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Table of Contents    
Year : 2021  |  Volume : 69  |  Issue : 5  |  Page : 1417-1420

Acute Lead Encephalopathy Secondary to Ayurvedic Medication Use: Two Cases with Review of Literature

Department of Neurosciences, Kokilaben Dhirubhai Ambani Hospital and Medical Reseacrh Center, Mumbai, Maharashtra, India

Date of Submission15-May-2020
Date of Decision13-Aug-2020
Date of Acceptance17-Oct-2020
Date of Web Publication30-Oct-2021

Correspondence Address:
Tushar P Raut
Department of Neurosciences, Kokilaben Dhirubhai Ambani Hospital and Medical Research Center, Mumbai, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.329591

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 » Abstract 

Ayurvedic medicine is an ancient and traditional system of health care. It is safe but inadvert and unsupervised use can lead to serious health complications. Lead is a common constituent of these medicines. Here authors describe two cases of lead encephalopathy as a result of long-term ayurvedic medication intake. First case was a 54-year-old female taking ayurvedic medications since long time presented with acute confusional state and memory disturbances with abdominal pain. MRI brain showed symmetric basal ganglia and cortical signal changes and edema with significantly elevated lead levels in blood. She responded to chelation therapy with oral penicillamine with complete clinical and radiological resolution. Second case presented was a 45-year female taking ayurvedic medications for hypertension presented with headaches and rapid deterioration in sensorium leading to coma and death. MRI brain showed diffuse cerebral edema with basal ganglia signal changes with elevated lead levels in blood. These two cases highlight the need for increased awareness that some Ayurvedic medicines may contain potentially harmful levels of lead and people who use them are at risk of developing associated toxicity which can even be fatal.

Keywords: Ayurvedic, encephalopathy, lead
Key Message: Toxin induced encephalopathy can manifest as subacute cognitive and behavioural changes or as a fulminant encephalopathy potentially life threatening. It should always be considered a s a differential when other causes like infection, metabolic etc have been ruled out. Detailed history,clinical examination and radiological findings on MRI can lead to early diagnosis, treatment and a better outcome.

How to cite this article:
Raut TP, Gholap G, Shaikh S, Mani J, Sanghvi D, Bhatt M. Acute Lead Encephalopathy Secondary to Ayurvedic Medication Use: Two Cases with Review of Literature. Neurol India 2021;69:1417-20

How to cite this URL:
Raut TP, Gholap G, Shaikh S, Mani J, Sanghvi D, Bhatt M. Acute Lead Encephalopathy Secondary to Ayurvedic Medication Use: Two Cases with Review of Literature. Neurol India [serial online] 2021 [cited 2022 May 28];69:1417-20. Available from: https://www.neurologyindia.com/text.asp?2021/69/5/1417/329591

Ayurvedic medicine (also known as Ayurveda) is India's primary and traditional system native to Indian healthcare system.[1] Ayurvedic formulations are based on herbal products which are safe but often include toxic metals and other elements based on Rasa Shastra practice.[2] These elements are believed to restore good health and normal function to the human body. A 2015 published survey of people who use Ayurvedic preparations showed that 40 percent had elevated blood levels of lead and some had elevated blood levels of mercury and other heavy metals.[3] Lead poisoning affects multiple organs like skeletal system, hematological, neurological, gingiva and kidneys. In the central nervous system, the lesions are thought to be the result of vascular injury.[4] Lead encephalopathy in adults is uncommon and due to ayurvedic medications is even more rare. According to a survey by State Adult Blood Lead Epidemiology and Surveillance (ABLES), the national prevalence rate of BLLs ≥10 μg/dL declined from 26.6 adults per 100,000 employed in 2010 (among 37 states) to 20.4 in 2013 (among 29 reporting states).[5]

Lead acts as a cellular toxin by inhibiting mitochondrial respiration. The increased resistance of the adult to encephalopathy and ataxia is believed to be caused by the capacity of the mature brain to sequestrate lead away from its mitochondrial site of action within the cerebral and cerebellar neurons.[6] Here authors would like to describe two cases of Lead poisoning due to long-term ayurvedic medication intake presenting as acute encephalopathy of varying severity.

