miosis in 43% of children exposed to OP pesticides, isolated CNS effects (stupor and coma) in the absence of peripheral muscarinic effects, incidences of seizures varying from 8% to 22%, and weakness and hypotonia (seen in 70% to 100% of victims) often in the absence of glandular secretions The clinician should be prepared for subtle and sometimes significant differences in children from the classic cholinergic toxidrome seen in adults Disposition and Prognosis The disposition of exposed patients depends on severity of symptoms and route of exposure Most patients presenting after vapor exposure manifest peak toxicity by the time of hospital arrival with only miosis, which may persist for up to weeks These children may be discharged After dermal exposure, symptom onset may lag up to 18 hours, even after thorough skin decontamination, and most experts recommend a 24-hour observation period even for initially asymptomatic victims The prognosis for full recovery from even severe nerve-agent poisoning appears to be good with timely life-support interventions and adequate antidotal therapy Apneic patients have recovered ventilatory function within hours, and once consciousness was regained, muscle weakness and obtundation have resolved over a few days, whereas miosis and subtle mental status effects have persisted for several weeks Significant histologically demonstrable neuropathologic changes in brain tissue persisting after acute exposures are typically seen only in exposed individuals who exhibited seizure activity during the acute cholinergic crisis Nerve agents appear not to cause intermediate syndrome (IMS), a syndrome of weakness, especially of cranial nerve–innervated muscles (neck flexors and respiratory muscles) and limb muscles seen in survivors of Sri Lankan suicide attempts involving OP insecticides Two acutely poisoned Japanese nerve-agent casualties, one from the Tokyo attack and one from an earlier attack in Matsumoto, developed organophosphate-induced delayed neurotoxicity, or OPIDN (also called organophosphate-induced delayed polyneuropathy, or OPIDP), a delayed polyneuropathy resulting in long-term and in some cases permanent upper motor neuron lesions with spasticity and hyperreflexia However, these are the only known cases associated with nerveagent exposure, and it is likely that extremely high exposures are necessary to cause this delayed neuropathy Exposure or suspected exposure to nerve agents has also been associated with a syndrome that has been called chronic organophosphate-induced neuropsychiatric disorders (COPIND) and, more recently, organophosphorus ester–induced chronic neuropathy (OPICN), a constellation of neurobehavioral and neurologic effects including defective