Indian Journal of Radiology and Imaging Indian Journal of Radiology and Imaging

: 2003  |  Volume : 13  |  Issue : 3  |  Page : 261--270

Computerised tomographic evaluation of orbital lesions : Pictorial essay

RB Dubey, NP Tara, KN Sisodiya 
 Department of Radiodiagnosis, Pravara Rural Medical and Hospital, Loni BK, 413736, Tal, Rahata Ahmednagar, India

Correspondence Address:
R B Dubey
Department of Radiodiagnosis, Pravara Rural Medical and Hospital, Loni BK, 413736, Tal, Rahata Ahmednagar

How to cite this article:
Dubey R B, Tara N P, Sisodiya K N. Computerised tomographic evaluation of orbital lesions : Pictorial essay.Indian J Radiol Imaging 2003;13:261-270

How to cite this URL:
Dubey R B, Tara N P, Sisodiya K N. Computerised tomographic evaluation of orbital lesions : Pictorial essay. Indian J Radiol Imaging [serial online] 2003 [cited 2021 Jan 28 ];13:261-270
Available from:

Full Text

Orbital lesions include wide spectrum of pathology ranging from orbital trauma cyst, vascular anomalies and metastasis to tumours (benign and malignant). These lesions are challenging problems frequently faced by radiologists and ophthalmologist alike.

The vision of man has enabled him to make enormours progress and emerge as supreme species. The basic anatomical unit of vision, ocular apparatus is housed in a four sided pyramid - The orbit.

The anatomic relation of the orbit to the paranasal sinuses make it susceptible to pathologies of the adjacent sinuses apart from intraorbital pathologies. CT provides us excellent delineation of the bony orbit and the adjoining soft tissues.

A broad spectrum of orbital lesions produce few and deceptive symptoms like proptosis, diplopia and visual defects. CT helps to disclose the enigma posed by these symptoms and accurately discern the number, size, nature and extent of the orbital lesions.

CT technique : The usual technique is to obtain a lateral scannogram and take contiguous 2 mm thickness sections at 2 mm interval for both axial and coronal planes prior to and after administration of intra venous (ionic/nonionic) contrast media (1.5cc/kg). Axial sections are obtained with a gantry angulation of -10 to the orbitomeatal base line. The images of patients with trauma are studied in bone window setting to assess fractures. Soft tissue window is used to assess orbital soft tissue injuries.

Anatomical Consideration

The shape of the bony orbit is like a four sided pyramid with a long central axis extending medially and superiorly from its anterior base to its posterior apex. The orbits are bounded by the nasal cavity and ethmoid sinuses medially, the maxillary sinuses inferiorly, the frontal sinus and anterior cranial fossa superiorly, the middle cranial fossa posteriorly and laterally, and the extra-cranial temporal fossa laterally. The orbits may be divided into intraconal and extraconal portions. The muscle cone is defined by superior, medial, lateral and inferior recti and the aponeurotic intermuscular membrane which connects them.

40-50% of the globe normally lies behind the interzygomatic line. A perpendicular drawn from the anterior margin of the globe to the line measures less than 21 mm normally.

The outer margin of the globe is formed by scleral investment. The anterior margin of the globe is defined by the cornea centrally, which is continuous with the sclera. The choroid lies inside the sclera within the retina forming the innermost layer. Together, all the three layers are seen as a high density boundary to the globe which normally enhances with IV contrast.

Lens : The lens is seen as a hyperdense biconvex structure in the anterior portion of the globe.

The orbital septum which is continuous with the periorbital tissue extends from the antero-medial and lateral orbital rim to insert on the tarsal plates of the eyelids.

Optic nerve: The optic nerve lies along the central axis of the orbit. The optic nerve is contained within a sheath which is formed by all meningeal layers, continuous with those in the intracranial cavity.

Various orbital lesions can be followed up. CT diagnosis can be correlated with histopathological reports and surgical findings. It helps in defining the incidence of orbital lesions, their age and sex distribution their natural history and pathophysiological features that affect their management and prognosis.

