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Thread: Ten frequently asked questions concerning cure of spinal cord injury

  1. #601
    abrelsford,

    This company is donating all the cord blood for our clinical trials. Check out their website- https://www.stemcyte.com/

  2. #602
    So does anyone know where the trials with the cord/lithium stand as of now? also what is the significance of the lithium?

    Finally, more for Dr. Young: I understand there is no way to know for sure, but do you believe that there will be as you put a "stage 3 cure" in the next 10 years?

  3. #603
    Quote Originally Posted by havok View Post
    So does anyone know where the trials with the cord/lithium stand as of now? also what is the significance of the lithium?

    Finally, more for Dr. Young: I understand there is no way to know for sure, but do you believe that there will be as you put a "stage 3 cure" in the next 10 years?
    Havok, I'm no expert but you can learn a lot from watching this video http://www.ustream.tv/channel/june-open-house and reading this thread http://sci.rutgers.edu/forum/showthread.php?t=189319. The thread starts out as a joke but gets more informative as it grows. Just make sure wait for published results before jumping to any conculsion.

  4. #604
    So I reviewed all of this stuff and your right it does clear things up some. I do have a few more questions though

    1) How can UCBMC+lithium+MUSE all help to repair spinal cord injuries when other researchers insist that the myline has to be restored, the blockers turned off and the cavity in the injury removed(or regrown)? I refer mostly to what those at irvine are saying in the reeves-irvine projects.

    2) has the UCBMC+lithium shown any signs of recovery other than walking? ie is it shown potential to increase function/feeling of bladder, bowels and sexual function?

    3) the surgery that is used called decompression, is this used to remove the injured tissue in the spinal cord?

    4) would these be able to work on people who have an injury that is several vertibre long?

    5) if the trials prove successful, how long would it take for it to be available to patients in hospitals?

    Thanks and sorry for all the questions

    edit: Sorry one more question, does the method require that the lithium be used for the rest of the patients life or the progress will degenerate?
    Last edited by havok; 08-18-2012 at 06:15 PM.

  5. #605
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    Advances in medical science

    Dr. Young:

    The data for the original talking points is approaching data nearly 10 years old. Would you revise or update any of it?

  6. #606
    Quote Originally Posted by Cris View Post
    Dr. Young:

    The data for the original talking points is approaching data nearly 10 years old. Would you revise or update any of it?
    I will try to do so soon. Wise.

  7. #607
    Pacific DAWN (DisAbled Women’s Network,) is doing a new
    project, "Research from Patients' Perspective".
    We would like to connect with SCI people from Canada who wants to participate in our project . Please contact us: sciresearchfpp@gmail.com
    The goal of our project is to promote research valuable for people with chronic SCI.
    Quote Originally Posted by Wise Young View Post
    Over the years, many questions recur repeatedly every few days. Let me try to recap some of these questions to stimulate discussion. Please ask and comment...

    1. Will there be a cure for spinal cord injury?
    • The answer to this question of course depend on one's definition of a cure. If a cure means eradication of spinal cord injury, I think that it is unlikely in my lifetime. If a cure means complete restoration of all function to "normal" or pre-injury levels for all people with spinal cord injury, I think that that this is unlikely because we probably will not have therapies that can completely reverse aging and changes of the body due to the injury. On the other hand, I believe that there will be effective therapies that will restore function to people with spinal cord injury, including touch and pain sensations, bladder and bowel function, erection and ejaculation, and motor control including long-distance walking. Several years ago, I tried to get around the problem of the definition of "cure" by proposing that a person would be cured if a well-informed observer cannot tell that a person has had spinal cord injury. This does not necessarily mean that the person has been completely restored to pre-injury levels or all functions are normal.

