Anesth Analg 2005;101:916-919
© 2005 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000175208.76574.54
GENERAL ARTICLES
Transient Global Amnesia After General Anesthesia
Ryan J. Bortolon, MD,
Margaret R. Weglinski, MD, and
Juraj Sprung, MD, PhD
Department of Anesthesiology, Mayo Clinic College of Medicine, Mayo Clinic, Rochester, Minnesota
Address correspondence and reprint requests to Juraj Sprung, MD, PhD, Department of Anesthesiology, Mayo Clinic Mayo Clinic College of Medicine, Mary Brigh 2–752 200 First Street SW, Rochester, MN 55905. Address electronic mail to sprung.juraj{at}mayo.edu.
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Abstract
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Transient global amnesia (TGA) is an amnestic syndrome, clinically dramatic but benign in nature. The hallmark of TGA is brief inability to form new memories and recall past memories despite otherwise normal neurological function. In a significant number of patients with TGA a stressful precipitating factor can be identified. We report two cases of TGA after uneventful general anesthesia. Anesthesia per se does not appear to be a direct trigger of TGA, as our first patient had a second anesthetic the next day without recurrence of TGA. Because the presentation of TGA can be dramatic and may mimic an acute cerebral ischemic event, a thorough neurologic evaluation should be pursued.
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Introduction
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Transient global amnesia (TGA) is a clinically dramatic, but poorly understood, amnestic syndrome. The hallmark of TGA is short-term inability to form new memories despite otherwise normal neurological function (1) (Table 1). The amnesia frequently involves recent and remote events, with the extent of memory loss varying from person to person (2–4). The memory loss is often accompanied by repetitive questioning and temporal disorientation ("Where am I? Why am I here?") while other neurologic functions, such as alertness, complex manual tasks, and other higher cognitive functions are preserved. The symptoms typically last from 30 min to 24 h (5). The reported annual incidence ranges from 3 to 32 per 100,000 persons (6). The overall incidence of TGA in Rochester, Minnesota is 5.2 per 100,000 residents per year (2). TGA usually affects patients between 50 and 60 yr of age, with a slightly increased incidence in females (2,7). The incidence of TGA for the population older than 50 yr of age in Rochester, Minnesota is 23.5 per 100,000 per year (2). In a significant number of cases a stressful precipitating factor can be identified (5,7,8) and excessive exertion preceding onset is present in 33.4% of cases (2). There are only 3 reports of TGA associated with general anesthesia in the literature (1,9,10). We report two cases of TGA after general anesthesia.
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Case Reports
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Case 1
A 67-yr-old man underwent evaluation for left shoulder pain and paresthesias along the left C5-C6 dermatome. The neurologist diagnosed mild weakness of the left arm external rotators, and an electromyogram showed evidence of a left C7 radiculopathy with active denervation. Based on these findings magnetic resonance imaging (MRI) of the cervical spine was ordered. Because of severe pain associated with neck extension, an initial attempt to perform the MRI was unsuccessful and was rescheduled under general anesthesia.
The patient's medical history was significant for coronary artery disease, migraine headaches, and depression with hallucinations. His electrocardiogram showed normal sinus rhythm with a ventricular rate of 70 bpm. His preoperative medications included atorvastatin, hydrocodone, ibuprofen, and calcium. After receiving 100 µg of fentanyl the patient was positioned on the MRI table. General anesthesia was induced with 200 mg of propofol IV and a laryngeal mask airway (LMA) was inserted. Anesthesia was maintained with 1.2% of isoflurane and a 50:50 percent mixture of nitrous oxide and oxygen. During induction, his arterial blood pressure decreased from 180/90 mm Hg to 110/70 mm Hg. His oxyhemoglobin saturation was 98% throughout the course of anesthesia. After the 50-min MRI was completed the patient emerged from anesthesia smoothly and the LMA was removed without coughing or straining. No benzodiazepines were given before or throughout the course of anesthesia. Approximately 30 min after entering the postanesthesia recovery room, he was awake and appeared comfortable. However, he was unable to recall having an MRI or the reason for scanning. After a 50-min stay in the recovery room he was sent to the outpatient recovery area. Forty-five minutes later the nurse contacted the anesthesiologist because the patient was continuing to ask the same questions repeatedly and did not know where he was or how he got there. When the anesthesiologist visited the patient she found him sitting in bed awake, alert, and calm, but oriented to person only. He did not remember meeting the anesthesiologist before. He could not recall names of close family friends or where his children lived. He repeatedly asked where he was and why he was there and despite being answered, he would ask the same questions again a few minutes later. His wife estimated that he had lost his memory of the last 5 yr. The patient's wife stated that the patient never before had a similar event.
