Abnormal Fixational Eye Movements in Amblyopia

Shaikh, Aasef G.; Otero‐Millan, Jorge; Kumar, Priyanka; Ghasia, Fatema F.

doi:10.1371/journal.pone.0149953

Cited by 72 publications

(115 citation statements)

References 34 publications

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“…Our previous studies have shown that patients without nystagmus have increased fixational saccade amplitude and inter-saccadic drift compared to controls. (Shaikh et al 2016) We have also found increased slow phase velocity in patients with FMN compared to the inter-saccadic drift velocity in amblyopic patients without nystagmus and controls. (Kang et al submitted under review) During occlusion therapy, the amblyopic eye is the viewing eye.…”

Section: Eye Movement Parameters and Clinical Outcomesmentioning

confidence: 50%

“…Differential value (velocity signal) was further smoothened with Savitzkey-Golay filter, a function that can be applied to a set of digital data points for the smoothing purpose. (Shaikh et al 2016) Fixational saccades and quick phases of nystagmus were identified using an unsupervised clustering method (Otero-Millan, Castro et al 2014). Drifts were defined as epochs between fixational saccades and blinks.…”

Section: Introductionmentioning

confidence: 99%

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Fixation instability in amblyopia: Oculomotor disease biomarkers predictive of treatment effectiveness

Scaramuzzi

Murray

Otero‐Millan

et al. 2019

Progress in Brain Research

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Fusion Maldevelopment Nystagmus (FMN) is one of the most common subtypes of pathologic nystagmus seen in children. The National Institutes of Health Committee on Eye Movement and Strabismus classification has recommended utilizing a new etiologic description from 2001, replacing the term latent nystagmus. This type of nystagmus has initially been called latent because its severity increases, or became evident when an eye is covered. However, it is now known that true latent nystagmus is rare, with the majority of patients have manifest latent nystagmus seen with both eyes uncovered as identified on eye movement recordings. (Abadi and Scallan 2000) Amblyopia is a neurodevelopmental disorder that occurs due to de-correlated binocular input to the visual cortex. Investigations in non-human primate models have revealed that loss of horizontal binocular connections within area V1 in infancy is the necessary and sufficient cause of FMN. (Tychsen et al. 2010) The new terminology describes the strong correlation with a binocular fusion maldevelopment that occurs during the infancy, like strabismus, amblyopia or any monocular vision deprivation. (Tychsen 1992) Studies by the pediatric eye investigator group have compared part-time occlusion to full-time occlusion and found similar levels of improvement in visual acuity. Thus the current standard of treatment is part-time occlusion ranging from 2-6 hours/eye depending on the severity of amblyopia. (Holmes et al. 2003) The slow phase velocity (SPV) of FMN increases under monocular viewing conditions and therefore in patients with FMN occlusion was initially considered contraindicated because it could enhance the nystagmus intensity or amplitude. (Duke-Elder and Wybar 1973) Successively evidence was provided in a small cohort of patients that a significant improvement of visual acuity was obtained with full-time patching during all waking hours. (von Noorden al. 1987) Similarly, Simonsz demonstrated a compensatory drift changes in nystagmus direction and lower magnitude over days of full-day occlusion in 5 patients with latent nystagmus.(Simonsz 1989) Despite good compliance, up to 40% of children treated by occlusion therapy have residual amblyopia. Some baseline risk factors that predict the presence of residual amblyopia include severe amblyopia at time of diagnosis and older age at treatment initiation. (PEDIG Group 2011) Amblyopes are known to have increased fixation instability.(Niechwiej-Szwedo et al. 2012; Subramanian et al. 2013). This instability could be due to the presence of FMN. Amblyopic patients without nystagmus have an increase in the amplitude of fixational saccades with increase inter-saccadic drift, which contributes to the instability in both the fellow and amblyopic eye. (Shaikh et al 2016; Shi et al 2012; Chen et al 2018)In the current manuscript, we characterized the fixational eye movement waveforms of amblyopic patients. We hypothesize that the presence of FMN and increase slow phase velocity in patients with nystagmus would predict treatment respo...

