Acta Ophthalmologica 2015
developing myopia during early adulthood have reported prospectively on myopic shifts and biometry. These studies have been performed in microscopists and medical or engineering students, who have been shown to develop adult onset myopia (Lin et al. 1996; McBrien & Adams 1997; Kinge et al. 1999), but authors did not report on lens power change with age, although those studies showed that the myopic shifts found were smaller than expected for the increase in axial length, thus pointing to possible loss of lens power during those adult years. Full prospective data of refractive change and biometry, including anterior chamber depth and lens thickness, were available in one of these studies (Kinge et al. 1999), so the lens power could be calculated with Bennett’s equation (Bennett 1988). As can be seen in the Table 1, the 3-year growth of approximately 0.4 mm in axial length that would represent a myopic shift in spherical equivalent of about 1.2 dioptres did not match the actual myopic shift found of 0.50 dioptres because the lens lost about 0.40–0.80 dioptres of power. It can then be seen that the lens continues to compensate for axial elongation in early adult years. Interestingly, the compensation is less evident in progressing myopes, as emmetropes or hyperopes show greater loss of lens power than progressing myopes in the same period. The lens thins and flattens curvatures in children up to age 10, and from
then on, the lens increases in axial thickness, steepens front and back curvatures and loses internal effective refractive index (Brown’s lens paradox). The increase in axial thickness can be seen in the follow-up of the current study, and interestingly, although curvatures may be steepening slightly with age in these engineering students, the lens is losing power probably because of changes in its internal structure, as has been discussed before (Iribarren et al. 2012). The fact that the lens seems to be losing more power in baseline emmetropes or hyperopes than in myopic subjects is possibly related to the changes seen in lens power loss during myopia development in previous studies (Iribarren et al. 2012; Mutti et al. 2012). A 0.77 dioptres change in 3 years represents a rate of lens power loss of 0.26 dioptres per year, which compares well with the rate of lens power loss in SCORM emmetropic schoolchildren of 0.29 dioptres per year (Iribarren et al. 2012). It could then be that the rate of lens power loss does not slow up much after age 10 and is still present during early adult life in subjects prone to develop myopic shifts, like these engineering students in Norway. It would be interesting to analyse lens power loss prospectively in population-based studies in younger and older adults according to refractive groups as has been done in CLEERE and SCORM studies in schoolchildren.
Table 1. Refraction and ocular components according to refractive error groups at baseline. Baseline
Initially myopic
Initially emmetropic
Initially hyperopic
Spherical equivalent (dioptres) Axial length (mm) Anterior chamber depth (mm) Lens thickness (mm) Corneal radius (mm) Lens power (dioptres)
2.29 24.37 3.6 3.5 7.78 23.29
0.12 23.54 3.6 3.56 7.83 23.72
1.08 23.1 3.39 3.62 7.9 24.34
Follow-up at 3 years Spherical equivalent (dioptres) Axial length (mm) Anterior chamber depth (mm) Lens thickness (mm) Corneal radius (mm) Lens power (dioptres)
2.96 24.75 3.59 3.58 7.79 22.92
0.38 23.93 3.61 3.63 7.83 22.95
0.84 23.32 3.43 3.66 7.88 23.75
Change after 3-year follow-up Spherical equivalent (dioptres) Axial length (mm) Anterior chamber depth (mm) Lens thickness (mm) Corneal radius (mm) Lens power (dioptres)
0.67 0.38 0.01 0.08 0.01 0.37
0.5 0.39 0.01 0.07 0 0.77
0.24 0.22 0.04 0.04 0.02 0.60
e234
References Bennett AG (1988): A method of determining the equivalent powers of the eye and its crystalline lens without resort to phakometry. Ophthalmic Physiol Opt 8: 53–59. Iribarren R, Morgan IG, Chan YH et al. (2012): Changes in lens power in Singapore Chinese children during refractive development. Invest Ophthalmol Vis Sci 53: 5124–5130. Kinge B, Midelfart A, Jacobsen G & Rystad J (1999): Biometric changes in the eyes of Norwegian university students–a three-year longitudinal study. Acta Ophthalmol Scand 77: 648–652. Lin LL, Shih YF, Lee YC et al. (1996): Changes in ocular refraction and its components among medical students–a 5-year longitudinal study. Optom Vis Sci 73: 495–498. McBrien NA & Adams DW (1997): A longitudinal investigation of adult-onset and adult-progression of myopia in an occupational group. Refractive and biometric findings. Invest Ophthalmol Vis Sci 38: 321–333. Mutti DO, Mitchell GL, Sinnott LT et al. (2012): Corneal and crystalline lens dimensions before and after myopia onset. Optom Vis Sci 89: 251–262.
