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integration processing, imparting effective and efficient asymptomatic place-in-space homeostasis. However, various peripheral and central pathologies disrupt this required func- tional adjustment, often leading to persistent visually mediat- ed vertiginous outputs including impaired correction and ad- aptation to postural control perceptions of vection and OKS- mediated ocular motor phases. This proximal impairment in turn leads to the advancement of the distal outputs of large postural sway patterns and symptoms of dizziness, vertigo, or nausea. Peripheral abnormalities, especially involving the ves- tibular end organ, may result in visual motion hypersensitivi- ty; individuals become abnormally dependent upon the visual system for posture and balance control, leading to an exces- sive response to variations in visual field motions. Central vestibular abnormalities also are associated with sensitivity to OKS. Central origin of OKS-related hypersensitivity has also been reported in those without a diagnosis of a central disease. Pollak and colleagues reported 37.5% of patients without neurological, psychiatric, cardiovascular, or pharma- cological etiology of dizziness and OKS-related hypersensi- tivity presented with scattered cortical hemispheric white mat- ter abnormalities compared to 7% in controls without OKS- related hypersensitivity (p = 0.009) [32]. A potential con- founder in this study was an age-related increase in prevalence of white matter lesions in the study population (31% for age 40–49 vs 83% for age > 70), as 67% of the OKS-related hy- persensitivity group was thought to have symptoms related to a vascular cause [32]. Furthermore, it was theorized that a global multifocal distribution of white matter abnormalities was likely more predictive of OKS-related hypersensitivity than the specific etiology of the white matter lesions them- selves. However, these findings were not replicated in a recent imaging trial comparing patients with OKS-related hypersen- sitivity to healthy controls [33]. OKS-related hypersensitivity is found in defined central disorders, especially when related to conditions that cause multifocal brain dysfunction such as traumatic brain injury [34, 35•]. Wright and colleagues found OKS-related symptoms were greater in patients with mild traumatic brain injury compared to healthy controls (p = 0.020) [36••]. Similar to MdDS, psychopathologies such as depression and anxiety [37, 38] have been associated with OKS-related hypersensitivity. OKS-mediated hypersensitivity, also referred to as visual vertigo (VV), is often confused with other ocular motor- related symptoms including oscillopsia; differentiating the two is crucial since their diagnosis and management are quite distinct [39]. Oscillopsia is also an illusionary disorder; howev- er, instead of the perception of vection (self-motion) experi- enced for patients with VV, oscillopsia is the sense that the visual field is in motion or unstable. The onset of oRead less