ORIGINAL ARTICLE
Year : 1984 | Volume
: 32 | Issue : 5 | Page : 343--346
Senile macular degeneration in Northern India
IS Jain, P Prasad, Amod Gupta, Jagat Ram, SP Dhir
Department of Ophthalmology, Postgraduate Institute of Medical Education and Research, Chandigarh, India
Correspondence Address:
I S Jain
Department of Ophthalmology, Postgraduate Institute of Medical Education and Research, Chandigarh
India
How to cite this article:
Jain I S, Prasad P, Gupta A, Ram J, Dhir S P. Senile macular degeneration in Northern India.Indian J Ophthalmol 1984;32:343-346
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How to cite this URL:
Jain I S, Prasad P, Gupta A, Ram J, Dhir S P. Senile macular degeneration in Northern India. Indian J Ophthalmol [serial online] 1984 [cited 2023 Mar 28 ];32:343-346
Available from: https://journals.lww.com/ijo/pages/default.aspx/text.asp?1984/32/5/343/27507 |
Full Text
Senile macular degeneration (SMD) is an age related process accounting for considerable visual loss in older people. Prevalence of SMD has been variably reported as 8.8% and 29.3%.[1],[2] However, it has been considered a rarity amongst the coloured races.[3] Although primarily degenerative in nature, systemic and local risk factors have been incriminated.[4],[5],[6] Both these facts prompted us to undertake a study of SMD in the North Indian Population.
MATERIALS AND METHODS
Patients over the age of 50 years were screened for macular changes, covering the period between July, 1981 to Feb. 1983. A complete R medical history of ocular and systemic problems was noted. The best corrected distance and near visual acuity was recorded. Biomicroscopic examination was performed in each case after adequate pupillary dilatation to assess lens changes. The macula was examined in detail with direct ophthalmoscopy. Macular changes were graded according to the criteria used in Framingham eye study.' Fluorescein angiography was carried out in few selected cases. The individual macular changes viz pigment and drusens were graded according to the severity and scored accordingly [Table 1]. From- these, macular degeneration as a whole was graded as pigment change score plus drusen score [Table 2]. All disciform degenerations were grouped in the severe form of SMD [Table 2]. In assessing the risk factors two variables were studied i.e., refractive errors and senile lenticular changes. Eighty five age related controls were also studied. Emmeteropia was defined as between -0.5 Dsp and +0.5 Dsph. in phakics and between +9.50 Dsph to + 10.00 Dsph in aphakes. Senile cataracts were classified as axial and peripheral. Axial cataract included those opacities within 2mm of central axis and peripheral those with opacities beyond 2 mm zone.
OBSERVATIONS
We detected 100 cases of SMD from a total of 2122 patients who were screened during the period of study. The prevalence rate of SMD was 4.7%. Of these, 85 were of dry and 15 disciforrn in nature. Thus disciform degeneration accounted for 15% of all SMD and was seen in 0.7% of the population. SMD was bilateral in 67 patients and unilateral in 33. Distance vision was found to decrease commensurately with increasing severity of SMD (Pshow that SMD in coloured races is not as rare as reported by Schatz.[3] Disciform macular degeneration (DMD) accounted for higher percentage of SMD (15%) in our study as opposed to both the caucasion and the black African groups[7]. The reason for this apparent susceptibility of the North India population to SMD remains to be solved.
Although distance and near vision decreased with increasing severity of disease, 61 eyes (36.5%) had a visual acuity of 6/9 orbetter. This feature has not been highlighted in other series since SMD was diagnosed by them only if vision was less than 6/9. This disparity between ophthalmoscopic grading and visual loss shows that clinical picture is not reliable indicator of amount of visual loss due to SMD. An increase in severity of SMD with age and progressive lens changes supports the observations that it is an age related process.
Risk Factors
The Framingham eye study[2] identified systemic blood pressure, height, vital capacity, left ventricular hypertrophy and interim history of lung infection as risk factor in SMD . A case controlled study 6 revealed that SMD had an age related increase and related to hypertension. It was also stated that hypermetropia may predispose to SMD and myopia may have a protective influence.[6] A similar study estimated the relative odds of having hypermeteropia among the SMD group versus the control as 2.4%.[4]
The present study supports the observations of the above two series in that hypermetropia was seen in almost twice as many cases as controls.
For the first time, the type of cataract has been shown to have an effect on SMD. Peripheral cataracts are more often associated with SMD and probably predispose to the development of disease. Central cataract on the other hand may have protective influence by cutting of solar rays from reaching the macula in aged susceptible eyes. Studies have[8],[9] demonstrated histopathological changes in the chorio-capillaries of aging eye i.e. thickening of intercapillary septa, narrowing of the lumen and acellularity of the capillaries. These changes, disturb the heat dissipating mechanism of the choroidal blood flow and render the retina more susceptible to light induced heat damage.[10]
SUMMARY
Senile macular degeneration (SMD) is an age related process supposedly rare in the colored races. All patients over the age of 50 years were studied clinically for macular degeneration. Of these, 100 cases were detected over a period of 2 years, (Prevalence 4.7%). Disciform degeneration accounted for a high proportion of cases (15%). SMD was found to affect significantly both distance and near vision. Hypermetropia was seen more often in these cases (70%) as opposed to controls (40%). SMD occurred more frequently in association with peripheral cataracts whereas central cataracts appeared to protect the macula from degeneration.
References
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| 2 | Kahn, H.A, Leibowitz H.M., GanleyJ.P., KiniM.S., Colton T., 1977. Amer. J. Epidemiol., 106: 33 |
| 3 | Schatz H., 1975. Int. Ophthalmol. Clin., 15: 169 |
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| 7 | Gregorz, Joffel., 1978. Brit. J. Ophthalmol., 62: 547 |
| 8 | Kornzweig A, 1977. Ann. Ophthalmol., |
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| 10 | Parver L.M., Auver C., Capenter D.O.,1980. Amer. J. OphthalmoL, 89: 641 |
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