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Section: Eye Movement Parameters and Clinical Outcomesmentioning

confidence: 50%

Section: Introductionmentioning

confidence: 99%

Fixation instability in amblyopia: Oculomotor disease biomarkers predictive of treatment effectiveness

Scaramuzzi

Murray

Otero‐Millan

et al. 2019

Progress in Brain Research

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“…An interesting and surprising finding is the increased fellow eye's response in the deep SC. Although we didn't record eye movements in the scanner, several previous studies found dysfunctions of fixational drifts and microsaccades of the amblyopia eye but not of the fellow eye during monocular viewing conditions (Gonzalez, Wong et al 2012, Subramanian, Jost et al 2013, Chung, Kumar et al 2015, Shaikh, Otero-Millan et al 2016). However, it might be possible that the fellow eye had improved fixational eye movements (e.g.…”

Section: Discussionmentioning

confidence: 99%

Layer-specific Loss and Compensation of Parvocellular Response in Subcortical Pathways of Adult Human Amblyopia

Wen

Wang

et al. 2020

Preprint

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Abnormal visual experience in critical period causes amblyopia or lazy eye, reducing visual abilities even with corrected optics. A long-standing question is where in the human visual system does the amblyopic deficit arise. In particular, whether amblyopia induces selective deficits of the magnocellular (M) or the parvocellular (P) geniculostriate pathways, and whether the more ancient retinotectal pathway is also affected. Technical limitations to non-invasively measure layer-specific activity in human lateral geniculate nucleus (LGN) and superior colliculus (SC) hampered efforts in addressing these questions. In the current study, using lamina-resolved 3T and 7T fMRI and visual stimuli selectively activating the M and P pathways, we investigated layer-specific response properties of the LGN and the SC of amblyopia patients and normal controls. With stimuli presented to the amblyopic eye, there was a stronger response loss in the P layers than in the M layers of the LGN. Compared to normal controls, amblyopic eye's response to the P stimulus was selectively reduced in the superficial SC, while the fellow eye's response was robustly increased in the deep SC. Selective P response deficits of amblyopia were also observed in the visual pulvinar, early visual cortex, and ventral but not dorsal visual streams. These results provide strong in vivo evidence in adult amblyopic patients for selective deficits of parvocellular functions in the visual thalamus, and additionally reveal response deficits to the amblyopic eye and neural compensation to the fellow eye in the retinotectal pathway. Highlights• Parvocellular response loss in the LGN P layers, visual pulvinar and ventral visual stream • Selective amblyopic deficits of the parvocellular pathway • Amblyopic eye's response decreased in the superficial SC • Fellow eye's response increased in the deep SC • Amblyopic deficits and neural compensation in the retinotectal pathway

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“…The finding of reduced microsaccade amplitude and frequency in TS differed from that in subjects with disorders of visual system such as amblyopia [37], refractive error [38], or degenerative disorders such as Parkinson’s disease or progressive supranuclear palsy [26, 27]. Disorders of visual system such as amblyopia increases the amplitude of microsaccades and reduces its frequency; refractive error affects the amplitude of microsaccades [37, 38]; the degenerative disorder such as Parkinson’s disase and progressive supranuclear palsy increases the amplitude of microsaccades and increases their frequency [26, 27].…”

Section: Discussionmentioning

confidence: 99%

“…Disorders of visual system such as amblyopia increases the amplitude of microsaccades and reduces its frequency; refractive error affects the amplitude of microsaccades [37, 38]; the degenerative disorder such as Parkinson’s disase and progressive supranuclear palsy increases the amplitude of microsaccades and increases their frequency [26, 27]. …”

Section: Discussionmentioning

confidence: 99%

Fixational eye movements in Tourette syndrome

et al. 2017

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Studies of saccadic eye movements in subjects with Tourette syndrome (TS) have provided additional evidence that there is a link between TS symptoms and deficits in fronto-striato-thalamic networks. These studies revealed impaired timing and inhibition of saccades. We compared fixational eye movements, such as microsaccades and ocular drifts, in subjects with TS and healthy controls.We measured horizontal and vertical eye positions with video-oculography in 14 subjects with Tourette syndrome. We found reduced microsaccade amplitude but increased time between adjacent microsaccades (intersaccadic interval). Hence, the rate of microsaccades was reduced in subjects with TS compared to controls. Measure of ocular stability during intersaccadic intervals revealed increased drift velocity and increased variance in eye position. We hypothesize that increased activity of the direct fronto-striatal pathway and the resulting reduction in basal ganglia outflow targeting the superior colliculus fixation zone affect the rate and amplitudeS of microsaccades in subjects with TS. The resulting impairment in frontal eye field fixation leads to increased drifts during intersaccadic interval in subjects with TS. Possible clinical implication for these results is that fixational eye movements can be objective biological markers of TS.

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Abnormal Fixational Eye Movements in Amblyopia

Cited by 72 publications

References 34 publications

Fixation instability in amblyopia: Oculomotor disease biomarkers predictive of treatment effectiveness

Fixation instability in amblyopia: Oculomotor disease biomarkers predictive of treatment effectiveness

Layer-specific Loss and Compensation of Parvocellular Response in Subcortical Pathways of Adult Human Amblyopia

Fixational eye movements in Tourette syndrome

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