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Journal of the Optical Society of America A


  • Vol. 20, Iss. 9 — Sep. 1, 2003
  • pp: 1681–1693

High blood pressure and visual sensitivity

Alvin Eisner and John R. Samples  »View Author Affiliations

JOSA A, Vol. 20, Issue 9, pp. 1681-1693 (2003)

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The study had two main purposes: (1) to determine whether the foveal visual sensitivities of people treated for high blood pressure (vascular hypertension) differ from the sensitivities of people who have not been diagnosed with high blood pressure and (2) to understand how visual adaptation is related to standard measures of systemic cardiovascular function. Two groups of middle-aged subjects—hypertensive and normotensive—were examined with a series of test/background stimulus combinations. All subjects met rigorous inclusion criteria for excellent ocular health. Although the visual sensitivities of the two subject groups overlapped extensively, the age-related rate of sensitivity loss was, for some measures, greater for the hypertensive subjects, possibly because of adaptation differences between the two groups. Overall, the degree of steady-state sensitivity loss resulting from an increase of background illuminance (for 580-nm backgrounds) was slightly less for the hypertensive subjects. Among normotensive subjects, the ability of a bright (3.8-log-td), long-wavelength (640-nm) adapting background to selectively suppress the flicker response of long-wavelength-sensitive (LWS) cones was related inversely to the ratio of mean arterial blood pressure to heart rate. The degree of selective suppression was also related to heart rate alone, and there was evidence that short-term changes of cardiovascular response were important. The results suggest that (1) vascular hypertension, or possibly its treatment, subtly affects visual function even in the absence of eye disease and (2) changes in blood flow affect retinal light-adaptation processes involved in the selective suppression of the flicker response from LWS cones caused by bright, long-wavelength backgrounds.

© 2003 Optical Society of America

OCIS Codes
(170.4470) Medical optics and biotechnology : Ophthalmology
(330.0330) Vision, color, and visual optics : Vision, color, and visual optics
(330.4300) Vision, color, and visual optics : Vision system - noninvasive assessment
(330.5510) Vision, color, and visual optics : Psychophysics
(330.7320) Vision, color, and visual optics : Vision adaptation

Original Manuscript: October 4, 2002
Revised Manuscript: February 21, 2003
Manuscript Accepted: April 23, 2003
Published: September 1, 2003

Alvin Eisner and John R. Samples, "High blood pressure and visual sensitivity," J. Opt. Soc. Am. A 20, 1681-1693 (2003)

