A<unk>  in the developing brain involves excitotoxicity, oxidative stress, and inflammation, which accelerate cell death through necrosis or apoptosis, depending on the region of the brain and severity of stroke. The pathophysiology of<unk>  may include thrombosis and thrombolysis, and vascular reactivity. Apoptosis mechanisms may have a more prominent role in developing an ischemic brain injury in<unk>  humans than in adult brain ischemia, as a majority of cells die in the environment where edema developed after a<unk> . There is an increased inflammatory response after hypoxia-ischemia, which corresponds to extensive neuronal apoptosis. Apoptosis involves the mitochondrial release of cytochrome c and apoptosis-inducing factor (AIF), which activate caspase-dependent and –independent execution pathways, respectively. Injury may also occur due to O2 accumulation via the production of O2 by microglia, a type of glial cell that are responsible for immune response in the CNS, but their role in injury after<unk>  is still relatively unknown. As observed by Alberi, et al., progressive atrophy in the ipsilateral hemisphere over three weeks after the stroke occurred, suggesting that a<unk>  has long-lasting effects on neuronal viability and the potential for a prolonged therapeutic window for alleviating the progression of cell death.
Neonatal stroke
Neonatal meningitis
Neonatal encephalopathy
Neonatal seizure
Shaken baby syndrome
Pediatric stroke
Intraventricular hemorrhage
Neonatal diabetes