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Transient Global : Complication of Cerebral Angiography

1 1 Lee R . Wales , 2 and Asher A. Nov

Transient global amnesia is a disorder of mentation in injecti on of 6 ml / sec for 11 ml. The pati ent received a total of 80 ml which there is an abrupt onset of loss and disorien­ of Conray-60 including test injecti ons. tation without change in consciousness. The disorder in­ Several minutes later, the patient looked at the examiners and volves events and activities of the present and recent past, asked who they were and where she was. She did not remember but leaves personal identification intact. There is no asso­ why she was in the hospital or why she was undergoing the stu dy. Transient slurring of speech was noted which cleared immediately. ciated focal or sensory deficit [1]. An episode usually lasts Th e catheter was withdrawn on recogniti on of the complication. for several hours. Memory returns to normal with residual Neurologic examinati on after angiography was unchanged with amnesia for the period of time from the onset to recovery. the exception of amn esia. The patient was confused and upset. She No consistent precipitating factors have been reported. was unable to the date or year, to retain numbers, or recall While series have been published associating the syndrome th e name of the hospital or objects shown to her for more than a to a number of possible causative mechanisms [1-3], we few minutes. Her automatic memory regarding her age, name, and know of no previous reports in the radiologic literature address was fully intact. Her preangiographic neurologic status describing total global amnesia as a complication of cerebral returned within 24 hr. angiography. Our experience with this syndrome forms the An giography revealed an avascular extraaxial mass in the right basis of this communication. cerebellopontine angle. There were no findings of atherosclerosis, spasm, or emboli. Surgery revealed a cholesteatoma. She had an uneventful recovery with return of strength on the right and no Case Reports further memory deficits.

Case 1 Case 2 A 27-year-old woman was referred for progressive neurologic symptoms of right-sided numbness, weakness, and " tingling." A 62-year-old man had a right upper lobe squamous cell carci­ Symptoms of objective vertigo, marked proximal muscle weakness, noma. No metastatic disease was found. Four months after radiation and dec reased coordination were noted. Her medical history and a therapy, he developed Jacksonian seizures of the ri ght arm which general physical examination were unremarkable. Neurologic ex­ progressed over a short peri od to right hemiparesis. Physical ex­ amination revealed right hemiparesis and subjective sensory dis­ amination revealed ri ght hemiparesis, ri ght , and turbance. Unenhanced and enhanced computed tomography and dysarthria. Decadron was begun. A CT scan revealed a left pari etal metrizamide (CT) c isternography revealed a low density right cer­ mass with surrounding edema and minimal mass effect. ebellopontine angle mass causing deformity of the stem and As resecti on was contemplated, cerebral arteriography was per­ quadrigeminal plate cistern. form ed via the femoral approach using a 5 French polyeth ylene Cerebral angiography was perform ed from the femoral approach catheter. The right common carotid , left common carotid, and left with a 5 French polyethylene catheter with frequent flushing with vertebral arteri es were stu died with a common carotid injection rate heparinized saline using a closed system. The right vertebral artery of 6 ml / sec for 12 ml. The vertebral artery was injected at a rate of was catheterized and rapid seri al filming was perform ed in the 6 ml / sec for 9 ml. The total amount of contrast materi al (Conray- anteroposterior, lateral, and base projections. Three injections of 60) admin istered during this study was 80 ml with duration of Conray-60 were made at the rate of 6 ml /sec for a total of 9 ml. examination being 55 min. Subsequently, in catheterizing the left carotid artery, the left verte­ Shortly