In a previous discussion, we promised to explore the pathophysiological mechanisms behind amblyopia and delve into why this condition develops. In this article, we will examine the human visual cortex, its structure and function, and discuss the molecular basis of amblyopia. Finally, we will briefly touch on potential future amblyopia treatments for this condition.
Our Sight is Born Naïve
At birth, the human brain is still in the early stages of development, and the visual pathway system, including the visual cortex, is no exception. While this may sound intriguing, it is difficult to directly study the developmental processes within the human brain, which is why much of the research on visual development has been conducted using animal models over the past 50 years. Still, due to the intricacy of the human visual cortex, no other mammal makes an excellent model for visual development and knows every detail of amblyopia.
Animal Models for Vision Development: Exploring Human Visual Cortex and Amblyopia
Most experts on this topic agree that the visual cortex of kittens and monkeys is closest to humans. Why might that be the case? Because both are predators, requiring strong abilities to determine distance and assess depth. This skill is made possible by binocular vision, where the position of the eyes plays a vital role. However, when comparing the developmental timelines of the visual system across species, we observe differences that are critical in understanding amblyopia and visual development.
For instance, the visual cortex in cats is structurally similar to that in humans. The anatomy of the visual cortex in these animals shares many characteristics with humans, making them valuable subjects for studying the condition of amblyopia. Most of the research aimed at understanding amblyopia has focused on this similarity. It has been observed that the maturation of the visual cortex differs among species. In kittens, it is complete by about 8 weeks; in monkeys, by about 8 months; and in humans, it continues to mature until about 8 years of age.
These differences in the timing of visual development are essential for understanding how amblyopia develops and why it is so incredibly impactful in humans during the critical period of visual system maturation.
Critical Period for Vision Development
Critical periods in vision development are well established. The current studies have recently shown that amblyopia improvement is possible beyond this crucial window. Still, treating amblyopia within the first 8 years of life is best for optimal outcomes. Another key principle is that the earlier the amblyopia develops, the more difficult it is to treat. This is especially true for sensory deprivation amblyopia caused by congenital cataracts, which are very hard to treat if the cataract is not removed within the first few months after birth.
Unbalanced Eye Inputs in Vision Development: Impact on Synaptic Connections and Binocular Vision
Visual development during synaptogenesis heavily relies on environmental influences, wherein synaptic connections are within the brain. In normal, healthy visual conditions, eye inputs are equally strong and bring robust synaptic connections. However, in amblyopia cases, if the input into the two eyes is not equal-for example, if in the two eyes, there are different refractive differences or other contributing factors visual brain favors the eye that transmits a more clearly focused image. This balance in the eyes prevents proper visual development and is exacerbated by binocular vision disturbance and a lack of synaptic plasticity in the visual cortex.
Effect of Unbalanced Inputs of the Eyes in Amblyopia
It is ultimately true that unbalanced eyes can significantly impact the visual development of an individual, and this leads to amblyopia. It is when one eye can send a more precise signal than the second. In this situation, the brain favours a stronger eye and hinders the proper synaptic connection to the weaker eye. Such an imbalance disrupts binocular vision, can cause long-term vision deficit eyes and prevent depth perception.
The Preference of the Brain and Lack of Binocular Vision
In the case of amblyopia, the brain will favour the more prominent eye with more developed input. The resulting insufficient visual development in the less dominant, or amblyopic eye, continues over time due to the interference caused by its feedback on the clearer vision from the stronger eye. Eventually, it leads to failure in developing binocular vision because stereopsis- depth perception will not be created. The neuroplasticity of the visual cortex plays a significant role here, as the brain rearranges to rely on the dominant eye, causing the condition of amblyopia and brain reorganization.
Amblyopia Treatments: Activation of the Amblyopic Eye
In the clinical treatment of amblyopia, strategies such as patching the stronger eye or using vision therapies, such as Amblyo Play, are used to stimulate the amblyopic eye. These methods work very well in young children, especially before age 8. These treatments promote visual development in the amblyopic eye by forcing the weaker eye to work. But what happens once the critical period for vision development has passed?
Beyond the Critical Period: Amblyopia Treatment in Adolescence and Adulthood
Traditionally, it was thought that treatment for amblyopia after the critical period was ineffective. However, recent clinical studies have shown that improvements can still be made in adolescents and adults. The mechanisms behind these improvements are poorly understood, although animal model research has provided some insights.
For example, in studies with kittens, where one eye was sutured closed early in life to induce amblyopia, it has been shown that the function of the amblyopic eye can be restored. The kitten’s visual cortex can be “reset,” eliminating amblyopia even after the critical developmental period. The process appears to involve the “noisy” retinal signals from the deprived eye, which, when suppressed, prompt the brain to reboot the visual cortex, similar to the state it was in at birth.
Revolutionary Treatment for Amblyopia: Resetting the Visual Cortex with TTX
How can we safely close the retinal input from the amblyopic eye without hurting it? An answer may come from tetrodotoxin, a neurotoxin very potent. TTX is derived from certain fishes, such as the fugu. It inhibits nerve signal conduction. In one study, researchers administered TTX in the eyes of kittens and effectively “rebooted” the visual cortex in the brain to demonstrate that, even after the critical period has passed, amblyopia is treatable by resetting the visual system.
While far from ready for human use, this approach provides the first proof of principle for pharmacological amblyopia therapy in adults and highlights the vast potential of these molecular mechanisms of amblyopia as a basis for future amblyopia therapies.
Conclusion
Amblyopia is a challenge to vision development, mainly during critical periods of visual maturation. Traditionally, methods like patching and vision therapy have been effective for infants and toddlers. However, recent studies have shown that treating adult amblyopia is viable. Research using animal models has indicated that restoring function in the amblyopic eye is possible even after the critical period by reactivating the visual cortex.
EyeX Vision Therapy is emerging as one of the most hopeful answers, combining state-of-the-art techniques with individually designed plans. Our therapy encourages the brain’s plasticity to stimulate the proper use of amblyopic eyes and offers a systematic approach to correcting vision deficits among children and adults alike.
Although the findings are preliminary, they open the door to novel pharmacological and digital therapies such as EyeX Vision Therapy for adult amblyopia. Such developments will likely change the treatment modalities and offer new hope for visual improvement in individuals of all ages.
If you wish to transform your vision with EyeX! Take the first step to download the app and look at the future of amblyopia treatments available at EyeX.