Orbital Trauma

Traumatic lesions constitute a major group of orbital lesion.

A blow to the face or head may result in injury to the osseous orbit and the orbital soft tissue. Most of the times clinical examination of orbit is not possible due to the soft tissue oedema or haematoma.

Therefore CT by virtue of its ability to detect soft tissue and bony abnormalities simultaneously, is able to define exactly the lesion in its anatomical extent. CT is able to demonstrate herniation of soft tissue contents into the roof of the maxillary sinus [28]. Coronal scans are invaluable in depicting the bony fragments in such blowout fracture [38]. CT also helps in detecting unsuspected fractures of the orbital apex. Damage to the globe and optic nerve produces deformity of the eyeball and intraocular haemorrhage which is clearly demonstrated by CT.

Direct damage to the optic nerve and bleeding within the subarachnoid, subdural or intradural space can lead to the loss of vision, due to either primary optic nerve injury or secondary optic nerve injury by vascular compression. In fracture of the orbital floor, trapping of the inferior rectus, inferior oblique, fat and connective tissue and in fracture of medial wall, entrapment of medial rectus are better appreciated on coronal view [38]. Pneumo-orbit is also been associated with the fractures. Collection in the frontal, ethmoidal and maxillary sinuses was also noted. Blunt trauma to the orbit can lead to dislocation of lens as is seen in [Figure 1].

Foreign Bodies

CT demonstrates precise anatomic location of foreign bodies within the globe and sequela there of like ruptured globe, retinal detachment, lens disruption or vitreous haemorrhage in patients who may be difficult to examine clinically.

Unsuspected fragment in retrobulbar or intracranial location can be detect by CT [9]. Low density foreign bodies which can be missed on routine X-ray can be clearly seen on CT.

Prognostic information may also be obtained by CT in penetrating injuries to the globe [35] caused by foreign bodies.

With non-opaque foreign bodies such as a wood splinter. CT may also show only the granulomatous reaction or focal air density. Exact anatomical localization facilitates surgical planning for its removal.

Vascular Lesions

Cavernous Haemangioma

Cavernous haemangiomas is one of the most common benign intraorbital lesions and occurs in the 2nd -5th decade and is characterized by proptosis, difficulty in ocular motility and has a slowly progressive course. Most are located within the muscle cone. CT demonstrates the cavernous haemangiomas as a homogenously dense mass with smooth margins which shows uniform contrast enhancement. They do not deform the globe. It can be easily demarcated form the adjacent optic nerve and the muscles [22].


They are most often extraconal in location and present at a younger age (2nd decade). They have slow, progressive growth and are more likely to cause haemorrhage leading to pain and rapidly progressive proptosis. On CT they are diffuse hyperdense masses with irregular margins and show mottled contrast enhancement [23].

Inflammation and Abscess

Most common causes are sinus related, secondary to ethmoid sinusitis typically affecting children and young adults [18] and spread from adjacent dacryocystitis or mid facial infective focus.

Orbital septum acts as a barrier to prevent preseptal cellulitis from extending back into the orbital soft tissues. The infection may extend into the orbit proper along venous pathway or through the orbital wall periosteum. Infection within the orbit can be intraconal, extraconal or subperrosteal. Most cases of post septal cellutlitis are limited to extraconal space [7]. Intraorbital abscess obliterate the soft tissue planes that exit between the optic nerve, orbital fat, rectus muscles and wall of the orbit.

CT can demonstrate extent and source of infection. It not only shows bony changes and concomitant sinus involvement but the orbital soft tissue changes are also seen well like thickening and irregularity of extraocular muscles along retrobulbar enhancing inflammatory soft tissue lesion [Figure 2] & [Figure 3]. Intracerebral extension of orbital abscess can also be very well shown by CT.

Acute periorbital cellulites usually shows septal swelling proptosis, scleral thickning and subperiosteal abscess. Frontal lobe cerebritis and epidural inflammation are also shown well by CT. Delayed or inadequate treatment leads to complications like cerebritis, cerebral abscess, cavernous sinus thrombosis and blindness [41].


