Residual Visual Function after Loss of Both Cerebral Hemispheres in Infancy

Werth, Reinhard

doi:10.1167/iovs.06-1141

Cited by 16 publications

(14 citation statements)

References 54 publications

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“…36,55,56 Despite the absence of subcortical-cortical connections due to total loss of the ipsilesional visual cortex, the relatively spared axoplasmic flow and structural integrity of the retinocollicular and retinogeniculate pathways projected from the contralesional eye in the current animal model may be helpful in examining residual visual functions that are mainly mediated by the subcortical visual nuclei, such as blindsight. 55,[57][58][59][60] Although our current MRI data supported the hypothesis that both the eye and the brain's visual pathway were affected by neonatal HI, it is currently uncertain the relative contributions of altered structural and physiological integrity in the visual system to visual impairment. Vision testing was not performed on the current albino Sprague-Dawley rat model because of the intrinsically low visual acuity of normal albino rats, 61 leaving limited room to quantitatively and reliably assess visual performance impairment and/or recovery.…”

Section: Discussionsupporting

confidence: 58%

Long-Term Effects of Neonatal Hypoxia-Ischemia on Structural and Physiological Integrity of the Eye and Visual Pathway by Multimodal MRI

Chan

Kancherla

Fan

et al. 2014

Investigative Ophthalmology & Visual Science

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Section: Discussionsupporting

confidence: 58%

Long-Term Effects of Neonatal Hypoxia-Ischemia on Structural and Physiological Integrity of the Eye and Visual Pathway by Multimodal MRI

Chan

Kancherla

Fan

et al. 2014

Investigative Ophthalmology & Visual Science

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“…The dominant role of the cortical pathway, and the minimal role of a subcortical pathway, is reinforced by studies of children. Neuroimaging of visual cortex, combined with eye movement recordings, has shown absence of visually driven pursuit or OKN in cerebrally blind infants (87,88).…”

Section: Maldevelopment In V1 Is Passed On To Medial Temporal and Medmentioning

confidence: 99%

The Neural Mechanism for Latent (Fusion Maldevelopment) Nystagmus

Tychsen

Richards

Wong

et al. 2010

Journal of Neuro-Ophthalmology

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Latent nystagmus (LN) is the by-product of fusion maldevelopment in infancy. Because fusion maldevelopment--in the form of strabismus and amblyopia--is common, LN is a prevalent form of pathologic nystagmus encountered in clinical practice. It originates as an afferent visual pathway disorder. To unravel the mechanism for LN, we studied patients and nonhuman primates with maldeveloped fusion. These experiments have revealed that loss of binocular connections within striate cortex (area V1) in the first months of life is the necessary and sufficient cause of LN. The severity of LN increases systematically with longer durations of binocular decorrelation and greater losses of V1 connections. Decorrelation durations that exceed the equivalent of 2-3 months in human development result in an LN prevalence of 100%. No manipulation of brain stem motor pathways is required. The binocular maldevelopment originating in area V1 is passed on to downstream extrastriate regions of cerebral cortex that drive conjugate gaze, notably MSTd. Conjugate gaze is stable when MSTd neurons of the right and left cerebral hemispheres have balanced binocular activity. Fusion maldevelopment in infancy causes unbalanced monocular activity. If input from one eye dominates and the other is suppressed, MSTd in one hemisphere becomes more active. Acting through downstream projections to the ipsilateral nucleus of the optic tract, the eyes are driven conjugately to that side. The unbalanced MSTd drive is evident as the nasalward gaze-holding bias of LN when viewing with either eye.

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“…The dominant role of the cortical pathway, and the minimal role of a subcortical pathway, is reinforced by studies of children. Neuroimaging of visual cortex, combined with eye movement recordings, have shown absence of visually-driven pursuit or OKN in cerebrally-blind infants (Tychsen, 1996, Werth, 2007). …”

Section: Discussionmentioning

confidence: 99%

Duration of binocular decorrelation in infancy predicts the severity of nasotemporal pursuit asymmetries in strabismic macaque monkeys

et al. 2008

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Purpose-Strabismus in human infants is linked strongly to nasotemporal asymmetries of smooth pursuit, but many features of this co-morbidity are unknown. The purpose of this study was to determine how the duration of early-onset strabismus (or timeliness of repair) affects the severity of pursuit asymmetries in a primate model. Methods-Binocular image decorrelation was imposed on infant macaques by fitting them with prism goggles on day 1 of life. The goggles were removed after 3 weeks (n=2), 12 weeks (n=2) or 24 weeks (n=3), emulating surgical repair of strabismus in humans at 3, 12, and 24 months of age, respectively. Two control monkeys wore plano lenses. Several months after the goggles were removed, horizontal smooth pursuit was recorded using binocular search coils and a nasal-bias index (NBI) was calculated.Results-Each animal in the 12-and 24-week groups developed a constant, alternating esotropic strabismus and a nasotemporal asymmetry of pursuit when viewing with either eye. Spatial vision was normal (no amblyopia). The 3-week duration monkeys were indistinguishable from control animals; they had normal eye alignment and symmetric pursuit. In the 12-and 24-week monkeys, the longer the duration of binocular decorrelation, the greater the pursuit asymmetry: for 15 deg/s target motion, the NBI in the 12-week and 24-week animals was 16 X and 22 X greater respectively, than that in the 3 week animals (ANOVA, p = 0.03).Conclusions-Binocular decorrelation in primates during an early period of fusion development causes permanent smooth pursuit asymmetries when the duration exceeds the equivalent of 3 months in human. These findings support the conclusion that early correction of infantile strabismus promotes normal development of cerebral gaze pathways.

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Residual Visual Function after Loss of Both Cerebral Hemispheres in Infancy

Abstract: Neural structures in the midbrain, including the superior colliculi and the pretectum, seem to be able to mediate visual function in the foveal and macular regions. These structures are, however, unable to mediate the presence of a functional visual field beyond 5 degrees eccentricity.

Cited by 16 publications

References 54 publications

Long-Term Effects of Neonatal Hypoxia-Ischemia on Structural and Physiological Integrity of the Eye and Visual Pathway by Multimodal MRI

Long-Term Effects of Neonatal Hypoxia-Ischemia on Structural and Physiological Integrity of the Eye and Visual Pathway by Multimodal MRI

The Neural Mechanism for Latent (Fusion Maldevelopment) Nystagmus

Duration of binocular decorrelation in infancy predicts the severity of nasotemporal pursuit asymmetries in strabismic macaque monkeys

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