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Thread: Tendon Lengthening

  1. #1

    Tendon Lengthening

    TENDON LENGTHENING FOR MUSCLE CONTRACTURES
    Wise Young, Ph.D., M.D.
    W. M. Keck Center for Collaborative Neuroscience
    Rutgers, State University of New Jersey, Pisacataway, NJ 08854
    Email: wisey@pipeline.com, Updated: 21 June 2006

    Several people have written to me about tendon lengthening to relieve spasticity. I thought that it might be useful to describe and comment on the procedure.

    Spasticity and Contractures. Spasticity induces and is aggravated by muscle contractures. Muscles contain receptors called spindles that monitor tension and feeds back to the spinal cord to maintain muscle length. Injury to the spinal cord increases excitabilty of neural circuits that control muscle tension. Spastic muscles resist changes of tension by contracting. Prolonged and continuous muscle spasticity may lead to muscle contracture or shortening of muscles. Contractures interfere with standing and walking. While drugs such as baclofen and tizanidine moderates spasticity, they usually cannot moderate muscle contractures.

    Treatments of contractures. Clnicians use three ways to relieve spasticity muscle contractures. One is to inject a toxin called Botox which damages motor nerves and, in high doses, the motoneurons that innervate muscles. The other is to inject phenol, a chemical, that damages both motor and sensory nerves. A third way is to cut the muscle tendon and lengthen the tendon to relieve the tension on the muscle. The first two methods damage motoneurons or axons, sometimes irreversibly, and may cause weakness of muscles. For people who have some muscle function, tendon lengthening is the method of choice.

    Tendon lengthening. The basic tendon lengthening procedure involves cutting the tendon partway at two points and a cut down the middle of the tendon. This allows the two halves of the tendon to be slid along each other and then sewed together, as illustrated in the diagram below. The procedure is simplified for illustrative purposes but it shows how the cuts (left image) can allow two strands of tendon to be slid alongside each other (middle image), and sewed together (right image). Note that there are other ways to cut the tendon, including methods that involving creating four strands and splicing these strands together. Once healed, the tendon is longer and the cut parts will fill out with scar tissues.

    Strength of repaired tendons. Tendon lengthening procedures have been carried out for many decades. In fact, I use to participate in such surgeries for children with cerebral palsy and idiopathic toe walking (Source). Children who undergo tendon lengthening even of big musles such as the leg flexors (Source) can return to athletic activities. Many athletes of course rupture their tendons, undergo tendon repair, and then return to their previous activity. Repaired tendons have a scar and the strength of the scar depends on how it healed. The tendon should be immobilized for about four weeks the healing to take place (Source). Properly healed tendons are reasonably strong.

    Complications. Making the tendons too long or not lengthening the tendon sufficiently can result in weakening of the muscle (Source) or insufficient resolution of the spasticity. Both surgical experience and judgment is required to get the proper lengthening without significantly weaking the muscle. For obvious reasons, it is not good to go in numerous times to repair the tendon. Repeated surgeries and scar tissues will cause stiffening of the tendon and lost of elastic recoil. Muscle weakness due to immobilization and non-use may be a problem and full function may not return to pre-operative levels for as long as 9 months after surgery, even with intensive physical therapy (Source). The change in one muscle group may affect the balance of other muscles, resulting in abnormal gait (Source).

    In summary, tendon lengthening surgery has been practiced for many decades. The procedure does reduce spasticity of major muscle groups and well-healed tendons are strong enough to permit renewal of athletic activity. However, the operation requires experience and good surgical judgment. Like all operations of this nature, complications may occur. Immobilization of the tendon is important for proper healing. Overlengthening, repeated operations, and muscle weakness may occur. The advantages of tendon lengthening is that it may correct specific orthopedic problems and spasticity without damaging nerves or motoneurons.
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    Last edited by Wise Young; 06-22-2006 at 09:59 AM.

  2. #2
    "Tendon lengthening procedures have been carried out for many decades. In fact, I use to participate in such surgeries for children with cerebral palsy."

