Perinatal stroke (PS) causes hemiparetic cerebral palsy (CP) and lifelong disability. Compensatory changes in the nonlesioned hemisphere may mediate residual function and represent targets for neuromodulation. Region-based approaches may reveal relationships between cortical thickness of nonlesioned primary motor/sensory cortices and motor function. This study uses surface-based morphometry to explore cortical alterations in the nonlesioned hemisphere in children after perinatal stroke. Children aged 6-19 with MRI-confirmed unilateral perinatal stroke and CP underwent T1-weighted anatomical imaging. Participants were classified as arterial ischemic stroke (AIS; n=36), periventricular venous infarction (PVI; n=38), or typically developing controls (TDC; n=53). Group differences in cortical thickness (distance between grey/white matter boundary and pial surface), grey matter volume, gyrification and sulcal depth and relationships between these morphology metrics and validated measures of motor/executive function were explored. Group comparisons revealed less cortical thickness, greater gyrification, and greater surface area in the nonlesioned hemisphere in both AIS and PVI as compared to TDC. Greater volume and sulcal depth were observed in the nonlesioned hemisphere for AIS. The PVI group showed greater volume in the cingulate cortex and less volume in the precuneus relative to TDC. The AIS group showed more widespread differences than the PVI group in volume and other cortical surface parameters when compared with TDC. Only modest correlations were observed between morphometric changes and clinical function. We suggest that broad differences in structural developmental plasticity occur in the nonlesioned hemisphere after perinatal stroke, particularly the larger lesions seen with AIS, and may represent novel targets for therapeutic neuromodulation.