Stroke

Stroke is the second leading cause of death worldwide and an important cause of disability in adulthood². Strokes can lead to decreased visual acuity, visual field loss, ocular motility abnormalities, and visuospatial perception deficits.^1,3

Up to 70% of patients develop acutely decreased visual acuity after a stroke¹. The reported percentage of patients with visual field loss after a stroke varies widely, ranging from 45 to 92% acutely and 8–25% chronically¹. In these, 50% arose from occipital stroke, 30% from parietal, 25% from temporal, and 5% from damage to the optic tract and/or lateral geniculate nucleus². The reported prevalence of ocular motility dysfunction after stroke ranges from 22 to 70%¹. Ocular motility dysfunction includes strabismus, gaze palsy, nystagmus, and vergence deficits. 

A prospective multicentre cohort study reported that 52% of patients with stroke had visual field loss, 47% had visual field loss as the sole visual symptom, and only 10% had no visual symptoms⁴. The type of strokes that most commonly caused visual field loss were occipital and parietal lobe strokes⁴. Homonymous hemianopia is the most reported form of visual field loss following stroke^3,4. In fact, in some types of stroke, vision loss can be the only presenting symptom. For example, Lauda et al performed a retrospective study and concluded that acute brain infarction occurred in 23% of 213 patients with branch/central retinal artery occlusions and vision loss was the only presenting symptom in 90% of these patients⁵. 

Ischaemia is the causative factor in 93.3% of transient ischaemic attack patients presenting with transient monocular vision loss³. Transient monocular visual loss or amaurosis fugax is an acute episode of ischemic origin in which one eye has profound visual loss, followed by full recovery within one hour⁶. Transient monocular visual loss most often occurs in the setting of retinal ischemia secondary to carotid embolism, and thus, it is considered a transient ischemic attack originating in the carotid arteries⁶. Transient visual loss due to retinal ischemia has an incidence of 14 per 100000 people per year⁷. It increases the risk of subsequent vascular events (strokes and myocardial infarction) within the first week⁷. This stroke rate remains high at 13% (10 times higher than the general population) for 3.5 years post retinal ischemia⁷. 

Besides transiently, retinal ischaemia can also occur permanently due to branch retinal artery occlusion (BRAO), central retinal artery occlusion (CRAO), or rarely ophthalmic artery occlusion^3,10,3,8. Over 75% of patients with central retinal artery occlusion (CRAO) experience associated decreased visual acuity³ and 30% of patients with CRAO present an acute cerebral ischaemia⁹. 

Stroke may affect the efferent visual system, i.e eye movements and pupils. Forms of visual impairment due to lesions external to the visual pathway include ptosis, diplopia, internuclear ophthalmoplegia, one-and-a-half syndrome, gaze palsies, saccadic intrusions, impaired smooth pursuits, and nystagmus³. 

Stroke in the brainstem and cerebellum, for example, may present with distinct neuro-ophthalmic  characteristics³. Acute onset of cerebellar vertigo and dizziness could be associated with cerebellar stroke¹¹. A stroke in the posterior inferior cerebellar artery (PICA) is characterized by several clinical findings related to nystagmus and central ocular motor signs¹¹. Anterior inferior cerebellar artery (AICA) stroke can manifest as at least eight different types, most often with a combined impairment of vestibular and audiological functions¹¹. Superior cerebellar artery (SCA) infarctions are associated with vertigo in about 50 % of patients, and in 25 % there is a spontaneous nystagmus to the side of the lesion¹¹. The key to the diagnosis is a careful neuro-ophthalmological and neuro-otological examination to look for cerebellar ocular motor signs, including nystagmus and ocular tilt reaction¹¹.

1. Ghannam ASB, Subramanian PS. Neuro-ophthalmic manifestations of cerebrovascular accidents. Curr Opin Ophthalmol. 2017;28(6):564-572. doi:10.1097/ICU.0000000000000414
   
   

2. World Health Organization - www.who.int/news-room/fact-sheets/detail/the-top-10-causes-of-death

3. Pula JH, Yuen CA. Eyes and stroke: the visual aspects of cerebrovascular disease. Stroke Vasc Neurol. 2017;2(4):210-220. doi:10.1136/svn-2017-000079
   
   
4. Rowe FJ, Wright D, Brand D, et al. A prospective profile of visual field loss following stroke: prevalence, type, rehabilitation, and outcome. BioMed Res Int. 2013;2013:719096. doi:10.1155/2013/719096
   
   
5. Lauda F, Neugebauer H, Reiber L, Jüttler E. Acute Silent Brain Infarction in Monocular Visual Loss of Ischemic Origin. Cerebrovasc Dis. 2015;40(3-4):151-156. doi:10.1159/000437274
   
   
6. Bidot S, Biotti D. Transient monocular blindness: Vascular causes and differential diagnoses. J Fr Ophtalmol. 2018;41(4):e129-e136. doi:10.1016/j.jfo.2017.12.002
   
   
7. Chen CS, Varma D, Lee A. Arterial Occlusions to the Eye: From Retinal Emboli to Ocular Ischemic Syndrome. Asia-Pac J Ophthalmol Phila Pa. 2020;9(4):349-357. doi:10.1097/APO.0000000000000287
   
   
8. Biousse V, Nahab F, Newman NJ. Management of Acute Retinal Ischemia: Follow the Guidelines! Ophthalmology. 2018;125(10):1597-1607. doi:10.1016/j.ophtha.2018.03.054
   
   
9. Fallico M, Lotery AJ, Longo A, et al. Risk of acute stroke in patients with retinal artery occlusion: a systematic review and meta-analysis. Eye Lond Engl. 2020;34(4):683-689. doi:10.1038/s41433-019-0576-y
   
   
10. Fiester P, Baig SA, Patel J, Rao D. An Anatomic, Imaging, and Clinical Review of the Medial Longitudinal Fasciculus. J Clin Imaging Sci. 2020;10:83. doi:10.25259/JCIS_49_2020
    
    
11. Bodranghien F, Bastian A, Casali C, et al. Consensus Paper: Revisiting the Symptoms and Signs of Cerebellar Syndrome. Cerebellum Lond Engl. 2016;15(3):369-391. doi:10.1007/s12311-015-0687-3