laloux et a!. (1992); Lin et a!. (1993); Matsuda et a!. (Guidotti, Anzalone, Morabito, & Landi, 1989); 12% (Muller, 1990); (1993); Sakashita, Sugimoto, Taki, and Matsuda (1993); Stillhard et a!. 13% (Fisher, 1982; Melo, Ferro, & Paiva, 1994); 14% (Mazzucchi et al., (1990); Tanabe et a!. (1991); Volpe, Herscovitch, Raich1e, Hirst, & Gaz­ 1980); 15% (Matias-Guiu, Casquero et a!., 1987); 16% (Rollinson, zaniga (1983). 1978); 18% (Accurti & Proli, 1988; Caplan, 1985; Shuping, Rollinson, 24. Low incidence (Crowell et al., 1984; Fisher & Adams, 1964; & Toole, 1980); 19% (Gandolfo et al., 1992; Melo et a!., 1992); 22% Frederiks, 1993; Hinge et al., 1986; Nausieda & Sherman, 1979; Shup­ (Hinge et a!., 1986); 23% (Muller & Mase, 1981); 24% (Miller, Pe­ ing, Rollinson, & Toole, 1980); high incidence (Jensen & Olivarius, tersen, Metter, Millikan, & Yanagihara, 1987); 25% (Cattaino, Querin, 1980; Mathew & Meyer, 1974). Pomes, & Piazza, 1984; Laurent et a!., 1990; Nausieda & Sherman, 25. Occlusion (Araga et a!., 1989; Ladurner et al., 1982); aneurysm 1979); 26% (Frederiks, 1990); 30% (Rowan & Protass, 1979); 37% (Fo­ (Rosenberg, 1979); lesions (Laterra, Gebarski, & Sackellares, 1988; gelholm et al., 1975); 38% (Guyotat & Courjan, 1956, cited in Poser & Poser & Ziegler, 1960; Robinson & Long, 1972; Rumpl & Rumpl, Ziegler, 1960); 40% (Tukel, 1977); 42% (Heathfield et al., 1973); 57% 1979); embolism (Kadota, lrino, Nishide, Kaneda, & Hashimoto, 1981; (Mathew & Meyer, 1974). Milandre et a!., 1990; Shuttleworth & Wise, 1973; Steinmetz & Vroom, 14. 1.9% (Columbo & Scarpa, 1988); 2.5% (Hinge & Jensen, 1990; 1972); hypertension (Ghidoni et a!., 1988); platelet aggregation Muller, 1990); 2.7% (Gandolfo et al., 1992); 3.0% (Guidotti et a!., (Matias-Guiu et a!., 1989); hematoma (Chatham & Brillman, 1985; 1989; Hodges & Warlow, 1990b); 3.3% (Hofstad & Gjerde, 1985); Moonis et al., 1988); high cholesterol (Matias-Guiu, Davalos, Antem, & 3.4% (Miller, Petersen, Metter et al., 1987); 4.2% (Matias-Guiu, Cas­ Codina, 1984); scleroderma (Nishida et a!., 1990); hemorrhage (Bo­ quero, Alvarez, & Bonaventura, 1987); 4.7% (Hinge et a!., 1986). gousslavsky & Regli, 1988; Jacome & Yanez, 1988; Landi, Giusti, & 15. Within one day (Hodges & Ward, 1989; Stillhard et al., 1990; Guidotti, 1982; Sandyk, 1984); high hematocrit levels (Matais-Guiu, Stracciari, Rebucci, & Gallassi, 1987; Wilson et al., 1980); several days Masague, & Codina, 1985); angiography (Caplan, 1985; Cochran, to weeks (cf. Hodges & Ward, 1989; Gallassi et a!., 1986; Ghidoni et a!., 1983; Cochran, Morrell, Huckman, & Cochran, 1982; Frank, 1981, as 1988; Laine, Portin, & Koski, 1984; Mazzucchi et a!., 1980; Mazzucci cited in Markowitsch, 1983; Giang & Kido, 1989; Haas, 1983; Juni & Parma, 1990; Ponsford & Donnan, 1980; Regard & Landis, 1984; et a!., 1992; Minuk, Melancon, Tampieri, & Ethier, 1990; Pexman & Roman-Campos et al., 1980; Stillhard et a!., 1990; Stracciari, Ciucci, & Coates, 1983; Reichter, Belt, & Stevens, 1986; Shuttleworth & Wise, Bissi, 1987; Stracciari, Rebucci, & Gallassi, 1987; Zinelli et a!., 1988). 1973; Wales & Nov, 1981). 