What is the physiology and anatomy of the eye. How does light travel through the eye and get processed by the brain. What is the role of the nervous system in vision. How do the photoreceptors in the eye work at the cellular level.

The Evolution of Human Vision

Vision is one of the five senses that the human body uses to interpret its surroundings. In the past, our primitive ancestors had what is called “dichromatic vision,” allowing for the interpretation of only UV light and red light. About 30 million years ago, the trichromatic part of vision came into existence due to the evolution of opsin genes.[1] Humans can now see black, white, red, green, and blue, as well as the colors in between this spectrum, as the retina and the brain are equipped to differentiate them. The journey from an object to a synapse in the most posterior part of the brain is a fascinating one that we will explore.

The Physics of Vision

Vision cannot be discussed without understanding the physical properties of optics. The eye receives light that is then transduced into energy. This energy travels through the optic nerve as an action potential and reaches specific nuclei in the brain, where it is processed. But how does the light get into the eye to be processed into an action potential and sent to the brain?

The eye is composed of a series of lenses and spaces that give focus to images, just like a camera. It is made up of the vitreous humor, aqueous humor, the crystalline lens, and the cornea, each with its own refraction index (the average being 1.34, due to the content of these tissues).[2][3] Light travels in the air in the form of waves, and the term “refraction index” refers to the relation between the velocity of light in the air compared to its velocity when it travels across an object. Light travels at a velocity of 300,000 km/s in the air, and the index of refraction of air is 1, the same value as in a vacuum. This refraction index changes when light travels through objects, as it gets slower going through glass, for example. From this, we can infer that light gets slower and its trajectory gets modified slightly as it goes through the eye, and that any disease affecting the refractive properties of the eye will significantly alter vision.

The Role of the Crystalline Lens

When light waves come across a spherical lens, these waves converge into a focal point, and in the eye, this focal point is projected towards a single area, which is the retina. For this to happen, the crystalline lens must be a dynamic structure. The lens is a capsule filled with water and filamentous proteins, and it has a stretched configuration when at rest. If we imagine this light wave coming across this stretched, very flat lens, then we can assume that light will go farther into the eye because the refraction index is lower. With this crystalline configuration, we can see things clearly even though they are far away because they get projected further into the eye. But when we focus on a closer object, the lens has to change its shape into a more spherical one, in order for the light waves to converge into a closer point, as discussed earlier. This is accomplished by the parasympathetic system. The nervous system plays a role here, as the parasympathetic system is in charge of constricting fibers in the ciliary muscle. Contraction of these muscle fibers makes the crystalline lens become rounder, allowing for the accommodation reflex to be accomplished.[4]

The Cellular Level of Vision

At the heart of these organic devices is the visual pigment rhodopsin, a modified molecule of vitamin A. This molecule, which consists of allylic carbons, contains a great deal of conjugated, pi electrons. Recall in organic chemistry an allylic group is a carbon atom singly bonded to another carbon atom, which is in turn double bonded to a carbon atom. The electrons within these alternating pi bonds of the rhodopsin molecule are not as well-defined as the electrons in a saturated carbon chain (no double bonds) or in a singly double-bonded (think simple structure) molecule of ethylene (aka ethene, C2h5).[5]

Rhodopsin consists of the protein scotopsin and the photoreactive chromophore retinal, which is derived from vitamin A. Retinal is covalently bound to one of the protein’s lysine residues in a protonated Schiff base (-N+=CH-). The chromophore is the light-absorbing center of the molecule. It functions by facilitating the absorption of photons to potential energy, which supplies the energy needed to allow isomerization of the chromophore molecule from cis to trans (180-degree rotation). Although the reaction mechanism is involved, it can be summarized as:

1. Photons elevate electrons within the conjugated pi system to higher energy orbitals (dictated by the level of resonance within the chromophore).
2. The molecule rotates around the double-bond, changing from cis to trans configuration.

By the end of the mechanism, the

The Retina and the Optic Nerve

The retina is a complex and highly organized tissue that lines the back of the eye. It contains two main types of photoreceptor cells: rods and cones. Rods are responsible for vision in low light conditions, while cones are responsible for color vision and high-acuity vision in bright light. When light enters the eye, it passes through the cornea, pupil, and lens before reaching the retina, where it is absorbed by the photoreceptor cells.

The photoreceptor cells convert the light energy into electrical signals, which are then transmitted through the optic nerve to the brain. The optic nerve is a bundle of nerve fibers that carries visual information from the retina to the brain’s visual processing centers, such as the thalamus and the primary visual cortex.

The Visual Pathway to the Brain

The visual information transmitted through the optic nerve is processed in a series of structures within the brain. The first stop is the thalamus, where the information is relayed to the primary visual cortex, located in the occipital lobe of the brain. Here, the visual information is processed and analyzed, allowing us to perceive and interpret the visual world around us.

The primary visual cortex is responsible for basic visual functions, such as detecting edges, color, and motion. From there, the visual information is sent to higher-order visual processing areas, where more complex visual tasks, such as object recognition and spatial awareness, are carried out.

The Importance of Vision

Vision is a crucial sense that allows us to navigate and interact with our environment. It plays a vital role in our daily lives, from recognizing faces and objects to reading, driving, and engaging in sports and other activities. Understanding the physiology and anatomy of the eye, as well as the complex neural pathways involved in visual processing, is essential for gaining a deeper appreciation of this remarkable sense and for developing treatments and technologies to address vision-related issues and disorders.

