Organophosphate neuropathy …

Michael T Pulley MD PhD

Peripheral Neuropathies

Updated 04.02.2024
Released 10.06.1999
Expires For CME 04.02.2027

Organophosphate neuropathy

Author: Michael T Pulley MD PhD

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Editor: Louis H Weimer MD

Organophosphate neuropathy

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Introduction

Overview

In this article, the author details the clinical manifestations resulting from organophosphate poisoning. Although there has been great concern about the effects of “nerve gas,” definite exposure to these chemicals in combat has been limited, and the manifestations have not been well studied. This article focuses on the clinical features of acute and intermediate syndromes of organophosphate poisoning and on organophosphate-induced delayed polyneuropathy, which develops only after exposure to certain specific chemicals.

Key points

	• Organophosphate poisoning occurs because of exposure to pesticides, either through occupational contact or intentionally in suicide attempts.
	• The neuropathy associated with organophosphate intoxication is delayed in onset and may occur even when initial symptoms from exposure are mild.

Historical note and terminology

Organophosphate compounds are used as chemical warfare agents (nerve gas), petroleum additives, insecticides, lubricants, antioxidants, flame retardants, and plastic modifiers. The best characterized peripheral neuropathy caused by these compounds in humans is that due to triorthocresyl phosphate, although exposure to other organophosphates such as chlorpyrifos, mipafox, trichlorfon, and leptophos may cause a similar neuropathy. Despite the multiple uses of these compounds, group exposure in the occupational setting is rare. Intoxication typically occurs due to accidental pesticide exposure from agricultural spraying. This may occur in individuals mixing or applying the pesticide or through dermal exposure from those working in the fields shortly after spraying (23). Exposure to and possible toxicity from organophosphorus compounds have also been reported in sheep dippers (16). Most organophosphate esters are quickly degraded in the environment. Pesticides containing organophosphate are also intentionally ingested in suicide attempts and, in some locations, are the most common cause of organophosphate poisoning (02). In one case, attempted injection of malathion seemed to cause focal injury of the median nerve in a delayed fashion (13). A report indicated that intentional subcutaneous injection of chlorpyrifos caused a severe case of organophosphorus poisoning (34).

Clinical manifestations

Presentation and course

Type 1 organophosphate syndrome (38) is primarily due to excessive muscarinic stimulation. These effects are always present within 1 day of exposure and frequently within hours. The specific organophosphate and the degree of exposure determine the intensity of the acute syndrome. Typical muscarinic symptoms include nausea and vomiting, diarrhea, sweating, salivation, micturition, and tachycardia or bradycardia. Extreme cases may cause CNS involvement with nervousness, emotional lability, fatigue, decreased alertness, cognitive impairment, convulsions, and coma. Rarely, behavioral change may be the only manifestation. Previous exposure to organophosphate with a resultant decrease in functional acetylcholinesterase may increase the susceptibility, on subsequent exposure, to developing the acute syndrome.

The intermediate or type 2 organophosphate syndrome (10; 01) is due to the overstimulation of nicotinic acetylcholine receptors in skeletal muscle and occurs within 12 to 96 hours of exposure. It is termed intermediate because it follows the muscarinic symptoms and precedes peripheral neuropathy. There may be an interval of 1 to 4 days between the acute and intermediate syndromes, during which the patient is symptom-free. Although neuropathy is discussed more frequently, it probably occurs less often than the type 2 syndrome. Respiratory insufficiency is usually the initial feature. This is followed by proximal muscle and neck flexor weakness. Distal extremity strength is usually preserved but there may be involvement of the cranial muscles (including extraocular muscles). Sensory function remains intact but dystonic posturing is occasionally seen. Recovery starts to occur 5 to 15 days after exposure and proceeds from the cranial muscles to the respiratory muscles, proximal limb muscles, and lastly to the neck flexors. Atropine does not prevent or treat the intermediate syndrome (38) as the drug is specific for muscarinic receptors. There is no correlation between the development of the type 2 syndrome and the later appearance of neuropathy.

