Introduction

Transient global amnesia (TGA) is characterized by the sudden onset of an anterograde and some retrograde amnesia that usually lasts about 6 h but may last up to 24 h [1]. The differential diagnosis includes seizure, stroke (especially in the posterior circulation), medication effect, and metabolic disorders. The history and clinical setting can help distinguish the etiology.

We report a case of transient acute amnesia following aneurysm coiling secondary to thromboembolism.

Case Report

A 56-year-old woman who had a history of smoking, underwent head computed tomography angiogram (CTA) for complaints of headache (never thunderclap) and visual changes. She was referred to our institution when the CTA revealed an unruptured 5 mm left superior cerebellar artery narrow-necked aneurysm. After discussing the risks and benefits, the patient elected to have the aneurysm treated. The next day she underwent coil embolization of the aneurysm. No abnormalities of the circle of Willis were present and no significant atherosclerotic plaques were present in the vessels catheterized. No balloon-assistance was used. During the procedure, she received 1 mg midazolam, 120 mg propofol, and 10 mg vecuronium. She received 8000 units of intravenous heparin during the procedure to maintain the activated clotting time between 250 and 300. Upon awakening from anesthesia, the patient was confused and had memory loss.

On examination, the patient knew her name but did not recall where she was and the name of her neurosurgeon whom she had met the day before. Mental status was notable for 0/3 on three word recall at 3 min. She knew the month and year. She repeatedly asked, “Where am I?” despite being told where she was. She could not recall her age. Her anterograde memory deficit was greater than the retrograde memory loss. For example, she could not remember why she was in the hospital despite being reminded several times. She was able to recite seven consecutive numbers correctly shortly after hearing them. She had preserved language. Cranial nerves, motor strength, sensation, and cerebellar testing were normal.

TGA, anesthetic effect, and thromboembolic complication after aneurysm coiling were at the top of the differential diagnoses. Since the patient’s symptomatology could be localized to the posterior circulation where a thromboembolic complication might have occurred, the patient was started on abciximab with a 0.25 mg/kg bolus. A brain MRI was ordered to determine whether there was any evidence of ischemia with the plan to discontinue abciximab if negative.

Prior to obtaining the MRI, she developed chest pressure that radiated with severe pain into the back. The differential diagnoses for chest pressure with radiation to the back after undergoing angiography included aortic dissection, myocardial infarction, and abciximab side effect. Given the concern for dissection, abciximab infusion was stopped. The patient underwent a CT angiogram of the chest, ECG, and serial measurement of serum troponin levels. All tests were unremarkable. Shortly, after stopping the abciximab infusion her chest and back pain resolved. The following day she underwent an MRI of the brain. Her MRI revealed two small foci of restricted diffusion and T2/fluid attenuated inversion recovery hyperintensity within the right mesial temporal lobe as well as tiny foci with similar signal characteristics within the posterior left occipital lobe and left mesial temporal lobe. (Fig. 1) The day after her procedure she could remember 3/3 words after five minutes, although she was amnestic for the previous days events. Ten days after the procedure she and her family were called and noted no residual deficits.

Fig. 1
figure 1

MRI of the brain Axial MRI diffusion weighted imaging (a, d), ADC (b, e), and fluid attenuated inversion recovery (e, f) demonstrate two small foci of diffusion restriction in the right mesial temporal lobe and one tiny foci of diffusion restriction in the left mesial temporal lobe. There is also small focus of diffusion restriction in the medial left occipital lobe

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Discussion

Our case highlights the importance of the history and clinical setting when determining the cause of acute memory loss. The differential diagnosis of TGA includes transient ischemic attack/stroke, seizure, and medication effect. Medication effect was felt to be lower on the differential diagnoses because our patient was fully alert, and drowsiness would have been expected if the symptoms had been related to residual drug effect. The patient had no history of seizures and there were no abnormal stereotypical movements to suggest transient epileptic amnesia. Further, transient epileptic amnesia is shorter in duration and associated with recurrent attacks [2].

While our patient did not have many of the vascular risk factors that should be considered when evaluating whether ischemia is mimicking TGA, she did undergo a procedure that substantially increases the risk of stroke. Our patient underwent coiling in the distribution of the posterior circulation which increased the likelihood that ischemia was the cause of the symptoms. Thromboembolic complications of coiling occur in approximately 8.5 % of patients [3]. In our patient, slow flow within the aneurysm with increased stasis, a phenomenon observed in rapidly expanding aneurysms, may have been a facilitating factor in the production of thromboembolism. When diffusion-weighted MRI is performed after coiling, 57 % of patients have evidence of silent thromboembolic events [4]. The MRI in our patient demonstrated bilateral medial temporal lobe ischemia in addition to ischemia in the occipital lobe consistent with small emboli after coiling as the underlying etiology.

A strategically located stroke can present in a similar manner to TGA [5]. Diencephalic amnesia can occur from bilateral medial thalamic infarctions [6]. High resolution imaging studies have demonstrated diffusion weighted imaging lesions selectively in the CA-1 region of the hippocampus in TGA patients [1]. Single-photon emission computed tomography (SPECT) scan during TGA have shown reduced blood flow in either the medial temporal lobes or diencephalon [7, 8]. Involvement of the mesial temporal structures (which usually receive supply from posterior cerebral artery), explains the clinico-anatomic correlation between the location of the signal change, the procedure, and symptoms of memory loss. While TGA has been associated with lesions in the CA-1 region of the hippocampus on diffusion-weighted MRI and mesial temporal reduction in blood flow, the concomitant lesion in our patient’s occipital lobe confirms emboli rather than TGA as the underlying cause. Further, knowledge of vascular anatomy and pattern recognition can aid in differentiating pathologies that cause diffusion weighted change in the hippocampus on MRI [9].

Abciximab, a glycoprotein IIb/IIIa receptor antagonist, is a potent inhibitor of platelet aggregation. Abciximab was used in this patient and has become our institutional preference in this clinical setting because it has been shown to be a safe and effective treatment for thromboembolic complications associated with endovascular interventions, including coiling of intracranial aneurysms [10]. After abciximab was started, our patient developed chest pain radiating to the back. Serious causes were excluded including aortic dissection and myocardial infarction. The temporal relationship of resolution of chest/back pain with stopping abciximab suggests causal relationship. In fact, chest pain occurs in 11.4 % and back pain in 17.6 % [11]. The cause of chest and back pain in patients receiving abciximab remains unknown.

While several series have reported thromboembolic complications during aneurysm coiling, this case uniquely demonstrates that ischemia in the posterior circulation should be considered in the differential diagnosis of acute amnesia, especially in situations predisposing to thromboembolism such as coiling. Abciximab can be used to treat thromboembolic complications related to coiling, but it can be occasionally associated with chest pain and back pain.