    I had this done behind the knees back in '73, shot up 6" almost over night!

  3. #3
    Senior Member zillazangel's Avatar
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    VERY helpful information, thank you!!

    Chad has been in bed so much lately that his foot is contracted, pointing down (like a ballerina). When he was in his chair every day, most of the day, the pressure on his feet from his foot plate and from his standing wheelchair, kept his ankles supple and they did not contract. But he has been in bed for so much of the time the last year or so that his ankles, especially his right for some reason, is really tight. Is that surgery appropriate for him? I'd hate to do any surgery on him just because he is so unwell so much of the time.

    I have been trying to diligently do range of motion and REALLY concentrate on the feet/ankles, but I don't feel like I'm making much of a difference frankly.

    Any advice? And even if not, thanks so much for the post.

    Ami
    Wife (8 years) to Chad (C4/5 since 1988), Mom to a Medium Boy, Owner of a Standard Poodle and a Pit Bull
    Blog: http://ItWasntFunnyAtTheTime.blogspot.com

  4. #4
    Hi Wise,

    thanks for the interesting info

    Just wondering though........I had always thought that the effects of botox were temporary and that also to allow the tendon after surgery to completely heal, that botox was essential to completely iradicate mobility through, say spasm ( which the discomfort of surgery would heighten too ) ?

  5. #5
    Quote Originally Posted by Cherrylips
    Hi Wise,

    thanks for the interesting info

    Just wondering though........I had always thought that the effects of botox were temporary and that also to allow the tendon after surgery to completely heal, that botox was essential to completely iradicate mobility through, say spasm ( which the discomfort of surgery would heighten too ) ?
    cherry, I wrote a lengthy review of botox but unfortunately I dropped my computer and it is being repaired right now. As soon as I get back my computer, I will post the review.

    Wise.

  6. #6
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    Tendon lengthening

    Dr.,


    I'm a c3-4 incomplete quad 6 years out. I have very limited use of my left arm and left thumb for typing, dialing, etc. I get ranged daily

    My problem is tone and muscle contraction are taking over my body.

    I've had a tone problem for a long time, but it's become progressively worse, and now it's at the point where I'm losing my ability to operate my chair, dial my phone, type on the computer, etc. My tendons are shortening. My hands are knarled and my left arm is becoming increasingly difficult to straighten. I've lost my ability to feed myself and brush my teeth. It's also affecting my abs and chest muscles and ability to breath.

    We've done x-rays, CT scans, endless bloodwork, urine samples, Botox, and I have made a trip to Houston TIRR - Dr. Francisco - to consult with a spasticity specialist . I have a Baclofen pump implanted. It does nothing for my torso but helps some with my legs. I take 32mg Zanaflex daily. An MRI ruled out a syrinx.

    I'm not blocked or impacted, no pressure sores, and no Foley problems. My body is so stiff, I can't sit totally upright in my chair, and I sit on my tailbone, which is sore all the time.

    My docs are at a loss. No one has even mentioned tendon shortening or contracted muscles. I've gleaned that by reading this site. I go to Johns Hopkins. Any ideas for another place to get others involved?

  7. #7

    Effects of Botox on Motoneurons

    Quote Originally Posted by Cherrylips
    Hi Wise,

    thanks for the interesting info

    Just wondering though........I had always thought that the effects of botox were temporary and that also to allow the tendon after surgery to completely heal, that botox was essential to completely iradicate mobility through, say spasm ( which the discomfort of surgery would heighten too ) ?
    Cherry,

    That is an interesting use of botox. I had not heard of this before but it does make sense.



    Effects of Botox on Motoneurons
    Wise Young, Ph.D., M.D.
    W. M. Keck Center for Collaborative Neuroscience
    Rutgers, State University of New Jersey, Piscataway, NJ 08540
    Email: wisey@pipeline.com, last updated 6/22/06

    Many people have asked questions about Botox or botulinum toxin that is now commonly used to treat spasticity and other conditions.