Independent of the development of the type 1 or type 2 syndromes, a central-peripheral axonopathy may develop with exposure to some organophosphates. Case reports and case series of intentional chlorpyrifos ingestion highlighted that the CNS effects might be prominent and overshadow the neuropathy (35; 28). Nayak and colleagues correctly termed this disease process a myeloneuropathy (26). The neuropathy is not related to the inhibition of acetylcholinesterase. Neuropathy may not occur until 7 to 21 days after exposure and, therefore, has been labeled organophosphate-induced delayed polyneuropathy. Although it occurs less frequently than cholinergic syndromes, it causes significant morbidity. Most organophosphates used in agriculture do not cause organophosphate-induced delayed polyneuropathy. Compounds that frequently cause subtle or unappreciated cholinergic symptoms are the ones that seem to cause the most dramatic cases of neuropathy. Such cases frequently involve low-level chronic exposure.

In contrast to most toxic central-peripheral axonopathies, the onset of organophosphate-induced delayed polyneuropathy is subacute. The patient usually reaches the nadir by 2 weeks after onset and sometimes sooner. The initial manifestations of organophosphate-induced delayed polyneuropathy include painful paresthesias in the feet and cramping pain in the calf muscles; however, motor symptoms and signs predominate. There is early weakness of the leg muscles with foot drop. Later, the intrinsic hand muscles are affected, and the proximal muscles are spared until later in the disease course. There is typically evidence of sensory loss with careful examination. There may be gait ataxia that is disproportionate to the degree of weakness or sensory loss. The Achilles reflex is always absent, but the degree of CNS dysfunction determines the activity of the other reflexes. Autonomic or cranial nerve dysfunction is rarely present.

A case report of a patient with severe manifestations of organophosphate-induced delayed polyneuropathy highlights many of the above features in terms of symptoms, disease course, and central versus peripheral involvement and demonstrates that it can be very severe with long-term sequelae (22).

There are reports of an association between chronic, low-level organophosphate exposure (in the absence of cholinergic toxicity) and a sensory neuropathy distinct from organophosphate-induced delayed polyneuropathy (16). However, in a well-designed study that carefully looked at exposure to chlorpyrifos and evaluated clinical and electrophysiologic parameters, no association with sensory neuropathy was discovered (03). A study looking at electrophysiologic parameters in farm workers in Indonesia exposed to organophosphate pesticides found that 44 or 64 had neuropathy, with 41 having motor neuropathy and only 19 having sensory neuropathy (27).

Prognosis and complications

Recovery from the acute and intermediate syndromes is usually complete as long as there is good supportive care. By 1 week after organophosphate exposure, only 40% to 60% of acetylcholinesterase content is regenerated. However, this is usually adequate for functional recovery. Cognitive and behavioral abnormalities may persist after recovery from the acute syndrome.

Good recovery usually occurs in those patients with mild organophosphate-induced delayed polyneuropathy. With more severe deficits, residual foot drop, claw hand deformity, or atrophy may persist. The effects on central (distal dorsal column and corticospinal) axons are frequently revealed after recovery from the peripheral neuropathy. Long-term deficits include ataxia and spasticity and these are more frequent than persistent dysfunction from neuropathy.

Biological basis

Etiology and pathogenesis

Intoxication typically occurs due to accidental pesticide exposure from agricultural spraying. This may occur in individuals mixing or applying the pesticide or through dermal exposure from those working in the fields shortly after spraying (23; 20). Exposure to chemical warfare agents has been proposed to be associated with the development of peripheral neuropathy, but the evidence is very limited (15).

Absorption of organophosphates may take place through the respiratory and gastrointestinal tracts as well as through the skin. Once absorbed, the action of organophosphate is to irreversibly inhibit acetylcholinesterase in erythrocytes and nervous tissue by phosphorylation. Acetylcholine cannot be degraded and builds up, resulting in excessive stimulation of both muscarinic and nicotinic receptors. There are acute (type 1) and intermediate (type 2) syndromes based on the receptor preferentially affected.