Arterial blood gas values with sodium, potassium, and glucose concentrations were normal. The patient's neurosurgeon was consulted and he found no abnormalities suggestive of a vertebrobasilar ischemic event. He suspected the patient was having an episode of TGA. The patient was admitted, given 100 mg of thiamine, and hydrated with normal saline. His amnesia gradually improved throughout the evening so that by 10 h after the onset of his TGA episode his cognitive function was back to baseline.
As the patient's MRI showed moderate left foraminal disk protrusion at C5-C6 and narrowing of the left C6-C7 foramen, he underwent left C5-C6 hemilaminectomy the following morning. His anesthetic course was unremarkable and he had no further episodes of amnesia. He was discharged from the hospital 2 days later. Before discharge his wife spoke to the neurosurgeon regarding her concerns about her husband's slowly progressive change in personality over several months before his episode of TGA. She observed that he was more easily irritated, more aggressive, and less decisive. When driving in the car he seemed to be less certain of where he was going. She questioned if his recent episode of TGA was another manifestation of possible early cognitive decline. When approached with these concerns the patient denied any problems. The patient returned 6 wk later and underwent neuropsychometric testing, awake electroencephalogram, MRI of the head, and extensive laboratory studies for treatable causes of memory and behavior changes. All results were nondiagnostic.
Case 2
A 74-yr-old male with a history of a bladder tumor underwent transurethral bladder resection under general anesthesia. The patient's medical history was significant for noninsulin-dependent diabetes mellitus, stable coronary artery disease, and migraine headaches controlled with non-opioid medications. His preoperative medications included metformin, enalapril, and acetaminophen/butalbital/caffeine as needed.
Before induction of anesthesia, vital signs were stable with arterial blood pressure of 151/68 mm Hg, heart rate 72 bpm, and oxyhemoglobin saturation of 97%. Anesthesia was induced with 250 µg fentanyl and 150 mg of propofol IV, and 100 mg succinylcholine was given for muscle relaxation. After endotracheal intubation, anesthesia was maintained with sevoflurane and a 50:50 percent mixture of nitrous oxide and oxygen. The patient experienced a brief period of moderate hypotension (mean arterial blood pressure, 61 mm Hg), which was treated with ephedrine, shortly after induction of anesthesia. The anesthetic course was stable throughout the remainder of the procedure. After the 50-min procedure, the patient emerged uneventfully from anesthesia. His immediate postanesthesia recovery was uneventful, he appeared comfortable, and he was discharged to the outpatient waiting area.
On arrival to the outpatient area the nurse noted that the patient was disoriented with regard to place and time. The patient was oriented to self and knew his family members. Over the next hour he continued to be disoriented despite multiple attempts at reorientation. He repeatedly asked the same questions such as: "Where am I? What day is it? Why am I here?" The patient otherwise displayed normal level of alertness and no other neurological abnormalities were noted. Blood gases, serum glucose, and electrolytes were all within normal limits. A subsequent neurological consultation also resulted in no additional findings. Computed tomography of the head was unremarkable. A follow-up examination performed 8 h after the event revealed a complete recovery of mental status.
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Discussion
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TGA is characterized by a sudden memory loss of recent and/or remote events and transient inability to acquire new knowledge. The dramatic presentation of acute change in personality, such as in our two patients, after emergence from general anesthesia, creates a puzzling and frightening situation for both the patient's family and the anesthesiologist.
Several etiologies of TGA have been postulated, but the underlying causes remain obscure. These include TGA being either a form of seizure or transient ischemic attack (TIA) in the territory of the posterior cerebral circulation, especially in the hippocampus and other parts of the limbic system related to short-term memory function (11,12) (Table 1). Others have proposed that TGA may be caused by TIA in the area of vertebrobasilar arterial distribution (13). However, none of the above mechanisms can explain the absence of neurologic signs or symptoms during TGA (11). Occasional association of TGA with Valsalva-like activities has led to the investigation of retrograde transmission of rapid venous flows into the cerebral venous system leading to temporary ischemia in the territory of the temporal lobe, hippocampus, and diencephalon (14–16). In support of this hypothesis, two studies using transcranial duplex sonography revealed that up to 72.9% of patients with TGA had jugular venous incompetence (16,17). Finally, the association of migraine headaches with TGA adds to further speculation that TGA patients may be susceptible to cerebral vasoconstrictors and that a similar underlying mechanism is shared between TGA and migraine headaches.
