CASE REPORT
Progression of Normal-Tension Glaucoma After Ventriculoperitoneal Shunt to Decrease Cerebrospinal Fluid Pressure Brian H. Chen, MD, MS,* Mitchell D. Drucker, MD,* Kenneth M. Louis, MD,w and David W. Richards, MD, PhD*
Purpose: To report a case of worsening normal-tension glaucoma immediately following ventriculoperitoneal (VP) shunt placement to lower cerebrospinal fluid pressure (CSFP). Methods: The clinical records of the patient were reviewed retrospectively. Observations were made and collated as the case progressed. Results: A 93-year-old white woman previously diagnosed with normal-tension glaucoma underwent placement of a VP shunt with a Codman-Hakim programmable valve for normal pressure hydrocephalus. Shortly after the procedure, progressive visual field loss was noted in both eyes and new optic disc hemorrhages were seen in the patient’s right eye. The hemorrhages resolved, but the patient had recurrent complaints of poor gait, memory, and mentation. The CSFP was lowered by reprogramming the CodmanHakim valve. The patient’s visual fields again worsened in both eyes and a new disc hemorrhage was seen in the right eye. A year later, a new disc hemorrhage was seen in the patient’s left eye. The CSFP was raised by reprogramming the VP shunt. Before the placement of the VP shunt, no optic disc hemorrhages had been observed. Conclusion: This case suggests that relatively low CSFP is a contributor to worsening normal-tension glaucoma, probably by increasing translaminar pressure gradient of the optic nerve. Key Words: ventriculoperitoneal shunt, cerebrospinal fluid, normal-tension glaucoma
(J Glaucoma 2016;25:e50–e52)
T
here is mounting evidence that cerebrospinal fluid pressure (CSFP) plays an important role in the pathogenesis of glaucoma.1 This may be due to an abnormally high translaminar gradient between the intraocular pressure (IOP) and the retrolaminar cerebrospinal fluid. A high translaminar pressure gradient may affect orthograde and retrograde axoplasmic flow2 or central retinal vein compression, shear, and wall thickening,3 among other factors. This report describes a case of worsening normal-tension
Received for publication May 7, 2014; accepted September 19, 2014. From the *Department of Ophthalmology, Morsani College of Medicine, University of South Florida Eye Institute; and wDepartment of Neurosurgery, Morsani College of Medicine, University of South Florida, Tampa, FL. Disclosure: The authors declare no conflict of interest. Reprints: David W. Richards, MD, PhD, Department of Ophthalmology, Morsani College of Medicine, University of South Florida Eye Institute, 12901 Bruce B. Downs Blvd., MDC 21, Tampa, FL 33612 (e-mail: [email protected]). Copyright r 2014 Wolters Kluwer Health, Inc. All rights reserved. DOI: 10.1097/IJG.0000000000000186
glaucoma in a patient who had ventriculoperitoneal (VP) shunting to lower CSFP for normal pressure hydrocephalus.
CASE REPORT A 93-year-old white woman, who has been followed for wellcontrolled normal-tension glaucoma since May 2000, presented for follow-up in October 2008. She had cataract extraction with posterior chamber intraocular lenses in both eyes 2 years earlier. Before the October 2008 visit, optic disc (Drance) hemorrhages had never been seen. On exam, her vision was 20/25 in both eyes, and IOPs were 10 mm Hg in the right eye, and 11 mm Hg in the left eye. Her central corneal thickness was 516 mm in the right eye and 509 mm in the left eye. The patient’s optic disc photographs are presented in Figure 1. The patient’s visual fields (Humphrey Field Analyzer, SITA Standard 24-2) remained stable with IOPs consistently low, treated with timolol 0.5% in both eyes twice daily and latanoprost 0.005% in both eyes at bedtime. She was intolerant to brinzolamide and brimonidine Five months after the October 2008 visit, the patient complained of forgetfulness, difficulty walking, headaches, and poor overall mentation. She had a computed tomography scan of the head that showed enlarged lateral and third ventricles and had a neurosurgical evaluation. She then underwent lumbar puncture and cisternogram and was diagnosed with normal pressure hydrocephalus. Of note, her gait and mental function symptomatically improved after lumbar puncture. VP shunting was discussed and offered at that time but declined by the patient and family. In September 2011, the patient continued to complain of gait disturbance and poor memory. Her neurosurgeon (K.M.L.) implanted a VP shunt with a Codman-Hakim programmable valve (DePuy Synthes, Warsaw, IN) set at 120 mm H2O to lower CSFP. Immediately after the procedure, her gait and mental function improved. She underwent ophthalmic examination 1 month after placement of the VP shunt, and 2 optic disc hemorrhages were noted in the right eye (Fig. 1). Her visual fields also worsened in both the eyes. In October 2011, the neurosurgeon increased the CSFP to 200 mm H2O via the Codman-Hakim valve because of development of subdural hygromas. The patient returned for ophthalmic examination and the disc hemorrhages in the right eye had resolved. In November 2011, the patient returned to the neurosurgeon with a recurrent complaint of poor balance and memory; the VP shunt setting was decreased from 200 to 180 mm H2O; a month later (December 2011) from 180 to 160 mm H2O; a month later (January 2012) from 160 to 150 mm H2O; another month later (February 2012) from 150 to 140 mm H2O. This improved the patient’s gait, mentation, and relieved her headaches. Six months later (August 2012) the patient was noted to have a new optic disc hemorrhage in the right eye, and again worsening visual field in both the eyes (Figs. 1, 2). One year later (September 2013), a third episode of new optic disc hemorrhage was seen in the left eye (Fig. 1). Visual fields had worsened in both the eyes (Fig. 2). At this point, in light of worsening visual fields despite low IOP and maximum tolerated medical therapy, the development of
e50 | www.glaucomajournal.com J Glaucoma Volume 25, Number 1, January 2016 Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved.
J Glaucoma
Volume 25, Number 1, January 2016
Normal-Tension Glaucoma After Ventriculoperitoneal Shunt
FIGURE 1. Optic disc photographs of the (A) right and (B) left eye prior (March 2009) to VP shunt. C, Disc hemorrhages (arrows) are seen in the right eye 1 month (October 2011) after VP shunt. D, A new disc hemorrhage (arrow) is seen in the right eye 10 months later (August 2012). E, Disc hemorrhage (arrow) is seen in the left eye 2 years (September 2013) after VP shunt. VP indicates ventriculoperitoneal. new disc hemorrhages after lowering CSFP, and the patient being a poor candidate for surgical therapy, the neurosurgeon raised the CSFP in September 2013 to 150 mm H2O. In November 2013, no disc hemorrhages were seen. A summary of the patient’s clinical course, IOP, presence of disc hemorrhage, CSFP, and visual field MD is presented in Figure 2.
DISCUSSION Volkov4 presented the idea that CSFP may be involved in the pathogenesis of glaucomatous optic neuropathy in the
Summary of Clinical Course Intraocular Pressure (mm Hg)
16 14 12 10 8 6 4
OD
Visual Field Mean Deviation (dB)
CSFP by VP shunt (mm H2O)
2
OS
0 10/27/08
10/27/09
10/27/10
200 190 180 170 160 150 140 130 120 110 10/27/08
10/27/09
10/27/10
10/27/11
10/27/12
10/27/11
10/27/12
(4.82)
-5
(10.36)
-10
(11.84) (10.99)
-15
(10.67) (10.87)
(11.01) (11.05)
-20
(10.67)
OD (PSD)
-25 -30 10/27/08
(7.75)
OS (PSD)
(7.63)
(9.67) (7.73)
(3.53)
10/27/09
10/27/10
10/27/11
10/27/12
Optic disc exam with no optic disc hemorrhage detected in either eye VP Shunt placed/adjusted Optic disc hemorrhage detected
FIGURE 2. Summary of the clinical course. CSFP indicates cerebrospinal fluid pressure; VP, ventriculoperitoneal.
