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Neuroradiology (2000) 42: 145148 Springer-Verlag 2000

H E A D A N D N E C K R A DI O L OG Y

I. Alorainy

Senile scleral plaques: CT

Received: 18 February 1999 Accepted: 14 June 1999

I. Alorainy Montreal General Hospital, Department of Diagnostic Radiology, 1650 Cedar Avenue, Room D5 137, Montreal, Quebec, Canada H3G 1A4 I. Alorainy ( ) Department of Radiology, College of Medicine, King Saud University, PO Box 9047, Riyadh 11413, Saudi Arabia e-mail: alorainy@ksu.edu.sa, Tel.: + 9 66-1-4 67 19 99, Fax: + 9 66-1-4 67 17 46

Abstract I studied the CT appearances and the distribution of 109 asymptomatic calcified senile scleral plaques in 49 patients (98 eyes). The vast majority were just anterior to the insertion of the horizontal rectus muscles. The calcified plaques are variable in size, can be single or multiple, involve one or both eyes, and are only seen in elderly patients. Beam-hardening artifact and forward protrusion beyond the confines of the sclera are uncommon but potentially confusing features. Confusion with other pathology is unlikely with awareness of the pla-

ques' asymptomatic nature and their clinical and CT appearances. Key words Eye, calcification Plaques, senile Computed tomography

Introduction
Senile scleral plaques (SSP) are well known to ophthalmologists since their description by Rolandi in 1915 [1]. Clinically, they are circumscribed, grayish, oblong areas in the sclera posterior to the limbus and slightly anterior to the insertion of the extraocular muscles, usually the horizontal recti [24]. They are seen characteristically in asymptomatic elderly patients. The principal pathologic change is hyaline degeneration of the sclera [3, 5, 6]. Several theories have been proposed to explain the pathogenesis, but none is proved [6]. Only calcified SSP are seen on CT. Despite the extensive literature on the clinical and histopathologic features, their appearance and distribution on imaging have seldom been a subject of interest in the English-language literature [7, 8]. This report aims to provide a detailed account of the CT appearances and the patterns of distribution. The potential pitfalls and the rare complications are discussed.

Materials and methods


I reviewed 49 consecutive patients with incidental calcified SSP identified on CT head (44 patients) or orbits (5) from May to August 1998. The CT head examinations were not for ophthalmological indications; the symptoms of the patients who had CT of the orbits were not attributable to SSP. The patients were included in the study on the basis of the typical location of the lesions, without ophthalmological examination. The age and sex of the patients and the site, shape, and pattern of distribution of the calcified SSP were analyzed. In the cases of head CT, axial 7-mm slices and a 7-mm table increment were used. Spiral mode in the axial plane was used for orbital CT, with slice thickness 3 mm and pitch 1, with reconstruction in the coronal and sagittal planes, using 3-mm slices and the site and shape of the calcification was confirmed in all three planes. The scans of all patients were viewed on a workstation. The window level and width were manipulated to confirm the calcified SSP and exclude scanning artifacts. Because of remarkable variability with different window settings and lack of reproducibility, no attempt was made to measure the size of the calcified SSP; however, it was classed subjectively as small, medium, and large. A permutation test was conducted for statistical significance.

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a
Fig. 2 Three different sizes of calcified SSP in the same patient. Magnified view of the orbits from a head CT on a 93-year-old woman with headache demonstrates small, medium, and large calcified plaques just anterior to the insertion of the right lateral, left lateral, and both medial recti, respectively. Mild beam-hardening artifacts (arrows) are seen posterior to the large medial plaques. Note also slight forward bulging of the medial plaques, especially on the right, beyond the outer border of the sclera

b
Fig. 1 a, b A 74-year-old woman with incidental calcified SSP and sclerochoroidal calcification. a Magnified view of CT of the head at the level of the superior recti shows bilateral punctate calcification, presumably calcified SSP, at the insertion of the superior rectus, towards the periphery rather than the center of the muscles' attachment. b At a lower level, there is ill-defined calcification of the sclera and choroid posteriorly. Note significant volume averaging due to the relatively thick slice

