Postchiasmal Visual Field Defects in Multiple Sclerosis

To solve vision issues in patients with multiple sclerosis, you may have to look beyond the anterior and posterior segments.

By Christine Ma, BSc

A 48-year-old Hispanic woman was referred for a comprehensive eye exam. She had a primary complaint of difficulty reading in low light conditions. She was diagnosed with multiple sclerosis (MS) 15 years ago and needed a baseline eye exam before the physician treating her MS could start her on oral fingolimod (Gilenya, Novartis) for MS flare-ups. The patient’s ocular history was unremarkable, with no past optic neuritis diagnosis, surgery, or trauma.


Multiple sclerosis (MS) is an inflammatory neurodegenerative disease that causes demyelination of axons within the central nervous system. Patients with MS can present with ocular manifestations secondary to inflammation and demyelination in the visual pathway. Often, the first symptoms of MS are related to the eyes or vision. MS can be associated with optic neuritis, chronic optic neuropathy, and postchiasmal visual field defects. It can affect higher-order cortical processing and cause eye movement abnormalities, such as diplopia, nystagmus, and internuclear ophthalmoplegia. It has also been found to be associated with ocular inflammatory disease, such as uveitis.1

1. Hickman SJ, Raoof N, McLean RJ, Gottlob I. Vision and multiple sclerosis. Mult Scler Relat Disord. 2014;3(1):3-16.


The patient was correctable to 20/20 OD and OS at distance and near. Pupils were equal, round, and reactive to light, and no afferent pupillary defect was noted. Confrontation visual fields were full to finger counting in both eyes. No color deficiency was detected OD or OS, but a red cap test revealed color desaturation in the right eye compared with the left.

The patient’s blood pressure was 113/64. Slit-lamp microscopy revealed nasal pinguecula in both eyes; otherwise, the anterior segment exam was unremarkable. Intraocular pressure (IOP) measurements as measured with the Icare ic100 tonometer (Icare USA) were 10 mm Hg OD and 11 mm Hg OS. Widefield retinal images were taken with the Daytona (Optos) (Figure 1). An area of inferotemporal peripheral degeneration 1.5 x 1.5 disc diameters was noted OD only. The rest of the posterior segment evaluation was normal in both eyes.

Baseline macular optical coherence tomography (OCT) imaging showed normal presentation (Figure 2). Borderline inferior retinal nerve fiber layer (RNFL) thinning was observed OD; borderline temporal RNFL thinning was observed OS (Figure 3). The patient was determined to be safe to start the MS medication and was informed to return to clinic 1 month after initiating fingolimod.

Figure 1. Inverted widefield retinal images OD (A) and OS (B).


Eleven days later, the patient returned with a sudden onset of blur OD. The patient described it as a blurry gray spot nasal to the center of vision that did not move or change. The patient was also experiencing tenderness around the right upper eyelid. At this visit, the patient had not yet started fingolimod therapy. Pupils were equal, round, and reactive to light with no afferent pupillary defect. The red cap test was unchanged. Confrontation fields in both eyes were full to finger counting. The patient reported some pain on upgaze and left and right gaze OD only. IOP measurements were within normal range (OD 11 mm Hg, OS 13 mm Hg). Anterior segment examination was unremarkable. Posterior segment evaluation did not reveal lens or macular involvement. There was no optic disc pallor in either eye. Repeated macular and optic nerve head OCTs were stable to baseline.

Figure 2. Baseline OCT macular thickness maps (A) and horizontal B-scans (B).

Figure 3. Baseline OCT optic nerve head and retinal nerve fiber layer analysis.

The patient returned 3 weeks later for a 30-2 frequency doubling technology (FDT) perimetry threshold visual field to map out visual field loss, and it appeared that the patient has a left homonymous hemianopsia (Figure 4). On the hemispatial neglect test, the patient was asked to copy a drawing of a clock and a house. The test did not reveal neglect on either drawing. The patient was also instructed to draw a vertical line across two horizontal lines (Figure 5A). The vertical line drawn was off to the left, indicating a slight midline shift to the left (Figure 5B). The physician treating the patient’s MS was informed of the exam results, and magnetic resonance imaging (MRI) was suggested to identify the lesion. At this time, the patient had been on fingolimod therapy for a couple of weeks.

Figure 4. Baseline 30-2 FDT perimetry threshold visual field OD (A) and OS (B)


The patient underwent MRI. The physician treating her MS identified that the patient’s field loss was due to an MS flare-up, and she was placed on intravenous (IV) steroids for 3 days to relieve her symptoms. At her most recent eye care visit, 1 month after starting fingolimod therapy, macular OCT revealed no macular edema related to the drug. The patient still had residual visual field loss nasal to fixation OD and scattered shallow defects temporally OS on 30-2 FDT perimetry threshold visual field (Figure 6). Resolution of the patient’s left homonymous hemianopsia was secondary to her resolving MS episode.

