Post by Tmasgio on Aug 19, 2008 6:58:18 GMT -6
I have often wondered why some people with a spinal cord injury have Nerve pain while others do not. I read this wonderful explanation by Dr. Wise Young with Rutgers University.
Dr. Youngs explanation:
It was only since the mid-1990’s that doctors even accepted that such pains are real, instead of “phantom” or “imaginary” pain. However, doctors and of course people with injuries have known about this pain for most of history. Because nobody had an explanation for it, doctors dismissed it as being imaginary.
The pain is real and it comes from neurons in your spinal cord or brain. It occurs when people lost sensory input. So, if you cut a peripheral nerve (or cut off a leg), the loss of sensory input result in the appearance of neuropathic pain, usually in the area where sensation was lost. It happens with diabetic neuropathy, where there is degeneration of sensory fibers. It occurs after damage to the brain, such as after a stroke.
When you damage the sensory fibers (axons) to the spinal cord, the axons become disconnected from the neurons and surrounding axons that have not been injured sprout additional branches and fill in the vacated spots on the neurons. In the process, the neuron becomes hyperexcitable (overexcitable) and fire burst of action potentials (the signals that neurons use to communicate with each other. These bursts are regarded by the brain as pain.
Most of the drugs that are being used to treat neuropathic pain were initially developed as anti-epileptic drugs that reduce spontaneous activity of neurons. So, the pain is a result of abnormal activities of the neurons that are relaying signals to the brain. Studies of denervated neurons suggest that they do become hyperexcitable.
Gunshot wound induced spinal cord injury does have a higher incidence of neuropathic pain than other causes of spinal cord injury. One possibility is that gunshot wounds has a propensity to damage some fibers and leave others intact, resulting in a higher likelihood of sprouting axons that can contribute to pain. Another possibility is that the bullet is more inflammatory and inflammation is known to make neurons hyperexcitable.
In animal studies, we have found that given rats high-dose methylprednisolone reduces the development of neuropathic pain behavior. Methylprednisolone is well known to suppress sprouting of axons. However, because the National Acute Spinal Cord Injury Study (NASCIS) trial did not include patients with gunshot wounds (because surgeons were pessimistic that these cases will respond to any therapy), we could not recommend methylprednisolone to people with gunshot wounds.
A majority of people with gunshot wounds don't get methylprednisolone and I wonder sometimes whether this is because they are not getting methylprednisolone. For that reason, I have started another topic that asks who has neuropathic pain and received or did not receive methylpednisolone. I presume that you did not.
Regardless of the cause, the treatment is similar at the present. The first line of therapy is amytryptiline (Elavil). Then gabapentin (neurontin). If gabapentin doesn’t work, most doctors try Lyrica. Cannabinoids have been reported by many to be beneficial. Finally, if all else fails, opioids may work but very high doses are needed and fentanyl patches are popular.
There is likely to be future therapies that manipulate the excitability of neurons genetically, changing expression of ionic channels.
Dr. Youngs explanation:
It was only since the mid-1990’s that doctors even accepted that such pains are real, instead of “phantom” or “imaginary” pain. However, doctors and of course people with injuries have known about this pain for most of history. Because nobody had an explanation for it, doctors dismissed it as being imaginary.
The pain is real and it comes from neurons in your spinal cord or brain. It occurs when people lost sensory input. So, if you cut a peripheral nerve (or cut off a leg), the loss of sensory input result in the appearance of neuropathic pain, usually in the area where sensation was lost. It happens with diabetic neuropathy, where there is degeneration of sensory fibers. It occurs after damage to the brain, such as after a stroke.
When you damage the sensory fibers (axons) to the spinal cord, the axons become disconnected from the neurons and surrounding axons that have not been injured sprout additional branches and fill in the vacated spots on the neurons. In the process, the neuron becomes hyperexcitable (overexcitable) and fire burst of action potentials (the signals that neurons use to communicate with each other. These bursts are regarded by the brain as pain.
Most of the drugs that are being used to treat neuropathic pain were initially developed as anti-epileptic drugs that reduce spontaneous activity of neurons. So, the pain is a result of abnormal activities of the neurons that are relaying signals to the brain. Studies of denervated neurons suggest that they do become hyperexcitable.
Gunshot wound induced spinal cord injury does have a higher incidence of neuropathic pain than other causes of spinal cord injury. One possibility is that gunshot wounds has a propensity to damage some fibers and leave others intact, resulting in a higher likelihood of sprouting axons that can contribute to pain. Another possibility is that the bullet is more inflammatory and inflammation is known to make neurons hyperexcitable.
In animal studies, we have found that given rats high-dose methylprednisolone reduces the development of neuropathic pain behavior. Methylprednisolone is well known to suppress sprouting of axons. However, because the National Acute Spinal Cord Injury Study (NASCIS) trial did not include patients with gunshot wounds (because surgeons were pessimistic that these cases will respond to any therapy), we could not recommend methylprednisolone to people with gunshot wounds.
A majority of people with gunshot wounds don't get methylprednisolone and I wonder sometimes whether this is because they are not getting methylprednisolone. For that reason, I have started another topic that asks who has neuropathic pain and received or did not receive methylpednisolone. I presume that you did not.
Regardless of the cause, the treatment is similar at the present. The first line of therapy is amytryptiline (Elavil). Then gabapentin (neurontin). If gabapentin doesn’t work, most doctors try Lyrica. Cannabinoids have been reported by many to be beneficial. Finally, if all else fails, opioids may work but very high doses are needed and fentanyl patches are popular.
There is likely to be future therapies that manipulate the excitability of neurons genetically, changing expression of ionic channels.
