# Isolated Aphasia From a Left Parietotemporal Infarct Secondary to a Patent Foramen Ovale: A Case Report

## TL;DR

A rare case of isolated aphasia caused by a brain infarct linked to a patent foramen ovale is presented, emphasizing the need for thorough neurological and cardiovascular evaluation.

## Contribution

This case report highlights the rare occurrence of isolated aphasia due to a left parietotemporal infarct secondary to a patent foramen ovale.

## Key findings

- Isolated aphasia can result from a left parietotemporal infarct without typical stroke symptoms.
- Patent foramen ovale may be a cryptogenic source of ischemic stroke presenting as isolated aphasia.
- Multidisciplinary evaluation and early intervention are crucial for optimal outcomes in such cases.

## Abstract

Isolated aphasia (IA) as the sole manifestation of stroke is rare and is often attributed to metabolic, toxic, or psychiatric disorders. Without typical stroke symptoms, such as hemiplegia or cranial nerve deficits (CND), IA can be easily overlooked. We present the case of a 41-year-old male accountant with a history of hyperlipidemia who presented to the emergency department with the sudden onset of an inability to read or speak, accompanied by confusion and anxiety. On examination, he had no CNDs, and his strength, sensation, reflexes, and cerebellar function were normal. His vital signs, blood glucose, and initial computed tomography (CT) scan were unremarkable, and his National Institute of Health Stroke Scale (NIHSS) score was 3. The patient declined tissue plasminogen activator (tPA) therapy. Computed tomography angiography (CTA) showed no intracranial stenosis, but magnetic resonance imaging (MRI) confirmed an acute infarct in the left parietal and temporal lobes within the middle cerebral artery (MCA) distribution. Further evaluation with a bubble study during echocardiography revealed a right-to-left interatrial shunt consistent with a patent foramen ovale (PFO). He was started on dual antiplatelet therapy, a statin, and speech therapy. Neurology and cardiology specialists recommended outpatient PFO closure and placement of an implanted loop recorder for arrhythmia monitoring. At discharge, the patient showed a significant improvement in his aphasia, though occasional recurrences persisted. This case highlights a rare presentation of ischemic stroke with IA, a condition that is more often attributed to stroke mimics such as metabolic or functional causes. Comprehensive neurological and cardiovascular evaluations are essential, particularly given the strong association between IA and cardioembolic sources such as PFO. Early multidisciplinary intervention is crucial to optimize outcomes, as this case illustrates the importance of identifying and addressing cryptogenic causes of IA to prevent recurrent strokes.