    2. When will a cure be available?
    • Some therapies are restoring substantial function to some people. These are what I call the first generation therapies which include treatments like weight-supported treadmill ambulation training, decompression and untethering of a spinal cord that is compressed. Some preliminary data suggest that certain cell transplants such as olfactory ensheathing glia transplants will restore 4-8 levels of sensory function and 1-2 levels of motor function. None of these therapies can be construed as a cure. Second generation therapies are beginning to come into clinical trial and should be available in a few years. These include nasal mucosa olfactory ensheathing glia, Schwann cell transplants, and perhaps even embryonic stem cells. The latter unfortunately have been mired in political debate and has already been delayed by 4 years. In addition, several therapies such as Nogo receptor blockers and Nogo antibodies, glial-derived neurotrophic factor, chondroitinase, and other treatments are being developed for clinical trial and may come on line within a year or two. The timing of such treatments depends on the availability of funding for clinical trials. But, if sufficient funding were available, I think that some of these treatments will be shown to be effective and will be available in 4 years. Finally, third generation therapies will be closer to the "cure". These include possible combination cell transplant therapies with growth factors and other treatments that stimulate regeneration of the spinal cord. These should produce more recovery in more people. For example, cell transplants combined with drugs such as glial-derived neurotrophic factor, chondroitinase ABC, and cAMP/rolipram have been reported to produce significantly better regeneration in rats compared to individual treatments. The rate at which these treatments get into clinical trial depend on the amount of funding available for clinical trial. If funding were made available, I think that some of third generation therapies will be available as soon as 8 years from now.

    3. Will a cure work for chronic spinal cord injury?
    • Yes, I believe so for the following reasons. First, much animal and human data suggest that regeneration of relatively few axons can restore function such as walking, bladder function, and sexual function. This is because the spinal cord contains much of the circuitry necessary to execute and control these functions. Probably about 10% of the axons in the spinal cord are necessary and sufficient to restore some of these functions. Second, animal studies suggest that axons continue to try to regrow for long periods of time after injury. Treatments that provide a path for growth, that negate some of the factors that inhibit growth, and that stimulate axonal growth can restore function. Third, while chronic spinal cord injury studies in animals are still very limited, the fact that many people continue to recover some function years after injury provide hope that these therapies will also work in chronic spinal cord injury. However, it is important to provide some caveats concerning recovery. Recovery may be limited by muscle atrophy and other changes in the body. Likewise, there is a phenomenon called "learned non-use" where neural circuits may turn off after prolonged periods of non-use. Intensive exercise and physical therapy will be necessary to reverse these changes.

    4. What can I do now to be ready for the cure?
    • The first and foremost concern of people with spinal cord injury should be to take care of their body and try to prevent muscle and bone atrophy and other changes that may prevent recovery of function. This is difficult but people need to engage in disciplined exercise that maintains their muscle and bone, take care of their skin, bladder, and bowels. People should avoid procedures that cause irreversible loss of peripheral nerve and other functions. On the other hand, it is important to weigh the benefits of procedures such as tendon transfers which can provide greater functionality and independence for people with weak hands. Likewise, certain procedures such as Mitrofanoff and bladder augmentation to reduce bladder spasticity may provide greater independence but may not be easily reversible. Finally, many studies have shown that people with the highest levels of education after injury are more likely to have better quality of life and health. It is important that people do not neglect their brain, the most important part of their body.

    5. What can I do about spasticity, spasms, and neuropathic pain?
    • Many people suffer from spasticity (increased tone), spasms (spontaneous movements), and pain or abnormal sensations (in areas below the injury site where there is diminished or absent sensation). These problems arise from disconnection of the brain from the body. Neurons in the spinal cord that have been disconnected tend to become hyperexcitable. Spasticity is the most common manifestation. Several treatments will reduce spasticity. The most commonly used drug is baclofen (a drug that stimulates GABA-B receptors in the spinal cord). Oral doses of baclofen up to 120 mg/day will reduce spasticity for most people. However, due to side-effects, some people cannot tolerate high oral doses and must take combinations of drugs, including clonidine or tizanidine which activate alpha-adrenergic receptors. In general, while these drugs reduce spasticity, they are typically not effective in preventing spasms without causing significant weakness. Taking too much anti-spasticity drug may reduce the muscle tone to the extent that muscle atrophy will occur. So, people should titrate the dose of anti-spasticity drugs so that they continue to have some tone. Few drugs are effective against spasms. One possible drug is neurontin (gabapentin) which is an anti-epileptic drug. Neuropathic pain probably results from increased excitability of spinal neurons that have been disconnected from sensory signals and may manifest in "burning", "freezing", or "pressure" type pain, usually in areas where normal sensation is absent or greatly diminished. Neurontin is reduces neuropathic pain in some people but people generally accomodate to the drug and higher doses are necessary over time. In some people, low doses (20 mg/day) of the anti-depressant drug amitryptaline (Elavil) may be useful in taking the edge off neuropathic pain. However, for many people, none of the oral drugs are sufficient to control spasticity, spasms, or neuropathic pain. For people with severe spasticity, a pump that delivers baclofen directly to the spinal cord through an implanted catheter may be effective and necessary. In about 15% of people, however, none of these therapies are sufficient to control spasms and neuropathic pain.

