Category: Vision

A person undergoes many changes within their eyes during infancy that are crucial for being able to have the best possible vision. At birth, a baby’s vision is very inferior when compared to an adult. This is because most elements of the eye are very underdeveloped and need to undergo changes as the baby ages in order to mature and function as they would in an adult. When first born the infant’s vision will be extremely vague and not contain any colour besides black and white. Although their vision at this point is very poor, they do still have the ability to see vaguely. This shows that most of the development of the eye takes place prenatally however most of the components of the eye are very immature at birth which is why during infancy a lot of changes take place allowing maturation of parts of the eye so they can function correctly. Without changes in axial length, cornea and lens shapes, an increase in the number of certain cells and many other factors the persons vision would remain unclear and without colour throughout their lives and therefore causing lots of problems with carrying out everyday tasks and having an intensely bad effect on their quality of life. Many experiments have taken place which has shown how the eyes develop during the first year of a child’s life and correlating strongly to visual acuity, colour vision and contrast sensitivity improvement.

When a child is born its visual acuity will be at around 6/120, however, as the infant grows its visual system will develop and by 4 months will be at around 6/60. At 6 months the expected acuity will be around 6/36 and by 1 year will be 6/18. From this, we can see visual acuity improves very rapidly in the first year of a person’s life. Visual acuity is very important as it shows how clearly a person can see and how well they can distinguish between more than one image, letter or number. At birth the ability to distinguish is not yet available, however, objects that are 8-10 inches away from them will be where the baby aims its focus towards. During this first month, their eyes will begin working as a team but every so often one eye may move out of sync with the other eye but this is normal and not a definite sign of amblyopia. Over the next few months, visual acuity will improve rapidly with infants being able to move their eyes together faster and having a sharper vision.

Experiments have taken place in the past that show this, for example in 1978 it was found that acuity increased from 1.5 cycles per degree at one month to 20 cycles per degree at 12 months. In a more recent experiment where swept spatial frequencies were used to measure acuity, there was an increase from 4.5 cycles per degree at one month to about 20 cycles per degree at 12 months. The development of visual acuity correlates with how the shape and systems within the eye mature. As we know that infants are usually hyperopic which can be due to their eyeballs being too long or the cornea and lens not having the correct shape and therefore not bending light rays so that they focus on the retina, but behind the retina instead.

The cornea is responsible for around 70% of the eyes refraction and around 42D of the eyes power (Sridhar, 2018). An evaluation in 2004 concluded that infants at birth have very curved corneas but they flatten rapidly up to the age of six months. (Isenberg et al, 2004) Hence, this may be a factor contributing to why there is a big increase in visual acuity from 6/120 to around 6/36. Cone cells are important for observing fine detail as they have a high visual acuity due to them being so close together so when light from two positions close together hit two cones in the fovea two separate action potentials are sent to the brain. An experiment in 2012 showed that at birth foveal cones are very immature and do not contain OCT bands that are usually seen in the photoreceptors of an adult fovea. The cones grow longer and pack together whilst moving to form the fovea in the middle of the retina. Cone cells provide a system that has a high spatial resolution which helps give a high visual acuity, for example, each cone cells connects to one ganglion cell. Therefore, this is another factor contributing to why visual acuity increases over the first year of an infant’s life. The axial length has been shown to increase by an average of 1.2mm from three months to nine which improves visual acuity as it helps the eye to focus images on its retina as it is likely images were being focused behind the eye before the eye grew.

Contrast sensitivity is nowhere near being perfect at birth due to an underdeveloped visual system. By the age of twelve months, components of the eye will have become more mature and therefore give a much higher contrast sensitivity compared to when firstborn. Contrast sensitivity is very important as it helps distinguish an item from its background. When light is a limiting factor or there is a situation where it is difficult to see, such as a foggy day, contrast sensitivity will help to continue doing tasks without being hindered by the inability to identify where an object is. High spatial frequency channels give the finer details of an object or image whereas low spatial frequency channels give information regarding the overall structure and how intensity gradually changes across it. Both frequency channels are very important in order to make up the full image.

An experiment took place which examined the change in contrast sensitivity in human infants. It was found that in low spatial frequencies the contrast sensitivity increased at a very fast rate up to ten weeks of age but then began to level off and remain fairly constant up to around 40 weeks. The contrast sensitivity values found ranged from 4.7 to 30 between the ages of 2 and 4 weeks. Results were also obtained which showed acuity increase from the first 8 weeks where it was 2.5 to 9 c/degree and increased to between 10 and 20 c/degree at 30 weeks. High spatial frequency development and grating acuity develop until around 30 weeks as well. (Norcia, Tyler, Hamer, 1987) In another experiment where infants provided a sweep VEP estimate of contrast sensitivity, it was shown that contrast sensitivity developed very fast in younger infants and then increased at a slower rate after around 16 weeks. Contrast sensitivity for a higher cycle per degree grating followed the same pattern but the initial sensitivity was smaller. (Allen, Tyler, Anthony) When the sweep VEP method was used in infants the contrast threshold advanced from a 7% contrast in the first month to around 0.5% at 2 months when low spatial frequencies were used. There was also a slow increase in spatial frequency when using grating acuity as in the first month there was around 5 c/degree but by 8 months spatial frequency had reached 16.3 c/degree. At all spatial frequencies, there had been a major increase from birth to nine weeks, however, after nine weeks contrast sensitivity remained fairly constant at low spatial frequencies but continued to increase at high spatial frequencies.

All experiments that have been tested to see the development of contrast sensitivity usually give results showing an increase in contrast sensitivity as the infant ages. This will be due to the infant’s eye changing and becoming more advantageous. At one month an infant usually has very short dendrites and unmyelinated cells which can both contribute to low contrast sensitivity. Rods in the eye are quite mature by two months which allows the infant to distinguish between black and white. By 10 weeks the amount of rhodopsin present is around 50% of adult levels. (Fulton et al, 1999)

Colour vision allows images or objects to be distinguished depending on their wavelengths. It is fairly crucial as it helps identify objects from their backgrounds as colour aids in seeing their borders. It also makes it much easier to recognise an object you may be looking for in a place full of other similar looking objects, therefore saving a lot of time and energy. Visible light is part of the electromagnetic spectrum and is made up of a stream of photons that all travel at the speed of light. Around 75% of the light that reached the eye actually get to the fovea which is where visual acuity is best, the highest light intensities are responded to and where the highest population of cone cells is found. Around 25% is responded to by the inner region and the rest are taken by the cones in the outer region.

At birth infants can only see in black, grey and white, they do not possess the ability to see any other colours yet. Red is the first colour that will be seen by an infant as their eyes mature, and eventually, by five months, it is believed that an infant can see the full spectrum of colours. It has been shown that two-month-old infants can discriminate varying intensities of red from a white backdrop proving that by two months infants are dichromatic. Following experiments showed that at least L and M cones are present and functioning by three months of age. This means long and medium wavelengths can be responded to and allows colour discrimination. This explains why red is the first colour to be seen by infants as it has the longest wavelength in the colour spectrum. Data has been provided which gives evidence to show short-wavelength cone cells are present at four to six weeks of being born, but for reasons such as the retina still developing, the immature dendrites and the optic nerve not being completely myelinated, the cone cells sensitivities are suppressed in the majority of infants. In a small proportion of infants, however, there is supporting the idea that functioning short-wavelength cones which show very little sensitivity but are still functional. As the majority don’t have functioning S cone cells at 2 months, we can assume this is why infants are dichromatic until around five months of age.

There is a maximum of three different cones present in a human eye, each is responsible for either red, blue or green by working over a spectrum of wavelengths and light intensities. In order to recognise a specific colour, the brain must receive information from two or more cones at the same time. The reason for being able to see colour at 2 months is a result of the colour pathway beginning to operate at two or three months of age. As the fovea develops the foveal cones continue to lengthen and cell bodies are piled up in order to have the densest layer of cells it can. (Provis, Dubis, Maddess, Carroll) This is important as cones contain pigments and other transduction elements which allow photons to be converted into the form of electrical signals which can be sent to the brain through the optic nerve. In an experiment, it is shown that maximum saturated photoreceptor responses had an increase of approximately 0.18 log units from six weeks to four months. This will also be a key factor why infant vision is almost mature by four months.

