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Neuro-ophthalmic Manifestations of Cerebrovascular Accidents

Info: 8542 words (34 pages) Dissertation
Published: 10th Dec 2019

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Tagged: PhysiologyNeurology

Purpose of review

Ocular functions can be affected in almost any type of cerebrovascular accident (CVA) creating a burden on the patient and family and limiting functionality. The present review summarizes the different ocular outcomes after stroke, divided into three categories: vision, ocular motility, and visual perception. We also discuss interventions that have been proposed to help restore vision and perception after CVA.

Recent findings

Interventions that might help expand or compensate for visual field loss and visuospatial neglect include explorative saccade training, prisms, visual restoration therapy (VRT), and transcranial direct current stimulation (tDCS). VRT makes use of neuroplasticity, which has shown efficacy in animal models but remains controversial in human studies.


CVAs can lead to decreased visual acuity, visual field loss, ocular motility abnormalities, and visuospatial perception deficits. Although ocular motility problems can be corrected with surgery, vision, and perception deficits are more difficult to overcome. Interventions to restore or compensate for visual field deficits are controversial despite theoretical underpinnings, animal model evidence, and case reports of their efficacies.


homonymous hemianopia, ocular motor dysfunction, stroke, visual rehabilitation, visual restoration therapy


Cerebrovascular accidents (CVAs) occur from decreased cerebral perfusion that results in neuronal death. According to the American Stroke Association, there are three types of strokes: ischemic, hemorrhagic, and transient. Ischemic strokes constitute 85% of all CVAs and can be thrombotic, with blood clots forming locally in the artery, or embolic, where one or more blood clots formed elsewhere, either in the heart, aorta, carotid arteries, or in the venous system with arterial crossover (paradoxical strokes). Ischemic strokes can also happen without clot formations in cases of cerebral hypoperfusion because of systemic shock. Hemorrhagic stroke may be caused by intraparenchymal or subarachnoid hemorrhage, whereas transient ischemic attacks (TIAs) are transient episodes of neurologic dysfunction, regardless of duration, caused by focal brain ischemia without acute infarction [1,2].

Whatever the cause of the stroke, consequences can vary from minor transient focal neurological deficits to permanent damage or even death. Any part of the body can be affected by stroke, and the eyes are no exception. In fact, the majority of CVAs


have ocular manifestations whether they involve the afferent pathways (vision), efferent pathway (eye movements), or both [3–7].

The present article aims at reviewing all the ocular manifestations that can happen after a CVA with a focus on new interventional methods thataim atrestoring visionand ocularfunction after CVAs (Table 1).


Clinically up to 70% of patients will develop acutely decreased visual acuity after a stroke [8–14], and this vision loss can be multifactorial. Siong [15] found

a b

Department of Ophthalmology, Department of Neurology and


Department of Neurosurgery, University of Colorado School of Medicine, Aurora, Colorado, USA

Correspondence to Prem S. Subramanian, MD, PhD, Professor of Ophthalmology, Neurology, and Neurosurgery, 1675 Aurora Ct, Mail Stop F731, Aurora, CO 80045, USA. Tel: +1 720 848 2500; fax: +1 720 848 5014; e-mail: Prem.subramanian@ucdenver.edu

Curr Opin Ophthalmol 2017, 28:564–572 DOI:10.1097/ICU.0000000000000414

The majority of patients with cerebrovascular accident (stroke) have visual dysfunction.

Injury to the visual system from stroke causes decreased quality of life.

Recovery of function often occurs but is variable, and no standard therapeutic interventions exist.

Restoring neurological function, rather than compensating for lost ability, may be possible but will likely require multimodal therapy and extended training for patients.

15% of 113 Hong Kong Chinese stroke patients had visual acuity less than 0.5log MAR and noted unilateral visual field defects in 26.5% of patients and bilateral defects in 11%. In a broad review of visual impairment after stroke, 75% of patients were noted to have normal vision, whereas 18.9% had difficulty watching television or reading, 1.2% were not able to read or watch television at all, and 0.6% were almost blind [7]. Although a large prospective UK study found reading problems in 177/915 (19.3%) of patients, only a minority had decreased acuity as the cause [16].

Factors that contribute to decreased vision include reduced contrast sensitivity (reported in up to 60% of patients after strokes affecting the parietal, temporal and occipital cortices [17,18]), perception defects, convergence insufficiency, visual field defects, reduced stereopsis, and dry eye from poor blinking or facial nerve palsies. Three studies have noted that the ‘drop’ in vision in many patients was related to dirty, lost, or broken glasses [9–11]. Decreased visual acuity because of cortical blindness from bilateral occipital lobe infarcts is rare [7].

Littleisreportedontherecoveryofcentralvision following stroke. Rowe [16] showed that 43% of stroke patients had partial improvement in reading abilities while 11% had complete recovery.


The reported percentage of patients with visual field loss after a stroke varies widely, ranging from 45 to 92% acutely and 8–25% chronically [9,19–28]. In localizing the visual field defects, Pambakian and Kennard reported 50% arose from occipital stroke, 30%fromparietal,25%fromtemporal,and5%from damage to the optic tract and/or lateral geniculate nucleus[29].Zhangetal.reportedsimilarfindingsin a cohort of over 850 patients [30]. Several smaller studies have demonstrated that up to 57% of stroke patients have persistent visual field defects, with contralateral homonymous hemianopsias and quadrantinopsias being most common [21–27].

In 2013, Rowe reported the results of a prospective study involving 915 patients throughout the United Kingdom to look at the visual outcome of patients with stroke (VIS study). Visual field loss was the sole visual symptom in 47.2% of the patients. The most common type of visual field loss was complete or partial homonymous hemianopia in 57 and 19.5%, respectively, followed by homonymous quadrantanopia, constricted visual fields scotomas, cortical blindness, and temporal crescent defect [9]. In an analysis of an acute stroke database of 11 900 patients, Ali et al. found 60.5% of patients had acute visual impairment. Complete recovery occurred in 42.6 and 45.0% patients by 30 and 90 days, respectively. Only 5.8% (693 patients) were judged to have had a preexisting visual problem [28]. A major limitation of this study is the precise nature of the visual deficit was not known and could include visual field loss and other problems.