    6. How can I exercise and will it do any good?
    • Exercise in a paralyzed person is difficult and some specialized equipment may be necessary and useful for exercising the muscles. First, most people have standing frames where they can stand for an hour or two every day. Second, functional electrical stimulation (FES) can be used to activate their leg muscles and the legs can be stimulated to pedal an exercise bike. Third, standing and walking in a swimming pool is the cheapest and possibly most cost-effective way for a person to stand and walk. Fourth, weight-supported treadmill ambulation training has been shown to improve walking recovery. Finally, people should think about setting aside a month or two every year where they would essentially engage in full-time training. During the rest of the year, they need to maintain the gains that they have achieved by spending an hour or so per day on exercising. Although there have been few formal studies of the subject, many people with spinal cord injury have reported significant increases in the girth of their legs when they use FES regularly.

    7. What is osteoporosis, its mechanisms and consequences, and ways to reverse it?
    • Osteoporosis is loss of calcium in bone that occur throughout the skeletal system, particularly in the pelvis and legs below the injury site. The mechanism is not understood but appears to be related to disuse and the loss of gravitational and other stresses on the bone. In acute spinal cord injury, bone begins to decalcify within days after spinal cord injury, with significant increases in calcium in the urine (hypercalciuria) within 10 days. The pattern of bone loss is 2-4 times greater those seen in people on prolonged bedrest without spinal cord injury, similar to the bone loss seen in postmenopausal women. The loss of bone is not effectively reversed by increased dietary calcium intake alone. Parathyroid hormone level is generally low in the first year but increases above normal after the first year. Substantial (25-43%) decreases in bone mineral densities occur in the leg bones occur within a year and may exceed 50% loss by 10 years while bone density may increase in the arms after 4 months in paraplegic patients, compared to tetraplegics. Some studies suggest that people with spasticity have less bone loss than those who are flaccid. Losses in bone result in increased fracture rates. The Model Spinal Cord Injury System, for example, reported a 14% incidence of fracture by 5 years after injury, 28% and 39% by 10 and 15 years, usually in the most demineralized bone. People with complete spinal cord injury and paraplegia have 10 times greater fracture rates than those with incomplete injury or tetraplegia. Weight-bearing and bicycling with functional electrical stimulation will reverse osteoporosis when started within 6 weeks after injury. However, such programs are less effective in people with chronic spinal cord injury. Some preliminary studies suggest that treatment bisphosphonates (Pamidronate) and parathyroid hormone (Teriparatide) can prevent or reduce osteoporosis and fracture rates in people with chronic spinal cord injury. http://www.emedicine.com/pmr/topic96.htm

    8. What is autonomic dysreflexia, its mechanisms and consequences, and treatments?
    • Autonomic dysreflexia (AD) refers to increased activity of the sympathetic nervous system, associated with profuse sweating, rash, elevated blood pressure, and vasodilation above the injury level. People with AD commonly develop a headache caused by vasodilation of brain blood vessels. Heart rate falls and vision may be blurred. Nasal congestion may be present. Between 40-90% of people with spinal cord injury suffer from AD and is more severe in people with spinal cord injury above T6. AD can be triggered by many potential causes, including bladder distension, urinary tract infection, and manipulation of the bowel and bladder system, pain from any source, menstruation, labor and delivery, sexual intercourse, temperature changes, constrictive clothing, sunburns, and insect bites. When AD occurs, doctors usually catheterize the bladder to ensure adequate urinary drainage, check for fecal impaction manually using lidocaine jelly as a lubricant, and eliminate all other potential causes of irritation to the body. Treatment includes use of calcium channel blocker Nifedipine (Procardia 10 mg capsule) to reduce blood pressure or adrenergic alpha-receptor blocking agent phenoxybenzamine (10 mg twice a day), mecamylamine (Inversine 2.5 mg orally). Diazoxide (Hyperstat 1-3 mg/kg). Often doctors in emergency room may not know how to handle AD crises in people with spinal cord injury and therefore it is important for people to know the treatments. http://www.emedicine.com/pmr/topic217.htm