Figure 5. Hemispatial neglect test (A) and midline shift (B).

Figure 6. FDT threshold visual field OD (A) and OS (B) after IV steroid treatment.


The patient’s findings were most consistent with an afferent visual pathway postchiasmal lesion, causing a left homonymous visual field defect. Postchiasmal lesions can occur at the optic tract, the lateral geniculate nucleus, or the optic radiations.1 Symptomatic homonymous hemianopic defects are rare in MS patients, occurring in 0.5% to 3.5% of cases. Asymptomatic field defects are more common.2,3 Plant et al studied 18 patients with relapsing-remitting MS and found that only large postchiasmal lesions are likely to cause symptomatic homonymous visual field defects and that the prognosis for visual field recovery after treatment is promising. Of 18 patients with homonymous visual field defects in that series, complete visual field recovery occurred in 14.4 Full resolution of visual field defects can happen as early as 2 weeks after onset.5 Although the patient in this case did not have full resolution of her homonymous hemianopsia, her visual field defects improved dramatically after 3 weeks.


Complications associated with multiple sclerosis include postchiasmal lesions, which may in turn cause homonymous visual field defect.

When MS relapses occur, high-dose IV corticosteroids can be effective. Typically, 1 g IV methylprednisolone is administered for 3 days. High doses of oral steroids have been shown to be just as effective as IV steroids for relapse episodes.6 However, patients recover on IV steroids and benefit most from IV treatment within 15 days of relapse. High-dose steroids are primarily used short term for acute MS flare-ups, whereas IV interferon beta, the most common treatment for MS, reduces relapse rates and decreases new plaque formation.

The patient in this case experienced resolution of her symptoms after being treated with IV steroids for 3 days. She continued taking fingolimod, a once-daily immunosuppressive agent used to prevent and treat relapsing-remitting MS. Macular edema is a documented ocular side effect of fingolimod. With discontinuation of treatment, complete resolution of macular edema has been confirmed on OCT.7


Although the patient’s anterior segment, posterior segment, and OCT all came out clear in this case, it provides evidence that MS can affect parts of the visual pathway beyond the eye. All patients with MS are at risk for ocular manifestations throughout the course of their disease. Therefore, it is important to know what types of tests are available to assess how MS is affecting the visual pathway. It has been reported that postchiasmal lesions are not always associated with symptoms and are often not discovered until a neuroradiologic exam or a necropsy are performed.8

For cases in which clinical manifestations are not present, visual evoked potential testing would be a valuable tool to objectively detect conduction delays of demyelination in the visual pathway. Subjective testing of visual fields may better characterize the condition if the patient experiences visual symptoms. OCT can provide an estimation of RNFL axonal damage or neuronal injury.2 OCT is an especially important tool if the patient is undergoing MS treatment that has ocular side effects. Early detection of acute attacks or relapses can prompt more rapid treatment with IV methylprednisolone to decrease symptoms and improve vision in MS patients.

1. Hickman SJ, Raoof N, McLean RJ, Gottlob I. Vision and multiple sclerosis. Mult Scler Relat Disord. 2014;3(1):3-16.

2. Kolappan M, Henderson APD, Jenkins TM, et al. Assessing structure and function of the afferent visual pathway in multiple sclerosis and associated optic neuritis. J Neurol. 2009;256(3):305-319.

3. Law SW, Lee AW, Chen CS. Multiple sclerosis presenting with homonymous hemianopia. Aust Fam Physician. 2009;38(10):795-796.

4. Plant GT, Kermode AG, Turano G, et al. Symptomatic retrochiasmal lesions in multiple sclerosis: clinical features, visual evoked potentials, and magnetic resonance imaging. Neurology. 1992;42(1):68-76.

5. Gündüz K, Cansu K, Bulduklar S, Saatçi I. Homonymous hemianopsia as the initial manifestation of multiple sclerosis. Ophthalmologica. 1998;212(3):215-220.

6. Le Page E, Veillard D, Laplaud DA, et al. Oral versus intravenous high-dose methylprednisolone for treatment of relapses in patients with multiple sclerosis (COPOUSEP): a randomised, controlled, double-blind, non-inferiority trial. Lancet. 2015;386(9997):974-981.

Christine Ma, BSc
• fourth year student, Pacific University College of Optometry, Forest Grove, Ore.
• financial disclosure: none relevant