after retraction of the catheter, the patient began ques­ bral artery was transiently entered on two occasions and small test tioning the angiographic team as to where he was and who the injections given. Separate anteroposteri or and lateral filming of the examiners were. He was disoriented to time and place. He did not left extern al carotid artery was performed with an injection rate of remember the angiographic procedure or the reason for his current 2 ml/ sec for a total of 7 ml. The left internal carotid artery was admission . The patient did remember his prior hospitalization and filmed in th e anteroposterior and lateral projections, each with an the diagnosis of lung carcinoma. Even after careful explanation,

Received July 29, 1980; accepted after revision November 6 , 1980. ' Department of Radiology, Harborview Medical Center, University of Washington, School of Medicine, Seattle, WA 98104. 2Present address: Department of Radiology, Evergreen General Hospital, 12040 N.E. 128th , Kirkland, WA 980 33. Address reprint requests to L. R. Wales. AJNR 2:275-277, May/ June 1981 0195- 6108/ 81 / 0203- 0275 $00.00 © American Roentgen Ray Society 276 WALES AND NOV AJNR:2, May/ June 1981

confusion recurred within minutes. Automatic memory for name, consistent precipitating factors have been noted [1 , 2, 12]: age, and address were intact. He was fully alert. Neurologic ex­ In a recent series by Mathew and Meyer [3], 14 patients aminati on in the angiographic suite revealed only his original neu­ with transient global amnesia, aged 40-92 years, were rologic defi c it and amnesia. Several hours after the procedure, his studied for a mean interval of 30 months. Thirteen of their resolved. patients had one or more risk factor for cerebral vascular An giographic findings demonstrated a left parietal avascular disease (hypertension, cardiac abnormalities, diabetes mel­ mass. No macroscopic emboli or spasm were noted . The patient litus, and hyperlipidemia). Clinical evidence for vertebral received radiation therapy but died 2 months later of diffuse meta­ static disease. An autopsy was not perform ed. basilar insufficiency was demonstrated in 11 cases. Cere­ bral angiography in 12 patients demonstrated lesions pre­ dominantly in the vertebral basilar system. In contradistinc­ Discussion tion to some earlier studies, eight of their patients had The neuroanatomy of amnesia is complex and controver­ recurrent attacks. Other studies have also reported multiple sial [4]. Bilateral lesions in the medial temporal lobe in attacks of total global amnesia [16, 17]. In the Mathew and humans produce a severe amnestic syndrome with perma­ Meyer [3] study, the patients with recurrent attacks showed nent antegrade amnesia (impaired ability to acquire infor­ permanent memory impairment on follow-up examination. mation , that is, to learn or form new [5]) and The type and incidence of complications secondary to retrograde amnesia (impaired ability to recall events and catheter cerebral arteriography have been well described other information that had been well established for a short [18-21]. In a recent review of 5,000 cases, Mani et al. [18] peri od prior to the injury [6- 8]). Early memories and mem­ noted that 43 (93%) of the 46 complications related to the ori es for technical skills remain intact and there is no loss of central nervous system were transient. The major compli­ general intelligence or complex perceptual abilities [7]. cations were visual, motor, or cerebellar. Scoville and Milner [7] found that medial temporal lobe The presumed mechanism for most complications has resecti on produced memory defects only when the hippo­ been embolism from the catheter and guide wire, athero­ campus was included. The pathologic studies of Korsakoff matous debris, or thrombus from the cardiac wall [18, 19]. syndrome and posterior cerebral artery occlusion supported A report of memory disturbance during angiography [22] the as an important structure in amnesic syn­ described transient visual abnormalities in six with two cases dromes, however animal studies failed to support this inter­ of