Myeloneuropathy due to copper deficiency

Clinical and MRI findings after copper supplementation

Laura Bolamperti, Maurizio A. Leone, Alessandro Stecco, Monica Reggiani, Mario Pirisi, Alessandro Carriero, Francesco Monaco

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Acquired copper deficiency constitutes an under-recognised cause of myelopathy. Aim of the study was to describe the clinical and imaging features at admission and after copper supplementation of a patient with acquired copper deficiency myeloneuropathy. A 73-year-old woman presented with anaemia and signs of posterior column dysfunction. Somatosensory evoked potentials showed impaired central pathway conduction. Serum copper and caeruloplasmin levels were low. Nerve conduction assessment revealed axonal polyneuropathy. Spinal magnetic resonance imaging (MRI) showed posterior column hyperintensity. Diffusion tensor imaging disclosed decreased fractional anisotropy (FA) corresponding to the hyperintensity. Copper supplementation normalised the haematological picture, whereas vibratory sensitivity was only slightly improved. Control MRI revealed a slight hyperintensity at C1-C2 level; FA values normalised. In conclusion, in acquired copper-deficiency-associated myelopathy, correction of blood and MRI alterations precedes that of neurological manifestations, which may remain suboptimal.

Original languageEnglish
Pages (from-to)521-524
Number of pages4
JournalNeurological Sciences
Volume30
Issue number6
DOIs
Publication statusPublished - Dec 2009

Fingerprint

Copper
Magnetic Resonance Imaging
Spinal Cord Diseases
Anisotropy
Ceruloplasmin
Diffusion Tensor Imaging
Somatosensory Evoked Potentials
Polyneuropathies
Neural Conduction
Neurologic Manifestations
Anemia
Serum

Keywords

  • Copper deficiency
  • Magnetic resonance imaging
  • Myelopathy
  • Neuropathy
  • Subacute combined degeneration

ASJC Scopus subject areas

  • Clinical Neurology
  • Psychiatry and Mental health
  • Dermatology

Cite this

Myeloneuropathy due to copper deficiency : Clinical and MRI findings after copper supplementation. / Bolamperti, Laura; Leone, Maurizio A.; Stecco, Alessandro; Reggiani, Monica; Pirisi, Mario; Carriero, Alessandro; Monaco, Francesco.

In: Neurological Sciences, Vol. 30, No. 6, 12.2009, p. 521-524.

Research output: Contribution to journalArticle

Bolamperti, L, Leone, MA, Stecco, A, Reggiani, M, Pirisi, M, Carriero, A & Monaco, F 2009, 'Myeloneuropathy due to copper deficiency: Clinical and MRI findings after copper supplementation', Neurological Sciences, vol. 30, no. 6, pp. 521-524. https://doi.org/10.1007/s10072-009-0126-7
Bolamperti, Laura ; Leone, Maurizio A. ; Stecco, Alessandro ; Reggiani, Monica ; Pirisi, Mario ; Carriero, Alessandro ; Monaco, Francesco. / Myeloneuropathy due to copper deficiency : Clinical and MRI findings after copper supplementation. In: Neurological Sciences. 2009 ; Vol. 30, No. 6. pp. 521-524.
@article{635760d7f332407c98f8e4e0f7a86f28,
title = "Myeloneuropathy due to copper deficiency: Clinical and MRI findings after copper supplementation",
abstract = "Acquired copper deficiency constitutes an under-recognised cause of myelopathy. Aim of the study was to describe the clinical and imaging features at admission and after copper supplementation of a patient with acquired copper deficiency myeloneuropathy. A 73-year-old woman presented with anaemia and signs of posterior column dysfunction. Somatosensory evoked potentials showed impaired central pathway conduction. Serum copper and caeruloplasmin levels were low. Nerve conduction assessment revealed axonal polyneuropathy. Spinal magnetic resonance imaging (MRI) showed posterior column hyperintensity. Diffusion tensor imaging disclosed decreased fractional anisotropy (FA) corresponding to the hyperintensity. Copper supplementation normalised the haematological picture, whereas vibratory sensitivity was only slightly improved. Control MRI revealed a slight hyperintensity at C1-C2 level; FA values normalised. In conclusion, in acquired copper-deficiency-associated myelopathy, correction of blood and MRI alterations precedes that of neurological manifestations, which may remain suboptimal.",
keywords = "Copper deficiency, Magnetic resonance imaging, Myelopathy, Neuropathy, Subacute combined degeneration",
author = "Laura Bolamperti and Leone, {Maurizio A.} and Alessandro Stecco and Monica Reggiani and Mario Pirisi and Alessandro Carriero and Francesco Monaco",
year = "2009",
month = "12",
doi = "10.1007/s10072-009-0126-7",
language = "English",
volume = "30",
pages = "521--524",
journal = "Neurological Sciences",
issn = "1590-1874",
publisher = "Springer-Verlag Italia s.r.l.",
number = "6",

