LEITERS

management of retinoblastoma patients. We presently use it in fewer than 10% of all patients with retinoblastoma and, in a series treated with the betatron, chemotherapy was used extremely rarely. Our present management of retinoblastoma does not include chemotherapy unless there is documented extraocular disease.

Drs. Schipper and Alberti have raised the important issue of the role of chemotherapy in inducing second tu­mors. We and they are all aware that the increasing num­ber of reports, especially in Hodgkins disease, have im­plicated chemotherapy as inducing second tumors. The interesting aspect of retinoblastoma is the demonstration that these second tumors occur despite no chemotherapy or, indeed, no radiation therapy being given.

DA VID H. ABRAMSON, M.D. New York, New York

Dear Editor:

The paper "Digital subtraction carotid angiography and retinal artery obstruction" by Shah et al (Ophthalmology 1985; 92:68-72) failed to discuss two key references related to this subject l

,2 (see also reference 3 below). In addition to the work of Kollarits (their reference 12),

Tomsak et all found that 10 of 13 patients with central retinal artery occlusion had ipsilateral carotid disease in a retrospective study using conventional angiography.

Wilson et al2 found that 67% of patients (their Table III) had angiographically documented ipsilateral carotid disease associated with central artery occlusion.

These other studies should be brought to the attention of Shah and co-workers and to your readers.

References

ROBERT L. TOMSAK, MD, PhD Cleveland, Ohio

1. Tomsak RL, Hanson M, Gutman FA. Carotid artery disease and central retinal artery occlusion. Cleve Clin Q 1979: 46:7.

2. Wilson LA, Warlow CP, Russell RW. Cardiovascular disease patients with retinal arterial occlusion. Lancet 1979: 1 :292-4.

3. Tomsak RL, Hanson M, Gutman FA. Carotid artery disease and retinal artery occlusion. Lancet 1979: 1:1084.

Dear Editor:

We wish to thank Dr. Tomsak for bringing these works of his group and Wilson et al to our attention. The omis­sion of these is certainly an oversight, as they are both important contributions and emphasize the high corre­lation between retinal arterial obstruction and arterio­graphically proven carotid artery atherosclerosis.

In contrast to previous reports, carotid evaluation in our studyl was performed in a series of essentially con­secutive patients with retinal arterial obstruction, rather than subgroups selected out for such. In the cited com­munication of Tomsak and associates, 48% of patients with central retinal artery obstruction underwent conven-

tional carotid arteriography, while Wilson and colleagues evaluated 60% of people with retinal arterial obstruction in a similar fashion. Although digital subtraction carotid angiography does not have the accuracy of conventional carotid arteriography in detecting ulcerated plaques and other small lesions, we believe that our series of consec­utive evaluations more precisely reflects the incidence of moderate to large carotid stenoses associated with retinal arterial obstruction than previous publications.

Reference

HARSHAD G. SHAH, MD GARY C. BROWN, MD

RICHARD E. GOLDBERG, MD Philadelphia, Pennsylvania

1. Shah HG, Brown GC, Goldberg RE. Digital subtraction carotid an­giography and retinal arterial obstruction. Ophthalmology 1985: 92: 68-72.

Dear Editor:

The cause of acute blepharoptosis in diabetes mellitus is mostly an oculomotor never palsy. I found, however, a considerable number of diabetics with ptosis of slow onset and progressive course without a neurogenic origin. I studied the relation of this type of hitherto not described ptosis to the degree of retinal microangiopathy.

I compared 204 consecutive adult, white diabetics (89 non-insulin dependent, lIS insulin-dependent) with 204 white age- and sex-matched controls existing in a normal refraction polyclinical population. Excluded from the study were neurogenic, endocrinological, neuromuscular, inflammatory, iatrogenic, congenital and senile causes of ptosis. I measured the width of the palpebral fissure (WPF) in a standardized way with a calibrated bar in a spacious room with normal room illumination. Extreme attention was paid to the prevention of contraction of the frontalis and orbicularis oculi muscles. The measuring was carried out before judging the state of fundus microangiopathy.

The mean WPF of the control group was 9.8 mm, with a standard deviation of 0.96 mm (men, 10.1 mm; women 9.7 mm) and an insignificant effect of age «50 years: mean WPF, 10.3 mm; > 70 years: mean WPF, 9.6 mm).

There appeared to be a significant relationship between the degree of diabetic retinal microangiopathy, and the degree of ptosis. In background retinopathy the mean WPF was decreased to a mean of 8.4 mm, and in prolif­erative retinopathy the WPF was highly significant de­creased to a mean of 6.0 mm. In the most severe form of diabetic proliferative retinopathy a WPF of 4 mm was not an uncommon finding.

This type of slowly starting progressive ptosis of the upper eyelid is quite distinct from the well known ptosis in diabetic oculomotor palsy and involutional ptosis. The upper eyelid crease remains intact even in extreme ptosis. Electromyography of the levator muscles depicted no neurogenic signs. Neither could local edema or sympa­thetic denervation be assigned as the cause. Special atten-

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OPHTHALMOLOGY • SEPTEMBER 1985 • VOLUME 92 • NUMBER 9

tion was paid to the eventual coexistence of a (partial) Horner syndrome. A sympathetic denervation of levator muscles and pupil was ruled out by topical application of cocaine and low-dose adrenalin in selected cases of dia­betes and controls.

The levator muscles are in a continuous state of con­traction during awake conditions and need a continuous abundant blood supply. Diabetic microangiopathy con­curs with chronic tissue hypoxia, and I presume that it is the chronic progressive lack of sufficient oxygenation of the levator muscles that causes the here described ptosis. Electromyography of the levator muscles is not helpful in finding this condition. In at least one other disease the cause of chronic progressive ptosis is ascribed to microan­giopathy and local tissue hypoxia (by thickened capillary basal membranes): Kearns Disease. 1

,2 Thickening of the capillary basal membranes is a well known feature in di­abetes3 and is also related to local and general hypoxia as

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are other factors which affect tissue oxygenation in dia­betes mellitus.

References

L. A. K. BASTIAENSEN, MD, PhD Tilburg, The Netherlands

1. Stadhouders AM, Bastiaensen LAK, Jaspar HHJ, Ter Laak HJ. Some new obseNations on ragged-red fibres in chronic progressive extemal ophthalmoplegia (CPEO). In: Huber A, Klein D, eds. Neurogenetics and Neuro-Ophthalmology. (Developments in Neurology vol. 5) Am­sterdam: Elsevier North-Holland Biomedical Press, 1981; 223-7.

2. Bastiaensen LAK, Stadhouders AM, Ter Laak HJ, et al. Keams-Sayre syndrome; remarks on the pathogenesis with reference to a case with dwartism and calcification of basal ganglia. Neuro-Ophthalmol 1984; 4:55-63.

3. Jackson RL, Ide CH, Guthrie RA, James RD. Retinopathy in adoles­cents and young adults with onset of insulin-dependent diabetes in childhood. Ophthalmology 1982; 89:7-13.