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Year : 2019  |  Volume : 8  |  Issue : 4  |  Page : 281-283

Poisoned to paralysed: A case of organophosphate induced delayed neuropathy

Department of General Medicine, JSS Medical College, JSS AHER, Mysuru, Karnataka, India

Date of Submission24-Aug-2019
Date of Acceptance23-Sep-2019
Date of Web Publication16-Dec-2019

Correspondence Address:
Dr. Sindhu Rao Malla
Room No.408, JSS PG Residents Hostel, Beside JSS Hospital, Ramachandra Agrahara, Mysore, Karnataka -570 025
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Source of Support: None, Conflict of Interest: None


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Organophosphate (OP) compound poisoning is a global public health problem and is a social calamity, especially in a developing country like India. Acute cholinergic crisis and intermediate syndrome after OP compound consumption are well-known and well-documented. Delayed neurological complications of organophosphate compound poisoning are rare. In the following case report, we present a case of a middle-aged man who was treated successfully for organophosphate compound poisoning and subsequently readmitted after two weeks with features of weakness of both upper and lower limbs suggesting delayed neuropathy.

How to cite this article:
Mahesh M, Malla SR, Venkatesh CR, Tandure V. Poisoned to paralysed: A case of organophosphate induced delayed neuropathy. J NTR Univ Health Sci 2019;8:281-3

How to cite this URL:
Mahesh M, Malla SR, Venkatesh CR, Tandure V. Poisoned to paralysed: A case of organophosphate induced delayed neuropathy. J NTR Univ Health Sci [serial online] 2019 [cited 2020 Jul 13];8:281-3. Available from: http://www.jdrntruhs.org/text.asp?2019/8/4/281/273137

  Introduction Top

Organophosphate (OP) compound poisoning is one of the major health problems worldwide and accounts for a large number of fatalities, especially in India. As per World Health Organization (WHO), every year, there are 3 million cases of OP compound poisoning, out of which 250,000 cases result in death.[1] Its clinical course runs in 3 phases: a) acute cholinergic crisis, b) intermediate syndrome, and the rarely encountered c) organophosphate induced delayed polyneuropathy (OPIDN).

Herein we describe the case of a young male farmer who had ingested chlorpyrifos with suicidal intention, and after treatment survived the acute phase and had no intermediate syndrome. However, he developed pain and weakness over all 4 limbs, 17 days after the initial exposure to the toxin. Nerve conduction studies confirmed the diagnosis of axonopathy. The patient was treated symptomatically and with physiotherapy, after which he showed significant improvement.

  Case Report Top

A 42-year-old male patient presented to the Medicine Out Patient Department with complaints of weakness over both lower limbs of 3 days' duration. There was also pain in both lower limbs since the same period. He reported inability to walk without support and difficulty in standing from sitting position since 3 days. The weakness gradually progressed to involve both the upper limbs. History was suggestive of proximal weakness more than distal weakness with no involvement of sensory system, bowel or bladder. There was no history of fever, vomiting or loose stools prior to this.

Neurological examination revealed muscle power of 2/5 proximally and 4/5 distally as per Medical Research Council muscle strength grading scale [See [Figure 1]. Hypotonia of both lower limbs was present. Bilateral knee jerks were present, but diminished and ankle jerks were absent. Bilateral plantar response was flexor. Fasciculations were present over biceps brachii. There was no cranial nerve involvement or sensory deficit. Gait assessment showed waddling gait. Other systems examination was unremarkable.
Figure 1: The patient, when he attempts to lift his arm, has to use the support of the other arm

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The patient also had recent history of consumption of organophosphate insecticide i.e. chlorpyrifos approximately 60 ml with suicidal intention, for which he was admitted in the intensive care unit in our hospital, after which he developed cholinergic crisis with toxic myocarditis. He had been treated as per protocol with gastric lavage, atropine, pralidoxime and supportive measures. After 2 weeks of appropriate treatment, patient had made a complete recovery and was discharged from the hospital.

The presentation was resembling that of Guillain Barre Syndrome, hence lumbar puncture was done and CSF analysis was normal. Nerve conduction studies showed motor axonopathy of bilateral tibial nerves with sensory axonopathy of left ulnar, superficial peroneal, and right sural nerves, and radiculopathy of bilateral common peroneal nerves.

The patient was initiated on daily physiotherapy after which his pain and weakness gradually reduced. At the time of discharge, he was able to walk without support and was able to stand from sitting position.

  Discussion Top

Organophosphate compound poisoning manifests as three well-defined clinical phases. The initial phase constitutes the acute cholinergic crisis. This occurs due to inhibition of the enzyme acetylcholinesterase which leads to accumulation of acetylcholine in the synaptic junction causing excessive stimulation of cholinergic receptors.