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  1. R. Klein, B. E. Klein, S. C. Tomany, K. J. Cruickshanks, “The association of cardiovascular disease with the long-term incidence of age-related maculopathy: the Beaver Dam Eye Study,” Ophthalmology 110, 636–650 (2003). [CrossRef] [PubMed]
  2. L. Hyman, A. P. Schachat, Q. He, M. C. Leske, “Hypertension, cardiovascular disease, and age-related macular degeneration. Age-Related Macular Degeneration Risk Factors Study Group,” Arch. Ophthalmol. 118, 351–358 (2000). [CrossRef] [PubMed]
  3. R. Klein, B. E. Klein, S. E. Moss, S. M. Meuer, “The epidemiology of retinal vein occlusion: the Beaver Dam Eye Study,” Trans. Am. Ophthalmol. Soc. 98, 133–141 (2000).
  4. L. Bonomi, G. Marchini, M. Marraffa, P. Bernardi, R. Morbio, A. Varotto, “Vascular risk factors for primary open angle glaucoma: the Egna–Neumarkt Study,” Ophthalmology 107, 1287–1293 (2000). [CrossRef] [PubMed]
  5. I. Dielemans, J. R. Vingerling, D. Algra, A. Hofman, D. E. Grobbee, P. T. de Jong, “Primary open-angle glaucoma, intraocular pressure, and systemic blood pressure in the general elderly population. The Rotterdam Study,” Ophthalmology 102, 54–60 (1995). [CrossRef] [PubMed]
  6. T. Y. Wong, R. Klein, B. E. Klein, J. M. Tielsch, L. Hubbard, F. J. Nieto, “Retinal microvascular abnormalities and their relationship with hypertension, cardiovascular disease, and mortality,” Surv. Ophthalmol. 46, 59–80 (2001). [CrossRef] [PubMed]
  7. S. S. Hayreh, “Duke–Elder lecture. Systemic arterial blood pressure and the eye,” Eye 10, 5–28 (1996). [CrossRef]
  8. I. A. Bhutto, T. Amemiya, “Choroidal vasculature changes in spontaneously hypertensive rats—transmission electron microscopy and scanning electron microscopy with casts,” Ophthalmic Res. 34, 54–62 (2002). [CrossRef] [PubMed]
  9. A. Harris, H. S. Chung, T. A. Ciulla, L. Kagemann, “Progress in measurement of ocular blood flow and relevance to our understanding of glaucoma and age-related macular degeneration,” Prog. Retin. Eye Res. 18, 669–687 (1999). [CrossRef] [PubMed]
  10. C. Delaey, J. Van De Voorde, “Regulatory mechanisms in the retinal and choroidal circulation,” Ophthalmic Res. 32, 249–256 (2000). [CrossRef] [PubMed]
  11. G. A. Cioffi, E. Granstam, A. Alm, “Ocular circulation,” in Adler’s Physiology of the Eye, 10th ed., P. L. Kaufman, A. Alm, eds. (Mosby, St. Louis, Mo., 2003), pp. 747–784.
  12. K. Polak, L. Schmetterer, C. E. Riva, “Influence of flicker frequency on flicker-induced changes of retinal vessel diameter,” Invest. Ophthalmol. Visual Sci. 43, 2721–2726 (2002).
  13. G. Michelson, A. Patzelt, J. Harazny, “Flickering light increases retinal blood flow,” Retina 22, 336–343 (2002). [CrossRef] [PubMed]
  14. J. Kiryu, S. Asrani, M. Shahidi, M. Mori, R. Zeimer, “Local response of the primate retinal microcirculation to increased metabolic demand induced by flicker,” Invest. Ophthalmol. Visual Sci. 36, 1240–1246 (1995).
  15. M. Kondo, L. Wang, A. Bill, “The role of nitric oxide in hyperaemic response to flicker in the retina and optic nerve in cats,” Acta Ophthalmol. Scand. 75, 232–235 (1997). [CrossRef] [PubMed]
  16. J. J. Steinle, D. Krizsan-Agbas, P. G. Smith, “Regional regulation of choroidal blood flow by autonomic innervation in the rat,” Am. J. Physiol. Regul. Integr. Comp. Physiol. 279, R202–R209 (2000). [PubMed]
  17. C. E. Riva, P. Titze, M. Hero, B. L. Petrig, “Effect of acute decreases of perfusion pressure on choroidal blood flow in humans,” Invest. Ophthalmol. Visual Sci. 38, 1752–1760 (1997).
  18. A. Luksch, E. Polska, A. Imhof, J. Schering, G. Fuchsjager-Mayrl, M. Wolst, L. Schmetterer, “Role of NO in choroidal blood flow regulation during isometric exercise in healthy humans,” Invest. Ophthalmol. Visual Sci. 44, 734–739 (2003). [CrossRef]
  19. G. Fuchsjager-Mayrl, A. Luksch, M. Malec, E. Polska, M. Wolst, L. Schmetterer, “Role of endothelin-1 in choroidal blood flow regulation during isometric exercise in healthy humans,” Invest. Ophthalmol. Visual Sci. 44, 728–733 (2003). [CrossRef]
