Mydriasis

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.

Drugs that can cause mydriasis include:

• Stimulants (typically monoaminergics) such as amphetamines, cocaine, MDMA, and mephedrone.
• Anticholinergics such as diphenhydramine, atropine, hyoscyamine, and scopolamine antagonize the muscarinic acetylcholine receptors in the eye. Blocking acetylcholine receptors reduces the pupillary 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 pupillary 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.[6]
• Serotonergics such as LSD, psilocybin mushrooms, mescaline and 2C-B. These drugs are typically hallucinogens. Similarly, selective serotonin reuptake inhibitors can cause mydriasis.
• Dissociatives such as dextromethorphan (an SSRI and sigma-1 agonist).
• Certain GABAergic drugs, such as phenibut and GHB.
• Adrenergic agonists, such as phenylephrine and cyclomydril.[7] Adrenergic agonists may be used if strong mydriasis is needed in surgery.[8] Norepinephrine is a hormone and neurotransmitter that regulates the involuntary muscles of the autonomic nervous system, including dilation of the pupil aperture via the muscles of the iris. Hence adrenergic agonists mimic the activity of norepinephrine, which is how they induce mydriasis.

Natural release of the hormone oxytocin can cause mild to moderate mydriasis.

Long term effects of drugs can also cause mydriasis, for example opioid withdrawal.

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.