title: Cervical MRI of subacute myelo-optico-neuropathy.
abstract: METHODS
  Case study.
  
  
  OBJECTIVE
  Subacute myelo-optico-neuropathy (SMON) is a severe neuro-degenerative disorder caused by poisoning due to over-dose and prolonged oral administration of clioquinol; this disorder was more frequent during 1957-1970. It is characterized by axonal degeneration and gliosis in the cervical gracile fasciculus. Recently, copper-deficient myelo-neuropathies presenting similar symptoms (that is, painful dysesthesia/paresthesia in the lower limbs, ataxia, spastic paraplegia, autonomic disorders and visual impairment) were reported. Magnetic resonance imaging (MRI) of these patients detected T2-weighted hyperintensities in the cervical spinal cord. An unbalanced zinc-copper metabolism was suggested as one of the candidate pathogenesis of clioquinol toxicity because of its metal-chelating ability. The aim of this study was to present MRI findings of old SMON patients and to compare them with those of current copper-deficient myelo-neuropathies.
  
  
  METHODS
  Japan.
  
  
  METHODS
  We conducted and analyzed cervical and brain MRIs of seven old SMON patients who contracted the disorder during the 1960s. Serum iron, magnesium, copper, zinc and ceruloplasmin levels were also measured.
  
  
  RESULTS
  Cervical T2-weighted MRIs showed mild volume loss and faint hyperintensities in the dorsal columns, which might reflect residual gliosis. Brain fast fluid-attenuated inversion-recovery images and tractography were normal. Current levels of serum copper and zinc were within almost normal ranges.
  
  
  CONCLUSIONS
  Although fainter, the abnormal T2 MRI signals we observed were similar to and occurred in the same locations as those reported in copper-deficient myelo-neuropathy patients. We suggest that these findings are useful to study the mechanism of clioquinol toxicity before using it to treat neurodegenerative diseases such as Alzheimer's disease.
authors.affiliation: Department of Neurology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan. enkimura@kumamoto-u.ac.jp
authors.forename: E
authors.initials: E
authors.lastname: Kimura
authors.forename: T
authors.initials: T
authors.lastname: Hirano
authors.forename: S
authors.initials: S
authors.lastname: Yamashita
authors.forename: T
authors.initials: T
authors.lastname: Hirai
authors.forename: Y
authors.initials: Y
authors.lastname: Uchida
authors.forename: Y
authors.initials: Y
authors.lastname: Maeda
authors.forename: M
authors.initials: M
authors.lastname: Uchino
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000871:Anthelmintics / Q000506:poisoning; D002614:Chelating Agents / Q000506:poisoning; D007464:Clioquinol / Q000506:poisoning*; D003300:Copper / Q000097:blood / Q000172:deficiency*; D005260:Female; D006801:Humans; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D008875:Middle Aged; D009901:Optic Nerve Diseases / Q000175:diagnosis / Q000209:etiology / Q000473:pathology*; D010523:Peripheral Nervous System Diseases / Q000175:diagnosis / Q000209:etiology / Q000473:pathology*; D013116:Spinal Cord / Q000187:drug effects / Q000473:pathology*; D013118:Spinal Cord Diseases / Q000175:diagnosis / Q000209:etiology / Q000473:pathology*
chemical_list: D000871:Anthelmintics; D002614:Chelating Agents; D003300:Copper; D007464:Clioquinol