PMCCPMCCPMCC

Search tips
Search criteria 

Advanced

 
Logo of brjopthalBritish Journal of OphthalmologyVisit this articleSubmit a manuscriptReceive email alertsContact usBMJ
 
Br J Ophthalmol. 2007 October; 91(10): 1257–1258.
PMCID: PMC2000993

Ageing and visual field data

Short abstract

Knowledge is sparse

Keywords: ageing, visual field data

No human function lasts forever. The progressive and inevitable decay of both sight and hearing, perhaps the two noblest human senses, is a good example of how the insults of time affect us all, in spite of modern medical advances. Research groups throughout the world are continually searching for ways to extend the average lifespan, allowing humans to live even well beyond the age of 100. This scientifically aided extension of life is not without consequences, especially if the natural deterioration processes underlying different human organs are not seriously considered. The sense of vision serves as a good example of this. It has been calculated, based on both histological (counting the optic nerve axons) and functional (data from different perimetric techniques) studies,1,2,3,4,5,6,7,8 that every human being loses on average approximately 5000 to 9000 optic nerve fibres per year (fig 11).). Progressive retinal nerve fibre layer thinning has also been shown with modern imaging techniques.9,10 Considering that a normal optic nerve is composed of one million to one and a half million optic fibres, upon reaching the hypothetical age of 200 a very limited number of retinal ganglion cells and nerve fibres would remain. This would probably lead to a condition of “physiological” blindness, unless truly effective neuroprotective agents were available at that time.

figure bj117978.f1
Figure 1 Number of axons in 60 normal optic nerves, plotted against age. These data were pooled from seven clinical studies: open circle, Balaszsi et al1; cross, Johnson et al2; closed circle, Jonas et al3; open triangle, Kupfer et al4; closed ...

Philosophical and ethical considerations aside, the influence of ageing on vision, but more specifically on visual field (VF), is quite important for a variety of reasons: (1) accurate normative age corrected parameters are needed to establish whether or not VF test results from subjects differing in age are within normal limits, thus avoiding false interpretations; (2) several ocular diseases that progressively affect the VF, such as chronic glaucoma, typically occur at an advanced age and thus knowing the influence of physiological visual function decay becomes diagnostically imperative; (3) other age related factors (such as fatigue, subject reliability, quickness of reflex, senile miosis, progressive lens opacity, etc) play an important part in VF testing, and should be extensively known and always taken into consideration.

To date, there are only a few published studies that assess the influence of ageing on VF data. Most of these papers are based on cross sectional studies and consider patients with progressive diseases like glaucoma. The limit of these studies is the difficulty in determining whether or not the worsening of VF parameters is due to advancing of age, ocular disease progression or a combination of both. More than 20 years ago, Haas et al11 reported that the differential light sensitivity begins to decline in youth and continues to gradually decrease throughout life at a rate of 0.58 dB per decade.11 Spry and Johnson analysed 562 eyes from clinically normal subjects who had previously been recruited for other studies.12 The rate of mean sensitivity loss was 0.43 dB/decade before 53.4 years, and 1.02 dB/decade after that age (fig 22).). Interestingly enough, this study showed that the linear age coefficients used in several VF devices tend to overestimate sensibility changes due to age in younger subjects, whereas they underestimate them in older subjects, thus missing early defects in the first group and overcalling them in the latter.

figure bj117978.f2
Figure 2 Distribution of mean sensitivity by decade. (Adapted from Spry and Johnson12.)

An additional point that needs to be clarified is whether or not all perimetric techniques are affected to the same extent by age. Six different methods of VF testing were considered to address this issue in a recent study.13 In considering the three most currently used methods, short wavelength automated perimetry (SWAP) showed the largest age effects, followed by frequency doubling technology (FDT), and lastly by standard automated perimetry (SAP). This information should be kept in mind when interpreting VF data from different testing techniques.

In this issue of the BJO, Rudolph and Frisén14 report an interesting longitudinal study based on a group of neuro‐ophthalmic patients with non‐progressive VF defects caused by chiasmal syndromes (see pages 1276–8). This paper is based on a different cohort of subjects, in comparison with studies involving typical glaucoma patients with defects that tend to progress over time. Patients were tested using high‐pass resolution perimetry (HRP), a non‐conventional VF testing method that is thought to selectively analyse the parvocellular visual pathway by means of special ring‐shaped targets of increasing size till perception.15 It has been previously demonstrated that HRP minimum angle of resolution and retinocortical neural channels (corresponding to retinal ganglion cells and respective axon projections to the brain) are closely related, thus providing very important information on structural damage based on functional data.16,17

