Wise Young
02-15-2005, 09:34 PM
From a post by Sherman Bryton (http://carecure.org/forum/showthread.php?t=21142)
Dr. Young-
I apologize for these 2 very elementery questions-
- in order to restore sensation, that is if you stepped on a nail, is replacing the axons or neurons at the damaged spinal cord site all that is needed? Would communication be restored, or does there have to be re-growth out of the spinal cord and down the peripheral nerves, down to the foot?
- The term, " infarction". If somebody has an infarct to their arm or leg for instance due to trauma or injury, what are the potential repercussions? Is having a spinal avm which forms an abnormal communication between the anterior spinal artery to a vein without the prerequisite capillaries, resulting in an increase in pressure gradient, and the draining spinal veins, the same thing or result as infarction? Would a cord surface avm causing venous dilation and pressure be attributible to an infarction, or just ischemia?
Sherman,
Don't apologize. Your questions are neither elementary nor trivial. Let me try to answer them.
1. Sensory neurons, interneurons, and motoneurons. Sensory axons come from two places: the dorsal root sensory ganglia (DRG) and spinal neurons in the dorsal horn of the spinal cord. Axons are "replaced" but regrown from neurons. If the neurons are gone, then you have to replace the neurons. Let me first try to describe in words where the sensory axons come from and where they go, as well as interneurons in the spinal cord. I drew a crude picture to illustrate below.
The DRG neurons are situated just outside the spinal column. The ganglia look like a little pimple on the nerves entering the cord. DRG neurons have axons that bifurcate, forming two branches. The peripheral branch goes to the skin, bone, and muscle, to collect sensory information. The central branch goes into the spinal cord and bifurcates into a branch that goes into the gray matter of the spinal cord. One branch makes a synapse with the sensory neurons in the dorsal horn of the spinal cord while the other branch goes into the dorsal columns which goes all the way to the brainstem where it makes synapses with the dorsal column nuclei. The dorsal column nuclei then send axons cross the midline and go to the thalamus in the brain. The dorsal column axons carry most proprioceptive information, i.e. touch and position sense. They are without any question the largest cells in the body. Some of them stretch from your toes to your brain. In a whale, the axons may be as long as 100 feet. The peripheral sensory axons would not be affected by a spinal cord infarct.
Spinal sensory interneurons are located in the dorsal horn of the gray matter in the spinal cord. They send axons that cross the midline in the spinal cord and ascend in the lateral spinocortical tract to the brain. They carry mostly pain and temperature sensations. Most of the spinal sensory interneurons also send axons to the motoneurons. They are what cause reflexive movements, i.e. the knee or ankle jerk.
ยช Inhibitory spinal interneurons are located in the middle part of the spinal cord and receive signals from the brain as well as sensory signals from the dorsal root ganglia axons. When spinal cord injury reduces the signals from brain to the inhibitory interneurons, one gets enhanced reflex activity or spasticity.
Motoneurons are located in the ventral horn of your spinal gray matter. They send their axons out the ventral root into the peripheral nerve and innervate muscle. A spinal cord infarction will damage motoneurons. When the motoneurons die, their axons of course will also die. Therefore, when one replaces the motoneurons, the motoneurons have to send their axons out the ventral root and grow in the peripheral nerve all the way back to the muscle. If you still have spasticity in a given muscle, that means that some of your motoneurons are not dead. By the way, a lot of people assume that flaccidity means that motoneurons are dead but that may not necessarily be true. It is possible that the motoneurons are alive but inactive. You can, for example, make yourself flaccid by damaging the spinal neurons that are responsible for reflexes, depriving the motoneurons of excitatory input and thereby reducing motoneurons activity.
2. Infarction. Ischemia usually does not affect axons as much as they do neuronal cell bodies. The oligodendroglial cells that myelinate axons tend to be damaged by ischemia but they usually regenerate. Likewise, Schwann cells that myelinate peripheral axons may be injured by ischemia (from compressing the nerves) but the axons themselves are usually not damaged unless the compression is very long and severe. The term infarction usually means severe tissue damage. So, in your case, I expect that you have mostly gray matter damage that probably affected the neurons in your lumbosacral spinal cord. If so, you should have less pain and temperature sensation but have some intact touch and position sense.
3. Arteriovenous malformations damage the spinal cord in two ways. First, because the blood goes directly from the artery to the vein, it "steals" blood from the spinal cord. So, your spinal cord was not functioning well due to lack of blood flow. Second, the arterial pressure goes directly into the veins, increasing venous pressure and causing them to dilate. Third, ischemia itself causes the spinal cord to swell. Combined with the pressure of the dilated veins, this reduces blood flow to the spinal cord further. So, all of these factors probably contributed to severe ischemia that probably killed a bunch of neurons in your lumbosacral cord.
So, spinal cord ischemia will damage neurons that are inside the spinal cord. Severe ischemia may affect axons that are passing through the spinal cord but axons tend to be more resistant to ischemia than cells. Dorsal root ganglion neurons and the peripheral branches of their axons are not likely to be affected by ischemia. Motoneurons are sensitive to ischemia. If they die, their axons also die. If motoneurons are replaced, they must send axons out the ventral root to the muscles if they are to replace the function of motoneurons.