Copyright
r
1970s. Attention has been recently focused on the pressure gradient between the intraocular space and the retrobulbar space. The lamina cribrosa of the optic nerve head defines the border between these spaces, and the pressure difference is called the translaminar pressure gradient.1 Yablonski and colleagues hypothesized that low CSFP around the optic nerve may induce glaucomatous optic neuropathy. He experimentally decreased the intracranial pressure 5 cm H2O below atmospheric pressure by cannulation of the cisterna magna in cats. The IOP in 1 eye was left unaltered, whereas in the other eye it was lowered to slightly above atmospheric pressure by cannulation of the anterior chamber. After 3 weeks, the optic disc in the eye that had an unaltered IOP showed glaucomatous optic neuropathy, whereas no changes were seen in the eyes that had lowered IOP.5 The translaminar pressure gradient depends not only on the pressure difference between the intraocular and the retrobulbar spaces, but also on the thickness of the lamina cribrosa.6 It has been shown that the lamina cribrosa thins in advanced stages of glaucoma, and this may be one of the reasons for increased risk of progression of glaucoma in eyes with advanced glaucoma.7 Recent studies have shown that CSFP measured by lumbar puncture was significantly lower in patients with normal-tension glaucoma and in primary open-angle glaucoma than in control subjects.8,9 Our patient’s course suggests that stable glaucoma was worsened by decreasing the CSFP. We believe that this is the first report of apparent worsening of glaucoma after VP shunt placement. After CSFP lowering, our patient exhibited glaucomatous disease progression in a variety of ways. Optic disc hemorrhages are a known marker for disease progression10,11 as is worsening visual field loss. It is possible that visual field progression occurs before the onset of disc hemorrhage.12 In the case presented, the optic disc hemorrhages correspond to worsening visual fields and to time intervals of lower CSFP. In clinical practice, a disc hemorrhage not only indicates that the disease is active and progression is likely, but also demands increased vigilant surveillance, and may require additional therapy. These optic disc hemorrhages are known to resolve without treatment. Our patient provided a difficult management challenge as a balance between symptomatically improving her headaches, gait, memory, and mentation versus slowing the progression of normal-tension glaucoma. More work is needed to apply this information clinically. These include a noninvasive method to measure CSFP, perhaps using tympanometry through the inner ear, ophthalmodynamometry, or an intrathecal pressure sensitive catheter; alternative medical or surgical treatment for abnormally low CSFP; and determination of whether other
2014 Wolters Kluwer Health, Inc. All rights reserved.
www.glaucomajournal.com |
Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved.
e51
Chen et al
J Glaucoma
diseases, both ocular and systemic, are associated with low CSFP. A prospective study of optic nerves in glaucoma patients who have VP shunts placed should be considered. REFERENCES 1. Jonas JB. Role of cerebrospinal fluid pressure in the pathogenesis of glaucoma. Acta Ophthalmol. 2011;89:505–514. 2. Anderson DR, Hendrickson A. Effect of intraocular pressure on rapid axoplasmatic transport in monkey optic nerve. Invest Ophthalmol Vis Sci. 1974;13:771–783. 3. Morgan WH. Central venous pulsations: new findings, clinical importance and relation to cerebrospinal fluid pressure. J Glaucoma. 2013;22(suppl 5):S15–S16. 4. Volkov VV. Essential element of the glaucomatous process neglected in clinical practice. Oftalmol Zh. 1976;31:500–504. 5. Yablonski M, Ritch R, Pokorny KS. Effect of decreased intracranial pressure on optic disc. Invest Ophthalmol Vis Sci. 1979;18:165. 6. Jonas JB, Berenshtein E, Holbach L. Anatomic relationship between lamina cribrosa, intraocular space, and cerebrospinal fluid space. Invest Ophthalmol Vis Sci. 2003;44:5189–5195.
Volume 25, Number 1, January 2016
7. The AGIS Investigators. The Advanced Glaucoma Intervention Study (AGIS): 7. The relationship between control of intraocular pressure and visual field deterioration. Am J Ophthalmol. 2000;130:429–440. 8. Berdahl JP, Allingham RR, Johnson DH. Cerebrospinal fluid pressure is decreased in primary open-angle glaucoma. Ophthalmology. 2008;115:763–768. 9. Berdahl JP, Fautsch MP, Stinnett SS, et al. Intracranial pressure in primary open angle glaucoma, normal tension glaucoma, and ocular hypertension: a case-control study. Invest Ophthalmol Vis Sci. 2008;49:5412–5418. 10. Drance SM, Fairclough M, Butler DM, et al. The importance of disc hemorrhage in the prognosis of chronic open angle glaucoma. Arch Ophthalmol. 1977;95:226–228. 11. Prata TS, De Moraes CG, Teng CC, et al. Factors affecting rates of visual field progression in glaucoma patients with optic disc hemorrhage. Ophthalmology. 2010;11:24–29. 12. De Moraes CG, Prata TS, Liebmann CA, et al. Spatially consistent, localized visual field loss before and after disc hemorrhage. Invest Ophthalmol Vis Sci. 2009;50: 4727–4733.
e52 | www.glaucomajournal.com Copyright r 2014 Wolters Kluwer Health, Inc. All rights reserved. Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved.
