Transient global amnesia after cerebral angiography still occurs: Case report and literature review.

Transient global amnesia is considered a very rare complication of diagnostic cerebral angiography, and has been reported only in a limited number of case reports more than 15 years ago. We describe a patient experiencing transient global amnesia following cerebral digital subtraction angiography. While the condition by definition is self-limiting, its differential diagnoses may cause severe morbidity and/or mortality if left untreated. It is therefore important to build and maintain awareness of transient global amnesia as a possible complication of cerebral angiography.

Introduction

Transient global amnesia (TGA) is an amnesic syndrome characterized by the abrupt onset of both anterograde and retrograde memory loss and lasting 2-24 hours. Its clinical features were first described by Ribot and Benon in 1882 and 1909 (1, 2), while Fischer and Adams introduced the official term and proposed diagnostic criteria in the 1960s (3). Key features of TGA include inability to form new memories and retrieve memories of past events, while exhibiting no other cognitive impairments or focal neurological or epileptic signs (4). The condition is self-limiting, with full resolution of symptoms within 24 hours.

While TGA is often preceded by emotional or physical stress (5, 6), its underlying pathophysiology is still unclear. Recent high-resolution MRI neuroimaging has revealed highly focal, transient lesions in the memory-associated CA1 field of the hippocampus in the acute stages of TGA (7, 8). Several possible underlying causes have been suggested, including migraine-related mechanisms, venous-flow abnormalities, hypoxic-ischemic events, epilepsy-related activity, cortical spreading depression, and psychological factors (4).

The following describes a patient experiencing TGA after diagnostic cerebral digital subtraction angiography (DSA). This phenomenon has been reported only a limited number of times, the last time more than 15 years ago (9). With this case report, we wish to renew and increase awareness of this rare complication and its uncertain pathophysiology.

Case report

A 53-year-old man was admitted for a scheduled followup DSA following an episode of subarachnoid hemorrhage (SAH) and subsequent coiling of a basilar-tip aneurysm six months prior (see Figure 1a, Figure 1b). After coiling of the aneurysm, the patient received standard treatment: 75mg acetylsalicylic acid daily for two months and 60mg nimodipine six times daily until day 21 post-ictus because of light vascular spasms observed during the coiling procedure. The patient was otherwise regarded as healthy, without any other history of disease, and suffered no significant sequelae after the SAH.

Figure 1a

The patient's cerebral angiogram before the coiling procedure.

Figure 1b

The patient's cerebral angiogram, immediately after coiling.

The physical examination and vital parameters prior to the followup DSA were unremarkable. The followup DSA was performed under local anesthesia with two injections, each with a volume of 7 ml of nonionic iohexol (Omnipaque ®, GE Healthcare), injected by hand in the left vertebral artery using a 5 fr. JB1-catheter. This demonstrated a normal course and caliber of the left vertebral artery, the distal right vertebral artery, the basilar artery, and the posterior circulation. Coil compaction into the neck of the aneurysm was noted consistent with a Raymond-Roy type B recurrence (see Fig. 1C). No vascular spasms were observed. Conscious sedation was not administered.

Figure 1c

The patient's cerebral angiogram one year after coiling.

Two hours after the procedure, the patient developed sudden-onset global amnesia. A detailed neurological examination revealed that the patient was awake and alert, partly oriented in personal data, but not in location or time. He did not know the reason for his hospital admission, what tests and procedures had been performed, or how or when he had been transported to the hospital.

The patient was unable to acquire and retain new memories and repeated the same questions concerning his situation over and over again. He could state his address and the names of family members, but could not recall his profession or when he had last seen his family. While being fully aware of his memory loss and expressing puzzlement over his condition, he did not show any signs of anxiety. The remaining detailed neurological examination was otherwise unremarkable, without any other focal neurological signs or symptoms. The patient was tentatively diagnosed with TGA and transferred to the neurosurgical semi-intensive unit for further observation. Knowing the self-limiting and benign nature of TGA, no additional neuroimaging procedures were performed. The condition gradually improved and was fully resolved after 22 hours. A clinical control one week after the angiography revealed no cognitive or neurological deficits. During the control, the patient stated that the last thing he remembered before awakening in the semi-intensive unit was being prepped for the angiography.

Discussion

The symptoms presented in the above-described case comply with the diagnostic criteria for TGA proposed by Caplan (10): anterograde amnesia, no clouding of consciousness or loss of personal identity, no other cognitive impairment or focal or epileptic signs, no recent history of head trauma or seizures, and full resolution within 24 hours.

