Copper Deficiency Myelopathy

Kumar, Neeraj; Crum, Brian A.; Petersen, Ronald C.; Vernino, Steven; Ahlskog, J. Eric

doi:10.1001/archneur.61.5.762

Cited by 82 publications

(69 citation statements)

References 18 publications

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“…Low serum copper was identified and the patient showed improvement following copper injections. Our findings were consistent with other case reports [2] and case series where copper deficiency caused such clinical presentation in absence of radiological and hematological findings [1,3].…”

Section: Discussionsupporting

confidence: 93%

Copper Deficiency Myeloneuropathy Mimicking Subacute Combined Degeneration Following Bariatric Surgery

Ismail¹,

Om²,

Ss³

2014

Journal of Neurology and Neurological Disorders

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Section: Discussionsupporting

confidence: 93%

Copper Deficiency Myeloneuropathy Mimicking Subacute Combined Degeneration Following Bariatric Surgery

Ismail¹,

Om²,

Ss³

2014

Journal of Neurology and Neurological Disorders

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“…The absorption of copper in humans takes place in the stomach and proximal duodenum. 1 Copper deficiency is a well-recognized cause of several hematological manifestations, such as normocytic, macrocytic, and rarely microcytic anemia as well as leukopenia, which may have been attributed to myelodysplasia before the copper deficiency state is detected. 2 Given its ubiquitous distribution, dietary deficiency of copper is rare and is commonly secondary to bariatric surgery, malabsorption, and nephrotic syndromes.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, copper deficiency may represent a complication of zinc, penicillamine, alkali therapy, and parenteral nutrition without copper supplementation. 1 However, in a significant percentage of patients the etiology of copper deficiency remains undetermined even after a careful history taking and extensive laboratory researches. Neurological manifestations of copper deficiency have been described only in the last years and can occur even in the absence of blood count abnormalities.…”

Section: Discussionmentioning

confidence: 99%

Copper deficiency myelopathy: A report of two cases

Plantone

Primiano

Renna

et al. 2014

The Journal of Spinal Cord Medicine

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Context: Copper deficiency myelopathy represents an often underdiagnosed, acquired neurological syndrome, clinically characterized by posterior column dysfunction. The main causes of copper deficiency are bariatric surgery, increased consumption of zinc, and malabsorption. However, even after a careful history taking and extensive laboratory researches, the etiology of copper deficiency remains undetermined in a significant percentage of cases. Patients affected by copper deficiency myelopathy usually present with sensory ataxia due to dorsal column dysfunction and sometimes with mild leg spasticity. In such patients, spinal cord magnetic resonance imaging (MRI) may show hyperintense lesions in T2-weighted sequences involving the posterior columns of cervical and thoracic cord. These MRI findings are not distinguishable from those of subacute combined degeneration associated with vitamin B12 deficiency. Findings: Here, we describe two patients with gait ataxia and sensory symptoms in which a diagnosis of copper deficiency myelopathy was made. Both patients showed a significant clinical, neuroradiological, and neurophysiological improvement after proper supplementation therapy. Conclusion: The patients herein described underline the importance to include serum copper and ceruloplasmin levels as part of the myelopathy diagnostic workup, especially in the cases of otherwise unexplained subacute myelopathy involving the posterior columns. Since copper deficiency myelopathy is a progressive syndrome, early diagnosis is mandatory in order to promptly provide a proper supplementation therapy and, thus, prevent an irreversible neurological damage.

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“…5,7,9,10,19,20 The hematologic deficits, however, generally correct within 2 months of beginning treatment.…”

Section: Discussionmentioning

confidence: 99%

Copper Deficiency as Cause of Unexplained Hematologic and Neurologic Deficits in Patient with Prior Gastrointestinal Surgery

Ricker

Muench

2006

The Journal of the American Board of Family Medicine

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Copper is a trace mineral essential to hematopoiesis and to the structure and function of the nervous system. Copper deficiency is a rare cause of anemia, leukopenia, and myeloneuropathy, but should be considered in the differential diagnosis in a patient with prior gastrointestinal surgery. We report the case of a 51-year-old woman admitted for nonspecific neurologic symptoms ultimately found to be due to copper malabsorption. Case ReportsA 51-year-old female presented to the emergency department complaining of numbness and tingling in her distal lower extremities that had progressively worsened over the previous 4 weeks and had begun to affect her fingers 2 days before presentation. In addition, the patient stated that over the past 2 weeks she had experienced a progressively worsening shortness of breath, generalized weakness, fast heartbeat, and light-headedness.She had undergone a gastrectomy 16 years ago with Roux-en-Y and partial small bowel resection for treatment of Zollinger-Ellison syndrome as well as a Whipple procedure for chronic pancreatitis. Since her surgeries, she received vitamin B12 supplementation intramuscularly and was converted to oral supplementation several months before her presentation in the emergency department.On presentation, the patient's vital signs included a temperature of 36.7°C, blood pressure of 121/84, pulse of 80, respiratory rate of 18, oxygen saturation of 100% on room air, and weight of 43.2 kg. Initial neurological evaluation revealed diminished sensitivity to light touch and vibration and decreased proprioception in her toes and ankles. Her Babinski's reflex was positive bilaterally, and her Romberg was strongly positive. Her patellar and brachioradialis deep tendon reflexes were hyperreflexic bilaterally, but Achilles tendon reflexes were normal. Her cranial nerves were intact, and her sensation of pain and temperature were normal. Her motor strength was normal, but she had significant difficulty walking because of her sensory deficits. The physical examination was otherwise unremarkable.Laboratory tests in the emergency department included a hematocrit of 17% (normal range, 33% to 44.6%) with a mean corpuscular volume (MCV) of 105.9 fL (normal range, 80 to 96 fL). At this point, the patient was admitted for management of anemia and further evaluation of neurologic symptoms. She received a transfusion of 2 units of packed red blood cells, which brought her hematocrit up to 27%. She was also started on 100 mcg of vitamin B12 intramuscularly daily and 1 mg of folate orally daily.The patient's neurological and laboratory findings were initially attributed to vitamin B12 or folate deficiency, given her history of gastrointestinal surgery and recent conversion to oral vitamin B12 supplementation. However, her vitamin B12 and folate levels were available by the third day of hospitalization, with a vitamin B12 level of 738 pg/mL (normal range, 200 to 950 pg/mL) and folate level greater than 24 ng/mL (normal level, Ͼ0.9 ng/mL). Methylmalonic acid was 0.77 mol/L (normal lev...

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Copper Deficiency Myelopathy

Abstract: Patients presenting with otherwise unexplained myelopathies should have their serum ceruloplasmin level measured.

Cited by 82 publications

References 18 publications

Copper Deficiency Myeloneuropathy Mimicking Subacute Combined Degeneration Following Bariatric Surgery

Copper Deficiency Myeloneuropathy Mimicking Subacute Combined Degeneration Following Bariatric Surgery

Copper deficiency myelopathy: A report of two cases

Copper Deficiency as Cause of Unexplained Hematologic and Neurologic Deficits in Patient with Prior Gastrointestinal Surgery

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