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Show Photo and Video Essay Section Editors: Kimberly M. Winges, MD Michael J. Gilhooley, MA, MB, BChir, DPhil Chiasmal Injury in Silent Pituitary Apoplexy Without Evidence of Mass Effect Ragini Phansalkar, PhD, Sylvia E. Villarreal Navarro, MD, Homer Chiang, MD, Heather E. Moss, MD, PhD FIG. 1. Case 1. A. Initial T1-weighted axial MRI. B. 30-2 automated visual field testing. C. Ganglion cell deviation maps on macula OCT. D. Follow-up T1-weighted coronal MRI. E. Initial T1-weighted coronal MRI. School of Medicine (RP), Stanford University, Palo Alto, California; and Departments of Ophthalmology (SEVN, HC, HEM) and Neurology & Neurological Sciences (HEM), Stanford University, Palo Alto, California. Funded by NIH P30 026877, unrestricted grant from Research to Prevent Blindness to the Stanford Department of Ophthalmology. The authors report no conflicts of interest. Address correspondence to Heather E. Moss, MD, PhD, Spencer Center for Vision Research, 2370 Watson Court, MC 5353, Palo Alto, CA 94303; E-mail: hemoss@stanford.edu Phansalkar et al: J Neuro-Ophthalmol 2024; 44: e187-e189 C ase 1: A 69-year-old man presented with a 2-year history of progressive blurry vision in the left eye and pain in the left side of his face and forehead. An MRI of the orbits showed an empty sella and a 4.1 · 2.0 · 1.7 cm mass in the left middle cranial fossa lateral to the cavernous internal carotid artery and abutting the left optic nerve (Fig. 1A). The initial review of the MRI suggested a normal optic chiasm. Prolactin was found to be elevated at 2,815 ng/mL, and the patient was started on cabergoline for e187 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Photo and Video Essay revealed nasal ganglion cell complex (GCC) thinning in the right eye and diffuse GCC thinning in the left eye (Fig. 1C). This chiasmal pattern of visual field defect and right eye optic nerve damage, which were not accounted for by the left cranial fossa lesion, prompted repeat imaging of the optic chiasm. A second MRI of the brain performed 4 months after the first showed that the chiasm was distorted with downward displacement and revealed that the sella contained a tumor-associated cyst (Fig. 1D). Although the mass, which was now displaying small areas of liquefactive necrosis, extended to the left superior orbital fissure and displaced the native pituitary gland rightward, it did not seem to be exerting a mass effect on the optic chiasm or tract. Although the patient had received cabergoline between these 2 MRIs, repeat evaluation of the first MRI showed similar observations of a “sagging” optic chiasm without evidence of mass effect (Fig. 1E), indicating that this finding was not a result of treatment. Case 2: A 44-year-old man presented following an incidental finding of a pituitary mass on a computed tomography scan performed for dental evaluation. MRI of the brain showed an expanded sella containing a T2 hyperintense 1.6 · 1.0 cm mass with liquefactive necrosis, abutting the medial aspects of the internal carotid arteries bilaterally (Fig. 2A). Like the previous case, the initial read of the MRI reported no compression of the optic chiasm. The patient did not report any vision loss and had normal visual fields (Fig. 2B); however, on macula OCT, he had focal superonasal GCC thinning in the right eye and mild nasal GCC thinning in the left eye (Fig. 2C), consistent with preperimetric ganglion cell injury in a chiasmal pattern. A second MRI 4 months later also showed that no elements of the patient’s mass were in contact with the chiasm. On further review, both MRIs revealed downward displacement of the chiasm (Fig. 2D). INTERPRETATION OF FINDINGS FIG. 2. Case 2. A. Initial T1-weighted coronal MRI. B. 30-2 automated visual field testing. C. Ganglion cell deviation maps on macula OCT. D. Follow-up T1-weighted coronal MRI. prolactinoma. Visual field testing conducted 2 months after initial presentation showed incomplete temporal field loss in the right eye as well as complete temporal field loss in the left eye (Fig. 1B). Optical coherence tomography (OCT) e188 Here, we report 2 cases of pituitary adenoma with MRI showing unexplained sagging or downward displacement of