Determining the prevalence of visual field loss can be difficult and is most likely underestimated becausemanypatientswhodevelopMCAstrokeswill havedecreasedlevelsofconsciousnessandareunable to report vision loss. In bilateral occipital lobe infarcts, patients can develop anosognosia (Anton Syndrome) and will deny vision loss [31,32]. Many visual field defects can be missed if confrontational visual field testing alone is used [33]. In a prospective study of 32 patients, 62% failed to recognize their right- or left-sided visual field defect [34], and in the VIS Study, only 45% of patients with visual field loss reported symptoms [9].


Complete recovery of visual field loss after an ischemic attack has been reported in 44% of patients, whereas partial recovery can reach up to 72% [20,25,28,35–38]. All of these studies, however, are limited by the duration of follow up and the method of assessing visual fields.

Spontaneous recovery usually occurs within the first 3 months, and in a series of 254 patients, 55% showed improvement in the first month, whereas recovery was unlikely after 6 months [20]. However, after 6 months, fixation patterns in patients with homonymous hemianopia change; many develop compensatory mechanisms and produce a series of hypometric saccades into the blind field until they find the object of intent [39–41]. Pediatric patients with hemianopia may have a compensatory exotropia or head turn toward the side of the visual field defect which will cause anomalous correspondence

Table 1. Ocular manifestations of different cerebrovascular occlusions

Anterior (70%) Ophthalmic artery Ocular ischemic syndrome
Anterior cerebral artery Case reports of ocular motor and eyelid closing apraxia due to involvement of branches to the supplementary motor area and corpus callosum

Anterior communicating Aneurysms can compress the supero-anterior portion of the optic artery              chiasm causing bilateral homonymous hemianopsia or the

poseterior portions of the optic nerves.

Middle cerebral artery Homonymous hemianopia


Hemineglect (nondominant hemisphere)

Conjugate deviation to the side of the lesion,

Decrease reflexive saccades

Voluntary saccades and memory driven saccades opposite to the lesion (FEF, PEF, DLPFC, temporal lobe),

Suppression of caloric induced nystagmus (temporal lobe)

Suppression of antisaccades

Ocular motor apraxia (bilateral FEF)

Apraxia of eyelid openings

Convergence insufficiency

Anterior choroidal Homonymous quadruple sectoranopia artery

Posterior communicating Artery Aneurysm Third nerve palsy, pupil involving

Posterior (30%) Posterior cerebral artery Congruous contralateral homonymous hemianopia, Macular sparing if anterior

Macular homonymous hemianopia if posterior

Cortical blindness if bilateral often with Anton syndrome or visual anosagnosia

Unilateral temporal crescent visual field loss

Balint’s syndrome (simultagnosia, optic ataxia, ocular motor apraxia)

Lateral posterior choroidal artery Horizontal, homonymous sectoranopia

Thalamoperforating Vertical gaze palsy arteries/percheron artery


Top of the basilar Dorsal midbrain syndrome

Vertical gaze palsy (upgaze and downgaze)

Convergence insufficiency

Convergence spasm

Convergence retraction nystagmus on upgaze

Pseudosixth due to failure of ocular abduction

Collier sign or lid retraction

’Plus minus sign’

Ocular tilt reactions in which there is a head tilt to the ipsilateral shoulder with incyclotorsion of the higher eye that is the contralateral eye

Skew deviation, ocular torsion, and abnormal estimation of the visual vertical.

Small, fixed, and slightly reactive to light

Light near dissociation Correctopia Iridae

Table 1 (Continued)

Caudal Lesions: third nerve palsy

Basilar artery Nuclear third nerve palsy:

ipsilateral third nerve palsy þ contralateral ptosis and superior rectus dysfunction

If the nuclear lesion is rostral, it will involve the Edingar Westphal nucleus leading to pupillary involvement with muscle sparing.

Fascicular Third nerve:

Superior cerebellar peduncle (Nothnagel’s Syndrome): ipsilateral 3rd nerve palsy þ cerebellar ataxia.

Lesions at the Red Nucleus (Benedikt’s Syndrome): ipsilateral 3rd nerve palsy and contralateral involuntary movement.

Lesion at the cerebral peduncle (Weber’s syndrome): ipsilateral

3rd nerve palsy and contralateral hemiplegia

Claude syndrome: distal territory of the mesencephalon, leading to contralateral hemiparesis, contralateral ataxia, and contralateral hemiplegia of the lower face, tongue, and shoulder in addition to ipsilateral oculomotor nerve palsy

Horizontal gaze palsy,

Internuclear ophthalmoplegia

One and a half syndrome

Vertical gaze palsy

Contralateral fourth nerve palsy

Anterior cerebellar artery Lateral pontine Syndrome

Gaze holding and pursuit deficit

Horner’s syndrome

Skew deviation

Sixth nerve nucleus: Ipsilateral gaze palsy þ ipsilateral facial nerve palsy

sixth nerve fasciculus: ipsilateral abduction deficit

Eight and a half syndrome: one and a half syndrome þ facial palsy

Foville syndrome: ipsilateral gaze palsy, facial palsy, facial hypoesthesia, peripheral deafness, Horner’s syndrome and contralateral hemiparesis, ataxia, pain, and thermal hypoesthesia

Millard–Gubler or ventral pontine syndrome: sixth nerve palsy, ipsilateral facial palsy, probably involving the root fibers and with contralateral hemiplegia or hemiparesia resulting from involvement of the corticospinal tract

Vertebral Arteries: Wallenberg syndrome (lateral medullary syndrome)

Ipsilateral impairment of pain and temperature on the face and contralateral impairment in the body

Ipsilateral horner

Skew deviation/ocular tilt reaction

Ipsilateral lateropulsion Ipsipulsion of saccade

tilt of the vertical normal towards side of the lesion Horizontal nystagmus beating away from lesion

Upbeat nystagmus

Ocuopalatine myoclonus

Superior cerebellar Saccadic contrapulsion artery

Tilt of the vertical normal away from the side of the lesion

Table 1 (Continued)

Posterior inferior cerebellar artery

Vestibular nystagmus
Lateral medullary syndrome

Saccadic dysmetria (hyper o hypometria)

Gaze evoked, rebound, downbeat nystagmus

Periodic alternating nystagmus

Impaired VOR suppression

Square wave jerk



to develop and thus overcome the complete visual field defect without diplopia [42,43].

