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Thread: The Meaning of Flaccidity and Muscle Atrophy after Spinal Cord Injury

  1. #51
    Senior Member MikeC's Avatar
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    Dr Young, thanks for the detailed reply. I've always thought that the therapists that tried e-stim on me should know that it doesn't work on people with 'lower level injuries.' I guess I was wrong and I appreciate them trying it. Thanks again. Mike
    T12 Incomplete - Walking with Crutches, Injured in Oct 2003

  2. #52
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    Dr Young,
    Excellent post. Thanks for the detailed response.

    I spent some time at a few hospitals in Taiwan, early, post-injury. The test with the needle recordings you referred to sounds very familiar. I don't have any numbers, but I just remember the doctor saying that the results were bad. LOL...whatever that means. To this day, I can't get a reflex reaction.

    Very intersting about the spinal shock; I've heard that term used quite a bit during the first year of injury. Even more interesting is the lack of experience with MRI techs and DTA tests in the US. I'll look into getting this scan.

    thanks
    Walk

  3. #53

    Spasms

    Dr. Young,

    I'm new to this forum; I stumbled across it looking for some answers to my sudden bout of uncontrollable spasms. I am a c5-c6 level incomplete quad. I spent my rehab at the Long Beach, CA VA hospital where I still receive the bulk of my care. I'm currently having issues with really severe muscle spasms that seem to originate from my bladder. I usually wear a condom cath but have switched to a foley which has helped but not stopped. The Dr. wants me to start using baclofen but I don't want to use something that makes me loopy which it does; besides I want to find the cause and treat it not just throw pills at it. Can a spastic bladder be cured? If yes then how?

  4. #54
    Quote Originally Posted by c5c6quadtrapp View Post
    Dr. Young,

    I'm new to this forum; I stumbled across it looking for some answers to my sudden bout of uncontrollable spasms. I am a c5-c6 level incomplete quad. I spent my rehab at the Long Beach, CA VA hospital where I still receive the bulk of my care. I'm currently having issues with really severe muscle spasms that seem to originate from my bladder. I usually wear a condom cath but have switched to a foley which has helped but not stopped. The Dr. wants me to start using baclofen but I don't want to use something that makes me loopy which it does; besides I want to find the cause and treat it not just throw pills at it. Can a spastic bladder be cured? If yes then how?
    Have you tried Ditropan? Wise.

  5. #55
    I've been taking Toviaz and Rapaflo together for the past several weeks. My bladder spasms aren't nearly as bad as they used to be.
    I'm not sure if it's Toviaz by itself or the combination that's working - I was on Rapaflo by itself before and it made no difference.

  6. #56
    Quote Originally Posted by EastRando View Post
    I've been taking Toviaz and Rapaflo together for the past several weeks. My bladder spasms aren't nearly as bad as they used to be.
    I'm not sure if it's Toviaz by itself or the combination that's working - I was on Rapaflo by itself before and it made no difference.
    EastRando,

    Thanks for your post. Taviaz is made by Pfizer (fesoterodine fumarate). It is very similar to an older drug called Detrol (Source). Approved in 2008 (Source), fesoterodine comes in both regular and extended release tablets (4 and 8 mg).

    The approval of Toviaz is based on two large 12-week Phase III clinical studies of 1,964 OAB patients. In these studies, patients showed up to an 88 percent median reduction in urge urinary incontinence with Toviaz 8 mg versus 50 percent with placebo. Treatment with Toviaz 8 mg reduced the number of urinations per day by up to 19 percent compared to an 11 percent reduction with placebo treatment. Reductions in wetting accidents with Toviaz were seen as early as week two of treatment and maintained over 12 weeks.

    In clinical studies, the most commonly reported adverse event was dry mouth (incidence of 7 percent for placebo; 19 percent for Toviaz 4 mg; 35 percent for Toviaz 8 mg). Most cases of dry mouth were mild to moderate with less than one percent of patients discontinuing Toviaz due to dry mouth. There was a low incidence of constipation (2 percent with placebo; 4 percent with 4 mg; 6 percent with 8 mg). Toviaz was evaluated for up to three years in open-label studies, with an adverse event profile similar to that seen in previous trials.
    Wise.