  20. G. Garhofer, K. H. Huemer, C. Zawinka, L. Schmetterer, G. T. Dorner, “Influence of diffuse luminance flicker on choroidal and optic nerve head blood flow,” Curr. Eye Res. 24, 109–113 (2002). [CrossRef] [PubMed]
  21. N. D. Wangsa-Wirawan, R. A. Linsenmeier, “Retinal oxygen: fundamental and clinical aspects,” Arch. Ophthalmol. 121, 547–557 (2003). [CrossRef] [PubMed]
  22. R. M. Berne, M. L. Levy, Cardiovascular Physiology, 8th ed. (Mosby, St. Louis, Mo., 2001).
  23. A. C. Guyton, J. E. Hall, Textbook of Medical Physiology, 10th ed. (Saunders, Philadelphia, Pa., 2000).
  24. A. Eisner, G. A. Cioffi, H. M. Campbell, J. R. Samples, “Foveal flicker sensitivity abnormalities in early glaucoma: associations with high blood pressure,” J. Glaucoma 3, S19–S31 (1994). [CrossRef] [PubMed]
  25. A. Eisner, J. R. Samples, “Flicker sensitivity and cardiovascular function in healthy middle-aged people,” Arch. Ophthalmol. 118, 1049–1055 (2000). [CrossRef] [PubMed]
  26. A. Eisner, “Flashed stimuli and the suppression of flicker response from long-wavelength-sensitive cones: integrating two separate approaches,” J. Opt. Soc. Am. A 18, 2957–2968 (2001). [CrossRef]
  27. A. Eisner, D. I. A. Macleod, “Flicker photometric study of chromatic adaption: selective suppression of cone inputs by colored backgrounds,” J. Opt. Soc. Am. 71, 705–717 (1981). [CrossRef] [PubMed]
  28. G. B. Arden, T. E. Frumkes, “Stimulation of rods can increase cone flicker ERGs in man,” Vision Res. 26, 711–721 (1986). [CrossRef] [PubMed]
  29. R. Pflug, R. Nelson, P. K. Ahnelt, “Background-induced flicker enhancement in cat retinal horizontal cells. I. Temporal and spectral properties,” J. Neurophysiol. 64, 313–325 (1990). [PubMed]
  30. I. D. Cadenas, E. S. Reifsnider, D. Tranchina, “Modulation of synaptic transfer between retinal cones and horizontal cells by spatial contrast,” J. Gen. Physiol. 104, 567–591 (1994). [CrossRef] [PubMed]
  31. A. Eisner, A. G. Shapiro, J. A. Middleton, “Equivalence between temporal frequency and modulation depth for flicker response suppression: analysis of a three-process model of visual adaptation,” J. Opt. Soc. Am. A 15, 1987–2002 (1998). [CrossRef]
  32. J. Pokorny, V. C. Smith, B. B. Lee, T. Yeh, “Temporal sensitivity of macaque ganglion cells to lights of different chromaticity,” Color Res. Appl. 26, S140–S144 (2000). [CrossRef]
  33. P. A. Sample, “Short-wavelength automated perimetry: its role in the clinic and for understanding ganglion cell function,” Prog. Ret. Eye Res. 19, 369–383 (2000). [CrossRef]
  34. J. M. Wild, “Short wavelength automated perimetry,” Acta Ophthalmol. Scand. 79, 546–559 (2001). [CrossRef]
  35. A. Eisner, D. F. Austin, J. R. Samples, “Short wavelength automated perimetry and tamoxifen use,” Br. J. Ophthamol. (to be published).
  36. A. J. Adams, R. Rodic, R. Husted, R. Stamper, “Spectral sensitivity and color discrimination changes in glaucoma and glaucoma-suspect patients,” Invest. Ophthalmol. Visual Sci. 23, 516–524 (1982).
  37. M. B. Gorin, R. Day, J. P. Costantino, B. Fisher, C. K. Redmond, L. Wickerham, J. E. Gomolin, R. G. Margolese, M. K. Mathen, D. M. Bowman, D. I. Kaufman, N. V. Dimitrov, L. J. Singerman, R. Bornstein, N. Wolmark, D. Kaufmann, “Long-term tamoxifen citrate use and potential ocular toxicity,” Am. J. Ophthalmol. 125, 493–501 (1998). [CrossRef] [PubMed]