The most common cause of an intraocular mass is the orbital pseudotumor [1]. It usually presents with a triad of proptosis, pain and impaired ocular movement. Age at presentation is between 10 and 40 years. It is one of the most common cause of unilateral exophthalmos [1] but bilateral pseudotumors are also common [5]. Pathologically two types of pseudotumors are described, an acute form in which the reaction is that of vasculitis with vessel wall necrosis and fibrinoid changes and chronic inflammatory process with diffuse infiltration of the affected tissues with lymphocytes, plasma cells, macrophages and eosinophils. The classical CT findings described is that of contrast enhancing uveal-scleral thickening [1].

Uveal-scleral thickening may obliterate the insertion of the optic nerve at the papilla and insertions of tendons of rectus muscles. Pseudotumours are usually moderately enhancing, isodense to slightly hyperdense lesion [Figure 4][Figure 5]. The pseudotomuour may present as uveal-scleral thickening or as isolated discrete mass without uveal-scleral thickening as an obliteration of all retrobulbar soft tissue planes, as a thickening of rectus muscles or as a lacrimal mass[29]. It can mimic optic nerve sheath meningioma or manifest as myositis involving one or multiple muscles[5].

Regressions of the lesions were seen on administration of steroids.

Thyroid Orbitopathy

Graves diseases is an autoimmune disorder resulting [17] in excess secretion of thyroid hormones by the thyroid gland. It commonly presents in 4th to 5th decade of life and affects women four times more frequently than men. It is the most common cause of thyrotoxicosis.

The classical clinical signs are prominent stare, mild proptosis, eyelid retraction and lid lag. Pain is not the feature of thyroid orbitopathy.

Graves disease usually presents as enlargement of extraocular muscle due to inflammatory infiltration and proliferation of connective tissues in the soft tissues of the orbit. It mimics pseudotumour clinically and histopathologically.

When the condition occurs in association with thyrotoxicosis, orbital fat content may increase [31]. The increase in the volume of the orbital tissues produces proptosis. Thyroid exophthalmos occurs in hyperthyroid and euthyroid patients and is usually bilateral. It is unilateral in 5-10% of cases [31].

Though CT is not necessary for diagnosis of Grave's disease, it has been useful in indicating the degree of muscle involvement, its bilaterally and it has also proved useful in diagnosis, in the absence of clinical or laboratory evidence [6]. It is also useful for evaluating result of orbital decompression surgery.

The inferior and medial recti are usually involved in approximately 3/4th of cases whereas the superior and lateral recti are involved in approximately of the cases [33]. However, any or all extraocular muscles may be involved in nearly any combination, but if isolated lateral rectus enlargement is seen, then other etiologies should be considered [6]. In the direct sagittal CT sections, the inferior and superior recti are visualized in their entire length, so that minimal changes of Grave's disease can be recognized [36].

The enlarged extraocular muscles tapers at the insertions [Figure 6]. They show homogenous enhancement on administration of IV contrast [Figure 7]. The insertions of extraocular muscles into the sclera are normal. Upon the treatment with antithyroid drugs the symptoms regressed.

Dermoid Cyst

Sequestration of ectoderm in the wall o f the orbit during the embryogenesis leads to the formation of dermoid cysts. The desquamated contents consist of laminated keratin and cholesterol crystals.

Usually presentation is in infancy with a painless nodule, most commonly located in the superotemporal and occasionally in the supranasal part of the orbit [19].

Clinically it is firm, smooth and non-tender. Posterior margins are easily palpable Globe is neither displaced or proptotic. Dermoid cysts can extend into the anterior cranial fossa or into the orbit with displacement of the orbital periosteum.

On CT dermoid cysts have well defined margins and appear cystic, with the density of their center ranging from CSF to that of fat [2] [Figure 8]. On contrast enhanced scan, the central portion remains same in density [Figure 9]. CT reveals characteristic benign lesion and its intraorbital and intracranial extension. Treatment is surgical excision for cosmetic purpose.

