Toxins Causing Miosis
Organophosphates and carbamates are the primary toxins causing miosis through acetylcholinesterase inhibition, while opioids also produce characteristic pinpoint pupils through direct CNS effects. 1, 2
Organophosphates and Carbamates
These cholinesterase inhibitors cause miosis as part of a broader cholinergic syndrome:
Organophosphates (found in pesticides, nerve agents like sarin and VX, and some medications) irreversibly inhibit acetylcholinesterase, resulting in parasympathetic excess that includes miosis as a hallmark sign, along with bradycardia, bronchospasm, bronchorrhea, hypersalivation, lacrimation, urination, diarrhea, vomiting, and diaphoresis 1
Miosis and rhinorrhea are the most common clinical findings in individuals acutely exposed to organophosphate nerve agents 3
Carbamates produce similar cholinergic effects but spontaneously dissociate from acetylcholinesterase (reversible inhibition), causing the same miotic response through the same mechanism 1
The miosis results from excessive acetylcholine accumulation at parasympathetic nerve endings in the iris sphincter muscle, causing sustained pupillary constriction 1
Topical ocular exposure to organophosphates (such as sarin or VX) produces dose-dependent miosis that can persist for 24-48 hours or longer, accompanied by impaired visual function 4, 5
Clinical Context
High-dose exposures lead to acute cholinergic crisis with pinpoint pupils, while chronic low-level exposures may not produce visible miosis but can still cause neurodevelopmental harm 1
The severity and duration of miosis correlates with the specific organophosphate agent, with nerve agents like VX and sarin producing particularly severe and prolonged pupillary constriction 4, 6
Opioids
Opioids produce characteristic miosis through a distinct mechanism:
Morphine and other full opioid agonists cause miosis even in total darkness through direct action on the Edinger-Westphal nucleus in the midbrain 2
Pinpoint pupils are a classic sign of opioid overdose, though this finding is not pathognomonic as pontine lesions can produce similar findings 2
Marked mydriasis rather than miosis may occur in severe opioid overdose due to hypoxia and brainstem dysfunction, representing a critical distinction in overdose situations 2
The miotic effect results from mu-opioid receptor stimulation in the CNS, not from peripheral cholinergic effects 2
Botulinum Toxin (Does NOT Cause Miosis)
Important caveat: Botulinum toxin blocks acetylcholine release and causes descending flaccid paralysis but does not produce miosis because it prevents acetylcholine release rather than causing accumulation 7, 8. This distinguishes botulism from organophosphate/carbamate poisoning, which have opposite effects on acetylcholine availability.