In a previous discussion, we promised to explore the specific pathophysiological mechanisms behind amblyopia and delve into the reasons this condition develops. In this article, we will take a closer look at the human visual cortex, examining its structure and function, and discuss the molecular basis of amblyopia. Finally, we will briefly touch on potential future 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 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 a particularly good model.
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 probably closest to humans. Why might that be the case? Simply 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.
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 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 important for understanding how amblyopia develops and why it is so especially 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 improvement in amblyopia is possible even beyond this critical window. Still, it is considered best to treat amblyopia within the first 8 years of life for optimal outcomes. Another key principle is: the earlier the amblyopia develops, the more difficult it is to treat. This is especially true for 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 the environmental influences, wherein synaptic connections within the brain. In normal healthy visual conditions, both eye inputs are equally strong and bring about equally 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-the 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.
Effect of Unbalanced Inputs of the Eyes in Amblyopia
Visual development during synaptogenesis heavily relies on the environmental influences, wherein synaptic connections within the brain. In normal healthy visual conditions, both eye inputs are equally strong and bring about equally 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-the 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.
The Preference of the Brain and Lack of Binocular Vision
In the case of amblyopia, the brain will favor 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 input on clearer vision from the stronger eye. Eventually, it leads to failure in developing binocular vision because stereopsis- depth perception will not be created.
Amblyopia Treatments: Activation of the Amblyopic Eye
In 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 the age of 8. By forcing the weaker eye to work, these treatments promote visual development in the amblyopic eye. 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 even adults. The mechanisms behind these improvements are not well 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 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 as a basis for future amblyopia therapies.
Conclusion
Amblyopia is a challenge to vision development, especially when it occurs 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 now a viable option. Research using animal models has indicated that it is possible to restore function in the amblyopic eye even after the critical period by reactivating the visual cortex.
Among them, 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 proper use of amblyopic eyes and offers a systematic approach in correcting vision deficits among children and adults alike.
Although the findings are preliminary, they open up the door to novel pharmacological therapies and digital therapies such as EyeX Vision Therapy for adult amblyopia. Such developments are likely to change the treatment modalities and offer new hope for visual improvement in individuals of all ages.