  38. For each of the three types of hypertensive retinopathy characteristics—vascular sclerosis, focal arteriolar constriction, and arteriovenous narrowing—grades were assigned on a five-point scale. For each characteristic, a score of 0 signified that the vasculature was indistinguishable from that of a young healthy person, a score of 1 signified a minimal difference, a score of 2 signified a more marked difference, and a score of 3 signified more difference yet, by itself enough to indicate a high probability of past or present vascular disease. No person tested had a score of 4, and two people were excluded from the study on the basis of sclerosis scores of 3. The distributions of scores for each subject group are given next. The numbers in parentheses refer to the number of subjects assigned a score of 0, 1, or 2, respectively. Focal arteriolar constriction: normotensive subjects (22, 5, 2), hypertensive subjects (22, 4, 1), and tamoxifen subjects (25, 5, 0). Arteriovenous narrowing: normotensive subjects (20, 7, 2), hypertensive subjects (21, 4, 2), and tamoxifen subjects (24, 6, 0). Vascular sclerosis: normotensive subjects (12, 12, 4), hypertensive subjects (15, 9, 3), and tamoxifen subjects (15, 15, 0).
  39. A. Eisner, “Multiple components in photopic dark adaptation,” J. Opt. Soc. Am. A 3, 655–666 (1986). [CrossRef] [PubMed]
  40. A. Eisner, J. R. Samples, H. M. Campbell, G. A. Cioffi, “Foveal adaptation abnormalities in early glaucoma,” J. Opt. Soc. Am. A 12, 2318–2328 (1995). [CrossRef]
  41. The specific order of testing depended on many considerations, some of which are specified in the text. The 1.6-log-td, 580-nm background preceded the 3.6-log-td, 580-nm background so that the dynamics of recovery of SWS-cone-mediated sensitivity could be assessed after a sudden large increase of background illuminance.40(The dynamics of recovery were affected by tamoxifen.35) The use of a 2.0-log-td, 580-nm background was based on preliminary results that suggested that the crossover points of an MWS–LWS-cone mechanism and an SWS-cone mechanism might differ between the hypertensive and the normotensive subject groups. (This suggestion was not verified on prospective testing.) The 2.0-log-td background preceded all other backgrounds by default, given all the other constraints. The 2.6-log-td, 580-nm background was used in order to assess the effects of background illuminance on flicker sensitivity under conditions in which departures from Weber’s law would not be great. There were several practical reasons for merging the protocols for two investigations (one concerning cardiovascular function and the other concerning effects of tamoxifen). Many of the same subjects served as controls for each investigation, and a second nonhypertensive subject group (the tamoxifen subjects) was used prospectively to confirm and to interpret effects from the normotensive subject group.
  42. P. M. Pearson, W. H. Swanson, “Chromatic contrast sensitivity: the role of absolute threshold and gain constant in differences between the fovea and the periphery,” J. Opt. Soc. Am. A 17, 232–243 (2000). [CrossRef]
  43. Measurements taken before 2 min were used to show that 440-nm sensitivities had stabilized by 2 min and to verify that SWS cones mediated detection at 440 nm.
  44. A 560-nm, rather than a 540-nm, test was used to eliminate any possibility, however remote, of detection of the test stimulus via SWS cones.
  45. SWAP 30-2 fields were administered for three normotensive subjects, six high-blood-pressure subjects, and two tamoxifen subjects.
  46. L. Wilkinson, G. Blank, C. Gruber, Desktop Data Analysis with SYSTAT (Prentice-Hall, Upper Saddle River, N.J., 1996).
  47. All the variables listed in Table 1were used in conducting a factor analysis for the normotensive subjects’ data. The number of factors was chosen a priorito be four, and a Varimax rotation was used. The first three factors were readily identified as (1) an SWS-cone-sensitivity factor, (2) a flicker-sensitivity factor, and (3) a factor that reflected sensitivities mainly for test wavelengths ranging from approximately 500 to 560 nm on the 2.0-log-td, 580-nm background. The fourth factor was less well defined but reflected sensitivities mainly on the 3.6-log-td, 580-nm background. Because the normotensive group’s maximal sensitivity in the 500- to 580-nm range occurred at 540 nm for the 2.0-log-td, 580-nm background, factor 3 can be identified with an MWS–LWS cone mechanism. Sensitivity to a 580-nm test on the 2.0-log-td 580-nm background was represented approximately equally in factors 2 and 3, and it was the only non-flicker-sensitivity variable with appreciable representation in factor 2.
