Journal of Neuro-Ophthalmology, September 1981, Volume 1, Issue 3

Visual loss and bitemporal hemianopsia.

}. Clin. Neufo-ophthdlmol. 1: 231-235, 198 I. Neuroradiological Clinical Pathological Correlations Visual Loss and Bitemporal Hemianopsia ROBERT M. QUENCER, M.D. Case History A 36-year-old. nondiabetic, nonhypertensive fe­male presented with a chief complaint of 6 months of poor vision in her left eye. There was no asso­ciated headache, eye pain, ~r diplopia. Visual acu­ity was 20/15 on the right and 20/40 on the left. There was a 1+ Marcus Gunn pupil on the left and a bitemporal hemianopsia with a small left central scotoma. Funduscopic examination showed normal vessels with no evidence of optic atrophy. The remainder of the neurological examination, the general physical examination, and all laboratory values, including the serum prolactin level, were normal. The radiological evaluation included com­puted tomography (Fig. 1), skull films (Fig. 2), and cerebral angiography (Fig. 3). Discussion Noncontrast computed tomography shows an isodense anterior suprasellar mass (Fig. 1) which, on contrast enhanced computed tomography, en­hances uniformly (Figs. Ib-ld). There is no evi­dence of extension into the optic canals or orbits. On the coronal scan, the enhancement within the sella is seen to be identical with the suprasellar enhancement, so it is difficult to determine on the basis of the enhancing characteristics alone whether the lesion originated within or outside of the pituitary fossa. This distinction is of critical importance in the radiological differentiation of a primary sellar mass (such as pituitary adenoma) from other parasellar masses. Close inspection of the floor of the sella shows no evidence of a widened, thinned, or sloped sellar floor. The lateral skull film (Fig. 2) is normal. Carotid angiography From the Department of Radiology, University of Miami School of Medicine, Jackson Memorial Hospital. Miami. Florida. September 1981 (Figs. 3.1 and 3b) shows elevation of both AI seg­ments of the anterior cerebral arteries and a faint homogeneous tumor stain in the suprasellar area. The radiologic differential diagnosis of a mass lesion in the suprasellar area includes the follow­ing: pituitary adenoma, craniopharyngioma, glioma of the optic chiasm or hypothalamus, aneu­rysm, subarachnoid cyst, metastasis, epidermoid tumor, chordoma, or meningioma. On the basis of the CT, plain films, and angiography, the proper diagnosis can be made. Pituitary adenomas can be divided into two groups according to size: those tumors greater than 1 cm (macroadenomas) which most frequently present radiographically as intra- and suprasellar masses and those less than 1 cm (microadenomas) which present basically as intrasellar masses. The microadenomas, most commonly prolactin-secret­ing tumors,' are isodense or hypodense on non­contrast CT,1,2 but reports concerning their en­hancing characteristics vary. Some investigators feel that the majority of microadenomas remain hypodense:1 on contrast enhanced CT, while others have shown enhancement in over 50"!c, of these tumors.' Chromophobe adenomas, the most com­mon type of macroadenoma, display a range of density characteristics, the most common being that of a slight inhomogeneous mass of minimally increased density on noncontrast CT.~·:' which shows either uniform, patchy, or ring-like en­hancement on contrast enhanced CT."" However, neither the increased density on noncontrast CT nor the enhancement on contrast-enhanced CT should be considered an invariable sign of these pituitary adenomas, because some may be largely cystic or necrotic and present as a low-density mass and some (up to 20%) may not significantly enhance on contrast-enhanced CT. Because of this wide variation in the CT characteristics of pituitary adenoma, other radiographic criteria, particularly the size and configuration of the sellar, are used to 231 232. (b) Figures 1. -d. Computed tomography. Noncontrast computed tomography (NCcn in the axial plane (a) shows an isodense mass (M) in the anterior portion of the suprasellar cistern. Note the lack of surrounding cerebral edema. Contrast-en­hanced computed tomography (CEcn in the axial (b) and coronal planes (c and d) shows a homogeneously enhancing, well-defined suprasellar mass (arrowheads). Section c is 0.5 cm anterior to d and includes a portion of the anterior clinoids. In d note the draping of the third ventricle (3) over the mass and that there is a similar degree of enhancement within the pituitary fossa and both cavernous sinuses ",beled p and s, respectively) as there is within the mass. Journal of Clinical Neufo-ophthalmology Quencer arrive at a proper diagnosis. In this case, the lack of sellar enlargement makes the diagnosis of a pituitary adenoma highly unlikely, for only rarely can an adenoma greater than 1 cm be present in the absence of sel1ar changes.7 A craniopharyngioma frequently has tumoral calcification, low-density cystic areas, an irregular September 1981 growth pattern, and non-uniform contrast en­hancement. When these features are present, the diagnosis of a craniopharyngioma is very sugges­tive on the basis of the CT alone. None of these characteristics is seen in Figure 1. Suprasel1ar gliomas, arising from either the optic chiasm or hypothalamus, show some features sim- 233 VisU.l1 Loss and Bitemporal Hemianopsia Figure 2. uleral skull Film. The presence of a normal sella turcica as suggested by CT is confirmed on this lateral skull film. The cortical