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Table of Contents
CASE REPORT
Year : 2022  |  Volume : 4  |  Issue : 1  |  Page : 46

“Sudden” visual loss caused by a transitional meningioma in a young female


1 Department of Ophthalmology, Penido Burnier Institute, Campinas, Brazil
2 Department of General Medicine, Ribeirão Preto University, Ribeirão Preto, São Paulo, Brazil

Date of Submission14-Aug-2022
Date of Acceptance23-Aug-2022
Date of Web Publication22-Sep-2022

Correspondence Address:
Gabriel Peres De Vitto
Jorge Krug Street, 162, Apartment 71, Campinas
Brazil
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/pajo.pajo_42_22

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  Abstract 


Intracranial tumors are known to have a broad clinical spectrum. Meningiomas are the second-most common benign tumors, usually affecting women in their sixth or seventh decade of life. The World Health Organization (WHO) classified them into three grades, and Grade 1 meningiomas are considered benign neoplasias. Despite being benign, they are usually located in noble areas of the brain, most frequently in the parasagittal area, followed by the falx, the sinus cavernosus, tuberculum sellae (5%–10%), lamina cribrosa, foramen magnum, and torcular zones, and are important causes of sequelae to the patient. We herein present the case of a young patient who experienced overnight visual loss. Literature shows that several factors are related to visual recovery, which is divided into phases and occurs in approximately 23%–80% of the cases. For the WHO grade 1 tumors, the standard treatment is complete excision of the mass, and it is possible to supplement treatment with stereotactic radiotherapy in atypical, malignant, or recurrent meningioma.

Keywords: Epidemiology, intracranial meningioma, subtype, visual loss, World Health Organization grade I meningiomas


How to cite this article:
De Vitto GP, Nogueira Costa MA, Abreu EB, De Vitto MP. “Sudden” visual loss caused by a transitional meningioma in a young female. Pan Am J Ophthalmol 2022;4:46

How to cite this URL:
De Vitto GP, Nogueira Costa MA, Abreu EB, De Vitto MP. “Sudden” visual loss caused by a transitional meningioma in a young female. Pan Am J Ophthalmol [serial online] 2022 [cited 2023 May 28];4:46. Available from: https://www.thepajo.org/text.asp?2022/4/1/46/356713




  Introduction Top


Meningiomas are one of the most common benign primary intracranial tumors, representing between 13% and 26% of all intracranial tumors.[1] They stem from Arachnoid cap cells, a subgroup of arachnoid cells, that are highly metabolic.[1] They commonly affect women around their sixth or seventh decade of life, with a female: male ratio of 3:2–2:1.[1] There are a few known risk factors described in literature such as deletion in the NF2 gene related to neurofibromatosis type 2, ionizing radiation used for the treatment of tinea capitis of the scalp, or cranial radiotherapy, and the presence of progesterone receptors, which explains the prevalence in the female population.[1]

The World Health Organization (WHO) created a histological classification for meningiomas, and WHO grade 1 meningiomas are the most common ones.[2],[3],[4] Notwithstanding the fact that they are considered benign tumors, the WHO grade 1 meningiomas have been reported as the cause of severe and extensive neurological deficits.[2],[3],[4] Grade 1 tumors can be divided into nine different subtypes.[2],[3],[4] A study, which assessed 83,000 cases of meningiomas in the United States between 2004 and 2015, found that 78,000 of them were WHO grade I, and only 2000 (2.7%) were the transitional subtype.[2],[3],[4]


  Case Report Top


A 26-year-old female presented on April 7, 2022, complaining of sudden visual loss of the left eye (LE). Additional to the visual loss, the patient was referred to a 1-year evolution of intense headache crises, including one at the night she lost her vision.

Ophthalmologic showed a Snellen best-corrected visual acuity (BCVA) of 20/20 in the right eye (RE) and hand movement in the LE. Slit-lamp examination revealed clear conjunctiva, transparent cornea, phakic, and the absence of anterior chamber reaction in both eyes (OU). Fundus examination of the RE revealed physiologic cupping and preserved macular brightness, arterioles, and venules with normal color, sheen, and course. In the LE 2-3+/4 + optic nerve pallor, preserved macular brightness, arterioles, and venules with normal color, sheen, and course [Figure 1].
Figure 1: Fundus picture of RE and LE, showing the discrepancy of disc color with a pallor disc in the LE. RE: Right eye LE: Left eye

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Optical coherence tomography (OCT) of the macula and optic disc region, angiography, retinography, and magnetic resonance imaging [Figure 2] were performed.
Figure 2: Magnetic resonance imaging of the brain showing a lesion in the anterior clinoid area

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LE OCT showed a macula with normal anatomy, and an optic disc with important loss of retinal nerve fiber layer (RNFL), increased cup/disc area ratio, and important loss of ganglion cell layer. RE showed no alterations in both macular and optic disc OCT. Angiography in OU had no alterations.

