through the lumen. this mechanism is exploited therapeutically to achieve negative balance in wilson's disease, which involves an excess of copper. diagnosis the diagnosis of copper deficiency may be supported by a person's report of compatible signs and symptoms, findings from a thorough physical examination, and supportive laboratory evidence. low levels of copper and ceruloplasmin in the serum are consistent with the diagnosis as is a low 24 hour urine copper level. additional supportive bloodwork findings also include neutropenia and anemia. mri imaging may demonstrate increased t2 signal of the dorsal column–medial lemniscus pathways. treatment copper deficiency is a very rare disease and is often misdiagnosed several times by physicians before concluding the deficiency of copper through differential diagnosis (copper serum test and bone marrow biopsy are usually conclusive in diagnosing copper deficiency). on average, patients are diagnosed with copper deficiency around 1.1 years after their first symptoms are reported to a physician. copper deficiency can be treated with either oral copper supplementation or intravenous copper. if zinc intoxication is present, discontinuation of zinc may be sufficient to restore copper levels back to normal, but this usually is a very slow process. people with zinc intoxication will usually have to take copper supplements in addition to ceasing zinc consumption. hematological manifestations are often quickly restored back to normal. the progression of the neurological symptoms will be stopped and sometimes improved with appropriate treatment, but residual neurological disability is common.