Dr. Young-
I apologize for these 2 very elementery questions-
- in order to restore sensation, that is if you stepped on a nail, is replacing the axons or neurons at the damaged spinal cord site all that is needed? Would communication be restored, or does there have to be re-growth out of the spinal cord and down the peripheral nerves, down to the foot?
- The term, " infarction". If somebody has an infarct to their arm or leg for instance due to trauma or injury, what are the potential repercussions? Is having a spinal avm which forms an abnormal communication between the anterior spinal artery to a vein without the prerequisite capillaries, resulting in an increase in pressure gradient, and the draining spinal veins, the same thing or result as infarction? Would a cord surface avm causing venous dilation and pressure be attributible to an infarction, or just ischemia?
Sherman,
Don't apologize. Your questions are neither elementary nor trivial. Let me try to answer them.
1. Sensory neurons, interneurons, and motoneurons. Sensory axons come from two places: the dorsal root sensory ganglia (DRG) and spinal neurons in the dorsal horn of the spinal cord. Axons are "replaced" but regrown from neurons. If the neurons are gone, then you have to replace the neurons. Let me first try to describe in words where the sensory axons come from and where they go, as well as interneurons in the spinal cord. I drew a crude picture to illustrate below.
The DRG neurons are situated just outside the spinal column. The ganglia look like a little pimple on the nerves entering the cord. DRG neurons have axons that bifurcate, forming two branches. The peripheral branch goes to the skin, bone, and muscle, to collect sensory information. The central branch goes into the spinal cord and bifurcates into a branch that goes into the gray matter of the spinal cord. One branch makes a synapse with the sensory neurons in the dorsal horn of the spinal cord while the other branch goes into the dorsal columns which goes all the way to the brainstem where it makes synapses with the dorsal column nuclei. The dorsal column nuclei then send axons cross the midline and go to the thalamus in the brain. The dorsal column axons carry most proprioceptive information, i.e. touch and position sense. They are without any question the largest cells in the body. Some of them stretch from your toes to your brain. In a whale, the axons may be as long as 100 feet. The peripheral sensory axons would not be affected by a spinal cord infarct.
Spinal sensory interneurons are located in the dorsal horn of the gray matter in the spinal cord. They send axons that cross the midline in the spinal cord and ascend in the lateral spinocortical tract to the brain. They carry mostly pain and temperature sensations. Most of the spinal sensory interneurons also send axons to the motoneurons. They are what cause reflexive movements, i.e. the knee or ankle jerk.
ยช Inhibitory spinal interneurons are located in the middle part of the spinal cord and receive signals from the brain as well as sensory signals from the dorsal root ganglia axons. When spinal cord injury reduces the signals from brain to the inhibitory interneurons, one gets enhanced reflex activity or spasticity.
Motoneurons are located in the ventral horn of your spinal gray matter. They send their axons out the ventral root into the peripheral nerve and innervate muscle. A spinal cord infarction will damage motoneurons. When the motoneurons die, their axons of course will also die. Therefore, when one replaces the motoneurons, the motoneurons have to send their axons out the ventral root and grow in the peripheral nerve all the way back to the muscle. If you still have spasticity in a given muscle, that means that some of your motoneurons are not dead. By the way, a lot of people assume that flaccidity means that motoneurons are dead but that may not necessarily be true. It is possible that the motoneurons are alive but inactive. You can, for example, make yourself flaccid by damaging the spinal neurons that are responsible for reflexes, depriving the motoneurons of excitatory input and thereby reducing motoneurons activity.
2. Infarction. Ischemia usually does not affect axons as much as they do neuronal cell bodies. The oligodendroglial cells that myelinate axons tend to be damaged by ischemia but they usually regenerate. Likewise, Schwann cells that myelinate peripheral axons may be injured by ischemia (from compressing the nerves) but the axons themselves are usually not damaged unless the compression is very long and severe. The term infarction usually means severe tissue damage. So, in your case, I expect that you have mostly gray matter damage that probably affected the neurons in your lumbosacral spinal cord. If so, you should have less pain and temperature sensation but have some intact touch and position sense.
3. Arteriovenous malformations damage the spinal cord in two ways. First, because the blood goes directly from the artery to the vein, it "steals" blood from the spinal cord. So, your spinal cord was not functioning well due to lack of blood flow. Second, the arterial pressure goes directly into the veins, increasing venous pressure and causing them to dilate. Third, ischemia itself causes the spinal cord to swell. Combined with the pressure of the dilated veins, this reduces blood flow to the spinal cord further. So, all of these factors probably contributed to severe ischemia that probably killed a bunch of neurons in your lumbosacral cord.
So, spinal cord ischemia will damage neurons that are inside the spinal cord. Severe ischemia may affect axons that are passing through the spinal cord but axons tend to be more resistant to ischemia than cells. Dorsal root ganglion neurons and the peripheral branches of their axons are not likely to be affected by ischemia. Motoneurons are sensitive to ischemia. If they die, their axons also die. If motoneurons are replaced, they must send axons out the ventral root to the muscles if they are to replace the function of motoneurons.