More than 50% of patients with homonymous hemianopia will not achieve adequate recovery of visual function. Rehabilitative methods have centered on both compensatory use of the remaining visualfield and attempting to restorefunction inthe hemianopic field. This latter goal remains elusive and controversial.

Trainingprotocolshavebeendevised toincrease awareness of the blind area; patients are instructed to make organized saccades into the blind hemifield [19,44]. Exploratory saccade training (EST), using a software program that generated a random array of digits where the patient was asked to move the cursor toward a specific digit without over or undershooting, was shown to improve saccadic behavior, natural search, and scene exploration on the blind side and was associated with subjective improvement in activities of daily living [45]. In a separate randomized trial employing a systematic, anticipatory scanning strategy [46&], patients demonstrated subjective improvement in mobility-related activities but not in reading, visual counting, and visual search [47&&]. Other interventions have integrated auditory stimuli into the visual scanning training procedure [48,49,50&].

Another approach is to make use of optical aids, by applying binocular prisms directed with base out away from the blind field. A prerequisite for these prism to work is to have gaze directed into the prism [51], and improved visual task performance but not in activities of daily living has been shown [52]. High power monocular sector prisms are an alternative, as the function in all directions of gaze and are commercially available; improved function including return to driving has been shown [53,54]. Nonetheless, a recent study of 87 patients showed the use of prisms and visual search training was not superior to standard care in increasing the visual field area afterstroke, and prisms were associated ahigh (69%) incidence of headaches [55&&]. A case report using computerized technology (Google Glass) has demonstrated the potential of such methods to expand the visual field [56&].

The above interventions compensate for but do not restore lost visual field. Restorative therapies purport to stimulate cortical neuroplasticity, a method supported by adult animal models of vision deprivation [57–59]. Sabel et al. devised a computerbased method (NovaVision) to stimulate the border zone of visual field defects, where improvement through retraining was most likely to occur. In their initial report, 30% of treated patients with retrochiasmal lesions showed improvement in visual field, and there was a shift in the transition zone of 5 to 68 among VRT-trained patients [60]. Similar improvements were demonstrated in subsequent studies [61,62]. Using a different visual discrimination training strategy, Cavanaugh and Huxlin found that 17 patients who underwent training recovered 108 deg2 of vision on average, whereas 5 untrained patients improved over an area of 16 deg2 [63&&].

Subsequent critiques of these methods postulated that patients had developed adaptive saccadic compensationratherthanatrueincreaseinthevisual field.HortonclaimedthatSabelandhisgroupdidnot report fixation losses, false positives, and false negatives,andthattheiruseofblindspotmonitoringwas inadequate to detect small saccades [64]. Indeed, small case series of patients treated with various flickering stimulus regimens seemed to show that responses in the blind field were not improved when fixation was monitored by methods different from those used in NovaVision restoration therapy [40].

Nonetheless, more accurate and reproducible target detection has been shown in patients treated with dual static and kinetic stimulation [65,66]. Also, vision restoration therapy combined with transcranial direct current stimulation (tDCS) was found to be superior to vision restoration therapy alone [67,68]. A recent pilot study by Sabel’s group showed that a combination of tDCS and VRT is well tolerated and seems to be more effective than standard vision training procedures [69&]. A confirmatory, larger-sample, controlled, randomized, and double-blind trial is now underway to compare real-tDCS-augmented versus sham-tDCS-augmented visual field training in the early vision rehabilitation phase [69&]. Finally, some critics have advocated delaying any therapy to avoid the mistaken conclusion that an intervention has been useful, because improvement may have been spontaneous. However, early intervention in hemiparetic patients improves outcomes, and to take advantage of neuroplasticity, early treatment with the goal of visual field restoration also may be justified [68,70,71&,72].

In conclusion, the efficacy of VRT and other interventions in expanding visual fields post strokes remains inconclusive despite animal data and human experience that support neuroplasticity in human visual systems.


The reported prevalence of ocular motility dysfunctionafterstrokerangesfrom22to70%[19,21,73–76]. Ocularmotilitydysfunctionincludesstrabismus,gaze palsy, nystagmus, and vergence deficits.


Strabismus after strokes is related to cranial nerve palsies, supranuclear palsies, internuclear ophthalmoplegia, skew deviations, ocular tilt reactions, and other abnormalities of ocular motor control. Prospective studies of patients with strokes have noted that strabismus can occur in 16.5 to 50% of patients [21,73,75–77]. Rowe reported that strabismus was mainly present with cortical strokes (69%), and 56.5% of patients with strabismus had only one ocularmotilityabnormality.Themostcommonstrabismus type was exotropia, seen in 74% of strabismic patients [73]. In a mixed population of stroke (129) andheadinjury(84)patients,Fowlerreportedthat89 (37%)ofpatientshadocularalignmentproblemsbut that only 32 (36% of those with strabismus) had symptoms, either because of the small deviation or because of decrease in vision or perception [75]. Interestingly,anidenticalrateofsymptomaticdiplopia with strabismus was found in the VIS UK Study [73]. Sixth and third nerve palsies are more common in stroke than fourth nerve palsy [10,73]. Within the spectrum of oculomotor nerve palsy, the medial rectus subnucleus may be affected in isolation [78–80].