 » Case Presentation Top

Case 1

A 54-year-old female known case of diabetes mellitus and systemic hypertension on medications came to emergency department with 2 weeks history of acute confusional state, disorientation, forgetfulness and irrelevant talking. There was history of abdominal pain colicky in nature since 2 months. CT Abdomen pelvis was normal and endoscopy suggestive of mild antral gastritis for which she was initiated on proton pump inhibitors. There was history of long-term multiple ayurvedic medication consumption for her diabetes and hypertension. Patient procured it from ayurved practioner and were dispensed as tablets.

Clinical examination revealed hypertension. Pallor was present. Patient was confused, disoriented and restless with difficulty in understanding complex commands. Plantar response was extensor. Gait was ataxic. Complete hemogram revealed hemoglobin of 8.4 gram% with microcytic hypochromic picture. Biochemical tests including renal and liver function tests were normal. MRI Brain study suggestive of multiple T2 FLAIR hyperintensities in putamen, thalami and subcortical white matter with gyral edema [Figure 1]. DWI revealed subtle diffusion restriction in left occipital lobe [Figure 2]. CSF study revealed 5 cells (mononuclear) with proteins of 15 mg% and normal sugars. CSF cultures were negative. EEG electroencephalogram revealed mild slowing of background. Blood toxin anaylsis revealed elevated lead levels in blood (105 μg/dL). All her ayurvedic medications were stopped and patient was given symptomatic treatment. Oral chelation therapy started which included oral D penicillamine 250 mg twice a day. Gradually abdominal pain and confusional state resolved. Patient was given oral chelation therapy for 3 months with periodic monitoring of lead levels. Repeat MRI Brain at 3 months showed complete resolution of signal changes previously seen [Figure 1] and [Figure 2]. Clinically patient had a normal neurological examination at follow-up.
Figure 1: (a-d): Axial FLAIR MRI images at presentation (top row: a, b) and follow up (bottom row: c, d). MRI at presentation (a, b) shows hyperintense signal and edema in the deep grey nuclei and cerebral cortices. Cerebral cortical edema is asymmetric and prominent on the right side at the vertex (arrows). Also seen is left frontal subcortical edema (arrow head). MRI at follow up (c, d) shows complete resolution of signal alteration and edema

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Figure 2: Diffusion weighted images (a, c) with corresponding ADC maps (b, d) show focal left occipital restricted diffusion (arrows) with interim resolution at follow up imaging

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Case 2

A 45-year-old female known case of hypertension was taking medications for her blood pressure from ayurvedic practioner since 6 months. Patient developed headaches since 3 weeks followed by multiple episodes of vomiting and drowsiness. She presented to emergency with extreme stupor. Vitals examination revealed hypertension and bradycardia. Glasgow coma scale (GCS) was E2M3V2 (7/15). Fundus examination revealed papilledema. Plantar response was extensor. CBC revealed Hb of 9.5 gram % with microcytic picture. Renal and liver profile was normal. MRI Brain suggestive of diffuse cerebral edema, gyral swelling with basal ganglia signal changes [Figure 3]. CSF Study revealed cell count of 4 cells with normal protein and sugar. Meningitis biofire and aerobic cultures were negative. Patient initiated on injection mannitol, antiepileptics and hydration. Lead levels were 140 μg/dL. Patient became comatose and succumbed to the illness.
Figure 3: (a) T2 WI showing symmetric basal ganglia signal changes and cortical edema. (b) T2 FLAIR showing diffuse cortical edema (arrows) and chinking of ventricles (arrows)

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 » Discussion Top

Ayurvedic preparations contain lead and/or mercury at 100 to 10,000 times greater than acceptable limits.[7] Excess levels of lead leads to production of free radicals which subsequently causes oxidative damage of cellular components including DNA and cell membranes.[8] It interferes with DNA transcription, enzymatic synthesis of vitamin D, and enzymes that maintain the integrity of the cell membranes. Lead results in denaturation of enzymes such as deltaaminolevulinic acid dehydratase (ALA-D) and ferrochelatase which are important for heme synthesis. Inhibition of pyrimidine 5'-nucleotidase can prevent the degradation of ribosomal RNA in red blood cells leading to basophilic stippling on a peripheral smear, a classic finding which can be apparent at BLLs of ~50 μg/Dl.[9] Basophilic stippling of erythrocytes is reported in 91% of patients by Whitfield et al.[10] but was seen in only 40% of cases reported by Greengard et al.[11] Basophilic stippling couldn't be demonstrated in either of our cases.

