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Ten frequently asked questions concerning cure of spinal cord injury

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    EDD, my advice is for people to wait. Yes, I think that the OEG transplants are producing some sensory improvement for some people but it is not a cure. In the coming years, there will be more and better therapies, including combination therapies that should restore much more function. I know that waiting is hard. Wise.

    Originally posted by EDD:

    HiDr Young,
    Im new to this site im 1 year 2months injury and this is my second post.

    Question: You say that Olfactory ensheathing glial (OEG)cells are giving 4-8 levels Sensory and 1-2 levels Motor function. I am T12 does this mean that i have a chance of gaining all function cause I do know that the spinal cord ends at L1 and it is only roots after that. Surly this surgery is enough for me to be able to regain major function that my injury is so low down.

    This Wheelchair is a pain in the butt


      I know this is probably not the right place to ask BUT
      I am a grandfather with a 9 week old grandson that has just been diagnosed with Cerebrel Palsy. I am trying to look at all options that may assist him to have a full and productive life. I have read about Dr Hongyuns work in China with Spinal injuries. Can you tell me whether this same techniques are available for Cerebrel Palsy, if not do you know of any other good work being done to assist people with Cerebrel Palsy.
      Thanks Ross


        Rangi100, I am sorry that your grandson has cerebral palsy. Olfactory ensheathing glia are special cells that appear to stimulate regeneration and has been extensively investigated for improving regeneration in spinal cord injury. I am not aware of any evidence or rationale for use of olfactory ensheathing glia for cerebral palsy. Cerebral palsy is a complex condition where there has been damage or failure to develop of parts of the central nervous system. The term cerebral palsy implies damage to the brain while the terms spina bifida, spinal meningomyelocoele relate to the defects on development of the spinal cord.

        Most research on cerebral palsy focus on preventing the condition. So, for example, there are many studies of conditions that may lead to cerebral palsy and drugs that may reduce the incidence of the condition. However, there is some studies of constraint-induced movement therapy in young children with cerebral palsy (Eliasson, et al., 2005; Gordon, et al., 2005), various therapies to address spasticity associated with cerebral palsy (Chin, et al., 2005; Satila, et al., 2005), orthopedic procedures and orthoses that improve gait (Saraph, et al., 2005; Terjesen, et al., 2005).

        From my reading of magazine articles, I remember that Sweden has quite advanced approaches towards physical therapy and training of children with cerebral palsy. Likewise, I think that they use an orthosis called second skin (a polyester lycra device that provides support and resistance to certain movements and may help improve motor control and reduce spasticity). I am not aware of any stem cell or other cell-based therapies that have been tried in people with cerebral palsy. We do have a number of members of this site that have cerebral palsy.

        What kind of cerebral palsy does your grandson have? Is there spontaneous movement, i.e. athetoid? In my opinion, it is very important not to neglect language and intellectual development. Because they are physically more apparent, too much attention is paid to the motor control and spasticity. Many children with cerebral palsy are intelligent and do well.


        References Cited

        Eliasson AC, Krumlinde-sundholm L, Shaw K and Wang C (2005). Effects of constraint-induced movement therapy in young children with hemiplegic cerebral palsy: an adapted model. Dev Med Child Neurol 47: 266-75. The aim of this study was to evaluate the effects of a modified version of constraint-induced (CI) movement therapy on bimanual hand-use in children with hemiplegic cerebral palsy (CP; age range 18 mo to 4 y) and to make a comparison with conventional paediatric treatment. Twenty-one children (13 females, eight males) completed the CI therapy programme and 20 children (12 males, eight females) served as a control group. Children in the CI therapy group were expected to wear a restraint glove for 2 hours each day over a period of 2 months. The training was based on principles of motor learning used in play and in motivational settings. To evaluate the effect of treatment, the Assisting Hand Assessment (AHA) was used. Assessments took place on three occasions: at onset, after 2 months, and 6 months after the first assessment. A significant interaction was found between group and AHA measure (ANOVA, F(2,74) = 5.64, p = 0.005). The children who received CI therapy improved their ability to use their hemiplegic hand significantly more than the children in the control group after 2 months, i.e. after treatment. Effect size was high after treatment and remained medium at 6 months. As the treatment was tailored to each child's capacity and interests, little frustration was experienced by the children. Neuropediatric Research Unit Q2:07, Astrid Lindgren Children's Hospital, SE-171 76 Stockholm, Sweden.