  48. The threshold elevation from a 2.0- to a 3.6-log-td background did not appear to differ between groups for an SWS-cone mechanism (p=0.380for 440-nm tests), but it may have differed for an MWS–LWS cone mechanism (p= 0.050for 560-nm tests).
  49. The rank order correlations between MAP/HR and logfl. sens.580-logfl. sens.640were computed for the 2.6- and for the 3.6-log-td 580-nm backgrounds. For the normotensive subjects, these rank-order correlations were, respectively, Spearman r=-0.19and Spearman r=0.14.For the high-blood-pressure subjects, the rank-order correlations were, respectively, Spearman r=-0.03and Spearman r=-0.11.
  50. Among normotensive subjects, MAP2-MAP1=-3.3± 1.0 mm Hg (p=0.003),and HR2-HR1=-3.4± 0.6 bpm (p<0.001).Among hypertensive subjects, MAP2-MAP1=-2.4±0.9 mm Hg (p=0.015),and HR2-HR1=-2.5±1.1 bpm (p=0.033).Among tamoxifen subjects, MAP2-MAP1=0.0±0.7 mm Hg (p= 0.99),and HR2-HR1=-2.3±0.8 bpm (p=0.007).
  51. A. Stockman, L. T. Sharpe, “The spectral sensitivities of the middle- and long-wavelength-sensitive cones derived from measurements in observers of known genotype,” Vision Res. 40, 1711–1737 (2000). [CrossRef] [PubMed]
  52. Adding age to the regression equation for ΔFSλ would not have improved the fit of the regression line to the data; the overall correlation would have changed from R=0.57to R=0.58.Nor was age itself correlated with ΔFSλ (Spearman r=-0.09).Age may have been weakly correlated with MAP2/HR2(Spearman r=0.30,p=0.18).
  53. For the normotensive subjects, the regression equation was ΔFSλ=1.20-0.40(MAP2/HR2)+0.29 ΔT.For the tamoxifen subjects, the regression equation was ΔFSλ= 0.96-0.24(MAP2/HR2)+0.29 ΔT.
  54. The rank order correlation between MAP2/HR2and ΔT was Spearman r=-0.02for the normotensive subjects and Spearman r=-0.12for the tamoxifen subjects.
  55. The correlation between an increase of heart rate and a reduction of mean deviation would have remained significant if the data from subjects who were administered 30-2 visual fields were excluded from the calculation.
  56. Among normotensive subjects, MAP3-MAP2=-0.8± 0.8 mm Hg (p=0.27),and MAP3/HR3-MAP2/HR2= 0.017±0.018 mm Hg/bpm (p=0.37).Among tamoxifen subjects, MAP3-MAP2=-0.1±0.7 mm Hg  (p= 0.94),and MAP3/HR3-MAP2/HR2=-0.022± 0.016 mm Hg/bpm (p=0.19).
  57. It is possible that the regression model could have been refined still further. When the normotensive subjects were classified by the presence or absence of arteriovenous narrowing, and this categorical factor was added to the three quantitative factors (MAP2/HR2,ΔT, and Δ(MAP/HR), all four factors were significant in an analysis of covariance (p=0.001,p=0.003,p=0.016,and p=0.021,respectively). Arteriovenous narrowing was associated with more selective suppression of the response from LWS cones.
  58. A. Eisner, M. L. Klein, J. D. Zilis, M. D. Watkins, “Visual function and the subsequent development of exudative age-related macular degeneration,” Invest. Ophthalmol. Visual Sci. 33, 3091–3102 (1992).
  59. S. L. Graham, S. M. Drance, “Nocturnal hypotension: role in glaucoma progression,” Surv. Ophthalmol. 43, S10–S16 (1999). [CrossRef] [PubMed]
  60. S. S. Hayreh, “Role of nocturnal arterial hypotension in the development of ocular manifestations of systemic arterial hypertension,” Curr. Opin. Ophthalmol. 10, 474–482 (1999). [CrossRef]
  61. G. Bellini, E. Bocin, A. Cosenzi, A. Sacerdote, R. Molino, N. Solimano, G. Ravalico, “Oscillatory potentials of the electroretinogram in hypertensive patients,” Hypertension 25, 839–841 (1995). [CrossRef] [PubMed]
  62. W. H. Swanson, J. Pokorny, V. C. Smith, “Effects of chromatic adaptation on phase-dependent sensitivity to heterochromatic flicker,” J. Opt. Soc. Am. A 5, 1976–1982 (1988). [CrossRef] [PubMed]
