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Retrosplenial Stroke Mimicking Transient Global Amnesia

An 89-year-old, right-hand-dominant female was brought to hospital by her family for acute confusion. The patient was fully independent at home, without cognitive impairment, and had a history of essential tremor, glaucoma, and hypertension. Her medications were irbesartan and amlodipine. She reported sudden-onset dizziness, headache, nausea, and a feeling that her “brain was not working as it should be” during volunteer work. She was aware that her memory was not at baseline; she could not recall in detail any events leading up to or during the episode. Roughly 1 hour later, she experienced some improvement and attempted to return home. She reported feeling disoriented, taking multiple detours and wrong turns on her way home. She was brought to hospital a few hours later by her sons. They reported that the patient repeatedly asked the same questions and did not remember events from earlier in the day. On examination, her vital signs were normal. Mini-Mental State Examination (MMSE) score was 26/30 with deficits in orientation to time, spontaneous recall, and inability to draw intersecting pentagons. The remainder of her neurological exam was entirely normal. Non-contrast computed tomography and computed tomography angiography of the head and neck showed chronic white matter microvascular ischemic changes and multiple areas of intracranial and extracranial stenosis with no acute abnormalities (not shown). She was kept in hospital overnight with a working diagnosis of transient global amnesia (TGA). Electroencephalogram performed the following day found mild intermittent left temporal slowing without any epileptiform discharges. Brain magnetic resonance imaging (MRI) did not show any hippocampal abnormality but instead revealed acute left retrosplenial ischemia (Figure 1). Her headache, dizziness, and nausea had completely resolved. Repeat examination revealed an MMSE score of 30/30 with no neurological deficits. She was discharged with outpatient follow-up, including a 24-hour Holter monitor which revealed sinus rhythm and occasional premature atrial complexes but no atrial fibrillation. She had an echocardiogram 6 months prior which showed mild left ventricular hypertrophy, left atrial dilation, and trace mitral regurgitation. Although no clear etiology for her stroke was established, the mechanism was thought to be atheroembolic given her imaging findings. She was maintained on aspirin and lipid-lowering therapy for secondary stroke prevention. This case presents an example of a left-sided retrosplenial stroke mimicking TGA. TGA is a benign syndrome characterized by an acute episode of anterograde amnesia that resolves within 24 hours. This classically presents as a patient repeatedly asking the same questions and being unable to orient to their current situation. Patients may also experience retrograde amnesia, though this is typically less pronounced than the anterograde amnesia. Awareness and domains of cognition other than memory characteristically remain intact. Associated nonfocal symptoms may include headache, dizziness, and nausea, which were seen in our case. Memory deficits caused by acute stroke often present with accompanying focal deficits that can be used to clinically exclude TGA. Stroke in the hippocampus, thalamus, caudate, and fornix (isolated or in combination) have been shown to present with a primary amnestic deficit, which makes these lesions difficult to distinguish from TGA. MRI diffusion-weighted imaging (DWI) is the best study to differentiate between stroke and TGA. Hippocampal punctate enhancement may be seen in TGA, which is distinct from typical cerebrovascular-associated lesions. The retrosplenial region is composed of the retrosplenial cortex and cingulate bundle. Both structures play a significant role in learning and memory: the cingulate bundle is a component of the Papez circuit, and the retrosplenial cortex shares connections with the anterior thalamus and hippocampus. Anterograde amnesia caused by a lesion in the retrosplenial region was coined “retrosplenial amnesia” by Valenstein et al., who reported the first case of this phenomenon caused by a ruptured arterio-venous malformation in 1987. Since then, several other cases caused by hemorrhagic stroke have been reported. In contrast, there have been very few cases of retrosplenial amnesia caused by ischemic stroke. Lesions to the retrosplenial cortex have also been shown to cause deficits in spatial memory in both animal and human models. We conducted a systematic literature review of all cases of anterograde amnesia caused by unilateral ischemia of the