Mechanism of Toxicity

Like all organophosphates, cyclosarin inhibits the enzyme acetlycholinesterase (AChE), causing overstimulation by a build-up of acetylcholine. Acetlycholinesterase is necessary for normal control of nerve impulse transmission.

Potential for Exposure

Opportunities of exposure to chemical warfare nerve agents, such as cyclosarin include:

• On the battlefield
• To civilians as a threat by a terrorist group
• An accident involving current demilitarization efforts

Signs and Symptoms of Poisoning

All cholinesterase inhibitors produce similar symptoms:

• Salivation
• Lacrimation (tears)
• Hypothermia
• Tremors
• Altered neuromuscular function
• Neuropathological lesions
• Long-term deficits in cognitive function and behavior
• Seizures
• Paralysis
• Respiratory Failure and death

Most long-term effects are unknown, and are the subject of current animal studies. Current data suggest that, even after treatment, long-term effects include memory impairment, epileptic seizures, and central neuropathy. (Filiat 1999)
 

Treatment

Following exposure to cyclosarin, the best therapy is immediate treatment with an
anticholinergic drug, such as atropine. Anticholinergeric drugs counteract the effect of excessive build-up of acetylcholine. In addition it is helpful to administer an oxime-reactivator of acetlycholinesterase, such as pralidoxime, obidoxime, or methoxime.

References

CBWInfo.com. 2003. Factsheets on Chemical and Biological Warfare Agents: CF
(http://www.cbwinfo.com/Chemical/Nerve/GF.shtml) Accessed 5/4/2008

Filliat et al. 1999. Improvement with anticholinergic and antiglutamatergic therapeutics, Neurotoxicology. 20:535-550.

Krejcova-Kunesova G, Bartosova L, Kuca K. 2005. Signs of cyclosarin-induced neurotoxicity and its pharmacological treatment with quaternary pyridinium-oximes reactivators. Toxicology. 216(1):32-40