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Journal articles on the topic 'Organophosphate induced delayed neuropathy'

Author: Grafiati

Published: 4 June 2025

Last updated: 1 August 2025

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1

Eyer, P. "Review : Neuropsychopathological changes by organophosphorus compounds — a review." Human & Experimental Toxicology 14, no. 11 (1995): 857–64. http://dx.doi.org/10.1177/096032719501401101.

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1 Available literature dealing with neuropsychopathologi cal changes after exposure to organophosphate insecti cides is reviewed. 2 Subacute neurological sequelae following acute organophosphate intoxication include the 'intermediate syndrome', probably a myopathy elicited by excess acetylcholine, and the 'organophosphate-induced delayed neuropathy' (OPIDN), which is caused by particularly neurotoxic organophosphates that inhibit neuropathy target esterase. 3 Long-term toxic effects affecting behaviour as well as mental and visual functions are occasionally observed after exposure to high dose

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2

Vasconcellos, Luiz Felipe R., Ana Cláudia Leite, and Osvaldo J. M. Nascimento. "Organophosphate-induced delayed neuropathy: case report." Arquivos de Neuro-Psiquiatria 60, no. 4 (2002): 1003–7. http://dx.doi.org/10.1590/s0004-282x2002000600022.

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Organophosphate induced delayed neuropathy (OPIDN) is an uncommon clinical condition. It occurs in association with the ingestion of great amounts of organophosphate after the stimulation of cholinergic receptor. The clinical picture is characterized by a distal paresis in lower limbs associated with sensitive symptoms. Electrodiagnostic studies show a motor axonal neuropathy. Involvement of the central nervous system may occur. We describe a 39 years-old female patient who developed hyperesthesia associated with lower limbs paresis, fourteen days after she had ingested a Dichlorvos-based inse

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3

Basak, PM, MM Begum, MJ Islam, FA Khan, HS Das, and KI Jahan. "Organophosphate Induced Delayed Neuropathy (OPIDN)." TAJ: Journal of Teachers Association 27, no. 1 (2018): 62–63. http://dx.doi.org/10.3329/taj.v27i1.37617.

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4

Shukla, Abhiranjan, Dharampal Anand, and Ravindra Urkude. "Organophosphate induced delayed pure motor neuropathy." Journal of Neurology, Neurosurgery & Psychiatry 88, no. 5 (2017): e1.43-e1. http://dx.doi.org/10.1136/jnnp-2017-316074.45.

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5

Prasai, Pratik, Jitendra Thakur, and Karuna Tamrakar Karki. "Organophosphorus Poisoning Induced Delayed Poly-axonal Motor Neuropathy: A Case Report." Eastern Green Neurosurgery 4, no. 1 (2022): 27–29. http://dx.doi.org/10.3126/egn.v4i1.51012.

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Organophosphate being the lethal compound and easily available insecticide in the developing countries has significant potential health risk. The morbidity related to organophosphate poisoning as delayed peripheral neuropathy, extra pyramidal syndromes and neuropsychiatric manifestations are still the major consequences of secondary neuronal damage. Herein, we present a case of 23 year old lady who ingested organophosphate in the context of suicidal attempt and presented with motor neuropathy after 4 weeks.

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6

International, Journal of Medical Science and Advanced Clinical Research (IJMACR). "Organophosphorus (Chlorpyrifos) Toxicity Causing Delayed Induced Neuropathy and Myelopathy - Rare Case Report." International Journal of Medical Science and Advanced Clinical Research (IJMACR) 8, no. 2 (2025): 42–47. https://doi.org/10.5281/zenodo.15239883.

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<strong>Abstract</strong> Organophosphate (OP) poisoning is the most common poisoning in India, accounting for almost half of the hospital admissions due to poisoning. Delayed neuropathy is initiated by an attack on a nervous tissue esterase. Although uncommon, delayed neurotoxicity has been consistently reported in literature. This mechanism is implicated not only in damaging peripheral nervous system but also in causing central processes leading to myelopathy. We report a case report of 35year old male who came to our hospital with delayed neurological manifestations of organophosphorus pois

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7

Akçay Yalbuzdag, Şeniz. "Organophosphate induced delayed neuropathy: a case report." Türkiye Fiziksel Tıp ve Rehabilitasyon Dergisi 63, no. 1 (2017): 88–91. http://dx.doi.org/10.5606/tftrd.2017.13549.

