{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T23:40:03Z","timestamp":1777938003041,"version":"3.51.4"},"reference-count":13,"publisher":"SAGE Publications","issue":"6","license":[{"start":{"date-parts":[[1997,1,1]],"date-time":"1997-01-01T00:00:00Z","timestamp":852076800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Mult Scler"],"published-print":{"date-parts":[[1997,1]]},"abstract":"<jats:p>Previous case reports demonstrated the presence of Leber's hereditary optic neuropathy (LHON) associated mitochondrial (mt) DNA mutations in patients presenting with prominent optic neuritis (PON). By screening the mtDNA, we have excluded vie presence of these mutations in 22 patients with PON, indicating that the frequency of these mutations is less than 4.5% in our selected patient population. Reviewing the clinical data of these patients revealed that severe optic nerve atrophy developed in association with both the benign and the severely disabling form of Multiple Sclerosis (MS). This observation suggests that the prominent feature of ON in MS may be related to local factors or to a selective vulnerability of the optic nerve in some patients. However, it also may be a consequence of a deleterious process associated with inflammatory demyelination in the central nervous system (CNS) of another, genetically probably distinct subgroup of severely disabled patients.<\/jats:p>","DOI":"10.1177\/135245859700200603","type":"journal-article","created":{"date-parts":[[2017,1,17]],"date-time":"2017-01-17T08:26:17Z","timestamp":1484641577000},"page":"279-282","source":"Crossref","is-referenced-by-count":15,"title":["Screening for Leber's hereditary optic neuropathy associated mitochondrial DNA mutations in patients with prominent optic neuritis"],"prefix":"10.1177","volume":"2","author":[{"given":"Bernadette","family":"Kalman","sequence":"first","affiliation":[{"name":"Department of Neurology, Thomas Jefferson University, Philadelphia, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jose Luis","family":"Rodriguez-Valdez","sequence":"additional","affiliation":[{"name":"Department of Neurology, Thomas Jefferson University, Philadelphia, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ursula","family":"Bosch","sequence":"additional","affiliation":[{"name":"Department of Neurology, Thomas Jefferson University, Philadelphia, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fred D","family":"Lublin","sequence":"additional","affiliation":[{"name":"Department of Neurology, Thomas Jefferson University, Philadelphia, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[1997,1,1]]},"reference":[{"key":"atypb1","unstructured":"1 Perkins GD, Rose FC. 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