  63. A. Stockman, D. I. A. MacLeod, J. A. Vivien, “Isolation of the middle-and long-wavelength sensitive cones in normal trichromats,” J. Opt. Soc. Am. A 10, 2471–2490 (1993). [CrossRef]
  64. W. H. Swanson, “Chromatic adaptation alters spectral sensitivity at high temporal frequencies,” J. Opt. Soc. Am. A 10, 1294–1303 (1993). [CrossRef] [PubMed]
  65. I. O. Haefliger, J. Flammer, J. L. Beny, T. F. Luscher, “Endothelium-dependent vasoactive modulation in the ophthalmic circulation,” Prog. Ret. Eye Res. 20, 209–225 (2001). [CrossRef]
  66. L. Schmetterer, K. Polak, “Role of nitric oxide in the control of ocular blood flow,” Prog. Ret. Eye Res. 20, 823–847 (2001). [CrossRef]
  67. M. T. Gewaltig, G. Kojda, “Vasoprotection by nitric oxide: mechanisms and therapeutic potential,” Cardiovasc. Res. 55, 250–260 (2002). [CrossRef] [PubMed]
  68. D. Xin, S. A. Bloomfield, “Effects of nitric oxide on horizontal cells in the rabbit retina,” Visual Neurosci 17, 799–811 (2000). [CrossRef]
  69. D. C. Hood, “Lower-level visual processing and models of light adaptation,” Annu. Rev. Psychol. 49, 503–535 (1998). [CrossRef] [PubMed]
  70. K. Jandrasits, A. Luksch, G. Soregi, G. T. Dorner, K. Polak, L. Schmetterer, “Effect of noradrenaline on retinal blood flow in healthy subjects,” Ophthalmology 109, 291–295 (2002). [CrossRef] [PubMed]
  71. B. Falsini, C. E. Riva, E. Logean, “Flicker-evoked changes in human optic nerve blood flow: relationship with retinal neural activity,” Invest. Ophthalmol. Visual Sci. 43, 2309–2316 (2002).
  72. A. Eisner, J. R. Samples, “Profound reductions of flicker sensitivity in the elderly: can glaucoma involve the retina distal to ganglion cells?” Appl. Opt. 30, 2121–2135 (1991). [CrossRef] [PubMed]
  73. A. Eisner, S. A. Fleming, M. L. Klein, W. M. Mauldin, “Sensitivities in older eyes with good acuity: cross-sectional norms,” Invest. Ophthalmol. Visual Sci. 28, 1824–1831 (1987).
  74. J. S. Werner, V. G. Steele, “Sensitivity of human foveal color mechanisms throughout the life span,” J. Opt. Soc. Am. A 5, 2122–2130 (1988). [CrossRef] [PubMed]
  75. J. S. Werner, M. L. Bieber, B. E. Schefrin, “Senescence of foveal and parafoveal cone sensitivities and their relations to macular pigment density,” J. Opt. Soc. Am. A 17, 1918–1932 (2000). [CrossRef]
  76. C. A. Johnson, A. J. Adams, J. D. Twelker, J. M. Quigg, “Age-related changes in the central visual field for short-wavelength-sensitive pathways,” J. Opt. Soc. Am. A 5, 2131–2139 (1988). [CrossRef] [PubMed]
  77. G. Haegerstrom-Portnoy, “Short-wavelength-sensitive-cone sensitivity loss with aging: a protective role for macular pigment?” J. Opt. Soc. Am. A 5, 2140–2144 (1988). [CrossRef] [PubMed]
  78. B. R. Hammond, B. R. Wooten, D. M. Snodderly, “Preservation of visual sensitivity of older subjects: association with macular pigment density,” Invest. Ophthalmol. Visual Sci. 39, 397–406 (1998).
  79. T. Sharma, A. Galea, E. Zachariah, M. Das, D. Taylor, M. Ruprah, V. Kumari, “Effects of 10 mg and 15 mg oral procyclidine on critical flicker fusion threshold and cardiac functioning in healthy human subjects,” J. Psychopharmacol. 16, 183–187 (2002). [CrossRef] [PubMed]
  80. I. Hindmarch, “Instrumental assessment of psychomotor functions and the effects of psychotropic drugs,” Acta Psychiatr. Scand. Suppl. 380, 49–52 (1994). [CrossRef] [PubMed]
  81. S. Curran, “Critical flicker fusion techniques in psychopharmacology,” in Human Psychopharmacology, I. Hindmarch, P. D. Stonier, eds. (Wiley, Chichester, West Sussex, UK, 1990), pp. 21–38.
  82. B. R. Hammond, R. M. Warner, K. Fuld, “Blood pressure and sensitivity to flicker,” J. Psychophysiol. 9, 212–220 (1995).
  83. A. M. McKendrick, A. J. Vingrys, D. R. Badcock, J. T. Heywood, “Visual field losses in subjects with migraine headaches,” Invest. Ophthalmol. Visual Sci. 41, 1239–1247 (2000).

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