|Year : 2000 | Volume
| Issue : 2 | Page : 144--8
Neurologic complications of dropsy : from possibility to reality.
S Prabhakar, D Khurana, KD Gill, S Choudhary, V Lal, CP Das
Departments of Neurology and Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India., India
Departments of Neurology and Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.
Epidemic dropsy, which results from the accidental ingestion of mustard oil adulterated with argemone oil, has been associated with certain neurologic symptoms. The occurrence of objective neurologic involvement has, however, precluded this illness. We report two cases, who were victims of epidemic dropsy in the recent outbreak in India and showed objective neurologic deficit in the form of brachial neuritis.
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Prabhakar S, Khurana D, Gill K D, Choudhary S, Lal V, Das C P. Neurologic complications of dropsy : from possibility to reality. Neurol India 2000;48:144-8
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Prabhakar S, Khurana D, Gill K D, Choudhary S, Lal V, Das C P. Neurologic complications of dropsy : from possibility to reality. Neurol India [serial online] 2000 [cited 2022 Jan 19 ];48:144-8
Available from: https://www.neurologyindia.com/text.asp?2000/48/2/144/1558
Epidemic dropsy results from the accidental ingestion of mustard oil adulterated with oil extracted from the seeds of Argemone mexicana (Mexican poppy/prickly yellow poppy). Lyon reported the first four cases of argemone oil poisoning from Bombay in 1877., Various epidemics have been reported, in India from Calcutta (1877), Assam, Bihar, Eastern U.P, Orissa, Madhya Pradesh, Gujrat and Delhi since then., Epidemics have also been reported from Rangoon, Fiji, Mauritius, North west Cape districts of South Africa, Madagascar and Australia.,,,,, The South African epidemic was unique, being associated with consumption of adulterated wheat flour. Epidemics in India have usually been reported between July and September. The epidemic in 1998 in Delhi and other parts of the country also started in August and was possibly the largest in India so far. Its fatal consequences have been linked to its propensity to cause a hypoalbuminaemic state with resultant intractable oedema ('dropsy'). The organs chiefly affected in this malady are the eyes, heart and the subcutaneous tissues. Although some investigators have documented few neurologic signs, but objective evidence of neurologic involvement has never been reported. We report two patients of the same family who were victims of the recent outbreak of epidemic dropsy in India, with neurologic complications which were hitherto unheard of.
Case 1: JL, 21 year male, had been consuming food cooked in mustard oil bought in Delhi when he developed loose stools. Despite the diarrhoea, he continued its consumption for the next 10-12 days. Fifteen days later he had pain in both shoulders, which was followed 4-5 days later by difficulty in raising both arms sideways. Wasting around both shoulders was also noticed which was progressive. On examination, besides an unremarkable general physical, there was bilateral wasting of the deltoids, supraspinatus and infraspinatus muscles [Figure. 1a] and [Figure. 1B] with a power of 1/5 in the supraspinatus bilaterally, 0/5 in the deltoids bilaterally, 2/5 and 3/5 in the right and left infraspinatii respectively. The biceps reflex was absent on the right side, while the rest of the reflexes were sluggish in the upper limbs. The plantars were flexor and sensory examination revealed a pansensory loss on skin over deltoids on both sides. Investigations carried out revealed a normal haemogram with an ESR of 50. Serum albumin was 7.3gm% with an albumin-globulin ratio of 2.3. Rest of biochemistry was within normal limits. Neuroelectrophysiologic studies were also conducted [Table I]. MRI of the brachial plexus was normal. Ocular tonometry showed a normal intraocular pressure.
Case 2: SP, 32 year male, brother of JL,consumed food in similar circumstances as JL and developed pedal swelling upto the ankles and fever in addition to diarrhoea. He developed pain in left shoulder 15-20 days later, followed by difficulty in raising the left arm. Wasting around the left shoulder was also noticed. On examination, pitting pedal oedema upto the ankles was seen. There was wasting of the rhomboids, supraspinatus, infraspinatus and deltoid muscles on the left side [Figure. 2a] and [Figure. 2B]; Power in left shoulder abductors was 3/5. His deep tendon reflexes were however intact and plantars were flexor. No objective sensory loss was found. On investigating, he had a haemoglobin of 7.5 gm% and an ESR of 45mm. The serum albumin was 5.5gm% and albuminglobulin ratio was 1.7. MRI of the brachial plexus was normal. Neuroelectrophysiologic profile is shown in [Table I]. The wife of SP also consumed the same food and later succumbed to the illness. The culpable oil was screened for various toxins by spectrofluorometery and high levels (11.5 gm/ml) of sanguinarine were detected.
