Impaired energy-dependent processes underlie acute lead neuropathy

Authors

  • Arun V. Krishnan MBBS, PhD,

    Corresponding author
    1. Translational Neuroscience Facility, School of Medical Sciences, University of New South Wales, Room 313, Wallace Wurth Building, Sydney, New South Wales 2052, Australia
    • Translational Neuroscience Facility, School of Medical Sciences, University of New South Wales, Room 313, Wallace Wurth Building, Sydney, New South Wales 2052, Australia
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  • Susanna B. Park PhD,

    1. Neuroscience Research Australia and Prince of Wales Clinical School, University of New South Wales, Sydney, Australia
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  • William Huynh MBBS,

    1. Neuroscience Research Australia and Prince of Wales Clinical School, University of New South Wales, Sydney, Australia
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  • Cindy S.-Y. Lin PhD,

    1. Translational Neuroscience Facility, School of Medical Sciences, University of New South Wales, Room 313, Wallace Wurth Building, Sydney, New South Wales 2052, Australia
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  • Robert D. Henderson MBBS, PhD,

    1. Department of Neurology, Royal Brisbane Hospital, Brisbane, Australia
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  • Matthew C. Kiernan MBBS, DSc

    1. Neuroscience Research Australia and Prince of Wales Clinical School, University of New South Wales, Sydney, Australia
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Abstract

Introduction:

The mechanisms of lead neuropathy remain unexplained. A 48-year-old painter presented after undertaking a 3-week project of paint removal without the use of a protective mask. Two weeks later, he developed fasciculations, weakness, and muscle wasting. Nerve conduction studies demonstrated a motor neuropathy. A high serum lead level was identified, leading to a diagnosis of acute lead neuropathy.

Methods:

To investigate the pathophysiology, nerve excitability studies were undertaken acutely and in convalescence. Studies were undertaken at baseline and after the induction of limb ischemia.

Results:

Prominent abnormalities of excitability were noted, including a rightward shift of stimulus–response curves, reduction in depolarizing threshold electrotonus, and increased refractoriness. These changes became more severe with limb ischemia, and there was abolition of the superexcitable period and increased refractoriness.

Conclusions:

We identified prominent changes in nerve excitability in lead neuropathy. The results suggest that there is impairment of axonal energy-dependent processes in lead neuropathy. Muscle Nerve, 2012

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