borders of the floor, anterior wall and poste­rior wall of the sella. the volume of the sella, and the posterior clinoids are all normal. There is no evidence of bony hyperos­tosis nor is there any abnormal calcification in the suprasellar or parasellar areas. ilar to the case presented here, i.e., tumoral en­hancement and no associated changes of the sellar floor. As Figure 1 shows, the mass is located in the anterior suprasellar space which rules out a hypo­thalamic glioma, since those tumors present in the posterior to middle suprasellar space. A chiasmal glioma is possible on the basis of the CT and plain skull findings; however, the homogeneous, non­malignant, persistent stain seen at angiography (Fig. 3) would be unusual for a glioma. An aneurysm of the anterior cerebral artery should be considered a possibility with an isodense suprasellar enhancing lesion and a normal-appear­ing sella, but this diagnosis is clearly ruled out by the results of angiography. A subarachnoid cyst is not a tenable diagnosis because these congenital lesions are nonenhancing, cerebrospinal fluid equivalent-density masses which are avascular an­giographically. A metastatic deposit to the base of the brain or the pituitary gland is very unlikely because there is no edema on CT, there are no malignant angiographic characteristics, and there is a lack of associated bone destruction. An epi­dermoid tumor which typically has low-density areas within a partially calcified, irregularly en­hancing, avascular mass is a poor diagnostic pos­sibility, as is a chordoma which invariably shows bone destruction of the skull base.~ Figures 3a and 3b. Cerebral angioj;:raphy. An early arterial phase from a right carotid injection (al shows elevation of bothA, st'gmt'nts of tht' anterior c('ft'bral arteries (arrows). A late arterial to early capillary phase of a left carotid injection (b l shows a homog('n('ous vascular stain (arrowht'ads) with no t'vid('nce of malignant vascularity (i.e.. no laking or pooling of contrast and nI' ('arly dr.lIning vt'ins). Small vt'ssds (opt'n arrowht'ad) arising from the supraclinoid left internal carotid were identified as feeding vessels to the mass. The stain persisted into the venous phase of the arteriogram. Vertebral and external carotid ini"(li(lnf~ wen' normcll. Journal of Clinical Neuro-ophthalmology Meningiomas vary in their CT charactl'ristics according to cell type, but the vast majority ,He isodense or of a greater density than surrounding brain; they are well defined; and they demlJnstr.1te moderate to marked homogeneous contrast.!' Al­though bony hyperostosis when present is .1 help­ful sign in diagnosing meningiom.1s, its .1bsence should not eliminate.1 meningioma as.1 possibility. Neither the lack of c.llcification in the tumor nor the lack of edema is .lg,linst meningiom.1 since calcification is seen in only approxim.1tely 30% of meningiomas,~ .md surrounding edem.1 is present in only 50%.111 Besides satisfying the m.1jor CT criteria for a meningioma, an important finding is the lack of sellar enlargement or erosion of the floor, indicating that this mass arose outside rather than within the pituitary fossa. A diagnosis of a suprasellar meningioma was considered most likely on the basis of the CT and skull series. The angiogram added further weight to that diagnosis by demonstrating elevation of the AI segments of the anterior cerebral arteries typical of an extra­axial mass and the classic homogeneous and per­sistent stain of a meningioma (Fig. 3). At surgery, a meningioma arising from the dia­phragma sella was found and completely removed. Histological examination showed a meningothelial type meningioma. References 1. Gardeur, D, Naidich, T. P., and Metzger, J.: CT analysis of intrasellar pituitary adenomas with em­phasis on patterns of contrast enhancement. Neu­roradiology 20: 241-247, 1981. September 1981 Quencer 2. Wolpert, S. M., Post, K. D., Biller, B. J.. and Molitch, M. E.: The value of computed tomography in eval­uating patients with prolactinomas. Radiology 131: 117-119,1 979. 3. Hillal, S. K., Ganti, R., and Ascherl, G.: Normal and abnormal CT anatomy of the intrasellar structures. Presented at the 17th Annual Meeting of the Amer­ican Society of Neuroradiology, Toronto, Canada, May 1979. 4. Hatam, A., Bergstrom, M., and Greitz, T.: Diagnosis of sellar ,md para sellar lesions by computed tomog­raphy. Neuroradiology 18: 249-258, 1979. 5. Nadich, T. P., Pinto, R. S., Kushner, M. J., et a!.: Evaluation of sellar and parasellar masses by com­puted tomography. Radiology 120: 91-99, 1976. 6. Sakoda, K., Mukada, K., Yonezawa, M., et a!.: CT scan of pituitary adenomas. Neuroradiology 20: 249-253, \981. 7. Rothman, L. M., Sher, J., Quencer, R. M., and Ten­ner, M. S.: Intracranial ectopic pituitary adenoma. /. Neurosurg. 44: 96-99, 1976. 8. Quencer, R. M.: Unilateral sixth nerve paresis. /. Clin. Neuro-ophthalmol. 1: 57-62, 1981. 9. Vassilouthis, ]., and Ambrose, ].: Computerized to­mography scanning appearances of intracranial meningiomas. /. Neurosurg. 50: 320-327, 1979. 10. Smith, H. P., Challa, V. R., Moody, D. M., and Kelly, D. L.: Biological features of meningiomas that deter­mine the production of cerebral edema. Neurosur­gery 8: 428-433, 1981. 11. Gyldensted, C, and Karle, A.: Computed tomogra­phy of intra- and juxtasellar Lesions. Neuroradiology 14: 5-13,1977. Write for reprints to: Robert M. Quencer, MD., De­partment of Radiology (R-130). University of Miami School of Medicine, P.O. Box 0\6960, Miami, Florida 33101. 235