|Pupil dilated for examination by ophthalmologist|
|Classification and external resources|
|OMIM||159420 159410 106240|
Mydriasis (//) is the dilation of the pupil, usually defined as when having a non-physiological cause, but sometimes defined as potentially being a physiological pupillary response. Non-physiological causes of mydriasis include disease, trauma, or the use of drugs. Normally, as part of the pupillary light reflex, the pupil dilates in the dark and constricts in the light to respectively improve vividity at night and to protect the retina from sunlight damage during the day. A mydriatic pupil will remain excessively large even in a bright environment. The excitation of the radial fibres of the iris which increases the pupillary aperture is referred to as a mydriasis. More generally, mydriasis also refers to the natural dilation of pupils, for instance in low light conditions or under sympathetic stimulation.
An informal term for mydriasis is blown pupil, and is used by medical providers. It is usually used to refer to a fixed, unilateral mydriasis, which could be a symptom of raised intracranial pressure.
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There are two types of muscle that control the size of the iris: the iris sphincter, composed of circularly arranged muscle fibers, and the iris dilator, composed of radially arranged muscle fibers. The sphincter is innervated by (signaled by nerves of) the parasympathetic nervous system; the dilator by the sympathetic nervous system. Sympathetic stimulation of the adrenergic receptors causes the contraction of the radial muscle and subsequent dilation of the pupil. Conversely, parasympathetic stimulation causes contraction of the circular muscle and constriction of the pupil.
The mechanism of mydriasis depends on the agent being used. It usually involves either a disruption of the parasympathetic nerve supply to the eye (which normally constricts the pupil) or overactivity of the sympathetic nervous system (SNS).
Parasympathetic fibers travel with cranial nerve III, the oculomotor nerve, to innervate the circular layer of muscle of the eye (sphincter pupillae). Damage to this nerve typically manifests itself as mydriasis, because the sympathetic supply to the pupil, which causes mydriasis, remains unaffected, and therefore unopposed.
Multiple central nervous system disorders e.g. epilepsy, stroke, and impending brain herniation are known to lead to temporal mydriasis as well. A brain catastrophe, or a rapidly increasing brain mass, can cause compression of the oculomotor nerve.
In cases of head injury or orbit trauma (eye injury), the iris sphincter (the muscle responsible for closing the pupil) or the nerves controlling it can be damaged, reducing or eliminating the normal pupillary light reflex.
Ketorolac is used as an analgesic and a mydriastic agent during cataract surgery. Anticholinergics such as atropine, hyoscyamine, and scopolamine antagonize the muscarinic acetylcholine receptors in the eye. By blocking these receptors, the pupils are no longer capable of constriction and dilation results. Such alkaloids present in many plants of the family Solanaceae may also induce mydriasis when used[medical citation needed]
Drugs that increase overall serotonin levels in general are capable of causing mydriasis in the same way as the 5-HT2A-mediated psychedelics. This is because serotonin itself is naturally responsible for normal 5-HT2A stimulation. Hence, in sufficient quantities serotonin is mydriatic and can even be mildly psychedelic[medical citation needed], though the potentially fatal serotonin syndrome usually ensues before the psychedelia becomes overly-pronounced. Examples of such drugs include MDMA (as well as other MDxx compounds), fenfluramine, chlorphentermine, stimulants (including cocaine and amphetamines), and some antidepressants (such as SSRIs, SNRIs, and MAOIs). Natural serotonin-boosting supplements such as L-Tryptophan and 5-HTP are also capable of this, but usually only in excessive doses.
The neurotransmitter norepinephrine regulates many physiological processes in the body and brain. One of them is the autonomic constriction and contraction of certain muscles. The psychoactive drug cocaine potently inhibits the normal reuptake of norepinephrine into presynaptic nerve terminals, resulting in an increased level of extracellular norepinephrine. Amphetamines also potently release and prevent the reuptake of norepinephrine. The released norepinephrine then proceeds to bind to adrenergic receptors, and the biological effects of norepinephrine finally occur. When a solution of cocaine is dropped into the eye, this process takes place and the end result is dilation of the pupil. Cocaine itself is not typically used for this task, however. Any potent norepinephrine reuptake inhibitor or release agent should be capable of such an effect.
A mydriatic is an agent that induces dilation of the pupil. Drugs such as tropicamide are used in medicine to permit examination of the retina and other deep structures of the eye, and also to reduce painful ciliary muscle spasm (see cycloplegia). Phenylephrine (e.g. Cyclomydril) is used if strong mydriasis is needed for a surgical intervention. One effect of administration of a mydriatic is intolerance to bright light (photophobia). Purposefully-induced mydriasis via mydriatics is also used as a diagnostic test for Horner's syndrome.
- Mydriasis in Farlex medical dictionary. In turn citing:
- The American Heritage Medical Dictionary (2007)
- Mosby's Dental Dictionary, 2nd edition.
- Mydriasis in Farlex medical dictionary. In turn citing: Mosby's Medical Dictionary, 8th edition.
- "Traumatic Brain Injury". American Association of Neurological Surgeons. Retrieved 27 March 2012.
- Saenz-de-Viteri, Manuel; Gonzalez-Salinas, Roberto; Guarnieri, Adriano; Guiaro-Navarro, María Concepción (2016). "Patient considerations in cataract surgery – the role of combined therapy using phenylephrine and ketorolac". Patient Preference and Adherence. Volume 10: 1795–1801. doi:10.2147/PPA.S90468. ISSN 1177-889X.
- "Common eye diseases and their management", Galloway/Amoako/Browning, Springer science 2006, 3rd edition, p196