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Transient Global Amnesia: Complication of Cerebral Angiography

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Transient Global Amnesia: Complication of Cerebral Angiography 275 Transient Global Amnesia: 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 memory 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 An episode usually lasts Th e catheter was withdrawn on recogniti on of the complication.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 recall 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 facial weakness, 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 brain 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 retrograde amnesia 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 memories [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 hippocampus 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].
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