The organophosphate-induced delayed polyneuropathy may be triggered by certain esterase enzymes but prevented by others. Neuropathy target esterase inhibition is felt to play a role in the genesis of organophosphate-induced delayed polyneuropathy. In fact, evaluating the toxicity potential of organophosphorus pesticides is based on an assay that measures the inhibition of chick neuropathy target esterase (06; 11). Organophosphate-induced delayed polyneuropathy may be prevented in experimental animals by inhibiting neuropathy target esterase but promoted by inhibiting another esterase known as M200 (25). The activity of lymphocyte neuropathy target esterase has been followed serially in a case of organophosphate-induced delayed polyneuropathy and found to be reduced (21). Neuropathy target esterase localizes to the inner face of the endoplasmic reticulum (14). It has been shown to play a role in phosphatidylcholine homeostasis, and derangement may affect membrane stability and contribute to problems with axonal transport (14). Studies in hens have shown that neurofilament change may be an early event in the evolution of organophosphate-induced delayed polyneuropathy (33). The same investigators showed that the inhibition of organophosphate-induced delayed polyneuropathy correlated with lack of alteration in neurofilament proportions, suggesting a possible pathogenic role (32). Although some organophosphorus compounds inhibit calcium-activated ATPases, this activity does not relate to induction of organophosphate-induced delayed polyneuropathy (05). Investigators have demonstrated abnormalities of mitochondrial complex I activity that correlate with changes in neuropathy target esterase and clinical effects in the preferred animal model (30).

Diagnostic workup

Although electrophysiologic testing is a sensitive indicator for organophosphate exposure, it does not accurately reflect the severity. Shortly after organophosphate exposure, spontaneous repetitive motor action potentials following the initial compound motor action potential are elicited by a single stimulus (37; 29). The ability to elicit spontaneous repetitive motor action potentials is a sensitive indicator of organophosphate exposure but does not reflect the degree of intoxication. With the onset of weakness, a decremental response to repetitive nerve stimulation is seen. The maximal reduction in motor potential amplitude typically occurs with the second potential, unlike myasthenia gravis, in which the decrement is typically maximal by the fourth response. In the case of mild intoxication, rapid stimulation rates may be required to demonstrate decrement. In addition, decrement may be followed by increment, and spontaneous repetitive motor action potentials are usually present. With more severe exposure, spontaneous repetitive motor action potentials may be absent, and decrement is evident even with slow rates of stimulation (07).

Electrophysiologic testing in organophosphate-induced delayed polyneuropathy reveals evidence of sensorimotor axonal neuropathy. Although motor symptoms are most prevalent, sensory conduction abnormalities are more dramatic and appear earlier. Sensory nerve action potentials are reduced in amplitude or absent, whereas the motor conduction studies are either normal or reveal minimal slowing of conduction velocity. Needle EMG reveals evidence of acute and chronic denervation in the distal and occasionally proximal limb muscles. EMG is normal in patients with the intermediate syndrome (36).

Routine clinical laboratory values are typically unrevealing. A study suggested there may be utility of using enzymes such as beta-glucuronidase, neuropathy target esterase, amylase, and lipase in addition to hematological indicators such as CBC, CRP, lactate dehydrogenase, and CPK in the diagnosis of organophosphate poisoning for diagnosis and prognosis (31). Acetylcholinesterase levels in erythrocytes are depressed with recent exposure to organophosphate, and levels below 20% of normal are associated with severe weakness. However, the variability of normal erythrocyte acetylcholinesterase levels makes a single determination difficult to interpret, and serial measurements showing a progressive decline in activity are most helpful. The acetylcholinesterase level is not predictive of future development of organophosphate-induced delayed polyneuropathy, and levels may have returned to normal by the time testing is performed as enzyme regeneration occurs at the rate of 1% per day. There appears to be little diagnostic value in performing pseudocholinesterase levels. The CSF protein level is normal or slightly elevated, and the fluid is acellular.

Management

Supportive measures are discussed in Peripheral neuropathies: supportive measures and rehabilitation.

