|Year : 2013 | Volume
| Issue : 1 | Page : 70-72
Acute reversible Parkinsonism following accidental exposure to organophosphate insecticide
A. S. Praveen Kumar, D. K. S. Subrahmanyam
Department of Medicine, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry, India
|Date of Submission||15-Oct-2011|
|Date of Acceptance||21-Nov-2011|
|Date of Web Publication||6-Feb-2013|
A. S. Praveen Kumar
Department of Medicine, JIPMER, Pondicherry
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Organophosphate insecticide (OPI) poisoning is one of the most common poisonings seen in rural south India. OPIs act by inhibiting acetylcholine esterase enzyme activity and thereby increasing acetylcholine at synapses. The usual neurological complications of OPI compounds are acute cholinergic crisis, intermediate syndrome, and delayed sensorimotor polyneuropathy. Extrapyramidal symptoms, though very rare, can also occur following OPI exposure. Parkinsonism is a movement disorder that develops as a consequence of reduced function of the dopaminergic neurons within the basal ganglia. The etiology of parkinsonism is multifactorial, with both genetic and environmental determinants. The development of typical parkinsonism following brief inhalational OPI exposure is very rare and there are only a few reports in the literature. We report a 50-year-old male who presented with cholinergic crisis following acute accidental inhalational exposure to chlorpyriphos, an OPI compound; he developed features of parkinsonism on day 6 of hospital admission, but recovered completely without treatment in 7 days.
Keywords: Acetylcholinesterase, cogwheel rigidity, chlorpyriphos, organophosphate insecticide, parkinsonism
|How to cite this article:|
Kumar AP, Subrahmanyam D. Acute reversible Parkinsonism following accidental exposure to organophosphate insecticide. Int J Nutr Pharmacol Neurol Dis 2013;3:70-2
|How to cite this URL:|
Kumar AP, Subrahmanyam D. Acute reversible Parkinsonism following accidental exposure to organophosphate insecticide. Int J Nutr Pharmacol Neurol Dis [serial online] 2013 [cited 2020 Aug 6];3:70-2. Available from: http://www.ijnpnd.com/text.asp?2013/3/1/70/106999
| Introduction|| |
The organophosphate insecticides (OPI) are chemical substances that act by inhibiting the acetylcholinesterase enzyme (AChE) activity. This action results in accumulation of acetylcholine and overstimulation of acetylcholine receptors in the synapses of the autonomic nervous system, neuromuscular junctions, and central nervous system (CNS).  Chlorpyriphos (CPF) is broad-spectrum OPI compound and exerts extensive, long-lasting, AChE inhibition. The occurrence of extrapyramidal symptoms and typical Parkinsonism More Details is very unusual following brief inhalational exposure to OPI. The reason why parkinsonism develops in only some patients following OPI exposure is uncertain. Whether it is related to a genetic susceptibility to develop parkinsonism on environmental exposure to OPI or to a specific agent of OPI is an unanswered question. We report a case of transient reversible acute parkinsonism following brief inhalational exposure to the OPI chlorpyriphos; the parkinsonism symptoms subsided completely without treatment.
| Case Report|| |
A 50-year-old farmer presented to our emergency department with history of profuse sweating, salivation, altered sensorium, and difficultly in breathing following a brief exposure to an organophosphate insecticide (OPI) compound. He had had accidental inhalational exposure to chlorpyriphos while spraying the crops in his fields. He was not a professional sprayer. On examination, his pulse rate was 72/min, blood pressure 130/80 mmHg, respiratory rate 24/min, and pupils around 3 mm in diameter. He had weakness of the neck muscles and respiratory paradox at presentation. Respiratory system examination showed bilateral rhonchi with minimal crepitations. The systemic examination was normal. Laboratory investigations revealed normal liver and renal function tests. The electrocardiogram and chest x-ray were normal.