isolated memory disturbance. Two cases of total global pretati on [4]. Horel [4] recently reviewed the literature on amnesia occurred during coronary angiography while the amn esi a and proposed that the hippocampus, fornix, and catheter was in the aortic arch. Amnesia ensued presumably mamillary bodies are not the source of amnesia in brain secondary to embolization of catheter thrombus after arterial injury. He proposes that the symptoms are produced by pressure through the catheter became clamped and aspi­ involvement of a system closely associated with the temporal ration was performed to clear it [23]. No obvious problems neocortex. This includes the temporal cortex and its white in catheter technique were noted during our cases. Ather­ matter extensions. These tracts connect the brain stem as omatous emboli are a well known complication of catheter well as the basal ganglia, medial thalamus, and orbitofrontal angiography [24, 25]. This is a possible cause in case 2. cortex. The vascular supply to this region is predominantly The recent finding of intrinsic particles in five commonly vi a the posterior cerebral artery. used water-soluble contrast media in Europe suggests an­ Clinically, disorders of memory have been associated with other possible source of emboli [26]. The multiplicity (the a wide variety of conditions. Amnesia has been a manifes­ mean number of particles greater than 5 J.Lm was 302 / ml tati on of bilateral hippocampal infarction, trauma to the contrast medium) of small emboli would more likely affect diencephalotemporal regions, spontaneous subarachnoid the territories supplied by both posterior cerebral arteries, hemorrhage and Wernicke-Korsakoff syndrome, among the region thought by Horel [4] to be responsible for amne­ many others [5, 9]. Amnesi a of sudden onset and transitory sia. Both our cases occurred within 10 days using the same duration occurs with temporal lobe seizures, electroconvul­ lot of contrast media. Due to the retrospective recognition sive treatm ent, postconcussive states, and the syndrome of of this by separate angiographers, we did not have a chance total global amnesia; all but the first and last are easily to analyze the contrast agent. No other neurologic compli­ distinguishabl e on clinical grounds [5, 9]. cations were noted in the time period where this lot of Total global amnesi a is a syndrome which has elicited contrast material was used. Reviewing our clinical material numerous reports [9-1 6] including a detailed description of for 10 years, no other cases of total global amnesia were 1 7 pati ents by Fisher and Adams [1]. The clinical presen­ identified. Spasm related to catheter manipulation or con­ tation in their cases is rather stereotyped. The patient is trast material would seem unlikely as a mechanism in our usually a man in the fifth or sixth decade who is suddenly patients, as spasm was not seen on the angiograms. unable to form new memori es. He is unable to perform Toxic effect of contrast material on the brain was reported routine tasks, and characteristically shows concern over the with early contrast media and very high-dose modern agents disability, incessantly repeating the same questions. There [27, 28]. Opening of interendothelial junctions at the capil­ is a striking inability to learn new material without impairment lary level with alteration in the blood-brain barrier and leak­ of remote memory. The patient is well aware of his own age of contrast material into the parenchyma [29] was noted. identity and the neurologic examination is unremarkable. Microscopic findings included swelling of perivascular as­ The episode usually lasts from 30 min to several hours. After trocytic filaments, ballooning of mitochondria, and lesions recovery, there is amnesia for the period of the attack. No of myelin fibers [28]. AJNR:2. May/ June 1981 TRANSIENT GLOBAL AMNESIA 277