Correspondence: Rafael Iribarren Department of Ophthalmology Centro Medico San Luis San Martın de Tours 2980 1425 Buenos Aires, Argentina Tel/Fax: +54 11 4393 1844 Email: [email protected]
Cerebrospinal fluid pressure trends in diseases associated with primary open-angle glaucoma David Fleischman,1,2 John Berdahl,3 Sandra S. Stinnett,1 Michael P. Fautsch4 and R. R. Allingham1 1
Duke Eye Center, Durham, NC, USA; Department of Ophthalmology, University of North Carolina, Chapel Hill, NC, USA; 3Vance Thompson Vision, Sioux Falls, SD, USA; 4 Department of Ophthalmology, Mayo Clinic, Rochester, MN, USA 2
doi: 10.1111/aos.12551
Editor, ecent studies implicate reduced CSFP as a risk factor for POAG,
R
Acta Ophthalmologica 2015
while an increased CSFP is appreciated in patients with ocular hypertension (OHT) (Berdahl et al. 2008; Ren et al. 2010; Wang et al. 2012; Yang et al. 2014). The lamina cribrosa serves as the boundary between two differentially pressurized compartments – the intra-ocular and subarachnoid spaces. It is suspected that the difference between the pressures within these two compartments enacts a net force across the lamina, perhaps resulting in glaucomatous damage to the ganglion cell axons. In OHT, an elevated CSFP would provide a protective counterbalance against elevated intra-ocular pressure (IOP). The purpose of this study was to identify trends in CSFP in different diseases. If decreased CSFP is associated with POAG, and increased CSFP with OHT, individual diseases that have a particular CSFP profile may help explain associations with POAG or OHT. This was a retrospective chart analysis from the Mayo Clinic’s medical records system of all patients who underwent a diagnostic lumbar puncture from 1996 to 2009. The study was approved by the Mayo Clinic Institutional Review Board (IRB) and was compliant with HIPAA. Information abstracted from this search included opening CSFP, as well as up to 15 diagnoses. Patients with medical conditions, head trauma or those taking medications known to alter CSFP were excluded. Patients were deidentified immediately following extraction. Individual patients were given randomized identifiers as part of the deidentification protocol at the Mayo Clinic. Patients were grouped as ‘Disease’ or ‘Non-disease’ groups. CSF parameters were grouped by patient age, and the means were compared using a twotailed t-test. Statistical significance was set at p < 0.05, testing that the difference of the means between the two groups was not dissimilar. ‘Electronic medical records of 33 922 patients with a history of having an LP during a thirteen-year period were extracted. Of these, 13 719 patients met entry criteria. Nine different disease groups were evaluated (Table 1). Multiple sclerosis (MS), cerebellar degeneration, Alzheimer’s, diabetes mellitus (DM) and atherosclerosis showed some association with CSFP,
Table 1. Mean cerebrospinal fluid pressure with standard deviation for diseased and non-diseased groups. Texts in yellow highlight and red indicate statistical significance. Statistical significance determined by Student’s t-test determination of difference in means between the disease and nondisease groups.
CVA, Cerebrovascular accidents.
but no consistent results were obtained in all age groups within a single disease. Our study failed to find consistent trends in CSFP differences between diseased and non-disease groups. Some exceptions were noted such as a trend towards a relative increase in CSFP in middle and older age in patients with multiple sclerosis and a elevated CSFP in younger patients with diabetes and atherosclerosis. A reduced CSFP was found in patients aged 40–69 with cerebellar degeneration and Alzheimer’s disease. In Alzheimer’s age >70, a trend towards elevated CSFP was noted.