The patient presented to our emergency medical services department with cholinergic crisis within 4 hours of symptom onset. His pulse and blood pressure were stable. The respiratory rate was 24/min. The arterial blood gas (ABG) analysis showed respiratory alkalosis (pH 7.50), with pO 2 78 mmHg, pCO 2 38 mmHg, and SpO 2 of 98% in room air. He was immediately intubated in view of the respiratory muscle weakness and shifted to the emergency medical intensive care unit for mechanical ventilator support. We administered atropine and pralidoxime according to the hospital protocol. On day 3, the patient became oriented to commands. With the ventilator support, atropine, and pralidoxime he recovered from the cholinergic crisis and was weaned off the mechanical ventilator on day 4 of hospital admission.
On day 6, the patient developed rigidity and bradykinesia, with tremor both hands. He was conscious and oriented to commands. On examination, he displayed an expressionless face with decreased blinking rate, monotonous speech, rest tremor, and cogwheel rigidity, with flexion at the elbows and a rigid posture [Figure 1] and [Figure 2]a. The deep tendon reflexes were normal, with mute plantar response bilaterally. MRI brain (done on day 8, after recovery from parkinsonism) was normal.
|Figure 1: Photograph showing fixed flexion at the elbows and the rigid body posture of the patient on the bed|
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|Figure 2: (a) Photograph of patient on day 3 of parkinsonism showing mask-like face and rigid posture. (b) The patient 1 week after discharge from hospital|
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The patient was kept under observation. From day 3 onward he started showing gradual improvement in the symptoms, and he recovered completely in 7 days without any treatment. We did not administer any treatment for the extrapyramidal symptoms as he showed signs of recovery from day 3 of parkinsonism. At the follow-up visit, 1 week after discharge from hospital, he was completely normal [Figure 2]b.
| Discussion|| |
This patient, who was not a professional sprayer, suffered inhalational exposure to OPI. He manifested parkinsonism-like features 6 days later and recovered completely within a week without any specific treatment. Since his MRI brain was normal and there was no family history of Parkinson disease (PD) we attribute his extrapyramidal manifestations to acute OPI exposure. The central nervous system manifestations of acute OPI exposure are anxiety, restlessness, ataxia, convulsions, respiratory depression, and coma, apart from the usual neurological complications. Neurological manifestations of OPI exposure may also include choreoathetosis, opisthotonos, torticollis, facial grimacing, tongue protrusion, extrapyramidal symptoms, and typical parkinsonism. ,, The first report of parkinsonism following OPI exposure was in 1978 by Davis et al.  In 1999 Bhatt et al. reported five patients with OPI-induced parkinsonism, among whom four cases occurred following inhalational exposure to OPI. 
The excessive acetylcholine activity due to prolonged and irreversible inhibition of acetylcholinesterase during OPI poisoning may alter the dopamine activity within the basal ganglia and substantia nigra, resulting in the exposed person exhibiting parkinsonism-like features.  Bhatt et al. suggested that the lack of response to levodopa-carbidopa in their patients might imply dopamine receptor blockade rather than mere deficiency of dopamine production. 
The exact latent period before onset of parkinsonism following OPI exposure is uncertain and varies in different reports. The shortest duration reported was 1 day and longest duration was 2 months after OPI exposure, but in most of the reports ,,,,,, patients have developed parkinsonism within a week of OPI exposure. The phosphate-containing OPI compounds such as chlorpyriphos appear to exhibit more neurotoxicity than other compounds. ,,, The imaging findings in OPI-induced parkinsonism vary from normal appearance , to symmetric signal changes in the putamen and caudate nucleus.  In our patient, MRI brain (T1W and T2W images) was done on day 8 after onset of parkinsonism and it was normal.
OPI-induced acute parkinsonism is a reversible phenomenon. Management should be decided on a case-by-case method as there is no consensus on treatment. There are reports of recovery from OPI-induced parkinsonism without any treatment. ,,, Treatment can be undertaken if the symptoms are prolonged and distressing. The selection of the suitable drug for the management of OPI-induced parkinsonism is also a challenging task. The drugs reported to be effective in case reports of OPI-induced parkinsonism are bromocriptine, benzhexol,  amantadine, , and biperidine.  According to Bhatt et al levodopa was not effective in the treatment of OPI-induced parkinsonism in their series.
In conclusion, reversible parkinsonism-like features can occur following brief inhalational OPI exposure and these features can improve without specific intervention.
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[Figure 1], [Figure 2]