A Mechanistic Elucidation of Pseudobulbar Palsy Secondary to Artery of Percheron Infarction

Abstract

Introduction: Pseudobulbar palsy (PBP) is an upper motor neuron syndrome traditionally attributed to bilateral corticobulbar tract injury caused by multifocal vascular, demyelinating, or degenerative pathology. The emergence of PBP following a single-vessel occlusion—specifically, an infarction of the Artery of Percheron (AOP)—presents a striking clinical and anatomical paradox. The AOP, a rare variant of the posterior cerebral circulation, supplies both paramedian thalami and often the rostral midbrain, making its occlusion a unique model for studying bilateral motor deficits arising from a unilateral vascular event.

Purpose: This study aims to elucidate the mechanistic relationship between AOP infarction and pseudobulbar palsy, investigating how a single ischemic lesion can produce a bilateral upper motor neuron syndrome. It seeks to integrate vascular anatomy, corticobulbar pathway organization, and thalamic-mesencephalic network function into a unified explanatory framework that accounts for both structural and functional aspects of this rare neurological presentation.

Methodology: A comprehensive literature review was conducted, focusing on neuroimaging studies of AOP infarction published from 2019 onwards. 

Result/Conclusion: Analysis of published evidence supports a dual-mechanism model in which PBP arises through either structural tract damage or functional disconnection, depending on infarct distribution within the AOP territory. Cases with midbrain involvement typically demonstrate direct corticobulbar tract injury, whereas isolated thalamic lesions produce PBP through disruption of motor relay networks, resulting in “functional de-efferentation” of brainstem motor nuclei. The study proposes a unified spectrum of injury bridging these mechanisms, highlighting the AOP infarction as a natural experiment revealing the interdependence of vascular architecture and supranuclear motor network integrity. This framework not only clarifies the pathophysiology of AOP-related PBP but also underscores the broader principle that vascular anomalies can expose latent bilateral vulnerabilities in motor control systems, offering new avenues for targeted neuroimaging research and clinical interpretation.