Physiology, Vision – StatPearls – NCBI Bookshelf

Introduction

Vision is one of the five senses the body uses to interpret its surroundings. In the past, our primitive ancestors had what is called “dichromatic vision,” allowing for interpretation of only UV light and red light. About 30 million years ago, the trichromatic part of vision came to existence due to the evolution of opsin genes.[1] Humans can now see black, white, red, green, and blue, as well as the colors in between this spectrum since the retina and the brain are equipped to differentiate them. What happens between an object and a synapse in the most posterior part of the brain is the fascinating journey that we will cover.

Issues of Concern

Physical Properties of Vision

Vision cannot be discussed without knowing the physical properties of optics. The eye receives light that then is traduced into energy. That energy goes into the optic nerve as an action potential and travels to specific nuclei in the brain, where it is processed. But, how does that light get into the eye to be processed into an action potential to be sent to the brain?

The eye is composed of a series of lenses and spaces that give focus to images, just as a camera does. It is composed of the vitreous humor, aqueous humor, the crystalline lens, and the cornea, and each of these has its own refraction index (the average being 1.34, because of the content of these tissues). Light travels in the air in the form of waves. The term “refraction index” refers to the relation between the velocity of light in the air compared to its velocity when it travels across an object. Light travels at a velocity of 300,000 km/s in the air.

The index of refraction of air is 1, the same value as in a vacuum. This refraction index changes when light travels through objects, as it gets slower going through glass, for example. With all of the above then we can infer that light gets slower and its trajectory gets modified slightly as it goes through the eye, and it can be also inferred that every disease that affects the refractive properties of the eye will significantly alter vision. [2][3]

When light waves come across a spherical lens, these waves converge into a focal point, and in the eye, this focal point is projected towards a single area, which is the retina. For this to be accomplished, the crystalline lens must be a dynamic structure. The lens is a capsule filled with water and filamentous proteins; it has a stretched configuration in resting. So, if we imagine this light wave coming across this stretched, very flat lens, then we can assume that light will go farther into the eye because the refraction index is lower. With this crystalline configuration, we can see things clearly even though they are far away because they get projected further into the eye. But when we focus a closer object, then the lens has to change its shape into a more spherical one, in order for the light waves to converge into a closer point, as discussed earlier. This is accomplished by the parasympathetic system. So the nervous system has a role here! Yes, because the parasympathetic system is in charge of constricting fibers in the ciliary muscle. Contraction of these muscle fibers makes the crystalline lens become rounder, as will be discussed later. All of these processes have to be intact for the accommodation reflex to be accomplished.[4]

Cellular Level

At the heart of these organic devices is the visual pigment rhodopsin, a modified molecule of vitamin A. This molecule, which consists of allylic carbons, contains a great deal of conjugated, pi electrons. Recall in organic chemistry an allylic group is a carbon atom singly bonded to another carbon atom, which is in turn double bonded to a carbon atom. The electrons within these alternating pi bonds of the rhodopsin molecule are not as well-defined as the electrons in a saturated carbon chain (no double bonds) or in a singly double-bonded (think simple structure) molecule of ethylene (aka ethene, C2h5).[5]

Rhodopsin consists of the protein scotopsin and the photoreactive chromophore retinal, which is derived from vitamin A. Retinal is covalently bound to one of the protein’s lysine residues in a protonated Schiff base (-N+=CH-). The chromophore is the light-absorbing center of the molecule. It functions by facilitating the absorption of photons to potential energy, which supplies the energy needed to allow isomerization of the chromophore molecule from cis to trans (180-degree rotation). Although the reaction mechanism is involved, it can be summarized as:

• Photons elevate electrons within the conjugated pi system to higher energy orbitals (dictated by the level of resonance within the chromophore).

• The molecule rotates around the double-bond, changing from cis to trans configuration.

• By the end of the mechanism, the excited electrons’ energy levels have fallen back to the ground state.[6]

At the reaction completion, the chromophore has changed to the more stable trans configuration. Thus, within rhodopsin, light absorption leads to a chemical reaction that forces part of the rhodopsin molecule to translocate, changing protein conformation, and exposing active sites. This activated form of rhodopsin is known as metarhodopsin II. Before it can get to the metarhodopsin phase, rhodopsin decays through a series of intermediates, and these changes occur in the matter of milliseconds. Metarhodopsin II activates many copies of the G protein transducin (by replacing transducin’s GDP with GTP). Many activated transducin complexes activate cyclic nucleotide phosphodiesterase (PDE), which can itself hydrolyze 1000 molecules of cGMP to 5′-GMP per second. cGMP-gated channels in the plasma membrane of these rods (or cones) allow sodium ion influx at high cGMP concentrations; this is balanced by cation exchanger-mediated glutamate efflux, maintaining cell depolarization in dark conditions. At low cGMP concentrations, these channels close, stopping sodium ion influx and reducing glutamate efflux, all leading to cell hyperpolarization in light conditions. Thus, light-induced rod/cone state changes lead to hyperpolarization of the photoreceptor cells. Conversely, photoreceptor cells without the presence of light exist in the depolarized state. [7][8][9]

After this cascade of events, the enzyme rhodopsin kinase quickly binds metarhodopsin II, phosphorylating and halting its activity. The protein arrestin binds phosphorylated metarhodopsin II. Metarhodopsin II is unstable and will split within minutes, leading to opsin and free trans-retinal. Trans-retinal is transported to pigment epithelial cells that convert trans-retinal back to 11-cis-retinal, which eventually is recombined with opsin within cones/rods to reform rhodopsin. Guanylate cyclase restores cGMP concentration, and the cone/rod is ready to respond to another light exposure event.[9]

Additionally, phototransduction is subject to regulation by a calcium-mediated pathway to quickly diffuse a large gradient response, which is important in events such as sudden flashes of light in the dark. In dark conditions, the intracellular calcium level is high due to calcium diffusion through cGMP-gated channels. Lack of frequent light response leads to higher intracellular cGMP concentrations and allows more calcium to enter the cell per second. Calcium ion binding to rhodopsin kinase increases the rate of rhodopsin phosphorylation, reducing transducin activation. Calcium ion binding to guanylate cyclase accelerates the restoration of cGMP concentration. And calcium ion binding to calmodulin increases cGMP affinity to its gated channel.

