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Visual display terminal (VDT) use reduces the blink rate and increases the number of incomplete blinks. However, the exact mechanisms causing DED development from VDT use have yet to be clearly described.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Purpose<\/jats:title>\n                    <jats:p>The purpose of the study was to conduct a review on pathophysiological mechanisms promoting VDT\u2010associated DED.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A PubMed search of the literature investigating the relationship between dry eye and VDT was performed, and relevance to pathophysiology of DED was evaluated.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Findings<\/jats:title>\n                    <jats:p>Fifty\u2010five articles met the inclusion criteria. Several pathophysiological mechanisms were examined, and multiple hypotheses were extracted from the articles. Visual display terminal (VDT) use causes DED mainly through impaired blinking patterns. Changes in parasympathetic signalling and increased exposure to blue light, which could disrupt ocular homeostasis, were proposed in some studies but lack sufficient scientific support. Together, these changes may lead to a reduced function of the tear film, lacrimal gland, goblet cells and meibomian glands, all contributing to DED development.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Visual display terminal (VDT) use appears to induce DED through both direct and indirect routes. Decreased blink rates and increased incomplete blinks increase the exposed ocular evaporative area and inhibit lipid distribution from meibomian glands. Although not adequately investigated, changes in parasympathetic signalling may impair lacrimal gland and goblet cell function, promoting tear film instability. More studies are needed to better target and improve the treatment and prevention of VDT\u2010associated DED.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/aos.15150","type":"journal-article","created":{"date-parts":[[2022,4,20]],"date-time":"2022-04-20T00:57:35Z","timestamp":1650416255000},"page":"861-877","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":52,"title":["Review on the possible pathophysiological mechanisms underlying visual display terminal\u2010associated dry eye disease"],"prefix":"10.1111","volume":"100","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6161-9171","authenticated-orcid":false,"given":"Ketil","family":"Fj\u00e6rvoll","sequence":"first","affiliation":[{"name":"Institute of Clinical Medicine, Faculty of Medicine University of Oslo  Oslo Norway"},{"name":"Department of Medical Biochemistry Oslo University Hospital  Oslo Norway"},{"name":"Department of Plastic and Reconstructive Surgery 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