Mydriasis

How is pupillary dilation regulated?

Pupillary dilation is mediated by the pupillary dilator muscle (m. dilatator pupillae). Its muscle fibers are arranged radially (like rays) within the stroma of the iris. This muscle is innervated by the sympathetic pathway, which consists of several sequential levels:

• Central pathway: descends from brain structures (the hypothalamus) down the brainstem to the spinal cord.
• Spinal center: located in the lateral horns of the spinal cord at the Th1 segment level (ciliospinal center of Budge).
• Preganglionic fibers: emerge from the spinal cord and ascend along the sympathetic trunk (truncus sympathicus).
• Ganglion: impulse transmission occurs in the superior cervical ganglion (ganglion cervicale superius).
• Postganglionic fibers: form a plexus around the internal carotid artery (a. carotis interna), enter the cranial cavity and the orbit, and reach the radial muscle of the iris.

What neurological lesions cause mydriasis?

Mydriasis can result from complete lesion of the oculomotor nerve (n. oculomotorius, CN III). In this case, pupil dilation is caused by weakness of the pupillary sphincter, which is normally innervated by the parasympathetic fibers of this nerve.

In oculomotor nerve palsy, mydriasis is accompanied by absent pupillary light reflex and loss of accommodation (due to ciliary muscle insufficiency). A characteristic triad of symptoms is also observed:

• Ptosis (drooping of the upper eyelid) — occurs due to paresis of the levator palpebrae superioris muscle and lack of opposition to the orbicularis oculi muscle.
• Fixed eye deviation (turned downward and outward) — caused by the unopposed contraction of the lateral rectus and superior oblique muscles.
• Pupil dilation.

Isolated paresis of the internal eye muscles (sphincter and ciliary muscle) results in internal ophthalmoplegia, where the eyeball retains mobility, but the pupil becomes fixed and completely unreactive to light.

Toxic and pharmacological significance

Changes in pupillary reactions are an important diagnostic sign in intoxications and when assessing side effects of therapy.

• Psychoactive substances (PAS): Marked pupil dilation is characteristic of intoxication with cocaine, psychostimulants, and cannabinoids. Opioid intoxication causes pupil constriction (miosis), but during withdrawal (abstinence syndrome), the opposite reaction occurs—marked mydriasis accompanied by lacrimation, tachycardia, chills, and myalgia.
• Medications: Mydriasis is induced by anticholinergic agents (atropine, trihexyphenidyl/cyclodol, antiasthmatic drugs). In overdose, pupil dilation is combined with agitation, tachycardia, tremor, and delirium. A similar side effect (along with dry mouth, tachycardia, and urinary retention) is caused by antipsychotics and tricyclic antidepressants (TCAs), which block muscarinic acetylcholine receptors.

In which diseases is mydriasis observed?

Mydriasis is one of the clinical signs of rabies (hydrophobia) in adults. In rabies, pupil dilation is observed alongside prominent salivation, hydrophobia, psychomotor agitation, hallucinations, and seizures.

Class and exam questions

What else to study on this topic

• Oculomotor nerve (CN III)
• Miosis (pupil constriction)
• Autonomic Nervous System
• Withdrawal syndrome

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