Case Presentation: A 76-year-old female was brought to the emergency department after being found wandering and attempting to inappropriately access locked buildings. Bystanders witnessed a ground-level fall without loss of consciousness. She had flown to Denver two days prior and had a 12-hour period of unaccounted wandering from her hotel. On exam, she had left upper extremity pronator drift and a lip laceration. She was alert and oriented to person, place, and time. She was completely unaware of this memory gap and unconcerned about spending the night outside in downtown Denver. Past medical history included hypertension and hyperlipidemia, and she was on appropriate medication. Collateral from her friend, husband, and primary care doctor confirmed she had normal baseline cognition, and all were concerned with her disinhibition regarding the overnight events.Encephalopathy workup ruled out metabolic, infectious, and toxic causes. CT head was unremarkable; CT angiogram head/neck revealed severe right M1 and left P1 stenosis. MRI showed multifocal acute infarcts in the right middle cerebral artery (MCA) territory, including the caudate, putamen, corona radiata, external capsule, and subinsular white matter. The stroke etiology was presumed to be artery-artery embolism from M1 stenosis with downstream ischemia. She had a normal EKG and no evidence of right-to-left interatrial shunt on echocardiogram, mildly elevated lipid panel, normal glucose levels. She was outside the thrombolysis and thrombectomy windows.She was treated with 21 days of dual antiplatelet therapy followed by aspirin monotherapy and vascular surgery follow-up. She was discharged after 3 nights with cognition near baseline. Medication adjustments included increasing rosuvastatin dose.
Discussion: This case demonstrates a rare presentation of retrograde amnesia following a right MCA stroke. While anterograde amnesia and confabulation have been reported after acute ischemic stroke, retrograde amnesia is less documented.The MCA supplies the lateral frontal, parietal, and temporal lobes, as well as some subcortical structures. While surprising that she had limited focal deficits on exam, her period of amnesia and disinhibition can be explained by the locations of infarcts. Multifocal infarcts in the caudate, putamen, corona radiata, external capsule, and subinsular white matter can disrupt communication between the frontal cortex, temporal lobe, thalamus, and limbic structures, explaining disinhibition and retrograde amnesia. Additionally, lesions in the right caudate and putamen have been associated with autobiographical and episodic memory deficits. Ischemia to the corona radiata and external capsule disrupts their connections to the temporal lobe, causing “disconnection syndrome”. Moreover, the white matter hyperintensities seen in strokes of this distribution can impair memory and cognition.
Conclusions: This case outlined retrograde amnesia as a neurocognitive deficit following multifocal infarcts in the right MCA. Although there is limited evidence of strokes of this nature causing amnesia, the role of subcortical and white matter regions in memory formation, executive functioning, and cognitive processing provides evidence for how strokes of this distribution can cause retrograde amnesia. The patient’s improvement at discharge suggests potential reversibility, though long-term follow-up was limited.