Glaucoma is the leading cause of irreversible blindness in the world and is characterized by the progressive loss of retinal ganglion cells and their axons. Elevated intraocular pressure (IOP) is a major risk factor, but in normal pressure glaucoma (NTG) static IOP is normal. The article proposes a dynamic imbalance hypothesis of trans-lamina cribrosa pressure difference (TLCPD) based on circadian fluctuations of IOP and cerebrospinal fluid pressure (CSFP). This imbalance arises from abnormal pulse synchronization between IOP and CSFP, such as phase mismatch, amplitude mismatch, or abnormal frequency. Ganglion cell damage occurs through mechanical stress on the lamina cribrosa and metabolic dysfunction, including disruption of the ocular glymphatic system, leading to activation of the programmed axonal degeneration pathway. Phase mismatch dominates in NTG, while amplitude and frequency mismatch dominate in primary open-angle glaucoma (POAG). The hypothesis suggests 24-hour monitoring of IOP and CSFP, animal experiments, new markers such as transient TLCPD peak, and therapies such as regulation of CSFP or modulation of the degeneration pathway.