        Chin TY, Nattrass GR, Selber P and Graham HK (2005). Accuracy of Intramuscular Injection of Botulinum Toxin A in Juvenile Cerebral Palsy: A Comparison Between Manual Needle Placement and Placement Guided by Electrical Stimulation. J Pediatr Orthop 25: 286-291. Most clinicians who perform botulinum toxin A injections for children with cerebral palsy do so using the "free-hand" or manual technique without using radiologic or electrophysiologic guidance to aid needle placement. The objective of this study was to investigate the accuracy of manual needle placement compared with needle placement guided by electrical stimulation. A total of 1,372 separate injections for upper and lower limb spasticity were evaluated in 226 children with cerebral palsy. The accuracy of manual needle placement compared with electrical stimulation was acceptable only for gastroc-soleus (>75%); it was unacceptable for the hip adductors (67%), medial hamstrings (46%), tibialis posterior (11%), biceps brachii (62%), and forearm and hand muscles (13% to 35%). The authors recommend using electrical stimulation or other guidance techniques to aid accurate needle placement in all muscles except the gastroc-soleus. Further study is needed to determine whether more accurate injecting will lead to better functional outcomes and more efficient use of botulinum toxin A. From *Department of Orthopaedics, Royal Children's Hospital, Melbourne, Australia; daggerUniversity of Melbourne, Melbourne, Australia; and double daggerHugh Williamson Gait Analysis Laboratory, Royal Children's Hospital, Melbourne, Australia.

        Satila H, Iisalo T, Pietikainen T, Seppanen RL, Salo M, Koivikko M, Autti-Ramo I and Haataja R (2005). Botulinum Toxin Treatment of Spastic Equinus in Cerebral Palsy: A Randomized Trial Comparing Two Injection Sites. Am J Phys Med Rehabil 84: 355-365. Satila H, Iisalo T, Pietikainen T, Seppanen RL, Salo M, Koivikko M, Autti-Ramo I, Haataja R: Botulinum toxin treatment of spastic equinus in cerebral palsy: A randomized trial comparing two injection sites. Am J Phys Med Rehabil 2005;84:355-365. OBJECTIVE:: To explore the clinical relevance of injection site by comparing two different injection techniques in children with cerebral palsy who have spastic equinus gait. DESIGN:: A total of 19 children (13 boys, 6 girls; range, 1 yr 6 mos to 7 yrs; nine hemiplegics, eight diplegics, two quadriplegics; levels I to IV with the Gross Motor Function Classification System) participated in the study. The children were randomized into two groups: the proximal group received a botulinum toxin A injection into the proximal part of both heads of the gastrocnemius, and the distal group received a botulinum toxin A injection into the mid-belly of the muscle bulks. A single-point injection of BOTOX, 3 units/kg per site, was used. Assessments of active and passive range of motion, dynamic muscle length (modified Tardieu scale), calf tone (modified Ashworth scale), and video gait analysis (Observational Gait Scale) were performed before treatment and 3, 8, and 16 wks posttreatment. RESULTS:: Active and passive dorsiflexion and calf tone in both groups and Observational Gait Scale total scores in the distal group improved at all time points. The median change from baseline values in Observational Gait Scale initial foot contact and total scores at 8 wks showed a significant difference favoring the distal group, but the clinical relevance remained tenuous. CONCLUSIONS:: Using the methods described, no major changes in main outcome measures were associated with changing the injection site. From the Departments of Paediatric Neurology (HS, MK) and Physiatry (TI, TP, RLS), Tampere University Hospital, Tampere, Finland; the Departments of Paediatric Neurology (HS) and Physiatry (MS), Central Hospital of Kanta-Hame, Hameenlinna, Finland; the Paediatric Neurology Unit, Hospital for Children and Adolescents, Helsinki, Finland (IAR); the Finnish Office for Health Care Technology Assessment, STAKES, Helsinki, Finland (IAR); and the School of Public Health, University of Tampere, Tampere, Finland (RH).