Symptoms of adult lead poisoning are variable depending on duration of exposure. The usual manifestations of lead poisoning in adults are colic, anemia, and peripheral motor neuropathy. The adult form of lead encephalopathy is rarer than the pediatric form[12] and can present with serious neurodeterioration and even death.[13] Lead encephalopathy can present in acute and chronic forms.[14] Acute lead encephalopathy presents pathologically as cerebral edema whereas in chronic lead encephalopathy, extensive tissue destruction with cavity formation and thickening of the veins with cellular disorganization of their walls is seen.[15] All this can lead to edema, gliosis, hemorrhage, neuronal loss, and perivascular proteinaceous exudate. Patients present with headache, vomiting, ataxia, convulsions, paralysis, stupor, and coma in acute forms[16] whereas in chronic encephalopathy, patients present with memory and concentration disturbances, headache, psychiatric symptoms, diminished libido, syncope, tremor, seizure and ataxia. In severe conditions, cerebral or cerebellar edema may develop; such patients may present with vomiting, apathy, stupor, coma, paralysis, and death.

The symptoms of lead toxicity usually appear at BLLs of 40-60 μg/dL in adults. Over the last 25 years, numerous cases of lead toxicity associated with Ayurvedic medicine have been reported in the literature.[17] Whitfield et al. (1972) reported the largest series of 23 adults with lead encephalopathy.[10] Ten of these patients had altered sensorium; 18 of them had seizures. Bhaskara rao et al. reported 2 cases with lead encephalopathy presenting as seizures and abdominal complaints with good response to chelation treatment.[18] Atre et al.[19] reported a case of lead encephalopathy due to ayurvedic medication presenting as acute onset short-term memory loss, loss of appetite, apathy and imbalance with hyperreflexia and spasticity. Our first case presented with acute onset confusional state, disorientation, memory disturbances and lead colic. Second case presented with rapid worsening of sensorium leading to coma and ultimately death.

Neuroimaging especially magnetic resonance imaging MRI can give some clue of toxin-induced encephalopathy. Schroter et al. reported high signal intensities in the periventricular white matter, basal ganglia, insula, posterior thalamus, and pons.[20] Perelman et al.[13] reported MR imaging findings such as cerebellar edema, suggested by an enlarged cerebellum with the disappearance of the cerebellar fissure and protrusion. Mani et al.[15] reported high signal intensities in both thalami on T2 weighted MR images. Tuzun et al.[21] reported low signal intensities on T1-weighted images and high signal intensities on T2-weighted images located bilaterally and symmetrically in thalami, lateral putamen, claustrum, and insula. Bhaskara rao et al. reported 2 cases with MRI showing bilateral symmetric involvement of the thalamus and lentiform nucleus, subcortical white matter and external capsule.[18] Both our cases showed cortical and basal ganglionic signal changes except the edema was serious in the second case. In the first case we could demonstrate reversal of signal changes post-treatment.

Management varies widely and includes oral chelation with D-penicillamine or DMSA (Dimercapto succinic acid) or intravenous infusions of Calcium EDTA, Na-EDTA (Ethylene diamine tetraacetic acid) or dimercaprol. In some instances combination therapy is administered. The current reference range for acceptable BLLs in healthy individuals without excessive exposure to environmental sources of lead is <10 μg/dL for children and <25 μg/dL for adults. To date, there are no clinical trials that define the optimal management although it is generally accepted that the first step is to identify and remove the source of the exposure. Chelation therapy should be initiated when the BLL is >80 μg/dL in asymptomatic and >50 μg/dL in symptomatic adults and should be continued until the BLL is <50 μg/dL. We used oral D penicillamine in our case with normalization of lead levels post-treatment. Timely diagnosis and identification of source of exposure are critical in preventing the long-term consequences of lead poisoning. Detailed medication history is essential in cases with unknown cause of encephalopathy.

In a case of rapidly progressive encephalopathy with no identifiable cause, toxin-induced encephalopathy should be suspected especially with MRI findings showing symmetric basal ganglia, cortical and subcortical white matter signal change. Prompt elimination of toxin and initation of chelation treatment may prevent neurological worsening and result in complete clinical recovery.

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Conflicts of interest

There are no conflicts of interest.