Gaze palsy

Gaze palsy is the most common ocular motility disturbance after stroke and has been reported in 18–44% of patients with CVA [21,74,81–83]. It can be isolated or associated with other motility problems. Horizontal gazepalsies aremoreprevalentthan vertical, and complete palsies are more common than partial [73,74]. The presence of conjugate eye deviation on CT scan is associated with worse outcome [84] and higher NIH stroke severity scale score [85] in patients with acute ischemic stroke, and this predictive status remains despite interventions such as thrombolysis [86&].


Prevalence of nystagmus after stroke is likely underestimated, as many studies do not report nystagmus when assessingstrokeoutcomes [87];inone study, it was present in 24% of 407 patients with posterior circulation stroke [13]. Unsurprisingly, cerebellar stroke has the strongest association with acute findings of nystagmus [76,88]. Although the onset of nystagmus with focal neurological deficits is highly diagnostic for stroke [89&], 11% of patients with isolated vertigo or dizziness (in which nystagmus often is present) were noted to have stroke in a recent study of 221 patients [90].


Convergence insufficiency (CI) is quitecommon after stroke; Cilsby [21] reported its presence in 55% of stroke cases, whereas Rowe noted that in 109 CVA patients with reading difficulties, 54% had impaired nearpointofconvergence(NPC)morethan6cm,and 28% had NPC more than 10cm [16]. Siong reported reduced convergence (>15cm) in 21% of cases [15].


Full recovery from CVA-associated cranial nerve palsies may occur in 7–28.5% of patients, and nearly all (92%)havesomeimprovement,withsixthnervepalsy being most likely to resolve completely [16,28,73,74]. Indeed, database analysis suggests some recovery occurs in all patients with horizontal gaze paresis [28]. More broadly, prospective data showed partial recovery of cranial nerve palsies in 43% and complete recovery in 22.5% of affected stroke patients; nystagmus improved partially in 42% whereas gaze palsy improved completely in 6% and partially in66%[73].


Higher order cognitive deficits may lead to visual disturbancesafterstroke, asmay lack of awareness of visual information. Visual hemifield neglect, or visual anosognosia, is seen commonly middle cerebral artery (MCA) stroke of the nondominant hemisphere. Studies usually do not separate visual, spatial, and auditory neglect. Although visual neglect is more often seen in right MCA strokes, even in left MCA stroke there is contralesional attentional impairment that can be recorded [91].

The reported prevalence of visual neglect after strokes ranges from 14 to 82% [92–96], with this broad range attributable to the use of different methods of assessment, different inclusion criteria, and different areas of the brain being affected.

Other perceptual deficits reported in the literature include cerebral achromatopsia [97], optic ataxia [98], simultagnosia [99], extinction [92], and visual hallucinations [17,94,95,96,100] In a series of 189 stroke patients age at least 65 years, 93 (49.2%) had one or more visual perceptual problems [101]. A lower prevalence of 20% was described in a population of 323 stroke patients of all ages [100]; in thisstudy,visualhallucinationswereseenin4%and visual agnosia in 2.5% of patients. Visual and tactile attentional testing of 454 patients in the United Kingdom with subacute stroke was performed and demonstrated contralateral (left) visual extinction in 28% of participants with right hemisphere stroke versus only 6.8% of participants with right visual extinction from left hemisphere stroke [102].


Recovery of visual neglect across several studies ranges from 29% to 78% [25,28,103]. Visual neglect has been correlated with a longer stay in hospital and poorer prognosis for functional recovery [103]. Recovery is mostly seen within 3 months post onset with approximately 10% full recovery within the first 2 weeks [25,28]. When CVA patients undergoing visual restoration therapy were asked (19 prospectively, 121 retrospectively) about visual hallucinations, they reported a median duration of 28 days and recovery within 90 days [36].

As with visual field defects, interventions to improvehemifieldneglecthavebeenstudiedbuthave inconclusive results. Right half field patching studies showeda positive butinconsistent trend toward effectiveness [104–106]. Smooth pursuit eye movement therapytowardtheneglectedfieldwasfoundeffective inachievingsomefunctionalimprovementinpatients with neglect in the setting of subacute stroke [107,108].However,arandomizedtrialwasconducted among 21 patients with acute (<14 days) stroke and left-sidedneglectandshowednobenefitforcombined hemifield eye patching and optokinetic stimulation [109]. Other suggested therapies include videogame [110]andvirtualrealitytraining[111].Visualscanning training similar to that discussed with visual field defects has also been studied and found to be effective in overcoming visual neglect, although functional improvement was not assessed [112,113]. Prism adaptation was found effective in some case reports [114], but randomized controlled studies did not show any functional benefits of prisms in patients with neglect [115–117]. Results of cognitive therapy are similarly inconclusive [118]. Recent assessments of tDCS suggestitmay behelpful[119,120],especially whencombinedwithothertreatmentmodalities[121&,122,123].


The majority of patients with stroke will experience either transient or permanent visual deficits. This review serves as an overview of the most recent and important data that outlines the prevalence of defects in the visual, perceptual, and oculomotor systems following CVAs. We paid special attention to the interventions that are thought to help restore or compensate for visual field loss and visuospatial neglect. This isacontroversialtopic,anddata aswell as expert opinions are still not conclusive on whether these interventions are useful, but clinical evidence supports the potential use of noninvasive brain stimulation in combination with other optical, cognitive, or plasticity-training therapies to improve the visual outcomes.