Development

The surface of the human retina contains about three million cones and one hundred million rods, but there are just 1.5 million ganglion cells; meaning that for every ganglion cell, there are sixty rods and two cones. Cones transmit color information, whereas rods have greater sensitivity to low-light conditions. However, the distribution of rods and cones tends to be different depending on the part of the retina. In the central retina, for example, there are almost only cones and a lot of ganglion cells making synapses, which explains why the central retina confers the highest visual acuity. In contrast, in the peripheral retina, there are more rods than cones, and the visual acuity in these peripheral regions is decreased. There are several different types of ganglion cells: W, X, and Y ganglion cells. Some of these are responsible for detecting changes in color intensity (cones), and some are more specialized in detecting changes in contrast (rods). These differences depend on the part of the retina in which the ganglion cells are receiving the stimuli.[10]

The interneural connections of ganglia (bipolar cells) allow for low-level visual processing, adjusting the gain of the signal to transmit light gradients rather than absolute light intensity. Thus, relative differences within the light field and the object’s visual patterns are emphasized, as opposed to binary hit/miss signal information. This process is crucial because rods and cones can distinguish light intensity varying by ten orders of magnitude; however, the ganglia of the optic nerve can only transmit about 1% of this range.[11]

Color vision results from the combination of signals from three pigment types within cones: red, green, and blue pigments that correspond to cone types L, M, and S (RGB-LMS), respectively. Those colors correspond to the wavelengths of peak light absorption intensities of the modified chromophores. Remember, excited electrons are vital to producing Schiff-base modifications, which can be further classified as red shift or blue shift modifications.

Red shift or blue shift modifications denote whether the shift is toward peak absorptions at longer or shorter wavelengths, respectively. The average absorption maxima for 11-cis-retinal occurs at a wavelength of 380nm. If an experimenter were to expose 11-cis-retinal to EM radiation at this wavelength, the 11-cis-retinal would most readily absorb energy, as opposed to with an EM radiation at a wavelength of 280nm. Studies have demonstrated that when retinal is chemically modified to exhibit a more conjugated, distributed pi-electron system, redshift Schiff-base modification is observed. This means the visual pigment exhibits more significant resonance than before, and light is maximally absorbed in a longer wavelength. In contrast, when retinal is chemically modified to exhibit a less conjugated, less distributed pi-electron system, blue shift Schiff-base modification is observed. Here, the visual pigment exhibits less significant resonance than before, and light is maximally absorbed in a shorter wavelength. L cones have peak absorptions at 555-565 nm, M cones at 530-537 nm and S cones at 415-430 nm.[12]

Thus, color vision arises from the shifted cones’ peak absorption levels and ultimately the brain’s interpretation of the composition of these points of wavelength absorption. The entire pathway is sometimes referred to as the retinoid cycle.

Organ Systems Involved

The sense of vision involves the eye and the series of lenses of which it is composed, the retina, the optic nerve, optic chiasm, the optic tract, the lateral geniculate nuclei in the thalamus and the geniculocalcarine tract that projects to the occipital cortex.

Mechanism

The information coming from the ganglion cells of the retina reaches the optic nerves, and then the action potentials travel to a region called the optic chiasm (where the optic nerve fibers of both eyes cross in the midline and then form the optic tract). The direction of the visual information here is slightly different, as the ipsilateral temporal side of it passes directly into the ipsilateral part of the cortex, whereas the nasal part of vision gets crossed to the contralateral part of the brain, traveling to the opposite occipital cortex. Therefore, downstream to the optic chiasm, every optic tract has information from both eyes, from the temporal ipsilateral part of the visual field and the nasal contralateral part of it. This visual information then gets integrated into the lateral geniculate nuclei of the thalamus and then projects to the visual cortex. Before visual information reaches the thalamus, it can also travel to other structures such as the pretectal nuclei and the superior colliculus in the brainstem (to generate visual reflexes to focus on certain objects) or to the suprachiasmatic nuclei of the hypothalamus (to regulate the circadian rhythms), etc.[13][14]

When the information reaches the thalamus, it has to be ordered like paperwork in an office. So, to accomplish this task, the lateral geniculate nucleus has six layers of neural networks so that information can be integrated and put in order. Layers II, III, and V receive information from the ipsilateral temporal visual field, and layers I, IV and VI receive information from the contralateral nasal visual fields. To make it more interesting, layers I and II are made of magnocellular neurons, and layers III, IV, V, and VI are made of parvocellular neurons. The retina also contains magnocellular and parvocellular neurons, which are subtypes of the ganglion cells (the cells that receive information at the end of the retinal visual pathway). In the retina, the “magnocellular” type of ganglion cells receive information about black and white contrast and rapid changes in object positions, and the “parvocellular” type of neurons receive information about color. So the lateral geniculate nucleus has two layers of neurons dedicated exclusively to the integration of information about black and white contrast and visual field changes, and it has four layers assigned to the combination of color. From here, all of these color and contrast cues go to the visual cortex, where the information is then processed and interpreted.[15]

Related Testing

When evaluating an ophthalmologic complaint, it is very important to delineate the timing of the onset of symptoms. Ocular symptoms may be sudden or progressive, unilateral or bilateral, be associated with pain, photophobia, or discharge. To gain insight from the patient´s medical history, previous ocular conditions, and medications, history of recent ocular surgery or general surgery, the attending clinician must ask intentionally, otherwise, there could be missing information. 

