Organophosphorus (OP) compounds, with their lipophilicity, are responsible for a spectrum comprising of acute cholinergic symptoms, intermediate syndrome, as well as delayed neurological sequelae in the form of OP-induced delayed neuropathy and subsequently, myeloneuropathy with predominantly thoracic cord affection, manifested on partial recovery of the neuropathy. The pathogenesis of this myeloneuropathy in humans is still not well perceived.To determine the onset and course of development of delayed myeloneuropathy in patients of OP poisoning.Twelve patients of OP ingestion presenting with delayed myeloneuropathy were evaluated with prior history, examination, MR imaging, nerve conduction and electromyography studies, and various evoked potentials to elicit the pattern of disease manifestation and progression.Among the included patients, a majority had consumed chlorpyrifos and permethrin composition, a majority had undergone gastric lavage. Five (41.7%) had experienced acute worsening and 8 (66.7%) patients had developed intermediate syndrome. OPIDN had appeared after a median of 4 (1-8) weeks after the poisoning. All patients had lower limb hypertonia with wasting and distal more than proximal weakness with pure motor or sensorimotor involvement. MRI showed thoracic cord atrophy in 3 (25%) patients. Motor-evoked potential with reduced amplitude was noted in lower limbs on lumbar stimulation but absent on cortical stimulation.Various animal models have shown similar patterns of neurotoxicity in OP poisoning with predominant thoracic cord pathology. Further research in humans may be undertaken to elicit the pathogenesis, thereby improving the treatment modality.