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8

Gao, Zhaobing, Qiang Ding, Xin Xie, Bernard Attali, and Jian Li. "TRPA1 channel mediates organophosphate-induced delayed neuropathy." Proceedings for Annual Meeting of The Japanese Pharmacological Society WCP2018 (2018): PO1–1–124. http://dx.doi.org/10.1254/jpssuppl.wcp2018.0_po1-1-124.

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9

GLYNN, P. "A mechanism for organophosphate-induced delayed neuropathy." Toxicology Letters 162, no. 1 (2006): 94–97. http://dx.doi.org/10.1016/j.toxlet.2005.10.012.

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10

Qiang, D., X. Xie, and Z. Gao. "New insights into the organophosphate-induced delayed neuropathy." Journal of the Neurological Sciences 381 (October 2017): 153–54. http://dx.doi.org/10.1016/j.jns.2017.08.451.

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11

Rao, Bangam Rajendra Prasad, Lalatendu Mohanty, Himavanta Kampali, et al. "Organophosphate-induced delayed neuropathy: A rare case presentation." Journal of Integrative Medicine and Research 2, no. 1 (2024): 33–36. http://dx.doi.org/10.4103/jimr.jimr_46_23.

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Abstract: Organophosphate-induced delayed neuropathy (OPIDN) is a rare clinical condition. It occurs in association with ingestion of large amount of organophosphorus compound. The clinical picture is characterized by transient paraesthesia, tingling, and numbness usually confined to the distal parts of the limbs, describes as gloves and stockings pattern of sensory impairment, followed by symmetrical motor weakness, which is flaccid type, starts distally in the lower limbs first then ascends to involve upper limbs. The sensory and motor disturbances are usually mild and seen distally, but in

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12

Gautam, Sandesh, Sanjaya Sapkota, Rajeev Ojha, et al. "Delayed myelopathy after organophosphate intoxication: A case report." SAGE Open Medical Case Reports 10 (January 2022): 2050313X2211043. http://dx.doi.org/10.1177/2050313x221104309.

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Organophosphate-induced delayed neuropathy, a central-distal axonopathy, passes through latent, progressive, static and improvement phases. During the improvement phase, the peripheral nerves regenerate unmasking the spinal cord lesion with myelopathic features. We report a case of a 16-year-old male who developed myelopathy 6 weeks following chlorpyrifos poisoning. He had a motor weakness of 4/5 in bilateral hips and 3/5 in bilateral knees and ankles. Spasticity and exaggerated reflexes with ankle clonus were present in the lower limbs. Sensory and the upper limb motor examinations were all n

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13

Inozemtsev, V. A., I. A. Nelga, I. V. Medvetsky, et al. "History of Foreign Studies of Organophosphate Induced Delayed Neuropathy." Journal of NBC Protection Corps 4, no. 2 (2020): 177–88. http://dx.doi.org/10.35825/2587-5728-2020-4-2-177-188.

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Сertain organophosphates are highly toxic and can be used as chemical warfare agents. However, some classes of organic phosphorus compounds can cause so-called delayed neurotoxicity. Since the discovery of this phenomenon in 1899, extensive research has been conducted on delayed neurotoxicity caused by organophosphates. Mass poisoning of residents of the United States and Morocco in the last century demonstrated the high danger of substances that cause neurotoxicity, and gave a powerful impetus to research into this phenomenon. In addition to delayed effects, some phosphorus compounds potentia

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14

Thomas, T. C., Y. Ishikawa, M. G. McNamee, and B. W. Wilson. "Correlation of neuropathy target esterase activity with specific tritiated di-isopropyl phosphorofluoridate-labelled proteins." Biochemical Journal 257, no. 1 (1989): 109–16. http://dx.doi.org/10.1042/bj2570109.

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Neuropathy target esterase (NTE) is a membrane-bound carboxylesterase activity that has been proposed as the target site for initiation of organophosphate-induced delayed neuropathy. This activity is identified by its resistance to treatment with Paraoxon and sensitivity to co-incubation with Paraoxon and Mipafox. Sucrose-density-gradient centrifugation of membrane-associated proteins isolated from chick-embryo brains identified three proteins, Mr 161,000, 116,500 and 103,000, that were labelled with [3H]di-isopropyl phosphorofluoridate in an NTE-like manner and that co-migrated with NTE. The

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15

Malla, SindhuRao, Mahadevaiah Mahesh, ChilkundaRaviprakash Venkatesh, and Varsha Tandure. "Poisoned to paralysed: A case of organophosphate induced delayed neuropathy." Journal of Dr. NTR University of Health Sciences 8, no. 4 (2019): 281. http://dx.doi.org/10.4103/jdrntruhs.jdrntruhs_87_19.