  7. #57
    My husband, who is 55 years old, has arthritis. A piece of his spinal disc broke off into his nerve. This piece of protein is moving around his nerve, which caused severe pain. He had a nerve injection, which didn't eliminate the pain. The next day he had another nerve injection, which did finally work. (Supposedly this disc piece could take weeks, months or years to be absorbed into the body. Or the nerve might get used to it called nerve adaptation.) Meanwhile, it's about three weeks later and in the last week his legs have experienced severe muscle atrophy, mostly in one of his legs. In addition, he's broken out with a rash, little red (some bumpy) spots on his front, back, arms and thighs, one even on his ankle. He saw his internist, who said he hoped it wasn't an autoimmune problem and prescribed a topical cream, an antiinflammatory. Our doctor said if it doesn't work in a couple of weeks, he'll take a biopsy of the rash. In three days, my husband is seeing a neurologist about the atrophy. I'm feeling helpless and concerned that my doctor is moving too slowly on this issue. I've looked into doctor recommendations for a back doctor, a new internist, and a rheumatologist.

    Any suggestions on what we should do? Is this caused by damage to his nerve from the nerve injections? I'm at a loss and highly distressed. Thanks for any ideas and insights.

    Diane

  8. #58

    Please help!

    Hello,
    I am 25 years post-injury and still trying to get a clue (!) (By the way, I'm the gal that rode my handcycle across the US in 2000 to raise $ for the SCIProject - I've been married, divorced, and become a mother in the interim) Anyway -taking Anatomy & Physiology now so have a bit of a better understanding, but it's of course making me pursue all of those questions that I've had for years with new determination. So - in relation to the quote below, I am interested to know WHY I am flaccid, and WHERE I can maybe get some of the tests described below to find out? I am seriously atrophied from level of injury (T-10 or T-12ish) down. I am wondering what the chances may be of my having ANY viable muscle fibers left at this point; if so, what other treatments besides FES (as I am told I am "not a good candidate") may exist?
    Thanks a million!

    Quote Originally Posted by Wise Young View Post
    jv, yes, it is possible to have denervation without root damage. I listed several causes of flaccidity or atrophy of muscle. You can have loss of neurons, injury to the root, or injury to the peripheral nerve. I assume that you received an EMG test, showing denervation hypersensitivity of your muscles. This does suggest that you have some denervation of your muscles and, while this does tell you that you are losing some muscles, it does not tell you how much you have left or lost. Looking at the nerve roots can't really tell you whether they are damaged. You may have had damage to motoneurons in the spinal cord at or close to the injury site. So, what tests can one do to distinguish between the various causes of denervation:

    1. Somatosensory evoked potentials (SEP). SEP's are activated by stimulating a peripheral nerve and recording the response in the brain and spinal cord. If one sees a sensory volley heading into the spinal cord through the peripheral nerve in question, it means that the peripheral nerve is intact. Since both motor and sensory fibers travel in the peripheral nerve, the only places where the damage can be is at the ventral root or in the spinal cord.

    2. H-reflex. This is the test of the monosynaptic reflex in legs. This test stimulates the peripheral nerve which activates action potentials that head proximally and distally. The responses are recorded from the muscle innervated by the stimulated nerve. The action potential that travels distally will activate the muscle, producing a rapid M-response. The action potential that travels proximally will activate motoneurons in the spinal cord which then sends a second and later activation of the muscle, called H-response. If this response is intact, it would strongly indicate that the peripheral nerve, roots, and spinal cord are intact.

    3. Reflexes. An intact reflex can be detected on neurological examination. If, for example, we poke a pin into the hand or foot and the limb withdraws, this means that not only is sensory signal getting into the spinal cord, it is activating appropriate muscle responses.

    Wise.

    [Sorry, I made a small correction]

    [This message was edited by Wise Young on 11-18-03 at 07:24 PM.]

  9. #59
    Quote Originally Posted by abrelsford View Post
    Hello,
    I am 25 years post-injury and still trying to get a clue (!) (By the way, I'm the gal that rode my handcycle across the US in 2000 to raise $ for the SCIProject - I've been married, divorced, and become a mother in the interim) Anyway -taking Anatomy & Physiology now so have a bit of a better understanding, but it's of course making me pursue all of those questions that I've had for years with new determination. So - in relation to the quote below, I am interested to know WHY I am flaccid, and WHERE I can maybe get some of the tests described below to find out? I am seriously atrophied from level of injury (T-10 or T-12ish) down. I am wondering what the chances may be of my having ANY viable muscle fibers left at this point; if so, what other treatments besides FES (as I am told I am "not a good candidate") may exist?
    Thanks a million!
    Dear abrelsford,

    I believe that you are flaccid because your injury is at T10-T12. Your lumbar enlargement starts at about T10 and ends at T12. L1 is where most of your sacral cord is. Damage to T10-T12 will result in injury to your motoneurons and other neurons that are responsible for your reflex circuitry, therefore reducing or eliminating spasticity. It does not mean that all the neurons have been damaged but when enough of them are damaged, there is not enough to cause spasticity. Combined with loss of descending axons, the loss of local neurons result in flaccidity, which then leads to atrophy.