Orbital Cysticercosis.

Cysticercosis is a disease due to infestation by Cysticercosis cellulosae, the larval form of the parasitic tapeworm Tanenia solium. Clinically patients present with either a visible subconjunctival cyst or orbital signs (proptosis) due to an extraocular muscle cyst that is unresponsive to treatment with oral corticosteroids [32]. Most of the cases of orbital cysticercosis examined by CT show a cystic lesion near or within an extraocular muscle. A subconjuntival location can also be seen. A scolex can usually be identified within the cystic lesions in nearly one half of the patients by CT and is diagnostic [Figure 10],[Figure 11].

CT imaging may show diffuse myositis in the presence of a positive enzyme linked immunosorbent assay for anti cysticerecal antibodies, which is also diagnostic. Neurocysticercosis is generally associated with more morbidity than orbital cysticercosis. Patient with neurocuysticercosis may present with convulsions and show presence of multiple brain cysticercii i.e. ring-enhancing lesions with a central hyperdense lesion [32],[8]. The lesions showed regression after antihelminthic drug therapy.

Persistent hyperplastic primary Vitreous (PHPV)

PHPV is an important cause of congenital leukocoria [16]. It results form failure of involution of the embryonic intraocular vascular system. CT demonstrates a linear or triangular density, the residual hyaloid vascular system with connective tissue, extending from the posterior aspect of the lens to the back of the globe [Figure 12]. There also may be associated retinal detachment as a result of recurrent hemorrhage. A hyaloid remnant may be difficult to differentiate from retinal detachment when it is complete PHPV is unilateral and noncalcified. There usually is microphthalmos, deformity of the globe and lens, increased density of the vitreous body. (vitreous body is replaced by soft tissue which shows enhancement) [26] [Figure 13] that extends between the lens and the posterior globe [27]. When PHPV is bilateral it is usually part of optic dyspalsia such as Noerrie's disease (Congenital progressive occuloacoustic cerebral degeneration).

Intraocular Tumours


Retinoblastoma is the most common intraocular malignancy of childhood. The incidence has been reported to be 1 in15,000-30,000 live births [39]. The average age at the time of diagnosis is 18 months. The tumour is bilateral in 25-33% of patients [40] In bilateral cases there is a frequent familiar history. Retinoblastoma most commonly presents as leucokoria, strabismus, glaucoma or vision loss.

Retinoblastoma arises in the nuclear layer of thee retina as a primary malignant neuroectodermal neoplasm composed of small round or ovoid cells. It is characterized by multicentric origin, rapid growth and ability to invade the adjacent tissues. As the tumour outgrows its blood supply, cell necrosis occurs and DNA is relased, that has a propensity to form calcified complex and by virtue of this complex, it is identified radiologically [40]. Danziger et al [4] divided retinoblastoma into three tumour grades:

Grade I - tumour confined to the globe, usually hyperdense and calcified mass. Grade II - tumour extending retro orbitally into the soft tissue or involving the optic nerve. Grade III - tumour extending byond the confines of the orbit or intracranially.

They concluded that presence of calcification is a favorable prognostic sign. Intracranial extension and marked contrast enhancement indicates poor prognosis.

Retinoblastoma can involve the entire globe, diffusely infiltrating the vitreous and aqueous humour and is seen on CT as soft tissue density intraocular mass with calcification and enhancement on administration of intravenous contrast [Figure 14],[Figure 15]. In these cases, calcification may be difficult to detect and with effect difficult to differentiate from other causes of retinal thickening which present as leucokoria. Retinoblastomas can be associated with retinal detachment which can be distinguished from tumour mass with intravenous contrast, as most retinoblastomas with non-calcified portions enhance.

Johnson [14] has described trilateral retinoblastoma (bilateral retinoblastoma with associated pineal tumour) which can be deteted on CT by taking higher sections of the brain along with orbit.


