Diseases and Disorders

Lazy Eye: An Overview of Amblyopia

Shrika Vejandla


Amblyopia is a neurological disorder in which an eye fails to achieve normal visual acuity due to the brain choosing to ignore visual input from the weaker eye. It typically develops during infancy or childhood, and affects only one eye. As a result, it is commonly referred to as a “lazy eye”. Approximately 1.75% of the population is affected by amblyopia [1]. Those who have the disorder are unable to neurologically process inputs from one eye in their visual cortex, and over time,  end up favoring the other eye for the input. Its underlying neural mechanisms remain relatively unknown. Despite this, a multitude of therapies and treatments are available for those affected by amblyopia. This article aims to provide an overview of the processes of this disorder, as well as its currently available treatments. 

Symptoms and Risk Factors

Generally speaking, symptoms of amblyopia can be difficult to discern as they typically arise in infants and children. Amblyopia is the leading cause of vision loss in children [1]. A common cause of amblyopia is strabismus (failure of the two eyes to work together and align effectively); misaligned eyes are an indication of this disorder. Infants may display discomfort when one eye is covered, indicating the eye that is open is the origin of amblyopia [2]. Children with amblyopia may also have poor depth perception, indicating they cannot tell how far or near an object is [2]. Early detection and treatment of amblyopia are crucial, as it proved to be the best method in preventing long term vision problems of the affected child. It is crucial for parents to register their child for a comprehensive eye exam to determine whether they are affected by amblyopia. The chances of having amblyopia are significantly higher in children who were born prematurely, weighed smaller than usual at birth, had a family history of amblyopia, or have developmental disabilities [2].



The neural, physiological, and psychological aspects of amblyopia are yet to be well understood [3]. Amblyopia is defined as a decrease in visual acuity, though it correlates directly with a large scope of neural, sensory, and perceptual visual functions. It occurs when various visual functions do not develop properly at birth, likely due to a lack of adequate stimuli received from each eye, eye parallelism (both eyes working together in harmony), and integrity of the visual pathways within the brain [3]. These three functions are highly sensitive during the critical period, which is a stage after birth in which individuals are very receptive to environmental stimuli.

When the disorder affecting the visual function develops early, is severe, and not treated within the first years of life, it can lead to structural modification of the visual neuronal circuit, causing definite physical changes in cortical projections from the lateral geniculate nucleus (LGN), towards the visual cortex of the brain. This is what leads to the alterations of visual function in amblyopic eyes [3]. On the other hand, when the disorder in the visual function occurs later with lower intensity, the anatomy of the visual cortex is maintained, although it is still possible to have active suppression from neurons of the normal eye onto neurons of the affected eye. This neurological mechanism, therefore, inhibits the visual image of the affected amblyopic eye as an attempt to prevent disturbing the processes of the unaffected eye [3]. This further reinforces the fact that early diagnosis of amblyopia is absolutely necessary for allowing treatment to begin at a stage in which the visual neurological pathways are still open to change to external stimuli and recovery [3].


Types of Amblyopia 

There exist three types of amblyopia, each of which are classified by their underlying causes. 

  1. Strabismic amblyopia

Strabismic amblyopia is considered the most common type of the disorder. The eyes are poorly aligned (drift apart), resulting in the brain choosing to ignore input from the amblyopic eye in order to avoid double vision [3]. Strabismus also causes a significant amount of change or a loss in connectivity to the spatial information pathways to the cortex within the brain. This alters the spatial summation and suppressions of the received stimuli resulting in the prevention of integrated contours and shapes from both eyes [3]. In addition, a result of this is the motor dysfunction and misalignment of both eyes, which is a distinct quality of strabismic amblyopia. Strabismus amblyopia affects approximately 2-4% of the population [4].

  1. Refractive amblyopia

  Refractive, or anisometropic amblyopia,  is caused by unequal refractive errors in the two eyes, despite correct eye alignment. This occurs when the shape of one’s eye does not bend light correctly [4]. For example, one eye may be significantly nearsighted or farsighted, while the other can see well. Consequently, the brain relies on the eye that has less uncorrected refractive error and ignores the blurred vision from the other eye, causing amblyopia in that eye from disuse [4]. In refractive amblyopia, there is a slight disconnection of the affected eye in the primary visual cortex in the brain, leading to irregular competition amongst neurons [4]. In normal individuals and animals, cortical neurons respond to the stimulation of both eyes, as opposed to amblyopic individuals subject to the blurring of the image of one eye facing a smaller proportion of cortical neurons responding to stimuli from that affected eye. Cortical neurons that respond to stimuli of the affected eye do so because of their insensitive receptive fields and tendency to diffuse, which generates worse spatial resolution and contrast sensitivity [3].