    9. What is syringomyelia, its mechanisms and consequences, and treatments?
    • Syringomyelia is the presence of a cyst in the spinal cord, resulting from enlargement of the central canal. The central canal is typically tiny and not visible on magnetic resonance images (MRI) of the spinal cord. As many as 15% of people develop a syringomyelic cyst in their spinal cords with perhaps 5% showing symptoms of pain and loss of function associated with cyst enlargement, beginning as early as one month to as late as 45 years after injury. Pain is the most commonly reported symptom associated with syringomyelia. Other symptoms include increased weakness, loss of sensation, greater spasticity, and increased sweating. The symptoms can be aggravated by postural changes, Valsalva manuever (increasing pressure in the chest). It may also be associated with changes in bladder reflexes, autonomic dysreflexia, painless joint deformity or swelling, increased spasticity, dissociation of sensation and temperature, respiratory impairment. The cyst can be observed with MRI scans. It is usually associated with scarring of the meninges or arachnoid membranes of the spinal cord, observable with CT-scan with myelography. Surgical intervention is recommended when there is progressive neurological loss. Traditionally, syringomyelia has been treated with shunting of the cyst by placement of a catheter between the cyst and the subarachnoid space or pleural cavity. But shunting alone is frequently associated with shunt blockade within a year. More recent studies suggest that meticulous removal of adhesions with duroplasty (increasing the dura by grafting membrane) to re-establish subarachnoid cerebrospinal fluid flow is more effective and may result in elimination of the cyst in 80% of cases. One study has shown that transplantation of fetal tissues into the cyst can eliminate the cyst. http://www.emedicine.com/pmr/topic115.htm

    10. What is the effect of spinal cord injury on sexual function and what can be done to improve such function?
    • Most people with spinal cord injury above the T10 will continue to have reflex erections associated with stimulation. Some people may have prolonged erections called priapism. A majority can have ejaculation although increased stimulation including vibration may be required. In many people, ejaculation may be retrograde, i.e. the ejaculate goes into the bladder rather comes out, because the external sphincter may be open. Retrograde ejaculation should not be harmful or cause urinary tract infections. A serious associated complication of sexual intercourse in both men and women is the occurrence of autonomic dysreflexia (AD) with orgasm, with associated headaches and other symptoms of AD. These can be treated with drugs to lower blood pressure (see answer to AD above). In addition, sexual intercourse may be associated with increased spasticity and spasms. People with injuries below T10 may have damage to the spinal cord centers responsible for erection and ejaculation. Many techniques are available to increase erection, including drugs such as Sildenafil (Viagra), vacuum pumps, cock rings, and penile prostheses. Several studies have reported that women with "complete" spinal cord injury can achieve orgasms, possibly through neural pathways outside of the spinal cord.

  8. #608
    Originally Posted by Wise Young on 7/21/2004 (updated on 12/21/2012)

    I posted “Ten frequently asked questions concerning cure of spinal cord injury” over 8 years ago. Several people have asked me to update this post. I have done so.

    1. Will there be a cure for spinal cord injury?
    • The answer to this question of course depends on one's definition of a “cure”. If a “cure” means eradication of spinal cord injury, I think that such a cure would be unlikely in my lifetime. If a “cure” means complete restoration of all function to "normal" or pre-injury levels for all people with spinal cord injury, I think this is unlikely since we probably will not have therapies that can completely reverse aging and all changes of the body due to the injury. On the other hand, I believe that there will be therapies that will restore function to people with spinal cord injury, including touch and pain sensations, bladder and bowel function, erection and ejaculation, and motor control including long-distance walking. Several years ago, I tried to get around the problem of defining "cure" by proposing that a person is cured if a well-informed observer cannot tell that a person has had spinal cord injury. This does not necessarily mean that the person has been completely restored to pre-injury levels or all functions are normal. In my opinion, we have come closer this “cure” of spinal cord injury in recent years. Scientists have a better understanding of what is needed to restore function. The first clinical trials of therapies to regenerate chronic spinal cord injury have begun. It is not a matter of if we will achieve a “cure” but when. [/i]

