INTRODUCTION: Organophosphate (OP) poisoning is known to cause delayed neurological manifestations. Chlorpyrifos, an OP, causes a delayed syndrome that is characterized by a motor sensory polyneuropathy. Pure motor neuropathy with intact sensory conduction is rarely documented. Rapidly evolving delayed myelopathy is extremely uncommon. CASE REPORT: A healthy 15-year-old female was admitted to hospital with cholinergic crisis due to ingestion of a large dose of chlorpyrifos (OP). She was treated with atropine and recovered completely without any neurological symptoms or signs. She came to hospital 6 weeks later with upper and lower motor neuron signs involving the lower limbs without sensory loss. By the end of 7 weeks, there was urinary incontinence. At 2-month follow-up, she had progressive spasticity. Electrophysiological studies revealed a pure motor neuropathy. Spine magnetic resonance imaging showed early signs of thoracic cord atrophy. Other causes of myelopathy were excluded. CONCLUSIONS: Chronic neurotoxicity due to OP poisoning is dependent on several factors: chemical composition of the OP, dose systematized, and the administration of anitcholinergics for cholinergic crisis. The pathology of OP-induced delayed neuropathy involves a central-peripheral distal axonopathy. Peripheral distal axonopathy results in a predominantly motor polyneuropathy. Axonopathy of the central nervous system results in myelopathic features that makes for a poorer prognosis.
INTRODUCTION:Organophosphate (OP) poisoning is known to cause delayed neurological manifestations. Chlorpyrifos, an OP, causes a delayed syndrome that is characterized by a motor sensory polyneuropathy. Pure motor neuropathy with intact sensory conduction is rarely documented. Rapidly evolving delayed myelopathy is extremely uncommon. CASE REPORT: A healthy 15-year-old female was admitted to hospital with cholinergic crisis due to ingestion of a large dose of chlorpyrifos (OP). She was treated with atropine and recovered completely without any neurological symptoms or signs. She came to hospital 6 weeks later with upper and lower motor neuron signs involving the lower limbs without sensory loss. By the end of 7 weeks, there was urinary incontinence. At 2-month follow-up, she had progressive spasticity. Electrophysiological studies revealed a pure motor neuropathy. Spine magnetic resonance imaging showed early signs of thoracic cord atrophy. Other causes of myelopathy were excluded. CONCLUSIONS:Chronic neurotoxicity due to OP poisoning is dependent on several factors: chemical composition of the OP, dose systematized, and the administration of anitcholinergics for cholinergic crisis. The pathology of OP-induced delayed neuropathy involves a central-peripheral distal axonopathy. Peripheral distal axonopathy results in a predominantly motor polyneuropathy. Axonopathy of the central nervous system results in myelopathic features that makes for a poorer prognosis.