How does the human eye capture and process light. What are the key components involved in vision. How has vision evolved over time. What role does the nervous system play in vision. How do physical properties affect our ability to see.

The Evolution of Human Vision: From Dichromatic to Trichromatic

The human visual system has undergone significant changes throughout evolutionary history. Our primitive ancestors possessed dichromatic vision, which allowed them to interpret only ultraviolet (UV) and red light. This limited color perception served their basic survival needs. However, approximately 30 million years ago, a pivotal moment occurred in the evolution of human vision with the emergence of opsin genes.

The development of opsin genes led to the advent of trichromatic vision, dramatically expanding the color spectrum perceivable by humans. This evolutionary leap enabled our species to distinguish between black, white, red, green, and blue, as well as the myriad colors that exist between these primary hues. The ability to perceive such a wide range of colors significantly enhanced our ancestors’ ability to navigate their environment, identify food sources, and detect potential threats.

The Impact of Trichromatic Vision on Human Evolution

The shift from dichromatic to trichromatic vision had far-reaching implications for human evolution. Enhanced color perception likely contributed to:

• Improved food selection and foraging abilities
• Better detection of ripe fruits and edible plants
• Enhanced ability to spot camouflaged predators or prey
• More sophisticated social communication through facial expressions and body language
• Development of complex visual arts and symbolism

This evolutionary advancement in visual capability played a crucial role in shaping human cognitive development and social interactions, ultimately contributing to the complex societies we have today.

The Physical Properties of Vision: Understanding Light and Refraction

To comprehend the intricacies of vision, it’s essential to grasp the fundamental physical properties that govern how light interacts with the eye. Vision begins with light, which travels in the form of waves through the air at an astonishing speed of 300,000 kilometers per second.

When light enters the eye, it encounters several structures, each with its own refractive index. These structures include:

1. The cornea
2. The aqueous humor
3. The crystalline lens
4. The vitreous humor

The average refractive index of these ocular components is approximately 1.34. This value is crucial because it determines how light behaves as it passes through the eye.

The Concept of Refractive Index in Vision

Refractive index is a measure that compares the velocity of light in air to its velocity when passing through a medium, such as the structures of the eye. Air has a refractive index of 1, identical to that of a vacuum. As light enters the eye, its speed decreases, and its trajectory is slightly altered due to the higher refractive indices of ocular tissues.

This change in light behavior is fundamental to the focusing mechanism of the eye. Any condition that affects the refractive properties of ocular structures can significantly impact vision quality. For instance, corneal irregularities or changes in lens shape can lead to refractive errors such as myopia, hyperopia, or astigmatism.

The Eye as a Biological Camera: Focusing Light on the Retina

The human eye functions remarkably similarly to a sophisticated camera. Its primary goal is to focus incoming light onto a specific area – the retina. This process involves several key components working in harmony to create a clear, focused image.

The Role of the Crystalline Lens in Focusing

Central to the eye’s focusing mechanism is the crystalline lens. This remarkable structure is not static but dynamically adjustable. The lens is essentially a capsule filled with water and filamentous proteins. In its resting state, the lens maintains a stretched, flattened configuration.

When light waves encounter this flattened lens, they are refracted less severely, allowing the focal point to fall further back in the eye. This configuration enables clear vision of distant objects. However, for near vision, the lens must adapt its shape to bring closer objects into focus.

The Accommodation Reflex: Adapting to Near and Far Vision

The process by which the eye adjusts its focus for objects at varying distances is called accommodation. This reflex involves a complex interplay between the nervous system and the eye’s muscular structures.

For near vision, the parasympathetic nervous system plays a crucial role. It triggers the contraction of the ciliary muscles, which in turn causes the crystalline lens to adopt a more spherical shape. This increased curvature of the lens results in a higher refractive power, allowing light from nearby objects to be focused precisely on the retina.

The accommodation reflex is a testament to the eye’s remarkable adaptability. It allows us to shift our focus seamlessly between distant and near objects, a capability that is essential for many daily activities, from reading to driving.