Orbital rhabdomyosarcoma is the most common primary malignant orbital tumor in children and most common soft tissue malignancy of childhood [21]. The tumour is composed of striated muscle cells and is thought to arise from undifferentiated mesenchymal elements. They usually manifest clinically as rapidly progressive exophthalmos over days to weeks. Rhabdomyosarcoma may arise in adjacent paranasal sinuses and secondarily involve the orbit through the thin bony wall with destruction of the sinus. CT can differentiate between primary orbital rhabdomyosarcoma and that arising from paranasal sinuses [39], can also demonstrate intracranial, expidural and subarachnoid extension of the tumour [39] which is a poor prognostic sign associated with almost 100% recurrence rate. CT demonstrates a uniformly enhancing isodense to slightly hyperdense mass along the lateral aspect of the right orbit which is seen to infiltrate the retrobulbar fat and the lateral recuts muscle causing destruction of the lateral wall of the orbit and causing anterior displacement of the globe leading to proptosis [Figure 16][Figure 17].

Paranasal Sinus Carcinoma

The orbit is often involved by extension of malignant process in the adjoining structures. 40-50% of paranasal sinus carcinoma can involve the orbit. The thin osseous wall separating the orbit from the adjacent four paranasal sinuses offer little resistance to the direct spread of tumour.The most common sinus involved is the maxillary sinus followed by ethmoid, frontal and sphenoid sinuses. Ethmoidal carcinoma has a much higher incidence of orbital involvement, 35% at the time of presentation. Orbital signs are proptosis, diplopia, visual loss, paraesthesia etc.

Extension of the mass outside the sinus cavity into the face, other paranasal sinuses, adjacent orbit or intracranial contents is more typical of a carcinoma [Figure 18],[Figure 19]. They usually extend through the medial wall, floor anterior orbit or the inferior orbital fissure [12].

CT shows presence of sinus soft tissue mass in association with extensive bone destruction [10]. Tumour mass often shows enhancement on contrast enhanced scan.


Haematogenous metastasis to the orbit are common, representing 3-10% of orbital masses. In children, the tumours most frequently responsible for orbital metastasis are embryonal tumors, neuroblastoma, Ewing's sarcoma and Wilms tumor. In adults the breast in women and the lung in men are the primary sites in majority of the cases [11]. In the child orbit is more frequently involved and the globe less often. Whereas in adults 70% of metastasis are ocular and only 30% are orbital. Orbital metastatic lesion usually presents with an abrupt onset of proptosis, external ophthalmoplegia and orbital pain. Metastases to the orbit most often have indistinct boundaries [Figure 20] and are diffusely infiltrating. ON CT a mass or masses which may be ill-defined will be seen. Globe lesions involving the chorioid or retina are frequent in posterior segment and may extend into retrobulbar space [11]. Secondary retinal detachment with haemorrhage may be seen. Metastasis to the extraocular muscles, optic nerve or lacrimal gland may appear merely as enlargement of these structures, although irregularity of the borders and multifocality of these masses often allows distinction from primary benign lesions [11]. There is usually some degree of contrast enhancement [34] [Figure 21].

Optic Nerve Sheath Meningioma

Primary meningioma arise from the optic nerve sheath and less frequently from the periosteum of the orbital wall. Secondary orbital meningiomas may arise from sphenoid ridge or tuberculum sellae and extend into the orbit. The latter are more common. Primary optic nerve meningioma constitute about one third of primary optic nerve tumours. Bilateral lesion are often associated with neurofibromatosis. Intraorbital meningioma arises along the course of the optic nerve. It can be a sheath meningioma, intracanalicular meningioma or foraminal meningioma. (At the intracranial opening to the optic canal). Most commonly they occur in females (80%) in the third to fifth decade of life. They usually present with early visual loss followed by proptosis(37). Papilloedema and optic atrophy are the next sequelae. High resolution CT demonstrates the size of the optic nerve shadow and its components. Significant enlargement, whether of the nerve, subrachnoid space or arachnoid membrane is easily visualized.