the optic chiasm, without the chiasm coming into contact with the tumor, along with evidence of chiasmal injury on ophthalmic imaging. Nasal GCC thinning on macula OCT confirmed chiasmal injury in both these cases and visual field deficits in one case. In both these cases, imaging demonstrated evidence of either hemorrhage or necrosis as well as cystic components in the pituitary masses, which are radiological evidence of previous hemorrhage.1 These patients likely experienced asymptomatic or silent pituitary tumor apoplexy, leading to regression of a portion of the mass that was previously compressing the chiasm. Pituitary apoplexy is a clinical syndrome involving either hemorrhage or infarction of a pituitary tumor, which classically presents with a severe acute headache, nausea, and visual deficits.2 However, several studies have found that Phansalkar et al: J Neuro-Ophthalmol 2024; 44: e187-e189 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. Photo and Video Essay most cases involving either radiographic or surgical evidence of hemorrhage or infarction of a pituitary tumor were not associated with these symptoms.1,3 This asymptomatic presentation is known as silent or subclinical apoplexy (SPA). Visual impairment is a leading presenting symptom in patients with SPA. Zhang et al4 reported visual disturbances in 142 of 185 SPA patients, of which 46 had visual field defects. Liu et al3 also described visual deficit as being a common symptom, present in 70% of cases in another cohort of SPA patients. Although there have been accounts of such silent pituitary apoplexy presenting with chiasmal injury and bitemporal hemianopia, this is, to the best of our knowledge, the first report presenting MRI findings of a deviated chiasm without apparent involvement by a mass. Such downward herniation of the chiasm has also been reported to occur after surgical resection of pituitary adenomas.5 In our 2 cases, it cannot be determined whether the chiasmal compression occurred because of mass effect before apoplexy or the apoplexy event itself. This distinction is significant because acute visual impairment due to apoplexy can often be reversed with surgical removal of the hemorrhage.6 Our patients were not considered surgical candidates because of the delay between the suspected time of apoplexy and neuroimaging. Nevertheless, these cases demonstrate that pituitary apoplexy should be considered in cases of MRI findings of chiasmal abnormality or clinical evidence of chiasm dysfunction in the setting of known pituitary adenoma. In addition, this case highlights the importance of correlating brain imaging, ophthalmic imag- Phansalkar et al: J Neuro-Ophthalmol 2024; 44: e187-e189 ing, and visual testing in cases of suspected chiasmal injury, especially when chiasmal abnormality on MRI is subtle. STATEMENT OF AUTHORSHIP Conception and design: H. E. Moss, S. E. V. Navarro, R. Phansalkar, H. Chiang; Acquisition of data: H. E. Moss, S. E. V. Navarro, R. Phansalkar, H. Chiang; Analysis and interpretation of data: H. E. Moss, S. E. V. Navarro, R. Phansalkar, H. Chiang. Drafting the manuscript: S. E. V. Navarro, R. Phansalkar; Revising the manuscript for intellectual content: H. E. Moss, S. E. V. Navarro, R. Phansalkar, H. Chiang. Final approval of the completed manuscript: H. E. Moss, S. E. V. Navarro, R. Phansalkar, H. Chiang. REFERENCES 1. Mohr G, Hardy J. Hemorrhage, necrosis, and apoplexy in pituitary adenomas. Surg Neurol. 1982;18:181–189. 2. Bi WL, Dunn IF, Laws ER. Pituitary apoplexy. Endocrine. 2015;48:69–75. 3. Liu ZH, Chang CN, Pai PC, et al. Clinical features and surgical outcome of clinical and subclinical pituitary apoplexy. J Clin Neurosci. 2010;17:694–699. 4. Zhang F, Chen J, Lu Y, Ding X. Manifestation, management and outcome of subclinical pituitary adenoma apoplexy. J Clin Neurosci. 2009;16:1273–1275. 5. Thome C, Zevgaridis D. Delayed visual deterioration after pituitary surgery—a review introducing the concept of vascular compression of the optic pathways. Acta Neurochir. 2004;146:1131–1136. 6. McFadzean RM, Doyle D, Rampling R, Teasdale E, Teasdale G. Pituitary apoplexy and its effect on vision. Neurosurgery. 1991;29:669–675. e189 Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |