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Case Reports
. 2024 Jun 21;16(6):e62877.
doi: 10.7759/cureus.62877. eCollection 2024 Jun.

The Enigma of Delayed Neurotoxicity in Organophosphate Poisoning: A Case Report of Clinical Presentation With Normal MRI Findings

Jayksh Chhabra  1 , Akankshi Oberoi  1 , Neha Pandita  2 , Vinit Banga  2
Affiliations
Case Reports

The Enigma of Delayed Neurotoxicity in Organophosphate Poisoning: A Case Report of Clinical Presentation With Normal MRI Findings

Jayksh Chhabra et al. Cureus. .

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.

Keywords: intermediate syndrome; myelopathy; organophosphate induced delayed neurotoxicity; organophosphate induced polyneuropathy; organophosphate pesticide poisoning.

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Conflict of interest statement

Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work.

Figures

Figure 1
Figure 1. Timeline of onset of symptoms after OP ingestion
Image credits: Akankshi Oberoi and Jayksh Chhabra
Figure 2
Figure 2. Clinical features of an acute cholinergic crisis
Image credits: Akankshi Oberoi and Jayksh Chhabra
Figure 3
Figure 3. Mechanism of stages of OP poisoning
Ach, acetylcholine; AchE, acetylcholine esterase; NTE, neuropathy target esterase; OP, organophosphates; OPIDN, organophosphate-induced delayed neurotoxicity Image credits: Akankshi Oberoi and Jayksh Chhabra
Figure 4
Figure 4. Mechanism of OPIDN
NTE, neuropathy target esterase; OPIDN, organophosphate-induced delayed neurotoxicity; PNPLA-6, patatin-like phospholipase domain-containing protein 6; TRPA1, transient receptor potential cation channel member A1 Image credits: Jayksh Chhabra and Akankshi Oberoi
See this image and copyright information in PMC

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