Immediately after an episode of TGA, MRI is unlikely to identify any abnormality (11). However, Ay et al. (18) described a patient with TGA whose diffusion-weighted (DW) MRI showed increased signal in the splenium of the corpus callosum and left parahippocampal gyrus. DW MRI may detect similar signal abnormality in both TIA and TGA; however, ischemic lesions typically appear very soon after onset of ischemia and are usually larger than those after TGA. In contrast, TGA-associated DW MRI changes occur most frequently after a 24-hour delay (15). Furthermore, a positive lesion on DW MRI during TIA results in a lower "apparent diffusion coefficient" (ADC) compared with TGA. A pattern of decreased intensity on ADC maps is useful in the early detection of ischemic brain injury. One proposed therapeutic approach is to add antiplatelet therapy to all patients with TGA who have a proven DW MRI abnormality in addition to positive cerebrovascular risk factors (15). However, further studies will be required to clarify this approach.
The DW MRI findings in patients with TGA are consistent with Lewis's venous backflow (congestion) theory of TGA (11). However, venous backflow is a very frequent event in everyday life (during Valsalva maneuver, intense emotion, sexual activity), and during anesthesia (coughing); therefore TGA should be more frequent if this mechanism were the only explanation.
There are several conditions that may either resemble or be associated with TGA. One is transient epileptic amnesia (TEA), which may resemble TGA except episodes are shorter and more frequent (19). In addition, patients with TEA consequently develop epileptic symptoms, which clearly differentiate it from TGA (7,20). Second, several authors described association of migraine headaches with TGA in up to 14.1% of patients (2,7,20,21). Both our patients suffered from migraine attacks. Finally, Nausieda and Sherman (12) found that 6% of TGA patients develop dementia over a 3-year follow-up period. In fact, early dementia may present as TGA (22). Our first patient had a history of depression and demonstrated intermittent psychological changes several months before the hospitalization for MRI; however, subsequent neurobehavioral testing was nondiagnostic.
TGA has been described only rarely after general (1,9,10) or spinal (23,24) anesthesia. During general anesthesia, many factors may contribute to an episode of TGA. If one believes that the Valsalva maneuver may lead to venous backflow in the cerebral system, then the addition of large levels of positive end-expiratory pressure or prolonged episodes of coughing before tracheal extubation may, in fact, lead to higher transthoracic pressures, which may induce venous backflow in susceptible patients. Furthermore, perioperatively, patients may undergo substantial pain as well as emotional and physical stress; all of these conditions have been described as possible inducers of TGA (5). Certainly, the use of benzodiazepines during general anesthesia may also be associated with transient memory loss resembling TGA (25); however, this type of amnesia is purely anterograde with no effect on retrograde memory (26). Neither of our patients received benzodiazepines perioperatively. Knowing the benign course of TGA, it was decided in our first patient to proceed with surgery the following day. The perioperative course was uneventful and no repeated episodes of TGA were noted. Therefore, TGA in this patient cannot be associated with any specific aspect of anesthesia per se. Furthermore, considering the incidence of TGA in the general population, it is surprising that the incidence of TGA after general anesthesia is so rare (1,9,10). This is especially true considering the pathogenesis of TGA has more recently been attributed to cerebral venous hypertension resulting from retrograde jugular venous flow (17), which may occur during the coughing or Valsalva maneuvers that are frequently encountered perioperatively. Moreover, a possibility exists that less severe postoperative TGA episodes resolve even before they get detected or may be falsely interpreted as perioperative confusion.
In conclusion, patients with TGA usually have no associated neurologic abnormalities and the memory loss is short-lived. TGA is a benign clinical phenomenon, probably caused by a functional cerebral disturbance unrelated to cerebrovascular disease; however, its presentation may be dramatic immediately after surgery and differentiation from a cerebral ischemic event should be pursued. Anesthesia per se does not appear to be a direct trigger for TGA, as our first patient had a second anesthetic the following day without recurrence of TGA. It is important to differentiate between a TGA and a TIA resembling TGA, as the latter may require antiplatelet therapy.
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Footnotes
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Supported, in part, by the Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota.
Accepted for publication March 14, 2005.
