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Positron Emission Tomography Using 64-Copper as a Tracer for the Study of Copper-Related Disorders
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[Acquired copper deficiency myelopathy].

D Videt-Gibou1, S Belliard, J Rivalan

  • 1Service de neurologie, CHU Pontchaillou, rue Henri-Le-Guilloux, Rennes, France.

Revue Neurologique
|May 15, 2010
PubMed
Summary

Acquired copper deficiency can cause neurological issues like myeloneuropathy. Early copper supplementation may improve symptoms, even if delayed, and nephrotic syndrome is a potential complication.

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Area of Science:

  • Neurology
  • Hematology
  • Nephrology

Background:

  • Acquired copper deficiency presents with known hematological issues and emerging neurological manifestations.
  • Neurological symptoms include myeloneuropathy, sensory ataxia, and spastic gait, with electrophysiological and MRI findings indicating axonal sensorimotor neuropathy and dorsal column changes.
  • Causes include gastric surgery, excessive zinc, and malabsorption, though often idiopathic; early intervention is key to preventing deterioration.

Observation:

  • Two cases of acquired copper deficiency myeloneuropathy are presented, one with concurrent nephrotic syndrome and another with iron overload.
  • Treatment with copper supplementation resolved biological abnormalities.
  • One patient experienced significant neurological recovery, including ataxia resolution, after eight months of supplementation.

Findings:

  • Nephrotic syndrome may be an additional complication of acquired copper deficiency.
  • Delayed treatment does not invariably lead to poor neurological outcomes.
  • Copper supplementation can lead to significant neurological improvement.

Implications:

  • Highlights nephrotic syndrome as a potential consequence of acquired copper deficiency.
  • Suggests that neurological recovery from copper deficiency myeloneuropathy is possible even with delayed treatment.
  • Emphasizes the therapeutic potential of copper supplementation for neurological recovery.