This study explores the relationship between lesion location and volume and upper limb spasticity after stroke. Ninety-seven stroke patients (51 with spasticity) were included in the analysis (age = 67.5 ± 13.3 years, 57 males). Lesions were traced from computed tomography and magnetic resonance images and coregistered to a symmetrical brain template. Lesion overlays from the nonspastic group were subtracted from the spastic group to determine the regions of the brain more commonly lesioned in spastic patients. Similar analysis was performed across groups of participants whose upper limb (elbow or wrist) Modified Ashworth Scale (MAS) score ranged from 1 (mild) to 4 (severe). Following subtraction analysis and Fisher's exact test, the putamen was identified as the area most frequently lesioned in individuals with spasticity. More severe spasticity was associated with a higher lesion volume. This study establishes the neuroanatomical correlates of poststroke spasticity and describes the relationship between lesion characteristics and the severity of spasticity using mixed brain imaging modalities, including computed tomography imaging, which is more readily available to clinicians. Understanding the association between lesion location and volume with the development and severity of spasticity is an important first step toward predicting the development of spasticity after stroke. Such information could inform the implementation of intervention strategies during the recovery process to minimize the extent of impairment.

Introduction: Damage to the corticospinal tract (CST) from stroke leads to motor deficits. The damage can be quantified as the amount of overlap between the stroke lesion and CST (CST Injury). Previous literature has shown that the degree of motor deficits post-stroke is related to the amount of CST Injury. These studies delineate the stroke lesion from structural T1-weighted magnetic resonance imaging (MRI) scans, often acquired for research. In Canada, computed tomography (CT) is the most common imaging modality used in routine acute stroke care. In this proof-of-principle study, we determine whether CST Injury, using lesions delineated from CT scans, significantly explains the variability in motor impairment in individuals with stroke. Methods: Thirty-seven participants with stroke were included in this study. These individuals had a CT scan within the acute stage (7 days) of their stroke and underwent motor assessments. Brain images from CT scans were registered to MRI space. We performed a stepwise regression analysis to determine the contribution of CST injury and demographic variables in explaining motor impairment variability. Results: Using clinically available CT scans, we found modest evidence that CST Injury explains variability in motor impairment (R2adj = 0.12, p = 0.02). None of the participant demographic variables entered the model. Conclusion: We show for the first time a relationship between CST Injury and motor impairment using CT scans. Further work is required to evaluate the utility of data derived from clinical CT scans as a biomarker of stroke motor recovery.