Combined therapies of hypothermia and pharmacological agents or growth factors to improve neurological outcomes are most likely the next direction for damaged neonatal brains, such as after a stroke. Other Treatments
A successful use of urokinase in a newborn with an aortic clot has been reported, but the bleeding risks associated with thrombolytic agents are still unclear.Heparin, an anticoagulant, treatments have been used in cases of cerebro-venous sinus thrombosis (CVST) in order to stop thrombosis extension and recurrence, to induce thrombosis resolution, and to prevent further brain damage. In the case of extremely high intracranial pressure, surgical removal of hematoma may be beneficial. Prognosis
Of the infants that survive, there may be as many as 1 million a year that develop cerebral palsy, learning difficulties or other disabilities. Cerebral palsy is the most common physical disability in childhood, and it is characterized by a lack of control of movement. Other neurological defects that can occur after a neonatal stroke include hemiparesis and hemi-sensory impairments   Some studies suggest that when tested as toddlers and preschoolers, children who previously had neonatal strokes fall within normal ranges of cognitive development. Less is known about longer-term cognitive outcome, but there has been evidence that cognitive deficits may emerge later in childhood when more complex cognitive processes are expected to develop.
Risk factors
Many different risk factors play a role in causing a neonatal stroke. Some maternal disorders that may contribute to neonatal strokes include: autoimmune disorders, coagulation disorders, prenatal cocaine exposure, infection, congenital heart disease, diabetes, and trauma. Placental disorders that increase the risk of stroke include placental thrombosis, placental abruption, placental infection, and chorioamnionitis. Other disorders that may increase the risk of a neonatal stroke are blood, homocysteine and lipid disorders, such as polycythemia, disseminated intravascular coagulopathy, prothrombin mutation, lipoprotein (a) deficiency, factor VIII deficiency (hemophilia A), and factor V Leiden mutation. Infectious disorders such as central nervous system (CNS) infection or systemic infection may also contribute.Many infants who have a neonatal stroke also follow an uncomplicated pregnancy and delivery without identifiable risk factors, which exemplifies the necessity for further research on this subject. Mechanism
A neonatal stroke 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 neonatal stroke may include thrombosis and thrombolysis, and  vascular reactivity. Apoptosis mechanisms may have a more prominent role in developing an ischemic brain injury in neonatal humans than in adult brain ischemia, as a majority of cells die in the environment where edema developed after a neonatal stroke. 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.