The perineural location of the perioptic meningioma can be seen as a mass surrounding a relatively less dense center (Compressed optic nerve). On contrast scan there is usually marked enhancement of optic nerve sheath resulting in the "tram tract" appearance seen on axial section and "doughnut" appearance seen on cornonal view (hypodense nerve seen as central lucency surrounding by a hyperdense nerve sheath) [3],[30]. Calcification if present confirms the diagnosis [3]. Intraorbital meningioma can cause optic canal widening and hyperostosis which is better appreciated on bone window. Intracranial extension is also known and well seen on CT.

In [Figure 22],[Figure 23] CT reveals a well defined, round, hyperdense lesion along the intraorbital part of the optic nerve, which showed strong enhancement on intravenous administration. Diagnosis was confirmed histopathologically.

Ocular Melanoma:

Both benign and malignant melamomas occur more commonly in the older people and are rare in the pediatric population. They arise intraocularly and are classified according to their site of origin. Malignant melanoma of the uveal tract is the most common intraocular malignancy in adults, predominantly in the whites. Primary malignant melanoma of the choroid is nearly always unilateral. Patient usually presents with visual field defects, decreased visual acuity, pain or inflammation. On CT it is seen as a slightly hyperdense, polypoid, flat or a crescentic mass which extends into the vitrous and which may show slight enhancement. Associated retinal detachment is common [24].


The incidence of orbital involvement by lymphoma is approximately 1%. The lacrimal gland is the most frequent site of involvement in the orbit. It may be either due to systemic disease or may indicate primary site. Bilateral involvement can also be seen. The patient with lacrimal gland involvement, presents with lid swelling and a palpable mass. It may present as an infiltrative process in the retroconal space that obliterates the normal soft tissue planes. It can mimic a pseudotumour. On CT the lacrimal gland lymphoma appears as a hyperdense mass in the lacrimal fossa that shows enhancement on contrast administration. It also displaces the globe medially and forwards. It responds very well to radiotherapy [25].