The Molecular Basis of Vision: Rhodopsin and Light Sensitivity

At the molecular level, vision is made possible by a remarkable light-sensitive pigment called rhodopsin. This complex molecule plays a pivotal role in the initial stages of visual perception, converting light energy into electrical signals that can be interpreted by the brain.

The Structure and Function of Rhodopsin

Rhodopsin is a sophisticated molecular machine composed of two key components:

1. Scotopsin: A protein component that provides the structural framework
2. Retinal: A photoreactive chromophore derived from vitamin A

The retinal component is covalently bound to one of the lysine residues in the scotopsin protein via a protonated Schiff base (-N+=CH-). This unique arrangement is crucial for rhodopsin’s light-sensing capabilities.

The Light-Induced Isomerization of Retinal

When light strikes the rhodopsin molecule, it triggers a remarkable chain of events at the molecular level:

1. Photon absorption: The retinal chromophore absorbs incoming photons, elevating electrons within its conjugated pi system to higher energy orbitals.
2. Isomerization: The absorbed energy causes the retinal molecule to undergo a rapid isomerization, changing from its cis configuration to a trans configuration. This involves a 180-degree rotation around a specific double bond in the molecule.
3. Conformational change: The isomerization of retinal induces a conformational change in the entire rhodopsin molecule, initiating the visual signaling cascade.

This light-induced isomerization of retinal is the fundamental event that initiates the visual process at the molecular level. It’s an incredibly fast and efficient mechanism, capable of responding to even single photons of light in some cases.

The Retina: Where Light Becomes Electricity

The retina is a complex neural tissue lining the back of the eye, serving as the critical interface between the optical components of the eye and the neural processing of visual information. It’s here that light is converted into electrical signals, initiating the journey of visual information to the brain.

The Layered Structure of the Retina

The retina consists of several distinct layers, each playing a crucial role in visual processing:

1. Photoreceptor layer: Contains rods and cones, the primary light-sensitive cells
2. Outer nuclear layer: Houses the cell bodies of the photoreceptors
3. Outer plexiform layer: Where photoreceptors synapse with bipolar and horizontal cells
4. Inner nuclear layer: Contains the cell bodies of bipolar, horizontal, and amacrine cells
5. Inner plexiform layer: Where bipolar cells synapse with ganglion cells
6. Ganglion cell layer: Contains the cell bodies of ganglion cells, whose axons form the optic nerve

Photoreceptors: Rods and Cones

The retina contains two types of photoreceptors: rods and cones. Rods are highly sensitive to light and are responsible for vision in dim light conditions (scotopic vision). Cones, on the other hand, require more light to function but provide color vision and higher visual acuity (photopic vision).

There are three types of cone cells, each sensitive to different wavelengths of light:

• S-cones: Sensitive to short wavelengths (blue light)
• M-cones: Sensitive to medium wavelengths (green light)
• L-cones: Sensitive to long wavelengths (red light)

The combination of signals from these three cone types allows for the perception of a wide range of colors.

Visual Processing: From Retina to Brain

Once light has been converted into electrical signals by the photoreceptors, a complex chain of neural processing begins. This process involves several stages of information refinement and integration before reaching the visual cortex in the brain.

The Visual Pathway

The visual pathway from the retina to the brain involves several key structures:

1. Optic nerve: Formed by the axons of retinal ganglion cells, carrying visual information from the eye
2. Optic chiasm: Where the optic nerves from both eyes partially cross, allowing for binocular vision
3. Optic tract: Carries visual information post-chiasm to the lateral geniculate nucleus
4. Lateral geniculate nucleus (LGN): A relay center in the thalamus that processes visual information before sending it to the cortex
5. Optic radiations: Neural fibers carrying information from the LGN to the primary visual cortex
6. Primary visual cortex (V1): Located in the occipital lobe, this is where initial cortical processing of visual information occurs

Higher-Order Visual Processing

Beyond the primary visual cortex, visual information is further processed in various regions of the brain, including:

• V2 (secondary visual cortex): Involved in processing color, form, and motion
• V3: Contributes to global motion processing
• V4: Associated with color processing and form recognition
• V5/MT: Specializes in motion perception

These higher-order visual areas work together to create our rich, detailed perception of the visual world, integrating information about color, form, motion, and depth.