Epidemic dropsy results from intoxication with argemone oil resulting from its willful adulteration with mustard oil, which is possible by virtue of their similar colour. In the most recent Indian epidemic in 1998, the first case was reported on Aug. 5, 1998 and the epidemic lasted for seven weeks. 2178 cases were reported out of which 66 (3.2%) died. This was possibly the largest epidemic in India. As a preventive measure, the Government of India stopped the sale of mustard oil on Aug. 26, 1998.
Mukerjee et al had isolated a toxic substance from argemone seeds which was later identified as sanguinarine by Sarkar. Argemone seeds contain 2 physiologically active alkaloids; dihydrosanguinarine (~ 87%) and sanguinarine (~ 5%). The fact that argemone oil is responsible for epidemic dropsy has been established by several human feeding trials with argemone oil and argemone adulterated mustard oil, which reproduced symptoms similar to epidemic dropsy in human subjects. Dropsy, although commonly has an insidious onset, about 30% victims show an acute onset. Symptoms are usually swelling of the feet and legs (hence the term dropsy), fever which is either intermittent or continuous, diarrhoea, vomiting, anorexia, abdominal colic and epigastric discomfort. Symmetrical pitting oedema is the most common finding; erythema or rash over the oedematous parts, hepatomegaly (10%) and congestive cardiac failure (4%) being the others., Ocular manifestations occur as late manifestations, the commonest being glaucoma (11%), superficial retinal haemorrhages (6%) and disc oedema (3%) and bilateral central retinal vein occlusion. An age and sex specific distribution has also been observed, with males being more susceptible and subjects in the age group of 11-20 years in both males and females being more vulnerable to ocular involvement. Ocular electrophysiologic tests i.e. electroretinogram and visual evoked responses, have been reported to be normal. Skin biopsy shows a large number of young and dilated capillaries along with marked endothelial proliferation around the vessels, papillary and subpapillary oedema leading to loss of papillae. Neurological involvement in epidemic dropsy has been controversial although, paraesthesias and alteration in tender jerks have been reported.,,, Attempts to determine objective involvement of the nervous system have been futile.,, In our patients the clinical presentation and objective evaluation suggests a picture similar to brachial neuritis. The nerve conduction studies were performed on Nicolet Viking IV EMG Machine and results compared with normative data established for our laboratory. Case 1 showed abnormal axillary nerve conductions on both sides with a normal distal latency and marked reduction in CMAP amplitude on stimulation at Erb's point. Rest of the nerves showed normal conductions. EMG sampling of the right and left deltoids showed a neurogenic pattern with large amplitude motor unit action potentials (MUAPs), polyphasic MUAPs and a discrete interference pattern. Case 2 showed an abnormal conduction in the right axillary nerve with prolonged distal latency and reduction in the compound muscle action potential (CMAP) amplitude indicating subclinical involvement of the right brachial plexus. His left median and left ulnar nerve conductions also showed a marked reduction (52.4% and 44.5% respectively) in CMAP amplitude on proximal stimulation at Erb's point. EMG sampling of the left deltoid was neurogenic. One of the patients (JL) who has been on regular follow up showed marked improvement in muscle power at 6 months. His right supraspinatus and right deltoid had grades 4/5 and 4/5 power respectively (at admission power in right supraspinatus and right deltoid was 1/5 and 0/5 respectively). Sensory loss on skin over the right deltoid had also abated. At one year follow up, the same patient has shown almost complete recovery of power and sensory loss.
Numerous mechanisms have been propounded for the toxicity of argemone oil. Sanguinarine (the toxic principle) reduces the glycogen levels due to enhanced glycogenolysis leading to formation of glycogen-1-phosphate which enters the glycolytic pathway resulting in pyruvate accumulation. Increased pyruvate levels in blood uncouple oxidative phosphorylation. Other mechanisms include inhibition of Na+K+ ATPase of the heart by interacting with the cardiac glycoside receptor site of the enzyme leading to degenerative changes in cardiac muscle fibres and thereby cardiac failure,, enhanced production of reactive oxygen species and inhibition of pyruvate oxidation leading to increased blood pyruvate concentration. The latter hypothesis has not been established as yet. The occurrence of brachial neuritis in our patients is unlikely to be coincidental, by virtue of the fact that both members developed similar symptomatology under identical circumstances. This points an incriminating finger towards the adulterated oil. The oil was screened for various toxins, however only sanguinarine was detected by spectrofluorometery in high levels (11.5 gm/ml). The occurrence of brachial neuritis in the two brothers may possibily be related a genetic susceptibility to the effect of sanguinarine. The clinical and neuroelectrophysiologic profile indicates a predominant axonal damage. Such a finding has never been documented in the vast literature available. The exact mechanism however needs to be elucidated.
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