1Bernardino ME, Zimmerman RD, Citrin CM, Davis DO: Scleral Thicknening: A sing of orbital pseudotumor. Am J Roentgenol 1977; 129:703-706.
2Chawda SJ, Moseley IF: Computed tomography of orbital dermoids: a 20 year review. Clinic Radiol 1999; 54 (12): 821-825.
3Daniel DL, William AL, Syversten A, Gager WE, Harris GJ: CT recognition of optic nerve sheath meningioma: Abnormaal sheath visualization. Am J Neuroradiol 1982: 181-183.
4Danziger AA, Price HI: CT findings in retinoblastoma. Am J Radiol. 1979; 133: 783-785.
5Dresner, et al: Computed tomography of orbital myositis. Am J Radiol 1984: 143:671-674.
6Enzamann D, et al: Computed tomography in Grave's ophthalmopathy. Radiol 1976a: 118:615-620.
7Fernbach K, Sandra, Naidich TP: CT diagnosis of orbital inflmmation in children. Neuroradiology 1981;22:7-13.
8Gadkari SS, Bhabha SK, Jehangir RP, Adrianwala SD, Kirtane MV, Shah NA: Orbital cysticercosis. J Postgard MED 1992; 38: 200-201.
9Gaster RN, Duda EE: Localisation of intraocular foreign bodies by computed tomography. Opthalmic surgery 1980; 11:25-29.
10Hesselink JR, Weber AL, New PFJ, Roberson GH, Taveras JM: Evaluation of mucoceles of the paranasal sinuses with CT. Radiol 1979; 133: 397-400.
11Hesselink JR, Davis KR, Weber AL, Davis JM. Taveras JM: Radiological evaluation of orbital metastasis with emphasis on computed tomography, Radiol 1980; 137:363-366.
12Hesselink JR, Weber AL: Pathways of orbital extension of extraorbital neoplasma. J Comput Assist Tomogr 182 Jun: 6(3): 593-597.
13Jacobiec FA, Depot MJ, Kennerdell JS, Shults WT, Anderson RL, Alper M, Citrin CM, Trokel SL : Combined clinical and computed tomographic diagnosis of orbital glioma and meningioma, Ophthalmology 1984;91(2):137-155.
14Johnson DL, Chandra R, Fisher WS, Hammock MK, Mckeown CA: Trilateral retinoblastoma: ocular and pinearetinoblastoma. J Neurosurg 1985; 63:367-370.
15Intraocular Tumors, Kanski. J. 2000; 8: 337-338.
16Intraocular Tumors, Kanski, J. 2000; 8:341
17Disorders of the orbit, Kanski J. 2000; 14: 558
18Disorders of the orbit, Kanski J. 2000; 14:564
19Disorders of the orbit, Kanski J. 2000; 14: 572
20Disorders of the orbit, Kanski J. 2000; 14: 579
21Disorders of the orbit, Kanski J. 2000; 14: 581
22Atlas SW et al. The Orbit, Cra Com Tomo and MRI 1987; 3:124
23Atlas SW et al. The Orbit, Cra Com Tomo and MRI 1987; 3:126
24Atlas SW et al. The Orbit, Cra Com Tomo and MRI 1987; 3:128
25Atlas SW et al. The Orbit, Cra Com Tomo and MRI 1987; 3: 149-150
26Mafee MF, Goldberg FM, Valvassori GE, Capek M: Computerised tomography in evaluation of patients with persistent hyperplastic primary vitreous (PHPV). Radiology 1982: 145: 713-717.
27Mafee M.F., Goldberg MF : PHPV : Role of CT and MR imaging. Radiol Clin North Am 1987; 25: 683.
28Momose KJ, New PFJ, Grove AS and Scott WR: Use of computed tomography in ophthalmology. Radiology 1975; 115:361-368.
29Nugent RA, Lapointe JS, Rootman J.Robertson WD, Greab DA: Orbital dermoids: features on CT. Radiol 1987; 165:475-478.
30Peyster RG, Hoover ED, Hershey BL, Haskin ME: High resolution CT of lesions of the optic nerve. Am J Neuroradiol 1983; 4: 169-174.
31Peyster RG, Ginsburg F, Silber J, Adler L: Exophthalmos Caused by excessive fat : CT volumetric analysis and differential diagnosis. Am J Neuroradiol 1986; 7:35-40.
32Sekhar GC, Lemke BN: Orbital cysticercosis. Ophthalmology 1997; 104: 1599.
33Trokel SL and Hilal SK: Recognition and differential diagnosis of enlarged extraocular muscles in Computed tomography. Am J Ophthalmol 1979; 870:503-512.
34Weisberg LA: The computed tomographic findings in intracranial metastasis due to breast carcinoma. Comput Radiol 1986; 10(6): 297-306.
35Wiesman RA, Savino PI, Schurt L, Schatz NJ: Computed tomography in penetrating wounds of the orbit with retained foreign bodies. Arch Otolaryngol 1983; 109:265-268.
36Wing SD, et al: Direct sagittal computed tomography in Grave's ophthalmopathy. J Comput Assist Tomogr 1979;3:820-824.
37Wright JE, Call NB, Liaricos: Primary optic nerve meningioma. BR J Ophthalmol 1980; 64;553-558.
38Zilkha : Computed tomography of blow out fracture of the medial orbital wall. Am J Neuroradiol 1981; 427-429.
39Zimmerman RA, Bilanuik L.T. Littman P: Computed tomography of paediatric craniofascial sarcoma. CT : J Comput Tomogr 1978; 2:113-121.
40Zimmerman RA, Bilanuik LT : Computed tomography in evaluation of patients with bilateral retinoblastomas. CT: J Comput Tomogr 1979;3:251-257.
41Zimmerman RA. Bilanuik LT. CT of orbital infection and its cerebral complication. Am J Radiol 1980; 134:45-50.