The patient was sent to a neurosurgeon for evaluation, and underwent a neurosurgical procedure on May 18, 2022, in which a 2-cm dimension anatomy specimen was sent for histopathological analysis. The result of the histopathological analysis was compatible with transitional meningioma.

Her last ophthalmologic evaluation took place on July 28, 2022, and her visual acuity and her clinical examination were unaltered. The chosen conduct was to repeat the retinography and perform a visual perimetry evaluation, so these exams could be used as a comparison parameter in the follow-up consultations.


  Discussion Top


Meningiomas are known to be slow-growing tumors, frequently not associated with any symptoms, and are important causes of incidental findings in imaging.[1] They have a broad clinical spectrum that varies depending on the location of the tumor, and the tuberculum sellae represents 5%–10% of the possible locations.[1]

Clinical findings of headaches due to increased intracranial pressure, focal neurological deficits, or seizures are possible to be found.[2] Other symptoms such as visual loss, hearing loss, personality changes, confusion, and altered level of consciousness can be seen.[2]

As it is a slow-growing tumor, visual findings can be perceived later and appear as a complaint of a sudden loss of vision, but it is known that as the disease progresses, parts of the visual field are lost.[5],[6],[7]

The optical chiasm is a noble structure for visual physiology, its primary function is to allow registration of each hemifield on the contralateral visual cortex allowing binocular vision.[5] It is located in the suprasellar region and has important anatomical relationships with the third ventricle, forming part of its anterior floor, and also has relationships with the anterior communicating, and anterior cerebral arteries, hence, it is vulnerable to compression by several types of lesions, being the pituitary adenomas the most frequent ones.[5]

Visual loss secondary to chiasm compression is due to ischemic injury, conduction block, demyelination, and retrograde and anterograde degeneration.[5] The pattern of the visual field impairment relies on the portion of the optic tract that is being compressed, bitemporal vertical hemianopia is pathognomonic to chiasmal compression, and if the compression is in the cranial portion of the optic nerve, unilateral defects can be found.[5]

Visual recovery after surgery can range from no improvement to complete recovery.[5],[6],[7] Studies have shown that the best improvement in mean deviation was seen within one to 4 months postoperatively.[5],[6],[7] A few predictive factors for visual recovery following chiasmal decompression are known, such as duration of symptoms, preoperative mean deviation, RNFL thickness before surgery, visual evoked potential abnormalities, and electroretinography abnormalities.[5],[6],[7] However, evaluating and studying all of them is still a challenge.[5],[6],[7] Experts classify the recovery of visual impairment into three stages, the early postoperative phase, in which conduction begins to return; the intermediate phase, in which axons undergo remyelination and restoration of intracellular infrastructures; and the late phase, in which the neural network undergoes reorganization and collateral sprouting.[5],[6],[7]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal her identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Marosi C, Hassler M, Roessler K, Reni M, Sant M, Mazza E, et al. Meningioma. Crit Rev Oncol Hematol 2008;67:153-71.  Back to cited text no. 1
    
2.
Buerki RA, Horbinski CM, Kruser T, Horowitz PM, James CD, Lukas RV. An overview of meningiomas. Future Oncol 2018;14:2161-77.  Back to cited text no. 2
    
3.
Zhang T, Yu JM, Wang YQ, Yin DD, Fang LJ. WHO grade I meningioma subtypes: MRI features and pathological analysis. Life Sci 2018;213:50-6.  Back to cited text no. 3
    
4.
Lin DD, Lin JL, Deng XY, Li W, Li DD, Yin B, et al. Trends in intracranial meningioma incidence in the United States, 2004-2015. Cancer Med 2019;8:6458-67.  Back to cited text no. 4
    
5.
Danesh-Meyer HV, Yoon JJ, Lawlor M, Savino PJ. Visual loss and recovery in chiasmal compression. Prog Retin Eye Res 2019;73:100765.  Back to cited text no. 5
    
6.
Kerrison JB, Lynn MJ, Baer CA, Newman SA, Biousse V, Newman NJ. Stages of improvement in visual fields after pituitary tumor resection. Am J Ophthalmol 2000;130:813-20.  Back to cited text no. 6
    
7.
Pinzi V, Caldiera V, Schembri L, Cerniauskaite M, Fariselli L. Spontaneous resolution of visual loss due to optic pathway meningioma: A case report and a review of the literature. Brain Inj 2016;30:225-9.  Back to cited text no. 7
    


    Figures

  [Figure 1], [Figure 2]



 

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