Our two cases of an extremely rare, relatively localized 11 . Fi sher CM, Adams RD . Transien t global amnesia. Trans Am neurologic deficit with a normal contrast load of a modern Neurol Assoc 1958;83: 1 43-1 46 agent would mitigate against contrast toxicity as the cause. 12. Heathfield KWG, Croft TV, Swash M. Th e syndrome of transien t global amnesia. Brain 1973;96: 729-736 A unilateral lesion of one temporal region would more easily 13. Gilbert JJ, Benson OF. Transient global amnesia: report of two explain this syndrome resulting from one or several small cases with definite eti ologies. J Nerv Ment Dis 1972; 154: 461 - emboli affecting the opposite side. However, CT scans 464 revealed the temporal region to be grossly normal in both 14. Man-Son-Hing CT. An uncommon type of transient loss of cases. memory. Ca n Med Assoc J 1968;98:594-599 Of the three mechanisms postulated for total global am­ 15. Martin EA . Transient global amnesia. Ir J Med Sci 1970;3: nesia (emboli, spasm, or contrast toxicity), we think emboli 331-335 the most probable. On the basis of the neuroanatomy of 16. Steinmetz ES. Vroom SQ. Transient global amnesia. amnestic syndrome, bilateral distribution is necessary. Two (NY) 1972;22: 1193-1200 cases of total global amnesia within a 10 day period using 17. Poser CM, Siegler OK . Temporary amnesia as a manifestati on the same lot of contrast material would suggest the latter as of cerebral vascular insufficiency. Trans Am Neurol Assoc 1960;85: 221 -223 an agent. In light of the recent report regarding intrinsic 18. Mani RL, Eisenberg RL, McDonald EJ , et al. Compli cati ons of particulate matter in contrast media, emboli offer the most cerebral arteri ography: analysis of 5,000 procedures. I. Crite­ plausible explanation for this phenomenon. More work ri a and incidence. AJR 1978;1 3 1 :861-865 needs to be done on contrast agents used in the United 19. Silberman J, Cravioto H, Feigin I. Foreign body emboli following States to see if intrinsic particles are present in them, as cerebral angiography. Arch Neuro/ 1960;3: 711-717 has been described in Europe. 20. Takahashi M , Kawanani H. Complications of cath eter cerebral angiography: an analysis of 500 examinations. Acta Radiol [oiagJ (Stockh) 1972; 13: 248-258 21. Fi eld JR, Robertson JT, OeSaussure RL. Jr. Complications of REFERENCES cerebral angiography in 2000 consecutive cases. J Neurosurg 1. Fisher CM, Adams RD. Transient global amnesia. Acta Neurol 1962;19: 775-781 Scand 1964;9: 7 -83 22. deTriebolete N, Assai G, Obetson R. Syndrome de Korsakoff 2. Mayeuxr R. Sexual intercourse and transient global amnesia et cecite corticale transito ires apres angiographie vertebrale. (letter). N Engl J Med 1979;300 : 864 Schweiz Med Wochenschr 1975; 105: 1 506-1 509 3. Mathew NT, Meyer JS. Pathogenesis and natural history of 23. Shuttleworth EC , Wise GR. Transient global amnesia due to transient global amnesia. 1974;5 :303-311 arterial embolism. Arch Neuro/1 973;29: 340- 342 4 . Horel JA. Neuroanatomy of amnesia, a critique of hippocampal 24. Schwartz S, Waters L. Cholesterol embolization. Radiology memory hypothesis. Brain 1978; 101 : 403-445 1973;106:37-41 5. Victor M . The amnesic syndrome and its anatomical basis. Can 25. Lonni YGW. Matsumoto KK, Lecky JW. Postangiographic cho­ Med Assoc J 1969;100: 1115-1125 lesterol (atheromatous) embolization. Radiology 1969;93: 63- 6. Scoville WB. The limbic lobe in man. J Neurosurg 1954;11 : 65 64- 66 26. Winding O. Intrinsic particles in angiographic contrast media. 7. Scoville WB, Milner B. Loss of recent memory after bilateral Radiology 1980; 134: 31 7 - 320 hippocampal lesions. J Neurol Neurosurg Psychiatry 1957;20 : 27. Bassett RC, Rogers JS, Cherry GR, Cruzhit C. Th e effect of 11-21 contrast media on the blood-brain barrier. J Neurosurg 8. Penfield W , Milner B. Memory deficit produced by bilateral 1953;10:38-47 lesions in the hippocampal zone. Arch Neurol 1958;79:4 75- 28. Murphy OJ . Cerebrovascular permeability after meglumine io­ 497 thalamate administration. Neurology (NY) 1973;23: 926-936 9. Symonds C. Disorders of memory. Brain 1966;89:625-644 29. Broman T, Olsson O. The tolerance of cerebral blood vessels 10. Evans JH. Transient loss of memory, an organic mental syn­ to a contrast medium of the diodrast group. Acta Radiol drome. Brain 1966;89: 539-548 (Stockh) 1948;30: 326- 342