    What is Botox? Botox is the trade name of a drug derived from botulinum toxins, a powerful family of neurotoxins that selectively affects acetylcholinergic neurons, produced by a family of bacteria called clostridium bolutinum. This bacteria grows under anaerobic conditions in canned foods and can cause a condition called botulism. One of the most powerful and dangerous neurotoxins in nature, it use to kill in over 50% of people who developed botulinism before respirators were available (Source). Ingestion, inhalation, or injection of 200-300 picograms per kilogram is a lethal dose. Because 100 grams of the toxin would be sufficient to kill every person on earth, it has been the target of some speculation as a terrorist weapon (Source), particularly in milk (Source) but, because the molecule is rapidly degraded when heated or exposed to air and difficult to produce in quantity, the concern has been largely theoretical (Source).

    Botulinum toxin therapy. Botulinum toxin has been studied for many years. In 1949, Justinus Burgen discovered that the drug blocked neuromuscular transmission. Botulinum toxin was among the first neurotoxins to be used as a therapy. In the 1950's, it was used to eliminate facial wrinkles in actors. When injected in tiny amounts into muscle, the toxin binds to motor nerves, preventing release of neurotranmiters from the nerves to paralyze or weaken the muscle. The injection effects usually last only 3-4 months and repeated re-injections are necessary to maintain its effects for longe periods. Seven members of the botulinum toxin family (A-G) with three subtypes of the A group have been identifeid. In 1989, the U.S. FDA approved use of botulinum toxin A (BTX-A) to treat strabismus (eye movement), blepharospasm (spasmodic blinking), and hemifacial spasm (spasms of the face). In 2002, the FDA approved Botox use for treating facial wrinkles. BTX-A is marketed under the trade names of Botox and Dysport. Dysport is a different formulation of botulinum toxin A. Although not specifically approved for such indications, BTX-A is frequently used to treat urinary incontinence, anal fissures, spasticity, focal dystonias, and temporomandular joint pain. It has been used for treatment of neuromuscular pain, even though the toxin does not directly affect sensory nerves, because abnormal muscle activity may be associated with cramps (Source), including bladder pain (Source). Some animal data suggest that botulinum toxins may affect activity of nociceptive neurons. In 2000, the U.S. FDA approved the use of botulinum toxin B (BTX-B) for cervical dystonia, a condition of hyperactive muscle groups in the neck. A cheaper but less potent Chinese version of Botox is also available. Although the other versions of botulinum toxin (C-G) have not been approved, several synthetic versions and fragments of the toxin being tested (Source.

    Mechanism of action. BTX-A has three components, a heavy chain and two light chains. Injected in small amounts into muscles, the heavy chain of botulinum binds to the surfaces of motor nerves where it is endocytosed (the membrane inverts and is taken back into the cell). A recent study (Source) suggests that a membrane protein called SV2 is protein receptor for botulinum toxin. The heavy chain has turned out to be a useful tool for getting other molecules to be transported into cells (Source). The light chains of botulinum toxin are enzymes (proteases) that break down the SNAP-25 proteins in the SNARE family. These proteins are essential for release of acetylcholine (the neurotransmitter that activates muscles). Motor nerves treated with BTX-A tend to fill up and swell with unused acetylcholine vesicles. BTX-A and BTX-B reduce both all muscle activity, due to both voluntary and involuntary motor activity, usually within 24-48 hours and the paralysis lasts several months.

    Side-effects of Botox Therapies. Botulinum toxin treatments are associated with some complications. Muscle weakness is the most commonly reported side-effect. The injection site may be sore and tender. Flu-like symptoms may occur. Pain may be present in neighboring muscles. Some 20-30% of patients may report these side effects (Source). Injection of the toxin into the wrong muscle is of course a possibility. When injected into the neck or nearby structures, the toxin may affect ability to swallow and dry mouths (a side-effect of the toxin on nerves that stimulate saliva secretion). The beneficial effects of the drug may not appear for 7-10 days and the effects may last 4-6 weeks. When used repeatedly and more frequently than 12 weeks, the body will develop antibodies against botulinum toxins, reducing their effectiveness. Antibodies against the serum (anti-toxin) is one treatment of botulinum toxicity.

