Organophosphate-induced delayed neuropathy (OPIDN) is a rare, serious neurological consequence of organophosphate poisoning. Unlike acute toxicity, which causes cholinergic crises, OPIDN develops insidiously, often weeks after exposure, leading to progressive sensorimotor deficits. A 44-year-old African male pesticide applicator with nine years of organophosphate exposure presented with progressive lower limb weakness, gait disturbances, and paresthesia. The patient exhibited no signs of acute cholinergic symptoms. Neurological examination revealed symmetrical limb weakness, diminished deep tendon reflexes, and distal sensory deficits. Serum cholinesterase levels were decreased. Electrophysiological studies demonstrated axonal degeneration with demyelination, and MRI showed mild spinal cord atrophy. Other causes of neuropathy were excluded. He received supportive care, including physical therapy, pain and spasticity management, antioxidants, vitamins, and off-label intravenous methylprednisolone. Over four months, he regained partial functional improvement, with residual weakness and mild gait disturbance. Chronic low-level organophosphate exposure can cause OPIDN even without acute poisoning. Diagnosis relies on occupational history, neurological examination, and electrophysiological findings. Management is primarily supportive; off-label therapies such as methylprednisolone may reduce neuroinflammation and oxidative stress but are not part of standard care. Early recognition, timely preventive measures, and long-term rehabilitation are essential to improve functional outcomes and quality of life.
Gudisa Bereda (Tue,) studied this question.