Copper deficiency myelopathy is a neurological disorder caused by inadequate copper levels in the body. This acquired condition primarily impacts the nervous system, leading to spinal cord dysfunction. Copper is an important trace metal, serving as a component in enzymes necessary for the proper function of both the nervous system and bone marrow. When copper levels are too low, these vital processes are disrupted, resulting in neurological issues. The condition can resemble other neurological disorders, making accurate diagnosis important.
Understanding the Causes
Copper deficiency myelopathy develops when the body lacks sufficient copper, often due to absorption issues or excessive intake of substances that interfere with copper. A common cause is gastrointestinal surgery, particularly bariatric procedures like gastric bypass. These surgeries alter the digestive tract, reducing the surface area for nutrient absorption, including copper.
Excessive zinc intake can also lead to copper deficiency. Zinc and copper compete for absorption pathways in the small intestine. High levels of zinc induce a protein that traps copper within intestinal cells, preventing its entry into the bloodstream and depleting the body’s copper stores. While dietary copper deficiency is uncommon, malabsorption syndromes such as celiac disease can impair copper uptake.
Other less frequent causes include long-term parenteral nutrition lacking adequate copper supplementation, or certain kidney conditions like nephrotic syndrome, which can lead to excessive copper loss. In some instances, the exact reason for copper deficiency remains undetermined.
Recognizing the Symptoms
Copper deficiency myelopathy primarily affects the nervous system, leading to various neurological symptoms. Individuals often experience difficulties with balance and coordination, manifesting as an unsteady or spastic gait. This occurs because copper deficiency impairs the function of the dorsal columns of the spinal cord, which transmit sensory information.
Numbness and tingling sensations are common, particularly in the arms and legs. Weakness in the limbs can also develop, contributing to mobility issues. While myelopathy refers to spinal cord dysfunction, copper deficiency can also lead to other neurological problems like peripheral neuropathy, affecting nerves outside the brain and spinal cord, and sometimes optic neuropathy.
Beyond neurological signs, copper deficiency can also affect blood cell production. Patients may develop hematological abnormalities such as anemia (reduced red blood cells) or neutropenia (decreased white blood cells). These blood disorders can sometimes occur even before neurological symptoms become apparent.
Diagnosis and Treatment Approaches
Diagnosing copper deficiency myelopathy involves clinical evaluation, laboratory tests, and imaging studies. Blood tests are essential, focusing on measuring serum copper levels and ceruloplasmin. Low levels of both are strong indicators of deficiency. Zinc levels may be checked if excessive intake is suspected, and vitamin B12 levels assessed to rule out other conditions with similar neurological symptoms.
A thorough neurological examination helps assess nerve damage and identify specific neurological deficits. Imaging studies, particularly magnetic resonance imaging (MRI) of the spinal cord, can reveal characteristic changes. These often include signal abnormalities in the posterior columns of the cervical and thoracic spinal cord, which can resemble findings seen in vitamin B12 deficiency. These imaging patterns, combined with clinical presentation and blood test results, help confirm the diagnosis.
Treatment primarily involves copper supplementation to restore adequate levels. Oral copper supplements are the most common approach, with dosage adjusted based on deficiency severity and patient response. In severe cases, an initial brief course of intravenous copper may be considered to rapidly normalize stores before transitioning to oral therapy. Addressing any underlying causes is crucial, which may involve reducing excessive zinc intake, modifying dietary habits, or managing malabsorption issues. Early intervention is important because prompt copper repletion can often halt neurological deterioration and may lead to some symptom improvement, though complete reversal is not always achieved.