Central Post-stroke Pain: From Lesion Localization to Network Dysfunction and Assessment

Abstract

Central post-stroke pain (CPSP) is a neuropathic pain condition that can substantially impact sensory function, daily activities, and participation in rehabilitation after stroke. Although CPSP has traditionally been associated with thalamic lesions, accumulating evidence indicates that it is associated with disruption of a broader nociceptive network involving multiple brain regions and the white matter pathways connecting them. This network-based view has shifted the focus of neuroimaging research from individual lesion locations to the neural pathways and networks underlying CPSP. Experimental studies have further identified the potential roles of glial activation, altered γ-aminobutyric acidergic signaling, and maladaptive plasticity in the development of abnormal pain. Clinically, CPSP may emerge following the acute phase of stroke, raising the possibility of identifying patients at risk before pain becomes apparent. Quantitative sensory testing, particularly the assessment of cold sensation, may provide an early functional marker of subsequent CPSP. Furthermore, pain quality may provide information about the underlying mechanisms of pain and its subsequent clinical course. This review summarizes current evidence linking brain lesions, disrupted neural pathways, sensory dysfunction, and CPSP and discusses the potential of integrating neuroimaging with sensory assessment for early risk stratification.