1. Introduction
Stroke or cerebrovascular accident is estimated to occur in approximately 150,000 people per year in the UK, and disabilities following stroke affect about 300,000 [1]. Visual field loss is reported as occurring in 8–67% [2–7] although some visual field impairment is due to a previous stroke or preexistent ocular pathology [7]. Estimates vary widely as the proportion testing positive is highly dependent on the time after stroke. Visual field loss is a loss of part of the field of vision which may occur centrally or peripherally. However, following stroke, loss of visual field is more usually peripheral in nature. The most common type of visual field loss is that of homonymous hemianopia in which there is loss of the same half of the visual field in both eyes and which occurs in approximately two-thirds of those with visual field loss [7–9]. Other types of visual field loss may include inferior and superior quadrantanopia, constricted visual fields, scotomas, and altitudinal defects [10–15].
Visual field loss following stroke has largely been attributed to cortical strokes in which the visual pathway is damaged. The intracranial course of the anterior visual pathway includes the optic nerves which pass medially from the optic canals to form the optic chiasm and are supplied by branches of blood vessels from the ophthalmic artery and pial vessels from adjacent branches of the internal carotid artery [16–19]. The optic chiasm is formed by the mergence of the two optic nerves and receives its blood supply from an anastomosis of arterioles from the Circle of Willis [20–22].
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The posterior visual pathway extends from the optic chiasm through to the visual cortex. The optic tracts sweep laterally from the optic chiasm, passing around the ventral portion of the midbrain and encircling the hypothalamus posteriorly. The optic tracts obtain their blood supply via a pial plexus which is continuous anteriorly with that of the optic chiasm and fed partly from the posterior communicating artery and branches of the middle cerebral artery but mainly from the anterior choroidal artery [23]. The lateral geniculate body is located in the diencephalon and has a dual blood supply involving the anterior choroidal artery and lateral choroidal artery [23].
The optic radiations consist of superior, inferior, and central nerve fibre bundles. The superior and central bundles pass directly posteriorly through the posterior temporal and parietal lobes. The inferior bundle initially passes anteriorly to loop into the temporal lobe before passing posteriorly through the parietal lobe. The blood supply to the optic radiations is predominantly from the posterior and middle cerebral arteries [24]. The nerve fibres of the optic radiations terminate in the visual striate cortex (V1) which is located on the medial aspect of the occipital lobe, superior and inferior to the calcarine fissure. The cortex is supplied predominantly by the posterior cerebral artery and its calcarine branch. A parieto-occipital branch supplies the superior calcarine lip, a posterior temporal branch supplies its inferior lip, and a calcarine branch supplies the central region posteriorly. The middle cerebral artery may supply the posterior aspect of the calcarine sulcus with an anastomosis between posterior and middle cerebral arteries accounting for sparing of the macula in cases of posterior cerebral artery occlusion [24, 25].
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Pambakian and Kennard [26] reported visual field loss due to occipital lobe lesion in 40%, parietal lobe in 30%, temporal lobe in 25%, and 5% with damage to optic tract and lateral geniculate nucleus. Zhang et al. [10] reported the area of stroke as occipital lobe in 54%, optic radiations in 33%, tract in 6%, lateral geniculate nucleus in 1%, and 5% with multiple pathway segment involvement. Further reports state that most stroke related visual field loss related to occipital infarct [27–29].
Homonymous hemianopia on admission is linked to poor early survival and conversely around 10% [30] experience full spontaneous recovery within the first 2 weeks. Visual field defects seriously impact on functional ability and quality of life following stroke [31]. Patients with visual field defects have an increased risk of falling, impaired ability to read, poor mood, and higher levels of institutionalisation [32–36]. Visual field loss impacts on a patient’s ability to participate in rehabilitation, may ultimately result in poor long term recovery, and can lead to loss of independence, social isolation, and depression [4].
National guidelines in the UK recommend that every patient with stroke has a practical assessment of vision and examination of visual field [37, 38] with access to appropriate therapy. Treatment for visual field loss includes restitution, substitution, and compensatory options [39]. Compensatory options, in particular, have shown favourable effects on improved visual scanning into the hemianopic side [40, 41].
Previous studies on visual field loss following stroke have provided information on type of visual field loss, treatment options, or recovery in both clinical and experimental settings. The Vision In Stroke (VIS) study is a prospective observation study aimed at capturing data on types of visual impairment following stroke and to report the profile of those visual impairments in standard care clinical environments. One objective of this study is to prospectively evaluate the prevalence of visual field loss occurring in this prospective clinical population of stroke survivors with suspected visual impairment. This paper provides a review of the visual pathway and, from the clinical population, profiles visual field loss in terms of type and extent of visual field loss, site of causative lesion, the treatment options, and outcome.
