| Mydriasis | |
|---|---|
| Other names | Blown pupil[1] |
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| Dilated pupils caused by mydriatic drops instilled for adilated fundus examination | |
| Pronunciation | |
| Specialty | Ophthalmology,neurology |
Mydriasis is thedilation of thepupil, usually having a non-physiological cause,[3] or sometimes a physiologicalpupillary response.[4] Non-physiological causes of mydriasis includedisease,trauma, or the use of certain types ofdrugs. It may also be of unknown cause.
Normally, as part of thepupillary light reflex, the pupil dilates in thedark andconstricts in thelight to respectively improve vividity at night and to protect theretina from sunlight damage during the day. Amydriatic 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. Mydriasis is frequently induced by drugs for certainophthalmic examinations and procedures, particularly those requiring visual access to theretina.
Fixed, unilateral mydriasis could be a symptom of raisedintracranial pressure. The opposite, constriction of the pupil, is referred to asmiosis. Both mydriasis and miosis can be physiological.Anisocoria is the condition of one pupil being more dilated than the other.
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There are two types ofmuscle that control the size of theiris: theiris sphincter, composed of circularly arranged muscle fibers, and the irisdilator, composed of radially arranged muscle fibers. The sphincter is controlled by nerves of theparasympathetic nervous system, and the dilator by thesympathetic nervous system. Sympathetic stimulation of theadrenergic receptors causes thecontraction of theradial 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 theparasympathetic nerve supply to the eye (which normally constricts the pupil) or overactivity of thesympathetic 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.[5]
Amydriatic is an agent that inducesdilation of thepupil. Drugs such astropicamide are used inmedicine to permit examination of theretina and other deep structures of the eye. Mydriatics typically also have acycloplegic effect, reducing or paralyzing theaccommodation reflex which may also be used for certain ophthalmic examinations or treatments, such as reducing painfulciliary muscle spasm. One effect of administration of a mydriatic is intolerance to bright light (photophobia). Purposefully-induced mydriasis via mydriatics is also used as adiagnostic test forHorner's syndrome.
Mydriasis can be induced via modulation ofadrenergic orcholinergic signalling.
Drugs that can cause mydriasis include:
Natural release of the hormoneoxytocin can cause the pupils to dilate to a greater degree to stimulus but perhaps not directly causative of mydriasis.[9]
Long term effects of drugs can also cause mydriasis, for exampleopioid withdrawal.
It is not clear whether Marijuana use causes mydriasis, a survey of several studies produced conflicting findings and suggest the mydriatic effect can be related to other factors occurring with cannabis use.[10]
Parasympathetic fibers travel withcranial nerve III, theoculomotor nerve, to innervate the circular layer of muscle of the eye (sphincter pupillae). Damage to this nerve typically manifests itself as mydriasis, because thesympathetic supply to the pupil, which causes mydriasis, remains unaffected, and therefore unopposed.
Multiplecentral nervous system disorders e.g.epilepsy,stroke, and impendingbrain 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 ofhead injury ororbit trauma (eye injury), theiris sphincter (the muscle responsible for closing the pupil) or the nerves controlling it can be damaged, reducing or eliminating the normalpupillary light reflex.