The effect of CSFP on POAG risk would suggest a protective effect in patients with MS. MS is not closely linked to POAG, although younger male patients have an increased risk of developing POAG, a finding that did not extend >50 years of age (Bazelier et al. 2012). The CSFP elevation with age in patients with MS would make POAG risk less likely. Diabetes mellitus has been studied extensively in the context of POAG risk, with varying results. The LALES Group found a relationship between POAG and DM in a Hispanic population (Chopra et al. 2008). Conversely,
e235
Acta Ophthalmologica 2015
the OHTS Group revealed a protective link between DM and POAG (Gordon et al. 2002). Our study identified a significant CSFP elevation in younger diabetics, a relationship that did not extend beyond the age of 40. Lastly, a link between Alzheimer’s and POAG has been recently examined from the standpoint of retrolaminar CSFP dynamics (Wostyn et al. 2009). Our results identify a significant CSF pressure decrease in middle-age patients with Alzheimer’s disease that abruptly changes to a trend towards increased CSFP (albeit statistically insignificant). Whether this indicates a clinical association or holds significant clinical implications requires additional studies. Future research directed towards understanding CSFP trends in normal and disease populations, and incidence and progression trends in patients with POAG harbouring these respective diseases, may aid in elucidating our current association data.
Yang D, Fu J, Hou R et al. (2014): Optic neuropathy induced by experimentally reduced cerebrospinal fluid pressure in monkeys. Invest Ophthalmol Vis Sci 55: 3067– 3073.
Correspondence: David Fleischman, MD Duke Eye Center 2351 Erwin Road DUMC 3802 Durham, NC 27710 USA Tel: +1 919 684 6611 Fax: +1 919 668 7871 Email: david8fl[email protected]
Effect of myopic refractive error on the glaucoma diagnostic ability of cirrus high-definition optical coherence tomography Mi Sun Sung,1 Jin Ha Yoon,2 Hwan Heo1 and Sang Woo Park1
References Bazelier MT, Mueller-Schotte S, Leufkens HG, Uitdehaag BM, van Staa T & de Vries F (2012): Risk of cataract and glaucoma in patients with multiple sclerosis. Mult Scler 18: 628–638. Berdahl JP, Fautsch MP, Stinnett SS & Allingham RR (2008): Intracranial pressure in primary open angle glaucoma, normal tension glaucoma, and ocular hypertension: a case-control study. Invest Ophthalmol Vis Sci 49: 5412–5418. Chopra V, Varma R, Francis BA, Wu J, Torres M, Azen SP, Los Angeles Latino Eye Study Group. (2008): Type 2 diabetes mellitus and the risk of open-angle glaucoma: the LALES. Ophthalmology 115: 227–232. Gordon MO, Beiser JA, Brandt JD et al. (2002): The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol 120: 714–720. Ren R, Jonas JB, Tian G et al. (2010): Cerebrospinal fluid pressure in glaucoma: a prospective study. Ophthalmology 117: 259– 266. Wang NL, Xie XB, Yang DY et al. (2012): Orbital cerebrospinal fluid space in glaucoma: the Beijing intracranial and intraocular pressure (iCOP) study. Ophthalmology 119: 2065–2073. Wostyn P, Audenaert K & De Deyn PP. (2009): Alzheimer’s disease and glaucoma: is there a causal relationship? Br J Ophthalmol 93: 1557–1559.