Progression of Normal-Tension Glaucoma After Ventriculoperitoneal Shunt to Decrease Cerebrospinal Fluid Pressure Brian H. Chen, MD, MS,* Mitchell D. Drucker, MD,* Kenneth M. Louis, MD,w and David W. Richards, MD, PhD*
Purpose: To report a case of worsening normal-tension glaucoma immediately following ventriculoperitoneal (VP) shunt placement to lower cerebrospinal fluid pressure (CSFP). Methods: The clinical records of the patient were reviewed retrospectively. Observations were made and collated as the case progressed. Results: A 93-year-old white woman previously diagnosed with normal-tension glaucoma underwent placement of a VP shunt with a Codman-Hakim programmable valve for normal pressure hydrocephalus. Shortly after the procedure, progressive visual field loss was noted in both eyes and new optic disc hemorrhages were seen in the patient’s right eye. The hemorrhages resolved, but the patient had recurrent complaints of poor gait, memory, and mentation. The CSFP was lowered by reprogramming the CodmanHakim valve. The patient’s visual fields again worsened in both eyes and a new disc hemorrhage was seen in the right eye. A year later, a new disc hemorrhage was seen in the patient’s left eye. The CSFP was raised by reprogramming the VP shunt. Before the placement of the VP shunt, no optic disc hemorrhages had been observed. Conclusion: This case suggests that relatively low CSFP is a contributor to worsening normal-tension glaucoma, probably by increasing translaminar pressure gradient of the optic nerve. Key Words: ventriculoperitoneal shunt, cerebrospinal fluid, normal-tension glaucoma
(J Glaucoma 2016;25:e50–e52)
T
here is mounting evidence that cerebrospinal fluid pressure (CSFP) plays an important role in the pathogenesis of glaucoma.1 This may be due to an abnormally high translaminar gradient between the intraocular pressure (IOP) and the retrolaminar cerebrospinal fluid. A high translaminar pressure gradient may affect orthograde and retrograde axoplasmic flow2 or central retinal vein compression, shear, and wall thickening,3 among other factors. This report describes a case of worsening normal-tension
Received for publication May 7, 2014; accepted September 19, 2014. From the *Department of Ophthalmology, Morsani College of Medicine, University of South Florida Eye Institute; and wDepartment of Neurosurgery, Morsani College of Medicine, University of South Florida, Tampa, FL. Disclosure: The authors declare no conflict of interest. Reprints: David W. Richards, MD, PhD, Department of Ophthalmology, Morsani College of Medicine, University of South Florida Eye Institute, 12901 Bruce B. Downs Blvd., MDC 21, Tampa, FL 33612 (e-mail: [email protected]). Copyright r 2014 Wolters Kluwer Health, Inc. All rights reserved. DOI: 10.1097/IJG.0000000000000186
glaucoma in a patient who had ventriculoperitoneal (VP) shunting to lower CSFP for normal pressure hydrocephalus.
CASE REPORT A 93-year-old white woman, who has been followed for wellcontrolled normal-tension glaucoma since May 2000, presented for follow-up in October 2008. She had cataract extraction with posterior chamber intraocular lenses in both eyes 2 years earlier. Before the October 2008 visit, optic disc (Drance) hemorrhages had never been seen. On exam, her vision was 20/25 in both eyes, and IOPs were 10 mm Hg in the right eye, and 11 mm Hg in the left eye. Her central corneal thickness was 516 mm in the right eye and 509 mm in the left eye. The patient’s optic disc photographs are presented in Figure 1. The patient’s visual fields (Humphrey Field Analyzer, SITA Standard 24-2) remained stable with IOPs consistently low, treated with timolol 0.5% in both eyes twice daily and latanoprost 0.005% in both eyes at bedtime. She was intolerant to brinzolamide and brimonidine Five months after the October 2008 visit, the patient complained of forgetfulness, difficulty