}

TY - JOUR

T1 - Myeloneuropathy due to copper deficiency

T2 - Clinical and MRI findings after copper supplementation

AU - Bolamperti, Laura

AU - Leone, Maurizio A.

AU - Stecco, Alessandro

AU - Reggiani, Monica

AU - Pirisi, Mario

AU - Carriero, Alessandro

AU - Monaco, Francesco

PY - 2009/12

Y1 - 2009/12

N2 - Acquired copper deficiency constitutes an under-recognised cause of myelopathy. Aim of the study was to describe the clinical and imaging features at admission and after copper supplementation of a patient with acquired copper deficiency myeloneuropathy. A 73-year-old woman presented with anaemia and signs of posterior column dysfunction. Somatosensory evoked potentials showed impaired central pathway conduction. Serum copper and caeruloplasmin levels were low. Nerve conduction assessment revealed axonal polyneuropathy. Spinal magnetic resonance imaging (MRI) showed posterior column hyperintensity. Diffusion tensor imaging disclosed decreased fractional anisotropy (FA) corresponding to the hyperintensity. Copper supplementation normalised the haematological picture, whereas vibratory sensitivity was only slightly improved. Control MRI revealed a slight hyperintensity at C1-C2 level; FA values normalised. In conclusion, in acquired copper-deficiency-associated myelopathy, correction of blood and MRI alterations precedes that of neurological manifestations, which may remain suboptimal.

AB - Acquired copper deficiency constitutes an under-recognised cause of myelopathy. Aim of the study was to describe the clinical and imaging features at admission and after copper supplementation of a patient with acquired copper deficiency myeloneuropathy. A 73-year-old woman presented with anaemia and signs of posterior column dysfunction. Somatosensory evoked potentials showed impaired central pathway conduction. Serum copper and caeruloplasmin levels were low. Nerve conduction assessment revealed axonal polyneuropathy. Spinal magnetic resonance imaging (MRI) showed posterior column hyperintensity. Diffusion tensor imaging disclosed decreased fractional anisotropy (FA) corresponding to the hyperintensity. Copper supplementation normalised the haematological picture, whereas vibratory sensitivity was only slightly improved. Control MRI revealed a slight hyperintensity at C1-C2 level; FA values normalised. In conclusion, in acquired copper-deficiency-associated myelopathy, correction of blood and MRI alterations precedes that of neurological manifestations, which may remain suboptimal.

KW - Copper deficiency

KW - Magnetic resonance imaging

KW - Myelopathy

KW - Neuropathy

KW - Subacute combined degeneration

UR - http://www.scopus.com/inward/record.url?scp=70449533093&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=70449533093&partnerID=8YFLogxK

U2 - 10.1007/s10072-009-0126-7

DO - 10.1007/s10072-009-0126-7

M3 - Article

VL - 30

SP - 521

EP - 524

JO - Neurological Sciences

JF - Neurological Sciences

SN - 1590-1874

IS - 6

ER -