Clinical Toxinology Resources Home


Flaccid paralysis caused by neurotoxins affects skeletal muscles and respiration, not cardiac or smooth muscle. For species with potent postsynaptic neurotoxins, paralytic symptoms can develop within 3-15 minutes of the bite and major paralysis within 15-30 minutes, but such cases are the exception. In most cases, clinically detectable paralysis will not be apparent until at least one hour post-bite and may be delayed up to 24 hours. The cranial nerves are usually affected first, with ptosis often the first sign. Other common presenting signs are dysphonia, dysphagia, drooling and diplopia, the latter due to partial ophthalmoplegia. As paralysis progresses drooling may increase, ophthalmoplegia may become total, with fixed forward gaze, often associated with fixed dilated pupils. Limb weakness becomes apparent, the victim usually first noticing ataxic gait, then inability to walk, then stand or even sit up. The neck may become floppy (“broken neck” sign). Deep tendon reflexes will become reduced, then disappear. Respiratory distress develops and breathing may become shallow, rapid and cyanosis may be apparent. Complete respiratory failure will ensue, unless respiratory support is offered. Time from bite to respiratory failure is highly variable, from as little as 30 minutes (rare) to more than 24 hours, but commonly within 6-12 hours. Without antivenom therapy or anticholinesterases, the period of respiratory failure may vary from less than 24 hours, to several days, or even several weeks.

For those species with potent presynaptic neurotoxins, but low concentrations of postsynaptic neurotoxins, while symptoms and signs are the same, the rapidity of onset is usually slower, with first signs essentially never evident in less than one hour post-bite. Unless paralysis is diagnosed and halted at an early stage, using antivenom therapy, this type of paralysis is not reversible and days, weeks or months may elapse before axonal repair is sufficient for return of neuromuscular function.

In addition to the major features noted above, several other neurotoxic effects may occur. Of particular note are transient or permanent alteration to taste or smell, sometimes leaving the victim with permanent complete anosmia.