e236
1 Department of Ophthalmology, Chonnam National University Medical School and Hospital, Gwangju, South Korea; 2Occupational Lung disease Institute, Ansan, South Korea
doi: 10.1111/aos.12546
Editor, t is well known that peripapillary retinal nerve fibre layer (pRNFL) measurement using spectral-domain optical coherence tomography (SDOCT) may have limited utility in highly myopic eyes. To overcome the anatomically induced measurement error, several studies have investigated the diagnostic ability of macular measurements using various SD-OCT instruments in glaucoma patients with high myopia (Kim et al. 2011; Shoji et al. 2012; Akashi et al. 2013; Choi et al. 2013; Nakano et al. 2013). However, the conclusions still have been controversial. This study, therefore, aimed to assess the effect of myopic refractive error on the diagnostic ability of pRNFL and macular ganglion cellinner plexiform layer (mGCIPL) thickness measurements obtained through Cirrus HD-OCT by using a receiver
I
operating characteristic (ROC) logistic regression analysis. Patients with a history of cataract extraction surgery were excluded. The average, minimum and sectoral thicknesses of the mGCIPL were measured in an elliptical annulus around the fovea. In this study, direct modelling of the ROC curve proposed by Pepe et al. (Leisenring & Pepe 1998) was used to assess the influence of refractive error presented as spherical equivalent (SE) refractive error on the diagnostic ability of Cirrus HD-OCT after adjusting for age and optic disc area differences. Age, optic disc size and SE refractive error were considered as covariates in the ROC regression model. Because the SE refractive errors strongly correlated with axial length (r = 0.75; p < 0.001), only one could be considered as a covariate, and therefore, axial length was omitted from the analysis. The remaining two covariates, age and optic disc size, were controlled, as they may affect the diagnostic performance of OCT. In addition, to minimize the effect of glaucoma disease severity on the diagnostic ability, this study was conducted after excluding eyes with advanced glaucoma [mean deviation (MD) < 12 decibels (dBs)] as assessed by visual field examination. A total of 462 subjects (242 normal controls and 220 subjects with mild-tomoderate glaucoma) met inclusion criteria. A myopic SE refractive error ≥ 6D, and therefore high myopia, was present in 14.87% (36 subjects) and 16.37% (36 subjects) of the normal and glaucoma groups, respectively. After controlling for age and optic disc area, minimum mGCIPL thickness had the highest area under the ROC curve (AROC) value among all parameters (0.92), followed by inferior pRNFL thickness (0.91), average pRNFL thickness (0.91) and average mGCIPL thickness (0.89) (Table 1). When further evaluating the diagnostic ability in highly myopic subjects, minimum mGCIPL thickness and inferior pRNFL thickness had the highest AROC value (0.87). Comparisons between the best four parameters in highly myopic eyes did not reach the statistical significance. Table 1 shows AROC values for each diagnostic parameter at levels of SE refractive error chosen arbitrarily. There was a trend towards decreasing
Copyright of Acta Ophthalmologica (1755375X) is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
developing myopia during early adulthood have reported prospectively on myopic shifts and biometry. These studies have been performed in microscopists and medical or engineering students, who have been shown to develop adult onset myopia (Lin et al. 1996; McBrien & Adams 1997; Kinge et al. 1999), but authors did not report on lens power change with age, although those studies showed that the myopic shifts found were smaller than expected for the increase in axial length, thus pointing to possible loss of lens power during those adult years. Full prospective data of refractive change and biometry, including anterior chamber depth and lens thickness, were available in one of these studies (Kinge et al. 1999), so the lens power could be calculated with Bennett’s equation (Bennett 1988). As can be seen in the Table 1, the 3-year growth of approximately 0.4 mm in axial length that would represent a myopic shift in spherical equivalent of about 1.2 dioptres did not match the actual myopic shift found of 0.50 dioptres because the lens lost about 0.40–0.80 dioptres of power. It can then be seen that the lens continues to compensate for axial elongation in early adult years. Interestingly, the compensation is less evident in progressing myopes, as emmetropes or hyperopes show greater loss of lens power than progressing myopes in the same period. The lens thins and flattens curvatures in children up to age 10, and from
then on, the lens increases in axial thickness, steepens front and back curvatures and loses internal effective refractive index (Brown’s lens paradox). The increase in axial thickness can be seen in the follow-up of the current study, and interestingly, although curvatures may be steepening slightly with age in these engineering students, the lens is losing power probably because of changes in its internal structure, as has been discussed before (Iribarren et al. 2012). The fact that the lens seems to be losing more power in baseline emmetropes or hyperopes than in myopic subjects is possibly related to the changes seen in lens power loss during myopia development in previous studies (Iribarren et al. 2012; Mutti et al. 2012). A 0.77 dioptres change in 3 years represents a rate of lens power loss of 0.26 dioptres per year, which compares well with the rate of lens power loss in SCORM emmetropic schoolchildren of 0.29 dioptres per year (Iribarren et al. 2012). It could then be that the rate of lens power loss does not slow up much after age 10 and is still present during early adult life in subjects prone to develop myopic shifts, like these engineering students in Norway. It would be interesting to analyse lens power loss prospectively in population-based studies in younger and older adults according to refractive groups as has been done in CLEERE and SCORM studies in schoolchildren.
