Organophosphate polyneuropathy

Lotti, Marcello; Becker, Charles E.; Aminoff, Michael J.

doi:10.1212/wnl.34.5.658

Cited by 149 publications

(50 citation statements)

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“…Out of fifty patients 26% of the patients had mild depression of serum pseudocholinesterase levels and 42% of patients had moderate depression of serum cholinesterase levels and 32% of patients showed severe depressions of cholinesterase levels. 11,12 Mortality rates of 26% were observed in our study, 6% of the patients required ventilatory support and two patients (4%) developed Intermediate syndrome. Respiratory paralysis was the major cause of death.…”

Section: Discussionmentioning

confidence: 47%

Random blood sugar levels and pseudocholinesterase levels their relevance in organophosphorus compound poisoning

Rao

Raju

2016

Int J Community Med Public Health

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INTRODUCTIONOrganophosphorus and organocarbamate compounds are used as agricultural and household insecticides and in the eradication of animal ectoparasites and human lice infestations. Of the various substances used for suicidal attempts in India, organophosphates and organocarbamates form a majority group. Estimation of plasma cholinesterase (pseudo cholinesterase) has an advantage because the measurement is simpler and more accurate than estimation of erythrocyte cholinesterase.1,2 In acute poisoning, manifestations generally occur only after more than 50% of serum cholinesterase is inhibited. The severity or manifestations parallels the degree of inhibition of serum cholinesterase action. Reduction of serum cholinesterase activity to 20-50% is considered as mild poisoning and less than 10% in severe poisoning in between 10-20% moderate poisoning. In severe poisoning, return to normal levels requires about four weeks for plasma cholinesterase and three weeks to several months for RBC cholinesterase when PAM is not administered. ABSTRACTBackground: Most of the organophosphates used as the insecticides inhibit both pseudocholinesterase and acetylcholinesterase. Estimation of erythrocyte cholinesterase (acetylcholinesterase) is theoretically preferred, since it would indicate the degree of inhibition of synaptic cholinesterase (also acetyle-cholinesterase). Estimation of plasma cholinesterase (pseudo cholinesterase) has an advantage because the measurement is simpler and more accurate than estimation of erythrocyte cholinesterase. Methods:We studied fifty cases of organophsphorus poisoning directly admitted in acute medical care of Osmania General Hospital, Hyderabad, India. Results: Out of fifty patients 26% of the patients had mild depression of serum pseudo cholinesterase levels and 42% of patients had moderate depression of serum cholinesterase levels and 32% of patients showed severe depressions of cholinesterase levels. Mortality rates of 26% were observed in our study, 6% of the patients required ventilatory support and two patients (4%) developed intermediate syndrome. Respiratory paralysis was the major cause of death. Conclusions: Hyperglycemia at admission correlates with depression of pseudo cholinesterase levels in organophosphorus poisoning. Random blood sugar levels of >200 mg/dl at admission and depression in pseudocholinesterase levels <1000 U/L (p<0.005) are reliable parameters to predict mortality and ventilator requirement in organophosphorus poisoning.

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Section: Discussionmentioning

confidence: 47%

Random blood sugar levels and pseudocholinesterase levels their relevance in organophosphorus compound poisoning

Rao

Raju

2016

Int J Community Med Public Health

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“…Besides these manifestations of acute onset, some organophosphates may produce delayed neurotoxic ef fects on both the peripheral and central nervous system, even in the absence of acute cholinergic symptoms [7,8]. Indeed, experimental studies have shown that exposure to chemicals like desbromoleptophos might occur with out acute symptoms because the mean lethal dose is 50 times the neurotoxic dose [9].…”

Section: Discussionmentioning

confidence: 99%

“…In the literature a few cases of organophosphate-induced delayed polyneuropa thy (OPIDP) are reported, appearing after a variable period ranging from 1 to 5 weeks following initial expo sure [10][11][12][13]. One case has been reported as GuillainBarrd syndrome [12], The delay between exposure and onset of these late complications depends in part on the dose and the nature of the involved chemical [8,13]. The clinical picture of OPIDP is characterized by a distal, symmetric, and predominantly motor polyneuropathy with wasting and flaccid weakness mainly in legs and feet [8,11].…”

Section: Discussionmentioning

confidence: 99%

Ataxia as the Only Delayed Neurotoxic Manifestation of Organophosphate Insecticide Poisoning

Michotte

Dijck²,

Maes

et al. 1989

Eur Neurol

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A patient is reported presenting a cerebellar disorder developing about 5 weeks after acute exposure to an organophosphate insecticide. Initially no major cholinergic features were observed. The ataxia of delayed onset was not accompanied by clinical or electrophysiological signs of polyneuropathy. The possible pathogenetic mechanisms are reviewed and discussed. This case illustrates the need to closely monitor all patients intoxicated with such chemicals for at least 5 weeks. One should not only keep in mind the well-known late-onset polyneuropathy, but also the less frequent delayed central nervous system effects, even in the milder cases where initial signs of acetylcholine excess are only minimally present or lacking.

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“…Furthermore, an organophosphate-induced delayed polyneuropathy (OPIDP) may result from a distal dying back axonopathy [110], believed to be caused by phosphorylation of the enzyme neuropathy target esterase (NTE) [111]. OPIDP appears 1 to 3 weeks after exposure with cramping pain in the legs, paresthesias, and motor weakness.…”

Section: Nerve Agentsmentioning

confidence: 99%

Treatment of Neuroterrorism

Busl

Bleck

2012

Neurotherapeutics

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Bioterrorism is defined as the intentional use of biological, chemical, nuclear, or radiological agents to cause disease, death, or environmental damage. Early recognition of a bioterrorist attack is of utmost importance to minimize casualties and initiate appropriate therapy. The range of agents that could potentially be used as weapons is wide, however, only a few of these agents have all the characteristics making them ideal for that purpose. Many of the chemical and biological weapons can cause neurological symptoms and damage the nervous system in varying degrees. Therefore, preparedness among neurologists is important. The main challenge is to be cognizant of the clinical syndromes and to be able to differentiate diseases caused by bioterrorism from naturally occurring disorders. This review provides an overview of the biological and chemical warfare agents, with a focus on neurological manifestation and an approach to treatment from a perspective of neurological critical care.

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Organophosphate polyneuropathy

Cited by 149 publications

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Random blood sugar levels and pseudocholinesterase levels their relevance in organophosphorus compound poisoning

Random blood sugar levels and pseudocholinesterase levels their relevance in organophosphorus compound poisoning

Ataxia as the Only Delayed Neurotoxic Manifestation of Organophosphate Insecticide Poisoning

Treatment of Neuroterrorism

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