Results
There were 17 men (35 %) and 32 women, aged 7096 years (median 84 years). A total of 109 calcified SSP were identified in their 98 eyes. Calcified SSP were primarily identified just anterior to the insertion of the medial and lateral rectus muscles. Only one patient had calcification near the insertion of the superior rectus muscle bilaterally (Fig. 1 a); this patient also had calcification just anterior to the insertion of the lateral recti and

sclerochoroidal calcification involving the posterior half of both globes (Fig. 1 b). Of the 109 lesions, 66 (60 %) were small, 30 (28 %) medium, and 13 (12 %) large. In 31 patients (63 %) there was more than one calcified SSP, of equal size in 19 patients. Small, medium and large SSP were seen in 2 of 16 patients with three or more plaques (Fig. 2). All but six (5.5 %) of the 109 SSP were within the confines of the sclera. The other six had grown forward beyond the outer border of the sclera (Figs. 2, 3). Mild beam-hardening artifact was seen with 12 plaques (11 %) (Fig. 2), which were medium or large. The coronal and sagittal reformatted images revealed an elongated shape to the calcified SSP that corresponds to the shape of the insertion of the horizontal rectus muscles (Fig. 4). The patterns of distribution of calcified SSP are shown in Table 1. The most common pattern was bilateral calcification just anterior to the insertion of both medial and lateral rectus muscles (22 %). Next were bilateral calcification anterior to the insertion of the medial rectus (20 %) and isolated calcification anterior to the insertion of the left medial rectus (20 %). The most common site involved, alone or in combination, was the insertion of the left medial rectus muscle (P = 0.0049). Of the 109 SSP, 64 (59 %) were on the nasal (P = 0.0028) and 43 (39 %) on the temporal side. The remaining two (2 %) were at the insertion of the superior recti. In non patient were calcified plaques identified in relation to the insertion of the inferior rectus or the

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Fig. 4 An 85-year-old woman with incidental calcified SSP in relation to the insertion of the medial rectus muscles. A reformatted image in the coronal plane demonstrates the oblong shape and the vertical orientation of the plaques, which correspond to the shape of the muscle insertion Fig. 3 An 86-year-old man with incidental calcified SSP. An enlarged view of the orbits from CT of the head clearly demonstrates the anterior protrusion of the right medial calcified plaque. A small calcified plaque is seen close to the insertion of the left medial rectus (arrow). Note previous lens surgery on the left

superior or inferior oblique muscles. Both eyes were involved in 30 patients (61 %). Apart from sclerochoroidal calcification, no other orbital calcification, such as optic nerve head drusen, trochlear, ciliary body or optic nerve sheath calcification, was encountered.

Discussion
Senile scleral plaques are asymptomatic lesions frequently encountered in elderly patients in ophthalmoTable 1 Frequency of different patterns of plaques distribution

logical practice and appear as symmetrical, sharply demarcated, glassy slate-gray areas about 3 mm from the limbus and 2 mm anterior to the tendinous insertion of the rectus muscles [24, 6]. They have the same obliquity as the muscle insertion and their vertical is greater than their horizontal diameter [2, 3]. The affected sclera is semitransparent, allowing the pigment of the uvea to shimmer through [3, 6]. They are identified less often on CT than on clinical examination because only calcified lesions are seen on CT. Urrets Zavalia et al. [9] in 1937 reported the histological findings in SSP. Several other studies showed that the process is primarily degenerative, with focal loss of cellularity and increased hematoxylinophilia [3, 5, 6]. The episclera immediately external to the lesion contains unique fibers with a characteristic corkscrew ap-

Right eye Medial rectus + + + + + 28 (26 %)


a b a

Left eye Lateral rectus + + + + + + 24 (22 %)


a

Medial rectus + + + +

Lateral rectus + + +

Total patients (%) 49 (100 %) 11 (22.4 %) 10 (20.4 %) 10 (20.4 %) 4 (8.2 %)b 4 (8.2 %) 3 (6.1 %) 3 (6.1 %) 2 (4.2 %) 1 (2 %) 1 (2 %) Total lesions (%) 107 (98 %)b

+ 36 (33 %)

+ 19 (17 %)

Calcification just anterior to the insertion of these muscles One patient also had bilateral calcified plaques at the insertion of the superior rectus muscle and posterior sclerochoroidal calcification