walking, headaches, and poor overall mentation. She had a computed tomography scan of the head that showed enlarged lateral and third ventricles and had a neurosurgical evaluation. She then underwent lumbar puncture and cisternogram and was diagnosed with normal pressure hydrocephalus. Of note, her gait and mental function symptomatically improved after lumbar puncture. VP shunting was discussed and offered at that time but declined by the patient and family. In September 2011, the patient continued to complain of gait disturbance and poor memory. Her neurosurgeon (K.M.L.) implanted a VP shunt with a Codman-Hakim programmable valve (DePuy Synthes, Warsaw, IN) set at 120 mm H2O to lower CSFP. Immediately after the procedure, her gait and mental function improved. She underwent ophthalmic examination 1 month after placement of the VP shunt, and 2 optic disc hemorrhages were noted in the right eye (Fig. 1). Her visual fields also worsened in both the eyes. In October 2011, the neurosurgeon increased the CSFP to 200 mm H2O via the Codman-Hakim valve because of development of subdural hygromas. The patient returned for ophthalmic examination and the disc hemorrhages in the right eye had resolved. In November 2011, the patient returned to the neurosurgeon with a recurrent complaint of poor balance and memory; the VP shunt setting was decreased from 200 to 180 mm H2O; a month later (December 2011) from 180 to 160 mm H2O; a month later (January 2012) from 160 to 150 mm H2O; another month later (February 2012) from 150 to 140 mm H2O. This improved the patient’s gait, mentation, and relieved her headaches. Six months later (August 2012) the patient was noted to have a new optic disc hemorrhage in the right eye, and again worsening visual field in both the eyes (Figs. 1, 2). One year later (September 2013), a third episode of new optic disc hemorrhage was seen in the left eye (Fig. 1). Visual fields had worsened in both the eyes (Fig. 2). At this point, in light of worsening visual fields despite low IOP and maximum tolerated medical therapy, the development of
e50 | www.glaucomajournal.com J Glaucoma Volume 25, Number 1, January 2016 Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved.
J Glaucoma
Volume 25, Number 1, January 2016
Normal-Tension Glaucoma After Ventriculoperitoneal Shunt
FIGURE 1. Optic disc photographs of the (A) right and (B) left eye prior (March 2009) to VP shunt. C, Disc hemorrhages (arrows) are seen in the right eye 1 month (October 2011) after VP shunt. D, A new disc hemorrhage (arrow) is seen in the right eye 10 months later (August 2012). E, Disc hemorrhage (arrow) is seen in the left eye 2 years (September 2013) after VP shunt. VP indicates ventriculoperitoneal. new disc hemorrhages after lowering CSFP, and the patient being a poor candidate for surgical therapy, the neurosurgeon raised the CSFP in September 2013 to 150 mm H2O. In November 2013, no disc hemorrhages were seen. A summary of the patient’s clinical course, IOP, presence of disc hemorrhage, CSFP, and visual field MD is presented in Figure 2.
DISCUSSION Volkov4 presented the idea that CSFP may be involved in the pathogenesis of glaucomatous optic neuropathy in the
Summary of Clinical Course Intraocular Pressure (mm Hg)
16 14 12 10 8 6 4
OD
Visual Field Mean Deviation (dB)
CSFP by VP shunt (mm H2O)
2
OS
0 10/27/08
10/27/09
10/27/10
200 190 180 170 160 150 140 130 120 110 10/27/08
10/27/09
10/27/10
10/27/11
10/27/12
10/27/11
10/27/12
(4.82)
-5
(10.36)
-10
(11.84) (10.99)
-15
(10.67) (10.87)
(11.01) (11.05)
-20
(10.67)
OD (PSD)
-25 -30 10/27/08
(7.75)
OS (PSD)
(7.63)
(9.67) (7.73)
(3.53)
10/27/09
10/27/10
10/27/11
10/27/12
Optic disc exam with no optic disc hemorrhage detected in either eye VP Shunt placed/adjusted Optic disc hemorrhage detected
FIGURE 2. Summary of the clinical course. CSFP indicates cerebrospinal fluid pressure; VP, ventriculoperitoneal.