Table 1. Refraction and ocular components according to refractive error groups at baseline. Baseline
Initially myopic
Initially emmetropic
Initially hyperopic
Spherical equivalent (dioptres) Axial length (mm) Anterior chamber depth (mm) Lens thickness (mm) Corneal radius (mm) Lens power (dioptres)
2.29 24.37 3.6 3.5 7.78 23.29
0.12 23.54 3.6 3.56 7.83 23.72
1.08 23.1 3.39 3.62 7.9 24.34
Follow-up at 3 years Spherical equivalent (dioptres) Axial length (mm) Anterior chamber depth (mm) Lens thickness (mm) Corneal radius (mm) Lens power (dioptres)
2.96 24.75 3.59 3.58 7.79 22.92
0.38 23.93 3.61 3.63 7.83 22.95
0.84 23.32 3.43 3.66 7.88 23.75
Change after 3-year follow-up Spherical equivalent (dioptres) Axial length (mm) Anterior chamber depth (mm) Lens thickness (mm) Corneal radius (mm) Lens power (dioptres)
0.67 0.38 0.01 0.08 0.01 0.37
0.5 0.39 0.01 0.07 0 0.77
0.24 0.22 0.04 0.04 0.02 0.60
e234
References Bennett AG (1988): A method of determining the equivalent powers of the eye and its crystalline lens without resort to phakometry. Ophthalmic Physiol Opt 8: 53–59. Iribarren R, Morgan IG, Chan YH et al. (2012): Changes in lens power in Singapore Chinese children during refractive development. Invest Ophthalmol Vis Sci 53: 5124–5130. Kinge B, Midelfart A, Jacobsen G & Rystad J (1999): Biometric changes in the eyes of Norwegian university students–a three-year longitudinal study. Acta Ophthalmol Scand 77: 648–652. Lin LL, Shih YF, Lee YC et al. (1996): Changes in ocular refraction and its components among medical students–a 5-year longitudinal study. Optom Vis Sci 73: 495–498. McBrien NA & Adams DW (1997): A longitudinal investigation of adult-onset and adult-progression of myopia in an occupational group. Refractive and biometric findings. Invest Ophthalmol Vis Sci 38: 321–333. Mutti DO, Mitchell GL, Sinnott LT et al. (2012): Corneal and crystalline lens dimensions before and after myopia onset. Optom Vis Sci 89: 251–262.
Correspondence: Rafael Iribarren Department of Ophthalmology Centro Medico San Luis San Martın de Tours 2980 1425 Buenos Aires, Argentina Tel/Fax: +54 11 4393 1844 Email: [email protected]
Cerebrospinal fluid pressure trends in diseases associated with primary open-angle glaucoma David Fleischman,1,2 John Berdahl,3 Sandra S. Stinnett,1 Michael P. Fautsch4 and R. R. Allingham1 1
Duke Eye Center, Durham, NC, USA; Department of Ophthalmology, University of North Carolina, Chapel Hill, NC, USA; 3Vance Thompson Vision, Sioux Falls, SD, USA; 4 Department of Ophthalmology, Mayo Clinic, Rochester, MN, USA 2
doi: 10.1111/aos.12551
Editor, ecent studies implicate reduced CSFP as a risk factor for POAG,
R
Acta Ophthalmologica 2015
while an increased CSFP is appreciated in patients with ocular hypertension (OHT) (Berdahl et al. 2008; Ren et al. 2010; Wang et al. 2012; Yang et al. 2014). The lamina cribrosa serves as the boundary between two differentially pressurized compartments – the intra-ocular and subarachnoid spaces. It is suspected that the difference between the pressures within these two compartments enacts a net force across the lamina, perhaps resulting in glaucomatous damage to the ganglion cell axons. In OHT, an elevated CSFP would provide a protective counterbalance against elevated intra-ocular pressure (IOP). The purpose of this study was to identify trends in CSFP in different diseases. If decreased CSFP is associated with POAG, and increased CSFP with OHT, individual diseases that have a particular CSFP profile may help explain associations with POAG or OHT. This was a retrospective chart analysis from the Mayo Clinic’s medical records system of all patients who underwent a diagnostic lumbar puncture from 1996 to 2009. The study