Organophosphate (OP) poisoning is known to cause delayed neurological manifestations. Chlorpyrifos, an OP, causes a delayed syndrome that is characterized by motor sensory polyneuropathy. Pure motor neuropathy with intact sensory conduction is rarely documented. Rapidly evolving delayed myelopathy is extremely uncommon. A healthy 46-year-old male, known alcoholic and smoker without any comorbidities was admitted to the hospital with a cholinergic crisis due to ingestion of chlorpyrifos (OP). He was on mechanical ventilation for 20 days and treated with atropine, pralidoxime, and other supportive measures. After his sensorium improved, he noticed a flail type of weakness in both lower limbs. He also noticed weakness, thinning, and clawing in both hands. No history of (h/o) muscle twitching, bowel and bladder disturbances, and sensory system involvement. After 1 week, patient noticed truncal weakness and also stiffness in both lower limbs. On examination (o/E) he had spasticity in all four limbs. All reflexes are brisk with absent ankle reflex and bilateral extensor plantar. Electrophysiological studies revealed pure motor neuropathy. A spine magnetic resonance imaging (MRI) showed atrophy of the entire spinal cord. Other causes of myelopathy and neuropathy were excluded. The pathology of OP-induced delayed neuropathy (OPIDN) involves a central-peripheral distal axonopathy. The axonopathy is thought to be attributed to the inhibition of neuropathy target esterase (NTE) by phosphorylation and subsequent aging of NTE, causes Wallerian-type degeneration of the axon, followed by myelin degeneration of long and large diameter tracts of the peripheral and central nervous systems. Peripheral distal axonopathy results in predominantly motor polyneuropathy. Axonopathy of the central nervous system results in myelopathic features. Pure motor neuropathy with intact sensory conduction is rarely documented. Rapidly evolving delayed myelopathy is extremely uncommon which makes for a poorer prognosis.