 » References Top

Chopra A, Doiphode VV. Ayurvedic medicine. Core concept, therapeutic principles, and current relevance. Med Clin North Am 2002;86:75-89.  Back to cited text no. 1
Mikulski MA, Wichman MD, Simmons DL, Pham AN, Clottey V, Fuortes LJ. Toxic metals in ayurvedic preparations from a public health lead poisoning cluster investigation. Int J Occup Environ Health 2017;23:187-92.  Back to cited text no. 2
Breeher L, Mikulski MA, Czeczok T, Leinenkugel K, Fuortes LJ. A cluster of lead poisoning among consumers of Ayurvedic medicine. Int J Occup Environ Health 2015;21:303-7.  Back to cited text no. 3
Teo JG, Goh KY, Ahuja A, Ng HK, Poon WS. Intracranial vascular calcifications, glioblastoma multiforme, and lead poisoning. AJNR Am J Neuroradiol 1997;18:576-9.  Back to cited text no. 4
Alarcon WA, State Adult Blood Lead Epidemiology and Surveillance (ABLES) Program Investigators. Elevated blood lead levels among employed adults-United States, 1994-2013. MMWR Morb Mortal Wkly Rep 2016;63:59-65.  Back to cited text no. 5
Holtzman D, DeVries C, Nguyen H, Olson J, Bensch K. Maturation of resistance to lead encephalopathy: Cellular and subcellular mechanisms. Neurotoxicology 1984;5:97-124.  Back to cited text no. 6
Saper RB, Phillips RS, Sehgal A, Khouri N, Davis RB, Paquin J, et al. Lead, mercury, and arsenic in US- and Indian-manufactured Ayurvedic medicines sold via the Internet [published correction appears in JAMA 2008;300:1652]. JAMA 2008;300:915-23.  Back to cited text no. 7
Meyer PA, Pivetz T, Dignam TA, Homa DM, Schoonover J, Brody D, et al. Surveillance for elevated blood lead levels among children--United States, 1997-2001. MMWR Surveill Summ 2003;52:1-21.  Back to cited text no. 8
Valentine WN, Paglia DE, Fink K, Madokoro G. Lead poisoning: Association with hemolytic anemia, basophilic stippling, erythrocyte pyrimidine 5'-nucleotidase deficiency, and intraerythrocytic accumulation of pyrimidines. J Clin Invest 1976;58:926-32.  Back to cited text no. 9
Whitfield CL, Ch'ien LT, Whitehead JD. Lead encephalopathy in adults. Am J Med 1972;52:289-98.  Back to cited text no. 10
Greengard J. Lead poisoning in childhood: Signs, symptoms, current therapy, clinical expressions. Clin Paediatr 1966;5:269-75.  Back to cited text no. 11
Bressler JP, Goldstein GW. Mechanisms of lead neurotoxicity. Biochem Pharmacol 1991;41:479-84.  Back to cited text no. 12
Perelman S, Hertz-Pannier L, Hassan M, Bourrillon A. Lead encephalopathy mimicking a cerebellar tumor. Acta Paediatr 1993;82:423-5.  Back to cited text no. 13
Saryan LA, Zenz C. Lead and its compounds. In: Saryan LA, Zenz C, editors. Occupational Medicine. 3rd ed. St. Louis, Mo: Mosby; 1994. p. 506-41.  Back to cited text no. 14
Mani J, Chaudhary N, Kanjalkar M, Shah PU. Cerebellar ataxia due to lead encephalopathy in an adult. J Neurol Neurosurg Psychiatry 1998;65:797.  Back to cited text no. 15
Landrigan PJ, Todd AC. Lead poisoning. West J Med 1994;161:153-9.  Back to cited text no. 16
Centers for Disease Control and Prevention (CDC). Lead poisoning associated with ayurvedic medications--five states, 2000-2003. MMWR Morb Mortal Wkly Rep 2004;53:582-4.  Back to cited text no. 17
Rao JV, Vengamma B, Naveen T, Naveen V. Lead encephalopathy in adults. J Neurosci Rural Pract 2014;5:161-3.  Back to cited text no. 18
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Atre AL, Shinde PR, Shinde SN, Wadia RS, Nanivadekar AA, Vaid SJ, et al. Pre- and posttreatment MR imaging findings in lead encephalopathy. AJNR Am J Neuroradiol 2006;27:902-3.  Back to cited text no. 19
Schroter C, Schroter H, Huffmann G. Neurologic and psychiatric manifestations of lead poisoning in adults (case report and review of the literature) [in German]. Fortschr Neurol Psychiatr 1991;59:413-24.  Back to cited text no. 20
Tüzün M, Tüzün D, Salan A, Hekimoğlu B. Lead encephalopathy: CT and MR findings. J Comput Assist Tomogr 2002;26:479-81.  Back to cited text no. 21


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