Through all the research I have done I can conclude that infancy is a very important period for a person as it is when the eye undergoes the most rapid changes. A baby advances from having no colour vision at birth to being trichromatic within four to five months, having a visual acuity of 6/120 to 6/18 with twelve months and contrast sensitivity also showed a rapid increase within the year. We can also see which parts of the eyes are most responsible for the development of vision by seeing the correlations from previous experiments that have taken place.

“Keep your eye on the Ball”- a common saying that is not often taken literally, but Vision Training has been thought to give this phrase a more meaningful purpose. Vision Training, also known as Vision Therapy has been said to be one of the most controversial procedures in Vision Care to date. It has been used for a variety of purposes over the years from helping those with Learning Disabilities to helping correct conditions such as Amblyopia, Strabismus, and Accommodative issues. In past years, Olympic athletes have also been known to undergo a subtype of Optometric Vision Therapy called ‘Sports Vision Training’. The word ‘training’ here is preferred due to it being used to enhance skills and not correct a problem suggested from the word ‘therapy’. Sports Vision Training introduces methods that should hopefully enhance an athlete’s performance by looking at several qualities a great athlete should possess and working parts of the eye and brain to improve those skills. This sport-specific program has been debated to be able to greatly improve the performance of competitors in their field of play. But is there solid evidence to prove these training methods having a direct link with improved sports performance?

Firstly, let’s look at why even our top performers may need this extra training. It is common for some athletes who have no refractive errors and no physical issues to feel they are underperforming. When they feel they are physically trained to the best of their ability coaches can offer Vision Training as a possible solution to those who are not achieving the best results. For top performance, athletes have a much higher visual demand and are required to possess excellent visual abilities. These qualities include having a boosted dynamic visual acuity, which is the ability to see a moving object clearly and considers head movements. This needs to be optimal in sports like cricket with a fast-moving ball. Eye-tracking is also essential, which is where “keep your eye on the ball” comes into play, this helps improve balance and increases reaction time. They also require adequate peripheral vision, for example in football players must be able to keep moving with the ball whilst being aware of what is going on around them without turning their heads. Depth perception is also vital for some athletes, for example, divers, who must be able to judge the correct time to make body adjustments prior to hitting the water. Some other skills include hand-eye coordination and binocular vision, which are both important in making a great athlete.

An important way to look at the success of Vision Training in Sport would be to assess previous studies completed and weigh up if there is enough evidence to support Vision Training having a direct link to increased performance from those competing in the sport.

The first study entitled ‘Visual adaptations to sports vision enhancement training’ was written in 2006 by Michael F. Zupan- a professor at the United States Air Force Academy (USAFA). The study used 922 college athletes from the Academy and collected results over various years of the students participating in their Sports Vision Training Programme. One large aspect that was looked at was Accommodation speed and Vergence flexibility. One test completed was a Flipper Exercise where athletes viewed a card with multiple lots of three random letters while holding a set of ±2.00D flippers before their eyes at 0.3m from the card. They had to flip from plus lenses to minus lenses and each time read the letters out loud, this was repeated for 1 minute, and the sequence of letters was recorded by the athletes and they were given a score. Each time the lens was flipped, the eyes accommodation system had to re-adjust to be able to see the letters clearly.

Another aspect that was looked to be improved was Hand-eye coordination. This is a vital part of many sports and is the ability to use our hands and eyes simultaneously. One of the pieces of equipment used was the Accuvision 1000, and this helped complete two tests, fixator on and fixator active. Fixator on had the athletes touch a series of 60 lights across the Accuvision board at a rate of 2.78 targets per second. The number of hits, late hits and misses were recorded. This test was designed to test central and peripheral vision. Fixator active was very similar, however athletes were only to hit the targets when a green fixation light was present in the middle of the board, with the athlete being penalised for every incorrect hit.

Overall, the study states if two athletes of similar physical training compete, and one has had Sports Visual Training, that they are more likely to perform better due to a boosted visual system, which is agreeable to some degree, but it seems difficult to know of this would actually have an impact on their performance within their sports, as so many sports have different visual requirements as discussed earlier, and at no point does the study actually look at the athlete’s performance prior to and after the Vision Training.

A third study I chose to look at was ‘The Impact of a Sports Vision Training Programme in Youth Field Hockey Players’ by Sebastian Schwab and Daniel Memmert. This 2012 study was completed at the German Sport University of Cologne, and it aimed to improve visual performance of 34 male hockey players over a six-week period. They were split into two groups, one group would train as normal whilst the other group named the ‘intervention group’ would undergo a six-week visual training programme which utilised the following equipment Dynavision D2 Trainer, Eyeport, Vision Performance Enhancement Program, Hart Charts, and P-Rotator. The D2 board is designed to enhance hand-eye coordination, reduce reaction times and improve perception in the periphery. The Eyeport Vision Training System pushes the ocular muscles to their limits, requiring the hockey players to follow flashing blue and red lights in various directions. This helps to improve gaze motor activity as well as the skill of diverging and converging the eyes. Next, the Vision Performance Enhancement Program was used, which is an online software that trains various visual aspects, including; central and peripheral vision, stereopsis and dynamic visual acuity. The fourth station consisted of the athletes using Hart Charts. These are charts of a given distance between each other on the wall that have letters of varying sizes on each chart. The idea was for the hockey players to locate a specific order of letters on the chart, with the distance between the charts increasing between each session. The last station the athletes participated in was The P-RotatorThis machine is a rotating disc that moves in different directions and speeds. It has two rows of letters in a clock-like order and the hockey players need to identify given letters on the disc.

Both the control group and the intervention group were measured for reaction times at three different points; pre-test, post-test then finally a retention test to see if their skills were keeping up after the vision training.

From the results there is a clear increase in gap between the two groups. The control group results remain consistent for all three measurements, whereas the intervention group’s reaction time drops and only slightly increases during the retention test, which does show it has been effective if they can maintain an improved result.

After considering all factors from the studies and other sources, I think it is fair to say that Vision Training does have an impact on certain visual skills, especially reaction times. It is, however, very difficult to say whether the Vision Training has a direct link to an increased sporting performance, as so many other factors need to be considered. In study 2 there is an increase in batting average over the two years, but how can we directly link this to the Vision Training when there are so many other key things to consider including the Hawthorne Effect. This is a key aspect that needs to be considered, and it describes the effect of a greater performance of the athlete’s working harder, not visually, and as a result performing better in their sport due to them being watched and/or assessed. This could be true for some of the studies, especially Study 3 where one group is competing. Also, none of the studies considered using a placebo group, which in my opinion reduces the reliability of the results, as athlete’s could be performing better purely due to harder physical training, and not actually related to the Vision Training. Overall, I do not feel there is enough scientific evidence to support that the Vision Training directly improves the performance of an athlete. Since there is no solid evidence to either refute or back up the hypothesis, I think the most reasonable conclusion to make is that Vision Training is an effective way of improving certain visual skills for certain athlete’s, and this could possibly have an impact on their performance.

Optometry plays an important role in both diagnosing and managing binocular vision disorders. Binocular vision disorders have been associated with increased near-work symptoms1 and reduced academic achievement,2 while successful treatment of a binocular vision disorder has been associated with reduced adverse academic behaviours and reduced parental concern regarding academic achievement.3 A binocular vision assessment is therefore an important component of a routine optometric consultation.

Additionally, practitioners also need to know the effect a patient’s binocular vision status has on myopia-management. Deficiencies in various binocular vision functions have been associated with myopia progression. The various myopia-management strategies may also affect binocular vision, which may or may not be beneficial depending on the individual’s binocular vision status. For example, centre-distance multifocal soft contact lenses increase near exophoria,4 and while this may be beneficial for eso-related or accommodative insufficiency-related disorders, it is less beneficial for exo-related or accommodative excess-related disorders. It is therefore incumbent on the practitioner performing myopia-management to be aware of a patient’s binocular vision status and manage a patient’s binocular vision disorder. Management of a binocular vision disorder may involve choosing myopia-management strategies that are beneficial to a patient’s binocular vision status, performing vision therapy or referring to another practitioner specialising in vision therapy.

