What to do with conus spinal cord injury

[Wise Young]

Sherman Brayton posts:

Dr. Young-

If my spasticity originates in the muscles that I can contract voluntarily, that is the thigh muscles I got back after spinal shock and my spinal embolization, does this differ from someone having spasticity in muscles they cannot move voluntarily?
With my injury, paralysis seems to originate in the anal and saddle area. So if I had a anterior spinal avm just above the Conus, what cellular structures were most likely damaged from the prolonged ischemia from the venous congestion on the surface of the Pial spinal cord? It sometimes feel to me that my SCI is soo low, that it is not affecting my back, but the buttocks on down. Spasticity is strong until below the knees, especially with my right foot, where things get more flaccid and a case of footdrop remains. The left foot has some voluntary movement recovery, not so much individual toe movements, but the ability to bend my whole row of toes down, with a sliver of foot muscle aiding the push. The left foot is the complete opposite of my right's foot drop. The foot is hyper sensitive to touch, it tends to bend upwards. Flickers of sensation ( sometimes super, super sensitive to light touch, or tickle ) are all around the bottom of both feet and toes. Bowel and bladder routine still need care and catheterization, with my inability to fully void without a catheter. I can however flex one of my glutes on the left buttock, but I am not sure that this is the same as being able to provide an "anal wink". So I can still be considered an ASIA A patient. The mere fact that I can move once unmovable muscles below my injury, but cannot feel my anal area, puts me in a classification ( ASIA A ) that excludes me from many potential future trials, one being the treadmill harness bit. With such a low injury baring the marks of a complete SCI, bearing witness to exclusion criteria, this is why I am soo negative all the time. Dr. Young- when ischemia turns into spinal infarction over a prolonged period of time ( 4 weeks ), but under hospital care, given steroids for weeks and weeks until embolization restored adequate blood flow by obliterating the fistula, how much additional tissue is destroyed after the first day of paralysis? I mean that does all that time result in adding insult to injury, or are the nerves really damaged within the first few days, and after that they are all dead anyway? Or did the delay in receiving the embolization cause tissue death to spread and perhaps kill most neurons in the area for good? I remember the interventional neuroradiologist at NYU Med telling me, "that there might be some live tissue down there". This concerns me because it leads me to believe that the Conus area was damaged, and the majority of the tissue from the Conus down was destroyed, leaving me not with a sci with healthy tissue below the injury, like say a T6 sci, but a sci which really is full tissue death to the Conus area, with no cord below due to it's termination below the Conus.

Sherman,

I have started a new topic to address your question originally posted in another topic.

Your question is complex but let me start by saying that there is no point in agonizing over what happened and that the important issue is what you have and what it will take to restore function. I am not sure what happened except that ischemia damaged portions of your lower spinal cord from L1-S5. The conus contains most of the sacral neurons, including ones that innervate the foot (S1), bladder and penis (S2-3), and anal regions (S4-5). Please understand that the ASIA classification system does not predict functional recovery in cases like yours. I think that you need to be examined by a experienced neurologist/physiatrist to determine the distribution of your damage. One person that I recommend highly is John Ditunno at Jefferson in Philadelphia. At this point in your life, the cause is not as important as the solutions.

Let me begin by trying to guess what your level of injury is based on your description. You probably have had scattered gray matter damage to both your lumbar and sacral spinal cord. Your gluteal muscles are innervated by your L5, S1, S2 muscles. So, at least on your left side, you have some function in L5. The fact that you can move your left foot including some toes confirm that you have S1 on that side as well. Based on your description, I suspect that you have probably an S2 sensory level. Can you feel when your bladder is full? The fact that you seem to have some ability to avoid, even incompletely, suggest that part of left S2 is intact. Finally, the fact that your right foot is weak while your left foot shows some voluntary movement suggest that the you have had more damage to your right S1-S5 than your left. The fact that your left foot shows spasticity (toes moving up) suggest that you have preservation of your left L5-S1 motoneurons. Finally, while you do not say what is happening with your hip flexors and quadriceps, I presume that you can contract these on both sides, suggesting that most of your lumbar spinal cord is intact. So, in summary, I would guess that you have what would be equivalent to a left S1 level and perhaps right L4 level.

