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| CASE REPORT |
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| Year : 2021 | Volume
: 69
| Issue : 5 | Page : 1421-1423 |
Lead Encephalopathy with Distinctive Brain Magnetic Resonance Imaging Findings
Ameya Patwardhan1, Nalini Atchayaram1, Jitender Saini2, Manu S Girija1, Jagadish Annapureddy1, Mishab Alumkadavath3, Tanushree Chawla1, Leena Shingavi1, Seena Vengalil1
1 Department of Neurology, National Institute of Mental Health and Neurosciences, Bangalore, India
2 Department of Neuroimaging and Interventional Radiology, National Institute of Mental Health and Neurosciences, Bangalore, India
3 Department of Clinical Psychology, National Institute of Mental Health and Neurosciences, Bangalore, India
| Date of Submission | 25-Apr-2020 |
| Date of Decision | 15-May-2020 |
| Date of Acceptance | 13-Jul-2020 |
| Date of Web Publication | 30-Oct-2021 |
Correspondence Address:
Seena Vengalil
Department of Neurology, National Institute of Mental Health and Neurosciences, Bangalore - 560 029
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0028-3886.329588
Lead poisoning is a multisystem disorder, more commonly affecting children. Occupational exposure, traditional medicines, and contaminated alcohol have been associated with lead encephalopathy in adults. Herein, we report a patient of lead toxicity presenting to the emergency services as acute encephalopathy with symptomatic hyponatremia and chronic recurrent abdominal colic and vomiting. This 50-year-old battery mechanic had multisystem involvement with anemia, basophilic stippling, lead line on the gums, and chronic hypertension. The blood lead level was more than 65 mcg/dL. Computed tomography of the brain showed intracranial calcifications and the MRI brain showed bilateral symmetric involvement of the thalamus, basal ganglia, brainstem, and external capsule. His sensorium improved rapidly after the correction of hyponatremia, however, apathy and psychomotor slowing persisted. This case highlights the importance of recognizing clinical markers and characteristic imaging findings, which can provide clues to an early diagnosis of this otherwise rare clinical condition, and prompt chelation therapy and avoid further lead exposure.
Keywords: Intracranial calcifications, hyponatremia, lead encephalopathy, lead line
Key Messages: Lead encephalopathy should be considered in the differential diagnosis of subcortical cognitive impairment in adults with occupational exposure to lead. Clinical findings like lead lines and investigations like anemia and basophilic stippling may be clues to this potentially treatable encephalopathy. Distinctive imaging findings like intracranial calcifications and symmetrical involvement of the thalamus, basal ganglia, external capsule, and brain stem should kindle a high index of suspicion and prompt further investigations.
How to cite this article:
Patwardhan A, Atchayaram N, Saini J, Girija MS, Annapureddy J, Alumkadavath M, Chawla T, Shingavi L, Vengalil S. Lead Encephalopathy with Distinctive Brain Magnetic Resonance Imaging Findings. Neurol India 2021;69:1421-3 |
How to cite this URL:
Patwardhan A, Atchayaram N, Saini J, Girija MS, Annapureddy J, Alumkadavath M, Chawla T, Shingavi L, Vengalil S. Lead Encephalopathy with Distinctive Brain Magnetic Resonance Imaging Findings. Neurol India [serial online] 2021 [cited 2022 May 29];69:1421-3. Available from: https://www.neurologyindia.com/text.asp?2021/69/5/1421/329588 |
Lead is toxic to the hematopoietic, gastrointestinal, renal, nervous, cardiovascular, and reproductive systems. Lead neurotoxicity is more frequent and severe in children.[1] Adults develop lead toxicity following occupational exposure.[1] Acute lead encephalopathy presents as headache, vomiting, seizures, paralysis, ataxia, or coma while chronic exposure results in depression, behavioral changes, and cognitive impairment.[1] We report a case of acute exacerbation of chronic lead encephalopathy following occupational exposure.
