TY - JOUR
T1 - Hemisphere opposite to vascular trunk deviation is earlier affected by glaucomatous damage in myopic high-tension glaucoma
AU - Lee, Kyoung Min
AU - Kim, Martha
AU - Oh, Sohee
AU - Kim, Seok Hwan
N1 - Publisher Copyright:
© 2020 Lee et al.
PY - 2020/5
Y1 - 2020/5
N2 - Purpose To investigate whether the position of the central vascular trunk, as a surrogate of lamina cribrosa (LC) shift, is associated with the initial hemisphere of visual field defect in myopic high-tension glaucoma (HTG) eyes. Methods The deviation of the central vascular trunk was measured from the center of the Bruch's membrane opening (BMO), which was delineated by OCT imaging. The angular deviation was measured with the horizontal nasal midline as 0° and the superior location as a positive value. The initial hemisphere developing visual field defect was defined as three connected abnormal points (having a P value with less than 0.5% probability of being normal) appearing in only one hemisphere in pattern deviation plots. If those points were observed in both hemispheres initially, the eye was classified as bi-hemispheric visual field defect. Results Initially, 36 eyes (44%) had superior visual field defects, 27 (33%) inferior visual field defects, and 18 (22%) bi-hemispheric visual field defects. After a mean follow-up of 5 years, the number of bi-hemispheric visual field defects had increased to 34 (42%). A logistic regression analysis revealed that inferior deviation of vascular trunk was the only factor associated with initial inferior visual field defect (P = 0.001), while initial bi-hemispheric visual field defects were associated with worse mean deviation at initial visits (P<0.001). A conditional inference tree analysis showed that both the angular deviation (P<0.001) and initial mean deviation (P = 0.025) determined the initial hemispheres developing visual field defect. Conclusions Although both hemispheres were involved as glaucoma progression, the axons on the side counter to the vascular trunk deviation were damaged earlier in HTG. This finding implies the LC shift could add additional stress to axons exposed to high intraocular pressure.
AB - Purpose To investigate whether the position of the central vascular trunk, as a surrogate of lamina cribrosa (LC) shift, is associated with the initial hemisphere of visual field defect in myopic high-tension glaucoma (HTG) eyes. Methods The deviation of the central vascular trunk was measured from the center of the Bruch's membrane opening (BMO), which was delineated by OCT imaging. The angular deviation was measured with the horizontal nasal midline as 0° and the superior location as a positive value. The initial hemisphere developing visual field defect was defined as three connected abnormal points (having a P value with less than 0.5% probability of being normal) appearing in only one hemisphere in pattern deviation plots. If those points were observed in both hemispheres initially, the eye was classified as bi-hemispheric visual field defect. Results Initially, 36 eyes (44%) had superior visual field defects, 27 (33%) inferior visual field defects, and 18 (22%) bi-hemispheric visual field defects. After a mean follow-up of 5 years, the number of bi-hemispheric visual field defects had increased to 34 (42%). A logistic regression analysis revealed that inferior deviation of vascular trunk was the only factor associated with initial inferior visual field defect (P = 0.001), while initial bi-hemispheric visual field defects were associated with worse mean deviation at initial visits (P<0.001). A conditional inference tree analysis showed that both the angular deviation (P<0.001) and initial mean deviation (P = 0.025) determined the initial hemispheres developing visual field defect. Conclusions Although both hemispheres were involved as glaucoma progression, the axons on the side counter to the vascular trunk deviation were damaged earlier in HTG. This finding implies the LC shift could add additional stress to axons exposed to high intraocular pressure.
UR - http://www.scopus.com/inward/record.url?scp=85084865209&partnerID=8YFLogxK
U2 - 10.1371/journal.pone.0233270
DO - 10.1371/journal.pone.0233270
M3 - Article
C2 - 32421695
AN - SCOPUS:85084865209
SN - 1932-6203
VL - 15
JO - PLoS ONE
JF - PLoS ONE
IS - 5
M1 - e0233270
ER -