    Studies from Switzerland and Austria indicate that it is possible to prevent atrophy and maintain muscles with very high current stimulation applied through very large electrodes. There is controversy whether severely atrophied muscles can be restored. Nobody has yet figured out how to regenerate the spinal cord and motoneurons yet. Nevertheless, if one looks at atrophied muscles carefully, it is possible to see some muscle fibers.

    Over very long periods, atrophic muscles that are not stretched can become fibrotic (i.e. contracted with a lot of fibrous tissues in them). This may be more difficult to reverse. Studies of denervated muscles indicate that the longer the muscles have been denervated, the less efficiently nerves can reinnervate them. Christine Thomas [1-2] at the Miami Project did some innovative studies in 2003 transplanting motoneurons into the peripheral nerves of muscles and showing that they can prevent atrophy and perhaps restore atrophic muscles.

    Electrical stimulation alone does not seem to be sufficient to prevent atrophy in animals completely [3] but may delay and slow down the atrophy [4]. Electrostimulation is better than no stimulation [5]. There may be some factors (such as neuregulins) that can reduce or prevent atrophy [6]. One, however, must use implanted electrodes or high current applied with huge electrode pads to prevent burning the skin with so much current. Kern, et al. [7] had developed a high current stimulator and showed that they can prevent and even reverse strophy of chronically denervated muscles.

    Wise.

