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 [
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 [
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 [
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 [
Pambakian and Kennard [
Homonymous hemianopia on admission is linked to poor early survival and conversely around 10% [
National guidelines in the UK recommend that every patient with stroke has a practical assessment of vision and examination of visual field [
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.
The design of this study is a prospective multicentre observational case cohort study. The Vision In Stroke (VIS) group consists of local investigators from twenty UK hospital trusts who are responsible for assessing stroke patients and collecting patient data. The data is collated centrally at the University of Liverpool. The study has multicentre ethical approval via the National Research Ethics Service and is undertaken in accordance with the Tenets of Helsinki. The recruitment period for this study ran from May 2006 to April 2009 with followup to April 2010.
The target population was stroke patients suspected of having a visual difficulty. Referrals could be made from in-patient wards, rehabilitation units, community services, or out-patient clinics. Patients were given an information sheet and recruited after informed, written consent. Patients were excluded if they were unable to consent due to cognitive impairment, unwilling to consent, if their diagnosis was that of transient ischaemic attack, or if they were discharged without vision assessment.
Patients with suspected visual difficulty were identified using a screening form. Subsequently this was used as the referral form to the orthoptic service. A standardised investigation sheet was used for the eye assessment consisting of identification of known preexistent ocular pathology, symptoms and signs, investigation of visual field, ocular motility, and perceptual aspects. Visual fields were assessed qualitatively by traditional confrontation methods or quantitatively by Humphrey (Humphrey systems, Dublin, CA, USA) automated central and/or peripheral static perimetry or Goldmann/Octopus (Haag Streit Int, Switzerland) kinetic perimetry. Complete hemianopia was defined as macular splitting field loss involving all of the superior and inferior quadrants to one side of the visual field. Partial hemianopia was defined as macular sparing, incongruous, and/or partial hemifield involvement.
Visual acuity was assessed at near and distance fixation with Snellen or logMAR acuity tests. Low visual acuity was considered in two categories. The first defined low visual acuity as less than best corrected 6/12 Snellens acuity or 0.3 logMAR in accordance with UK driving standards [
Assessment of ocular alignment and motility consisted of cover test, evaluation of saccadic, smooth pursuit and vergence eye movements, retinal correspondence (Bagolini glasses), fusional vergence (20D or fusional range), stereopsis (Frisby near test), prism cover test, and lid and pupil function.
Perceptual deficits were recorded after questioning of the patient and/or carers and relatives. Inattention was assessed by means of a combination of assessments including line bisection, Albert’s test, cancellation tests, memory tests using verbal description, and drawing. Alexia was diagnosed where patients described an inability to read (despite being able to see the text) because of being unable to decipher the words or their meaning or being unable to make sense of the text.
Quality of life was undertaken using the Activities of Daily Living Dependent on Vision (ADLDV) questionnaire [
Stroke details were recorded from patient notes accounting for stroke laterality, type, and area involved. Ocular treatment details were recorded along with outcome. Reasons for nonattendance at review appointments included death, a move out of area, lost to followup, followup unwanted, or unknown.
Results were inputted to the statistical package SPSS version 19 (IBM SPSS Statistics, USA). Pearson chi squared test (
1345 patients were referred for visual assessment for this study. 915 patients were recruited, and 430 patients were excluded, the latter mainly due to inability to provide informed, written consent as required of the ethical approval for this study (Table
Reasons for exclusion.
Unable to consent | Discharged without assessment | Transient ischaemic attack | Unwilling to consent | Not available for assessment | Died | Other pathology | Failed to attend assessment | No reason provided |
---|---|---|---|---|---|---|---|---|
225 | 52 | 44 | 34 | 28 | 26 | 10 | 4 | 7 |
Frequency indicates the numbers of patients with age of onset of stroke.
Median duration from onset of stroke to initial baseline eye examination was 22 days (0–2543 days), the mean of 40.84 (SD 141.28) days being skewed by three outliers who were referred a number of years after the stroke onset. Stroke lesion was right sided in 448 patients (49%, i.e., right-sided brain), left sided in 348 (38%), and bilateral in 119 (13%). Infarcts accounted for 773 cases (84.5%) with the remainder due to haemorrhage.
Ethical approval allowed the documentation of visual diagnosis (if available) for excluded patients but not the documentation of full visual data. Of 430 excluded patients, 336 had outline visual data. Of these, 164 (48.8%) had visual field loss recorded and mainly of homonymous hemianopia type. 479 (52.3%) of 915 recruited patients had visual field loss. Thus, 51.4% of all patients referred to the VIS study (both recruited and nonrecruited patients) had visual field loss.
