ABSTRACT
Organophosphates (OP) are the most widely used pesticides globally and are misused for suicides because of their easy availability. It leads to functional impairment of distal segments of sensory and motor axons of peripheral nerves, as well as impacting the ascending and descending spinal tracts. It progresses through latent, progressive, static, and improvement phases. In the improvement phase, peripheral nerve regeneration occurs, revealing the spinal cord lesion with myelopathic features. The acute symptoms and treatments of OP poisoning have been extensively documented in the literature. Delayed neurotoxicity is a rare but debilitating condition that can manifest weeks after initial exposure. A high index of suspicion for OP-induced delayed neurotoxicity should be maintained in patients presenting with delayed neurological symptoms post-OP exposure, even with normal MRI findings. OP linked to delayed neuropathy include triorthocresyl phosphate, chlorpyriphos, malathion, fipronil, mipafox, matriphonate, and parathion. Among these, the most hazardous OP ester is tri-o-cresyl phosphate. We report a case of a 28-year-old male who developed neurotoxicity five weeks following OP poisoning with chlorpyrifos. Early diagnosis and symptomatic management are important for improving patient outcomes.
ABSTRACT
Neurological side-effects of linezolid manifesting as a posterior reversible leuco-encephalopathy syndrome (PRES) is rare. Early identification of this offending drug might reverse this catastrophic event. We report a 45-year-old female, who was diagnosed as a case of disseminated tuberculosis and was treated with antitubercular drugs (ATT), but later developed ATT-induced hepatitis. She was then put on modified ATT (moxifloxacin, terizidone, and linezolid). In the next two days she developed an altered sensorium. Brain imaging was suggestive of PRES. Linezolid was withdrawn, following which she showed an excellent clinical and radiological recovery.