Calcium inside the nerve cells (neurons) seems to be crucial in making pain chronic, according to a publication in the journal Neuron by researchers in Heidelberg, Germany. They discovered that in patients with persistent pain, calcium in the spinal cord neurons helps contact other pain-conducting neurons resulting in increased sensitivity to painful stimuli. This may explain how the pain memory is formed.
Chronic pain caused by inflammation, nerve injury, herniated disks, and other causes often leads to a persistent structural change in the nervous system. This pain often persists even after the original cause, such as a herniated disc, is removed. Many chronic pain patients including those with chronic migraine develop allodynia, an increased sensitivity which results in pain from touch and minor pressure. Migraine patients often cannot brush their hair or wear glasses because of such sensitivity. In people with chronic pain, too much calcium inside the neurons that transmit pain makes them react to activation of neurons that normally transmit sensation of touch, heat, and other non-painful sensations. This excess calcium enters the nucleus of the cell where the genetic material is located and it activates certain genes that promote pain. One of the researchers, Prof. Kuner said that “These genes regulated by calcium in the spinal cord are the key to the chronicity of pain, since they can trigger permanent changes.”
Blocking calcium in the cell seems to prevent such increased sensitivity. Mice in which the effect of the calcium in the cell nucleus is blocked did not develop hypersensitivity to painful stimuli or a pain memory despite chronic inflammation.
Interestingly, magnesium is a natural antagonist of calcium and I would speculate that its deficiency may also promote chronic pain.
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