    Effect of Botox on Motoneurons. BTX-A is generally considered to be a very long-acting reversible toxin. However, BTX-A may have toxic effects on motoneurons. In neonatal rats, the toxin has been reported to increase electrotonic coupling between motoneurons and other neurons (Source). BTX-A is well known to stimulate motor axonal sprouting in muscle. This may have some unanticipated effects. For example, in 2002, Millecamps, et al. (Source) reported that prior injection of BTX-A enhances locallly injected adenovirus retrograde gene transfer in motoneurons, apparently related to toxin-induced sprouting of the nerves and increasing the surface area of nerves exposed to virus. In 1977, Sumner (Source reported the BTX-A injected into the tongues of rats produced the same changes in motoneurons as cutting of the axon, with reductions in dendrite numbers and increase in abnormal dendrite appearance, increases in astrocytes around the motoneurons, and even presence of microglial cells that suggest an inflammatory response. Jung, et al. (Source) reported changes in gene expression in rat spinal motoneurons after chemodenervation with botulinum toxin.

    Effects of Botox on Muscle. Botox parayzes muscle by stopping acetylcholine release. Because the toxin is injected in small amounts that only affect the muscle in the immediate vicinity of the injection site, there is a decrease in muscle activity and strength. The toxin effect lasts for 4-6 weeks and the injections must be repeated to retain the effect. The mechanisms by which the muscle recovers strength from the toxin are not well understood but may be due to some or all of the following possibilities. First, the recovery of muscle strength may be due to sprouting axons from surrounding non-paralyzed motor nerves. After botox injections, motor axons do sprout extensively in the muscle. Second, the nerves may take several weeks to get rid of the BTX-A and transport additional SNAP-25 proteins to the end of the axon so that acetylcholine can be released. Third, surrounding muscle fibers may hypertrophy to make up for the paralysis of the muscle. Permanent weakness of muscle may occur, especially in muscles with already compromised voluntary activity.

    Advantage and Disadvantage. The advantage of Botox is its ease of administration. The doctor simply injects a tiny amount of the toxin into the muscle deemed to be overactive. Depending on the vantage point, the fact that Botox’s effects are not permanent may be an advantage or a disadvantage. To doctors and the companies that make money from the procedure, it is an advantage. For the patients, the reversibility of botox effects is also an advantage, particularly if the injection is made into the wrong place. To have to receive repeated injections every 3 months, however, is disadvantageous. A second disadvantage is botox paralyzes both voluntary and involuntary (spasticity and spasms) muscle activity. For patients who use or anticipate using the muscles, the weakness due to botox may contribute further dysfunction. Finally, the side-effects and the development of immune responses to the toxin are significant drawbacks of repeated injections.

    Limitations and Alternatives. Botox is useful only in situations where one or at most a few groups of muscles are overactive. It is not suitable as a treatment of widespread spasticity, spasms, and other abnormal activity affecting many muscle groups. Alternatives to botox for treatment of spasticity fall into three broad categories. The first are anti-spasticity, ant-epileptic/spasm, and other drugs that suppress central nervous system and muscle activity. These include baclofen and tizanidine. The second are surgical methods, such as lengthening tendons or even denervation. The third are chemical methods of damaging peripheral nerve connections to the muscle, such as phenol.

    Of note to afficionados of spinal cord injury therapies, bacteria are a rich source of other toxins (Source that may be of benefit for spinal cord injury. For example, clostridia bacteria produce C2 toxin, which binds to actin (Source). Others, such as C3, bind to proteins of the Rho family Source) that are responsible for mediating inhibitory effects of Nogo receptor activation on axonal growth (Source), a mechanism that has been hypothesized to be one of the reasons why axons cannot regenerate in the central nervous system.