Copyright
r
1970s. Attention has been recently focused on the pressure gradient between the intraocular space and the retrobulbar space. The lamina cribrosa of the optic nerve head defines the border between these spaces, and the pressure difference is called the translaminar pressure gradient.1 Yablonski and colleagues hypothesized that low CSFP around the optic nerve may induce glaucomatous optic neuropathy. He experimentally decreased the intracranial pressure 5 cm H2O below atmospheric pressure by cannulation of the cisterna magna in cats. The IOP in 1 eye was left unaltered, whereas in the other eye it was lowered to slightly above atmospheric pressure by cannulation of the anterior chamber. After 3 weeks, the optic disc in the eye that had an unaltered IOP showed glaucomatous optic neuropathy, whereas no changes were seen in the eyes that had lowered IOP.5 The translaminar pressure gradient depends not only on the pressure difference between the intraocular and the retrobulbar spaces, but also on the thickness of the lamina cribrosa.6 It has been shown that the lamina cribrosa thins in advanced stages of glaucoma, and this may be one of the reasons for increased risk of progression of glaucoma in eyes with advanced glaucoma.7 Recent studies have shown that CSFP measured by lumbar puncture was significantly lower in patients with normal-tension glaucoma and in primary open-angle glaucoma than in control subjects.8,9 Our patient’s course suggests that stable glaucoma was worsened by decreasing the CSFP. We believe that this is the first report of apparent worsening of glaucoma after VP shunt placement. After CSFP lowering, our patient exhibited glaucomatous disease progression in a variety of ways. Optic disc hemorrhages are a known marker for disease progression10,11 as is worsening visual field loss. It is possible that visual field progression occurs before the onset of disc hemorrhage.12 In the case presented, the optic disc hemorrhages correspond to worsening visual fields and to time intervals of lower CSFP. In clinical practice, a disc hemorrhage not only indicates that the disease is active and progression is likely, but also demands increased vigilant surveillance, and may require additional therapy. These optic disc hemorrhages are known to resolve without treatment. Our patient provided a difficult management challenge as a balance between symptomatically improving her headaches, gait, memory, and mentation versus slowing the progression of normal-tension glaucoma. More work is needed to apply this information clinically. These include a noninvasive method to measure CSFP, perhaps using tympanometry through the inner ear, ophthalmodynamometry, or an intrathecal pressure sensitive catheter; alternative medical or surgical treatment for abnormally low CSFP; and determination of whether other
2014 Wolters Kluwer Health, Inc. All rights reserved.
www.glaucomajournal.com |
Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved.
e51
Chen et al
J Glaucoma
diseases, both ocular and systemic, are associated with low CSFP. A prospective study of optic nerves in glaucoma patients who have VP shunts placed should be considered. REFERENCES 1. Jonas JB. Role of cerebrospinal fluid pressure in the pathogenesis of glaucoma. Acta Ophthalmol. 2011;89:505–514. 2. Anderson DR, Hendrickson A. Effect of intraocular pressure on rapid axoplasmatic transport in monkey optic nerve. Invest Ophthalmol Vis Sci. 1974;13:771–783. 3. Morgan WH. Central venous pulsations: new findings, clinical importance and relation to cerebrospinal fluid pressure. J Glaucoma. 2013;22(suppl 5):S15–S16. 4. Volkov VV. Essential element of the glaucomatous process neglected in clinical practice. Oftalmol Zh. 1976;31:500–504. 5. Yablonski M, Ritch R, Pokorny KS. Effect of decreased intracranial pressure on optic disc. Invest Ophthalmol Vis Sci. 1979;18:165. 6. Jonas JB, Berenshtein E, Holbach L. Anatomic relationship between lamina cribrosa, intraocular space, and cerebrospinal fluid space. Invest Ophthalmol Vis Sci. 2003;44:5189–5195.
Volume 25, Number 1, January 2016
7. The AGIS Investigators. The Advanced Glaucoma Intervention Study (AGIS): 7. The relationship between control of intraocular pressure and visual field deterioration. Am J Ophthalmol. 2000;130:429–440. 8. Berdahl JP, Allingham RR, Johnson DH. Cerebrospinal fluid pressure is decreased in primary open-angle glaucoma. Ophthalmology. 2008;115:763–768. 9. Berdahl JP, Fautsch MP, Stinnett SS, et al. Intracranial pressure in primary open angle glaucoma, normal tension glaucoma, and ocular hypertension: a case-control study. Invest Ophthalmol Vis Sci. 2008;49:5412–5418. 10. Drance SM, Fairclough M, Butler DM, et al. The importance of disc hemorrhage in the prognosis of chronic open angle glaucoma. Arch Ophthalmol. 1977;95:226–228. 11. Prata TS, De Moraes CG, Teng CC, et al. Factors affecting rates of visual field progression in glaucoma patients with optic disc hemorrhage. Ophthalmology. 2010;11:24–29. 12. De Moraes CG, Prata TS, Liebmann CA, et al. Spatially consistent, localized visual field loss before and after disc hemorrhage. Invest Ophthalmol Vis Sci. 2009;50: 4727–4733.
e52 | www.glaucomajournal.com Copyright r 2014 Wolters Kluwer Health, Inc. All rights reserved. Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved.