The International Myopia Institute5 (IMI) recommends the following tests be performed at a baseline examination and at follow-up visits to monitor changes with myopia-management strategies:

• Accommodative accuracy / response (lag or lead)
• Amplitude of accommodation
• Distance and near accommodative facility
• Distance and near heterophorias
• Near fixation disparity
• Accommodative convergence / accommodation (AC/A) ratio

The IMI also lists various clinical methods that can be used to measure these outcomes.5

In addition to these tests, the practitioner may also consider tests at baseline that aid in differential diagnosis of a binocular vision disorder. These include monocular accommodative facility, near point of convergence, negative and positive fusional reserves at distance and near and negative and positive relative accommodation (B+ and B-, respectively) at near.6

Much of the interest in binocular vision and myopia-management stems from differences in myopes compared to non-myopes for various aspects of binocular function, particularly accommodative function. Myopes tend to have a higher lag of accommodation and a lower amplitude of accommodation. This need for the myope to increase accommodative effort at near is a a contributing factor to other differences in binocular vision function, such as tendency towards esophoria and increased gradient AC/A ratio.

References

1. Borsting E, Rouse MW, Deland PN, et al. Association of symptoms and convergence and accommodative insufficiency in school-age children. Optometry 2003;74:25-34.
2. Shin HS, Park SC, Park CM. Relationship between accommodative and vergence dysfunctions and academic achievement for primary school children. Ophthalmic Physiol Opt 2009;29:615-624.
3. Borsting E, Mitchell GL, Kulp MT, et al. Improvement in academic behaviors following successful treatment of convergence insufficiency. Optom Vis Sci 2012;89:12.
4. Gong CR, Troilo D, Richdale K. Accommodation and Phoria in Children Wearing Multifocal Contact Lenses. Optom Vis Sci 2017;94:353-360.
5. Gifford KL, Richdale K, Kang P, et al. IMI – Clinical Management Guidelines Report. Invest Ophthalmol Vis Sci 2019;60:M184-m203.
6. Scheiman M, Wick B. Clinical management of binocular vision: heterophoric, accommodative, and eye movement disorders: Lippincott Williams & Wilkins; 2008.

This essay will explore the development of visual acuity and depth perception within the first year of an infant’s life. It explains the reason for the fast development of visual acuity within the first 6 months and the development of visual acuity based on how cone photoreceptors and the fovea mature to provide good resolution. OKR and VOR are also looked at for stabilising images. The development of depth perception using motion parallax and stereopsis is explained and along with the reasons for the age of onset of stereopsis.

Visual Acuity Infantile Development

Researchers Daphne Maurer and Telle L Lewis (Maurer and Lewis 2001) explained the rapid change in acuity within the first 6 months is due to the cone shape change. The cone changes to become a funnel shape preventing extra light from falling thorough and therefore allowing fine details to pass on to the visual cortex. Simons ( Simons 1993) using research from (Bach and Seefelder, 1914; Abramov et al, 1982; Hendrickson and Youdelis, 1984; Youdelis and Hendicson, 1986) that the spacing for cones in an adult is more densely packed than that of an infant, so as infants cones spacing decreases, less information is lost from the gaps, increasing fine detail and therefore increasing visual acuity.

In the parafovea, the rod cells have already matured, but the cone cells are still developing, Simons (Simons 1993) explains that initially cones are untapered so they are thinner and smaller at one end.

Foveal Maturation

Changes in the fovea aid visual acuity as it affects spatial vision. As the fovea matures, more light and information from the world is caught, more information is processed, so less of the world is blurry therefore improving the acuity for an infant and allowing them to gradually recognise faces and important detail.

The fovea at birth is immature, after which it shows rapid development which aids with visual acuity. Hendrickson and Youdellis (Anita E Hendrickson Christine Youdelis 1984) explain the fovea shows thinning in the inner nuclear and ganglion cell layers which leads to a central depression by centripetal migration forming the foveal pit. They also include that there is shallow depression one week after birth and the rods are still thick without outer segments. Researchers (Hendrickson and Drucker 1992) state that the inner retina within 5-8 days is nearly mature. Within these days, the basal layers of the axons of the photoreceptors elongate too, leading to a thicker photoreceptive layer.

Simons says (Simons 1993) as the axial length of Rhodopsin increases in the rod outer segment it leads to an increase in quantum catch therefore it leads to higher resolution. The chart shows maximum rhodopsin being produced post 6 months and rapid development within first 6 months disregarding preterm babies. As rhodopsin is important for transduction, more light is transduced into energy signals therefore more information reaches the visual cortex, and objects are seen with a greater acuity.

Neurons at birth are immature at birth. The lateral geniculate nucleus responsible for relay between the retina and the visual cortex neurons are visibly different, they have spiky textures and more dendrites in comparison to adult neurons, greatest spines are at 4 months, and reach adult spine level at 9 months. The maturation of neurons is important for transmitting information to the visual cortex and the continued development of visual post the early post- natal months could be attributed to the maturation of neurons, as greater fine detail is achieved.

In his book (Simons 1993) explained the importance of the development of vestibuloocular and optokinetic reflexes to maintain images on the retina, if they are moved, blurry images are seen lowering visual acuity. Head Movement causes this response. During head rotation, the visual field moves in the opposite direction, to maintain the image the eyes move in opposite direction to the head movement these are controlled by two reflexes:

Vestibulooculular reflex: the movement of the eyes

VOR gain (ratio eye velocity: Head velocity) determines the efficiency of VOR, a study (finocchio Preston and Fuschs 1991) cited in Simons book shows infants have higher gain than adults therefore allowing for short periods of head rotation.

Optokinetic reflex: Determine velocity for movement of eyes to ensure image is stabilised. It is dependent on development of visual acuity, contrast sensitivity and other such factors.

The importance of VOR and OKR for infants is that at birth, smooth pursuit and tracking has not yet developed and so to maintain image, the infant relies on these reflexes. Smooth pursuit only develops at about 3 months of age when both eyes can co-ordinate together.

Depth Perception in Infants

Depth perception is the ability to view objects in 3d using depth cues. Infants use monocular and binocular depth perception.

Motion Parallax is important for the development of monocular depth perception, by making head movements as explained earlier in OKR the closer objects move in the opposite direction. It is a monocular depth cue that relies on motion as proven ( Nawrot et al 2009) when infants discerned depth when using smooth pursuit. They also develop it close to the age of stereopsis

Nawrot (Nawrot and Nawrot) in their journal claim that motion parallax develops slightly before the onset of stereopsis and therefore prepares the cortical developments required for depth processing.

Stereopsis is a means of depth perception using binocular vision. It requires retinal disparity, this allows information about depth to be made. Due to the different geometrical positions of the eyes, different images are seen. The greater the difference between images, the closer the object is and vice versa.

(Simons 1993) in his book had defined onset stereopsis as the youngest age in which an infant is able to differentiate between images with and without binocular disparity. Using the diagram, it is concluded that onset stereopsis is shown as 3-5 months of age, however, some infants display stereopsis at as young as two months. Simons surmised the age for the sudden onset can be determined by various factors:

• Retinal maturation: cited from (Aslin and Dumais, 1980) but, there is no sudden increase in acuity from the retina, and therefore it cannot be the only factor. The maturation increases the retinal resolution, however Simon states at 2 months old, the spatial resolution is enough for stereopsis to occur.
• Vergence: Simons also cites research carried out by scientists (Aslin and Durmais 1980, Braddrick and Atkinson1983) in that Vergence Control is a factor for development of stereopsis, considering that postnatal vergence control improves greatly.
• Cortical Maturation: it is important for the coding of original visual information to be accurately depicted using depth disparity (Birch et al 1982, Atkinson 1984, Held 1988, Wilson 1988). Simons cites that a study (Huttonlocher et al 1982) that the development of synapses peaks between 2-8 months, this coincides with the onset of stereopsis. Due to the development of synapses, visual information is passed on the cortex, the disparity differences would be more visible and a more accurate depth perception can be carried out.

The fusion of the data received from the right and left eyes that causes depth disparity need to be analysed and combined, this process is carried out by binocular neurons in the visual cortex which need to be developed to work.

