Screening for peripheral neuropathy in chemical warfare victims

Holisaz, M T; Rayegani, Seyyed Mansoor; Hafezy, Rahmatollah; Khedmat, Hossein; Motamedi, Mohammad Hosein Kalantar

doi:10.1097/mrr.0b013e3280143c49

Cited by 16 publications

(7 citation statements)

References 14 publications

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“…More recently, in a cross‐sectional study in 100 CWA Iranian veterans, Holisaz et al . reported five patients suffering from axonal neuropathy, which is significantly higher than what is found in the normal population. In a cohort study of 74 OP‐poisoned patients 13 years post‐exposure, EMG and NCV were normal except for two severely affected patients .…”

Section: Discussionmentioning

confidence: 67%

Delayed Neurological Complications of Sulphur Mustard and Tabun Poisoning in 43 Iranian Veterans

Darchini-Maragheh

Nemati-Karimooy

Hasanabadi

et al. 2012

Basic Clin Pharma Tox

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Delayed neurotoxic complications of chemical warfare agents (CWA), such as sulphur mustard (SM) and tabun, in human beings have not been reported in detail. We thus aimed to investigate possible neurotoxic complications of these agents in Iranian veterans 22-27 years after exposure. After co-ordination with the veteran foundation and obtaining the approval of the medical research ethics committee, 43 Iranian veterans with late complications of CWA exposure during the Iran-Iraq conflict were studied after obtaining signed written informed consent. Demographic and clinical findings were recorded on pre-designed forms. Neurological examination was performed by a neurologist. Routine biochemical tests were performed for all the patients. Electromyography (EMG), nerve conduction velocity (NCV) and electroencephalography (EEG) were carried out as clinically indicated. The majority of the patients (38) had been exposed to SM and only five patients to tabun. Hyperaesthesia was the most objective finding (72.1%). Fatigue (93%), paraesthesia (88.3%) and headache (83.7%) were the most common subjective findings in the patients. Sensory nerve impairments, including paraesthesia (88.3%), hyperaesthesia (72.1%) and hypoesthesia (11.6%), were the most common observed clinical complications. EMG and NCV were impaired in seven patients (16.3%) who were all SM-exposed patients but did not show any significant correlation with organ complications. EEG was negative even in the seized patients. Cholesterol, LDL and triglyceride levels were significantly above the normal ranges. Late neurological complications of CWA, particularly SM poisoning, are considerable even after three decades of exposure and require medical attention.

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Section: Discussionmentioning

confidence: 67%

Delayed Neurological Complications of Sulphur Mustard and Tabun Poisoning in 43 Iranian Veterans

Darchini-Maragheh

Nemati-Karimooy

Hasanabadi

et al. 2012

Basic Clin Pharma Tox

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“…In another study conducted on four of 98 chemical warfare victims, with severe mustard gas exposure and mean age of 49.8 years, EMG findings revealed positive sharp waves as well as fibrillations. The motor unit action potential defects in these cases indicated presence of axonal polyneuropathy (33). …”

Section: Reultsmentioning

confidence: 90%

Environmental and Population Studies Concerning Exposure to Pesticides in Iran: A Comprehensive Review

Mostafalou¹,

Karami‐Mohajeri²,

Abdollahi³

2013

Iran Red Cres Med J

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Pesticides are widely used in Iranian agriculture and this has made a major toxicological concern among health professionals. The objective of this study is to explore national data about pesticides toxicity. All relevant databases such as Google Scholar, PubMed, and Scopus in a time period of 1960 to 2012 were searched for the keywords “Pesticides, Iran, Environment, and Population studies”. A total of 57 studies were found relevant and then included into study. Almost all non-experimental studies carried out in Iran were classified into two main categories of residue assessment in different samples and toxic effects on human. Depending on the dose and duration of exposure, toxic effects of pesticides have been studied in two classifications including acute toxicity or acute poisoning and chronic toxicity. High extent of pesticides have been used during the past decade in Iran while no enough proper studies were done to explore their possible toxic effects in the environment and the people.

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“…Long-term peripheral neuropathy was observed in victims of the Iran-Iraq conflict, which lasted from 1980 to 1988. This peripheral neuropathy seemed to correlate with OP chemical exposure; however, no CNS damage was reported (Holisaz et al 2007). Another study assessed the gross neuroanatomical structures with quantitative MRI (Houston et al 2001) in veterans of the Gulf War who were possibly exposed to sarin and cyclosarin (Heaton et al 2007).…”

Section: Organophosphate-induced Chronic Neurotoxicitymentioning

confidence: 99%

“…There is a well-established link between OP nerve agent exposure, neuropathological damage (Holisaz et al 2007) and long-term behavioral differences (McDonough et al 1986; Kadar et al 1995; Jamal 1997). A recent study echoed the link between sarin exposure and neuropathological alterations (Grauer et al 2008).…”

Section: Organophosphate-induced Chronic Neurotoxicitymentioning

confidence: 99%

Sarin (GB, O-isopropyl methylphosphonofluoridate) neurotoxicity: critical review

Abou‐Donia

Siracuse

Gupta

et al. 2016

Critical Reviews in Toxicology

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Sarin (GB, O-isopropyl methylphosphonofluoridate) is a potent organophosphorus (OP) nerve agent that inhibits acetylcholinesterase (AChE) irreversibly. The subsequent build-up of acetylcholine (ACh) in the central nervous system (CNS) provokes seizures and, at sufficient doses, centrally-mediated respiratory arrest. Accumulation of ACh at peripheral autonomic synapses leads to peripheral signs of intoxication and overstimulation of the muscarinic and nicotinic receptors, which is described as “cholinergic crisis” (i.e. diarrhea, sweating, salivation, miosis, bronchoconstriction). Exposure to high doses of sarin can result in tremors, seizures, and hypothermia. More seriously, build-up of ACh at neuromuscular junctions also can cause paralysis and ultimately peripherally-mediated respiratory arrest which can lead to death via respiratory failure. In addition to its primary action on the cholinergic system, sarin possesses other indirect effects. These involve the activation of several neurotransmitters including gamma-amino-butyric acid (GABA) and the alteration of other signaling systems such as ion channels, cell adhesion molecules, and inflammatory regulators. Sarin exposure is associated with symptoms of organophosphate-induced delayed neurotoxicity (OPIDN) and organophosphate-induced chronic neurotoxicity (OPICN). Moreover, sarin has been involved in toxic and immunotoxic effects as well as organophosphate-induced endocrine disruption (OPIED). The standard treatment for sarin-like nerve agent exposure is post-exposure injection of atropine, a muscarinic receptor antagonist, accompanied by an oxime, an AChE reactivator, and diazepam.

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Screening for peripheral neuropathy in chemical warfare victims

Cited by 16 publications

References 14 publications

Delayed Neurological Complications of Sulphur Mustard and Tabun Poisoning in 43 Iranian Veterans

Delayed Neurological Complications of Sulphur Mustard and Tabun Poisoning in 43 Iranian Veterans

Environmental and Population Studies Concerning Exposure to Pesticides in Iran: A Comprehensive Review

Sarin (GB, O-isopropyl methylphosphonofluoridate) neurotoxicity: critical review

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