Posterior reversible encephalopathy syndrome (PRES) is a clinicoradiological entity characterized by headache, seizures, visual deterioration, motor and cognitive deficits, and decreased level of consciousness among other symptoms and signs with imaging findings suggestive of vasogenic edema preferentially affecting the occipital and posterior temporal and parietal lobes. As the name suggests in the vast majority of cases, the syndrome is self-limiting and the deficits are reversible to a large extent. It is seen most commonly in periparturient patients and multiple theories have been proposed regarding its pathogenesis. It is widely thought to occur due to intermittent high blood pressures overwhelming the myogenic arm of cerebral autoregulation and in the setting of weaker neurogenic autoregulation in the posterior cerebral circulation being due to sparse innervation; the resulting hyperperfusion creates vasogenic edema. This can be compounded by deranged overcompensation causing hypoperfusion and endothelial dysfunction precipitating vasogenic edema through increased permeability. Various spinal pathologies and interventions can create pathophysiologic cascades that can combine to result in PRES; thus leading to often unforeseen morbidity. This review seeks to present in a narrative form (systematically searched literature) on PRES as a sequel to spinal pathologies or interventions.