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Thread: What can help improve recovery in a walking quad?

  1. #1

    What can help improve recovery in a walking quad?

    Dr. Young, do you think there is anything that could help a walking quad, 3yrs 10months post recovr faster? I can move almost everything in my body but its weak. I know Ive asked this question a lot but I dont know what else to do. I exercise n strecth everyday
    I received this question several weeks ago. Sorry about not answering. I had to think about this a lot.

    Let me start by discussing what a "walking quad" means. A person who is walking after spinal cord injury has enough axons passing through the injury site to activate the locomotor pattern generator. Relatively few axons are needed for this purpose. Sensory feedback is necessary for maintaining balance and posture. Many muscles may be weak or atrophied through prolonged non-use. The recovery may be stronger on one side than the other, thereby resulting in abnormal stress of joints and muscles that are weak. Spasticity often interferes with the movement but at the same time is important for the movement to occur. People often take drugs for spasticity and the drugs interfere with movements.

    If your recovery seem to have plateaued, what can and should you to do restart the recovery process?

    1. Check your medication. If you are taking anti-spasticity drugs, such as baclofen or tizanidine, the drugs may be causing weakness. In addition to reducing spasticity, anti-spasticity drugs weaken the muscles. If you are taking anti-spasticity medication or have a baclofen pump, you should discuss the situation with your doctor and consider lowering the dose so that it still controls your spasticity but gives you additional strength. There is some controversy about this and relatively few good studies (Source). The same may be true for anti-pain medications such as gabapentiin (neurontin). One possibility is to adjust your schedule of medication so that you take more at night (when you don't need to move) and reduce the dose during the day. Another possibility is to use alternative approaches to reducing spasticity (see below).

    2. Consider functional electrical stimulation of muscle. Muscle stimulation, particularly against resistance, strengthens your muscles. FES may also reduce spasticity. I have heard many people tell me that their spasticity is less after they have had a period of FES stimulation.

    3. Consider spinal cord stimulation. Several credible studies have shown that epidural stimulation of the lumbar cord with low frequency waves will activate the locomotor pattern generator in the spinal cord and greatly reduce the effort required and the speed of walking overground. There are only a few places in the United States that offers this kind of stimulation. One place in in Arizona and the other is in Vienna (Austria). See
    http://sci.rutgers.edu/forum/showthread.php?t=17601
    http://sci.rutgers.edu/forum/showthread.php?t=23383
    http://sci.rutgers.edu/forum/showthread.php?t=15424

    4. Consider 4-aminopyridine. There are many many posts concerning 4-aminopyridine or fampridine on this site. This is a potassium channel blocker that not only may improve the conduction of demyelinated axons but also increases the amount of neurotransmitter released per impulse that gets through. There is a phase 2 study in MS that shows that fampridine will reduce fatigue, increased strength and walking speed of people with MS. Do a search for 4-AP and you will find a lot of information on this. The drug is available through doctor subscription and can be dispensed by compounding pharmacies. Many people on this site take 4-AP.

    5. There are several new drugs that may help. One is HP184. This is a drug that apparently blocks both sodium and potassium channels and may have effects that are similar to 4-aminopyridine. Another theoretical possibility is to take a serotonin uptake blocker; these are antidepressive drugs that reduce the uptake of serotonin and since serotonin is an important neurotransmitter for activating the locomotor pattern generator, it is possible that such drugs may help reduce fatigue and improve walking. There are some reports that fluoxetine and maparotiline improves motor function in people after stroke (Source).
    There is a recent report that a drug called quipazine (which is a serotonin receptor agonist) helps mice with transected spinal cords walk better (Source). I am not suggesting that you take these drugs but just pointing out that there may be some pharmaceutical approaches that may be coming.

    There are other possibilities but let me just start with these and see where the discussion leads us.

    Wise.

  2. #2
    Senior Member mr_coffee's Avatar
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    Wise,

    Do you think 4-AP would be helpful for me, to get the signal strength stronger/faster in my bad leg? I'm about a year 1/2 post now, but i just recently discovered I have alot of push on my left side that actually kicks in my quads/hamstring/gastroc muscle all at once when I push against somthing. But the problem is i can't functinoally stimulate these muscles, my quads/hamstrings because if i'm sitting up, i can't fire them as quickly or at all somtimes.