| » Case Report | |  |
A 50-year-old man was brought to the emergency services with acute onset of altered sensorium of one day. This was preceded by abdominal colic and vomiting for three days. He had episodes of abdominal colic for four years and was detected to be hypertensive for six years. He worked in a battery manufacturing factory for 15 years and has handled lead-based chemicals without any personal protective gear. He also ate food with unwashed bare hands. Examination revealed pallor, sallow colored skin, and dark blue lead lines on the gums. He was drowsy, arousable, had no eye to eye contact, but responded to simple verbal commands. He had hypophonia and mild postural tremor of upper limbs with cogwheel rigidity. Investigations revealed anemia with hemoglobin of 9.1 g/dL (microcytic to macrocytic) with basophilic stippling, hemolysis, and relative monocytosis on blood smear [Figure 1]a. The serum sodium level was 120 mmol/L. Other electrolytes, renal, liver, and thyroid function tests were normal. The cerebrospinal fluid analysis was normal. Blood lead levels, measured by anodic stripping voltammetry was more than 65 mcg/dL. Computed tomography brain showed cortical, cerebellar, and cortical laminar calcification [Figure 1]b. Magnetic resonance imaging (MRI) brain showed symmetrical involvement of thalamus, basal ganglia, external capsule, subcortical white matter, and brainstem in form of hyperintensity on T2-weighted-fluid-attenuated inversion recovery (FLAIR/T2W) images [Figure 1]b. Electroencephalography (EEG) showed intermittent slowing. Motor and sensory conduction studies were normal. | Figure 1: (a): Peripheral smear showing microcytes (black arrow), macrocytes (dotted black arrow), and red cells with basophilic stippling (red arrow). (b): (Top panel): Non-contrast CT brain showing cerebellar (black arrow) and cortical laminar (white arrow) calcifications. (b) (Bottom panel): MRI brain showing the involvement of bilateral brainstem, basal ganglia, thalamus, external capsule, and subcortical white matter
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The patient was started on chelation with D-Penicillamine and correction of hyponatremia was done. He improved in sensorium, however, the neurocognitive assessment revealed impairment in working memory, category fluency, new learning ability, and disturbed expressive speech.
| » Discussion | | |
Lead poisoning is a well-recognized occupational health hazard, especially in the manufacturing of batteries, paints, ammunition, and construction materials.[1] In an earlier study, the majority of battery workers who developed lead toxicity were middle-aged with a job duration of 10–15 years.[2] Our patient is a middle-aged man, engaged in a lead-acid battery manufacturing unit for 15 years. Lead toxicity is more in workers who did not use personal safetywear.[2],[3] Our patient also did not use any protective clothing and used to have food with soiled hands. Blood lead levels increase with longer work shifts, increasing exponentially after 8 h of work.[3] Our patient used to have work shifts of 8 to10 h per day. Smoking has been associated with increased risk of lead toxicity,[2],[3] as seen in our patient. Smoking aggravates lead toxicity due to lack of handwashing before smoking, increased hand to mouth contact, and contamination of cigarettes by airborne lead dust and fumes.[3] In an earlier report, abdominal pain and nausea occurred in 38 and 32 of 40 patients, respectively.[2] Our patient had recurrent abdominal pain and vomiting for 4 long years, for which he had not undergone any evaluation and the present episode was also preceded by acute abdominal colic and vomiting. Around 30% of lead toxicity patients had hypertension in a previous study.[3] Our patient had hypertension for 6 years. This likely is secondary to alterations in the renin-angiotensin-aldosterone system, decreased production of nitric oxide, increase in vasoconstrictors like endothelin-3, or increase in reactive oxygen species with the rise of calcium in endothelial cells.[4] Neurological involvement may be characterized by edema, demyelination, or vascular injury and may manifest as convulsions, ataxia, peripheral neuropathy, cognitive impairment, ataxia, encephalopathy, and coma.[1]
Various patterns of involvement on CT and MR brain imaging have been reported in lead encephalopathy. CT brain imaging in our patient demonstrated cortical laminar and cerebellar calcifications. Reyes et al., have shown intracerebral calcifications in subcortical areas, vermis, cerebellum, and basal ganglia in three American adults who had dementia, peripheral neuropathy, back pain, and dizziness.[5] The patterns of calcifications noted were punctate, curvilinear, speckled, or diffuse.[5] They had normal calcium and phosphorus levels while two had elevated parathyroid hormone. Our patient had a curvilinear pattern of cerebellar and cerebral calcification. Tüzün et al., have reported thalamus, lateral putamen, claustral, and insular hypodensities bilaterally on CT brain in lead poisoning.[6]
MRI changes involve gray matter, subcortical white matter, or cortico-subcortical junction.[7] Occipital involvement is more common, signal changes may be seen in thalamus, basal ganglia, pons, insula, periventricular white matter, or cerebellum. Restricted diffusion along the margin of subcortical areas is rarely reported.[7] Atre et al. reported bilateral symmetrical involvement of the occipital lobe involving the gray-white matter junction, which resolved after chelation therapy.[8] Our patient had a similar picture with extensive changes in basal ganglia, thalamus, brain stem external capsule, and subcortical white matter.