Simons also uses research carried out on a monkey that depicts during the early stages of infancy, the neurons of both eyes at the entry of the striate cortex are overlapped and share synapses with the same cells, this causes the disparities to be wrongly processed and therefore stereopsis is unable to occur. Research carried out with cats (Timney 1981) suggests that the separation of these columns and the age of onset stereopsis are similar and therefore neural development too could be a factor for onset stereopsis.

The experiment (Birch et al 1982) carried out to investigate stereoacuity for crossed and uncrossed disparities indicates stereoacuity develops very early on between 3-6 months of an infants life, which is on par with stereopsis development, they also concluded that the difference between crossed and uncrossed disparities aren’t present post 6 months this shows that convergence isn’t a main factor for stereopsis. Birch et al also conclude that the data support the hypothesis that convergence is important for development of onset stereopsis: inaccuracy of convergence leads to a decrease in acuity for stereopsis both crossed and uncrossed disparities. In addition to this, it supports the idea that the visual cortex is important for the development of stereopsis as fixation and fusion are necessary. This further supports Simons conclusions.

Over the first year of life, many developments in the body occur including speech advancements, fine and gross motor movements, facial expressions and the fusion of bones. One of these advancements includes the progression of our eyesight- vision is a powerful sight that allows us to protect ourselves from the environment by reacting to stimuli; there is no doubt that as we get older, we gain more independence, such as being able to walk ourselves meaning it is essential that we are able to react to our environment in order to survive.

Vision is a combination of both incoming information from the environment and our knowledge of the world, consisting of many components- this includes visual acuity, depth and colour perception all of which gradually develop over the first year of life. A newborn does not have the visual abilities required for its environment, such as accommodation, and so gains information through the interpretation of its surroundings.

The human visual system develops rapidly over the first 12 months of life, advancing both in anatomy and function. Although newborns can detect changes in brightness, distinguish between stationary and kinetic objects in their visual fields (En.wikipedia.org, 2019), the ability to do so is very weak and improves with time. The cells that make up the visual cortex in an infant are not yet isolated by function and type, as they are in adults. Additionally, most of the cells are not yet coated with myelin, a white, fatty substance that aids neural transmission and the dendrites that reach multiple layers of the cortex are still short.

Colour perception

Colour perception is the ability to distinguish between different colours or alternate wavelengths. Rods and cones are essential cells that are a part of our eyes and assist our eyes in vision; rods detect light and are responsible for vision at low levels of light. Cones are mainly used for photopic vision and are capable of colour vision. There are three types of cones known as red, blue and green. Any absence of these cones results in colour blindness- all babies are colour-blind when they are born suggesting that these cells may still be developing. This may be due to most receptors not being coated in myelin that aids neural transmission as well as the dendrites still being short, causing slower transmission. Colour vision begins to develop within a week after birth and by 6 months a baby can see every colour that an adult can (Discovery Eye Foundation, 2019).

At 1 week, infants are able to discriminate long and medium wavelengths which may be due to the development of the light sensitive cones in the retina. However, infants at 1 month can not distinguish between short wavelengths due to the absence of S cones and such mechanisms in the visual cortex which still requires some advancements (Psyc.ucalgary.ca, n.d.).

Over the first 2 months, colour perception develops rapidly and by 3 months, an infant can start to see colours due to the strengthening of rods and cones, allowing the eye to respond to different wavelengths of light. It is firmly established that two-month-old infants are at least dichromatic, but there is no clear data on whether they are trichromatic. There are a few pieces of evidence to suggest that the basic sensory capacities required for color processing are different for infants than for adults, but specifics on the ontogenetic course are as yet unknown (Werner and Wooten, 1979)

By 2 months, the S cones have now become functional, allowing the infant to better discriminate between the shorter wavelength colours. At 4 months, an infant can categorise colours in the same way as an adult, demonstrating the advancements in retina and visual cortex allowing this to be made possible.

By 6 months, advances in the visual parts of the brain have taken place, allowing an infant to see colours similar to that of an adult, including most colours of the rainbow. Testing more than 40 babies, Skelton has found that, even at four months, they, like adults, need blues and yellows to be more intense to see them than reds and greens. Research by Franklin and her team has also shed light on a surprising phenomenon: babies can categorise colours (Davis, 2019). Franklin and her colleagues familiarized 179 babies ranging from 4 months to 6 months old with a particular hue, such as blue. Then, after less than a minute, the researchers presented the baby with a familiar color alongside a new color, such as green. If the baby stayed on green, the researchers considered it novel for the baby. In the end, the researchers concluded that the babies were able to discern five color categories: red, yellow, green, blue and purple (Staedter, 2017). This in turn proposes that at 6 months, a babies colour vision is similar to that of an adult as they can make out more complex shapes as well as a wider spectrum of colours than they could pre 6 months; this implies development in photoreceptors on the retina. By 6 months, rod outer segment length, rhodopsin content has increased so that rod-mediated visual sensitivity has become similar to that of adults (Hansen and Fulton, 2006) Their sensitivity is greatest to intermediate wavelengths such as yellow and green and less for shorter wavelengths such as blue or longer wavelengths such as red.

The images above demonstrates how newborns cannot see in colour- their vision is limited to simple shapes and minute colour. It consists of a blur with a single colour, demonstrating that they may just be able to make out their parents faces. Even at 6 months, although the vision is similar to that of an adult, the colour vision is not yet fully advanced and a distinct image is not fully seen, whereas the adult can clearly see a more complicated image with brighter colours and shadows. This is most likely to be due to the lack of development in their visual cortex as well as the growth of the rods and cones.

Depth perception at birth

Depth perception is the visual ability to perceive the world in three dimensions to see if objects are closer or father away then other objects. Depth perception occurs when our brain processes information from both eyes and joins them together to form a three-dimensional image; this is a requirement of both eyes- infants do not experience depth perception, suggesting that their eyes do not work together at birth. At 3 months of age, an infant can accommodate which allows them to discriminate small differences in object distance. Therefore, sensitivity to depth from motion is present very early in infancy (Kellman and Arterberr 1998) (Sciencedirect.com, 2019)

There are three visual cues that aid depth perception known as motion parallax, interposition and aerial perspective. Motion parallax occurs when we move our head back and forth. Objects at different distances will move at slightly different speeds. Our brains perceive this and give us cues about depth perception (Bedinghaus, 2019) In infants, dishabituation results indicate that infants may be sensitive to unambiguous depth from motion parallax by 16 weeks of age (Nawrot E, Mayo and Nawrot, 2009). Interposition is also known as overlapping and is a monocular trait, telling us which objects are closer or father away and finally, aerial perspective refers to the affect the atmosphere has on an object, causing farther away objects to seem hazy. For example, we can see clearly the keys on a laptop but if we were to look at mountains from a distance, they would seem blurry. In a newborn, aerial perspective hardly exists as the greatest they can see is a blur of the shape of their parents faces. This demonstrates that depth perception is non-existent at birth, due to the lack of visual cues present in addition to the eyes lacking the ability to work in duo.

At 2 to 3 months old, infants have some form of depth perception which is demonstrated through the ‘visual cliff’ experiment; researchers found that infants as young as 2 months showed changes in heart rate when lowered face down over the shallow and deep ends of the visual cliff. Specifically, the infants’ heart rates decreased when they were lowered over the deep end, and were unchanged when over the shallow end. (Condry and Yonas, 2019) (Spillman and Werner, 1989) suggesting an interest from the infants, therefore indicating they have an idea of depth perception. However, a limitation of this experiment is that infants cannot tell the experimenter what they witness, therefore, the heart rates may be unreliable due to a number of external factors having an influence over their vision.

