DirkUlbricht, Assistant en Neurologie, Centre Hospitalier de Luxembourg[email protected]
Submitted November 25, 2002
I read with great interest the article of Prodan et al. on the CNS
effects of copper deficiency and hyperzincemia. [1] The following points should be made. There is no clarity regarding the timing of the
MRIs or the modalities used. The distribution of lesions closely
resembles arterial borderzone territories and less than typical
demyelinizations at the ventricle border seen in MS. It is unclear whether the MR findings might represent ischemias acquired
during the periods with a really striking anemia. Secondly, we recently
had to switch treatment in a patient with Wilson’s disease who developed
a particular hematological copper deficiency syndrome after resection
of one kidney and nephrotic syndrome three years later. The MRI was
unchanged except for the sequelae of Wilson’s disease. So the MRI changes
may also be associated with the fluctuations induced by the copper
substitution. Was there any improvement in the patients’ neurological
state after hematological normalization (gait disturbances/ataxia/apraxia,
paresthesias)?
References
1. Prodan CI, Holland NR, Wisdom PJ, Burstein SA, Bottomley SS.
CNS demyelination associated with copper deficiency and hyperzincemia.
Neurology 2002; 59: 1453-1456.
I read with great interest the article of Prodan et al. on the CNS effects of copper deficiency and hyperzincemia. [1] The following points should be made. There is no clarity regarding the timing of the MRIs or the modalities used. The distribution of lesions closely resembles arterial borderzone territories and less than typical demyelinizations at the ventricle border seen in MS. It is unclear whether the MR findings might represent ischemias acquired during the periods with a really striking anemia. Secondly, we recently had to switch treatment in a patient with Wilson’s disease who developed a particular hematological copper deficiency syndrome after resection of one kidney and nephrotic syndrome three years later. The MRI was unchanged except for the sequelae of Wilson’s disease. So the MRI changes may also be associated with the fluctuations induced by the copper substitution. Was there any improvement in the patients’ neurological state after hematological normalization (gait disturbances/ataxia/apraxia, paresthesias)?
References
1. Prodan CI, Holland NR, Wisdom PJ, Burstein SA, Bottomley SS. CNS demyelination associated with copper deficiency and hyperzincemia. Neurology 2002; 59: 1453-1456.