Location
Philadelphia, PA
Start Date
17-4-2026 1:30 PM
End Date
17-4-2026 2:30 PM
Description
Introduction: Meningiomas are generally benign CNS tumors with a propensity to occur in individuals with predisposing risk factors, such as, neurofibromatosis type II. These tumors can arise via de novo mutations, or through inheritance via NF2, and SMARCB1 mutations. They can also arise idiopathically. In this case, A 33-year-old female presented to the ophthalmology clinic for a routine diabetic fundus exam. She also complained of worsening left eye (OS) vision, which had historically been her weaker eye. She had been a type II diabetic for 2.5 years with a most recent HbA1c of 13.6. The patient reported poor OS vision as a teenager and was prescribed glasses. Her poor OS vision had been attributed to amblyopia, likely refractive. At the time of her exam, now 3 years later, the patient presented with complete no light perception (NLP) vision OS. Per patient, vision had been worsening over the past year or so. Additional work-up was initiated and given the pattern of retinal nerve fiber layer (RNFL)/ganglion cell layer (GCL) loss, a compressive lesion was high on the differential hence an MRI brain and orbits with and without contrast was ordered. MRI revealed an eccentric left-sided suprasellar meningioma with encasement of the A1 segment of the anterior cerebral arteries as well as likely encasement of the prechiasmatic optic nerve with optic nerve atrophy. The mass appeared to be separate from the pituitary measuring 2.5 x 1.9 x 2.0 cm with a dural tail.
Methods: Sequential ocular examination and appropriate testing.
Results: Neurosurgery was consulted and given the tumor size, and proximity to critical structures, surgical resection/debulking via an orbital zygomatic approach was urgently performed. Biopsy of the lesion was confirmed by pathology to be a meningioma WHO grade 1. After resection, the patient’s visual acuity improved to seeing shadows. The patient was discharged with follow ups. 6 months post op, OS vision remained markedly compromised with now eccentric light perception vision, from an initial NLP.
Discussion: Case reports and literature review were performed.
On further review of her initial optical coherence tomography (OCT) imaging 3 years prior, early asymmetric GCL loss was noted, hence, the tumor was likely present for a long period of time, however, too small to cause substantial symptoms. The tumor compressed the A1 segment of the anterior cerebral artery, and even though it does not directly supply the optic nerve, the vessel's compression could potentially affect the microvasculature in the region. Specifically, the small pial vessels that contribute to the optic nerve's blood supply. The pathogenesis of visual impairment was likely primarily due to compression of the prechiasmatic optic nerve, where the tumor mass directly compressed the fine optic nerve fibers. This led to axonal damage, loss of retinal ganglion cells reflected by extreme RNFL thinning, and ultimately, optic nerve atrophy. This case highlights that albeit benign, meningiomas can be locally destructive hence clinicians should be alert to compressive lesions as a potential etiology for unexplained vision loss especially with corresponding changes to the RNFL, and GCL.
Embargo Period
6-4-2026
Included in
A Case of Extensive Suprasellar Meningioma Presenting with Insidious Visual Impairment
Philadelphia, PA
Introduction: Meningiomas are generally benign CNS tumors with a propensity to occur in individuals with predisposing risk factors, such as, neurofibromatosis type II. These tumors can arise via de novo mutations, or through inheritance via NF2, and SMARCB1 mutations. They can also arise idiopathically. In this case, A 33-year-old female presented to the ophthalmology clinic for a routine diabetic fundus exam. She also complained of worsening left eye (OS) vision, which had historically been her weaker eye. She had been a type II diabetic for 2.5 years with a most recent HbA1c of 13.6. The patient reported poor OS vision as a teenager and was prescribed glasses. Her poor OS vision had been attributed to amblyopia, likely refractive. At the time of her exam, now 3 years later, the patient presented with complete no light perception (NLP) vision OS. Per patient, vision had been worsening over the past year or so. Additional work-up was initiated and given the pattern of retinal nerve fiber layer (RNFL)/ganglion cell layer (GCL) loss, a compressive lesion was high on the differential hence an MRI brain and orbits with and without contrast was ordered. MRI revealed an eccentric left-sided suprasellar meningioma with encasement of the A1 segment of the anterior cerebral arteries as well as likely encasement of the prechiasmatic optic nerve with optic nerve atrophy. The mass appeared to be separate from the pituitary measuring 2.5 x 1.9 x 2.0 cm with a dural tail.
Methods: Sequential ocular examination and appropriate testing.
Results: Neurosurgery was consulted and given the tumor size, and proximity to critical structures, surgical resection/debulking via an orbital zygomatic approach was urgently performed. Biopsy of the lesion was confirmed by pathology to be a meningioma WHO grade 1. After resection, the patient’s visual acuity improved to seeing shadows. The patient was discharged with follow ups. 6 months post op, OS vision remained markedly compromised with now eccentric light perception vision, from an initial NLP.
Discussion: Case reports and literature review were performed.
On further review of her initial optical coherence tomography (OCT) imaging 3 years prior, early asymmetric GCL loss was noted, hence, the tumor was likely present for a long period of time, however, too small to cause substantial symptoms. The tumor compressed the A1 segment of the anterior cerebral artery, and even though it does not directly supply the optic nerve, the vessel's compression could potentially affect the microvasculature in the region. Specifically, the small pial vessels that contribute to the optic nerve's blood supply. The pathogenesis of visual impairment was likely primarily due to compression of the prechiasmatic optic nerve, where the tumor mass directly compressed the fine optic nerve fibers. This led to axonal damage, loss of retinal ganglion cells reflected by extreme RNFL thinning, and ultimately, optic nerve atrophy. This case highlights that albeit benign, meningiomas can be locally destructive hence clinicians should be alert to compressive lesions as a potential etiology for unexplained vision loss especially with corresponding changes to the RNFL, and GCL.