9 79 Amnesia after Femorocerebral Angiography J. H. W. Pexman 1 R. K. Coates 1 The charts and radiographs of 12 of 1 ,520 patients who developed amnesia after transfemoral cerebral angiography performed with local anesthesia and minimal sedation were retrospectively reviewed . In three younger patients , exacerbation of organic or idiopathic temporal lobe epilepsy was thought to be the cause of the amnesia, while the amnesia of the nine patients over 40 years old had the characteristics of transient global amnesia . Eight of the patients had had similar episodes before angiography , and three others had other evidence of vertebrobasilar disease . Emboli from atheromatous debris or catheter clot due either to catheter manipulation problems , an inexperienced operator, or the use of a large catheter were considered likely causes in 11 cases, while in three patients contrast emboli or toxicity may have been the etiologic factor. Amn esia after angiography is se ld o m mentioned in reviews of th e compli ca tion s of ce rebral angiogra phy performed by transfemoral cath eterizati on [1]. Wi shart [2] bri efly mentioned six cases in 231 ve rtebral angi ograms. Wales and Nov [3 ] described two cases of transient g loba l amn es ia compli cating cerebral ang iography . Memory d isturbance was described in nin e patients after ve rt eb ral angiography by de Tribo let et al. [4] , while two cases have been reco rd ed during coro nary angiog raphy w ith the catheter positi oned in the aorta [5]. Our expe rie nce is th at amn es ia is more co mmo n th an th e literature sugges ts; th is pape r presents 12 cases see n in our department over th e past 4 years. MClterials and Methods Received November 20, 198 1; accepted aft er revision December 1 , 1982. ' Departm ent o f Diag nostic Rad io logy, Vi c tori a Hospita l, London, Ontario, Canad a N6A 4G5 . Address reprint req uests to J . H . W. Pex man. AJNR 4 :979-983, July / AU9ust 1983 0 195-6108 / 83 / 0404-0979 $00 .00 © Ame ri can Roentgen Ray Society B etween Ap ril 1977 and Ap ril 1981 , 1,520 pati ents had ce reb ra l ang iog rap hy pe rfo rm ed by transfemoral cat hete ri zati o n under loca l a nesth esia w ith pre med ication using eith er 10 mg Valium o r 30 mg Serax given o rall y about 1 hr before th e angiog ram. Th e po ste ri o r c ircu lati o n was stu d ied in 1,3 2 1 of th e pati e nts. Fo rty pe rce nt o f th e pati ents we re examin ed fo r suspected carotid ste nosis, 11 % fo r poss ibl e vertebrobasi lar isc hemi a, 3 0 % fo r possible intrac ra ni al b leed in g, 10% fo r suspec ted brain tum o rs, and 9 % for misce ll aneo us reasons. One ne uroradiol og ist use d a red Kifa 6 Frenc h cath eter fo r 750 angiog ra ms. Th e oth e r neurorad io log ist ob tain ed 3 13 angiograms w ith a 7 .3 Frenc h Cook Head Hunte r cath ete r o n cases presentin g wi th tra nsient isc he mi c attacks and vertebral basi lar di sease , and used a M an i 5 Fre nch ca th ete r for th e o th er 4 57 a ng iog rams. Fo rt y-e ig ht ang iog rams we re obtain ed by a resid ent under supe rvisio n, and th e two ex perienced neurorad io log ists obta in ed th e oth er 1 ,472. Conray-260 was used in all cases ; the cath eters were frequ entl y flu shed with heparini zed sa li ne (4 ,000 U / L). Subc lavian o r inn om inate inj ec ti ons we re made in 519 pati ent s; se lec ti ve ve rt ebral injec ti o ns w ere made in 802. Fo r eac h subc lavian o r innom in ate a rtery se ri es, 10 ml o f co ntrast materi a l was used pe r injec ti on , whil e 2 '12 -6 ml o f co ntrast materi a l was inj ec ted eac h tim e a ve rt ebra l artery was se lec ti ve ly stu d ied . Th e to tal amo unt of co ntrast materi a l injec ted into th e ve rte bro basil ar c ircu lati o n by th e neuro rad io log ist using th e M ani and Cook ca th ete rs was 20 ml , and th e o th e r neuro rad io logist never injected more th a n 3 5 ml. If both ve rteb ral a rt eri es need ed to be ca th eteri zed, bot h in vest igators PEXMAN AND COATES 980 studi ed one before and th e oth er after th e anterior c irc ulation had been examin ed so th at th ere was a '/2-1 hr interva l betwee n th e two se ri es of vertebrobasil ar injections. Th e smallest artery cath eterized in eac h examin ation of the posterior c irc ulat ion is recorded in tabl e 1. Results Th e ce ntral nervous system (CNS) co mpli cati ons are li sted in table 2 and are div ided into four types as described TABLE 1: Relation of Catheter Size and Artery Injected to Amnesic Complications Artery Inj ected: Catheter Type and French Size Subclavian: Head Hunter 7.3 Kifa 6 Mani 5 Vert ebral: Head Hunter 7.3 Kifa 6 M ani 5 N o . Patie nt s Tolals 284 225 10 13 4 20 369 With Amnesic Complica ti ons (Ages) 5(57,57,59,64,72) o o o 5(22,36,43,43,62) 1 (65) Note.-A 12 th pati ent (ag ed 24) developed amn esia aft er a right ca rot id angiogram was obtain ed . TABLE 2: Central Nervous System Complications in 1 ,520 Patients after Femorocerebral Angiography Type Transient minor Transient major Perman ent Deaths Total No . (% ) 14 (0. 9) 17 (1.1) 3 (0.2) Notes Fi ve < 5 min; all < 20 min 12 amnesias < 24 hr; three strokes < 10 days; one cortica l blin dness < 24 hr; one hall ucination < 48 hr Two strokes; one internu c lear op hthalm op le9 ia 0 34 (2.2) AJNR:4, Jul. / Aug. 1983 by Mani et al. [1]. A transient minor co mplication lasted less th an 10 days and did not significantly affect the hea lth of th e patient, while a transient major compli cation was of th e same duration, but th e activity and hea lth of the patient were affected . A perman ent complication persisted for more th an 10 days . Technical problems during angiography were reco rded on our radiologic reports . The data concern ing amnes ia and other co mplications were recorded at the time of th e angiogram and from information supplied during our daily neuroscience case conferences. Details of the course of amnesia were derived retrospectively from the patients ' charts. Twelve patients developed sudden amnesia for recent events and could not remember where they were , why they were there, or what had happened to them (table 3). Frequently, they asked a question that they had asked just a few minutes before and to which they had been g iven an answer. Some felt vaguely th at something was wrong and others felt shivery . In three younger pati ents (cases 1-3), the amnesic episodes were thought to be due to a temporal lobe epilepsy because th e patients were more ag itated , restl ess, or belligerent, and because th ey had previously had a similar attack labe led as temporal lobe epilepsy. These patients, two men and one woman aged 22-36 years, had no evidence of ce rebrovascular disease. The temporal lobe epi lepsy was idiopathi c in one patient, the result of a viral encephaliti s in another, and produced by a th alamic g liom a in th e third . The amnes ia started during or at the end of the angiograms and lasted 3 , 6 , and 24 hr, respectively. The posterior c irc ulation was studied angiographically in two patients, but in the patient with the thalami c glioma on ly a right carotid angiogram was obtained . In this patient the right carotid artery supplied the right posterior cerebral artery. In nine older patients , six men and three women 43-72 years old (mean , 58 years), transient g lobal amnes ia developed after angiography . This was recognized during or at the end of angiography in eight patients, while in one patient (case 12), the amnesia was recognized only 8 hr after TAB LE 3: Etiologic Factors in Amnesia after Femorocerebral Angiography Case No . Temporal lobe epil epsy Transient globa l amn esia Cli nica l (C) or rad iologic (R) evidence of di sease in th e territory of th e posterior ce rebral basil ar and ve rtebral art eri es: Previous amn esic episode Other evid ence of ve rt ebrobasil ar disease Spasm Possible tec hnic al prob lems: Catheter manipul ati on Inexperien ced resident Bi g cath eter-7 .3 Frenc h in subc lavi an (S) or 6 French in ve rtebral (V) Poss ible contrast problems: " Bad batc h" .............. " Overdose " . . . . . . . . . . . . . . . . . . . . Right carotid ang iog raph y onl y: thi s supplied the ri ght posterior ce re bra l arte ry . 5 French Mani used . t X C 2 3 X X C C 5 6 X X X C C R R C C X X V S' X V V V 9 10 11 X X X X X X C R C RC C C C X S X X 8 8 8 V X X X 8 t 12 8 TOlals 3 9 8 7 1 4 2 68; 5V 2 AJNR:4. Jul. / Aug . 1983 ANGIOGRAPHIC AMNESIA angiography. The nine patients had both their anterior and posterior c irc ulations stud ied. Cases 4-7 and 10-12 had cl ini cal and/or radiologic evidence of cerebrovascular d isease. Five of the nine cases (cases 4 , 6-8 , and 12) also had had a previous episode of transient g lobal amnesia. The precise duration of that amnesia was diffi c ult to evaluate, but five patients had recovered within 4 hr and all had recovered by 24 hr. Seven patients (cases 1, 2, 6, 7, and 9 -1 1), questioned at various times during their hospital stay, could not recall the angiogram . Four patients (cases 3, 5, 8, and 12) were not asked if they cou ld remember the angiogram. Case 4 was amnesic for 3 hr after angiography, but later c laimed to remember the angiogram . One of the older patients, case 7, developed transient signs indicative of vertebrobasi lar ischemia during his amnesia. No new signs occurred in any other patient. Computed tomography (CT) was performed on all patients before angiography and was normal in all except case 2, the patient with the thalamic glioma. Clinical vertebrobasilar d isease and a history of transient global amnesia was prominent in those patients who developed transient g lobal amnesia after angiography. Seven (4 %) of 167 patients presenting with vertebrobasilar disease developed postangiographic transient g loba l amnesia. Excluding all patients who may conceivably have had temporal lobe ep il epsy, only one (0.1 % ) in 1,200 of those patients without vertebrobasilar disease developed postangiographic transient g lobal amnesia. A patient who developed postangiographic transient g lobal amnesia was at least 10 (and not more than 30) times more li kely to have a history of transient global amnesia than one who did not develop this complication. In case 4 , a patient with spasm of the basilar artery in whom it was important clinically to prove that a basilar tip aneurysm was present , four injections of 6 ml of contrast material were made into the left vertebral artery, and it was estim ated in this case that 30 ml of the total 50 ml of con trast agent used for the investigation entered the posterior circulation. Technical problems with catheter manipulation were recorded in four patients (cases 5, 7 , 10, and 11). All the amnesic compli cations occurred in the hands of experienced neuroradiologists with the exception of two of the younger patients (cases 1 and 3), who were catheterized by a resident under supervision. In five patients the amnesic episodes followed subclavian injections using a 7.3 French Head Hunter catheter . There were no episodes of amnesia when subclavian angiography was carried out using 6 French Kifa or 5 French Mani catheters. In five patients the amnesic episodes followed selective vertebral injections using a 6 French Kifa catheter. One patient developed amnesia after a selective vertebral injection with a 5 French Mani catheter. In the patient in whom the posterior cerebral artery originated from the carotid artery , the amnesic episode followed carotid angiography using a 7.3 Frenc h Head Hunter cathete r. When the re lation of catheter size and the sma llest artery injected in age-matched groups is studied (table 1), a soft size 6 catheter is safer than a stiff size 7.3 catheter in a subclavian 981 artery and a size 5 catheter is safer than a size 6 ca theter in a vertebral artery. Cases 6 and 9 developed amnesia with the same batch of co ntrast material (table 3), and at that time six of nin e consecutive patients developed complications. Five of th ese had neurologic comp li cations, and one had an all ergic co mplication. Three of the patients had the prese nting neurologi c symptoms reprodu ce d. The probability that two of fiv e consecutive patients wo uld develop amnesia afte r angiography when the approximate incidence of amnesi a is 1 % (12 in 1,520) is 9.7 X 10- 4 , and the probability of fiv e of nine patients developing neurologic comp li cations when our neurologi c compli cation rate is 2 .2% (table 2) is 6 x 10- 7 using binomi al probability . Three patients had a history of temporal lobe epilepsy and five patients had a hi sto ry of transient g loba l amn esia. Seven patients had either c lin ical or radiologic evidence of vertebrobasi lar disease (table 3). Overall , therefore , 11 of 12 patie nts had ev id ence of disease in th e territories of th e posterior ce rebral arteries; case 9 was the on ly exce ption . These 11 patients were regard ed as having " susceptibl e brains. " Situations likely to produce atheromatous debri s or catheter c lot emboli occurred in 11 cases (table 3). In thre e patients contrast emboli or to xicity may have contribu ted to the deve lopment of th e amnesia , and in case 9 it was most strong ly suspected. Thi s 60-year-old man presenting with amaurosis fug ax had no radiologic or c lini cal evid ence of vertebrobasilar disease , and his technically uneventfu l angiogram was obtained by an experienced operator using a 6 French Kifa catheter in the vertebral artery. Thi s pati ent was one of the six of nine consecutive patients who developed complications during ang iography using the same batch of contrast material. Discussion Transient global amn esia is a syndrome desc ribed by Fisher and Adams [6] in 1964 in which th ere is a sudden loss of memory for the present and recent past in individu als in or past middle age, and the patients cannot retain new facts although the remote memory is intact . Charac teristicall y, the patient keeps asking the same question. There is no loss of consc iousn ess, no physical signs , and th e pati ent recovers in several hours but has amnesia for th e period of th e attack. Single occ urren ces are the rul e but multipl e attacks have been reported [7 -9]. Th e authors speculated that th e cause of the transient global amnesia might be a localized ep ilepti c discharge in the temporal lobe, a th eo ry subsequently favored by few [10 , 11], or an ep isode of ischemia involving the limbic system of the medial temporal lobe. The generally accepted theory is that it is du e to transient vascular insufficiency of the arteries supplying th e medial temporal lobe [12]. Our series has two distinct groups of patients-a younger group of three labeled as tem poral lobe epi lepsy and an o ld er group of nin e classified as transient global amnesia . Of our 1 ,520 pati ents, 12 (0 .8% or one in 125) developed postangiographi c amn esia , yet thi s co mpli ca ti on is rarely recorded by others [1 -5]. Th e com pli cati o n rate for patients 982 PE XM AN AND CO ATE S with cereb rovascul ar disease and subarachn oid hemorrh age in the 2,316 cases of M ani and Ei senberg [1 3] was 1.7 % . They did not say wheth er am nesia occurred . Ei se nberg et al. [1 4] reported a co mplicati o n rate of 1.3% in 301 cases of cerebrovasc ul ar d isease, but they d id not attempt either ve rtebral or subc lavian catheteri zati o n. Th ey repo rted no am nes ic com pli cati ons. Alth o ug h our CN S complicati on rate was 2 .2% , we had a hi g h num ber of mino r transient CNS compli cations (0.9% ) compared w ith Mani et al. [1] , possibly due to o ur lig ht sedati on. Because o ur overa ll comp licati on rates are si mil ar to th ose of other investigators, we spec ul ate th at oth ers may not have recog nized amn esia d ue to heavie r sedation. We wo ul d hav e been un aware of these com pl icati o ns if th e pati ents had been premedicated with neuro lepta nalgesia [ 15] or Demerol or had th e in vesti gati on been pe rformed unde r general anesth es ia. The type of sedati o n used by M ani et al. [1 ] and by Ei se nberg et al. [ 14] is