        Saraph V, Zwick EB, Auner C, Schneider F, Steinwender G and Linhart W (2005). Gait improvement surgery in diplegic children: how long do the improvements last? J Pediatr Orthop 25: 263-7. Gait improvement surgery in ambulatory children with cerebral palsy performed as single-event multilevel surgery is today a well-established modality of treatment, but follow-up studies are lacking. Preoperative and follow-up gait analysis data of 32 diplegic children who underwent single-event multilevel surgery for gait improvement between 1995 and 1998 were evaluated retrospectively. Relevant sagittal plane kinematic parameters of the hip, knee, and ankle joint and time-distance parameters were considered for outcome measures in this study. Postoperative gait analysis was performed three times in all the cases: after discontinuation of the dynamic AFOs (mean 1.0 +/- 0.3 years), after discontinuation of the night splints (mean 2.3 +/- 0.7 years), and at least 1.5 years after discontinuation of physiotherapy and splints (mean 4.4 +/- 1.1 years). The aim of the study was to ascertain whether the improvements in gait function were maintained over these examinations. The authors found that gait function continued to change over 1, 2, and 3 years of follow-up. A general decrease in gait function was measurable in this collective between the first postoperative and the second postoperative evaluations. The results indicate that evaluation of gait improvement surgery in cerebral palsy performed at a minimum of 3 years after surgery would give the most predictive outcome of treatment. From the Pediatric Orthopedic Unit, Department of Pediatric Surgery, Medical University of Graz, Graz, Austria.

        Gordon AM, Charles J and Wolf SL (2005). Methods of constraint-induced movement therapy for children with hemiplegic cerebral palsy: development of a child-friendly intervention for improving upper-extremity function. Arch Phys Med Rehabil 86: 837-44. We delineate the methodology for constraint-induced movement therapy (CIMT) modified for children with hemiplegic cerebral palsy (CP) and describe important considerations that need to be made when testing this intervention in children. The resulting intervention evolved from piloting and testing it with 38 children with hemiplegic CP who were between the ages of 4 and 14 years. Thirty-seven successfully completed the treatment protocol. The intervention retains the 2 major elements of the adult CIMT (repetitive practice, shaping) and was constructed to be as child-friendly as possible. It involves restraining the noninvolved extremity with a sling and having the child engage in unimanual activities with the involved extremity 6 hours a day for 10 days (60 h). Specific activities are selected by considering joint movements with pronounced deficits and improvement of which interventionists believe have greatest potential. The activities are chosen to elicit repetitive practice and shaping. The intervention is conducted in groups of 2 to 3 children to provide social interaction, modeling, and encouragement. Each child is assigned to an interventionist to maintain at least a 1:1 ratio. CIMT can be modified to be child-friendly while maintaining all practice elements of the adult CIMT. The modified therapy is tolerated by most children. Further modifications will likely be required to hone in on the specific components of the intervention that are most effective before applying them to children who are most likely to benefit. Department of Biobehavioral Sciences, Teachers College, Columbia University, New York, NY 10027, USA.

        Terjesen T, Lie GD, Hyldmo AA and Knaus A (2005). Adductor tenotomy in spastic cerebral palsy. A long-term follow-up study of 78 patients. Acta Orthop Scand 76: 128-37. BACKGROUND: There is a risk of hip dislocation in children with spastic cerebral palsy. We evaluated the prophylactic effect of adductor tenotomy in patients with long-term follow-up. PATIENTS AND METHODS: Our material comprised 78 patients (46 boys) with a mean age of 8 (2-17) years who underwent adductor tenotomy during the period 1986-1991. 40 patients had spastic diplegia and 38 had quadriplegia. For patients who had further hip surgery, follow-up was until the next hip operation. Those who had not undergone further surgery were invited to a follow-up examination. The migration percentage (MP) was measured on the preoperative and follow-up radiographs. The radiographic result was termed good if MP at follow-up was reduced or had increased less than 10%. The follow-up period was 10 (1.6-16) years, with a mean of 6 years for patients with later hip surgery and 13 years without such surgery. RESULTS: The clinical outcome was good in 51 cases, poor in 12, and uncertain in 15. The radiographic result was good in 39 of the 53 patients with radiographs available both preoperatively and at follow-up. The patients with good radiographic results had lower preoperative MP than those with poor results (MP 34% versus 49%) and lower preoperative acetabular index. The mean increase in MP (worst hip in each patient) was 1.9% per year, which is considerably less than that in nonoperated patients. Further hip surgery was necessary in 27 patients, because of increasing MP in 14 cases and for clinical reasons in 13. INTERPRETATION: Adductor tenotomy reduced the trend towards lateral displacement of the hip joints. The operation had a favorable outcome in approximately two-thirds of the patients. The operation should be performed before the MP reaches 50%. Department of Orthopedics, Rikshospitalet University Hospital, NO-0027 Oslo, Norway.


          Dr. Young
          can you tell me what happens with spasticity and spasm after treatment when people get some movements back.


            Vlad, I don't really know. From the people that I have seen, it doesn't seem to make that much difference for spasticity and spasms. Wise.