So, if I were you, what would I do.
1. 4-aminopyridine. Ischemia damages a variety of cells in the spinal cord. It can also cause demyelination. So, the first thing that I would probably try is 4-aminopyridine. This is a drug that increases conduction in demyelinated axons. You can get it from compounding pharmacies. It would be of interest to see what additional sensations you get back. If you do get back additional sensory or motor function, it would strongly suggest that demyelination is part of your problem and remyelination therapy may help.
2. Walking exercise. You seem to have some proximal limb muscular control. So, you should be able to stand and walk. You would have to use a ankle-foot orthosis to lift your right foot but you can be able to avoid all of these by using something like the Glider 6000 which allows you to stand and walk without such prostheses. In China, they just used an elastic band to hold up the foot while stepping and a rolling frame to support weight. I was impressed by these devices and how much standing and walking the patients were doing in Kunming.
3. Reduce bladder spasticity. You sound as if you can initiate voiding even though it is not complete. You need to find out why this is the case, whether the sphincter is closing or the bladder is not contracting fully. There are now peripheral nerve bridging procedures using peripheral nerves to connect the pudendal nerves to the thoracic spinal cord, with reported successes. I think that these are not appropriate for you at the present and should only be applied as a last resort because they may produce irreversible peripheral nerve changes. I would try to figure out the best balance between bladder spasticity and control.
4. Swimming. This is probably the cheapest and the most effective way of getting on your feet, exercising your cardiovascular system, and reverse "learned non-use". I strongly suggest that you do this. This will also allow you to work out your upper body.
5. Keep a close eye on the stem cell research. At the present, embryonic stem cells are the only ones that have produced motoneurons in the spinal cord. Olfactory ensheating glial cells may promote remyelination and regeneration. You might have to wait a year or two before these trials get started in the United States. I hope that the confluence of state funding and the pressure to get stem cell trials going in New Jersey and New York will result in some clinicals trials in these two states in less than 2 years.

Wise.

P.S. I added a "not" in the bladder section and edited the section on stem cell research.

[This message was edited by Wise Young on 08-17-04 at 09:01 PM.]

[MikeC]

Dr Young, a few questions. Is conus different than Cauda Equina? If so, would you recommend different actions for someone with CES, specifically I was wondering if people with CES should try 4-aminopyridine?

Also, I assume that you have a typo in paragraph 3. - that you think the peripheral nerve bridging procedures are inappropriate for Brayton (you wrote they are appropriate even though the rest of your sentence indicates they should be a last resort). Thanks. Mike

T12 Incomplete - Walking with Walker, Oct 2003

[Wise Young]

MikeC, a cauda equina lesion is different from a conus injury. The conus is the tip of the spinal cord. Cauda equina is composed with only spinal roots. Note, however, that traumatic injury may damage both the conus and the cauda equina. Because Sherman seems to have quite a bit of feeling, I think that most of his lesion is confined to the conus. Please understand that the neurological examination is complicated and requires a very experienced neurologist or physiatrist to dissect out all the findings. Often in such cases, it is better to have two or more doctors do the examination and discuss the results.

Regarding 4-aminopyridine (4-AP, it might be worth a try. 4-AP affects both central and peripheral nerves. There is another drug called 4-diaminopyridine (4-DAP) that does not penetrate the blood brain barrier well but affects the peripheral nerve. If you respond to both 4-AP and DAP, it would be consistent with an effect on demyelinated roots.

Note that there has been some talk about using OEG transplants for cauda equina injuries. This is because several studies have shown that OEG will facilitate axonal regrowth back into the spinal cord from avulsed spinal roots. I think and hope that Jim Guest from the Miami Project is going to Beijing. Jim has been isolating OEG cells from the nose and he specializes in cauda equina injuries.

Thanks for spotting the typo. I corrected it.

Wise.