Cortical binocularity in convergent strabismus after section of the optic chiasm

Abstract

In convergent strabismus (esotropia) the spatial asynchrony of the two eye inputs unbalances the interocular interactions, leading to the functional advantage of the nondeviated eye and the inhibition of the esotropic eye. It may be argued that the strabismic suppression, if it is the effect of inhibitory interactions between the eyes, could be removed by interrupting the interocular pathways at the optic chiasm. After chiasmatic section, each eye is connected only to the ipsilateral cortex through the uncrossed retinal projections and so the functionality of each eye's input is no longer interfered with by interocular mechanisms. In strabismic cats submitted, as adults, to section of the optic chiasm, we performed electrophysiological recordings from the striate cortex. Results show that in these animals: (1) the cortical responsiveness to the strabismic eye is strikingly higher than in esotropes with an intact optic chiasm; (2) the effectiveness of stimulation of the deviated eye is not different from that of the nondeviated eye in driving neurons of corresponding cortex; (3) surprisingly, a high degree of binocular activation is present in the cortex ipsilateral to the deviated eye, while in the cortex connected to the nondeviated eye the greatest majority of neurons are monocularly driven. Cortical binocularity depends on the corpus callosum, which conveys the input from the nondeviated eye to the opposite cortex (which receives the direct strabismic input), but not vice versa. The asymmetry of callosal transmission parallels the morphological asymmetry of callosal connections that occur in convergent strabismus. All together the findings indicate that the impaired effectiveness of esotropic input does not result from developmental deficit of the strabismic afferents but, rather, from inhibitory influences that are actively exerted through the interocular pathways. Strabismic suppression may be accomplished by the same interocular mechanisms underlying binocular rivalry.

Visual Neuropsychology in Development: Anatomo-Functional Brain Mechanisms of Action/Perception Binding in Health and Disease

“…In children, binocularity emerges at about 3 months (Thorn et al, 1994), depending on ocular convergence (Downey et al, 2017), cortical maturation (Elberger and Smith, 1985), neural plasticity (Chalupa, 2004), specific neurotransmitters (Kameyama et al, 2010;Krahe and Medina, 2010), and corticocortical interactions, both in humans (Jurcoane et al, 2007) and other mammals (Dehmel and Lowel, 2014). The failure of one or more of these cortical mechanisms can contribute to the creation of the conditions for developing binocularityrelated functional deficits, such as strabismus (Berman and Murphy, 1981;Freeman et al, 1982;Di Stefano and Gargini, 2002). Together with binocularity, depth perception relies on a number of visual abilities, including shape/shade segregation, sensitivity to differential texture density, interposition of near/far surfaces, all of which start to be present between 4 and 7 months (Yonas et al, 2002), and it keeps progressing in parallel with the development of fine visuo-motor skills both in health (Braddick and Atkinson, 2013) and disease (Grant et al, 2014).…”

Does dominance of crossing retinal ganglion cells make the eyes cross? The temporal retina in the origin of infantile esotropia – a neuroanatomical and evolutionary analysis

“…Sectioning crossing retinal ganglion cell neurons at the midline of the optic chiasm of strabismic cats restores responsiveness of cortical neurons to the squinting eye. The binocular response was restored after sectioning all crossing retinal ganglion cells (Di Stefano & Gargini 2002). Apparently, in strabismus, the ipsilateral non-decussating projection from the temporal retina is suppressed.…”