    So if I would go on a leg curel machine, only my right leg would do the leg curel, and the signal seems to go around my left leg. But if I put a ball underneith my bad leg, and i focus really hard I can make that leg kick up, firing the quad muscles.

    Also if you get off 4-AP do you loose the benefits of it and is it covered by insurance?

    Thanks.

    -Cory
    Injured:10-16-04
    C7/C8, T1 incomplete;


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  3. #3
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    Quote Originally Posted by wise young
    Another theoretical possibility is to take a serotonin uptake blocker; these are antidepressive drugs that reduce the uptake of serotonin and since serotonin is an important neurotransmitter for activating the locomotor pattern generator, it is possible that such drugs may help reduce fatigue and improve walking.
    Could you expand on this ?

  4. #4
    I have not checked pubmed or anything yet on this, but the thought has occurred to me that new approaches/therapies could also concentrate on the amount of neurotransmitter synthesis and availability after SCI, as well as what happens to receptors at the synapse. Are they downregulated after injury and nonuse? What approaches might be feasible to encourage adequate neurotransmiter availability and binding? Have any trials explored acetylcholinesterase inhibitors or dietary supplements for Ach precursors?
    When return occurs, the muscle experiences fatigue not unlike what occurs in Myasthenia Gravis, although the mechanism in MG is autoimmune. It seems to me that neurotransmitter availability has to be a crucial factor. The muscle is there, and the nerve is there.
    Any thoughts?

    I edit to ask also about addressing the importance of remyelination in therapy. Obviously if axons regenerate but myelin is not adequate, recovery would be terrible. I know it has been suggested that progesterone aids in re-myelination, but am wondering if there is good research addressing repair of damage to myelin in axons.
    Last edited by Cripply; 05-18-2006 at 07:19 PM.

  5. #5
    Quote Originally Posted by IanTPoulter
    Could you expand on this ?
    There is a possibility that SSRIs improve functional outcomes by acting on an undiagnosed depression? I guess it is difficult to tell, difficult to design a good study to discern.

  6. #6
    mr_coffee,

    My remarks were obviously directed at a situation of a person who is a "walking quad" but is weak. You seem to have some axons crossing the injury site and may be able to partly activate your left leg extensors. I am not sure, however, which is the muscle that initially allows you to "push" your left leg if it is not the quadriceps. The extensor muscles are your quads (L2-L3), gastocnemius (L4-L5), and gluteus maximus (L5).

    In your case, FES cycling may be worthwhile trying. You should be able to stimulate your quads, anterior tibs, and gluteus in sequence to pedal the bike. This will also reinforce the cycle of extensor followed by flexor muscles: psoas (L2), anterior tibialis (L3-L4), hamstring (L4-L5). See http://www.wheelessonline.com/ortho/...the_lower_limb

    After you have built up the muscles a bit in both legs, I think that it is reasonable for you to start on the Glider daily, standing, bearing weight, and going through the motions. Weight supported ambulation would be next.

    4-AP might be helpful. There is no easy way to predict but most studies suggest that it probably will help most when you have some voluntary movement.

    Wise.

    Quote Originally Posted by mr_coffee
    Wise,

    Do you think 4-AP would be helpful for me, to get the signal strength stronger/faster in my bad leg? I'm about a year 1/2 post now, but i just recently discovered I have alot of push on my left side that actually kicks in my quads/hamstring/gastroc muscle all at once when I push against somthing. But the problem is i can't functinoally stimulate these muscles, my quads/hamstrings because if i'm sitting up, i can't fire them as quickly or at all somtimes.

    So if I would go on a leg curel machine, only my right leg would do the leg curel, and the signal seems to go around my left leg. But if I put a ball underneith my bad leg, and i focus really hard I can make that leg kick up, firing the quad muscles.

    Also if you get off 4-AP do you loose the benefits of it and is it covered by insurance?

    Thanks.

    -Cory

  7. #7
    Cripply, you must be a student of physiology to ask these questions.

    People who have spasticity and spasms obviously don't have to worry about their acetylcholinergic systems because the acetylcholinergic transmissions are obviously working.

    Flaccid muscles of course present a problem but that problem is perhaps not so much due to acetylcholine deficit as much as it is from denervation or muscle atrophy. The latter can be addressed with functional electrical stimulation. The former is problematical and may peripheral nerve regeneration (if the motoneurons are intact) or motoneuronal replacement. An alternative is to do a peripheral nerve bridge from the ventral root to another part of the spinal cord.