              Dr Young, there's no secret that you control the attention of the sci world, and far beyond. It is for this, and many other reasons I'm sure, that you must chose your words carefully..
              It is soon reaching the 1st anniversary of this thread. Unless previously posted elsewhere, to which I offer my apologies, I thought it only appropriate to keep you infinitely haunted by the only quandry that really matters to us: can we expect moderate recoveries by 2010?
              RULES OF RESPONSE:
              Cannot use the word; "depends".
              Cannot ask why I used the date; 2010.
              Cannot respond with another question.
              Cannot disappoint us.
              Cannot use the term "research money" more than once.

              Yes, we are trying our best too.



                Without putting any caveats on my comments, the answer is yes, I believe that there will be therapies that will restore more than "modest" amounts of function. First generation therapies produce some function or some people. Second generation therapies as those that produce more function in more people. What you received was the first generation therapy. The second generation therapies are beginning to be tested in clinical trials.



                  Tim C., good question.

                  Dr. Y, good answer.

                  Dr. Y, one more question: I have read that lower cervical and mid-thoracic injuries (above T-8) may respond to second generation therapies favorably since there is no loss of motorneurons. Is it possible that second generation could get some of these injury levels up on their feet?

                  I assume third generation will consist of replacement of lost/damaged motorneurons, correct?



                    I think that second generation therapies will help all spinal cord injured people. It is true that some people will need neuronal replacement and that will take stem cells or other therapies to produce that outcome. However, most people will benefit from axonal regeneration.



                      Dr. Young,
                      I keep reading the term "axonal regeneration". Is this currently available? Sally's problem is axonal loss. No injury, no tumors, little inflamation(controlled by IVIG). She needs axons. Some have regenerated since the onset of her illness (critical illness poyneuropathy). She continues to make very small gains 7 years post, but still not walking or weight bearing, except fullly supported on standing frame.

                      Is there any treatment currently available, anywhere in the world, that will help to hasten the regeneration of her axons?



                        Originally posted by linnburg1
                        Dr. Young,
                        I keep reading the term "axonal regeneration". Is this currently available? Sally's problem is axonal loss. No injury, no tumors, little inflamation(controlled by IVIG). She needs axons. Some have regenerated since the onset of her illness (critical illness poyneuropathy). She continues to make very small gains 7 years post, but still not walking or weight bearing, except fullly supported on standing frame.

                        Is there any treatment currently available, anywhere in the world, that will help to hasten the regeneration of her axons?
                        Regenerating axons is what most of spinal cord injury research has been all about. There are literally dozens, perhaps even hundreds, of treatments that have been reported to produce some regeneration in animal spinal cord injury models. I summarize these in many articles and posts that I have written for this site over the past three years. If you are having trouble finding them on the site, i can try to point some out.

                        Regarding Sally's situation, I assume that you are talking about her peripheral nerves and not spinal cord injury when you say "critical illness polyneuropathy". The reasons for peripheral neuropathy are not well understood. For example, it is not clear (at least to me, even though I follow the literature pretty carefully) why peripheral neuropathy occurs and what exactly happens when a person gets polyneuropathy, diabetic neuropathy, or even Guillian-Barre neuropathy. One of the reasons why we do not know is because rarely do we ever get to see the pathology of the nerves when this is happening. Few doctors would consider taking a biopsy of a peripheral nerve while neuropathy is happening. When we do see the nerves, it is usually long after the initial acute event. While there are animal models, we really don't know how closely the animal models mimic various human neuropathies.

                        There are several excellent web sites that explain peripheral neuropathy. One of the best is Diagnoses of neuropathies try to distinguish between three conditions:

                        1. Axonopathy. In this case, the axon itself is damaged but the neuron that gives rise to the axon remains intact. Generally, axonopathy affects the most distal part of the axon first and the axon dies back some distance. The axon must regrow back to restore function. Peripheral nerves do regenerate but it is much more limited is generally conceded. Recovery, however, can occur with about 10% of the peripheral axons regenerating.

                        2. Neuronopathy. In this case, the neurons that gave rise to the axons are damaged or have died. This can refer to either motoneurons (which are located in the gray matter of the spinal cord) or sensory neurons (which are located in the dorsal root ganglia just outside the spinal column). Note that when a dorsal root ganglion neuron dies, both the peripheral axon and the central axon (that goes into the spinal cord and up to the brain) die.

                        3. Myelinopathy. In this case, the cells that myelinate (ensheathes) axons die. For peripheral nerves, these cells are Schwann cells. If the axons are spared, recovery from remyelination by Schwann cells is often rapid, on the order of weeks, at most months, unless of course there is continuing demyelination.

