Brian can protect itself from ischemia and/or hypoxia by two distinct mechanisms which probably involve two separate systems of neurons in the CNS. The first ome mediates a reflex neurogenic neuroprotection, which is associated with oxygen-sensitive sympathoexcitatory reticulospinal neurons of rostral ventrolateral medula oblongata. It can be excited within seconds by reduction in blood flow or oxygen and initiate an oxygen conserving reflex. The second is conditioned central neurogenic neuroprotection, which is represented in intrinsic neurons in cerebellar fastigial nucleus. It can be initiated by electrical excitation of intrinsic neurons of fastigial nucleus and afford a persisting for almost two weeks neuroprotection. This mode of neuroprotection is not restricted to focal ischmia,it also protects the brain against global ischemia and excitotoxic cell injury. The ne-oruprotective mechanism of the system is associated with reduced excitability of cortical neurons, inhibition of the onset of necrosis and apoptosis of ischemic neurons, reduced expression of many detrimental factors including Caspase-3 and NF-kappaB, and reduced immunoreactivity of cerebral microvessels. Fastigial neucleus stimulation can also promote the recovery of neurological deficits and can somewhat improve the cognitive function. Some prelimilary observations of clinical application of fastigial nucleus electrical stimulation on protecting neurons from ischemic injury and treating patients with stroke are presented. Recommendations of further research on fastigial nucleus stimulation before its broad clinical practice are provided.