Athena Vale
The pupil is the black hole in the centre of the iris, which is the coloured part of the eye. The iris dilator muscle, also known as the dilator pupillae muscle, is a smooth muscle of the eye that runs radially in the iris. It is innervated by the sympathetic nervous system and is responsible for dilating the pupil, thus widening it and allowing more light to enter the eye. The iris sphincter and dilator muscles work together to control pupil size.
| Characteristics | Values |
|---|---|
| Name | Iris dilator muscle, pupil dilator muscle, pupillary dilator, radial muscle of iris, radiating fibers, dilator pupillae muscle |
| Type | Smooth muscle |
| Shape | Spokelike arrangement of modified contractile cells |
| Function | Controls pupil size, increases the size of the pupil to allow more light to enter the eye |
| Controlled by | Sympathetic nervous system, noradrenaline |
| Related conditions | Adie syndrome, Horner syndrome, Argyll Robertson pupils, Parinaud dorsal midbrain syndrome, Traumatic brain injury, Cataracts |
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What You'll Learn
The iris dilator muscle
When the α-receptors of the iris dilator muscle are stimulated, the muscle contracts and widens the pupil, allowing more light to enter the eye. Conversely, when the α-receptors are blocked, the muscle relaxes, causing pupillary miosis (constriction). There are nine subtypes of α-receptors: α1a, α1b, α1d, α2a, α2b, α2c, ß1, ß2, and ß3. Research suggests that α1-receptors are the primary mediators of dilation in the iris dilator muscle.
Several conditions can affect the function of the iris dilator muscle, including Adie syndrome (Holmes-Adie syndrome), which is characterised by a lack of response to light and a pupil that remains tonically dilated. Horner syndrome is another condition that can cause ptosis (drooping of the eyelid) and a constricted pupil due to a loss of sympathetic innervation to the eye. Traumatic rupture of iris muscles can also cause an irregularly shaped pupil.
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The sympathetic nervous system
The SNS fibres innervate tissues in almost every organ system, providing at least some regulation of functions such as pupil diameter, gut motility, and urinary system output and function. Messages travel through the SNS in a bidirectional flow, and efferent messages can trigger changes in different parts of the body simultaneously. For example, the SNS can accelerate heart rate, widen bronchial passages, decrease the movement of the large intestine, constrict blood vessels, activate goose bumps, start sweating, and raise blood pressure.
In the eye, the SNS causes the radial muscle of the iris to contract, leading to mydriasis (pupil dilation) and allowing more light to enter. The ciliary muscle relaxes, improving far vision. In the heart, the SNS increases the heart rate, the force of contraction, and the rate of conduction, allowing for increased cardiac output to supply the body with oxygenated blood.
The SNS is composed of many pathways that perform a variety of functions on various organ systems. The neurons of the SNS arise from neural crest cells that originate between the neural and non-neural ectoderm. They form the dorsal neural folds as the folds themselves form the neural tube. The SNS neurons arise from near the middle of the spinal cord in the intermediolateral nucleus of the lateral grey column, beginning at the first thoracic vertebra and extending to the second or third lumbar vertebra.
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Adie syndrome
The primary symptom of Adie syndrome is a dilated pupil that reacts slowly or not at all to light. This is known as a tonic pupil. Over time, the affected pupil tends to become smaller than the unaffected pupil, a condition called "little old Adie" pupil. The affected pupil will also constrict slowly when focusing on objects close by, a response known as the near response. This behaviour can be observed with a loupe or microscope, where some sectors of the sphincter muscles constrict while others do not, resembling the movement of an earthworm.
In terms of treatment, Adie syndrome is typically managed by an interprofessional team of medical experts. Low-concentration pilocarpine tests may be used to demonstrate cholinergic denervation supersensitivity in the affected eye.
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Traumatic rupture of iris muscles
The pupil is dilated by the iris dilator muscle, which is a smooth muscle of the eye. This muscle is innervated by the sympathetic nervous system, which acts by releasing noradrenaline, causing the muscle to contract and dilate the pupil, thus letting more light reach the retina.
