J Korean Ophthalmol Soc.  2010 May;51(5):721-727.

Comparision of Primary Vascular Dysregulation for Unilateral and Bilateral Eye Involvement in Normal Tension Glaucoma

Affiliations
  • 1Department of Ophthalmology, Samsung Medical Center, Sungkyunkwan University College of Medicine, Seoul, korea. ckee@skku.edu

Abstract

PURPOSE
To compare the clinical symptoms and signs of primary vascular dysregulation (PVD) for unilateral and bilateral eye involvement in normal tension glaucoma (NTG).
METHODS
The authors administered a questionnaire to assess PVD in patients with NTG. The answers to the 10-item questionnaire (cold hands, migraine, sleep latency, thirst, hypotension, orthostatic hypotension, emotional stress, drug sensitivity, vertigo, and systemic vasospasm) were compared between patients with unilateral involved NTG and bilateral involved NTG (N=61). The groups were classified again according to age (criteria: 55 years), sex, and mean deviation via standard automated perimetry (criteria: -6 dB).
RESULTS
The answers to the questionnaire between patients with unilateral involved NTG and bilateral involved NTG were not different at the level of statistical significance. In groups classified according to age, sex, and mean deviation, none of the answers to the questionnaire were different at the level of statistical significance between the groups.
CONCLUSIONS
Clinical symptoms and signs of PVD were not different between patients with unilateral or bilateral eye involvement in NTG. Systemic vascular factors may not be considered different between unilateral and bilateral eye involvement in NTG.

Keyword

Bilateral normal tension glaucoma; Primary vascular dysregulation; Unilateral normal tension glaucoma

MeSH Terms

Eye
Hand
Humans
Hypotension
Hypotension, Orthostatic
Low Tension Glaucoma
Migraine Disorders
Surveys and Questionnaires
Stress, Psychological
Thirst
Vertigo
Visual Field Tests

