Introduction

Ischemic stroke results from a transient or permanent reduction in cerebral blood flow that is restricted to the territory of a major brain artery. The reduction in blood flow in a specific region is, in most cases, caused by the occlusion of a cerebral artery either by an embolus or by local thrombosis. With an incidence of approximately 250 to 400 in 100,000 head of population aged 45 to 89 (Warlow, 1998) and a mortality rate around 30%, stroke remains the third leading cause of death in major industrialized countries. Hypoxic-ischemic and stroke injury to the perinatal brain is also a major clinical problem causing death in a large number of affected infants, recognized in about 1 per 4000 live term birth (Vannucci, 2000; Nelson and Lynch, 2004). More than 95 percent of infants who have a stroke survive to adulthood, and many have residual motor or cognitive disabilities (permanent neuropsychological handicaps including mental retardation, cerebral palsy, epilepsy, or learning disability) (Nelson and Lynch, 2004).

The immature brain has long been considered to be resistant to the damaging effects of hypoxia and hypoxia-ischemia (HI). However, it is now recognized that there are specific periods of increased vulnerability related to the developmental stage at the time of the insult. Much of our knowledge of the pathophysiology of cerebral HI is based on extensive experimental studies using in vitro and in vivo models relevant to mechanisms seen in humans. The major pathogenic mechanisms of brain injury following cerebral HI include excitotoxicity, inflammation, and apoptosis. This chapter will summarize most of the commonly used models in rodents (rat, mouse) and some of the recent data on developmental differences in the immature brain that create periods of selective vulnerability to hypoxia-ischemia, and are quite distinct from the responses in adult hypoxia-ischemia.

Your Heart and Nutrition

Your Heart and Nutrition

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