Papers of particular interest, published within the annual period of review, have been highlighted as: & of special interest

&& of outstanding interest

  1. Bevers MB, Kimberly WT. Critical care management of acute ischemic stroke. Curr Treat Options Cardiovasc Med 2017; 19:1952.
  2. Benjamin EJ, Blaha MJ, Chiuve SE, et al. Heart disease and stroke statistics2017 update: a report from the American Heart Association. Circulation 2017; 135:e146–e603.
  3. Pollock A, Hazelton C, Henderson CA, et al. Interventions for disorders of eye movement in patients with stroke. Cochrane Database Syst Rev 2011; (10):CD008389.
  4. Pollock A, Hazelton C, Henderson CA, et al. Interventions for age-related visual problems in patients with stroke. Cochrane Database Syst Rev 2012; (3):CD008390.
  5. Pollock A, Hazelton C, Henderson CA, et al. Interventions for visual field defects in patients with stroke. Cochrane Database Syst Rev 2011; (10):CD008388.
  6. Aldrich MS, Alessi AG, Beck RW, Gilman S. Cortical blindness: etiology, diagnosis, and prognosis. Ann Neurol 1987; 21:149–158.
  7. Sand KM, Midelfart A, Thomassen L, et al. Visual impairment in stroke patients – a review. Acta Neurol Scand 2013; suppl 127:52–56.
  8. Rowe F, Brand D, Jackson CA, et al. Visual impairment following stroke: do stroke patients require vision assessment? Age Ageing 2009; 38:188–193. 9. Rowe F; VIS Group UK. Symptoms of stroke-related visual impairment. Strabismus 2013; 21:150–154.
  1. Lotery AJ, Wiggam MI, Jackson AJ, et al. Correctable visual impairment in stroke rehabilitation patients. Age Ageing 2000; 29:221–222.
  2. Edwards DF, Hahn MG, Baum CM, et al. Screening patients with stroke for rehabilitation needs: validation of the poststroke rehabilitation guidelines. Neurorehabil Neural Repair 2006; 20:42–48.
  3. Hanna KL, Hepworth LR, Rowe F. Screening methods for poststroke visual impairment: a systematic review. Disabil Rehabil 2016; 60:1–13.
  4. Searls DE, Pazdera L, Korbel E, et al. Symptoms and signs of posterior circulation ischemia in the New England Medical Center Posterior Circulation Registry. Arch Neurol 2012; 69:346–351.
  5. Jerath NU, Reddy C, Freeman WD, et al. Gender differences in presenting signs and symptoms of acute ischemic stroke: a population-based study. Gend Med 2011; 8:312–319.
  6. Siong KH, Woo GC, Chan DY-L, et al. Prevalence of visual problems among stroke survivors in Hong Kong Chinese. Clin Exp Optom 2014; 97:433–441.
  7. Rowe F, Wright D, Brand D, et al. Reading difficulty after stroke: ocular and non ocular causes. Int J Stroke 2011; 6:404–411.
  8. Bulens C, Meerwaldt JD, van der Wildt GJ, Keemink CJ. Spatial contrast sensitivity in unilateral cerebral ischaemic lesions involving the posterior visual pathway. Brain 1989; 112:507–520.
  9. Santos dos NA, Andrade SM. Visual contrast sensitivity in patients with impairment of functional independence after stroke. BMC Neurol 2012; 12:90.
  10. Pambakian A, Currie J, Kennard C. Rehabilitation strategies for patients with homonymous visual field defects. J Neuroophthalmol 2005; 25:136–142.
  11. Zhang X, Kedar S, Lynn MJ, et al. Natural history of homonymous hemianopia. Neurology 2006; 66:901–905.
  12. Clisby C. Visual assessment of patients with cerebrovascular accident on the elderly care wards. Br Orthop J 1995; 52:38–40.
  13. Isaeff WB, Wallar PH, Duncan G. Ophthalmic findings in 322 patients with a cerebral vascular accident. Ann Ophthalmol 1974; 6:1059–1069.
  14. Gray CS, French JM, Bates D, et al. Recovery of visual fields in acute stroke: homonymous hemianopia associated with adverse prognosis. Age Ageing 1989; 18:419–421.
  15. Agrell BM, Dehlin OI, Dahlgren CJ. Neglect in elderly stroke patients: a comparison of five tests. Psychiatry Clin Neurosci 1997; 51:295–300.
  16. Cassidy TP, Bruce DW, Gray CS. Visual field loss after stroke: confrontation and perimetry in the assessment of recovery. J Stroke Cerebrovasc Dis 2001; 10:113–117.
  17. Haerer AF. Visual field defects and the prognosis of stroke patients. Stroke 1973; 4:163–168.
  18. Benedetti MD, Benedetti M, Stenta G, et al. Short term prognosis of stroke in a clinical series of 94 patients. Ital J Neurol Sci 1993; 14:121–127.
  19. Ali M, Hazelton C, Lyden P, et al. Recovery from poststroke visual impairment: evidence from a clinical trials resource. Neurorehabil Neural Repair 2013; 27:133–141.
  20. Pambakian AL, Kennard C. Can visual function be restored in patients with homonymous hemianopia? Br J Ophthalmol 1997; 81:324–328.
  21. Zhang X, Kedar S, Lynn MJ, et al. Homonymous hemianopias: clinicalanatomic correlations in 904 cases. Neurology 2006; 66:906–910.
  22. Adeyemo BO, Nesathurai S. The original description of Anton syndrome. PM R 2013; 5:74.
  23. Chen J-J, Chang H-F, Hsu Y-C, Chen D-L. Anton-Babinski syndrome in an old patient: a case report and literature review. Psychogeriatrics 2015; 15:58–61.
  24. Townend BS, Sturm JW, Petsoglou C, et al. Perimetric homonymous visual field loss poststroke. J Clin Neurosci 2007; 14:754–756.
  25. Celesia GG, Brigell MG, Vaphiades MS. Hemianopic anosognosia. Neurology 1997; 49:88–97.
  26. Farne´ A, Buxbaum LJ, Ferraro M, et al. Patterns of spontaneous recovery of neglect and associated disorders in acute right brain-damaged patients. J Neurol Neurosurg Psychiatr 2004; 75:1401–1410.
  27. Poggel DA, Muller-Oehring EM, Gothe J,€ et al. Visual hallucinations during spontaneous and training-induced visual field recovery. Neuropsychologia 2007; 45:2598–2607.
  28. Celebisoy M, Celebisoy N, Bayam E, Ko¨se T. Recovery of visual-field defects after occipital lobe infarction: a perimetric study. J Neurol Neurosurg Psychiatr 2011; 82:695–702.
  29. Goodwin D. Homonymous hemianopia: challenges and solutions. Clin Ophthalmol 2014; 8:1919–1927.
  30. Pambakian AL, Wooding DS, Patel N, et al. Scanning the visual world: a study of patients with homonymous hemianopia. J Neurol Neurosurg Psychiatr 2000; 69:751–759.
  31. Reinhard JI, Damm I, Ivanov IV, Trauzettel-Klosinski S. Eye movements during saccadic and fixation tasks in patients with homonymous hemianopia. J Neuroophthalmol 2014; 34:354–361.
  32. Loetscher T, Chen C, Wignall S, et al. A study on the natural history of scanning behaviour in patients with visual field defects after stroke. BMC Neurol 2015; 15:64.
  33. Kedar S, Zhang X, Lynn MJ, et al. Pediatric homonymous hemianopia. J AAPOS 2006; 10:249–252.
  34. Paysse EA, Coats DK. Anomalous head posture with early-onset homonymous hemianopia. J AAPOS 1997; 1:209–213.
  35. Trauzettel-Klosinski S. Rehabilitation for visual disorders. J Neuroophthalmol 2010; 30:73–84.
  36. Roth T, Sokolov AN, Messias A, et al. Comparing explorative saccade and flicker training in hemianopia: a randomized controlled study. Neurology 2009; 72:324–331.
  37. de Haan GA, Melis-Dankers BJM, Brouwer WH, et al. The effects of

