Since the initial clinical delineation of catatonia in 1874, two distinct conceptual frameworks have emerged: one viewing catatonia as a psychomotor disorder, rooted in Kahlbaum’s legacy, and the other interpreting it as a primarily motor phenomenon, aligned with the perspectives of Kraepelin and Bleuler. This historical dichotomy is reflected in contemporary investigations into the pathophysiological mechanisms of catatonia. Neuroimaging studies utilizing motor and behavioral rating scales, such as the Bush-Francis Catatonia Rating Scale, have highlighted alterations in dopamine-mediated cortical and subcortical motor circuits – specifically the basal ganglia, supplementary motor area, primary motor cortex, and cerebellum – as key neuronal correlates of catatonia. In contrast, studies employing the Northoff Catatonia Rating Scale, a scale integrating affective, motor, and behavioral criteria within a psychomotor framework, have identified disruptions in higher-order frontoparietal networks, including the prefrontal, orbitofrontal, and primary motor cortices, as well as the limbic system. These networks appear to be dysregulated by imbalances in glutamatergic and gamma-aminobutyric acid transmission, underscoring the complex interplay between motor, affective, and cognitive domains in the pathophysiology of catatonia. This chapter introduces the pathophysiology of catatonia from a systemic (network-based) perspective, irrespective of its association with mental or medical disorders.