Pathologic myopia has become one of the most common causes of irreversible blindness worldwide, and studies reported that myopia may be a risk factor for primary open angle glaucoma (POAG). The possible mechanisms for this association may be the trabecular meshwork function is damaged in myopia, increase the aqueous humor outflow resistance and resulted in intraocular pressure (IOP) increasing. Comparing with that of emmetropic eyes, the optic nerve head (ONH) in myopic eyes may also be more vulnerable to IOP changes. However, there are diagnostic problems to detect ONH damages in a highly myopic eye. The problems include the spatial contrast between the neuroretinal rim and optic cup is decreased, the examination of the retinal nerve fiber layer (RNFL) thickness is disturbed by the bright background in the parapapillary region, the optical coherent tomography (OCT) determination of the peripapillary RNFL thickness often is unreliable due to irregularities in the parapapillary region, and that visual field defects are not specific for an optic nerve damage but may be related to myopic macular lesions and posterior pole irregularities of the globe. To detect the progression of optic nerve damage in highly myopic eyes pose an even greater problem. Future research will focus on the biomechanical properties of the peripapillary border tissues, the physiologic and pathological role of the trans-lamina cribrosa pressure difference, and the role of Bruch’s membrane in the ONH. Clinical investigations may improve the OCT techniques to enhance the diagnostic precision to evaluate the optic nerve damage in highly myopic eyes. It is also necessary to conduct longitudinal studies and explore structural biomarkers that predispose a highly myopic to the development of a glaucomatous and non-glaucomatous optic neuropathy.