Visual Perception: Interpreting the Visual World

Visual perception goes beyond the mere detection of light; it involves the brain’s interpretation of visual signals to create a meaningful representation of our environment. This complex process encompasses various aspects of visual cognition and involves multiple regions of the brain working in concert.

Key Aspects of Visual Perception

Visual perception involves several interrelated processes:

1. Object recognition: The ability to identify and categorize objects based on their visual features
2. Depth perception: The interpretation of visual cues to perceive the three-dimensional structure of the environment
3. Color perception: The ability to distinguish and interpret different wavelengths of light as colors
4. Motion perception: The detection and interpretation of movement in the visual field
5. Face recognition: A specialized form of object recognition crucial for social interaction

The Role of Top-Down Processing in Vision

Visual perception is not just a bottom-up process of assembling visual features. It also involves top-down processing, where our prior knowledge, expectations, and attention influence how we interpret visual information. This explains phenomena such as:

• Visual illusions: Where our perception doesn’t match the physical reality of a stimulus
• Change blindness: The failure to notice significant changes in a visual scene
• Inattentional blindness: The failure to perceive an unexpected stimulus when attention is focused elsewhere

Understanding these aspects of visual perception highlights the complex interplay between sensory input and cognitive processing in shaping our visual experience of the world.

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

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Physiology, Eye – StatPearls – NCBI Bookshelf

Parker E. Ludwig; Rishita Jessu; Craig N. Czyz.

Author Information and Affiliations

Last Update: October 7, 2022.

Introduction

The proper function of the eye depends on its ability to receive and process energy from light in the environment, produce action potentials in specialized nerve cells, and relay those potentials through the optic nerve (cranial nerve II) to the brain. The cornea, iris, ciliary body, and lens all play a role in transmitting and focusing light onto the sensory component of the eye, the retina. Structures such as the choroid, aqueous and vitreous humor, and the lacrimal system are important for physiological balance, appropriate pressure maintenance, and nourishment of ocular tissues.[1]

Issues of Concern

Visual acuity relies on proper refraction or bending of light passing through structures of varying densities as the light is transmitted through the cornea, aqueous humor, lens, and vitreous humor before striking the retina. The lens is the adjustable component of the refractive system: its shape is altered by the contraction or relaxation of the ciliary muscle to focus on objects that are near or far.

Cellular Level

The retina is comprised of two types of photoreceptor cells: rods and cones. Rods are the cells primarily responsible for scotopic vision, or low-light vision. Rods are the more abundant cell-type of the retina and reach their maximum density approximately 15 to 20 degrees from the fovea, a small depression in the retina of the eye where visual acuity is highest. There are approximately 90 million rod cells in the human retina. The cones confer color vision and high spatial acuity and are the cell-type most activated at higher light levels when photopic vision predominates. The fovea has the highest density of cones and is free of rods. The human retina contains approximately 6 million cone cells. It should be noted that there is a visual field “blind spot” at the site of the optic nerve where photoreceptor cells are absent.

In comparing the photoreceptor cell types, rods have more photopigment and exhibit high amplification, highly convergent retinal pathways, and high sensitivity, while cones have a faster response with short integration times, are directionally selective, and exhibit high acuity. The term “bleaching” refers to the absorption of a photon by a pigment molecule. Rods are achromatic, meaning they contain one type of pigment, while cones are arranged in a chromatic organization of three different pigments. In the fovea, this arrangement takes on the form of what is referred to as the “cone mosaic.” Photopigment molecules are embedded in the membranes of photoreceptors.[1][2][3]