& compensatory scanning training on mobility in patients with homonymous visual field defects: a randomized controlled trial. PLoS ONE 2015; 10:e0134459.

One of the first randomized trials to look at visual rehabilitation with mobility outcomes.

  1. de Haan GA, Melis-Dankers BJM, Brouwer WH, et al. The effects of

&& compensatory scanning training on mobility in patients with homonymous visual field defects: further support, predictive variables and follow-up. PLoS ONE 2016; 11:e0166310.

Strong data to support structured rehabilitation to improve quality of life and mobility, even in the absence of a clear demonstration that objective visual field enlargement has occurred.

  1. Passamonti C, Bertini C, La`davas E. Audio-visual stimulation improves oculomotor patterns in patients with hemianopia. Neuropsychologia 2009; 47:546–555.
  2. Bolognini N, Rasi F, Coccia M, La`davas E. Visual search improvement in hemianopic patients after audio-visual stimulation. Brain 2005; 128:2830– 2842.
  3. Dundon NM, Bertini C, La`davas E, et al. Visual rehabilitation: visual scanning,

& multisensory stimulation and vision restoration trainings. Front Behav Neurosci 2015; 9:192.

Balanced discussion of the need for a multifaceted approach to visual rehabilitation.

  1. Pelak VS, Dubin M, Whitney E. Homonymous hemianopia: a critical analysis of optical devices, compensatory training, and NovaVision. Curr Treat Options Neurol 2007; 9:41–47.
  2. Rossi PW, Kheyfets S, Reding MJ. Fresnel prisms improve visual perception in stroke patients with homonymous hemianopia or unilateral visual neglect. Neurology 1990; 40:1597–1599.
  3. Apfelbaum HL, Ross NC, Bowers AR, Peli E. Considering apical scotomas, confusion, and diplopia when prescribing prisms for homonymous hemianopia. Trans Vis Sci Tech 2013; 4:2.
  4. Moss AM, Harrison AR, Lee MS. Patients with homonymous hemianopia become visually qualified to drive using novel monocular sector prisms. J Neuroophthalmol 2014; 34:53–56.
  5. Rowe FJ, Conroy EJ, Bedson E, et al. A pilot randomized controlled

&& trial comparing effectiveness of prism glasses, visual search training and standard care in hemianopia. Acta Neurol Scand 2016; 38:188. Visual search training, but not prisms, were found to improve visual quality of life as assessed by the VFQ-25. None of the techniques used by the authors led to objective visual field expansion, however.

  1. Trese MGJ, Khan NW, Branham K, et al. Expansion of severely constricted

& visual field using google glass. Ophthalmic Surg Lasers Imaging Retina 2016; 47:486–489.

Novel technology employment in a stroke patient- possible future uses exist.

  1. Huxlin KR, Pasternak T. Long-term neurochemical changes after visual cortical lesions in the adult cat. J Comp Neurol 2001; 429: 221–241.
  2. Huxlin KR, Pasternak T. Training-induced recovery of visual motion perception after extrastriate cortical damage in the adult cat. Cereb Cortex 2004; 14:81–90.
  3. Huxlin KR, Williams JM, Price T. A neurochemical signature of visual recovery after extrastriate cortical damage in the adult cat. J Comp Neurol 2008; 508:45–61.
  4. Sabel BA, Kasten E. Restoration of vision by training of residual functions. Curr Opin Ophthalmol 2000; 11:430–436.
  5. Jung CS, Bruce B, Newman NJ, Biousse V. Visual function in anterior ischemic optic neuropathy: effect of vision restoration therapy – a pilot study. J Neurol Sci 2008; 268:145–149.
  6. Mueller I, Mast H, Sabel BA. Recovery of visual field defects: a large clinical observational study using vision restoration therapy. Restor Neurol Neurosci 2007; 25:563–572.
  7. Cavanaugh MR, Huxlin KR. Visual discrimination training improves Humphrey

&& perimetry in chronic cortically induced blindness. Neurology 2017; 88:1856–1864.

This article showed improved performance on standard, clinically relevant tests of visual field after visual restoration training that controls for fixation. The clinical significance remains to be seen, but this study addresses many of the prior concerns about saccadic movements giving a false sense of improvement.