A complete physical examination is necessary, inquire about changes in vision with each eye, make a pupillary exam, evaluate extraocular muscle movements and if you are suspecting a CNS lesion or in the optic pathway, test the confrontation visual fields. 

Pupil Examination

Pupil abnormalities are one of the most common challenges faced by clinicians. In order to evaluate the pupillary function correctly, one must understand the principles of the physiology of the pupil. The pupil either dilates or constricts. The pupillary dilation is mediated by the sympathetic nervous system, the constricting function is mediated by the parasympathetic nervous system.

• The constricting pupillary pathway starts in the midbrain, there we can find the Edinger – Westphal nucleus. When the eye is exposed to a very near object or to light, this information travels through the optic nerve first, in order for the brain to integrate and process it. Just after the optic chiasm and before information processing at the level of the thalamus (lateral geniculate nuclei), visual information of space and light goes to the EW nucleus after making synapsis in the olivary nuclei. Then, the third cranial nerve acquires parasympathetic fibers originating in these nuclei and travel together. In the subarachnoid space, they travel in the dorsal part of the nerve, very near to the posterior communicating artery. When the oculomotor nerve enters the cavernous sinus, these fibers are configurated more peripherally. Then, the oculomotor nerve reaches the anterior part of the cavernous sinus and soon will reach the superior orbital fissure. Once it reaches the SOF, the oculomotor nerve divides into two divisions: a superior division that innervates the superior palpebrae levator muscle and the superior rectus. The inferior division of the third cranial nerve innervates the rest of the extraocular muscles, except for the lateral rectus (innervated by the abducens) and the superior oblique (innervated by the trochlear nerve). In the posterior aspect of the globe, there is the ciliary ganglion. Here, fibers from the third cranial pair synapse to give origin to the short ciliary nerves that will innervate the pupillary muscles and that will configure the lens alongside the pupil. The near triad is composed of miosis, convergence, and accommodation, this triad is under the influence of more than one brain area, namely the mesencephalic reticular formation, the raphe interpositus, and the superior colliculus.  

• The dilating pupillary pathway consists of a set of three neurons. The first-order neuron is located in the paraventricular nucleus of the hypothalamus and it travels along the lateral aspect of the brainstem to make synapsis with the second-order neurons located in the ciliospinal nuclei (of Budge), this nucleus extends from C8 to T12 and its fibers run along the lung apex and the subclavian artery and they ascend through the common carotid artery to the third-order neurons that constitute the stellate cervical ganglion. The neurons that originate from this ganglion travel along the internal carotid artery and external carotid artery. The internal carotid artery fibers innervate the Müller muscles and the pupillary dilator muscle; they run along the abducens nerve and the ophthalmic artery. The external carotid fibers innervate the sweat glands of the face. 

Anisocoria refers to the discrepancy between the size of both pupils. Physiologic anisocoria is a dilation difference of 1 mm or less between the two pupils. Anisocoria may be monocular or binocular, in miosis or mydriasis. 

– Monocular mydriasis: This results from damage to the parasympathetic fibers innervating the pupil. It can be localized to the oculomotor nerve fibers before they reach the ciliary ganglion or after they synapse with it. Always examine the complete function of the third cranial nerve, including the function of the superior and inferior division. Ask yourself if it is a complete or a partial third nerve palsy, is associated with pain, is there any pupil involvement, and if there are signs of abnormal regeneration. The two more common causes of a third nerve palsy are an intracranial aneurysm or an ischemic lesion. Other slow-growing lesions may cause an eye to go mydriatic, like a meningioma. When the ciliary fibers are damaged, they cause a tonic pupil. This means a pupil that stays in mydriasis but typically resolves a little when stimulated by the accommodation reflex. The third cranial nerve is resilient to traumatic injury. When there is a traumatic injury of the oculomotor nerve, there surely is damage to the abducens nerve and trochlear nerve as well. The Adie pupil, as its called, is more common in females, tends to be idiopathic, and may be associated with non-responsive deep tendon reflexes. This is called Holmes-Adie syndrome.

– Binocular mydriasis: These may result from excessive sympathetic stimulation. They may be physiological in the case of an anxiety attack. The concern is the overstimulation of the SNS by drugs, such as cocaine, tricyclic antidepressants, or sympathomimetics. Some cases might be secondary to iris injury or a systemic disease acting as a parasympatholytic such as botulism (never Myasthenia gravis). The bilateral optic neuropathy may present with bilateral mydriasis, as well as diabetic neuropathy.