Intermediate syndrome typically occurs 24-96 hours following an intense period of cholinergic symptoms and signs. It is due to failure of the neuromuscular junction as a result of prolonged over-stimulation of cholinergic receptors. It predominantly involves the cranial nerves and the proximal muscles such as neck and respiratory muscles. Recovery usually occurs within 5-18 days of its onset, unless it is complicated by cardiac arrhythmias or infections.[2]

Rarely, a delayed phase of peripheral neuropathy (OPIDN) is seen where the patient presents with vague distal muscle weakness and pain which may progress to paralysis. It is usually a pure motor or predominantly motor axonal neuropathy characterized by wrist drop and foot drop with minimal or no sensory loss and occurs 7-20 days after exposure to an OP agent. It is due to phosphorylation and inhibition of an enzyme called Neuropathy Target Esterase (NTE), which is located within the nervous tissue. It catalyzes the breakdown of endoplasmic reticulum-membrane phosphatidylcholine and plays an important role in membrane-phospholipid homeostasis, axonal transport and glial-axonal interactions.[3] In Organophosphate poisoning, there is phosphorylation and subsequent aging of at least 70% of NTE in the peripheral nerves.[4]

H Nand et al. reported a case of a young man who after complete recovery after OP compound consumption, presented with distal muscle weakness in the lower limbs 6 days after discharge. He had developed spastic paralysis.[5] Mundu et al. reported a case of a 22-year-old male who developed OPIDN with pyramidal tract involvement in the form of spastic paralysis with increased tone and exaggerated deep tendon reflexes.[6] In another report by Kobayashi et al., they presented a case of a 89-year-old man who after surviving the initial acute phase, developed severe distal muscle weakness and sensory disturbance, which rapidly progressed proximally.[7] In our case, patient predominantly had proximal muscle weakness with mild distal muscle weakness and no sensory disturbance.

The prognosis in mild neuropathy is good. However, in severe neuropathy, the patient will have slow recovery and usually have residual deficits. There is no definitive treatment for OPIDN. Experimental studies in animals have shown benefits of thiamine and high dose methyl prednisolone. However, in a follow-up study done by Senanyake, only physiotherapy was done and all the patients seen one year after poisoning were asymptomatic.[8]

This case is being reported due to its rare occurrence. Though OP compound poisoning is quite commonly encountered in most Indian hospitals, there are very few reports of late neuropathy syndrome. It is important that clinicians be aware of this entity and to keep this condition in one's mind during the follow up of patients who have recovered from OP compound poisoning.


We thank Dr. Nemichandra, MD, DM, Assistant Professor, Department of Neurology, JSSH for his help in nerve conduction study. We also thank Dr. K.C Shashidhara, MD, Associate Professor, Department of General Medicine for his inputs.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Narang U, Narang P, Gupta O. Organophosphorus poisoning: A social calamity. J Mahatma Gandhi Inst Med Sci 2015;20:46-51.  Back to cited text no. 1
  [Full text]  
Peter JV, Sudarsan TI, Moran JL. Clinical features of organophosphate poisoning: A review of different classification systems and approaches. Indian J Crit Care Med 2014;18:735-45.  Back to cited text no. 2
  [Full text]  
Clark RF. Insecticides: Organic phosphorus compounds and carbamates. In: Goldfrank LR, Flomenbaum NE, Lewin NA, Howland MA, Hoffman RS, Nelson LS, editors. Goldfrank's Toxicological Emergencies. New York: McGraw-Hill; 2002. p. 1346-60.  Back to cited text no. 3
Lotti M, Moretto A. Organophosphate-induced delayed polyneuropathy. Toxicol Rev 2005;24:37-49.  Back to cited text no. 4
Nand N, Agrawal HK, Bharti Komal, Chakrabarti D. Organophosphate induced delayed neuropathy. J Assoc Physicians India 2007;55:72-3.  Back to cited text no. 5
Mundu PA, Kumar M, Satapathy RP, Mitra JK. Organophosphate induced delayed neuropathy: A case report. Int J Contemp Med Res 2019;3:2289-91.  Back to cited text no. 6
Kobayashi S, Okubo R, Ugawa Y. Delayed polyneuropathy induced by organophosphate poisoning. Intern Med 2017;56:1903-5.  Back to cited text no. 7
Senanayake N. Tri-cresyl phosphate neuropathy in Sri Lanka: A clinical and neurophysiological study with a three year follow up. J Neurol Neurosurg Psychiatry 1981;44:775-80.  Back to cited text no. 8


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