not recorded. Palmer et al. [1 6] , w ho injected th e innominate and subc lavian arteri es, may not have noticed amnesic compli cations because of th e neuroleptanalges ia. Sil ent radio log ic emboli from cereb rofe moral ang iog raphy were desc ri bed by Cro nqvi st [17]. Ou r statistics for vertebral and subc lavian ang iog raphy suggest th at a small er, softer cath ete r will produce th e fewest complicati ons. Ei se nberg et al. [14] stated th at a 5 Frenc h cath ete r has a surface area onl y half th at of a 7 Frenc h cath eter , w hi c h would correspo ndi ngly dec rease th e potential for emboli , and th at the stiffer cath eters, wh ose torque facilitates cath eterizati on, may also damage th e intima by flailin g of th e cath eter tip . Wi shart [ 2] , wh o reco rd ed six cases of amnesia in 447 cases, used an 8 Frenc h Hinc k Head Hunter cath eter [1 8]. De Tribolet et al. [4 ], wh o desc ribed Ko rsakoff syndrome in nin e of 832 vertebra l angi ograms, used a 6.5 Fre nc h BD red cath eter, and we used a 7 .3 Frenc h Head Hunter in six of o ur cases. Lin [19] recomm ended onl y usi ng bigger Head Hunters fo r diffi c ult cases, preferring, as do M ani et al. [ 1] and Eisenberg et al. [1 4 ], the soft 5 Frenc h cath eter. Wishart [2 ] also stated th at most of hi s cases we re done by res idents, and M ani et al. [ 1] fo und in 5, 0 0 0 cases th at res idents prod uced 4 .5 tim es as many co mpli cati o ns as mo re experienced operato rs. Alth oug h Olivec ro na [20], w ho revi ewed a simil ar num ber of cases, d isag rees, comparisons suggest th at reside nts in Californ ia and Stock holm have sim il ar compli catio n rates. Two of our cases occ urred in th e hands of a resident . In Europe, fi ve commo n brands of contrast medi um have been fo un d to contain intrin sic parti c les [ 2 1]. In rub be rtipped via ls th ere are betwee n 6 1 and 369 partic les measurin g 5- 10 fLm, 45 to 183 measuring 10 - 3 0 fL m , and three to f ive measuring greater th an 30 fLm in va ri o us brand s in 1 ml of contrast mate ri al. Th ese small pa rtic les coul d embo li ze into th e territori es of both posterior cerebral arteri es, th e reg ions thoug ht by Horel [22] to be responsibl e fo r amnesia, and cou ld acco unt fo r our cases of am nesia in w hich verteb robasil ar disease or tempo ral lobe epil epsy was present in 1 1 of o ur 12 patients. Two cases described by Wales and Nov [3] occurred wh ile usi ng the same batc h of contrast medium (Con ray-60), and it was theo rized that th e compli- AJNR:4 , Ju l. / Aug . 1983 cati ons we re du e to contrast emboli . We had two simil ar cases associated wi th one batc h of co ntrast medium . On e of our cases of amn esia occ urred w hen about 30 ml of co ntrast materi al was inj ected into a ve rt e bra l artery to di ag nose a bas il ar aneurysm in th e presence of so me spasm. Th is amnesia may be d ue to contrast tox ic ity in a brain made susceptibl e by ath erosc lerosis and arteri al spasm. Tox ic effects of co ntrast medium ca n occ ur wi th v e ry hig h doses of mod ern age nts [23]. In 14 patients with tra nsient gl obal amnesia reported by Matth ew and Meye r [7] , 1 1 had c lini cal and 1 2 had rad iolog ic ev ide nce of vertebrobas il ar vasc ul ar di sease; and in our nin e cases of transient glo bal amnesia, seve n had c linical and three had rad iol og ic evid e nc e of vertebro basil ar disease. Five of our nine cases of transient global amnesi a had a previ ous amnesic epi sode, and all of our cases di ag nosed as temporal lobe epil epsy had had a simil ar epi sode. All th ese factors suggest th at th e re are areas in th e hi ppocampi made susceptibl e by disease processes that can be tri ggered either by an o perato r o r co ntrast-induce d factor. Ov e rd oses with di azepam may produce transi ent gl obal amnes ia [24] , but in our cases 10 mg oral Val ium or 30 mg Serax was c hose n to prod uce mild tranq uil izatio n with minimal drowsin ess. 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