    2. When will a cure be available?
    • First generation therapies are producing modest improvements in some people. These include functional electrical stimulation (FES), weight-supported treadmill ambulation training, decompression and untethering of compressed spinal cords. Second generation therapies include cell transplants and drugs shown to regenerate or improve function in animals. Many groups have transplanted human fetal spinal cords, olfactory ensheathing glia, olfactory mucosa, and autologous bone marrow stromal cells into people with spinal cord injury with only modest improvements of function. Geron started phase I trials of oligodendroglial precursor cells in subacute spinal cord injury in 2008 but abandoned the trial mid-stream in 2010. In 2008, Bioaxone completed Phase I/II trials showing the rho inhibitor Cethrin improves function when applied epidurally several days after spinal cord injury. In 2011, Novartis completed Phase I trials of Nogo antibody and is now considering phase II trials. Two new therapies for acute spinal cord injury (minocycline and riluzole) are showing promise in phase I/II clinical trials and may go to phase III trials. Stem Cell, Inc. and Neuralstem are testing fetal neural stem cells in chronic spinal cord injury. Miami Project will be testing Schwann cells in acute spinal cord injury. Finally, third generation therapies are combinations of cell transplant therapies with growth factors and growth inhibitor lockers to stimulate regeneration of the spinal cord. The first trials of such combination therapies have begun. ChinaSCINet is doing phase I/II clinical trials of umbilical cord blood mononuclear cells (UCBMC) and lithium, the first combination therapy for chronic spinal cord injury. Phase III trials are planned for 2013. A trial to test combination of UCBMC, lithium, and Cethrin is being planned. If successful, these trials may yield the first therapies restoring function in chronic spinal cord injury within a few years.

    3. Will a cure work for chronic spinal cord injury?
    • Yes, I believe so for the following reasons. First, much animal and human data suggest that regeneration of relatively few axons can restore function such as walking, bladder function, and sexual function. This is because the spinal cord contains much of the circuitry necessary to execute and control these functions. Probably about 10% of the axons in the spinal cord are necessary and sufficient to restore some of these functions. Second, animal studies suggest that axons continue to try to regrow for long periods of time after injury. Treatments that provide a path for growth, that negate some of the factors that inhibit growth, and that stimulate axonal growth can restore function. Third, while chronic spinal cord injury studies in animals are still very limited, the fact that many people continue to recover some function years after injury provide hope that these therapies will also work in chronic spinal cord injury. However, recovery may be limited by muscle atrophy and other changes in the body. Likewise, there is a phenomenon called "learned non-use" where neural circuits may turn off after prolonged periods of non-use. Intensive exercise and physical therapy will be necessary to reverse these changes.

    4. What can I do now to be ready for the cure?
    • The first and foremost concern of people with spinal cord injury should be to prevent muscle and bone atrophy and other changes that may prevent recovery of function. People must maintain their muscle and bone, skin, bladder, and bowels. Although several studies suggest that standing an hour a day 3 days a week does not prevent or reverse bone loss, I recommend that people stand at least an hour a day in a standing frame. People should not take so much anti-spasticity drugs that their muscles are flaccid. Spasticity is a form of exercise. People should avoid procedures that cause irreversible loss of peripheral nerves and other function. Likewise, certain procedures such as bladder augmentation to reduce bladder spasticity may provide greater independence but may not be easily reversible. Take antibiotics of urinary tract infections only when there are systemic signs of infection, such as fever. This reduces development of resistant bacterial strains. Finally, eat healthy foods and reduce weight. Obesity is not only unhealthy but prevents locomotor recovery.