An article detailed the importance of rehabilitative therapy after a severe case of peripheral neuropathy due to attempted suicide after drinking an organophosphate pesticide (17). Organophosphate poisoning is a medical emergency and can be fatal if not treated properly. Because there is a significant risk of respiratory failure, maintenance of a good airway is paramount and intubation may be required. Excessive secretions and vomiting are often present with altered awareness, and intubation may be necessary even when respiratory function is preserved.

Immediately after recognition, the affected individual should be removed from further exposure. Contaminated clothing should be removed, and the skin should be cleansed to prevent further absorption. In the case of ingestion, gastric lavage should be performed and cathartics administered. Reactivation of acetylcholinesterase may be accelerated by administering pralidoxime, which is most effective if given early in the course. Pralidoxime may prevent the emergence of the intermediate syndrome. Although the World Health Organization recommends the use of pralidoxime for organophosphate poisoning, a Cochrane review did not find evidence to support its use, and there was a suggestion that there may be harm, particularly in some cases (08). Fortunately, the muscarinic symptoms are typically relieved with atropine. However, the duration of atropine’s action is short, and it often must be readministered to prevent the recurrence of symptoms that may still be fatal. Because there is some evidence that administration of atropine to patients with respiratory insufficiency may be associated with an increased risk of ventricular arrhythmias, patients need to be adequately ventilated before it is given. Atropine is specific for muscarinic receptors and, therefore, has no effect on depolarizing neuromuscular blockade due to overstimulation of nicotinic receptors. A study found that the administration of packed red blood cells is beneficial in acute organophosphate poisoning, and the benefit is more pronounced with freshly obtained (fewer than 10 days) packed red blood cells (04).

References

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03: Albers JW, Garabrant DH, Schweitzer S, Garrison RP, Richardson RJ, Berent S. Absence of sensory neuropathy among workers with occupational exposure to chlorpyrifos. Muscle Nerve 2004;29(5):677-86. PMID 15116371
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05: Barber D, Hunt J, Ehrich M. Inhibition of calcium-stimulated ATPase in hen brain P2 synaptosomal fraction by organophosphorous esters: relevance to delayed neuropathy. J Toxicol Environ Health 2001;63:101-13. PMID 11393797
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13: Ergun S, Oztürk K, Su O, Gürsoy EB, Uğurad I, Yüksel G. Delayed neuropathy due to organophosphate insecticide injection in an attempt to commit suicide. Hand (N Y) 2009;4(1):84-7. PMID 18780003
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Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Michael T Pulley MD PhD

Dr. Pulley of the University of Florida, Jacksonville received consulting fees from Argenx, Alexion, and UCB/Ra.
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Editor

Louis H Weimer MD

Dr. Weimer of Columbia University has no relevant financial relationships to disclose.
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Former Authors

Alan R Berger MD

Patient Profile

Age range of presentation: 19 to 64 years
Sex preponderance: male=female
Heredity: none
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: agricultural workers

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Organophosphate neuropathy

Associated Disorders

Intermediate organophosphate syndrome
Type 1 organophosphate syndrome

Differential Diagnosis

other drug or toxin ingestion
Guillain-Barré syndrome
periodic paralysis
myasthenia gravis
other causes of central-peripheral distal axonopathy
- simple distal axonopathy

Organophosphate neuropathy …

Organophosphate neuropathy

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Diagnostic workup

Management

Special considerations

Pregnancy

Anesthesia

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview.
Start a Free Account
to access the full version.

Questions or Comment?

Also in This Category

Neuropathies associated with cytomegalovirus infection

Chronic inflammatory demyelinating polyradiculoneuropathy

Amyotrophic lateral sclerosis

Amiodarone neuropathy

Autoimmune autonomic neuropathy

Leukodystrophies

Neuroacanthocytosis

Peripheral nerve injuries

Organophosphate neuropathy

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Diagnostic workup

Management

Special considerations

Pregnancy

Anesthesia

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Neuropathies associated with cytomegalovirus infection

Chronic inflammatory demyelinating polyradiculoneuropathy

Amyotrophic lateral sclerosis

Amiodarone neuropathy

Autoimmune autonomic neuropathy

Leukodystrophies

Neuroacanthocytosis

Peripheral nerve injuries

This is an article preview.
Start a Free Account
to access the full version.