After Professor Peter Jannetta’s pioneering success in 1966 with microvascular decompression (MVD) on the facial and trigeminal nerves in the posterior fossa [1–3], this procedure has become the established treatment for hemifacial spasm and trigeminal neuralgia. Its surgical indications have gradually expanded to include glossopharyngeal neuralgia, intractable dizziness, tinnitus, and neurogenic hypertension among various cranial nerve diseases involving neurovascular conflicts, termed “neurovascular compression syndrome” (NVCS) [4, 5]. The oculomotor nerve, responsible for eye movement and pupil reflexes as the third cranial nerve originating from the midbrain, traverses through the heavily vascularized subarachnoid cisterns. Consequently, one might associate neurovascular conflicts with oculomotor nerve palsy (ONP), presenting clinically as diplopia, ophthalmoplegia, and anisocoria. However, beyond well-recognized causes such as posterior communicating artery (PCom) aneurysms leading to compressive ONP, little is known about ONP solely caused by non-aneurysmal vascular compression (nAVC) [6–8]. Cases treated with MVD for nAVC-induced ONP (nAVC-ONP) are exceedingly rare, with sporadic reports [9–23]. Yet, with advancements in high-resolution MRI and 3D post-processing techniques, the relationship between nAVC and ONP seems to be gradually unveiled [17, 24–26]. Consequently, the therapeutic value of MVD in such diseases is progressively emerging. This chapter presents five cases of MVD-treated nAVC-ONP from our center [27], accompanied by a preliminary discussion informed by existing literature on similar cases, aiming to explore this field further.