Mydriasis is the dilation of the pupil, usually having a non-physiological cause, or sometimes a physiological pupillary response. Non-physiological causes of mydriasis include disease, trauma, or the use of drugs.
|Pupil dilated for examination by ophthalmologist|
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, and 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).
Pupil diameter also increases in reaction to cognitive tasks requiring memory and attention, and this phenomenon is used as an indicator of mental activation (‘arousal’) in psychophysiological experiments.
- Stimulants such as amphetamines, cocaine, MDMA, and mephedrone.
- Anticholinergics such as diphenhydramine or scopolamine.
- Serotonergic hallucinogens such as LSD, psilocybin mushrooms, mescaline and 2C-B.
- Selective serotonin reuptake inhibitors.
- Dissociatives such as dextromethorphan.
- Opioid withdrawal.
- Certain GABAergic drugs, such as phenibut and GHB.
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.
Drug Induced MydriasisEdit
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). 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 can be induced via modulation of adrenergic or cholinergic signalling. Within the adrenergic system, norepinephrine is a hormone and neurotransmitter responsible for regulating physiological processes in the body, including the involuntary muscles of the autonomic nervous system (such as the dilation or constriction of the pupil aperture via the muscles of the iris). Modulation of norepinephrine signalling can induce mydriasis. For instance, the adrenoceptor agonist phenylephrine (e.g. Cyclomydril) is used if strong mydriasis is needed for a surgical intervention.
Alternatively, anticholinergics (in particular, antimuscarinics) such as atropine, hyoscyamine, and scopolamine antagonize the muscarinic acetylcholine receptors in the eye. Blocking acetylcholine receptors, reduces the pupilary muscles' ability to constrict and causes dilation (which is critical in eye surgery procedures such as cataract surgery which require uninterrupted access to the inner eye via the pupilary aperture, thus requiring that the eye be both paralyzed and anesthetized before the procedure can go ahead. The antimuscarinic, tropicamide, may be used as a mydriastic agent during surgery.
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