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16

Moussaoui, Salma, Salma El Ouadih, Anas Orgi, et al. "MRI findings in organophosphate-induced delayed neuropathy: A case report." Radiology Case Reports 20, no. 3 (2025): 1345–49. https://doi.org/10.1016/j.radcr.2024.11.038.

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17

Funk, Kathleen A., John D. Henderson, Chen-Hsuan Liu, Robert J. Higgins, and Barry W. Wilson. "Neuropathology of organophosphate-induced delayed neuropathy (OPIDN) in young chicks." Archives of Toxicology 68, no. 5 (1994): 308–16. http://dx.doi.org/10.1007/s002040050074.

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18

Masoud, Anwar, Ravi Kiran, and Rajat Sandhir. "Impaired Mitochondrial Functions in Organophosphate Induced Delayed Neuropathy in Rats." Cellular and Molecular Neurobiology 29, no. 8 (2009): 1245–55. http://dx.doi.org/10.1007/s10571-009-9420-4.

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19

Song, Fuyong, and Keqin Xie. "Calcium-dependent neutral cysteine protease and organophosphate-induced delayed neuropathy." Chemico-Biological Interactions 200, no. 2-3 (2012): 114–18. http://dx.doi.org/10.1016/j.cbi.2012.10.001.

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20

Kretzschmar, Doris. "PNPLA6/NTE, an Evolutionary Conserved Phospholipase Linked to a Group of Complex Human Diseases." Metabolites 12, no. 4 (2022): 284. http://dx.doi.org/10.3390/metabo12040284.

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Patatin-like phospholipase domain-containing protein 6 (PNPLA6), originally called Neuropathy Target Esterase (NTE), belongs to a family of hydrolases with at least eight members in mammals. PNPLA6/NTE was first identified as a key factor in Organophosphate-induced delayed neuropathy, a degenerative syndrome that occurs after exposure to organophosphates found in pesticides and nerve agents. More recently, mutations in PNPLA6/NTE have been linked with a number of inherited diseases with diverse clinical symptoms that include spastic paraplegia, ataxia, and chorioretinal dystrophy. A conditiona

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21

Masoud, A., and R. Sandhir. "Increased oxidative stress is associated with the development of organophosphate-induced delayed neuropathy." Human & Experimental Toxicology 31, no. 12 (2012): 1214–27. http://dx.doi.org/10.1177/0960327112446842.

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22

Glynn, Paul. "Axonal Degeneration and Neuropathy Target Esterase." Archives of Industrial Hygiene and Toxicology 58, no. 3 (2007): 355–58. http://dx.doi.org/10.2478/v10004-007-0029-z.

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Axonal Degeneration and Neuropathy Target EsteraseThis brief review summarises recent observations which suggest a possible mechanism for organophosphate-induced delayed neuropathy (OPIDN). Neuropathy target esterase (NTE) has been shown to deacylate endoplasmic reticulum (ER) membrane phosphatidylcholine (PtdCho). Raised levels of PtdCho are present in the brains of swiss cheese/NTE mutant Drosophila together with abnormal membrane structures, axonal and dendritic degeneration and neural cell loss. Similar vacuolated pathology is found in the brains of mice with brain-specific deletion of the

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23

Doherty, John D. "Screening Pesticides for Neuropathogenicity." Journal of Biomedicine and Biotechnology 2006 (2006): 1–13. http://dx.doi.org/10.1155/jbb/2006/70414.

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Pesticides are routinely screened in studies that follow specific guidelines for possible neuropathogenicity in laboratory animals. These tests will detect chemicals that are by themselves strong inducers of neuropathogenesis if the tested strain is susceptible relative to the time of administration and methodology of assessment. Organophosphate induced delayed neuropathy (OPIDN) is the only known human neurodegenerative disease associated with pesticides and the existing study guidelines with hens are a standard for predicting the potential for organophosphates to cause OPIDN. Although recent

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24

Lotti, M., A. Moretto, R. Zoppellari, R. Dainese, N. Rizzuto, and G. Barusco. "Inhibition of lymphocytic neuropathy target esterase predicts the development of organophosphate-induced delayed polyneuropathy." Archives of Toxicology 59, no. 3 (1986): 176–79. http://dx.doi.org/10.1007/bf00316329.

