Abstract DP067: Dissecting Spasticity After Acute Stroke: Relationship with Motor Recovery and Neural Mechanisms

Stroke is a leading cause of long-term disability, with most survivors showing upper limb motor impairment. Spasticity is a common outcome, marked by excessive muscle tone during quick joint extension. This can reduce range of motion, limit functional arm use, and cause pain. Despite the prominence of spasticity, its relationship to motor recovery and underlying neural mechanisms remains unclear. In this longitudinal study, we examine how post-stroke spasticity relates to upper limb motor recovery and investigate associated patterns of neuroanatomical injury (both lesions and networks). Methods: We recruited 59 acute stroke patients in the first week after stroke, all of whom underwent MR neuroimaging. Patients returned at 3 months to have upper limb spasticity measured with the Modified Ashworth Scale (MAS). Both times, upper limb motor impairment was measured with the Fugl-Meyer scale (FMA). We used (a) Voxel Lesion Symptom Mapping (VLSM) to link lesion location to presence of spasticity (MAS≥1) with and without FMA as a covariate and (b) Lesion Network Mapping (LNM) to quantify patients’ lesion connectivity in order to estimate spasticity-related disruptions of functional brain networks. Results: Patients showed recovery of motor impairment from acute (FMA: 31.1±3.1, mean±SEM) to subacute phase (FMA: 43.9±2.9). More severe impairment (lower FMA) in first week after stroke predicted development of spasticity (MAS≥1) at 3 months (Spearman’s ρ=-0.6, p=4.3×10 -7 , Fig.1a). Patients with spasticity at 3 months showed markedly less recovery of FMA (Fig.1b). Voxels associated with both spasticity and motor impairment centered on the corticospinal tract (CST); voxels uniquely associated with spasticity centered in basal ganglia (Fig.2). Lesions in patients with spasticity (vs. without) were connected to ext. capsule, operculum, and orbitofrontal cortex (OFC) (Fig.3). Discussion: In the first 3 months after stroke, the development of upper limb spasticity is associated with worse motor impairment and reduced recovery. The effect of CST damage on spasticity is compounded by lesions to basal ganglia. LNM associated spasticity with networks including OFC. Developing spasticity after acute stroke is thus associated with direct damage to CST but also damage to and connectivity with broader neuromodulatory networks including basal ganglia and OFC. Findings open the door to targeted neurorehabilitation, e.g. neuromodulation, to improve specific components of hemiparesis.