Mechanism

The photopigment in rods is called rhodopsin. Human rhodopsin is a G-protein-coupled receptor made up of 348 amino acids arranged in seven transmembrane domains, and its gene is located on chromosome 3. Rhodopsin consists of a protein called scotopsin and its covalently-bound cofactor, retinal. The chromophore retinal lies in a pocket formed by the transmembrane domains of scotopsin. Retinal is a vitamin A derivative produced from dietary beta-carotene. Inactive, retinal exists in the 11-cis-retinal conformation. Upon exposure to light, retinal is isomerized to all-trans-retinal leading to a series of changes in conformation to the form metarhodopsin II (Meta II). Meta II activates the G protein transducin, after which its alpha subunit is released. The transducin alpha subunit, bound to guanosine triphosphate (GTP), then activates cyclic guanosine monophosphate (cGMP) phosphodiesterase.  cGMP is hydrolyzed by cGMP phosphodiesterase which inhibits its activation of cGMP-dependent cation channels and causes hyperpolarization of the rod cell and consequent release of glutamate which depolarizes some neurons and hyperpolarizes others. Reversion of rods to their resting state involves rhodopsin kinase (RK), arrestin, a regulator of G protein signaling (RGS) protein, and closure of cGMP channels. The activity of transducin is partially inhibited by the phosphorylation of the rhodopsin cytosolic tail by RK. Arrestin then binds the phosphorylated rhodopsin to inactivate it further. The RGS protein increases the rate of GTP to GDP hydrolysis to convert transducin into its “off” state. cGMP-sensitive channel closure decreases the concentration of calcium ions, which stimulates calcium ion-sensitive proteins to activate guanylyl cyclase causing restoration of cGMP levels and plasma membrane depolarization.

In contrast to rods, there are three different types of cones: S-cones (short wavelength-sensitive), M-cones (medium wavelength-sensitive), and L-cones (long wavelength-sensitive). The S-cone photopigment gene is encoded on chromosome 7, while those of the M-cones and L-cones are on the X chromosome. All cone receptors contain the protein photopsin in modified conformations to enable activation by different wavelengths of light. The different types of photopsin, which are also opsins combined with retinal, are the cone equivalent of rhodopsin in rods. The absorption maxima for photopsin I, photopsin II, and photopsin III are for yellowish-green, green, and bluish-violet light respectively. The increased visual acuity associated with cones is due to their individual connections to the optic nerve, which enables improved distinction between isolated signals. As compared to rods, each step in the generation of a response to light in cones is less effective, and the reactions responsible for termination of such a light response are faster. Melanopsin is located in some ganglion cells of the retina and is responsible for non-visual responses to light such as the regulation of circadian rhythms and the pupillary reflex. The function of melanopsin is similar to that of invertebrate opsins, it absorbs light and triggers a cascade that allows the brain to generate and modify the body’s circadian rhythm. The absorption of blue light by melanopsin can disrupt the body’s circadian rhythm and can lead to insomnia. 

Signals from photoreceptor cells are transmitted through bipolar cells to the retinal ganglion cells (RGCs) in the innermost layer of the retina, which carry the signals through the optic nerve (composed of bundled RGC axons) to the brain. Retinal horizontal cells are responsible for providing inhibitory feedback to photoreceptor cells. It is interesting to note that light exposure has an inhibitory effect on photoreceptor neurotransmitter release; glutamate is released in states of darkness, causing depolarization of the membrane at rest, and its release is inhibited by photon absorption.[4][5][6][7][8]

Clinical Significance

Astigmatism refers to a blurring of vision due to the irregular curvature of the cornea or the lens. Compensation for such abnormalities is generally made through the use of extraocular lenses such as glasses or contact lenses, or refractive surgery. Myopia or nearsightedness is the result of an excessively long eyeball or thick lens. Hyperopia or farsightedness typically is due to an abnormally short globe or thin lens. Both types of visual disturbance are corrected using intra- or extraocular lenses and/or refractive surgery.

Glaucoma refers to a group of diseases that cause optic nerve damage due to increased intraocular pressure. Open-angle glaucoma is the most common type and is characterized by a normal angle between the iris and cornea (iridocorneal angle). Other types of glaucoma include closed-angle and normal-tension glaucoma. While some cases of glaucoma result from mutations of certain genes, the cause of primary glaucoma remain largely unknown. Glaucoma is usually associated with either an overproduction of aqueous humor or impairment in the drainage of aqueous.