Recent research shows that young infants are sensitive to motion parallax in visual displays but leaves open the question of whether infants use the information to perceive spatial layout. In this experiment, 6-month-old infants were translated horizontally in front of two objects that were attached to the infant’s movement. One object moved in the same direction as the motion of the infant and the other object moved in the opposite direction. This provided motion parallax information that the object that moved in the opposite direction was nearer in depth. Infants who viewed the display monocularly reached, in preference, the object that was apparently nearer. A control group of infants who viewed the display binocularly showed no such preference. These results provide the first direct evidence that young infants use the spatial information provided by motion parallax to perceive the relative distance of objects and to direct their actions accordingly. (Condry and Yonas, 2019)

Although depth perception reaches that to of an adult at 2 years, by 12 months, an infant can see the same as an adult. This development may be due to infants’ eyes working together to help form a three-dimensional image as both eyes view different angles, therefore, together they can help form an image with a certain depth. With physical improvements such as increased distances between the cornea and retina, increased pupil dimensions, and strengthened cones and rods, an infant’s visual ability improves drastically. (Walk, 1966)

Visual acuity at birth

Visual acuity refers to the sharpness of vision; it is usually measured by the ability to read numbers and letters from a specific distance and is affected by the refractive error of the patient. Most newborns are hyperopic therefore, their visual acuity on average is 6/240 to 6/60 (Wikipedia, 2019). The most common visual acuity test in newborns, is by testing their eye movements to a toy. However, through the use of the opticokinetic nystagmus response to striped patterns of varying width, investigators demonstrated that the newborn exhibits at least 20/150 vision (Volpe, 2008) This means that what a newborn can see at 20 feet, is what an adult can see at 150 feet, demonstrating that the vision is obviously not as sharp.

The image above demonstrates poor visual acuity in newborns. The pictures in the upper images demonstrate how groups of toys are seen by adults. The images in the lower tables show how groups of toys would be for newborns whose visual acuity is 25 times worse than that of an adult, at more than 45cm (Gwiazda et al., 2019). The cause of low visual acuity may be due to the refractive error a child is born with- most newborns are hyperopes, but the range varies to myopia as well causing visual acuity to be lower than an adult. This may be due to the shape, size and distributions of cone receptors on the retina. These changes improve the eye’s light capturing ability as well as its acuity (Psyc.ucalgary.ca, 2019). This demonstrates how visual acuity improves over the first 12 months of life.

In newborns, the cones are short and not as closely packed together than in adults- this means that light is less efficient in being absorbed. In addition to this, the cones in infants have a fat inner segment and a small outer segment, resulting in less visual pigment reducing the ability to capture light as demonstrated in figure 1 below. As the infant grows, the cells elongate, become more densely packed and migrate toward the center of the retina to form the fovea, the area of best acuity.

The image above demonstrates how acuity progresses throughout infanthood; visual acuity rapidly develops between birth and 3 months where its starts at 20/800 and rises, on average, to 20/200. After 3 months, there is a slow improvement between 3 months and 12 months where visual acuity has now reached similar to that of an adult, however, is still weak. By 3 years, an infant has now 20/20 vision due to the distribution of rods and cones being interchangeable to that of an adult.

Conclusion

To conclude, infant vision at birth is scarce with a blur and minute colour being visualised. Vision starts to develop from the day the infant is born with rods and cones strengthening, allowing an infant to interpret a wider variety of wavelengths of light; in addition to this, the visual cortex starts to develop, allowing the infant to receive impulses about its vision.

Visual acuity is extremely weak at birth with an average of 6/240 being seen. When in development, the distribution of rods and cones allow the ability of the infant to capture light to improve, which in turn, helps improve visual acuity. There is a rapid improvement between birth and 6 months, however, it slows down after 6 months but does not stop until 20/20 vision is achieved. This can be explained by the cones elongating and migrating closer together on the fovea, resulting in more defined input in the fovea. By 3 years, the visual acuity is equal to that of an adult who has perfect vision and a child can see in sync with an adult’s vision. However, there are different results from a number of different resources, making it difficult to understand the visual acuity in newborns, shining light on to whether there is a wider range of visual acuities present at birth.

Depth perception is non-existent at birth due to the infant lacking the ability to accommodate. However, depth perception begins to make its way into an infant’s vision as they start to use their ability to accommodate, which in turn results in objects from a selection of distances to be perceived more accurately than they could before. This may be due to our eyes having the ability to work binocularly, which is a trait that is essential in order to start perceiving our world at different depths.

We can see the world in colour due to receptors, known as rods and cones, which are found in our retina. They contain different pigments, which absorb certain wavelengths of light better than others. Rods do not mediate colour vision and are responsible for our ability to see in dim light as they have high photosensitivity. There are three types: blue-sensitive, green-sensitive and red-sensitive cones (short, medium and long wavelength cones with peak absorptions at 430, 530, 560nm.) When they are stimulated in different proportions we are able to see different colours. Although humans are born with all 3 types of cone cells, we are not able to see in colour at birth as parts of the brain receiving these nerve signals need to mature with age, along with the cone cells themselves.

Colour categorisation is a skill that infants develop early in life. Infants can distinguish between red and green at 2 months, and with time, between blues and yellows. An expert in colour vision, Franklin, devised a test that involved presenting infants with a coloured screen on which a dot appears. Both the dot and coloured screen may have been from the same colour category or a different colour category. It was observed how quickly the infant looked at the coloured dot. The speed at which they looked at the coloured dot helped to determine how different it appeared from the colour of the screen. Franklin and her team carried out another experiment involving 170 babies, being shown two squares of the same colour and two of different colours. This experiment helped to derive how many colour categories infants possess – they found that these categories were likely to be red, purple, yellow-brown, green and blue whilst other colour categories with pink and orange develop with language.

You can see that infants look more quickly towards a coloured dot when it comes from a different colour category. In other words, babies can tell that different colours of blue are all, well, “blue”. Colour categories, it seems, are not just down to language, they are in some way “hardwired”.

Contrast sensitivity measures the amount of contrast needed to detect the presence of a grating of different spatial frequencies, ranging from coarse to fine. Spatial frequency is measured in cycles per degree, and peak sensitivity is reached at 4 cycles/deg – this grating is resolved with only 1% contrast, whereas higher and lower spatial frequencies require higher contrast.

An experiment in which CSF’S were obtained longitudinally from infant monkeys (5-6 weeks postnatally) showed that with time, sensitivity increased at all spatial frequencies. (Boothe et al.,1980) However, sensitivity to low spatial frequencies become adult-like earlier than that for the high-frequency range. E.g, sensitivities for 1-5 cycles/deg reach adult levels by 20 weeks, compared to gratings greater than 15 cycles/deg which still improve at 40 weeks. These changes shift the CSF curve upwards (increasing sensitivity) and peak response shifts to the right (higher spatial frequencies. A 4:1 rule is devised because visual functions develop four times faster in a monkey than an infant, therefore we can relate these results to human visual development.

Changes in contrast sensitivity occur due to changes in the retina and the development of the visual cortex. Wilson (1988) suggested that migration of foveal cones produces a change in spatial scale and therefore a progressive shift of mechanisms turned towards higher spatial frequencies. The growth of the foveal cone outer segments causes an increase in mechanism sensitivity (Bernard, Edgar, 1995, p.54), as well as tighter packing of cones.

In the image above we can see the improvements in contrast sensitivity from 3 to 9 months, as the infant is able to see more low contrast elements and fine detail, and how similar this is to what the adult is able to see. Retinal factors take 4+ years to reach full adult maturity. Vision rapidly improves after birth because of the size, shape and density of cones found in the fovea. The cone length is 16x shorter in newborns. Visual acuity is further limited because the cone packing density is also 4x less in newborns which reduces spatial sampling.

Cone waveguide is not developed in the infant, meaning the cones do not have a funnel-like appearance, which is the waveguide property. The waveguide property allows light to enter only at one aperture and guides it into the interior space of the receptor.

The image shows the difference in a cone without the waveguide property on the left. When light enters this cone, it is not guided towards the interior space of the aperture and continues in a straight line. The cone with waveguide properties continually guides the light ray. Banks and Bennet (1988 ) estimated that the adult central foveal cone lattice absorbs 350 times more quanta than the newborn central foveal lattice, i.e for every quantum of light absorbed in newborn cones, roughly 350 quanta are effectively absorbed in adult foveal cones.

Post retinal factors also affect visual development. The speed of conduction depends on synapses and the structural properties of axons. When light focuses onto the retina, the optic nerve transports nerve impulses from receptors to the brain. A critical component is the thickness of the myelin sheath which acts as an electrical insulator. It causes the nerve impulses to ‘jump’ from one uninsulated node to the next, resulting in rapid saltatory conduction. However, myelination is incomplete at birth therefore vision is limited and improves during growth.