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25

Johnson, M. K., and D. J. Read. "Prophylaxis against and promotion of organophosphate-induced delayed neuropathy by phenyl di-n-pentylphosphinate." Chemico-Biological Interactions 87, no. 1-3 (1993): 449–55. http://dx.doi.org/10.1016/0009-2797(93)90074-9.

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26

Jati, Monalisa, and Ashmeet Kaur. "Isolated Hypoglossal Nerve Palsy: A Rare Complication of Organophosphate Poisoning." Acta Neurologica Taiwanica 33, no. 3 (2024): 123–26. http://dx.doi.org/10.4103/ant.33-3_112_0053.

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Abstract Purpose: This case report aims to describe a rare manifestation of isolated hypoglossal nerve palsy (HNP) resulting from organophosphate poisoning (OP), specifically organophosphate- induced delayed neuropathy (OPIDN). The primary objective of this case report is to highlight this unusual manifestation and discuss its potential underlying mechanisms, emphasizing the importance of timely diagnosis and appropriate management. Case Report: A 31-year-old male with a history of consuming a commercial chlorpyrifos formulation presented with acute organophosphate poisoning symptoms that impr

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27

Kokshareva, N. V., I. I. Tkachenko, V. E. Krivenchuck, et al. "Experimental correction of the delayed neuropathy induced by organophosphates." Toxicology Letters 88 (October 1996): 22. http://dx.doi.org/10.1016/s0378-4274(96)80079-8.

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28

Padilla, Stephanie, and Bellina Veronesi. "Biochemical and Morphological Validation of a Rodent Model of Organophosphorus-Induced Delayed Neuropathy." Toxicology and Industrial Health 4, no. 3 (1988): 361–71. http://dx.doi.org/10.1177/074823378800400308.

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Exposure to certain organophosphates (OPs) produces a delayed degeneration of the longest and largest nerve fibers (OPIDN). Until recently, investigators have used the chicken as the primary experimental model of OPIDN. Although the chicken is extremely sensitive to the ataxia associated with this neuropathy, it lacks an extensive biochemical, electrophysiological and pathological data-base. Because of this we set out to develop a rodent model of OPIDN with morphological and biochemical correlates similar to those seen in the chicken. Historically the rat had been labeled insensitive to OPIDN

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29

Petroianu, G., F. Hardt, M. Toomes, W. Bergler, and R. Rüfer. "High-dose intravenous paraoxon exposure does not cause organophosphate-induced delayed neuropathy (OPIDN) in mini pigs." Journal of Applied Toxicology 21, no. 4 (2001): 263–68. http://dx.doi.org/10.1002/jat.752.

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30

Honorato de Oliveira, Georgino, Vanessa Moreira, and Sheila Patricia Ribeiro Goes. "Organophosphate induced delayed neuropathy in genetically dissimilar chickens: studies with tri-ortho-cresyl phosphate (TOCP) and trichlorfon." Toxicology Letters 136, no. 2 (2002): 143–50. http://dx.doi.org/10.1016/s0378-4274(02)00295-3.

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31

Yu-Yuan, Li, and Wu Yi-Jun. "Changes of Neuropathy Target Esterase Affect Phospholipid Homeostasis in SK-N-SH Cells." Revista de Chimie 71, no. 8 (2020): 327–34. http://dx.doi.org/10.37358/rc.20.8.8306.

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Neuropathy target esterase (NTE), is a membrane protein located in the endoplasmic reticulum (ER). NTE has the activity of phospholipase B and can catalyze the deacylation of phosphatidylcholine (PC) and lysophosphatidylcholine (LPC) to glycerylcholine (GPC). It is phosphorylated and aged by organophosphorus compounds (OPs), that induce delayed neuropathy in humans and sensitive animals. Our previous study has reported that the disruption of ER phospholipid homeostasis caused by the NTE inhibition may contribute to the initiation of the organophosphate-induced delayed neurotoxicity (OPIDN), wh

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32

Knoll-Gellida, Anja, Leslie E. Dubrana, Laure M. Bourcier, et al. "Hyperactivity and Seizure Induced by Tricresyl Phosphate Are Isomer Specific and Not Linked to Phenyl Valerate-Neuropathy Target Esterase Activity Inhibition in Zebrafish." Toxicological Sciences 180, no. 1 (2021): 160–74. http://dx.doi.org/10.1093/toxsci/kfab006.