404 (84%) of the 479 recruited patients with visual field impairment complained of the symptom of visual field loss. Fifty-one patients (10.6% of 479 patients) had no visual symptoms. Visual field loss was the sole visual symptom in 226 patients (47.2%). 202 patients (42.2%) complained of additional visual symptoms including reading difficulty, blurred vision, diplopia, and visual perceptual abnormalities (hallucinations, spatial difficulties, impaired colour vision, and alexia) (Figure
Visual symptoms.
Assessment of visual field loss was by confrontation methods in 63% (
The most common type of visual field loss was found to be complete (
Types of visual field loss.
Type | Number (total: 479) | Percentage |
---|---|---|
Complete homonymous hemianopia | 259 | 54.5 |
Partial homonymous hemianopia | 79 | 16.6 |
Constriction | 44 | 9.3 |
Inferior quadrantanopia | 40 | 8.4 |
Superior quadrantanopia | 30 | 6.4 |
Hemianopia and contraquadrantanopia | 6 | 1.2 |
Scotoma | 5 | 1.0 |
Chequerboard | 3 | 0.6 |
Altitudinal | 3 | 0.6 |
Complete unilateral blindness | 2 | 0.4 |
Binasal hemianopia | 1 | 0.2 |
Bilateral homonymous hemianopia | 1 | 0.2 |
Temporal crescent | 1 | 0.2 |
Ocular pathology was noted in 17 patients (3.5%) with visual field loss including glaucoma (
The area of brain involved by the stroke and producing visual field loss was most commonly the occipital and/or parietal lobes (
Area affected by stroke lesion.
Area of brain (combined single and multiple sites of lesion) | Number (total: 1001) | Percentage |
---|---|---|
Occipital lobe | 225 | 22.5 |
Parietal lobe | 165 | 16.5 |
Middle cerebral artery | 81 | 8.1 |
Cerebellum | 79 | 7.9 |
Frontal lobe | 74 | 7.4 |
Brainstem | 69 | 6.9 |
Temporal lobe | 62 | 6.2 |
Thalamus | 58 | 5.8 |
Basal ganglia | 56 | 5.6 |
Lacunar | 35 | 3.5 |
Internal capsule | 29 | 2.9 |
Posterior cerebral artery | 21 | 2.1 |
Anterior circulation infarct | 16 | 1.6 |
Periventricular | 14 | 1.4 |
Intraventricular | 7 | 0.7 |
External capsule | 5 | 0.5 |
Anterior cerebral artery | 4 | 0.4 |
Posterior inferior cerebellar artery | 1 | 0.1 |
The types of visual field loss were compared for area of stroke lesion (Table
Area of brain stroke and recorded type of visual field loss.
Homonymous hemianopia | Homonymous quadrantanopia | Constricted loss | Scotoma | Altitudinal | Bilateral loss | Temporal crescent loss | |
---|---|---|---|---|---|---|---|
Frontal lobe | 5 | 2 | 1 | ||||
Parietal lobe | 20 | 6 | 6 | ||||
Temporal lobe | 1 | ||||||
Occipital lobe | 78 | 1 | 23 | 2 | 1 | 2 | |
Brainstem | 4 | 3 | |||||
Cerebellum | 4 | 2 | 2 | ||||
Basal ganglia | 7 | 2 | |||||
Thalamus | 2 | 1 | 2 | ||||
Internal capsule | 6 | ||||||
Periventricular | 4 | ||||||
Intraventricular | 3 | 1 | |||||
Lacunar | 4 | 2 | 1 | ||||
Anterior cerebral artery | 2 | 1 | |||||
Middle cerebral artery | 28 | 6 | 2 | ||||
Posterior cerebral artery | 15 | 4 | 1 | ||||
Anterior circulation infarct | 2 | 2 | 1 | ||||
Multiple brain areas | 158 | 18 | 16 | 2 | 2 | 5 | 1 |
151 patients (31%) had visual field loss as their sole visual impairment. In addition to a diagnosis of visual field loss, 328 patients had additional visual impairments. 28.6% (
Treatment was provided for 474 patients. No options for restitution treatment were provided. Compensatory options largely constituted advice on adaptive strategies using visual search exercises and visual field awareness for 250 patients (52.7%) or typoscopes (
Visual rehabilitation.
Treatment options | ||||||||
---|---|---|---|---|---|---|---|---|
Refraction | Peli prisms | Diplopia prisms | Occlusion | Low visual aids | Typoscope | Orthoptic exercises | Advice | |
Sole treatment option ( |
22 | 5 | 3 | 5 | 2 | 0 | 0 | 250 |
Multiple treatment option ( |
63 | 24 | 10 | 2 | 18 | 42 | 8 | 224 |
Advice consisted of raising awareness of visual field loss, reading strategies, scanning eye and head movements, use of lighting, compensatory head posture, and registration for visual impairment.
