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Progressive encephalopathy due to chronic exposure to lead

Encefalopatia progressiva por exposição crônica ao chumbo

A 70-year-old man reported a 2-year history of progressive gait imbalance and cognitive decline (memory, executive functions, and language impairment). A physical examination revealed spastic ataxia without peripheral involvement. The patient worked with car battery solutions for 40 years, until 13 years ago.11 Landrigan PJ, Todd AC. Lead poisoning. West J Med 1994;161(02): 153–159 He had several hospitalizations due to acute lead poisoning, with levels of lead in the blood and urinary delta-aminolevulinic acid of 162,8 g/dl and 20 mg/U (normal: up to 40 g/dl and 4,5 mg/U) respectively). Recent brain neuroimages showed typical findings of saturnism (▸Figure 1),22 Reyes PF, Gonzalez CF, Zalewska MK, Besarab A. Intracranial calcification in adults with chronic lead exposure. AJR Am J Roentgenol 1986;146(02):267–270 with normal bone profile blood tests. Therefore, chronic lead poisoning should be remembered as an environmental cause of leukoencephalopathy.22 Reyes PF, Gonzalez CF, Zalewska MK, Besarab A. Intracranial calcification in adults with chronic lead exposure. AJR Am J Roentgenol 1986;146(02):267–27055 Shih RA, Glass TA, Bandeen-Roche K, et al. Environmental lead exposure and cognitive function in community-dwelling older adults. Neurology 2006;67(09):1556–1562

Figure 1
Axial non-contrast computed tomography (CT) scan of the brain showing diffuse hypodensity in the deep white matter of both cerebral hemispheres with cerebellar and cerebral subcortical calcifications (A-C). Axial T2/fluid-attenuated inversion recovery (FLAIR) magnetic resonance imaging (MRI) scan showing confluent hypersignal in the periventricular, subcortical, and deep white matter of both cerebral hemispheres (D), the thalamus (E), and the cerebellar hemispheres (F), with hypointense areas involving the basal ganglia (E). Axial gradient echo (GRE) T2-weighted magnetic resonance imaging (MRI) scan showing subcortical white matter (G: arrows) with either microbleeds or mineralization in the basal ganglia (H) and cerebellar hemispheres (I: arrowheads).

References

  • 1
    Landrigan PJ, Todd AC. Lead poisoning. West J Med 1994;161(02): 153–159
  • 2
    Reyes PF, Gonzalez CF, Zalewska MK, Besarab A. Intracranial calcification in adults with chronic lead exposure. AJR Am J Roentgenol 1986;146(02):267–270
  • 3
    Mani J, Chaudhary N, Kanjalkar M, Shah PU. Cerebellar ataxia due to lead encephalopathy in an adult. J Neurol Neurosurg Psychiatry 1998;65(05):797–798
  • 4
    Manto M. Toxic agents causing cerebellar ataxias. Handb Clin Neurol 2012;103:201–213
  • 5
    Shih RA, Glass TA, Bandeen-Roche K, et al. Environmental lead exposure and cognitive function in community-dwelling older adults. Neurology 2006;67(09):1556–1562

Publication Dates

  • Publication in this collection
    09 Jan 2023
  • Date of issue
    2022

History

  • Received
    27 Jan 2022
  • Accepted
    01 May 2022
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