The authors report findings based on 28 patients who did not show significant deterioration in both normal and abnormal field areas over a median follow‐up period of 9 years. As the authors stated, these unexpected results were difficult to explain. Although the follow‐up period was quite long, it may be insufficient to adequately show the relation between age and HRP sensitivity. A persistent learning effect may partially explain the apparent lack of threshold deterioration over time in some patients. The authors show, however, that when a cross sectional representation of data is used, plotting HRT minutes of arc against age, a typical age related deterioration is evident. It is important to note that these results somewhat differ from SAP, which is currently the gold standard for VF testing. Studies with SAP in patients with glaucomatous damage have shown high variability in defective VF areas.18 As previously stated, the characteristics of glaucomatous defects significantly differ from neurological VF defects. Moreover, SAP seems to underestimate age related ganglion cell loss when compared to HRP.8 Further studies are definitely needed to show whether these discrepancies are due to different types of defects and/or to the different techniques used. Longitudinal studies based on extensive follow‐up results of normal subjects and patients with different ocular and neuro‐ophthalmic diseases would be of pertinent clinical interest. These types of studies, however, entail considerable practical difficulties. The article by Rudolph and Frisén paves the way as an exciting incentive for researchers to move forward in this intriguing and underdeveloped topic.

In closing, one of the main goals of modern medicine entails stopping or slowing down the detrimental effects of ageing on human functions. While the hunt for the fountain of eternal youth continues, science should not only be directed at halting deterioration, but also at helping humans to cope and accept inevitable age related changes, allowing them to age gracefully over time.

References

1. Balazsi A G, Rootman J, Drance S M. et al The effect of age on the nerve fiber population of the human optic nerve. Am J Ophthalmol 1984. 97760–766.766 [PubMed]
2. Johnson B M, Miao M, Sadun A A. Age‐related decline of human optic nerve axon population. Age 1987. 105–9.9
3. Jonas J B, Müller‐Bergh A, Schlötzer‐Schrehardt U M. et al Histomorphometry of the human optic nerve. Invest Ophthalmol Vis Sci 1990. 31736–744.744 [PubMed]
4. Kupfer C, Chumbley I, Downer J de C. Quantitative histology of optic nerve, optic tract and lateral geniculate nucleus of man. J Anat 1967. 101393–401.401 [PubMed]
5. Oppel O. Untersuchungen über die Verteilung und Zahl der retinalen Ganglienzellen beim Menschen. Graefes Arch Klin Exp Ophthalmol 1967. 1721–22.22
6. Potts A M, Hodges D, Shelman C B. et al Morphology of the primate optic nerve. Invest Ophthalmol 1972. 11980–988.988 [PubMed]
7. Quigley H A, Dunkelberger G R, Green W R. Chronic human glaucoma causing selectively greater loss of large optic nerve fibers. Ophthalmology 1988. 95357–363.363 [PubMed]
8. Frisén L. High‐pass resolution perimetry and age‐related loss of visual pathway neurons. Acta Ophthalmol 1991. 69511–515.515 [PubMed]
9. Alamouti B, Funk J. Retinal thickness decreases with age: an OCT study. Br J Ophthalmol 2003. 87899–901.901 [PMC free article] [PubMed]
10. Da Pozzo S, Iacono P, Marchesan R. et al The effect of ageing on retinal nerve fibre layer thickness: an evaluation by scanning laser polarimetry with variable corneal compensation Acta Ophthalmol Scand 2006. 84375–379.379 [PubMed]
11. Haas A, Flammer J, Schneider U. Influence of age on the visual fields on normal subjects. Am J Ophthalmol 1986. 101199–203.203 [PubMed]
12. Spry P G, Johnson C A. Senescent changes of the normal visual field: an age‐old problem. Optom Vis Sci 2001. 78436–441.441 [PubMed]
13. Gardiner S K, Johnson C A, Spry P G D. Normal age‐related sensitivity loss for a variety of visual functions throughout the visual field. Optom Vis Sci 2006. 83438–443.443 [PubMed]
14. Rudolph T, Frisén L. Influence of ageing on visual field defects due to stable lesions. Br J Ophthalmol 2007. 911276–1278.1278 [PMC free article] [PubMed]
15. Frisén L. A computer graphics visual field screener using high‐pass spatial frequency resolution targets and multiple feedback devices. Doc Ophthalmol Proc Ser 1987. 49441–446.446
16. Frisén L. High‐pass resolution perimetry: central‐field neuroretinal correlates. Vision Res 1995. 2293–301.301
17. Popovic Z, Sjostrand J. The relation between resolution measurements and numbers of retinal ganglion cells in the same human subjects. Vis Res 2005. 452331–2338.2338 [PubMed]
18. Spry P G, Johnson C A. Identification of progressive glaucomatous visual field loss. Surv Ophthalmol 2002. 47158–173.173 [PubMed]

Articles from The British Journal of Ophthalmology are provided here courtesy of BMJ Group