– Monocular miosis: This presentation arises from the disruption of the sympathetic innervation to the eye. Patients often present with Horner syndrome: is comprised of unilateral miosis, ptosis, and hemifacial ipsilateral anhidrosis. The clinical presentation may vary depending on the order neuron injured. First-order neuron injuries are very uncommon, unless the lesion is at the level of the medulla, being part of a Wallenberg syndrome. Lesion at the level of the ciliospinal nucleus comes from a Brown-Séquard syndrome, commonly. A Pancoast tumor, which is a tumor located a the lung apex, may cause Horner syndrome. Carotid dissection is a rather common cause of Horner syndrome and one should be very aware of this pathology. Note that the syndrome might not be complete in presentation, depending on the level of injury, one might find a partial Horner syndrome. Not every miotic eye is a Horner syndrome. It may be a chronic Adie pupil becoming miotic out of fatigue of the sympathetic nervous system.

– Bilateral miosis: Bilaterally small pupils are not uncommon. This results from a predominance in parasympathetic action over sympathetic action. It may be caused by sedating medications, lesions in the pons, lesions in the diencephalon or chronic reinnervation from a ganglionopathy. One pathology of concern is the Argyll-Robertson pupil. in which both pupils are miotic but are irregular. It is being said that the lesion responsible for this chronic syphilis manifestation is at the level of the midbrain, there’s no evidence supporting that theory.[16]

Clinical Significance

Improper Color Vision Recognition/Color Blindness

Many forms of color vision recognition abnormalities are present in the population, with most having a genetic origin. Very few individuals are truly color blind, but instead, individuals who are considered color-blind see a disrupted range of colors. The most common forms are protanopia and deuteranopia, conditions arising from loss of function of one of the cones, leading to dichromic vision. Protanopia is the loss of L cones (red) resulting in green-blue vision only. Deuteranopia is the loss of M cones (green) resulting in red-blue vision only. Both are X-linked alleles, therefore almost exclusively occurring in males, occurring with a prevalence of 1%. Loss of S cones does rarely occur in 0.01% of males and females. In these cases, one of the cones does not function, and one of the others is expressed instead in its place.

Similar to above, but not as severe in its symptoms, is the condition called “anomalous trichromatic vision” (tritanomaly), in which all three cones are present but the color vision is aberrant. The two common forms of color blindness, protanomaly and deuteranomaly, result in loss of L or M cones, respectively, and the lost cones are replaced with cones of intermediate spectral tuning. Both are X-linked and occur in 7% of males.[17]

Diseases affecting color vision but not affecting cones  

In addition to disorders of proper color recognition, many diseases in vision display phototransduction defects that affect many portions of the signal pathway and its regulation. Here, not only is color vision function decreased, but the monochromatic vision is worsened as well.

1. Congenital Stationary Night Blindness (CSNB)

One such disease is congenital stationary night blindness. It is a genetic defect resulting in functional cones but dysfunctional rods. In this disease, many potential culprits have been identified including abnormal rhodopsin, arrestin, rod transducin, rod phosphodiesterase, and rhodopsin kinase. Studies have demonstrated that in some populations of this disease, rods are permanently transmitting light signals. In CSNB, b-waves are reduced (in CSNB type 2) or absent (in CSNB type 1) during an electroretinogram (ERG). There are currently no treatments for this disorder. 

2. Retinitis Pigmentosa (RP)

Another disease affecting rod function is retinitis pigmentosa, which is a genetically inherited disease characterized by progressive degeneration of the retina, leading to blindness. Frequently, it begins in the early phase as night blindness. Vision loss first occurs in the periphery and progresses towards the center of vision, manifesting as tunnel vision. RP is associated with faulty rod functioning; if cones begin to be affected, then blindness eventually results. RP is characterized by reduced or absent a-waves and b-waves during an ERG. It has a prevalence of 1 in 3500 individuals.

3. Malnutrition-Associated

Deficiency in the essential nutrient vitamin A leads to night blindness, and this can eventually lead to permanent blindness through the deterioration of the receptor outer segments.

Experimental Therapies

Currently, there are no FDA-approved treatments for CSNB. However, the promise of gene-therapy interventions is on the horizon. Recently, FDA-approval was gained for retinal gene therapy (voretigene neparvovec) that utilizes the adeno-associated virus (AAV) and RPE65 gene, which can treat an uncommon form of RP called Leber congenital amaurosis (LCA). This was the first FDA-approved gene therapy for an inherited disorder.[18]

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Figure

Arteries of the Eye, Ophthalmic Artery; Internal Carotid Artery. Contributed by Gray’s Anatomy Plates

Figure

The Tunics of the Eye, Plan of retinal neurons. Contributed by Gray’s Anatomy Plates

Figure

Figure 1. (A) When light is incident on the skin (thick red arrow), most of it tends to get reflected back (thin red arrow), while the remaining gets refracted (oblique orange arrow), diffracted (yellow shooting arrows) or absorbed (crimson area). On (more…)

Figure

The retinoid cycle. Contributed by Arturo López de Nava, MS

Figure

Retina anatomy. Image courtesy Orawan

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Bouffard MA. The Pupil. Continuum (Minneap Minn). 2019 Oct;25(5):1194-1214. [PubMed: 31584534]

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Baden T, Osorio D. The Retinal Basis of Vertebrate Color Vision. Annu Rev Vis Sci. 2019 Sep 15;5:177-200. [PubMed: 31226010]

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Disclosure: Arturo Sánchez López de Nava declares no relevant financial relationships with ineligible companies.

Disclosure: Anisha Somani declares no relevant financial relationships with ineligible companies.

Disclosure: Baby Salini declares no relevant financial relationships with ineligible companies.

Human eye | Definition, Anatomy, Diagram, Function, & Facts

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human eye, in humans, specialized sense organ capable of receiving visual images, which are then carried to the brain.