                        Of course, a peripheral neuropathy can include all three of these components. All three cause loss of peripheral nerve function and a clinical neurological examination often is not sufficient but some obvious clinical important findings are sensory loss versus motor loss, the distribution of the neurological deficits, and the presence or absence of muscle atrophy. Nerve conduction studies can detect some partially demyelinated axons. The presence of pain or sensory hypersensitivity developing afterward would be suggestive of damage and regrowth of small and thin fibers that conduct pain. Finally, one frequently overlooks the sympathetic and parasympathetic peripheral nervous system effects of neuropathy and it is important that these be assessed in the clinical examination, including respiratory, bowel, bladder, and other autonomic functions.

                        Treatments for neuropathies to date have focused on prevention of further damage or compliations (Source), as opposed to enhancing recovery or regeneration. Many experimental treatments, however, have been shown to enhance peripheral nerve regeneration, including hormones (pregnenolone and others), growth factors (nerve growth factor or NGF, neurotrophin-3 or NT3), vitamins (B12, methylcobalmin), artemin, insulin-like growth factor or IGF-1, erythropoietin, and many other treatments.



                          Response to my post

                          Dr Young,
                          Of couse I showed utter disrespect to you and the professional world of neurology by posting such a bush question.
                          Please accept my apologies, I know you know me not to place such a desperate post.

                          But then again, you answered! ? !
                          You are remarkable.
                          Just to be sure, I have a team of lawyers carefully combing your response as we speak. lol. you have learned to choose your words carefully to say the least.
                          I also know recoveries will be available for us within the time projections you speak. I hope we can live up to your expectations too.
                          You already have inspired many blog-fuls of heroes within the CC community.


                            Last edited by Christopher Paddon; 7 Jul 2005, 4:33 AM.



                              Please, I don't think that you are showing disrespect at all. You should understand, however, that I don't have a crystal ball. My guess is as good as yours. All the information that I have is available on this site. You can judge as well as i can.

                              The main obstacle to progress in achieving restorative therapies for spinal cord injury has not been science but economics and politics. While I can talk about science until I am blue in the face, if the funding is not available to translate the science into therapies for people and there is political obstruction of therapies, the implementation of therapies may be delayed. That would be a shame.

                              As Christopher Reeve once said (paraphrasing from memory), "I think that I can accept it if scientists tell me that it is very difficult or impossible to regenerate the spinal cord but I cannot tolerate it when scientists say that it can be done but it is not happening because of funding or politics."

                              Two days ago, Senator Jon Corzine (who is running for governor of the state of New Jersey) announced his commitment to stem cell research and to making New Jersey the "cure corridor". I asked him what we can do to help him win the hearts and minds of New Jersey voters to this cause. He said to me that scientists must be careful not to take sides in politics because one cannot predict elections. He said that support of stem cell research and science that can help people should be bipartisan and should not be a political issue. He commented further that scientists may lose credibility is they take sides in politics.

                              I have been reflecting on his comment to me for the last day or so. As some people on these forums may have witnessed, over the past few years, I have become slowly but surely convinced that scientists must take a much greater role in educating society and our government. We must speak out or else those who are against science will eat our lunch. There is so much misinformation out there and I have come to realize that there are politicians who are against cure and science. The last four years in particular have convinced me that misguided politicians can do a great deal of harm people that I care very much about. We have lost four years in stem cell research because scientists hesitated to speak out strongly.

                              Scientists can no longer bury themselves in the laboratory and ignore what is happening outside. For 20 years, I did bury myself in the laboratory, believing that good science was necessary and sufficient. I still believe that it is necessary but I no longer think that good science alone is sufficient. If we discover therapies that work in animals but society and government does not do what is necessary to get the therapies to people, scientists must become involved in the process of moving the therapies to people.

                              Last edited by Wise Young; 8 Jul 2005, 7:46 AM.


                                siringomielia and future terapy

                                dear Dr.Wise

                                first i have no words for your work in the forum ; thank you very much for all you are doing for us in the world.

                                Second i have a dilemma : i'm t 5 complete asia A
                                my M.R N. show a big cavity at T6 with a syrinx from t5 to c3 ; my T-A.C.XRAY show about 20% anterior compression of the cord at T5 level- seven years ago i had posterior laminectomy with stabilitation by two Hurrington . Now ì'm in good shape i work eight hours day in my office and i do FES bycicle every day 20minuts in the pause and parastep one day a week. I would wait for the best terapy with an anterior decompression in one time but in your opinion is better to do now a anterior decompresiion and later future terapy . I have neuropatic pain but no loss function .

                                thank you so much!