Diquat poisoning review outlines brain injury mechanisms and treatment gaps
Experimental research and case reports link neurological injury after diquat poisoning to several interacting pathways, while leaving effective targeted treatments unresolved.
Based on the published abstract. The full paper may contain additional methods, results and limitations.
The 30-second takeaway
This review connects the neurological features of diquat poisoning with proposed mechanisms of brain injury. It describes impaired consciousness, convulsions and characteristic brain lesions, alongside interacting cellular pathways. Because the evidence combines experimental work with clinical case studies, it maps possible injury processes and treatment challenges without demonstrating an effective neuroprotective treatment.
Experimental studies and clinical case reports contribute different kinds of evidence. The abstract reports no controlled treatment-effect estimate, patient totals or follow-up lengths, so it cannot establish which intervention improves neurological recovery.
Clinical features described
Clinical descriptions included brainstem symptoms and lesions in the basal ganglia and brainstem on imaging. The abstract identifies these as characteristic findings, but does not report how often each occurred among patients.
Interacting injury pathways
The proposed mechanisms include oxidative stress, inflammation, altered cell recycling, cell-death signaling, mitochondrial dysfunction and neurotransmitter changes. The review describes them as interconnected, without identifying a single pathway that fully explains neurological injury.
The original publication
Toxicological effects of diquat on the central nervous system and associated treatment challenges.
Wang X, Liu Y, Yang M et al.
Neurotoxicology · 2025
- PubMed ID
- 41015091
- Record checked
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