GM-M Bumoko1, NH Sadiki2, A Rwatambuga7, K.P. Kayembe2, DL Okitundu1, Mumba Ngoyi, D3,4, J-JT Muyembe3,4, J-P Banea5, MJ Boivin6, and D Tshala-Katumbay1,4,7

1Department of Neurology, University of Kinshasa, Kinshasa, Congo-Kinshasa
2School of Public Health, University of Kinshasa, Congo-Kinshasa
3Department of Tropical Medicine, University of Kinshasa, Congo-Kinshasa
4Institut National de Recherches Biomedicales, Kinshasa, Congo-Kinshasa
5Department of Nutrition, School of Public Health & National Nutrition Program, Ministry of Health,
Kinshasa, Congo-Kinshasa
6Department of Psychiatry and Neurology/Ophthalmology, Michigan State University, East
Lansing, Michigan, USA
7Oregon Institute of Occupational Health Sciences and Department of Neurology, Oregon Health
& Science University, Portland, Oregon, USA

NIH-PA Author Manuscript

Published in final edited form as:
J Neurol Sci. 2015 February 15; 349(0): 149–153. doi:10.1016/j.jns.2015.01.007.

Abstract
We assessed the relationship between key trace elements and neurocognitive and motor impairments observed in konzo, a motor neuron disease associated with cassava cyanogenic exposure in nutritionally challenged African children. Serum concentrations of iron, copper, zinc, selenium, and neurotoxic lead, mercury, manganese, cadmium, and cobalt were measured in 123 konzo children (mean age 8.53 years) and 87 non-konzo children (mean age 9.07 years) using inductively coupled plasma mass spectrometry (ICPMS). Concentrations of trace elements were compared and related to performance scores on the Kaufman Assessment Battery for Children, 2nd edition (KABC-II) for cognition and Bruininks-Oseretsky Test, 2nd edition (BOT-2) for motor proficiency. Children with konzo had low levels of selenium, copper, and zinc relative to controls.
Selenium concentration significantly correlated with serum 8,12-iso-iPF2α-VI isoprostane (spearman r = 0.75, p < 0.01) and BOT-2 scores (r = 0.31, p = 0.00) in children with konzo.
Elemental deficiency was not associated with poor cognition. Mean (SD) urinary levels of thiocyanate were 388.03 (221.75) μmol/l in non-konzo compared to 518.59 (354.19) μmol/l in konzo children (p < 0.01). Motor deficits associated with konzo may possibly be driven by the combined effects of cyanide toxicity and Se deficiency on prooxidant mechanisms. Strategies to prevent konzo may include dietary supplementation with trace elements, preferentially, those with antioxidant and cyanide-scavenging properties.