    5. What can I do about spasticity, spasms, and neuropathic pain?
    • Many people suffer from spasticity (increased muscle tone), spasms (spontaneous movements), and neuropathic pain or other abnormal sensations (in areas below the injury site where there is diminished or absent sensation). These problems arise from disconnection of the brain from the body. Neurons in the spinal cord that have been disconnected tend to become hyperexcitable. Spasticity is the most common manifestation. Several drugs reduce spasticity. The most commonly used drug is baclofen (which stimulates GABA-B receptors in the spinal cord). Oral doses of baclofen up to 120 mg/day will reduce spasticity for most people. Due to side effects, some people cannot tolerate oral doses >120 mg/day and may require combinations of other drugs, such as clonidine or tizanidine, which activate alpha-adrenergic receptors. High doses of anti-spasticity drugs can cause muscle atrophy. So, people should titrate the dose of anti-spasticity drugs to maintain some muscle tone. Few drugs prevent spasms. Neurontin (gabapentin), an anti-epileptic drug used to treat neuropathic pain, seems to reduce spasms. Neuropathic pain results from increased excitability of spinal neurons that have been disconnected from sensory signals and may manifest in "burning", "freezing", or "pressure" type pain, usually in areas where sensation is absent or diminished. Neurontin reduces neuropathic pain but most people accommodate to the drug and very high doses may become necessary. For many people, low doses (20 mg/day) of the anti-depressant drug amitryptaline (Elavil) reduce neuropathic pain. Some require a pump to deliver baclofen or morphine directly to the spinal cord through an implanted catheter.

    6. How can I exercise and will it do any good?
    • Exercise in a paralyzed person is difficult and specialized equipment may be necessary and useful for exercising muscles. First, most people have standing frames where they can stand for an hour or two every day. Second, functional electrical stimulation (FES) can be used to activate their leg muscles and the legs can be stimulated to pedal an exercise bike. Third, standing and walking in a swimming pool is the cheapest and possibly most cost-effective way for a person to stand and walk. Fourth, weight-supported treadmill ambulation training has been shown to improve walking recovery. Finally, people should think about setting aside a month or two every year where they would essentially engage in full-time training. During the rest of the year, they can maintain the gains that they have achieved by spending an hour or so per day exercising. Although there have been few formal studies of the subject, many people with spinal cord injury have reported significant increases in the girth of their legs when they use FES regularly.

    7. What is osteoporosis, its mechanisms and consequences, and ways to reverse it?
    • Osteoporosis is loss of calcium in bone that occur throughout the skeletal system, particularly in the pelvis and legs that are paralyzed. The mechanism is not well understood but appears to be related to lack of weight-bearing. In acute spinal cord injury, bone begins to decalcify within days after spinal cord injury, with significant increases in calcium in the urine (hypercalciuria) within 10 days. The bone loss after spinal cord injury is 2-4 times greater those seen in people on prolonged bedrest without spinal cord injury and is similar to the bone loss seen in postmenopausal women. Increasing dietary calcium intake alone does not reverse the bone loss. Parathyroid hormone level is low in the first year but increases above normal after the first year after spinal cord injury. Substantial (25-43%) decreases in bone mineral densities occur in leg bones within a year and may exceed 50% loss by 10 years. Bone density may increase in the arms after 4 months in paraplegic patients, compared to tetraplegics. People with spasticity have less bone loss than those who are flaccid. Bone decalcification is associated with increased fracture rates. The Model Spinal Cord Injury System, for example, reported a 14% incidence of fracture by 5 years after injury, 28% and 39% by 10 and 15 years, usually in the most demineralized bone. People with complete spinal cord injury and paraplegia have 10 times greater fracture rates than those with incomplete injury or tetraplegia. Weight-bearing and bicycling with functional electrical stimulation will reverse osteoporosis when started within 6 weeks after injury. However, such programs are less effective in people with chronic spinal cord injury. Some preliminary studies suggest that treatment bisphosphonates (Pamidronate) and parathyroid hormone (Teriparatide) can prevent or reduce osteoporosis and fracture rates in people with chronic spinal cord injury. http://www.emedicine.com/pmr/topic96.htm

    8. What is autonomic dysreflexia, its mechanisms and treatments?
    • Autonomic dysreflexia (AD) refers to increased activity of the sympathetic nervous system, associated with profuse sweating, rash, elevated blood pressure, and vasodilation above the injury level. People with AD commonly develop a headache caused by vasodilation of brain blood vessels. Heart rate falls and vision may be blurred. Nasal congestion may be present. Between 40-90% of people with spinal cord injury suffer from AD and is more severe in people with spinal cord injury above T6. AD can be triggered by many potential causes, including bladder distension, urinary tract infection, and manipulation of the bowel and bladder system, pain from any source, menstruation, labor and delivery, sexual intercourse, temperature changes, constrictive clothing, sunburns, and insect bites. When AD occurs, doctors usually catheterize the bladder to ensure adequate urinary drainage, check for fecal impaction manually using lidocaine jelly as a lubricant, and eliminate all other potential causes of irritation to the body. Treatment includes use of calcium channel blocker Nifedipine (Procardia 10 mg capsule) to reduce blood pressure or adrenergic alpha-receptor blocking agent phenoxybenzamine (10 mg twice a day), mecamylamine (Inversine 2.5 mg orally). Diazoxide (Hyperstat 1-3 mg/kg). Often doctors in emergency room may not know how to handle AD crises in people with spinal cord injury and therefore it is important for people to know the treatments.http://www.emedicine.com/pmr/topic217.htm

