Perinatal arterial stroke is a cerebrovascular event occurring around the time of birth, with pathological or radiological evidence of focal arterial infarction mainly affecting the middle cerebral arterial territory, with an incidence of 1 in 2500 term births (Badve et al., 2012). Perinatal hypoxia–ischemia (HI) is a major cause of acute mortality, with an incidence of 2–4 per 1000 full term births (Vannucci, 2000). Perinatal brain injury induced by stroke and/or HI has been associated with permanent neuropsychological handicaps, including mental retardation, cerebral palsy, epilepsy or learning disability. No therapeutic method is available for perinatal encephalopathy apart from initiating hypothermia within 6 h after birth, but only 1 infant in 6 benefits (Azzopardi et al., 2009 and Gonzalez and Ferriero, 2009). Although these studies provide proof of concept that in this context cell death is both delayed and preventable, the protection is limited and there is still no treatment available for perinatal stroke or brain injury occurring in preterm and term infants. Clinical presentations (cause, severity, magnitude, and deteriorating speed), and inherent potentials (adaptation, preconditioning-tolerance, and intolerance) against an HI or ischemic insult are different from one infant to another. Consequently, it is incumbent on scientists in the field of neonatal brain injury to address the questions of therapeutic efficacy of an array of potential therapies in several developmentally appropriate models. Towards that end, a number of new models of neonatal HI and stroke have been introduced recently, the last being that reported by Tsuji et al. (2013). These models have been designed in the rat and mouse brain and most of them present a great variability in the lesion size and brain areas damaged, whereas this last reported model in the mouse is highly reproducible with a selective cortical infarction.