A formal PubMed literature search including (but not limited to) the following terms–“transient global amnesia,” “TGA,” ”amnesic syndrome,” “digital subtraction angiography,” and “cerebral angiography” in various combinations–uncovered only 15 case-report observations of isolated TGA following diagnostic cerebral angiography with nonionic contrast agent (9, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17) (see Table), the last of which was published in 1997 (9). A prospective analysis of 2,899 cerebral angiographies using nonionic contrast agents has shown a TGA complication rate of 0.002% (18), thus establishing TGA as a very rare and possibly underdiagnosed complication of cerebral angiography. Several proposed causes of TGA following cerebral angiography have been suggested, but the pathophysiology still remains unclear.

Publication	Author(s)	Journal	Title	Number of cases
1989	Giang DW, Kido DK	Radiology	Transient global amnesia associated with cerebral angiography performed with use of iopamidol (12)	2
1990	Minuk J, Me-lançon D, Tamp-ieri D, Ethier R	Radiology	Transient global amnesia associated with cerebral angiography performed with use of iopamidol (17)	1
1992	Juni J, Morera J, Lâinez JM, Es-cudero J, Ferrer C, Sancho J	Radiology	Transient global amnesia after cerebral angiography with iohexol (14)	1
1993	Brady AP, Hough DM, Lo R, Gill G	Canadian Association of Radiologists Journal	Transient global amnesia after cerebral angiography with iohexol (11)	2
1994	Schamschula RG, Soo MY	Australasian Radiology	Transient global amnesia following cerebral angi-ography with non-ionic contrast medium (16)	2
1995	Jackson A, Stewart G, Wood A, Gillespie JE	American Journal of Neuroradi-ology	Transient global amnesia and cortical blindness after vertebral angiography: further evidence for the role of arterial spasm(13)	5
1997	Meder JF, Mourey-Gerosa I, Blustajn J, Le-maignen H, De-vaux B, Fredy D	Acta Radiologica	Transient global amnesia after cerebral angiography. A case report (15)	1
1997	Woolfenden AR, O'Brien MW, Schwartzberg RE, Norbash AM, Tong DC	Stroke	Diffusion-weighted MRI in transient global amnesia precipitated by cerebral angiography (9)	1

Our patient had no history of migraine, seizures, or former episodes of transient amnesia, and he showed no change in consciousness or abnormal stereotypical movements suggesting epileptic activity during the amnesic event. This, combined with the duration of the episode, make both migraine and epilepsy unlikely causes.

Hypoxic-ischemic mechanisms, with bilateral ischemic lesions affecting areas in the medial temporal lobes that are involved in memory functions, have been advocated as explanations (8, 14, 19), while others dispute this (20). Our patient showed no signs of vascular spasms or reduced flow during angiography. He did not exhibit any other neurologic symptoms indicating ischemia on examination, specifically no motor or sensory symptoms. There were no visual abnormalities, aphasia/dysarthria, balance problems, or headache.

Others have indicated contrast-agent neurotoxicity as a causative factor of TGA (12, 21). TGA has been observed with both nonionic and ionic contrast agents, and reported three times as prevalent using the latter (18, 22). Why only a minor subset of patients experience TGA has been explained by an increased toxic effect due to pre-existing abnormalities of the blood-brain barrier (12, 23). In our case, an MRI performed two days before followup angiography showed no enhancement patterns suggestive of blood-brain-barrier damage. As the patient had experienced a minor subarachnoid bleeding and subsequent coiling of an aneurysm, minor defects cannot be ruled out, though they are not believed to be located temporally.

Some investigators have suggested micro-embolisms resulting from intrinsic particles in the contrast agent as responsible for TGA after angiography (24). As the contrast product was visually inspected prior to injection in our case, and no other signs of ischemia were observed, this was deemed an unlikely cause. Others have reported higher rates of TGA with contrast agent temperatures above room temperature (13). The contrast agent used in our case was administered at room temperature.

The definite pathophysiology of TGA in the described patient remains unclear, as it does for TGA in general. The underlying cause may be one of those discussed above or a combination of multiple factors.

Conclusion

Even though the mechanisms of angiography-induced TGA remain the subject of debate, the link between the procedure and the amnesic syndrome stands out as evident. While TGA by definition is self-limiting, its differential diagnoses (including stroke, intoxication, focal seizures, and transient global epilepsy) may cause morbidity and/or mortality if left untreated. It is therefore important to build and maintain awareness of TGA as a possible complication to cerebral angiography. Staff involved in treatment and care of this patient category should be trained to identify and distinguish the condition from its differential diagnoses.