The NIH Intramural Research Program: Opportunities for training and career development in neuroscience and beyond.

Perinatal stroke refers to a vascular insult—either arterial or venous—that occurs between approximately 20 weeks of gestation and the first 28 days of life []. Arterial ischemic stroke (AIS) is the most common form, affecting an estimated 1 in 4000 live births [, ]. Perinatal AIS often leads to long‐term neurological consequences, including motor, cognitive, and psychiatric impairments [, , ]. Among children with middle cerebral artery (MCA) strokes, approximately 20% develop dystonia [], a movement disorder characterized by involuntary muscle contractions, twisting movements, and abnormal postures []. Although the pathophysiology of dystonia in adults is associated with abnormal activation within motor circuits, the underlying mechanisms in children remain poorly understood [, , ]. Emerging evidence suggests involvement of the basal ganglia, thalamus, cerebellum, and disrupted sensorimotor integration [, , ]. Investigating such mechanisms in carefully matched cases—such as twins with perinatal stroke—can help disentangle the roles of lesion characteristics, brain plasticity, and individual variability in shaping outcomes. Twin with pediatric stroke offer a unique opportunity to control for genetic and early environmental factors and examine how similar injuries can lead to different outcome trajectories. Risk factors for perinatal stroke include twin pregnancy, maternal infections, placental disorders, and thrombophilia [, , ]. In twin pregnancies, risks are often related to pathological placental conditions that compromise blood flow and increase the likelihood of hypoxic‐ischemic events such as twin–twin transfusion syndrome or selective intrauterine growth restriction [, ]. These complications disproportionately affect monochorionic twins due to shared vascular structures and can increase the risk of perinatal stroke by 15‐fold [, , ]. Understanding how these early vascular insults interact with developmental plasticity is critical for explaining the divergent motor outcomes observed in affected twins. Neuroplasticity of the developing brain enables adaptive reorganization following injury by recruiting undamaged motor regions and alternative neural pathways to restore function [, ]. However, this plasticity may become maladaptive, reinforcing abnormal motor patterns that can give rise to dystonia. Dystonic symptoms typically emerge 6–12 months after stroke [, ], suggesting a delayed but pathological reorganization process. Notably, post‐stroke dystonia is much less common in adults than children, implying a vulnerability of the developing brain. Given that dystonia is a painful, disabling, and often treatment‐resistant motor disorder, elucidating its neural basis is critical for improving outcomes in children with perinatal stroke. Advanced neuroimaging offers powerful tools to investigate the mechanisms of adaptive and maladaptive neuroplasticity in the developing brain. Structural magnetic resonance imaging (MRI) enables characterization of lesion location, extent, and involvement of motor‐related regions, while diffusion tensor imaging (DTI) provides insight into white matter integrity and connectivity disruptions. Magnetoencephalography (MEG) provides millisecond‐level temporal resolution and precise spatial localization of brain activity when co‐registered with MRI. This enables the mapping of oscillatory dynamics (theta, gamma) underlying motor control processes relevant to dystonia. In this study, we leverage a rare case of monozygotic twins with perinatal stroke to examine how structural lesion characteristics identified on MRI relate to functional motor network alterations detected with MEG, while controlling for genetic and environmental confounds. This approach provides a unique window into the neurobiological mechanisms that drive divergent outcomes—including dystonia—following early brain injury.