A child with strabismus cannot align both eyes on the same object, and current treatments—surgery on the eye muscles—often fail to fix the underlying problem. This matters because the root cause of strabismus remains unknown. The researchers suspect the issue lies in faulty "oculoproprioception": the brain’s ability to sense each eye’s rotation via stretch receptors in the eye muscles. In healthy adults, passively rotating one eye in darkness makes the other eye mirror the movement. The team will test whether this coupling is weaker in 4- to 5-year-old children with strabismus, before surgery has altered the system. They will also map how the healthy brain coordinates eye movement, specifically how brain areas receiving proprioceptive signals drive brainstem circuits controlling eye muscles. If the hypothesis holds, it would shift strabismus from a mechanical problem of eye muscles to a neural one of misperceived eye position. This could lead to earlier, non-surgical interventions—such as sensory training or targeted therapies—that address the brain’s role in alignment. For children, that might mean better academic performance, sports participation, and social confidence. The work is fundamental science on a common condition, with clear potential to reshape clinical practice.
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Strabismus (squint or crossed eyes) is one of the most common and debilitating eye disorders in childhood. Individuals with this condition cannot align the two eyes to look at the same visual object. The current treatment is visual correction followed by surgery of the muscles that move the eyes in the eye sockets. This treatment does not work in everyone. In many children the eye misalignment persists and a majority of those treated do not regain normal vision. Visual problems may prevent the children from performing well academically, competing successfully in sports, and pursuing some occupations. The appearance of "crossed" eyes leads to low self-esteem and social difficulties. The reason the treatment does not work could be that it does not address the root cause of the disease. It is not known what causes strabismus. To precisely control where we look, the brain has access to information about the rotation of each eye in the eye sockets. One source of such information is called 'oculoproprioception'. It is provided by stretch receptors in the muscles that rotate the eye. We have observed in healthy adults that when one eye is passively rotated in complete darkness, the other eye mirrors this rotation, albeit with a smaller amplitude. We are proposing to test for the first time the hypothesis that the misalignment of the eyes in strabismus might be caused by inaccurate oculoproprioception. Answering this question is challenging for several reasons. First, animal models of strabismus are inadequate for understanding the role of oculoproprioception in human disease, as there are inter-species differences in anatomy and function. Second, because corrective strabismus surgery itself affects oculoproprioception, one would need to examine before surgical intervention, in early childhood. To address these challenges we propose to pool resources, knowledge, and expertise across several institutions. The project has two main aims. First, we will adapt behavioural tasks previously used in adults to assess whether the passive movement of one eye has a smaller impact on the movement of the other eye in 4- to 5-year-old children with strabismus relative to healthy controls. Second, we will identify how the healthy brain orchestrates the coupling between the movement of the eyes. The hypothesis is that brain areas that receive proprioceptive input, drive the activity of brainstem areas that control the extraocular muscles. Thus, the project will shed light on the cause of a clinical condition in humans at behavioural and neural levels. The outcomes will provide the basis for earlier assessment and a more effective intervention in strabismus.
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