was approved by the Mayo Clinic Institutional Review Board (IRB) and was compliant with HIPAA. Information abstracted from this search included opening CSFP, as well as up to 15 diagnoses. Patients with medical conditions, head trauma or those taking medications known to alter CSFP were excluded. Patients were deidentified immediately following extraction. Individual patients were given randomized identifiers as part of the deidentification protocol at the Mayo Clinic. Patients were grouped as ‘Disease’ or ‘Non-disease’ groups. CSF parameters were grouped by patient age, and the means were compared using a twotailed t-test. Statistical significance was set at p < 0.05, testing that the difference of the means between the two groups was not dissimilar. ‘Electronic medical records of 33 922 patients with a history of having an LP during a thirteen-year period were extracted. Of these, 13 719 patients met entry criteria. Nine different disease groups were evaluated (Table 1). Multiple sclerosis (MS), cerebellar degeneration, Alzheimer’s, diabetes mellitus (DM) and atherosclerosis showed some association with CSFP,
Table 1. Mean cerebrospinal fluid pressure with standard deviation for diseased and non-diseased groups. Texts in yellow highlight and red indicate statistical significance. Statistical significance determined by Student’s t-test determination of difference in means between the disease and nondisease groups.
CVA, Cerebrovascular accidents.
but no consistent results were obtained in all age groups within a single disease. Our study failed to find consistent trends in CSFP differences between diseased and non-disease groups. Some exceptions were noted such as a trend towards a relative increase in CSFP in middle and older age in patients with multiple sclerosis and a elevated CSFP in younger patients with diabetes and atherosclerosis. A reduced CSFP was found in patients aged 40–69 with cerebellar degeneration and Alzheimer’s disease. In Alzheimer’s age >70, a trend towards elevated CSFP was noted.
The effect of CSFP on POAG risk would suggest a protective effect in patients with MS. MS is not closely linked to POAG, although younger male patients have an increased risk of developing POAG, a finding that did not extend >50 years of age (Bazelier et al. 2012). The CSFP elevation with age in patients with MS would make POAG risk less likely. Diabetes mellitus has been studied extensively in the context of POAG risk, with varying results. The LALES Group found a relationship between POAG and DM in a Hispanic population (Chopra et al. 2008). Conversely,
e235
Acta Ophthalmologica 2015
the OHTS Group revealed a protective link between DM and POAG (Gordon et al. 2002). Our study identified a significant CSFP elevation in younger diabetics, a relationship that did not extend beyond the age of 40. Lastly, a link between Alzheimer’s and POAG has been recently examined from the standpoint of retrolaminar CSFP dynamics (Wostyn et al. 2009). Our results identify a significant CSF pressure decrease in middle-age patients with Alzheimer’s disease that abruptly changes to a trend towards increased CSFP (albeit statistically insignificant). Whether this indicates a clinical association or holds significant clinical implications requires additional studies. Future research directed towards understanding CSFP trends in normal and disease populations, and incidence and progression trends in patients with POAG harbouring these respective diseases, may aid in elucidating our current association data.
Yang D, Fu J, Hou R et al. (2014): Optic neuropathy induced by experimentally reduced cerebrospinal fluid pressure in monkeys. Invest Ophthalmol Vis Sci 55: 3067– 3073.