16. Croisile et a!. (1990); Frederiks (1990); Fujii, Sadoshima, and Fu­ 26. Stroke (Bender, 1956; Bogousslavsky & Regli, 1988; Ghika & jishima (1990); Hinge and Jensen (1990); Melo et a!. (1992); Palmer Bogousslavsky, 1990; Halsey, 1967; Heathfield et al., 1973; Logan & (1986). Sherman, 1983; Mathew & Meyer, 1974); cyst (Stracciari, Ciucci, & 17. Cantor (1971); Deisenhammer (1981); Evans (1966); Fisher Bissi, 1987); tumor (Araga et al., 1989; Cattaino et al., 1989; Collins & (1982); Gilbert (1978); Greene and Bennett (1974); Heathfield et a!. Freeman, 1986; Findler, Feinsod, Lijovetzky, & Hadani, 1983; Hartley, (1973); Hodges and Warlow (1990a, I990b ); Joynt, Satran, and Charl­ Heilman, & Garcia-Bengochea, 1974; Lisak & Zimmerman, 1977; Matias­ ton (1973); Kennedy, Ratnam, Freeman, and Ziegler (1979); Mathew Guiu et al., 1986; Meador et a!., 1985; Shuping, Toole, & Alexander, TRANSIENT GLOBAL AMNESIA 427

1980); hydrocephalus (Giroud et aI., 1987); neurosyphilis (Hall, 1982); defecating (8); neck extension (6); head retroflexion (5); infection (Nishida et aI., 1990; Pommer, Pilz, & Harrer, 1983). vertigo (3); working on a car (3); preparing dinner (2); play­ ing the piano (2); fishing (2); whiplash (2); hyperventila­ APPENDIX tion (2); preparing for a trip (2); singing (1); playing shuf­ Proximal Experiences Preceding TGA fleboard (I); cutting grass (1); hunting (I); carpentry work by Percent and Frequency (in Parentheses) (1); horseback riding (1); inspecting real estate (1); cough­ ing spell (I); push-starting a moped (1) Routine Activities: 10% (62) Heavy Physical Exertion: 19% (125) awakening in the morning (17); eating a meal (13); watch­ general farm work (44); general physical exertion (32); ing a movie (II); talking on the phone (5); watching tele­ swimming in cold water (13); athletic exercise (11); bicy­ vision (2); sitting (2); sunbathing (2); conversing (2); cling (11); chopping wood (8); vomiting (2); pitching hay attending church (1); praying on knees (1); standing up sud­ (1); gymnastics (1); playing football (1); installing a fire­ denly (1); discussing a manuscript (I); getting dressed (1); place (1) getting a haircut (1); riding a bus (I); riding a subway (1) Physical Pain: 10% (63) Emotional Stress: 15% (95) nonconcussive mild head injury (35); muscular pain (8); general emotional stress (49); intense argument (5); excit­ migraine attack (7); headache (4); abdominal pain (3); ing card game (4); arriving home from work (4); visiting chest pain (2); sinus pain (2); dental extraction (1); child­ a friend (4); sudden illness/injury to a friend or relative birth (1) (4); visiting a cemetery (2); business meeting (2); watch­ Medical Procedures: 5% (35) ing a sporting event (2); testifying in court (2); public angiography (17); general medical procedures (2); hospi­ speech (2); getting robbed (2); attending a memorial ser­ talization (2); spinal anesthesia (2); trigeminal ganglion vice for a spouse (1); receiving unpleasant news (I); at­ stimulation (2); pulmonary function test (2); treadmill test tending a party (1); tearful reunion with a child (1); busi­ (2); bronchoscopy (1); EEG exam (I); cystoscopy (1); cer­ ness foreclosure (1); relative's funeral (I); death ofspouse vical manipulation (1); excretory urography (1); nasogastric (1); getting fired (I); musical performance (1); harsh crit­ tube insertion (1) icism from boss (1); obscene phone call (1); witness to a Drugs: 1% (8) car accident (1); watching challenger explosion (I) chloroquine (3); diazepam (1); morphine (1); lorazepam Light to Moderate Physical Stress: 41% (268) (1); triazolam (1); clioquinol (1) sexual intercourse (52); driving (30); bathing in hot water (29); housecleaning (25); showering in hot water (20); gar­ (Manuscript received May 14, 1997; dening (20); at work (19); walking (18); shopping (9); revision accepted for publication December 9, 1997.)