Achromatopsia describes a partial or total absence of color vision. Usually, it is inherited in an autosomal recessive manner. Genetic mutations, most commonly in CNGA3, CNGB3, GNAT2, PDE6C, or PDE6H, cause inappropriate responses of cones to light exposure. This can mean a complete lack of functionality or a significant deficit.

Some of the most common retinal diseases include diabetic retinopathy (DR), and age-related macular degeneration (AMD). AMD exits in two forms: dry (atrophic) and wet (exudative or neovascular). In the majority of people, AMD starts as the dry form and in some individuals, it progresses to the wet type (15% to 20%). AMD is always bilateral, but not always the same form in both eyes. Also, the disease does not necessarily progress at the same rate in both eyes. Both AMD and DR involve degeneration of retinal structure which leads to disruption of the phototransduction pathway discussed. In diabetic retinopathy, blood vessels and neurons are damaged by an overaccumulation of glucose, and in severe disease, the proliferation of new blood vessels can further exacerbate visual impairments. In AMD, there is a buildup of damaged cellular components such as lipofuscin (intracellular) and drusen (extracellular). This leads to damage to the macula which causes dysfunctional central vision and can ultimately lead to complete blindness. Choroidal neovascularization can also exacerbate AMD. Many different genes have been implicated in the development and progression of AMD.

In contrast to achromatopsia, retinitis pigmentosa (RP) affects the rod cells of the retina. Rods are progressively lost as the disease advances, leading to difficulty seeing at night, and decreased peripheral vision which has been described as “tunnel vision”. Symptoms often begin in childhood and progressively worsen with age. Mutations in many genes have been shown to cause RP, with possible inheritance patterns including autosomal dominant, autosomal recessive, X-linked, and mitochondrial inheritance.[9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24]

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Figure

Schematic diagram of the human eye. Contributed by the Public Domain

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Disclosure: Parker Ludwig declares no relevant financial relationships with ineligible companies.

Disclosure: Rishita Jessu declares no relevant financial relationships with ineligible companies.

Disclosure: Craig Czyz declares no relevant financial relationships with ineligible companies.

The structure and functions of the human eye

The structure and function of the human eye

The human eye is an organ with a complex structure that allows us to receive almost 90% of information about the world. Its main task is to “transmit” the correct image to the optic nerve. The eye has a special structure, unlike other organs: it consists of peripheral, conductive and central parts. Each of its parts, each layer has its own functions, properties and purpose.

Structure of the eye

The eyeballs are located in the sockets, which reliably protect them from various injuries. The movement of the “apples” occurs due to six external muscles, which are attached to the sclera and bone tissue. The surface of the organ is regularly moistened thanks to the tears that are produced by the lacrimal gland and form a special film that creates a barrier to protect against external factors. The front of the eye is also protected by the eyelids, which prevent large amounts of germs, dust and pollution from entering it.

Shells

The eyeball has several shells, each of which has a specific function:

1. Conjunctiva. Completely transparent outer shell allowing normal eyeball movement.
2. Fibrous. It mainly consists of the sclera – a dense layer that provides protection to the organ and performs a supporting function. The anterior part of the fibrous membrane is called the cornea – this is its most sensitive area, which is the optical refractive medium.
3. Vascular. This shell provides normal blood supply to the organ of vision and trophism of the structures located inside the eye.
4. Mesh. This is the inner sheath, which is a multi-layered tissue made up of nerves. The macula is located in the retina and is responsible for central vision.

The choroid, in turn, also consists of several elements:

1. Choroid — performs a trophic function, closely contacts with the retina and sclera.
2. Ciliary body is a neuromuscular element that contributes to the natural hydration of the organ.
3. Iris is the element responsible for the color of the eyes. In the center of the iris is the pupil, which limits the amount of light rays perceived by a person.

Chambers

The eyeball has two fluid-filled chambers that are normally closely connected to each other through the pupil. Their main task is to bring the intraocular tissues to a normal state and participate in the conduction of light rays to the retina. The anterior chamber is located directly behind the cornea, while the posterior chamber is located behind the iris. Due to the regular formation and outflow of fluid, both chambers have the same volume. The formation of fluid occurs in the posterior chamber, and then it flows into the drainage system located in the anterior.