Our patient had an acute presentation due to hyponatremia, which improved after correction of hyponatremia. Hyponatremia might have been due to recurrent episodes of vomiting. Lead is known to cause chronic nephropathy and gout,[9] however, renal function tests and uric acid were normal in our patient. Lead encephalopathy may cause executive dysfunction, short-term memory impairment, and a multitude of psychiatric disturbances like anxiety, depression, and aggression.[10] Our patient had cognitive impairment involving working memory, category fluency, acquisition of new information, calculation difficulty, and disturbed expressive speech. There was no personality or behavior change. Treatment involves avoidance of further exposure and chelation with dimercaprol and succimer or D-Penicillamine,[1] though neurocognitive deficits may persist. Our patient has been advised to avoid further exposure and is on chelation therapy with D-Penicillamine.
| » Conclusion | | |
This case highlights the importance of occupational history and a detailed clinical evaluation in elucidating the etiology of a potentially treatable encephalopathy. Simple clues like lead lines on gums, anemia, and basophilic stippling, may suggest the diagnosis and distinctive imaging findings of intracranial calcifications could assist in the diagnosis.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| » References | | |
| 1. | Kim HC, Jang TW, Chae HJ, Choi WJ, Ha MN, Ye BJ, et al. Evaluation and management of lead exposure. Ann Occup Environ Med. 2015;27:30.  |
| 2. | Basit S, Karim N, Munshi AB. Occupational lead toxicity in battery workers. Pak J Med Sci 2015;31:775-80. |
| 3. | Ahmad SA, Khan MH, Khandker S, Sarwar AF, Yasmin N, Faruquee MH. Blood lead levels and health problems of lead acid battery workers in Bangladesh. Scientific World Journal 2014;2014:974104. doi: 10.1155/2014/974104. |
| 4. | Alghasham AA, Meki AR, Ismail HA. Association of blood lead level with elevated blood pressure in hypertensive patients. Int J Health Sci (Qassim) 2011;5:17-27. |
| 5. | Reyes PF, Gonzalez CF, Zalewska MK, Besarab A. Intracranial calcification in adults with chronic lead exposure. Am J Roentgenol 1986;146:267-70. |
| 6. | Tüzün M, Tüzün D, Salan A, Hekimoğlu B. Lead encephalopathy: CT and MR findings. J Comput Assist Tomogr 2002;26:479-81. |
| 7. | de Souza A, Narvencar KP, Desai PK, D'Costa Z, Nilajkar G. Adult lead encephalopathy. Neurol Res 2013;35:54-8. |
| 8. | 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. |
| 9. | Landrigan PJ, Todd AC. Lead poisoning. West J Med 1994;161:153-9. |
| 10. | Fenga C, Gangemi S, Alibrandi A, Costa C, Micali E. Relationship between lead exposure and mild cognitive impairment. J Prev Med Hyg 2016;57:E205-10. |
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