High frequency of asymptomatic visual field defects in subjects with transient ischaemic attacks or minor strokes

Falke, P; Abela, B. M.; Krakau, C. E. T.; Lilja, B.; Lindgärde, Folke; Maly, Pavel; Stavenow, Lars

doi:10.1111/j.1365-2796.1991.tb00389.x

Cited by 24 publications

(14 citation statements)

References 8 publications

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“…Visual field loss is reported in the acute period following stroke in 45–67% of patients [2, 30, 45, 46] and in the long term for 8–25% of patients following adjustment for recovery of visual field and morbidity [3, 47, 48]. 51.4% of all referred patients had demonstrable visual field loss with a prevalence of 52.3% for those formally recruited to the VIS study.…”

Section: Discussionmentioning

confidence: 99%

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A Prospective Profile of Visual Field Loss following Stroke: Prevalence, Type, Rehabilitation, and Outcome

Rowe

Wright

Brand

et al. 2013

BioMed Research International

127

119

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Aims. To profile site of stroke/cerebrovascular accident, type and extent of field loss, treatment options, and outcome. Methods. Prospective multicentre cohort trial. Standardised referral and investigation protocol of visual parameters. Results. 915 patients were recruited with a mean age of 69 years (SD 14). 479 patients (52%) had visual field loss. 51 patients (10%) had no visual symptoms. Almost half of symptomatic patients (n = 226) complained only of visual field loss: almost half (n = 226) also had reading difficulty, blurred vision, diplopia, and perceptual difficulties. 31% (n = 151) had visual field loss as their only visual impairment: 69% (n = 328) had low vision, eye movement deficits, or visual perceptual difficulties. Occipital and parietal lobe strokes most commonly caused visual field loss. Treatment options included visual search training, visual awareness, typoscopes, substitutive prisms, low vision aids, refraction, and occlusive patches. At followup 15 patients (7.5%) had full recovery, 78 (39%) had improvement, and 104 (52%) had no recovery. Two patients (1%) had further decline of visual field. Patients with visual field loss had lower quality of life scores than stroke patients without visual impairment. Conclusions. Stroke survivors with visual field loss require assessment to accurately define type and extent of loss, diagnose coexistent visual impairments, and offer targeted treatment.

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Section: Discussionmentioning

confidence: 99%

“…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.…”

Section: Introductionmentioning

confidence: 99%

A Prospective Profile of Visual Field Loss following Stroke: Prevalence, Type, Rehabilitation, and Outcome

Rowe

Wright

Brand

et al. 2013

BioMed Research International

127

119

View full text Add to dashboard Cite

show abstract

“…Indeed, visual impairments are often a first symptom in these pathologies (Benavente et al, 2001, Mead et al, 2002), and 57% of minor strokes are accompanied by subclinical visual field defects (Falke et al, 1991). Ocular ischemic syndrome, usually caused by severe obstruction of the carotid artery, involves vision loss due to chronically reduced arterial blood flow to the eye (Sturrock and Mueller, 1984).…”

Section: Introductionmentioning

confidence: 99%

Severity of middle cerebral artery occlusion determines retinal deficits in rats

Allen

Sayeed

Cale

et al. 2014

Experimental Neurology

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Middle cerebral artery occlusion (MCAO) using the intraluminal suture technique is a common model used to study cerebral ischemia in rodents. Due to the proximity of the ophthalmic artery to the middle cerebral artery, MCAO blocks both arteries, causing both cerebral and retinal ischemia. While previous studies have shown retinal dysfunction at 48 hours post-MCAO, we investigated whether these retinal function deficits persist until 9 days and whether they correlate with central neurological deficits. Rats received 90 minutes of transient MCAO followed by electroretinography at 2 and 9 days to assess retinal function. Retinal damage was assessed with cresyl violet staining, immunohistochemistry for glial fibrillary acidic protein (GFAP) and glutamine synthetase, and TUNEL staining. Rats showed behavioral deficits as assessed with neuroscore that correlated with cerebral infarct size and retinal function at 2 days. Two days after surgery, rats with moderate MCAO (neuroscore < 5) exhibited delays in electroretinogram implicit time, while rats with severe MCAO (neuroscore ≥ 5) exhibited reductions in amplitude. Glutamine synthetase was upregulated in Müller cells 3 days after MCAO in both severe and moderate animals, however, retinal ganglion cell death was only observed in MCAO retinas from severe animals. By 9 days after MCAO, both glutamine synthetase labeling and electroretinograms had returned to normal levels in moderate animals. Early retinal function deficits correlated with behavioral deficits. However, retinal function decreases were transient and selective retinal cell loss was observed only with severe ischemia, suggesting that the retina is less susceptible to MCAO than the brain. Temporary retinal deficits caused by MCAO are likely due to ischemia-induced increases in extracellular glutamate that impair signal conduction, but resolve by 9 days after MCAO.