Axon diameter is limited at birth and continues to grow throughout the first few years. A larger axon diameter means there is less resistance to ion flow, increasing the speed of nervous transmission. Maturation of these regions of the brain undergo conspicuous growth in infancy but may not completely mature until adulthood (suggested by postmortem studies).

Synaptogenesis is also important in neural development. They begin to form prior to week 27 of pregnancy and reach peak density after birth. In late pregnancy as well as early postnatal life, synaptic density increases within the primary visual cortex. Density doubles from 2 to 4 months of age, and declines after the age of one. Along with synaptogenesis, neurons increase their dendritic arborizations, extend their axons and myelination occurs. This is followed by a period called synapse elimination during which the nervous system fine-tunes neural connectivity; which involves eliminating interconnections between redundant or non-functional neurones. This continues for over a decade.

To summarise, vision over the first 12 months experiences a rapid improvement. The most important changes occur in the rapid infantile phase because of emmetropization, retinal factors, as well as post retinal factors involving the visual cortex, myelination and synaptogenesis. These factors combined to give rise to colour vision, improved contrast sensitivity and a higher VA in the first 12 months.

What is it?

Color vision deficiency, also known as color blindness, is a condition that affects an individual’s ability to differentiate between colors, specifically those of similar hues. The inability to distinguish between colors results from either a partial or total loss of color vision, depending on the type of color blindness present (National Institutes of Health [NIH], n.d.).

Symptoms

The most common indicator that someone has color blindness is the lack of ability to decipher between the three primary colors, red, yellow, and blue, or the lack of ability to decipher between colors of similar shades, such as dark blue and black (NIH, n.d.). In more severe cases of color blindness, such as when achromatopsia occurs, vision problems arise as additional symptoms (NIH, n.d.). Some vision problems that are apparent with severe color blindness are: photophobia (light sensitivity), side-to-side eye movements that appear to be involuntary, and a decrease in vision sharpness (NIH, n.d.). Farsightedness and nearsightedness have also been observed in people with more severe cases of color blindness, but when these occur, the person only has one or the other, never both (NIH, n.d.).

Types

Color blindness can be classified into two main types: incomplete or complete. Incomplete color blindness is the milder form where an individual can still see and differentiate between some colors (NIH, n.d.). Complete color blindness is the more severe form where an individual cannot see any colors within the visible spectrum of light, therefore that person only sees black, white, and shades of gray (NIH, n.d.). Incomplete color blindness can be further divided into two types: red-green color blindness, which is by far the most common, and blue-yellow color blindness, which is less common (NIH, n.d.). Individuals with red-green color blindness have trouble deciphering between red, yellow, and green (NIH, n.d.). Red-green color blindness affects males more often than females, affecting nearly one in twelve males and one in two-hundred females (NIH, n.d.). Red-green color blindness tends to affect people with a Northern European heritage more often than people with other ethnical backgrounds, for reasons still quite unclear (NIH, n.d.). Individuals with blue-yellow color blindness have trouble deciphering between varying shades of blue and green and between dark blue and black (NIH, n.d.). Blue-yellow color blindness affects both males and females equally, affecting nearly one in ten thousand individuals (NIH, n.d.). Blue-yellow color blindness does not appear to affect any specific ethnicity more than the other (NIH, n.d.).

Complete color blindness, also known as monochromacy or achromatopsia, can also be further divided into two categories: incomplete and complete (Neitz & Neitz, 2000). In incomplete achromatopsia, such as blue cone monochromacy, an individual only has one type of functioning cone out of three, so that individual’s ability to decipher between colors is extremely impaired (Neitz & Neitz, 2000). Blue cone monochromacy, specifically, is a rare type of color vision deficiency that affects males more often than females (NIH, n.d.). This type of color blindness only occurs in one out of every one hundred thousand individuals (NIH, n.d.). Blue cone monochromacy, even though characterized under complete color blindness, allows an individual to still see a single color, which is why it is classified as incomplete achromatopsia (Neitz & Neitz, 2000). In complete achromatopsia, such as rod monochromacy, an individual does not have any of the three types of cones functional (Neitz & Neitz, 2000). Without any of the three types of cones functional, an individual cannot see any color, only a grayscale. While it is possible that individuals with achromatopsia can see a single color, as mentioned previously, due to the possibility of the single functioning cone, it is not very common and most individuals’ color vision is completely absent (Neitz & Neitz, 2000).

Causes/ pathophysiology

When light enters the eye, in the form of a wave, it enters through the cornea, passes through the lens, where it is focused, and then travels to the retina (Mayo Clinic, 2018). The retina, a light-sensitive layer of tissue in the back of the eye, is connected to the optic nerve which transmits the visual signals processed within the retina to the brain (Neitz & Neitz, 2000). The retina includes two types of photoreceptor cells: rods and cones (Neitz & Neitz, 2000). The rods are responsible for vision in low-light environments, such as those that occur at night, whereas the cones are responsible for vision in bright-light environments, such as those that occur during the day (NIH, n.d.). Both the rods and the cones, through the utilization of pigments, allow the eyes to recognize and respond to varying wavelengths of light and transmit these visual signals to the brain (NIH, n.d.; Mayo Clinic, 2018). The light-sensitive pigment in the rods is rhodopsin, which is encoded by a gene on chromosome three (Neitz & Neitz, 2000). The light-sensitive pigment in the cones is opsin, which comes in three different types depending on the type of cone (NIH, n.d.). The pigments of both the rods and the cones contain chromophore 11-cis-retinal, which is the light-sensitive portion of the pigment (Neitz & Neitz, 2000). When light is absorbed by the eye, the 11-cis-retinal undergoes a conformational shape change which specifically stimulates the opsin of the cones, triggering biochemical reactions to occur and a neural signal to be sent to the brain about the light absorbed (Neitz & Neitz, 2000). The rods and cones are able to transmit the signals from visual stimuli to the brain because they contain chemicals that decompose through the biochemical reactions triggered by the activated opsin, which promotes the sending of the neural signal (Chaudhari & Shah, 2012).

The cones within the retina, which provide color vision, can be classified into three basic groups: “L” cones, “M” cones, and “S” cones (NIH, n.d.). The “L” cones are cones sensitive to long wavelengths of light, such as that from yellow-orange light, and they contain opsin encoded by the OPN1LW gene (NIH, n.d.). The “M” cones are cones sensitive to middle wavelengths of light, such as that from yellow-green light, and they contain opsin encoded by the OPN1MW gene (NIH, n.d.). The “S” cones are cones sensitive to short wavelengths of light, such as that from blue-violet light, and they contain opsin encoded by the OPN1SW gene (NIH, n.d.). The OPN1LW and OPN1MW genes are located on the X chromosome, whereas the OPN1SW gene is located on chromosome seven (NIH, n.d.). When individuals have mutations in any of their opsin genes, they have one of the inherited forms of color blindness. Abnormal opsin pigments within the “L” or “M” cones, or absence of either of these types of cones, results in red-green color blindness (NIH, n.d.). If both of these types of cones are absent but the “S” cone is still present, blue cone monochromacy results (NIH, n.d.). Since the genes for the opsin pigments in the “L” and “M” cones are encoded on the X chromosome, red-green color blindness and blue cone monochromacy are considered X-linked disorders (NIH, n.d.). Abnormal or absent opsin pigment within the “S” cone results in blue-yellow color blindness (NIH, n.d.). Since the gene for the opsin pigment in the “S” cone is encoded on chromosome seven, blue-yellow color blindness is considered an autosomal disorder (NIH, n.d.).

Acquired color vision deficiencies are not linked to chromosomal gene mutations and can occur throughout life from several factors, including: eye diseases and disorders, antibiotics, prescription medications, toxic chemicals, eye trauma and injury, age, and other physiological diseases and disorders (Chaudhari & Shah, 2012; NIH, n.d.). Macular degeneration, which is a degeneration of part of the retina, or other eye disorders which affect the retina, optic nerve, or visual cortex, can all cause color vision deficits in individuals when they arise (Chaudhari & Shah, 2012; NIH, n.d.). The side effects of specific antibiotics or prescription medications, such as high blood pressure medications, can also cause individuals’ perceptions of color to change when under use (Chaudhari & Shah, 2012). When individuals are exposed to certain toxic chemicals, such as carbon monoxide, fertilizers, styrene, or organic solvents, in a laboratory or other work space, they too put themselves at risk of color vision deficiencies (Chaudhari & Shah, 2012; NIH, n.d.). Eye trauma or injury only affects color vision when the damage is in the retina or portions of the brain that transmit, integrate, and process visual stimuli produced by colors (Chaudhari & Shah, 2012). A stroke is a common example of an injury that can cause damage to the parts of the brain involved in relaying and interpreting color stimuli (Chaudhari & Shah, 2012).