Traumatic rupture of the iris muscles can cause an irregularly shaped pupil. This type of injury can present in various ways depending on its location and severity. Tears at the pupillary border can damage the sphincter muscle, resulting in an atonic, mydriatic, or partially reactive pupil. Tears at the iris root can lead to iridodialysis, a separation of the iris from its attachment to the root. These tears can be full thickness through the iris stroma or only partial thickness, involving the posterior pigment epithelium and resulting in trans-illumination defects. Traumatic iris wounds do not heal on their own, and repairing them can be challenging.
The iris is a delicate structure that can be damaged by blunt, penetrating, or iatrogenic trauma. Penetrating wounds, either from foreign objects lacerating the eye or surgical trauma, are the primary cause of full-thickness iris defects. Iris defects may also be hereditary or created during certain eye surgeries or procedures. Traumatic iris damage can take several forms, including sphincter tears, iris chaffing, tears at the root of the iris, iridodialysis, transillumination defects, and traumatic aniridia, where the iris is extruded from the eye.
When repairing iris defects, it is important to evaluate the lens-bag-zonule complex for instability and check for iris atrophy, trans-illumination defects, synechiae, or exfoliative material in the other eye. A gonioscopy exam should be performed when there is no ocular laceration to check for tears in the iris root or peripheral anterior synechiae. Repair of iris lacerations should be delayed until an assessment of the posterior segment can be performed with ophthalmoscopy and/or a B-scan ultrasound.
Non-surgical management options for traumatic iris reconstruction include miotics like pilocarpine, brimonidine, carbachol, and contact lenses. However, pilocarpine has minimal or no action in cases of traumatic mydriasis and pupillary sphincter tears. Surgical techniques may involve the use of viscoelastic to safeguard the endothelium and facilitate suturing, as well as anterior chamber maintainers and pars plana infusion in eyes with previous vitrectomy.
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How pupil dilation is controlled
The pupil is the black hole in the center of the colored part of the human eye, also known as the iris. The iris has two muscles that control how the pupil opens and closes: the iris dilator muscle and the iris sphincter muscle. The dilator muscle, also known as the pupillary dilator, consists of a spoke-like arrangement of modified contractile cells called myoepithelial cells. These cells are stimulated by the sympathetic nervous system. When stimulated, the cells contract, widening the pupil and allowing more light to enter the eye. Conversely, when the α-receptors are blocked, the dilator muscle relaxes, causing the pupil to constrict.
The iris sphincter muscle, on the other hand, is a circular muscle that controls the closing of the pupil. It receives parasympathetic innervation via the short ciliary nerves, leading to pupillary constriction and accommodation. The parasympathetic fibers that serve the sphincter muscle originate from the Edinger-Westphal nucleus of cranial nerve III. The signal synapses in the ciliary ganglia and are terminated on muscarinic receptors of the muscle fibers. The sympathetic and parasympathetic systems work in opposition to constantly adjust the size of the pupil.
Several conditions can affect pupil dilation and constriction. Adie syndrome, for example, is characterized by a pupil that stays dilated and doesn't react normally to changes in light. Horner syndrome, a rare condition that affects the eyes and face, is another example. It can result in either a constricted pupil due to loss of sympathetic innervation or a dilated pupil due to damage to the parasympathetic nerves. Traumatic rupture of iris muscles can also cause an irregularly shaped pupil.
The pupil is the pathway that lets light reach the retina. The diameter of the pupil fluctuates in response to changes in luminance, accommodation, and various brain states related to arousal, locomotion, emotion, attention, and cognitive loads. Pupil dilation is also used as a reliable indicator of cortical arousal, which is modulated by the release of noradrenaline and acetylcholine.
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Frequently asked questions
The muscle that dilates the pupil is called the iris dilator muscle, or the pupillary dilator.
The iris dilator muscle is a smooth muscle that runs radially in the iris. It is made up of a spokelike arrangement of contractile cells called myoepithelial cells. When these cells are stimulated, they contract, widening the pupil and allowing more light to enter the eye.
The iris dilator muscle controls the size of the pupil by increasing or decreasing the amount of light that enters the eye. This is important for maintaining vision in different lighting conditions.
Damage to the iris dilator muscle can cause an abnormally small pupil, a condition known as Horner syndrome. Traumatic rupture of the iris muscles can also result in an irregularly shaped pupil.