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“…However, the nasal peripapillary retina contains a preponderance of crossed axons, and the temporal peripapillary retina contains a preponderance of uncrossed axons. 19 The results of this study showed that the superior, inferior, and nasal peripapillary retina in the contralateral eye was affected by the TRD of the RGC where the crossed fibers are located. Additionally, the superior, inferior, and temporal peripapillary retina in the ipsilateral eye was affected by the TRD of the RGC where the uncrossed fibers are located.…”

Section: Discussionmentioning

confidence: 81%

Long Term Transneuronal Retrograde Degeneration of the Retinal Ganglion Cells in Patients with Cerebral Infarction

Yıldız¹,

Yıldız²,

Acar³

et al. 2016

Turkiye Klinikleri J Ophthalmol

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A AB BS ST TR RA AC CT T O Ob bj je ec ct ti iv ve e: : The purpose of this study was to investigate the probable transneuronal retrograde degeneration (TRD) of the retinal ganglion cells (RGCs) in humans with cerebral infarction. In addition, the correlation between the laterality and severity of the retinal nerve fiber layer (RNFL) damage and other variables (laterality of hemispheric damage and arterial territory of the infarct) were analyzed. M Ma at te er ri ia al l a an nd d M Me et th ho od ds s: : Thirty consecutive patients were included. All of the subjects underwent complete ophthalmic examinations, including optical coherence tomography (OCT) and perimetry after diagnosis, and in the 6 th and 12 th months. The main outcome measures were the changes in the thicknesses of the RNFL, RGCs, and visual field (VF). The average thickness of the total macular RGCs and MD and PSD values analyzed in the perimetry (using the SITA Standard 24-2 Threshold Test) were taken into account. R Re es su ul lt ts s: : The RNFL thicknesses were reduced significantly in all four quadrants in the contralateral eyes, and in the superior, inferior, and temporal quadrants in the ipsilateral eyes at 12 months. However, the reduction of the RGCs' average total thickness was not statistically significant for either the ipsilateral or contralateral groups (p>0.05). The loss of the VF considering the mean MD measurements was statistically significant in the contralateral group (p=0.001) unlike in the ipsilateral group. C Co on nc cl lu us si io on ns s: : The RNFL thickness was reduced in both eyes at 12 months, providing evidence for TRD. The TRD was more pronounced in the nasal quadrant of the contralateral and temporal quadrant of the ipsilateral eye.K Ke ey y W Wo or rd ds s: : Brain infarction; retrograde degeneration; optic nerve; retinal ganglion cells; visual field tests Ö ÖZ ZE ET T A Am ma aç ç: : Çalışmanın amacı serebral infarkt hastalarında retinal ganglion hücrelerinin (RGH) olası transnöronal retrograde dejenerasyonunu (TRD) araştırmaktır. Retinal sinir lifi (RNFL) hasarının ciddiyeti ve tarafı ile diğer değişkenlerin arasındaki ilişkinin yanı sıra hemisferik hasarın tarafı ve infarkta sebep olan arter bölgesi de analiz edildi. G Ge er re eç ç v ve e Y Yö ön nt te em ml le er r: : Otuz ardışık hasta çalışmaya dahil edildi. Tüm hastalar tanı aldıktan sonra optik koherens tomografi (OKT) ve perimetriyi de içeren tam bir oftalmik muayeneden geçirildi ve tetkikler 6. ve 12. aylarda tekrarlandı. Çalışmanın ana amacı RSLT ve RGH tabakalarındaki kalınlık değişimleri ile görme alanındaki değişimleri değerlendirmekti. Ortalama total maküler RGH kalınlığı ve perimetri (SITA-Standart 24-2 eşik test) MD, PSD değerleri dikkate alındı. B Bu ul lg gu ul la ar r: : On ikinci ayda RSLT; kontralateral gözde dört kadranda; ipsilateral gözde ise superior, inferior ve temporal kadranlarda anlamlı derecede incelmiş idi. Ortalama total maküler RGH tabakasındaki incelme ipsilateral ve kontralateral göz için istatistiksel olarak anlamlı değil...

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High frequency of asymptomatic visual field defects in subjects with transient ischaemic attacks or minor strokes

Cited by 24 publications

References 8 publications

A Prospective Profile of Visual Field Loss following Stroke: Prevalence, Type, Rehabilitation, and Outcome

A Prospective Profile of Visual Field Loss following Stroke: Prevalence, Type, Rehabilitation, and Outcome

Severity of middle cerebral artery occlusion determines retinal deficits in rats

Long Term Transneuronal Retrograde Degeneration of the Retinal Ganglion Cells in Patients with Cerebral Infarction

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