    The main neurotransmitters of descending spinal motor systems are glutamate (excitatory), GABA (inhibitory), and serotonin (oscillatory). The last comes from brainstem and the locus coeruleus. Catecholaminergic neurotransmitters also appear to play a role in exciting the locomotor pattern generator, including norepinephrine. That is why the experiments were addressing serotonin-catecholamine uptake blockers.

    Yes, indeed regenerated axons need to be myelinated. If the endogenous cells are not sufficient, remyelination therapies may be necessary. The spinal cord is capable of remyelinating axons. We know this from people with MS. Oligodendroglia myelinate the axons but mature oligodendroglia are not able to remyelinate axons. This must be done by oligodendroglial precursors or O2A cells. The sources of these cells are not well understood. Some scientists believe that they arise from neural stem cell in the spinal cord. Unfortunately, remyelination is sometimes incomplete. Many therapies have now been shown to remyelinate the spinal cord after injury, including transplanted Schwann cells, olfactory ensheathing glia, bone marrow stem cells, oligodendroglia from neural stem cells or embryonic stem cells, and even myelinating antibodies (Rodriguez, et al.). It may be useful to try 4-aminopyridine which should improve conduction in demyelinated axons.

    Wise.

    Quote Originally Posted by Cripply
    I have not checked pubmed or anything yet on this, but the thought has occurred to me that new approaches/therapies could also concentrate on the amount of neurotransmitter synthesis and availability after SCI, as well as what happens to receptors at the synapse. Are they downregulated after injury and nonuse? What approaches might be feasible to encourage adequate neurotransmiter availability and binding? Have any trials explored acetylcholinesterase inhibitors or dietary supplements for Ach precursors?
    When return occurs, the muscle experiences fatigue not unlike what occurs in Myasthenia Gravis, although the mechanism in MG is autoimmune. It seems to me that neurotransmitter availability has to be a crucial factor. The muscle is there, and the nerve is there.
    Any thoughts?

    I edit to ask also about addressing the importance of remyelination in therapy. Obviously if axons regenerate but myelin is not adequate, recovery would be terrible. I know it has been suggested that progesterone aids in re-myelination, but am wondering if there is good research addressing repair of damage to myelin in axons.

  8. #8
    Dr Wise,

    Agreed that the cholinergic system works in spastic muscles, but what I was really addressing is the issue of fatigue. Why the muscle gets "fatigued" so quickly.
    Thanks for your detailed post.

  9. #9
    Quote Originally Posted by Wise Young
    5. There are several new drugs that may help. One is HP184. This is a drug that apparently blocks both sodium and potassium channels and may have effects that are similar to 4-aminopyridine. Another theoretical possibility is to take a serotonin uptake blocker; these are antidepressive drugs that reduce the uptake of serotonin and since serotonin is an important neurotransmitter for activating the locomotor pattern generator, it is possible that such drugs may help reduce fatigue and improve walking. There are some reports that fluoxetine and maparotiline improves motor function in people after stroke (Source).
    There is a recent report that a drug called quipazine (which is a serotonin receptor agonist) helps mice with transected spinal cords walk better (Source). I am not suggesting that you take these drugs but just pointing out that there may be some pharmaceutical approaches that may be coming.

    There are other possibilities but let me just start with these and see where the discussion leads us.

    Wise.

    Wise,

    I have Brown Sequard (C5/6) and have had a significant recovery. I walk full time with no problem. My left side is a bit weaker still than my right which limits things like running and my agility. I'm nearly 5 years post and definitely think I've reached a plateau.

    My question is would any of these drugs potentially have a postive effect on things like sensory issues or improvements in the movement of my left hand which is still at about 70%? I tried 4-AP years ago with little improvement.

    In a perfect world I'd still like to get closer to normal (pre-injury). Any advise would be appreciated...

  10. #10
    Dr. Wise, I too walk full time with crutches. C-5 7 yrs post. I don't take much baclfen 40mg a day. I did just get a FES bike and it makes a big differece. The day after i ride i always feel great and my spasms are very minimal. This has worked well for me. But i still fatigue quickly after walk or standing a while.
    Will a serotonin blocker affect my sleep. My brother takes serotonin to help him sleep. I will try it regardless.

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