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References
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- Kohase H, Yoshikawa F, Umino M. Transient global amnesia after general anesthesia [in Japanese]. Masui 1998;47:481–3.[Medline]
- Miller JW, Petersen RC, Metter EJ, et al. Transient global amnesia: clinical characteristics and prognosis. Neurology 1987;37:733–7.[Abstract/Free Full Text]
- Zeman AZ, Boniface SJ, Hodges JR. Transient epileptic amnesia: a description of the clinical and neuropsychological features in 10 cases and a review of the literature. J Neurol Neurosurg Psychiatry 1998;64:435–43.[Abstract/Free Full Text]
- Wermut W, Benert K. Transient global amnesia. Case report [in Polish] Neurol Neurochir Pol 1992;26:883–6.[Medline]
- Fisher CM. Transient global amnesia: precipitating activities and other observations. Arch Neurol 1982;39:605–8.[Abstract]
- Pantoni L, Lamassa M, Inzitari D. Transient global amnesia: a review emphasizing pathogenic aspects. Acta Neurol Scand 2000;102:275–83.[ISI][Medline]
- Zorzon M, Antonutti L, Mase G, et al. Transient global amnesia and transient ischemic attack. Natural history, vascular risk factors, and associated conditions. Stroke 1995;26:1536–42.[Abstract/Free Full Text]
- Hodges JR, Warlow CP. Syndromes of transient amnesia: towards a classification: a study of 153 cases. J Neurol Neurosurg Psychiatry 1990;53:834–43.[Abstract]
- Wood T, Donegan J. Transient global amnesia following general anesthesia. Anesthesiology 1985;62:807–9.[ISI][Medline]
- Yamaji A, Watanabe H, Tanaka K et al. A case of retrograde amnesia of 22 years, continued for 4 days following a general anesthesia accompanied by a permanent amnesia of these 4 days after the complete recovery from the retrograde amnesia [in Japanese]. Masui 1989;38:236–40.[Medline]
- Lewis SL. Aetiology of transient global amnesia. Lancet 1998;352:397–9.[ISI][Medline]
- Nausieda PA, Sherman IV. Long-term prognosis in transient global amnesia. JAMA 1979;241:392–3.[Abstract]
- Jensen TS, de Fine Olivarius B. Transient global amnesia: its clinical and pathophysiological basis and prognosis. Acta Neurol Scand 1981;63:220–30.[ISI][Medline]
- Akkawi NM, Agosti C, Rozzini L, et al. Transient global amnesia and disturbance of venous flow patterns. Lancet 2001;357:957.
- Tong DC, Grossman M. What causes transient global amnesia? New insights from DWI. Neurology 2004;62:2154–5.[Free Full Text]
- Sander D, Winbeck K, Etgen T et al. Disturbance of venous flow patterns in patients with transient global amnesia. Lancet 2000;356:1982–4.[ISI][Medline]
- Maalikjy Akkawi N, Agosti C, Anzola GP, et al. Transient global amnesia: a clinical and sonographic study. Eur Neurol 2003;49:67–71.[ISI][Medline]
- Ay H, Furie KL, Yamada K, Koroshetz WJ. Diffusion-weighted MRI characterizes the ischemic lesion in transient global amnesia. Neurology 1998;51:901–3.
- Kapur N. Transient epileptic amnesia: a clinical update and a reformulation. J Neurol Neurosurg Psychiatry 1993;56:1184–90.[Abstract]
- Hodges JR, Warlow CP. The aetiology of transient global amnesia: a case-control study of 114 cases with prospective follow-up. Brain 1990;113:639–57.[Abstract/Free Full Text]
- Tosi L, Righetti CA. Transient global amnesia and migraine in young people. Clin Neurol Neurosurg 1997;99:63–5.[ISI][Medline]
- Daniel ES. Early diagnosis and treatment of dementia presenting as transient global amnesia in a 76-year-old man. Prim Care Companion J Clin Psychiatry 2004;6:248–51.[Medline]
- Domingo I, Abad F, Velilla I. Amnesia global transitoria durante anestesia subaracnoidea. Rev Esp Anestesiol Reanim 1996;43:74–5.
- Dykes MH, Sears BR, Caplan LR. Transient global amnesia following spinal anesthesia. Anesthesiology 1972;36:615–7.[ISI][Medline]
- Ogg TW, Fischer HB, Bethune DW, Collis JM. Day case anaesthesia and memory. Anaesthesia 1979;34:784–9.[ISI][Medline]
- Ghoneim MM. Transient global amnesia: a cause for postanesthetic memory disorder. Anesth Analg 1998;87:980–1.
- Hinge HH, Jensen TS, Kjaer M, et al. The prognosis of transient global amnesia: results of a multicenter study. Arch Neurol 1986;43:673–6.[Abstract]
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Abstract
Introduction