    References Cited

    1. Thomas CK, Sesodia S, Erb DE and Grumbles RM (2003). Properties of medial gastrocnemius motor units and muscle fibers reinnervated by embryonic ventral spinal cord cells. Exp Neurol 180: 25-31. Department of Neurological Surgery, University of Miami School of Medicine, Miami, FL 33136, USA. cthomas@miami.edu. Severe muscle atrophy occurs after complete denervation. Here, Embryonic Day 14-15 ventral spinal cord cells were transplanted into the distal tibial nerve stump of adult female Fischer rats to provide a source of neurons for muscle reinnervation. Our aim was to characterize the properties of the reinnervated motor units and muscle fibers. Some reinnervated motor units contracted spontaneously. Electrical stimulation of the transplants at increasing intensity produced an average (+/- SE) of 7 +/- 1 electromyographic and force steps. Each signal increment represented the excitation of another motor unit. These reinnervated units exerted an average force of 12.0 +/- 1.5 mN, strength similar to that of control fatigue-resistant units. Repeated transplant stimulation depleted 17% of the muscle fibers of glycogen, an indication of some functional reinnervation. Reinnervated (glycogen-depleted), denervated (no cells transplanted), and control fibers were of histochemical type I, IIA, or IIB. Fibers of the same type were grouped after reinnervation. The proportion of fiber types also changed. Reinnervated fibers were primarily type IIA, whereas most fibers in denervated and control muscles were type IIB. Reinnervated fibers of each type had significantly larger cross-sectional areas than the corresponding fiber types in denervated muscles. These data suggest that neurons with different properties can reside in the unusual environment of the adult rat peripheral nerve, make functional connections with muscle, specify muscle fiber type, and reduce the amount that each type atrophies.
    2. Grumbles RM, Wood P, Rudinsky M, Gomez AM and Thomas CK (2002). Muscle reinnervation with delayed or immediate transplant of embryonic ventral spinal cord cells into adult rat peripheral nerve. Cell Transplant 11: 241-50. The Miami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami School of Medicine, FL 33101, USA. Muscle denervation is common in various neuromuscular diseases and after trauma. It induces skeletal muscle atrophy. Only muscle reinnervation leads to functional recovery. In previous studies, denervated adult rat muscles were rescued by transplantation of embryonic day 14-15 (E14-15) ventral spinal cord cells into a nearby peripheral nerve. In the present study, changes were made in the environment into which the cells were placed to test whether reinnervation was improved by: 1) prior nerve degeneration, induced by sciatic nerve transection 1 week before cell transplantation; 2) transplantation of 1 million versus 5 million cells; 3) addition of nerve growth factor (NGF) to the transplant. Ten weeks after cell transplantation, axons had grown from all of the transplants. The numbers of myelinated axons that regenerated into the tibial, medial (MG), and lateral gastrocnemius-soleus (LGS) nerves were similar across treatments. The mean diameters of large LGS axons (>6 microm) were significantly larger with nerve degeneration before transplantation. The mean diameters of MG and LGS axons were significantly larger with transplantation of 1 million versus 5 million cells. Silver-stained experimental and control lateral gastronemius (LG) muscles showed axons that terminated at motor end plates. Nodal and terminal sprouts were more common in reinnervated muscles (45-63% of all end plates) than in control muscles (10%). Electrical stimulation of the transplants induced weak contractions in 39 of 47 MG muscles (83%) and 33 of 46 LG muscles (72%) but at higher voltages than needed to excite control muscles. The threshold for MG contraction was lower with transplantation of 1 million cells, while LG thresholds were lower without NGF. The cross-sectional area of whole LG muscles was significantly larger with cell transplantation (immediate or delayed) than with media alone, but all of these muscle areas were reduced significantly compared with control muscle areas. These data suggest that delayed transplantation of fewer cells without NGF assists regeneration of larger diameter axons and prevents some muscle atrophy.
    3. Russo TL, Peviani SM, Durigan JL, Gigo-Benato D, Delfino GB and Salvini TF (2010). Stretching and electrical stimulation reduce the accumulation of MyoD, myostatin and atrogin-1 in denervated rat skeletal muscle. Journal of muscle research and cell motility 31: 45-57. Department of Physical Therapy, Federal University of Sao Carlos, Rodovia Washington Luis, Km 235, Sao Paulo, CEP 13565-905, Brazil. thiago_russo@yahoo.com.br. Denervation causes muscle atrophy and incapacity in humans. Although electrical stimulation (ES) and stretching (St) are commonly used in rehabilitation, it is still unclear whether they stimulate or impair muscle recovery and reinnervation. The purpose of this study was to evaluate the effects of ES and St, alone and combined (ES + St), on the expression of genes that regulate muscle mass (MyoD, Runx1, atrogin-1, MuRF1 and myostatin), on muscle fibre cross-sectional area and excitability, and on the expression of the neural cell adhesion molecule (N-CAM) in denervated rat muscle. ES, St and ES + St reduced the accumulation of MyoD, atrogin-1 and MuRF1 and maintained Runx1 and myostatin expressions at normal levels in denervated muscles. None of the physical interventions prevented muscle fibre atrophy or N-CAM expression in denervated muscles. In conclusion, although ES, St and ES + St changed gene expression, they were insufficient to avoid muscle fibre atrophy due to denervation.