As individuals get older, as with any other portion of the body, the retina and all its components involved in processing color stimuli become degraded and altered, which can cause partial loss of, or alterations to the color vision of the older individuals (Chaudhari & Shah, 2012). The nerves of the visual cortex, where color stimuli are processed, become neuropathic in physiological diseases such as Alzheimer’s disease, which can also result in color vision deficits (Chaudhari & Shah, 2012). In disorders such as diabetes, the pigments within the cones of the retina can get disturbed, the lens of the eye can get discolored, and there can be pathological changes in the neurons that transmit the visual stimuli (Chaudhari & Shah, 2012). Each of these three factors can play a role in causing color vision defects in the affected individuals. When an individual is a chronic alcoholic, his/her optic nerve can eventually atrophy, which also results in color vision changes as seen with the other physiological disorders, due to a loss of transmission of visual stimuli to the visual cortex in the brain (Chaudhari & Shah, 2012). In general, acquired color blindness occurs from an alteration in the retina or portions of the brain involved in deciphering colors.

Diagnosis

The most efficient, and widely-used way to diagnose color blindness is to get an eye exam done which includes the use of printed pseudoisochromatic plates to test for color vision deficiencies (Neitz & Neitz, 2000). These plates help to diagnose not only the severity of an individual’s color vision loss but also the type of color vision deficiency present (Fomins & Ozolinsh, 2011). Rabkin tables and Ishihara tests, forms of pseudoisochromatic plates, are used most often to diagnose red-green color deficiencies specifically (Fomins & Ozolinsh, 2011). All of the various pseudoisochromatic test plates, no matter what form, include an object of focus, often a number or shape, and a background (Fomins & Ozolinsh, 2011). Both the object and the background are comprised of patches of random sizes, colors, and hues which led to these test plates gaining the nickname “color camouflage” plates (Fomins & Ozolinsh, 2011). It is fairly common for difficulties to arise when children of younger ages get tested by these plates since they are more prone to misunderstanding directions or getting stressed by the testing environment and the pressure to get the “correct answer” (Fomins & Ozolinsh, 2011). Due to these difficulties, the pseudoisochromatic plate tests tend to be inconsistent and therefore less reliable, so new methods of diagnosis are being encouraged (Fomins & Ozolinsh, 2011).

Treatment

Inherited color blindness has no cure at this time, but scientists are working on ways to utilize gene therapy and other retinal therapeutics to reinstate color vision in those that have either partial or complete color blindness (Mayo Clinic, 2018). A relatively recent study at the University of Pennsylvania utilized gene therapy, mediated by a recombinant adeno-associated virus, in order to restore cone function and color vision in daylight in humans and animals, specifically canines, that had forms of achromatopsia (Komáromy et al., 2010). Various types of the promoter for the human form of red cone opsin, a protein involved in sensing light, was utilized in the gene therapy (Komáromy et al., 2010). This study helped provide insight into future ways gene therapy can be used to target malfunctioning rods and cones in the retina.

Since the use of gene therapy for inherited color vision deficiencies is still being developed and tested, individuals with this form are currently recommended to implement a colored filter over their glasses or place colored contacts into their eyes in order to get some color vision back (Mayo Clinic, 2018). If an individual has an acquired color blindness, rather than an inherited one, the treatment is much simpler. These individuals can be treated by taking measures to remove the source of infection or reduce the effects of the eye disorders that caused the acquired color vision loss. For example, one can discontinue a medication if it appears to cause color blindness as a side effect (Mayo Clinic, 2018). When acquired color blindness is treated correctly, individuals can often get some color vision back but typically not all the color-visualizing ability they had originally (Mayo Clinic, 2018).

Correlations with other diseases

Even though there is currently no known association between color vision deficiencies and disorders of the eye that cause blindness, there have been individuals who have experienced color blindness as a symptom of the blinding disorders (Neitz & Neitz, 2000). Some of the blinding disorders that have been known to cause color vision deficiencies, include: macular degeneration, as mentioned previously, glaucoma, and diabetic retinopathy (Neitz & Neitz, 2000). Color blindness often occurs in conjunction with other physiological diseases that do not directly cause blindness, however, to such a great extent that these diseases have been classified as causes of color vision deficiencies (Chaudhari & Shah, 2012). Individuals can get acquired color blindness as a symptom from Alzheimer’s, diabetes, and chronic alcoholism, as discussed previously, but also from Parkinson’s disease (Chaudhari & Shah, 2012).

As more studies are carried out, more information can be obtained on if there are other external factors, such as other physiological disorders, that correlate to color blindness. The information from these studies can allow insight into how to more-efficiently prevent the development of acquired color blindness. As novel information arises about both types of color blindness, acquired and inherited, diagnostic tests and treatment plans for both can also improve.

References

1. Chaudhari, D. K., & Shah, J. S. (2012). Pathophysiology of altered color perception. Research in Pharmacy.
2. Color vision deficiency – Genetics Home Reference – NIH. (n.d.). Retrieved from https://ghr.nlm.nih.gov/condition/color-vision-deficiency.
3. Fomins, S., & Ozolinsh, M. (2011). Multispectral analysis of color vision deficiency tests. Materials Science, 17(1), 104-108.
4. Komáromy, A. M., Alexander, J. J., Rowlan, J. S., Garcia, M. M., Chiodo, V. A., Kaya, A., … Aguirre, G. D. (2010). Gene therapy rescues cone function in congenital achromatopsia. Human Molecular Genetics, 19(13), 2581–2593. doi: 10.1093/hmg/ddq136
5. Neitz, M., & Neitz, J. (2000). Molecular genetics of color vision and color vision defects. Archives of ophthalmology, 118(5), 691-700.
6. Poor color vision. (2018, November 6). Retrieved from https://www.mayoclinic.org/diseases-conditions/poor-color-vision/symptoms-causes/syc-20354988.

Introduction

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There are several aspects of the optical system which contribute to normal visual development in infants, and retinal development is essential for this. Retinal factors take 4+ years to reach full adult maturity. Receptors are found in the fovea and peripheral parts of the retina.

Vision rapidly improves after birth due to changes in the size, shape and density of cones found in the fovea. The outer segment length of the cones in the fovea is 16x shorter in newborns compared to adults. Visual acuity is further limited because the cone packing density is also 4x less in newborns which reduces spatial sampling. (VVP infant vision,2018)

Cone waveguide is not developed in the newborn, meaning the shape of the cones do not have a funnel- like appearance, which is known as the waveguide property. The waveguide property allows light to enter only at one aperture, and guides it into the interior space of the receptor. (Banks MS, Bennett PJ, 1988, Dec;5(12):2059-79.)

The image shows the difference in a cone without the waveguide property on the left. When light enters this cone, it is not guided towards the interior space of the aperture and continues in a straight line. The cone with waveguide properties guides the light ray in the correct direction. Banks and Bennet (1988 ) estimated that the adult central foveal cone lattice absorbs 350 times more quanta than the newborn central foveal lattice, i.e for every quantum of light absorbed in newborn cones, roughly 350 quanta are effectively absorbed in adult foveal cones.

Post retinal factors also affect visual development. Myelination of axons is essential for rapid nervous transmission. The speed of conduction depends on synapses and structural properties of axons. When light focuses onto the retina, the optic nerve transports nerve impulses from photoreceptors in the fovea to the brain. A critical component is the thickness of the myelin sheath which acts as an electrical insulator. It causes the nerve impulses to ‘jump’ from one uninsulated node to the next, resulting in rapid saltatory conduction. However, myelination is incomplete at birth therefore vision is limited, and improves during growth.

