Having sight but no vision

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The blurring of vision in MS is synonymous with optic neuritis in most instances, however visual defects also occur secondary to lesions in the brain proper. These are often silent or misconstrued as the former.

Below is a pictorial representation of potential field defects based on the area of lesion location within the visual pathways of the brain:

Visual field - Wikipedia

Little is known of the evolution of these visual defects or their occurrence. Symptomatic vision loss due to lesions after the optic chiasm, unlike lesions in the optic nerve, cause a same sided visual field loss; called a homonymous visual field defect (HVFD). And unlike optic nerve lesions they present less frequently, although paradoxically MRI and autopsy studies have have shown that these visual pathways are involved by MS lesions in 30-90% of cases. Some of this may be due to the size of the MS lesions, with only the largest ones causing a symptomatic HFVD. It is also possible that HFVD are simply under-diagnosed.

In a review of PwMS presenting to their opthalmology unit in Switzerland with HVFD, Schmutz and Borruat found that partial HFVD (4-6 in the image above) was more frequent than complete HFVD (3 in the image above), as most of the MS lesions associated with HFVD were small and located within the optic radiations, which spread over a larger area.

After their occurrence most recovered in a relatively short time (on average 9 weeks), with a third of their studied cases showing a partial recovery on follow-up. Interestingly, they can also re-occur (see Figure below).

Figure: Recurrence of a homonymous visual field defect (HVFD). Top – inaugural left homonymous inferior quadrantanopsia, which disappeared completely after three months. Middle – 2 years later, recurrence of the left homonymous inferior quadrantanopsia, which this time resolved over four months. Bottom – 4 years after the initial episode, a second HVFD recurrence occurred with a bilateral inferior homonymous quadrantanopsia. Complete recovery of the HVFD was obvious after 3.5 months. MD = mean defect expressed in decibels (dB).

Therefore, in those with atypical presentations for optic neuritis a visual field perimetry examination would be helpful in picking up visual loss caused by lesion further along the visual axis.

Abstract

Swiss Med Wkly. 2020 Sep 17;150:w20319. doi: 10.4414/smw.2020.20319. eCollection 2020 Sep 7.

Homonymous visual field defects in patients with multiple sclerosis: results of computerised perimetry and optical coherence tomography

Lydia Schmutz ,François-Xavier Borruat

Aims of the study: Visual dysfunction is frequent in multiple sclerosis, usually resulting from retrobulbar optic neuritis or papillitis. Less frequently, demyelinating lesions can affect the retrochiasmal pathways. There are few reports of homonymous visual field defects (HVFD) in multiple sclerosis and little is known about their evolution. The purpose of this study was to better define both the clinical profile and the evolution of HVFD in patients with multiple sclerosis.

Methods: We performed a retrospective study of all multiple sclerosis patients who presented HVFD and were examined by automated static perimetry. A subset of patients benefited from macular assessment with optical coherence tomography (OCT). We also reviewed the worldwide literature on the subject.

Results: Twenty patients were retrieved from the neuro-ophthalmology database of the Hôpital Ophtalmique Jules-Gonin. There were 11 women and 9 men, and their average age was 35 ± 11 years. The relapsing-remitting form of multiple sclerosis was most common (18/20; 90%), the primary progressive form (1/20; 5%) and the secondary progressive form (1/20; 5%) were rare. HVFD were the presenting symptom of multiple sclerosis in seven patients (35%). The recovery was complete in 12/20 patients (60%), and the median time to recovery was 10 weeks (2-13 weeks). An incomplete recovery was found in 5/20 subjects (25%) and no recovery occurred in 3/20 subjects (15%). Magnetic resonance imaging disclosed a definite lesion explaining the HVFD in 7/11 patients: five within the optic radiations (71.4%), one within the optic tract (14.3%) and one within the lateral geniculate nucleus (14.3%). Our results were comparable to those compiled from our literature search (29 publications, totalling 70 cases). A recurrent episode of HVFD occurred in three patients (15%). OCT was performed in 10/20 patients. Retinal ganglion cell layer thickness was assessed and revealed a homonymous thinning in three patients, diffuse unilateral or bilateral thinning (resulting from previous episodes of optic neuritis) in six patients, and normal retinal ganglion cell layer thickness in one patient.

Conclusion: HVFD in multiple sclerosis are found mostly in young patients with relapsing-remitting multiple sclerosis, which is consistent with the epidemiology of multiple sclerosis. HVFD can be the first manifestation of multiple sclerosis and have a relatively good prognosis. Like optic neuritis, HVFD can recur. The incidence of HVFD in multiple sclerosis is unknown, as it is probably underdiagnosed. Systematic automated static perimetry and OCT could help to determine the true incidence of HVFD in multiple sclerosis.

About the author

Neuro Doc Gnanapavan

1 comment

  • I had presentation 2 in 2004 and my birth mother had presentation 4 in 1985 ish. She was never diagnosed but it seems possible she had MS. These presentations were not at the beginning of MS for either of us and we were both older than the Swiss cohort. As she died soon after and I had no symptoms then I didn’t question her much about her condition as I thought she’d probably had some kind of stroke. Pity.

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