Anatomy of the visual apparatus

Structures auxiliary to the eye

The eye is protected from mechanical injury by being enclosed in a socket, or orbit, which is made up of portions of several of the bones of the skull to form a four-sided pyramid, the apex of which points back into the head. Thus, the floor of the orbit is made up of parts of the maxilla, zygomatic, and palatine bones, while the roof is made up of the orbital plate of the frontal bone and, behind this, by the lesser wing of the sphenoid. The optic foramen, the opening through which the optic nerve runs back into the brain and the large ophthalmic artery enters the orbit, is at the nasal side of the apex; the superior orbital fissure is a larger hole through which pass large veins and nerves. These nerves may carry nonvisual sensory messages—e.g., pain—or they may be motor nerves controlling the muscles of the eye. There are other fissures and canals transmitting nerves and blood vessels. The eyeball and its functional muscles are surrounded by a layer of orbital fat that acts much like a cushion, permitting a smooth rotation of the eyeball about a virtually fixed point, the centre of rotation. The protrusion of the eyeballs—proptosis—in exophthalmic goitre is caused by the collection of fluid in the orbital fatty tissue.

It is vitally important that the front surface of the eyeball, the cornea, remain moist. This is achieved by the eyelids, which during waking hours sweep the secretions of the lacrimal apparatus and other glands over the surface at regular intervals and which during sleep cover the eyes and prevent evaporation. The lids have the additional function of preventing injuries from foreign bodies, through the operation of the blink reflex. The lids are essentially folds of tissue covering the front of the orbit and, when the eye is open, leaving an almond-shaped aperture. The points of the almond are called canthi; that nearest the nose is the inner canthus, and the other is the outer canthus. The lid may be divided into four layers: (1) the skin, containing glands that open onto the surface of the lid margin, and the eyelashes; (2) a muscular layer containing principally the orbicularis oculi muscle, responsible for lid closure; (3) a fibrous layer that gives the lid its mechanical stability, its principal portions being the tarsal plates, which border directly upon the opening between the lids, called the palpebral aperture; and (4) the innermost layer of the lid, a portion of the conjunctiva. The conjunctiva is a mucous membrane that serves to attach the eyeball to the orbit and lids but permits a considerable degree of rotation of the eyeball in the orbit.

The conjunctiva

The conjunctiva lines the lids and then bends back over the surface of the eyeball, constituting an outer covering to the forward part of this and terminating at the transparent region of the eye, the cornea. The portion that lines the lids is called the palpebral portion of the conjunctiva; the portion covering the white of the eyeball is called the bulbar conjunctiva. Between the bulbar and the palpebral conjunctiva there are two loose, redundant portions forming recesses that project back toward the equator of the globe. These recesses are called the upper and lower fornices, or conjunctival sacs; it is the looseness of the conjunctiva at these points that makes movements of lids and eyeball possible.

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The fibrous layer

The fibrous layer, which gives the lid its mechanical stability, is made up of the thick, and relatively rigid, tarsal plates, bordering directly on the palpebral aperture, and the much thinner palpebral fascia, or sheet of connective tissue; the two together are called the septum orbitale. When the lids are closed, the whole opening of the orbit is covered by this septum. Two ligaments, the medial and lateral palpebral ligaments, attached to the orbit and to the septum orbitale, stabilize the position of the lids in relation to the globe. The medial ligament is by far the stronger.

The muscles of the lids

Closure of the lids is achieved by contraction of the orbicularis muscle, a single oval sheet of muscle extending from the regions of the forehead and face and surrounding the orbit into the lids. It is divided into orbital and palpebral portions, and it is essentially the palpebral portion, within the lid, that causes lid closure. The palpebral portion passes across the lids from a ligament called the medial palpebral ligament and from the neighbouring bone of the orbit in a series of half ellipses that meet outside the outer corner of the eye, the lateral canthus, to form a band of fibres called the lateral palpebral raphe. Additional parts of the orbicularis have been given separate names—namely, Horner’s muscle and the muscle of Riolan; they come into close relation with the lacrimal apparatus and assist in drainage of the tears. The muscle of Riolan, lying close to the lid margins, contributes to keeping the lids in close apposition. The orbital portion of the orbicularis is not normally concerned with blinking, which may be carried out entirely by the palpebral portion; however, it is concerned with closing the eyes tightly. The skin of the forehead, temple, and cheek is then drawn toward the medial (nose) side of the orbit, and the radiating furrows, formed by this action of the orbital portion, eventually lead to the so-called crow’s feet of elderly persons. It must be appreciated that the two portions can be activated independently; thus, the orbital portion may contract, causing a furrowing of the brows that reduces the amount of light entering from above, while the palpebral portion remains relaxed and allows the eyes to remain open.

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Opening of the eye is not just the result of passive relaxation of the orbicularis muscle but also is the effect of the contraction of the levator palpebrae superioris muscle of the upper lid. This muscle takes origin with the extraocular muscles at the apex of the orbit as a narrow tendon and runs forward into the upper lid as a broad tendon, the levator aponeurosis, which is attached to the forward surface of the tarsus and the skin covering the upper lid. Contraction of the muscle causes elevation of the upper eyelid. The nervous connections of this muscle are closely related to those of the extraocular muscle required to elevate the eye, so that when the eye looks upward the upper eyelid tends to move up in unison.

The orbicularis and levator are striated muscles under voluntary control. The lids also contain smooth (involuntary) muscle fibres that are activated by the sympathetic division of the autonomic system and tend to widen the palpebral fissure (the eye opening) by elevation of the upper, and depression of the lower, lid.