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Abstract Environmental exposure to tricresyl phosphate (TCP) may lead to severe neurotoxic effects, including organophosphate (OP)-induced delayed neuropathy. TCP has three symmetric isomers, distinguished by the methyl group position on the aromatic ring system. One of these isomers, tri-ortho-cresyl phosphate (ToCP), has been reported for years as a neuropathic OP, targeting neuropathic target esterase (NTE/PNPLA6), but its mode of toxic action had not been fully elucidated. Zebrafish eleuthero-embryo and larva were used to characterize the differential action of the TCP isomers. The symmetr

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33

Makhaeva, Galina F., Vladimir V. Malygin, Nadezhda N. Strakhova, et al. "Biosensor assay of neuropathy target esterase in whole blood as a new approach to OPIDN risk assessment: review of progress." Human & Experimental Toxicology 26, no. 4 (2007): 273–82. http://dx.doi.org/10.1177/0960327106070463.

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Organophosphates (OPs) that inhibit neuropathy target esterase (NTE) with subsequent ageing can produce OP-induced delayed neuropathy (OPIDN). NTE inhibition in lymphocytes can be used as a biomarker of exposure to neuropathic OPs. An electrochemical method was developed to assay NTE in whole blood. The high sensitivity of the tyrosinase carbon-paste biosensors for the phenol produced by hydrolysis of the substrate, phenyl valerate, allowed NTE activity to be measured in diluted samples of whole blood, which cannot be done using the standard colorimetric assay. The biosensor was used to establ

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34

Masoud, Anwar, Ravi Kiran, and Rajat Sandhir. "Modulation of dopaminergic system and neurobehavioral functions in delayed neuropathy induced by organophosphates." Toxicology Mechanisms and Methods 21, no. 1 (2010): 1–5. http://dx.doi.org/10.3109/15376516.2010.529182.

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35

Johnson, M. K., I. Bird, and C. Meredith. "Phenyl di-n-pentylphosphinate: a convenient reactivatible inhibitor for studies on neuropathy target esterase (NTE) and protection against organophosphate-induced delayed polyneuropathy." Toxicology Letters 40, no. 2 (1988): 133–40. http://dx.doi.org/10.1016/0378-4274(88)90154-3.

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36

Choudhary, Sanjeev, and Kiran Dip Gill. "Protective effect of nimodipine on dichlorvos-induced delayed neurotoxicity in rat brain11Abbreviations: OP, organophosphate; NTE, neuropathy target esterase; OPIDN, organophosphate-induced delayed neuropathy; PAM, 2-pyridine aldoxime methiodide; SPM, synaptic plasma membranes; VOCC, voltage-operated calcium channels; TOCP, tri-o-cresyl phosphate; PSP, phenyl saligenin phosphate; and [Ca2+]i, intracellular calcium." Biochemical Pharmacology 62, no. 9 (2001): 1265–72. http://dx.doi.org/10.1016/s0006-2952(01)00762-6.

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37

Luo, Fang, Aaron F. Sandhu, Wiramon Rungratanawanich, et al. "Melatonin and Autophagy in Aging-Related Neurodegenerative Diseases." International Journal of Molecular Sciences 21, no. 19 (2020): 7174. http://dx.doi.org/10.3390/ijms21197174.

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With aging, the nervous system gradually undergoes degeneration. Increased oxidative stress, endoplasmic reticulum stress, mitochondrial dysfunction, and cell death are considered to be common pathophysiological mechanisms of various neurodegenerative diseases (NDDs) such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), organophosphate-induced delayed neuropathy (OPIDN), and amyotrophic lateral sclerosis (ALS). Autophagy is a cellular basic metabolic process that degrades the aggregated or misfolded proteins and abnormal organelles in cells. The abnormal regula

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38

Kelly, Sean S., Gail E. de Blaquière, Faith M. Williams, and Peter G. Blain. "Effects of multiple doses of organophosphates on evoked potentials in mouse diaphragm." Human & Experimental Toxicology 16, no. 2 (1997): 72–78. http://dx.doi.org/10.1177/096032719701600202.

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1 Male albino mice were injected s.c. with an organopho sphate (mipafox, ecothiopate or paraoxon). Treat ments were either a single injection or multiple daily injections with lower doses for 5 or 8 days. At 3 h after injection the activity of brain and diaphragm acet ylcholinesterase and of brain neuropathy target esterase (NTE) was measured. Also measured in the diaphragm at 3 h post dose was the duration of spontaneous miniature endplate potentials (eMEPPs), recorded extracellularly. 2 At 7 and 28 days after dosing action potentials and evoked endplate potentials, produced by stimulating th

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39

Chuang, Chia-Chang, Thy-Sheng Lin, and Ming-Che Tsai. "Delayed Neuropathy and Myelopathy after Organophosphate Intoxication." New England Journal of Medicine 347, no. 14 (2002): 1119–21. http://dx.doi.org/10.1056/nejm200210033471421.