    4. Lim JY and Han TR (2010). Effect of electromyostimulation on apoptosis-related factors in denervation and reinnervation of rat skeletal muscles. Muscle & nerve 42: 422-30. Department of Rehabilitation Medicine, Seoul National University College of Medicine, Seoul National University Bundang Hospital, Seoul, Republic of Korea. Electromyostimulation (EMS) has been utilized to reduce muscle atrophy, but its effect on denervated muscles is controversial. This study was performed to determine the effect of EMS on intramuscular changes and apoptosis during denervation and reinnervation following nerve damage. Rat sciatic nerves were denervated completely (CD) or partially (PD), and EMS was applied for 2 weeks. The same numbers of cases were followed without EMS. Nerve conduction studies, muscle weights, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay to measure apoptotic changes, and Western blot were done 4, 8, and 12 weeks after injury. TUNEL-positive nuclei of CD muscles (18.6 +/- 5.5%) were more prevalent than those of PD muscles (7.5 +/- 3.3%). The EMS group showed greater muscle weight, fewer positive nuclei (4.7 +/- 1.9%), and lower BAX and Bcl-2 expression levels compared with the non-EMS group at 4 weeks after PD but not after CD. Denervated muscle atrophy delayed by EMS may be linked with enhanced anti-apoptosis under the control of apoptosis-related factors.
    5. Marqueste T, Decherchi P, Desplanches D, Favier R, Grelot L and Jammes Y (2006). Chronic electrostimulation after nerve repair by self-anastomosis: effects on the size, the mechanical, histochemical and biochemical muscle properties. Acta Neuropathologica 111: 589-600. Laboratoire des Determinants Physiologiques de l'Activite Physique (UPRES EA 3285), Faculte des Sciences du Sport de Marseille-Luminy, Institut Federatif de Recherches Etienne-Jules MAREY (IFR 107), Universite de la Mediterranee (Aix-Marseille II), France. This study tests the effects of chronic electrostimulation on denervated/reinnervated skeletal muscle in producing an optimal restoration of size and mechanical and histochemical properties. We compared tibialis anterior muscles in four groups of rats: in unoperated control (C) and 10 weeks following nerve lesion with suture (LS) in the absence of electrostimulation and in the presence of muscle stimulation with either a monophasic rectangular current (LSEm) or a biphasic modulated current (LSEb). The main results were (1) muscle atrophy was reduced in LSEm (-26%) while it was absent in LSEb groups (-8%); (2) the peak twitch amplitude decreased in LS and LSEm but not in LSEb groups, whereas the contraction time was shorter; (3) muscle reinnervation was associated with the emergence of type IIC fibers and proportions of types I, IIA and IIB fibers recovered in the superficial portion of LSEb muscles; (4) the ratio of oxidative to glycolytic activities decreased in the three groups with nerve injury and repair; however, this decrease was more accentuated in LSEm groups. We conclude that muscle electrostimulation following denervation and reinnervation tends to restore size and functional and histochemical properties during reinnervation better than is seen in unstimulated muscle.
    6. Nicolino S, Panetto A, Raimondo S, Gambarotta G, Guzzini M, Fornaro M, Battiston B, Tos P, Geuna S and Perroteau I (2009). Denervation and reinnervation of adult skeletal muscle modulate mRNA expression of neuregulin-1 and ErbB receptors. Microsurgery 29: 464-72. Dipartimento di Biologia Animale e dell'Uomo, Universita di Torino, Torino, Italy. Skeletal muscle atrophy represents one of the main causes of poor outcome of microsurgical nerve reconstruction. Recent studies have pointed to the importance of the neuregulin/ErbB signaling pathway in the development and regeneration of the neuromuscular system. Here, we show by immunohistochemistry, RT-PCR, and Western blotting analyses, in an in vivo model of adult skeletal muscle denervation/reinnervation, that expression of Neuregulin1 (NRG1) and ErbB receptors is regulated by the innervation condition. We found out that a significant upregulation of the alpha-, but not beta-, isoform of NRG1, as well as of ErbB2, ErbB3, and ErbB4-cyt1 isoform occurs as a consequence of denervation of flexor digitorum muscles of the rat forelimb by median nerve transection. Moreover, after tubulization median nerve repair, and consequent muscle reinnervation, all messengers of the NRG1/ErbB system are promptly downregulated. Therefore, our results suggest the existence of a alpha-NRG1-mediated autocrine and/or paracrine trophic loop in skeletal muscles that is activated after denervation and promptly deactivated after nerve reconstruction. This myotrophic loop is a promising therapeutic target for the prevention of muscle atrophy. Yet, the recent demonstration of a similar alpha-NRG1-mediated gliotrophic loop in denervated Schwann cells provides a possible explanation for the effectiveness of muscle conduits for tubulization nerve repair.
    7. Kern H, Hofer C, Modlin M, Forstner C, Raschka-Hogler D, Mayr W and Stohr H (2002). Denervated muscles in humans: limitations and problems of currently used functional electrical stimulation training protocols. Artificial organs 26: 216-8. Ludwig Boltzmann Institute of Electrostimulation and Physical Rehabilitation, Department of Physical Medicine, Wilhelminenspital, Wien, Austria. helmut.kern@phys.wil.magwien.gv.at. Prior clinical work showed that electrical stimulation therapy with exponential current is able to slow down atrophy and maintain the muscle during nonpermanent flaccid paralysis. However, exponential currents are not sufficient for long-term therapy of denervated degenerated muscles (DDMs). We initiated a European research project investigating the rehabilitation strategies in humans, but also studying the underlying basic scientific knowledge of muscle regeneration from satellite cells or myoblast activity in animal experiments. In our prior study, we were able to show that high-intensity stimulation of DDMs is possible. At the beginning of training, only single muscle twitches can be elicited by biphasic pulses with durations of 120-150 ms. Later, tetanic contraction of the muscle with special stimulation parameters (pulse duration of 30-50 ms, stimulation frequency of 16-25 Hz, pulse amplitudes of up to 250 mA) can improve the structural and metabolic state of the DDMs. Because there are no nerve endings for conduction of stimuli, large-size, anatomically shaped electrodes are used. This ensures an even contraction of the whole muscle. Contrary to the current clinical knowledge, we were able to stimulate and train denervated muscle 15-20 years after denervation. The estimated amount of muscle fibers that have to be restored is about 2-4 million fibers in each m. quadriceps. To rebuild such a large number of muscle fibers takes up to 3-4 years. Despite constant stimulation parameters and training protocols, there is a high variation in the developed contraction force and fatigue resistance of the muscle during the first years of functional electrical stimulation.


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