In addition to the muscles already described, other facial muscles often cooperate in the act of lid closure or opening. Thus, the corrugator supercilii muscles pull the eyebrows toward the bridge of the nose, making a projecting “roof” over the medial angle of the eye and producing characteristic furrows in the forehead; the roof is used primarily to protect the eye from the glare of the sun. The pyramidalis, or procerus, muscles occupy the bridge of the nose; they arise from the lower portion of the nasal bones and are attached to the skin of the lower part of the forehead on either side of the midline; they pull the skin into transverse furrows. In lid opening, the frontalis muscle, arising high on the forehead, midway between the coronal suture, a seam across the top of the skull, and the orbital margin, is attached to the skin of the eyebrows. Contraction therefore causes the eyebrows to rise and opposes the action of the orbital portion of the orbicularis; the muscle is especially used when one gazes upward. It is also brought into action when vision is rendered difficult either by distance or the absence of sufficient light.

The outermost layer of the lid is the skin, with features not greatly different from skin on the rest of the body, with the possible exception of large pigment cells, which, although found elsewhere, are much more numerous in the skin of the lids. The cells may wander, and it is these movements of the pigment cells that determine the changes in coloration seen in some people with alterations in health. The skin has sweat glands and hairs. As the junction between skin and conjunctiva is approached, the hairs change their character to become eyelashes.

The glandular apparatus

The eye is kept moist by secretions of the lacrimal glands (tear glands). These almond-shaped glands under the upper lids extend inward from the outer corner of each eye. Each gland has two portions. One portion is in a shallow depression in the part of the eye socket formed by the frontal bone. The other portion projects into the back part of the upper lid. The ducts from each gland, three to 12 in number, open into the superior conjunctival fornix, or sac. From the fornix, the tears flow down across the eye and into the puncta lacrimalia, small openings at the margin of each eyelid near its inner corner. The puncta are openings into the lacrimal ducts; these carry the tears into the lacrimal sacs, the dilated upper ends of the nasolacrimal ducts, which carry the tears into the nose.

The evaporation of the tears as they flow across the eye is largely prevented by the secretion of oily and mucous material by other glands. Thus, the meibomian, or tarsal glands, consist of a row of elongated glands extending through the tarsal plates; they secrete an oil that emerges onto the surface of the lid margin and acts as a barrier for the tear fluid, which accumulates in the grooves between the eyeball and the lid barriers.

Anatomy and physiology of the eye | Likon – contact lenses and care products Kyiv.

23 Apr 2010

The eye socket is a bony cavity or cavity in which the eyeball is located. It consists of seven small bones that protect the eye from physical damage.

Adjacent Organs – The tissues surrounding the eye, including the eyelashes and eyelids, are called adjacent organs.

Eyelashes consist of several rows of short fluffy hairs located along the edge of the eyelids and perform the following functions:

by retaining particles of air dust, eyelashes prevent clogging of the eyes;

contribute to the rapid closure of the eyelids in case of damage.

Eyelashes are characterized by natural growth and loss. New eyelashes grow quickly.

Each eyelid consists of a movable plate of fibrous tissue that covers and opens the front of the eyeball. Outside, the eyelids are covered with skin, and inside – with a mucous membrane. By distributing tear fluid secreted by the lacrimal glands, the eyelids protect the eye from any foreign matter that could damage the cornea. There are also lacrimal openings on the eyelids through which tears are discharged.

Both eyelids are covered by a sensitive membrane, which is called the conjunctiva. The palpebral conjunctiva lines the inner surface of the eyelids and passes into the bulbar conjunctiva. The bulbar conjunctiva is located on the front of the eyeball (visible white part of the eye) and is in contact with the surface of the palpebral conjunctiva.

Since the conjunctiva is a continuous shell, contact lenses cannot be behind it, that is, behind the eye. The conjunctiva is in constant direct interaction with the lenses, so a healthy conjunctiva is essential for the successful use of contact lenses. When the eye is irritated, the blood vessels of the conjunctiva dilate and the eye turns red. The conjunctiva contains glands that help form the tear film to keep the surface of the eye moist.

The layer of water and nutrients on the cornea is called the tear film. This film is constantly produced and removed from the surface of the eye. The lacrimal glands of the eyelids participate in its formation, the outflow occurs through the lacrimal openings into the nasolacrimal duct and further into the nose. The tear film provides nutrition to the cornea in the form of oxygen, glucose, salts and minerals. It moisturizes the cornea and eyelids, preventing them from drying out, and also acts as a lubricant, making it easier for the eyelids to glide over the cornea. Foreign particles dissolve in the tear film and are removed from the surface of the eye. Dangerous microorganisms are exposed to antibacterial enzymes (lysozymes) of the tear. The tear film consists of three layers: an outer lipid (fatty) layer, a central aqueous layer, and an inner mucin layer, which helps to bond the film to the cornea.

The lipid layer is a fatty film that prevents the tear film from drying out. The water layer is a slightly alkaline solution (pH 7.35) consisting of water (98%), minerals and nutrients, enzymes, (ions), dissolved salts and proteins. This layer, which makes up up to 90% of the thickness of the tear film, provides the cornea with oxygen and nutrients. Mucinous (mucous) layer connects the tear film and corneal epithelium.

An important factor in adaptation to contact lenses is the chemical structure of the tear film, since the lenses lie on it. Typically, the film thickness is 7 µm. The average volume of tear fluid in the eye is 6 µl. 10-20 seconds would be enough for the entire tear film to evaporate, but we involuntarily blink every 5-10 seconds and restore the film.