    In summary, botox is botulinum toxin A, a potent neurotoxin made by the bacterium clostridium botulinus that grows in spoiled foods and still kills people. The toxin binds selectively to the surface of motor nerves and transfers inside the nerve where it breaks down proteins required for release of acetylcholine, the neurotransmitter responsible for muscle and secretory activity. The toxin selectively paralyzed muscles where it has been injected but the effects wear off.

  8. #8
    Quote Originally Posted by retusn
    Dr.,


    I'm a c3-4 incomplete quad 6 years out. I have very limited use of my left arm and left thumb for typing, dialing, etc. I get ranged daily

    My problem is tone and muscle contraction are taking over my body.

    I've had a tone problem for a long time, but it's become progressively worse, and now it's at the point where I'm losing my ability to operate my chair, dial my phone, type on the computer, etc. My tendons are shortening. My hands are knarled and my left arm is becoming increasingly difficult to straighten. I've lost my ability to feed myself and brush my teeth. It's also affecting my abs and chest muscles and ability to breath.

    We've done x-rays, CT scans, endless bloodwork, urine samples, Botox, and I have made a trip to Houston TIRR - Dr. Francisco - to consult with a spasticity specialist . I have a Baclofen pump implanted. It does nothing for my torso but helps some with my legs. I take 32mg Zanaflex daily. An MRI ruled out a syrinx.

    I'm not blocked or impacted, no pressure sores, and no Foley problems. My body is so stiff, I can't sit totally upright in my chair, and I sit on my tailbone, which is sore all the time.

    My docs are at a loss. No one has even mentioned tendon shortening or contracted muscles. I've gleaned that by reading this site. I go to Johns Hopkins. Any ideas for another place to get others involved?

    Stiff Man's Syndrome came to mind as I am reading your description. Do you have any diabetic symptoms, i.e. abnormally long elevated on glucose tolerance test? The reason why I ask is because the Stiff Man's Syndrome is a supposedly rare condition that is assoicated with autoimmune attack of GABA neurons in the central nervous system. The same antibody that attacks the GABA neurons also may attack pancreatic islet cells. It is just a fanciful notion but one possibility is that the spinal cord injury triggered the autoimmune condition because it may be exposed your immune system to cells and chemicals released from the injured spinal cord.

    I don't know of whether Johns Hopkins does the assay but it is an autoimmune disease that attacks inhibitory cells. There is an extensive literature on the subject. Several years ago, I wrote an article for Cando (which is no longer available) reviewing all that literature and called "Stiff Woman's Syndrome". I was struck by the coincidence that many people with spinal cord injury also develop diabetic symptoms.

    Wise.

  9. #9
    I've had two tendon surgeries on my left arm/wrist/hand for problems with cerebral palsy pre-SCI. The first wasn't so successful. The second was better. Bone was removed (including two knuckles) during the second surgery due to contractures which had bones out of joint with no hope of returning to previous position.

    I wear a customized splint to help keep my left wrist, hand and fingers in position at night.

    Five years ago, the tendons were lengthened on my lower leg and ankle. This was eight years post-SCI.

    At the same time, my ankle was fused into place at a 90 degree angle after a bad break of lower leg, ankle, foot. Had I been ab, I have no doubts the docs would not have fused my ankle and foot into place. I'm not ab, so they didn't.

    Don't mean to hijack the thread. Just be aware if you break bones you may receive more drastic treatment than if you're ab. With my ankle fused at the angle it is, I must use caution in positioning myself in bed or during transfers. That ankle and foot aren't going to flex or move without seriously breaking more bones. No foot flop or drop with that one. LOL

    The tendon lengthening can help. It's helped me a lot. It's prevented further contractures in my wrist, hand and fingers and also my ankle. I got more use out of my left hand than before the surgeries. As for my lower leg, ankle and foot? I'm only seeing visible contractures in my big toe (pointing up) and my other toes (pointing down and toward the sole of my foot) five years post surgery.

  10. #10

    multiple sclerosis and bilateral transfer

    i have m.s.. i am scheduled to have tendon lengthening and bilateral transfer. im wondering if you know any people with this desease who have had success, with this procedure. june 2009

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