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pearance. Their number, and the degree and extent of hematoxylinophilia, increase progressively with the size, and presumably the age, of the plaque [6]. Calcification is present in less than half the cases; the plaques then become brittle and can be shelled out [5]. The pathogenesis of SSP is not precisely known. Their site and orientation have led some investigators to propose a mechanical theory [4]. Atherosclerosis of the ciliary artery and dissection of the anterior part of the sclera have been suggested [6]. Scroggs and Klintworth [6] found a frequent association between scleral plaques and actinic elastosis of the conjunctiva overlying them, indicating that most eyes with plaques have received significant sun damage [6]. However, more than one factor may contribute. As in this study, SSP are rarely seen before the seventh decade [5]; the incidence increases with age [10]. The higher number of women may simply reflect the proportion of women in the population at this age being investigated by CT. Only one patient was found to have bilateral calcification, presumably in SSP, at the insertion of the superior rectus muscle. Plaques involving the insertion of the vertical muscles are very rare [7, 10]. As in previous clinical reports [2, 3], the medial side was more often involved than the lateral. The reason for this is not clear and not explained by the proposed pathogenetic theories. Lateral predominance was described in a small series [6]. Calcification is seen only in the large lesions and is thought to be a late sequel to cell loss [5]. Calcium carbonate, calcium phosphate, and calcium sulphate have been found in these lesions [6]. The calcification is considered dystrophic because it involves a degenerate tissue, despite normal serum calcium and phosphate levels, while metastatic ocular calcification occurs in normal tissues secondary to high serum calcium and phosphate levels [11]. Abnormalities of calcium and phos-

phate metabolism as in hyperparathyroidism, pseudohypoparathyroidism, vitamin D intoxication, and chronic renal failure are recognized causes of focal sclerochoroidal calcification [11, 12]. It is hypothesized that elevated cytoplasmic calcium levels will cause rise in the mitochondrial calcium levels and precipitation of hydroxyapatite crystals [11]. Very rarely, SSP can be sequestered and expelled, with a resulting scleral hole that mimics scleromalacia perforans [4]. Surgery has been performed to prevent impending perforation of the sclera at the site of a senile plaque [13]. While the majority of the plaques in this report were within the sclera, six had clearly grown forward beyond its confines. The causes of acquired orbital calcification are many and include severe trauma, infection, tumors, and inflammation [8, 11]. CT plays a major role in differential diagnosis [7, 8]. Many types of calcification can be differentiated from SSP by virtue of their site, such as optic nerve head drusen, choroidal osteoma, and trochlear calcification [7]. Unlike SSP, sclerochoroidal calcification can be idiopathic (dystrophic) or metastatic, involve both the sclera and choroid, and is not confined to muscle insertions. It is however, also seen in elderly patients, but usually involve the posterior sclera [11, 12]. Since one third of the calcified SSP are single they might be a source of confusion with foreign bodies in trauma, especially if associated with beam-hardening artifact, as seen in 11 %. The age of the patient, the oblong vertical orientation, the relation to rectus muscle insertion, and the presence of another plaque in the same or the other eye are helpful indicators. Simple clinical examination should be decisive.
Acknowledgements My thanks to Dr. Raquel delCarpio for reviewing the manuscript and to Professor James Hanley for statistical assistance.

References
1. Rolandi S (1915) Sulla presenza di speciali chiazzo nella sclera di probabile natura cartilaginea. Ann Ottal 44: 843857 2. Boshoff PH (1942) Hyaline scleral plaques. Arch Ophthalmol 28: 503506 3. Roper KL (1945) Senile hyaline scleral plaques. Arch Ophthalmol 34: 283291 4. Manschot WA (1978) Senile scleral plaques and senile scleromalacia. Br J Ophthalmol 62: 376380 5. Cogan DG, Kuwabara T (1959) Focal senile translucency of the sclera. Arch Ophthalmol 62: 604610 6. Scroggs MW, Klintworth GK (1991) Senile scleral plaques: a histopathologic study using energy-dispersive X-ray microanalysis. Hum Pathol 22: 557562 7. Murray JL, Hayamen LA, Tang RA, Schiffman JS (1995) Incidental asymptomatic orbital calcifications. J Neuroophthalmol 15: 203208 8. Yan X, Edward DP, Mafee MF (1998) Ocular calcification: radiologic-pathologic correlation and literature review. Int J Neuroradiol 4: 8196 9. Urrets Zavalia A, Maldonado Allende I, Obregn Oliva R (1937) Scleromalacia observed during the course of chronic porphyrinuria. Arch Oftalmol B Aires 12: 115137 10. Norn MS (1974) Scleral plaques. I. Incidence and morphology. Acta Ophthalmol 52: 96106 11. Schachat AP, Robertson DM, Mieler WF, Schwartz D, Augsburger J, Schatz H, Gass DM (1992) Sclerochoroidal calcification. Arch Ophthalmol 110: 196199 12. Sivalingam A, Shields CL, Shields JA, McNamara JA, Jampol LM, Wood WJ, Daubert G (1991) Idiopathic sclerochoroidal calcification. Ophthalmology 98: 720724 13. Carrol CP, Peyman GA, Raichand M (1980) Surgical management of senile scleromalacia. Ophthalmic Surg 11: 719721

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