  1. Horton JC. Disappointing results from Nova Vision’s visual restoration therapy. Br J Ophthalmol 2005; 89:1–2.
  2. Das A, Huxlin KR. New approaches to visual rehabilitation for cortical blindness: outcomes and putative mechanisms. Neuroscientist 2010; 16:374–387.
  3. Parkin BL, Ekhtiari H, Walsh VF. Noninvasive human brain stimulation in cognitive neuroscience: a primer. Neuron 2015; 87:932–945.
  4. Plow EB, Obretenova SN, Halko MA, et al. Combining visual rehabilitative training and noninvasive brain stimulation to enhance visual function in patients with hemianopia: a comparative case study. PM R 2011; 3:825–835.
  5. Miller NR, Subramanian PS. Should visual restoration therapy be used in patients with visual field loss? J Neuroophthalmol 2015; 35:319–322.
  6. Alber R, Moser H, Gall C, Sabel BA. Combined transcranial direct current

& stimulation and vision restoration training in subacute stroke rehabilitation: a pilot study PM R 2017. [Epub ahead print]

Open label (unmasked) study that shows potential efficacy of combined therapies.

  1. Frolov A, Feuerstein J, Subramanian PS. Homonymous hemianopia and vision restoration therapy. Neurol Clin 2017; 35:29–43.
  2. Melnick MD, Tadin D, Huxlin KR. Relearning to see in cortical blindness. & Neuroscientist 2016; 22:199–212.

Overview of current attempts to restore visual field.

  1. Liu N, Cadilhac DA, Andrew NE, et al. Randomized controlled trial of early rehabilitation after intracerebral hemorrhage stroke: difference in outcomes within 6 months of stroke. Stroke 2014; 45:3502–3507.
  2. Rowe F; VIS Group UK. Prevalence of ocular motor cranial nerve palsy and associations following stroke. Eye (Lond) 2011; 25:881–887.
  3. Rowe FJ, Wright D, Brand D, et al. Profile of gaze dysfunction following cerebrovascular accident. ISRN Ophthalmol 2013; 2013:264604–264608.
  4. Fowler MS, Wade DT, Richardson AJ, Stein JF. Squints and diplopia seen after brain damage. J Neurol 1996; 243:86–90.
  5. Su C-H, Young Y-H. Clinical significance of pathological eye movements in diagnosing posterior fossa stroke. Acta Otolaryngol 2013; 133:916–923.
  6. Maeshima S, Osawa A, Miyazaki Y, et al. Functional outcome in patients with pontine infarction after acute rehabilitation. Neurol Sci 2012; 33:759–764.
  7. Ogawa K, Suzuki Y, Takahashi K, et al. Clinical study of eleven patients with midbrain infarction-induced oculomotor nerve palsy. J Stroke Cerebrovasc Dis 2016; 25:1631–1638.
  8. Derle E, O¨ cal R, Kibaroglu S, Can U. Rare presentation of midbrain infarction: isolated medial rectus palsy. Eur Neurol 2015; 74:60–61.
  9. Yao Y, Hong W, Fan Z, et al. Isolated medial rectus palsy: rare presentation of mesencephalon infarction. J Stroke Cerebrovasc Dis 2017; 26:e53–e54.
  10. Tao W-D, Liu M, Fisher M, et al. Posterior versus anterior circulation infarction: how different are the neurological deficits? Stroke 2012; 43:2060–2065.
  11. Singer OC, Humpich MC, Laufs H, et al. Conjugate eye deviation in acute stroke: incidence, hemispheric asymmetry, and lesion pattern. Stroke 2006; 37:2726–2732.
  12. Fruhmann Berger M, Pross RD, Ilg UJ, Karnath HO. Deviation of eyes and head in acute cerebral stroke. BMC Neurol 2006; 6:23.
  13. Tijssen CC, Schulte BP, Leyten AC. Prognostic significance of conjugate eye deviation in stroke patients. Stroke 1991; 22:200–202.
  14. Schwartz KM, Ahmed AT, Fugate JE, et al. Frequency of eye deviation in stroke and nonstroke patients undergoing head CT. Neurocrit Care 2012; 17:45–48.
  15. Shah NH, Bhatt N, Tipirneni A, et al. Conjugate eye deviation on CT

& associated with worse outcomes despite IV thrombolysis. Neurohospitalist 2017; 7:74–77.

Demonstration of outcome prediction being possible from a simple data point regarding eye position on CT.

  1. Siddique MAN, Nur Z, Mahbub MS, et al. Clinical presentation and epidemiology of stroke: a study of 100 cases. J Med 2009; 10:86–89.
  2. Baier B, Dieterich M. Incidence and anatomy of gaze-evoked nystagmus in patients with cerebellar lesions. Neurology 2011; 76:361–365.
  3. Choi J-H, Park M-G, Choi SY, et al. Acute transient vestibular syndrome:

& prevalence of stroke and efficacy of bedside evaluation. Stroke 2017; 48:556–562.

The authors showed that bedside testing and even MRI may miss clinically relevant posterior fossa strokes.