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40

Lotti, Marcello, and Angelo Moretto. "Organophosphate-Induced Delayed Polyneuropathy." Toxicological Reviews 24, no. 1 (2005): 37–49. http://dx.doi.org/10.2165/00139709-200524010-00003.

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41

Jokanovic, Milan, Melita Kosanovic, and Petar Stukalov. "Organophosphate Induced Delayed Polyneuropathy." Medicinal Chemistry Reviews - Online 1, no. 2 (2004): 123–31. http://dx.doi.org/10.2174/1567203043480377.

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42

Milan Jokanovic, Bentham Science Publisher, Bentham Science Publisher Petar V. Stukalov, and Bentham Science Publisher Melita Kosanovic. "Organophosphate Induced Delayed Polyneuropathy." Current Drug Target -CNS & Neurological Disorders 1, no. 6 (2002): 593–602. http://dx.doi.org/10.2174/1568007023338879.

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43

Gutmann, Ludwig, and John B. Bodensteiner. "Organophosphate-induced delayed polyneuropathy." Journal of Pediatrics 123, no. 5 (1993): 837. http://dx.doi.org/10.1016/s0022-3476(05)80877-7.

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44

Dirik, Eray, and Kamer Mutafoğlu Uysal. "Organophosphate-induced delayed polyneuropathy." Pediatric Neurology 11, no. 2 (1994): 111. http://dx.doi.org/10.1016/0887-8994(94)90247-x.

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45

Coskun, Abuzer, Afsin Emre Kayipmaz, Sedat Ozbay, Osman Mahir Okur, Ilham Ozkan, and Sevki Hakan Eren. "Delayed organophosphate - induced polyneuropathy." Medical Science and Discovery 2, no. 4 (2019): 271–74. https://doi.org/10.36472/msd.v2i4.70.

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Introduction: Intoxication with organophosphate compounds used for pest control is common in Turkey. Organophosphate intoxication may occur during agricultural spraying, transport of organophosphate compounds, or domestic accidents, although suicide attempts are the most common way of intoxication. Case Presentation: We present a 23-year-old woman ingested a fistful of painkillers and drank a sip of an unknown syrup after having a quarrel with her family. Four hours later, she had been taken to a nearby hospital with nausea, vomiting, and abdominal pain, where she had been treated for drug int

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46

Chen, Chiao-Chien, and Lin-Fen Hsieh. "Delayed Neuropathy Due to Organophosphate Intoxication: A casereport." Rehabilitation Practice and Science 33, no. 4 (2005): 235–43. http://dx.doi.org/10.6315/2005.33(4)07.

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47

Karademir, M., F. Ertürk, and R. Koçak. "Two Cases of Organophosphate Poisoning with Development of Intermediate Syndrome." Human & Experimental Toxicology 9, no. 3 (1990): 187–89. http://dx.doi.org/10.1177/096032719000900312.

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Two cases of intermediate syndrome caused by organophosphorus poisoning are reported. Trichlorfon, propoxur (a carbamate pesticide) and fenthion were ingested in both attempts at suicide. After successful conventional therapy during the cholinergic phase, but before the time when the onset of delayed neuropathy might be expected, an intermediate syndrome developed. It affected the proximal limb muscles, neck flexors and respiratory muscles 2 d after pesticide ingestion. The two patients needed respiratory support. Recovery from the intermediate syndrome was complete in both patients, although

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48

Zhminko, Peter, and Natali Kokshareva. "Organophosphate-induced neuropathy and its experimental correction." Toxicology Letters 211 (June 2012): S137. http://dx.doi.org/10.1016/j.toxlet.2012.03.500.

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49

Kobayashi, Shunsuke, Reiko Okubo, and Yoshikazu Ugawa. "Delayed Polyneuropathy Induced by Organophosphate Poisoning." Internal Medicine 56, no. 14 (2017): 1903–5. http://dx.doi.org/10.2169/internalmedicine.56.7921.

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50

Moretto, Angelo. "Testing for Organophosphate-Induced Delayed Polyneuropathy." Current Protocols in Toxicology 00, no. 1 (1999): 11.5.1–11.5.14. http://dx.doi.org/10.1002/0471140856.tx1105s00.

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