Axon diameter also affects the speed of transmission, but it is limited at birth and continues to grow throughout infancy and childhood. A larger axon diameter means that there is less resistance to ion flow, increasing the speed of nervous transmission. Maturation of these regions of the brain undergo conspicuous growth during the first two years of life, but may not completely mature until adulthood (suggested by postmortem studies.) – T. Paus (1999)

Synaptogenesis is also important in neural development. They begin to form prior to week 27 of pregnancy and reach peak density after birth. During late pregnancy and early postnatal life, synaptic density increases within the primary visual cortex. Density doubles from 2 to 4 months of age, and declines after the age of one. Along with synaptogenesis, neurons increase their dendritic arborizations, extend their axons and myelination occurs. This is followed by a period called synapse elimination during which the nervous system fine tunes neural connectivity; which involves eliminating interconnections between redundant or non-functional neurones. This continues for over a decade. (VVP infant vision, 2018, slide 43)

To summarise, vision over the first 12 months experiences a rapid improvement. Although vision improves in the first few years of life, also known as the ‘slow juvenile phase’ the most rapid and critical changes occur during the rapid infantile phase due to emmetropization, retinal factors such as the development of cones and post retinal factors involving development of the visual cortex, myelination and synaptogenesis. These factors combined give rise to colour vision, improved contrast sensitivity and a higher visual acuity over the first 12 months of life.

To most people, they may seem like normal activities –catching a sunset, seeing the beautiful waves of a beach, or watching an artistic performance. Yet, for the 285 million human beings around the world who are blind or visually impaired, the full splendor of those moments can only be imagined or described. For those individuals, a sunset would just look like an orange blur, books can only be heard, and an image can only be viewed with the center of it blocked out. Many people in this category will never be able to see the full beauty of life.

What makes the number of visually impaired people so unsettling is that roughly 80% of visual impairment problems can actually be avoided. Many of these eye conditions, such as macular degeneration and cataracts, can be avoided or reduced by fixes as simple as a better diet. Vision impairment comes in many types; it affects every age and every place around the globe. It is often described as any vision problem that cannot be fixed without eyeglasses or contact lenses. Despite the fact that 90 percent of the visually impaired live in evolving countries, the developed world is not resistant to vision loss either.

In the European Association, 31,700 for every million individuals are visually impaired (3000 for each one million individuals of which are blind, and 28,700 for each million people of which have low vision). In the US, more than 6 million people have visual impairment of some sort. (‘Introduction to Eye Health”) While eyesight absolutely worsens with age — eighty two percent of humans dwelling with blindness are aged 50 and above — blindness doesn’t escape the young. It’s estimated that 1.4 million kids around the world are blind.

The largest of all forms of vision impairment (43%) is “uncorrected refractive errors,” which means poor vision that may need to be handled with eyeglasses or contacts. Other forms of vision impairment are largely age-related, such as cataracts, glaucoma, and macular degeneration. When blindness by itself is taken into consideration, the top three causes are cataracts, glaucoma, and macular degeneration. Refractive error implies that the state of your eye does not bend light effectively, bringing about a blurred picture. The fundamental sorts of refractive errors are myopia (near sightedness), hyperopia (farsightedness), and presbyopia (loss of close vision with age). Some symptoms of refractive error include a blurred vision and difficulty in reading something up close.

Myopia, otherwise called nearsightedness, is generally inherited and regularly found in youth. Nearsightedness regularly advances all through the high school years when the body is developing quickly. Hyperopia, otherwise called farsightedness, can likewise be inherited. Kids frequently have hyperopia, which may diminish in adulthood. In mellow hyperopia, far vision is clear while close vision is foggy. In further developed hyperopia, vision can be obscured at all distances. After the age of 40, the lens of the eye turns out to be increasingly stiff and does not flex as effectively. Subsequently, the eye loses its focusing capacity and it turns out to be progressively hard to properly see at short distance. This condition is called presbyopia. This natural maturing procedure of the lens can likewise be accompanied by myopia, hyperopia or astigmatism.

Astigmatism often happens when the front surface of the eye, the cornea, has an uneven curving of the light into the eye. Typically the cornea is smooth and similarly curved every which way, and light entering the cornea is centered similarly on all planes. In astigmatism, the front surface of the cornea is curved more in one way than in another. This variation from the norm may result in vision that is much similar to looking at a misshapen, wavy mirror. For the most part, astigmatism causes obscured vision at all distances.

A refractive error can be analyzed by an eye care professional amid a normal eye examination. Testing more often than not comprises of requesting that the patient reads a vision chart while testing an arrangement of lenses to expand a patient’s vision. Extraordinary imaging or other testing is infrequently needed. Refractive errors are generally treated utilizing restorative lenses, for example, eyeglasses or contact lenses. Refractive medical procedure, (for example, Lasik surgery) can likewise be utilized to address some refractive issue. Presbyopia, without some other refractive error, can sometimes be treated with retail reading glasses. There is no real way to back off or switch presbyopia. (Bixler)

A cataract is a blurring of the ordinarily clear lens of your eye. For individuals who have cataracts, seeing through shady lenses is somewhat similar to glancing through a chilly or misted up window. Obfuscated vision brought about by cataracts can make it progressively hard to read or drive a vehicle (particularly during the night). Most cataracts create when maturing or damage changes the tissue that makes up your eye’s lens. Some inherited hereditary disarranges that reason other medical issues can expand your danger of cataracts. Cataracts can likewise be brought about by other eye conditions, past eye medical procedures or conditions, for example, diabetes. Long period utilization of steroid meds, as well, can make cataracts evolve. Some ways to prevent cataract include having customary eye examinations, stopping smoking, and picking a solid eating routine. (“Cataracts”)

Macular degeneration (AMD) is a typical eye condition and a main source of vision misfortune among individuals aged 50 and above. It harms the macula, a little spot close to the center of the retina and the piece of the eye required for sharp, focal vision, which gives us a chance to see things that are straight ahead. In certain individuals, AMD progresses so gradually that vision misfortune does not happen for quite a while. In others, the illness advances quicker and may prompt lost vision in one or the two eyes. As AMD advances, an obscured region close to the center of vision is a typical side effect. After some time, the obscured zone may become bigger or you may create clear spots in your focal vision. Items may not have all the earmarks of being as shining as they used to be. Major causes of AMD are smoking and inherited genetics. (“Facts About Age Related Macular Degeneration”)

Diet is a critical piece of the day by day lifestyle decisions you make. Food you eat and the dietary enhancements you take influence the soundness of your eyes just as your general well-being. An eating routine high in immersed fat and sugar may expand your danger of eye illness. Then again, a solid diet including greens and organic products, for example, may help avoid certain eye infections and other medical issues. Cardiovascular sickness, diabetes and eye conditions including cataracts and age-related macular degeneration (AMD) have been appeared to happen less as often as in individuals who eat calories wealthy in nutrients, minerals, sound proteins, omega-3 unsaturated fats and lutein. (Jegtvig)

One way to naturally improve refractive errors is by doing eye exercises and stretches. A long-standing analysis of eye practices by optometrists and ophthalmologists is the nonattendance of logical research that shows eye activities can successfully lessen or dispose refractive errors and diminish your requirement for glasses or contact lenses.

David W. Muris, OD, one of the four specialists who built up the eye exercise methods, directed a clinical assessment of the item in his Sacramento, Calif., work on amid the fall of 1999. As indicated by Dr. Muris, the assessment included 21 individuals ages 14 to 80 with gentle myopia. Following a month and a half of eye stretches and exercises, nine of the 21 had ‘critical’ improvement and 11 had ‘moderate’ improvement in visual keenness. Seven disposed of their requirement for glasses or contacts, he stated, while 11 had ‘diminished reliance,’ which means they required their restorative lenses for less time than previously. (Murphy)

In conclusion, there are a lot of different forms of vision impairment that have different causes, symptoms, and methods for improvement. Methods such as having a better diet and quitting smoking can help in most vision impairment cases. Some vision impairment cases, such as macular degeneration, worsen with age which signals that this vision loss is mostly due to the aging of the eye. While other vision impairment issues, such as myopia, are mostly found in childhood and are inherited. The only real answer for the question “What causes vision impairment?” is: it depends on what type of vision impairment it is.