  1. Deprivation amblyopia

Deprivation amblyopia happens when eye diseases prevent the light stimulus from reaching the retina, thus forestalling the normal visual process [4].  This form of amblyopia often develops when a child has cataracts in one or both eyes that impair their vision [4]. Cataracts are rare but can be passed on due to reasons such as genetics, as a result of trauma, steroid use, or other childhood diseases. It also may occur due to anatomic deficits of the retina or optic nerve, or abnormal movement disorders of the eye (known as nystagmus) [3]. This deficit greatly impacts the visual processing system within the brain. The optic nerve is the second cranial nerve, which works to transfer visual information from the retina to the LGN in the visual cortex via neurons [3]. Similar to refractive amblyopia, the cortical neurons within the retina possess insensitive receptive fields, resulting in “unclear” information being sent to the visual cortex, ultimately forming a blurry image.



For children within the critical period, the gold standard of treatment of amblyopia is considered to be an eye patch for the better eye to force the visual cortex into using the weaker eye [5]. The deprivation of the fixating eye of vision forces the amblyopic eye to combat suppression and to use the visual cortex corresponding to the eye to recover neural connections, resulting in better visual acuity [5]. Other alternatives to patching an eye include optical penalization with atropine (muscle relaxant) eye drops, filters to blur the better eye, optical defocus using glasses or contact lenses, and dichoptic video games [5] [6]. These methods aim to lower the dependence on the visually fixated eye similar to the eye patch [5].

Treatments are still available for children beyond their critical period. Fortunately, while a young brain is more plastic than an adult brain, the adult brain is still capable of learning and recovering after injury, so it is clear that there is plasticity at a synaptic level, thus also at the level of cortical representation [3]. A brief reduction of gamma-aminobutyric acid-ergic (GABAergic) inhibition in the brains of rats has shown a window of plasticity in the visual system well after the normal closure of the critical periods, so several modes of augmentation of plasticity have been employed to create amblyopia therapy beyond the critical period of development [3]. For example, intrinsic augmentation can be achieved by manipulating the neurotransmitter systems that regulate synaptic plasticity in an environmental way. This occurs by the action of neurotransmitters in the brain such as norepinephrine and serotonin to disinhibit (suppress) cortical visual neurons. In addition, an individual can stimulate this effective system through prolonged dark exposure, caloric restriction, and with new or challenging visual tasks (perceptual learning).

Transcranial direct current stimulation (TDCS) and transcranial magnetic stimulation (TMS) have also been used in an effort to facilitate plasticity in stroke patients, as well as patients with amblyopia [3]. Nonetheless, it is important to note that further studies are needed to evaluate the efficacy and safety of these technologies [3].



Amblyopia is a treatable disorder and it is important for parents to regularly check on the habits and behaviors of their children to potentially detect amblyopia as early as possible. As much as it is crucial for an early diagnosis with amblyopia, there is plenty of room for improvement and recovery in those who are receiving treatments after their critical period. New treatment models in amblyopia offer hope for older patients to improve their visual acuity, due to their neuroplasticity that exists beyond childhood. Not only that, dichoptic treatments involving the use of video games provide unique, exciting tools for treatment and visual rehabilitation.


  1. Hashemi, Hassan. (30/07/2018). Global and regional estimates of prevalence of amblyopia: A systematic review and meta-analysis.  Strabismus: Volume 26. https://www.tandfonline.com/doi/abs/10.1080/09273972.2018.1500618?journalCode=istr20. Retrieved: 05/08/2020.

  2. National Eye Institute. (02/07/2019). Amblyopia (Lazy Eye). National Eye Institute: Research Today, Vision Tomorrow. https://www.nei.nih.gov/learn-about-eye-health/eye-conditions-and-diseases/amblyopia-lazy-eye. Retrieved: 05/08/2020.

  3. Zagui, Roberta. (25/06/2019). Amblyopia: Types, Diagnosis, Treatment, and New Perspectives. American Academy of Ophthalmology.  https://www.aao.org/disease-review/amblyopia-types-diagnosis-treatment-new-perspectiv. Retrieved: 05/08/2020.

  4. Boston Children’s Hospital Contributors. Amblyopia. Boston Children’s Hospital. http://www.childrenshospital.org/conditions-and-treatments/conditions/a/amblyopia. Retrieved: 05/08/2020.

  5. Bradfield, Yasmin. (01/03/2013). Identification and Treatment of Amblyopia. American Academy of Family Physicians. https://www.aafp.org/afp/2013/0301/p348.html. Retrieved: 05/08/2020.

  6. Dornbos, Brian. Neuroplasticity, Amblyopia and Emerging Treatments. Mivision Education. https://www.mieducation.com/pages/neuroplasticity-amblyopia-and-emerging-treatments. Retrieved: 05/08/2020.

  7. Sengpiel, Frank. (22/09/2014). Plasticity of the Visual Cortex and Treatment of Amblyopia. Cell: Current Biology. https://www.cell.com/current-biology/fulltext/S0960-9822(14)00664-2. Retrieved: 05/08/2020.

Shrika Vejandla

Shrika Vejandla

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