A patient with a defect in any layer of the tear film is ill-suited to wear contact lenses. The state of the tear film can be assessed in two ways: the Schirmer test uses strips of paper to indirectly determine the amount of water layer of the film, the disintegration time test (TDT) shows the time it takes for the tear film to evaporate from the surface of the cornea (normally 10–15 seconds).

The cornea is a transparent, avascular, highly sensitive, multi-layered, domed membrane that delimits the anterior chamber of the eye. Convex in the center, the cornea flattens at the point of transition to the sclera, which is called the limbus. The changing curvature of the cornea makes it difficult to measure and fit contact lenses. Therefore, contact lenses usually have different curvature: central peripheral.

Features of the anatomy and physiology of the child’s eye

The visual system of a child is different from the visual system of an adult and is constantly evolving.

How do newborn children see when they recognize their mother and why is the color of the eyes in the first days of life far from always final?

Anatomy and physiology of the organ of vision in children

The eyeball of a child is still too small, which is why the focusing of light rays does not occur on the retina, but behind it. So farsightedness at an early age is a natural physiological phenomenon!

Babies see objects blurry, they do not distinguish small details, they focus better at a distance of 20-25 cm. It is curious that this is the approximate distance to the mother’s face when she holds the baby at her breast.

With growth and development, farsightedness decreases and completely disappears by 6-7 years. The eyeball grows significantly during the first year of life, at the age of 5 it is almost the same as in an adult, but it is finally formed only by the age of 17–18.

Also, the retina, optic nerve, oculomotor muscles continue to actively form, the visual cortex of the brain develops – everything necessary not only for vision, but also for the perception and understanding of what is seen.

Children’s vision in different periods

Even in the womb (approximately 5 months), the baby reacts to light or its absence. In the first 2-3 weeks, the child focuses only on large objects. By the end of 1 month already distinguishes silhouettes.

From 2 months, the baby learns to focus his eyes, follow moving objects. He is especially good at catching bright objects with his eyes, because around the same period the child begins to perceive colors. Best distinguishes between red and yellow, later begins to see green and blue, and then other colors and shades.

At the age of three months, close objects become visible. And the baby also recognizes the faces of his closest relatives – those who are constantly in contact with him, repeats their facial expressions. From the 4th month of life, the baby distinguishes shapes and primary colors. From the 7th, he already sees various objects well: shape, size and color play a role. And from the 8th he recognizes familiar people, distinguishes their faces.

At 1–1.5 years old, children actively comprehend the world around them, but they still see a two-dimensional picture. And only when they start to crawl and walk – to move independently in space – binocular vision begins to form. Binocular, or stereoscopic, spatial vision is the ability to see with both eyes, when the brain “adds” a single three-dimensional image from what is seen. The process of development of binocular vision is fully completed at the age of 7–15 years.

It is important to remember that each child is unique and the described periods of development are individual, they may differ by 1-2 months. But if something bothers you in the development of your baby, be sure to seek help from a specialist, sign up for a diagnosis. After all, the sooner a problem is detected, the easier it is to fix it.

How children’s eyesight is checked

The ophthalmologist conducts the first examination immediately after birth. If there are no problems, vision is checked in the first month of life, 1 year, at the age of 3 and 5–6 years. At school, children undergo annual medical examinations.

Depending on the age, during the examination, the oculist notes whether the baby’s gaze is fixed on objects and whether he reacts to light, checks eye movement, face recognition, reactions to stimuli. For example, although immediately after birth, the child does not yet distinguish between objects and objects, but in the first 4-6 weeks of life, the reaction to light is checked – pupils constrict as a protective mechanism.

Preschoolers evaluate vision using special tables with images of objects: a mushroom, an asterisk, a horse, etc. Before that, you need to make sure that the pictures are familiar to the baby. They are asked to draw a well-known figure, for example, a circle (with one eye closed in turn). When they learn the alphabet, using a traditional table with letters.

Children sometimes do not complain to their parents about visual defects, simply because they do not know how objects should actually look. Poor vision delays development, which is why regular eye examinations are so important. Also, adults need to monitor alarming symptoms: the child squints, literally sticks his nose into the TV or tablet monitor, reads or looks at pictures at close range, complains of a headache, rubs his eyes, often stumbles, loses things.

Interesting and important to know!

• In the first months of life, the sensitivity of the cornea is reduced. If something gets into the eye, then newborns do not feel pain and do not react, which means that this may go unnoticed by parents. Foreign bodies – cilia, dust particles, villi – threaten with inflammation.

• Light is necessary for the proper development of eye muscles and pigmentation, but not direct sunlight at all. The baby’s lens is not yet fully formed. While it is developing, it is not protected from the harmful effects of ultraviolet radiation, so it is advisable to go for walks with a child in a panama hat, cap or in a stroller with a visor.

• At first, babies cry without tears – this is normal. But if in the first couple of months of life the mucous plugs that close the tear ducts do not resolve, you should contact an ophthalmologist.

• It often happens that immediately after birth, the iris in newborns is very light or even blue. This is due to the lack of pigmentation. The final color of the eyes is formed most often by the age of two.

• Children’s vision needs to be developed: hang different bright toys and moving mobiles at a distance of 20–30 cm, periodically change them to new ones; take the baby in your arms and show him things around; actively use different facial expressions in communicating with the child; put it in the crib in different ways so that the eyes do not squint in one direction.