  1. Doijiri R, Uno H, Miyashita K, et al. How commonly is stroke found in patients with isolated vertigo or dizziness attack? J Stroke Cerebrovasc Dis 2016; 25:2549–2552.
  2. Schendel K, Dronkers NF, Turken AU. Not just language: persisting lateralized visuospatial impairment after left hemisphere stroke. J Int Neuropsychol Soc 2016; 22:695–704.
  3. Umarova RM, Saur D, Kaller CP, et al. Acute visual neglect and extinction: distinct functional state of the visuospatial attention system. Brain 2011; 134:3310–3325.
  4. Becker E, Karnath H-O. Incidence of visual extinction after left versus right hemisphere stroke. Stroke 2007; 38:3172–3174.
  5. Linden T, Samuelsson H, Skoog I, Blomstrand C. Visual neglect and cognitive impairment in elderly patients late after stroke. Acta Neurol Scand 2005; 111:163–168.
  6. Brink Ten AF, Verwer JH, Biesbroek JM, et al. Differences between left- and right-sided neglect revisited: a large cohort study across multiple domains. J Clin Exp Neuropsychol 2016; 6:1–19.
  7. Appelros P, Karlsson GM, Seiger A, Nydevik I. Neglect and anosognosia after first-ever stroke: incidence and relationship to disability. J Rehabil Med 2002; 34:215–220.
  8. Bouvier SE. Behavioral deficits and cortical damage loci in cerebral achromatopsia. Cereb Cortex 2005; 16:183–191.
  9. Khan AZ, Crawford JD, Blohm G, et al. Influence of initial hand and target position on reach errors in optic ataxic and normal subjects. J Vis 2007; 7:8.1–16.
  10. Chechlacz M, Rotshtein P, Hansen PC, et al. The neural underpinings of simultanagnosia: disconnecting the visuospatial attention network. J Cogn Neurosci 2012; 24:718–735.
  11. Rowe F; VIS Group UK. Visual perceptual consequences of stroke. Strabismus 2009; 17:24–28.
  12. Beaudoin AJ, Fournier B, Julien-Caron L, et al. Visuoperceptual deficits and participation in older adults after stroke. Aust Occup Ther J 2013; 60:260–266.
  13. Chechlacz M, Rotshtein P, Demeyere N, et al. The frequency and severity of extinction after stroke affecting different vascular territories. Neuropsychologia 2014; 54:11–17.
  14. Karnath H-O, Rorden C. The anatomy of spatial neglect. Neuropsychologia 2012; 50:1010–1017.
  15. Ianes P, Varalta V, Gandolfi M, et al. Stimulating visual exploration of the neglected space in the early stage of stroke by hemifield eye-patching: a randomized controlled trial in patients with right brain damage. Eur J Phys Rehabil Med 2012; 48:189–196.
  16. Fong KN, Chan MK, Ng PP, et al. The effect of voluntary trunk rotation and half-field eye-patching for patients with unilateral neglect in stroke: a randomized controlled trial. Clin Rehab 2007; 21:729–741.
  17. Tsang MHM, Sze KH, Fong KNK. Occupational therapy treatment with right half-field eye-patching for patients with subacute stroke and unilateral neglect: a randomised controlled trial. Disabil Rehabil 2009; 31:630–637.
  18. Fong KNK. Smooth pursuit eye movement training improves recovery from functional neglect in individuals with postacute stroke. J Physiother 2015; 61:45.
  19. Kerkhoff G, Bucher L, Brasse M, et al. Smooth pursuit ‘bedside’ training reduces disability and unawareness during the activities of daily living in neglect: a randomized controlled trial. Neurorehabil Neural Repair 2014; 28:554–563.
  20. Machner B, Ko¨nemund I, Sprenger A, et al. Randomized controlled trial on hemifield eye patching and optokinetic stimulation in acute spatial neglect. Stroke 2014; 45:2465–2468.
  21. Mainetti R, Sedda A, Ronchetti M, et al. Duckneglect: Video-games based neglect rehabilitation. Technol Healthcare 2013; 21:97–111.
  22. Kim YM, Chun MH, Yun GJ, et al. The effect of virtual reality training on unilateral spatial neglect in stroke patients. Ann Rehabil Med 2011; 35:309– 315.
  23. Jutai JW, Bhogal SK, Foley NC, et al. Treatment of visual perceptual disorders post stroke. Top Stroke Rehabil 2003; 10:77–106.
  24. Priftis K, Passarini L, Pilosio C, et al. Visual scanning training, limb activation treatment, and prism adaptation for rehabilitating left neglect: who is the winner? Front Hum Neurosci 2013; 7:360.
  25. Facchin A, Beschin N, Daini R. Rehabilitation of right (personal) neglect by prism adaptation: a case report. Ann Phys Rehabil Med 2016; 60:220–222.
  26. Oh S-I, Kim J-K, Park S-Y. The effects of prism glasses and intensive upper limb exercise on hemineglect, upper limb function, and activities of daily living in stroke patients: a case series. J Phys Ther Sci 2015; 27:3941–3943.
  27. Vaes N, Nys G, Lafosse C, et al. Rehabilitation of visuospatial neglect by prism adaptation: effects of a mild treatment regime. A randomised controlled trial. Neuropsychol Rehabil 2016; 57:1–20.
  28. Champod AS, Frank RC, Taylor K, Eskes GA. The effects of prism adaptation on daily life activities in patients with visuospatial neglect: a systematic review. Neuropsychol Rehabil 2016; 32:1–24.
  29. Bowen A, Hazelton C, Pollock A, Lincoln NB. Cognitive rehabilitation for spatial neglect following stroke. Cochrane Database Syst Rev 2013; (9):CD003586.
  30. Elsner B, Kugler J, Pohl M, Mehrholz J. Transcranial direct current stimulation (tDCS) for improving activities of daily living, and physical and cognitive functioning, in people after stroke. Cochrane Database Syst Rev 2016; (3):CD009645.
  31. Yi YG, Chun MH, Do KH, et al. The effect of transcranial direct current stimulation on neglect syndrome in stroke patients. Ann Rehabil Med 2016; 40:223–229.
  32. Bang D-H, Bong S-Y. Effect of combination of transcranial direct current

& stimulation and feedback training on visuospatial neglect in patients with subacute stroke: a pilot randomized controlled trial. J Phys Ther Sci 2015; 27:2759–2761.

Further proof of concept.

  1. La`davas E, Giulietti S, Avenanti A, et al. a-tDCS on the ipsilesional parietal cortex boosts the effects of prism adaptation treatment in neglect. Restor Neurol Neurosci 2015; 33:647–662.
  2. Turgut N, Miranda M, Kastrup A, et al. tDCS combined with optokinetic drift reduces egocentric neglect in severely impaired postacute patients. Neuropsychol Rehabil 2016; 30:1–12.

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