Abstract 124: Beyond Thalamic Aphasia: Semantic and Memory Deficits Following Left Anterior Thalamic Infarct

Introduction Thalamic strokes account for approximately 2‐4% of all ischemic strokes and are associated with a broad spectrum of linguistic and cognitive symptoms. Infarcts in the anterior (tuberothalamic/polar artery) territory commonly result in confusion, memory deficits, executive dysfunction, and language impairment—particularly when the dominant hemisphere is involved. We report a case of left thalamic infarction who presented with transient cognitive‐linguistic dysfunction and brief unresponsiveness. Case Report 46‐year‐old left‐handed male with severe OSA and class III obesity presented to the emergency department following transient word‐finding difficulty and a brief episode of loss of consciousness. He was initially found unresponsive and snoring loudly and could not be awakened for a few minutes. Upon regaining consciousness, he was disoriented, unaware of his location, and had word‐finding difficulty. EMS noted several recurrent episodes of word‐finding difficulty during transport. By ED arrival, his language and cognition had returned to baseline.On examination, he was alert, oriented, and demonstrated no focal neurological deficits. CT head and CTA were unremarkable. A subsequent episode of transient aphasia was witnessed in the ED 2 hours later; speech was fluent with occasional paraphasia, lasting ∼90 seconds, after which he returned to baseline. MRI brain revealed restricted diffusion in the left thalamus, consistent with acute infarction predominantly involving the anterior territory. Transthoracic echocardiography revealed a large right‐to‐left shunt consistent with a patent foramen ovale. Telemetry showed no arrhythmia. He was started on secondary prevention and had no further episodes during hospitalization. Bedside testing the next day demonstrated fluent speech with intact naming, comprehension, and repetition. Inpatient neuropsychological testing revealed semantically related language deficits, including impaired single‐word retrieval with semantic paraphasic errors and impaired semantic/category fluency relative to intact phonemic fluency. His memory profile showed impaired learning and recall with little benefit from cues, suggesting impaired storage. Executive testing revealed impaired set‐shifting and complex figure copy, with other domains largely intact. Processing speed was below expectations, though attention was preserved.Given absence of traditional vascular risk factors, presence of a large PFO, and transient loss of consciousness, an embolic etiology with possible spontaneous recanalization of a top‐of‐the‐basilar or PCA branch occlusion was considered. Conclusion This case underscores the need to consider thalamic infarction in patients with transient, subtle, and non‐classical language and memory deficits—even in the absence of focal findings or abnormal CT imaging. The patient's higher baseline cognitive abilities made the subtle deficits more noticeable and underscore the varied neurocognitive presentations of anterior thalamic strokes. image