Optical structures

The eye perceives objects with the help of optical structures that react to the image and conduct light rays. The quality of vision depends on the state of these structures.

1. The cornea is essentially a lens that transmits and refracts light rays.
2. Lens focuses light rays and is responsible for their transformation into a nerve impulse.
3. Aqueous moisture and vitreous body also have refractive properties. The quality of vision depends on their transparency (or vice versa, cloudiness), that is, how clear a person sees the outlines of objects.

Basic functions

1. Central vision. The task of this function is to perceive small objects and details. It is by this indicator that ophthalmologists determine the overall visual acuity. For diagnostics, a special table with graphic elements of different sizes is used.
2. Peripheral . Forms a field visible to the eye with a constant direction of view. With the help of this function, a person can navigate in space, as well as see objects that fall into the extreme coverage areas.
3. Color . This is the ability of the organ of vision to perceive different colors and shades. Colors are divided according to the wavelength of radiation and are long-wave (shades of the red spectrum), medium-wave (green-yellow spectrum) and short-wave (violet, cyan, blue). If the eye normally perceives all three spectra, then it is able to perceive many intermediate shades that arise when the three primary colors are mixed.
4. Light perception . This function allows you to perceive and distinguish the brightness of the rays of light. Violation of light perception is a pathology and can be an early sign of various diseases.
5. Binocular . Binocular vision is responsible for the clear perception of one object with both eyes at once. This function works thanks to the cortical section of the analyzer.

Binocular function is fully developed by 6–15 years of age. In order for binocular vision to develop correctly, the following conditions must be met:

• symmetrical arrangement of the organs of vision;
• free movement of the oculomotor muscles – with normal muscle tone, a parallel arrangement of the visual axes should be ensured when the rays are projected onto the central region of the retina;
• equal value of the object in question in both organs;
• normal functioning of the retina, optic nerve and pathways.

To make sure that all visual functions develop correctly, it is important to see an ophthalmologist regularly from an early age. The doctor will monitor the development of visual functions and, if necessary, make timely corrections to avoid the development of pathologies.

Why the correct performance of visual functions is impaired

There are several factors that can have a negative impact on the functioning of visual functions:

1. Lack of regular consultations with an ophthalmologist . Vision should be checked once a year in order to prevent the development of diseases in time or to evaluate the effectiveness of the treatment.
2. Incorrect use or incorrect fitting of contact lenses. Do not sleep in the lenses, and do not walk in them for longer than indicated in the instructions for each model. Also, you can’t choose the means of correction on your own – this can only be done according to the prescription of an ophthalmologist. At least once a year, you need to undergo a re-diagnosis in order to change lenses in time if visual acuity has changed.
3. Incorrect light distribution. High-quality lighting while reading, drawing and any other work is very important for eye health.
4. No sunglasses. Regular exposure to sunlight can cause serious eye problems, so it is important to use sun lenses with a special coating that blocks UV rays. This is especially true in the mountains, as well as in regions with a large number of sunny days.
5. Malnutrition . It is important to eat fully, because with a lack of essential vitamins, early degeneration of the retina and the development of cataracts are possible.

You can undergo vision diagnostics and choose corrective means in Lensmaster optics stores.

Sources:

1. DelMonte, D. V., and Kim, T. (2011). Anatomy and physiology of the cornea. Journal of Cataract and Refractive Surgery, 37(3), 588–598. PMID: 21333881
2. Takahashi J., Miura K., Morita K., Fujimoto M., Miyata S., Okazaki K., Matsumoto J., Hasegawa N., Hirano Yu., Yamamori H., Yasuda Yu. , Makinodan M., Kasai K., Ozaki N., Onitsuka T. and Hashimoto R. (2021). Effects of age and gender on eye movement characteristics. Neuropsychopharmacology Reports, 41(2), 152–158. PMID: 33615745
3. Sridhar M.S. (2018). Anatomy of the cornea and ocular surface. Indian Journal of Ophthalmology, 66(2), 190–194. PMID: 2938075

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).