At present, long noncoding RNAs (lncRNAs) have become a new target for the treatment of cerebral ischemia-reperfusion injury. Accumulating evidence demonstrates that the lncRNAs can participate in the regulation of cerebral ischemia-reperfusion injury by affecting neuronal cell autophagy. This article aims to systematically review the effects of lncRNAs-mediated neuronal cell autophagy in brain deficiency from the perspective of autophagy, using “lncRNAs”, “neuronal autophagy” and “cerebral ischemia-reperfusion injury” as keywords. Studies have shown that lncRNAs can regulate important target genes at all stages of autophagy (induction, nucleation, extension, maturation, and autophagosome lysis), thereby regulating the level of autophagy and exerting neuroprotective effects. Understanding the autophagy regulation of lncRNAs and its mechanism of action in cerebral ischemia-reperfusion injury is expected to bring new hope for the treatment of ischemic brain injury.