    9. What is syringomyelia, its mechanisms and treatments?
    • Syringomyelia is the enlargement of the central canal in the spinal cord. The central canal is typically <1 mm and barely visible on magnetic resonance images (MRI) of the spinal cord. As many as 15% of people develop a syringomyelic cyst in their spinal cords after injury and 5% show symptoms of pain and loss of function associated with cyst enlargement, starting as early as one month and as late as 45 years after injury. Pain is the most commonly reported symptom. Other symptoms include increased weakness, loss of sensation, greater spasticity, and increased sweating. The symptoms can be aggravated by postural changes and Valsalva maneuver (increasing pressure in the chest). It may increase bladder reflexes, autonomic dysreflexia, painless joint swelling, spasticity, dissociation of sensation and temperature, and respiratory impairment. The cyst can be observed with MRI scans. It is usually associated with tethering or adhesions of meninges or arachnoid membranes of the spinal cord, observable with CT-scan with myelography. Surgical intervention is recommended for progressive neurological loss. Traditionally, surgeons have treated syringomyelia by shunting the cyst with catheter between the cyst and the subarachnoid space or pleural cavity. But shunting alone is frequently associated with shunt blockade within a year. More recent studies suggest that meticulous removal of adhesions with duroplasty (increasing the dura by grafting membrane) to re-establish subarachnoid cerebrospinal fluid flow is more effective and may result in elimination of the cyst in 80% of cases. One study has shown that transplantation of fetal tissues into the cyst can eliminate the cyst. http://www.emedicine.com/pmr/topic115.htm

    10. What is the effect of spinal cord injury on sexual function and what can be done to improve such function?
    • Most people with spinal cord injury above the T10 will continue to have reflex erections associated with stimulation. Some people may have prolonged erections called priapism. A majority can have ejaculation although increased stimulation including vibration may be required. Normally, sperm ejaculation goes forward (out) if the bladder sphincter is closed. However, dysfunction of the sphincter may result in retrograde ejaculation, i.e. the ejaculate goes into the bladder. Retrograde ejaculation is not harmful or cause urinary tract infections but prevent pregnancies. A serious complication of sexual intercourse in both men and women is autonomic dysreflexia (AD) with orgasms, causing headaches and other symptoms of AD. These can be treated with drugs to lower blood pressure (see answer to question 8 above). Sexual intercourse may also be associated with increased spasticity and spasms. People with injuries below T10 may have damage to spinal cord centers responsible for erection and ejaculation. Many techniques are available to increase erection, including drugs such as Sildenafil (Viagra), vacuum pumps, cock rings, and penile prostheses. Women with "complete" spinal cord injury may be able to achieve orgasms through neural pathways outside of the spinal cord.

  9. #609
    Thank you Dr Young for all your hard works and dedications in finding a cure for all of us SCI. Hope to here good news from your clinical trails.

  10. #610
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    Dr. Young,

    I noticed in a Times Union (Albany, NY) article that you were in Albany just this past week on a panel with longtime activist Paul Ricter & others advocating to get the Cuomo Administration to stop diverting money from a traffic ticket surcharge that was intended to go to spinal cord injury cure research but is instead going to the state's general fund...thanks to a decision by Gov. Paterson when he was in office.

    Thanks for lending your time & support! I wish I knew you were going to be in Albany...it would've been great to meet you...I live just nearby.
    C4/5 incomplete, 17 years since injury

    "The trick is in what one emphasizes. We either make ourselves miserable, or we make ourselves happy. The amount of work is the same.” - Carlos Castaneda

    "We live not alone but chained to a creature of a different kingdom: our body." - Marcel Proust

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