Following baseline assessment and diagnosis of visual field loss, 64 patients were discharged from eye care services. 56 patients were referred to other eye care services, and 359 were offered review appointments. Table
Outcome of visual field loss after followup.
Fifteen patients (7.5%) had a full recovery of field loss. 78 patients (39.2%) showed partial improvement of visual field, and two patients (1%) showed further loss of visual field. 104 patients had stable, unchanged visual field loss (52.3%). There was no identifiable factor found to be associated with those patients achieving full restoration of their visual field, partial restoration, or no improvement regardless of their age at stroke onset (
ADLDV responses were obtained from 63 patients with visual field loss at their first appointment. The overall mean score was 65.69 (SD 18.07), compared to a possible maximum score of 88. For those patients with visual field loss as their only visual difficulty, their mean score was 69.43 (SD 18.89). For those patients with visual field loss plus additional visual impairments, the mean score was 63.55 (SD 17.47). Despite a slightly lower mean score for those with combined visual impairments, there was no significant difference (
Quality of life measured with Activity of Daily Living Dependent on Vision questionnaire (maximum score of 88 indicating no impact).
Using a multiple linear regression model we analysed the relationship between the initial quality of life score and predictor variables of age at stroke onset, length of time from stroke onset to time of first eye examination, laterality, and type of stroke plus visual diagnosis. We obtained an overall
Visual field loss is reported in the acute period following stroke in 45–67% of patients [
A greater number of our patients had left-sided visual field loss. A slightly greater preponderance for left-sided visual field loss has also been reported in one previous large cohort study [
Most of our patients (
Notably, 51 patients (10%) did not complain of any visual field loss and seemed unaware or unaffected by this deficit in their daily lives. Previous reports have also identified that a number of patients are unaware of their visual field loss but who also continue to drive. Thus there is an impact to driving and road safety [
The brain imaging reports for our patients depicted either the area of stroke lesion, for example, occipital lobe, or the artery affected, for example, middle cerebral artery infarct. We noted multiple areas of the brain affected by stroke lesions in which visual field loss was documented. Typically we found cortical strokes were associated with visual field loss and particularly occipital, temporal, and parietal lobes plus middle and posterior cerebral artery infarcts. Unexpectedly, we also noted some stroke lesions to be reported in brainstem and cerebellar areas which are not associated with the visual pathway. In these cases, where previous stroke-related visual field loss was excluded, it has been assumed that the visual pathway was affected by an extension of the stroke that was not documented in the imaging report.
When considering the type of field loss and location of stroke lesion, homonymous hemianopia was more prevalent in occipital lobe and middle or posterior cerebral artery strokes. Quadrantic defects were more prevalent in occipital, parietal, and temporal lobe strokes. Homonymous scotomas, altitudinal defects, and temporal crescent defects were associated with occipital lobe strokes. Thus, we recommend that postchiasmatic visual field loss should be screened for in patients with strokes affecting occipital, parietal, and temporal lobes or middle and posterior circulation strokes. It is equally important to remember that anterior circulation strokes may also impact on the visual pathway causing homonymous defects but also unilateral visual field defects with retinal stroke or optic nerve damage.
There are three main approaches to visual rehabilitation: substitution, adaptation, or restitution [
The profile of visual rehabilitation offered to our patients was largely dependent on the individual needs of these patients, regardless of age or presence of cognitive or communication problems. Compensatory options aim to adapt for the visual field loss by altering the patient’s behaviour or their activity through exercises, training, and cues. In our study, treatment most frequently consisted of advice on adaptive visual search strategies. This encompassed improving awareness of the visual field loss and employing visual search strategies to promote the individual’s ability to scan to the impaired side by increasing head movements and fast eye movements [
Substitutive treatment options utilise devices or modifications to change the visual field such as prisms, eye patches, and magnifiers. Treatment with prisms involves expanding the visual field in lateral gaze [
Visual fields can recover spontaneously following damage to the geniculostriate pathway after cerebral infarction [
The problems specifically caused by hemianopia include hemianopic reading deficits [
Hemianopic alexia results from loss of parafoveal field area which cuts the perceptual window for reading [
Visual search problems include numerous hypometric saccades and frequent repetitions in to the hemianopic side [
The presence of persistent, complete homonymous hemianopia is reported as being associated with a poor prognosis for rehabilitation and survival [
It is not uncommon for stroke survivors to have coexistent visual inattention/neglect in association with their visual field loss particularly in right-sided hemisphere stroke lesions [
Quality of life data was gathered in 63 of our patients with visual field loss. The ADLDV questionnaire was utilised which specifically measures vision-related activities of daily living for visual recognition and ability to “see and do,” impact on mobility plus near vision activities such as reading and sorting money. Our patients with a normal visual status at baseline assessment had a mean ADLDV score of 81.6 : 88 is the maximum normal score. For those with solely visual field loss, the mean score was 69.43, and for those with other associated visual impairments, the mean score was 63.55. There was no significant difference for having a sole or multiple visual impairments, but there was considerable variability and overlap of scores between groups. Multiple regression analysis did not reveal any correlation for key variables such as gender, age at onset of stroke, the length of time from stroke onset to time of first eye examination, the visual diagnosis or laterality, and type of stroke. Confidence intervals for these variables contained the zero value, and thus it is possible for the correlation to be zero. It is however recognised that there are many other variables that may affect quality of life scores that are also independent of vision. Reduction in scores was across all levels of visual recognition, mobility, and near vision tasks. It is important to maximise compensation to visual field loss to enhance visual function and related activities of daily living. The knowledge that visual field loss significantly impacts on quality of life should underpin the requirement for appropriate screening and diagnosis of visual field loss and associated visual impairments following stroke.