Figure

  • Figure 1. Questionnaire about primary vascular dysregulation


Reference

References

1. Flammer J, Orgül S, Costa VP, et al. The impact of ocular blood flow in glaucoma. Pro Retin Eye Res. 2002; 21:359–93.
Article
2. Flammer J, Pache M, Resink T. Vasospasm, its role in the pathogenesis of disease with paticular reference to eye. Pro Retin Eye Res. 2001; 20:319–49.
3. Nicolela MT. Clinical clues of vascular dysregulation and its association with glaucoma. Can J Ophthalmol. 2008; 43:337–41.
Article
4. Gherghel D, Orgul S, Dubler B, et al. Is vascular regulation in the central retinal artery altered in persons with vasospasm? Arch Ophthalmol. 1999; 117:1359–62.
Article
5. Flammer J, Pache M, Resink T. Vasospasm, its role in the pathogenesis of diseases with particular reference to the eye. Prog Retin Eye Res. 2001; 20:319–49.
Article
6. Phelps CD, Corbet JJ. Migraine and low-tension glaucoma: a case-control study. Invest Ophthalmol Vis Sci. 1985; 26:1105–8.
7. Pache M, Krauchi K, Cajochen C, et al. Cold feet and prolonged sleep-onset latency in vasosapstic syndrome. Lancet. 2001; 358:125–6.
8. Teuchner B, Orgul S, Ulmer H, et al. Reduced thirst in patients with a vasospastic syndrome. Acta Ophthalmol Scand. 2004; 82:738–40.
Article
9. Orugul S, Kaiser HJ, Flammer J, Gasser P. Systemic blood pressure and capillary blood-cell velocity in glaucoma patients: a preliminary study. Eur J Ophthalmol. 1995; 5:88–91.
10. Pache M, Dubler B, Flammer J. Peripheral vasospasm and nocturnal blood pressure dipping-two distinct risk factors for glaucomatous damage? Eur J Ophthalmol. 2003; 49:164–8.
11. Chai E, Goldberg I, Chia A, et al. Visual field responses to a hand vibration stimulus. Surv Ophthalmol. 1999; 43:S79–86.
Article
12. Flammer J. Psychophysical mechanisms and treatment of vasospastic disorders in normal-tension glaucoma. Bull Soc Belge Ophthalmol. 1992; 244:129–34.
13. Wunderlich K, Zimmerman C, Gutmann H, et al. Vasospastic persons exhibit differential expression of ABC-transport proteins. Mol Vis. 2003; 9:756–61.
14. Waldmann E, Gasser P, Dubler B, et al. Silent myocardial ischemia in glaucoma and cataract patients. Graefes Arch Clin Exp Ophthalmol. 1996; 234:595–8.
Article
15. Surgiyama T, Utsunomiya K, Ota H, et al. Comparative study of cerebral blood flow in patients with normal-tension glaucoma and control subjects. Am J Opthalmol. 2006; 141:394–6.
16. Levene RZ. Low tension glaucoma: a critical review and new material. Surv Ophthalmol. 1980; 24:621–64.
Article
17. Feuer WJ, Anderson DR. Static threshold asymmetry in early glaucomatous visual field loss. Ophthalmology. 1989; 96:1285–97.
Article
18. Poinoosawmy D, Fontana L, Wu JX, et al. Frequency of asymmetric visual field defects in normal-tension and high-tension glaucoma. Ophthalmology. 1998; 105:988–91.
Article
19. Kim C, Kim TW. Comparision of risk factors for bilateral and unilateral eye involvement in normal-tension glaucoma. Invest Ophthalmol Vis Sci. 2009; 50:1215–20.
20. Cartwright MJ, Anderson DR. Correlation of asymmetric damage with asymmetric intraocular pressure in normal-tension glaucoma (low-tension glaucoma). Arch Ophthalmol. 1988; 106:898–900.
Article
21. Crichton A, Drance SM, Douglas GR, Schulzer M. Unequal intraocular pressure and its relation to asymmetric visual field defects in low-tension glaucoma. Ophthalmology. 1989; 96:1312–4.
Article
22. Park HJ, Choi BG. The quantitative evaluation of optic nerve head of normal tension glaucoma. J Korean Ophthalmol Soc. 2000; 41:1203–9.
23. Klein BE, Klein R, Linton KL. Intraocular pressure in an American community. The Beaver Dam Eye Study. Invest Ophthalmol Vis Sci. 1992; 33:2224–8.
24. Jonas JB, Berenshtein E, Holbach L. Lamina cribrosa thickness and spatial relationships between intraocular space and cerebrospinal fluid space in highly myopic eyes. Invest Ophthalmol Vis Sci. 2004; 45:2660–5.
Article
25. Collaborative Normal-Tension Glaucoma Study Group. Comparison of glaucomatous progression between untreated patients with normal-tension glaucoma and patients with therapeutically reduced intraocular pressure. Am J Ophthalmol. 1998; 126:487–97.
26. Drance S, Anderson DR, Schulzer M. Risk factors for progression of visual field abnormalities in normal-tension glaucoma. Am J Ophthalmol. 2001; 131:699–708.
Article
27. Kitazawa Y, Shirato S, Yamamoto T. Optic disc hemorrhage in low-tension glaucoma. Ophthalmology. 1986; 93:853–7.
Article
28. Lee DH, Kee C. abdominal, abdominal comparision in normal tension glaucoma with unilateral field loss. J Korean Ophthalmol Soc. 2008; 49:125–34.
29. Jonas JB, Papastathopoulos KI. Pressure-dependent changes of the optic disk in primary open-angle glaucoma. Am J Ophthalmol. 1995; 119:313–7.
Article
30. Park KH, Tomita G, Liou SY, Kitazawa Y. Correlation between abdominal atrophy and optic nerve damage in normal-tension glaucoma. Ophthalmology. 1996; 103:1899–906.
31. Burk RO, Rohrschneider K, Noack H, Volcker HE. Are large optic nerve heads susceptible to glaucomatous damage at normal intraocular pressure? A three-dimensional study by laser scanning tomography. Graefes Arch Clin Exp Ophthalmol. 1992; 230:552–60.
32. Tuulonen A, Airaksinen PJ. Optic disc size in exfoliative primary open angle, and low-tension glaucoma. Arch Ophthalmol. 1992; 110:211–3.
Article
33. Yim JH, Park SC, Kee CW. Evaluation of ocular risk factors related to asymmetric visual field defects in normal tension glaucoma. J Korean Ophthalmol Soc. 2008; 49:1507–14.
Article
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