Correspondence: David Fleischman, MD Duke Eye Center 2351 Erwin Road DUMC 3802 Durham, NC 27710 USA Tel: +1 919 684 6611 Fax: +1 919 668 7871 Email: david8fl[email protected]
Effect of myopic refractive error on the glaucoma diagnostic ability of cirrus high-definition optical coherence tomography Mi Sun Sung,1 Jin Ha Yoon,2 Hwan Heo1 and Sang Woo Park1
References Bazelier MT, Mueller-Schotte S, Leufkens HG, Uitdehaag BM, van Staa T & de Vries F (2012): Risk of cataract and glaucoma in patients with multiple sclerosis. Mult Scler 18: 628–638. Berdahl JP, Fautsch MP, Stinnett SS & Allingham RR (2008): Intracranial pressure in primary open angle glaucoma, normal tension glaucoma, and ocular hypertension: a case-control study. Invest Ophthalmol Vis Sci 49: 5412–5418. Chopra V, Varma R, Francis BA, Wu J, Torres M, Azen SP, Los Angeles Latino Eye Study Group. (2008): Type 2 diabetes mellitus and the risk of open-angle glaucoma: the LALES. Ophthalmology 115: 227–232. Gordon MO, Beiser JA, Brandt JD et al. (2002): The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol 120: 714–720. Ren R, Jonas JB, Tian G et al. (2010): Cerebrospinal fluid pressure in glaucoma: a prospective study. Ophthalmology 117: 259– 266. Wang NL, Xie XB, Yang DY et al. (2012): Orbital cerebrospinal fluid space in glaucoma: the Beijing intracranial and intraocular pressure (iCOP) study. Ophthalmology 119: 2065–2073. Wostyn P, Audenaert K & De Deyn PP. (2009): Alzheimer’s disease and glaucoma: is there a causal relationship? Br J Ophthalmol 93: 1557–1559.
e236
1 Department of Ophthalmology, Chonnam National University Medical School and Hospital, Gwangju, South Korea; 2Occupational Lung disease Institute, Ansan, South Korea
doi: 10.1111/aos.12546
Editor, t is well known that peripapillary retinal nerve fibre layer (pRNFL) measurement using spectral-domain optical coherence tomography (SDOCT) may have limited utility in highly myopic eyes. To overcome the anatomically induced measurement error, several studies have investigated the diagnostic ability of macular measurements using various SD-OCT instruments in glaucoma patients with high myopia (Kim et al. 2011; Shoji et al. 2012; Akashi et al. 2013; Choi et al. 2013; Nakano et al. 2013). However, the conclusions still have been controversial. This study, therefore, aimed to assess the effect of myopic refractive error on the diagnostic ability of pRNFL and macular ganglion cellinner plexiform layer (mGCIPL) thickness measurements obtained through Cirrus HD-OCT by using a receiver
I
operating characteristic (ROC) logistic regression analysis. Patients with a history of cataract extraction surgery were excluded. The average, minimum and sectoral thicknesses of the mGCIPL were measured in an elliptical annulus around the fovea. In this study, direct modelling of the ROC curve proposed by Pepe et al. (Leisenring & Pepe 1998) was used to assess the influence of refractive error presented as spherical equivalent (SE) refractive error on the diagnostic ability of Cirrus HD-OCT after adjusting for age and optic disc area differences. Age, optic disc size and SE refractive error were considered as covariates in the ROC regression model. Because the SE refractive errors strongly correlated with axial length (r = 0.75; p < 0.001), only one could be considered as a covariate, and therefore, axial length was omitted from the analysis. The remaining two covariates, age and optic disc size, were controlled, as they may affect the diagnostic performance of OCT. In addition, to minimize the effect of glaucoma disease severity on the diagnostic ability, this study was conducted after excluding eyes with advanced glaucoma [mean deviation (MD) < 12 decibels (dBs)] as assessed by visual field examination. A total of 462 subjects (242 normal controls and 220 subjects with mild-tomoderate glaucoma) met inclusion criteria. A myopic SE refractive error ≥ 6D, and therefore high myopia, was present in 14.87% (36 subjects) and 16.37% (36 subjects) of the normal and glaucoma groups, respectively. After controlling for age and optic disc area, minimum mGCIPL thickness had the highest area under the ROC curve (AROC) value among all parameters (0.92), followed by inferior pRNFL thickness (0.91), average pRNFL thickness (0.91) and average mGCIPL thickness (0.89) (Table 1). When further evaluating the diagnostic ability in highly myopic subjects, minimum mGCIPL thickness and inferior pRNFL thickness had the highest AROC value (0.87). Comparisons between the best four parameters in highly myopic eyes did not reach the statistical significance. Table 1 shows AROC values for each diagnostic parameter at levels of SE refractive error chosen arbitrarily. There was a trend towards decreasing
Copyright of Acta Ophthalmologica (1755375X) is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