There are a number of limitations to this study. The VIS study only includes those patients referred with suspected visual impairment and therefore is not representative of a full stroke patient cohort. Given that a number of our patients were asymptomatic it is possible that referrals were not made for other visually asymptomatic patients. The area of stroke lesion was based on the neuroimaging reports available at the time of recruitment for our patients. These documented either the main stroke lesion area or the artery affected. Therefore we may have missed documenting other areas affected by the stroke that were not specified on the scan report. For some of our patients with visual field loss but with imaging reports stating the site of stroke lesion in the cerebellum or brainstem, we have assumed a nonreported extension of the stroke to nearby areas in which the visual pathway may have been damaged.
Two-thirds of our assessments at baseline were by confrontation technique which we believe is reliable for detecting homonymous hemianopia and large defects but less reliable for smaller visual field defects. It is possible that the latter types of visual field loss were not detected. We were unable to obtain followup on all patients offered review appointments. This was due to patient death, moving out of area, loss to followup, or patient choice not to attend followup. As a pragmatic study, we chose to describe the outcomes of the patients who did attend followup, as data on 199 cases was felt of sufficient number to report on. However, there was variable followup of these patients from 2 weeks to 3 months, and thus it was not possible to plot consistent trajectories of visual field change over time. Furthermore there was insufficient data to enable us to plot percentage of recovery rates reliably over time. Such information would be useful in future longitudinal studies of visual fields.
Only 63 of our patients completed quality of life questionnaires which is a very small percentage of those with visual field loss. Completion of the ADLDV questionnaire was not a mandatory assessment in our study, and given that this was an unfunded study with limited clinical resources, the questionnaire was only completed if clinicians had sufficient time to do so. The low number undoubtedly limited the extent to which we could evaluate differences between groups for absence of visual field loss versus visual field loss only or visual field loss with other visual impairments. Future prospective studies and trials reporting outcomes for stroke patients with visual field loss should aim to incorporate quality of life and activity of daily living assessments as important outcome measures.
To our knowledge, this is the first large prospective cohort observation study of visual field loss in stroke survivors in the UK. 52% of our cohort had visual field loss, and 47% had visual field loss due to their recent stroke once preexisting visual field loss was accounted for. Most patients were aware of their visual field loss. However 10% were asymptomatic which may have implications to activities of daily living such as driving. Other symptoms attributed to coexistent visual impairment included diplopia and blurred vision. Visual symptoms relating to visual field loss included hallucinations and spatial awareness difficulties. Three-quarters had homonymous hemianopia. The area of stroke largely related to the type of visual field defects. Specifically, occipital, temporal, and parietal lobe strokes and middle and posterior cerebral artery strokes were linked to hemianopia, quadrantanopia, altitudinal, temporal crescent, and homonymous scotoma defects. Visual rehabilitation consisted of compensatory or substitutive options. Full resolution of visual field loss occurred for 8% of patients, partial improvement for 39%, and no recovery for 52%. Many patients had other visual impairments in addition to visual field loss. Regardless of this, vision-related activities of daily living were reduced in comparison to stroke survivors without visual impairment.
We recommend careful visual screening of stroke survivors to accurately diagnose presence of visual field loss and any other visual impairments so that prompt treatment can be instigated to maximise visual function and outcomes for these patients.
The authors have no conflict of interests.
The authors acknowledge Alison Price, Birmingham: Sandwell and West Birmingham NHS Trust; Linda Walker, Burnley: East Lancashire Hospitals NHS Trust; Carla Eccleston, Derby: Derby Hospitals NHS Trust; Leonie Robson, Lincoln: United Lincolnshire Hospitals NHS Trust; Sue Yarde, Taunton: Taunton and Somerset NHS Trust.