Recently, LeeAnn asked a number of cogent questions in a topic entitled Seeking lots of answers, relating to her 78-year old father who had spinal cord injury. I tried to answer some of the questions specifically for her father in the topic but include below my attempt to answer the more general questions. Please understand that I have written these answers rapidly and there are typographical and other potential errors. Also, many people may have different opinions regarding the mechanisms. However, it should be good point for more questions and more discussion.
Spinal cord injury causes much more than sensory loss and paralysis. In many cases, spinal cord injury causes pain and many other complications of interrupting connections between the brain and body.
Why.....does it hurt so much?
• Most people think that spinal cord injury causes only sensory loss and paralysis. Spinal cord injury causes pain and abnormal movements (spasticity and spasms). Over 50% of people say that they have pain after spinal cord injury. Pain is the sensory counterpart to increased excitability of the motor system or spasticity in the spinal cord. This is because many of the connections in the spinal cord are inhibitory (suppresses activity) and damage to the inhibitory systems and also reorganization of the spinal cord circuitry lead to increased excitability. This increased excitability result not only is spasticity and spasms but also the presence of spontaneous pain and abnormal feelings. See answer below regarding causes of neuropathic pain.
Why.....do my legs feel like they are in water?
• Altered sensations. Our sensory systems are not just conduits for sensations from the periphery to our brains. The brain and the spinal cord are constantly filtering signals. For example, we accomodate rapidly to sensations, so that we can ignore constant sensory input such as those resulting from clothing and shoes. At the same time, we also increase sensitivity. For instance, have you every wondered why people are ticklish, so that slight touch (even imaginary touches) can produce strong sensory responses. Because spinal cord injury damages not only the sensory connections but also the pathways the control sensory threshold, this may lead to a variety of abnormal sensations, such as the legs feeling like they are under water.
Why.....do my legs feel like they are freezing?
• The spinal cord interprets incoming signals and categorizes them into various classes of sensations, such as temperature, touch, position, movement, and pain. When the signals are something that the spinal cord is recognizes, the signals are relayed to the brain. However, some of the signals are absent or the controls of the signals are not functioning, the spinal cord send abnormal signals to the brain that may be recognized as "freezing", "burning", or "pressure" sensations.
Why.....do my hands and feet swell?
• Swelling of the feet. The spinal cord controls blood flow in the legs. Normally, when a person stands up, the blood vessels in the legs constrict to keep all the blood from pooling in the legs. Likewise, muscle activity squeezes the veins so that the blood is pushed up the veins (which have valves that prevent the blood from running backwards). This "pumping" action moves blood back into the body. These vascular reflexes are impaired after spinal cord injury. Blood pools in the legs when a person sits in a wheelchair. Fluid accumulate in the legs. If the person raises his or her legs, the fluid will run back into the body. Support hoses and even alternating expanding air pumps can help move blood and fluids out of the legs.
• Swelling of the hands is more unusual after spinal cord injury. Although it may be due to abnormal sympathic activity that is cause dilation of blood vessels in the hands, I have heard fewer complaints of hand swelling than feet swelling. This may be because the arms and hands are often higher than the heart (the source of blood flow) and there is less opportunity for pooling of blood in the hands.
Why.....do my wrists ache?
• Aching in various joints of the body is common after spinal cord injury. This is because people with spinal cord injury often overuse certain joints of their bodies. Aching of the shoulders, for example, is very common in people who use manual wheelchairs a lot. If the wrists are aching, this may be because of overuse or overexercise of the hands, for example, due to use of the hands to operate a wheelchair. However, these are consequences of use. While spinal cord injury can cause neuropathic pain that may be centered on the wrists, it is important to not blame all aches and pains on spinal cord injury. It is important to rule out causes of such pain before concluding that it is due to spinal cord injury. For example, a person may have carpal tunnel syndrome, i.e. a condition in which the tunnel through which the hand tendons and nerves pass through in the wrist is constricted, and surgery may be able to fix this and other joint problems.
Why.....does my bladder feel so spasmatic?
• Bladder spasticity is very common after spinal cord injury. Spinal cord injury damages spinal tracts from the brain that sense and control the bladder. The spinal cord circuits that control the bladder become abnormally excitable when this happens. For example, one powerful reflex of the bladder is to contract when it is filled with urine. Normally, the bladder will relax the sphincter at the neck of the bladder to allow the urine out. However, the sphincter may not relax on time. When the bladder contracts "spasmodically" but the sphincter does not relax, pressures rise in the bladder, sometimes forcing urine to go into the ureters, the tubes that go from the kidneys to the bladder. If the urine is infected, retrograde reflux (backward movement of urine) may cause kidney infections. Such infections is a leading cause of kidney damage and death after spinal cord injury. Several treatment approaches are used for bladder spasticity.
1. Catheterization. The bladder is catheterized through the uretha (the tube leading from the bladder to the outside, through the penis). Because an indwelling (constantly present) foley catheter placed in the urethra tends to cause infections, sterile intermittent catheterization has the lowest risk of urinary tract infections and is the recommended approach. For people with cervical spinal cord injury who have weak hands and cannot catheterize themselves, an indwelling catheter (that is always left in) is an option. Because an indwelling foley catheter (placed through the urethra) tends to increase the incidence of infections, it is preferable to use a suprapubic catheter (placed into bladder through the abdomenal wall above the pubis). Alternatively, a surgical procedure can use the appendix or a piece of intestine to form a conduit from the umbilicus (belly button) or abdomenal wall to the bladder. The former is called a Mitrafanoff procedure.
2. Treatment and prevention of urinary tract infections, bladder stones, and other causes of bladder irritation . Infections of the bladder (cystitis) and bladder stones increase bladder irritability and spasticity. Treatment and prevention of urinary tract infections will reduce spasticity. Note that bacteria in the urine (bacteriuria) does not necessarily mean urinary tract infection. Doctors use to treat all bacteriuria with antibiotics but this practice is being discouraged because constant or repeated antibiotic therapies encourages the development of antibiotic resistant bacteria. Antibiotics should be used only if there is evidence of infection, i.e. the presence of fever, blood cells in the urine, etc. One of the most effective methods of reducing urinary tract infections is to drink plenty of fluids, increasing urine volume which washes away bacteria and keep them from colonizing the bladder. Other methods include taking vitamin C, cranberry concentrates, mandelamine, and other chemicals that inhibit bacterial growth in the urine. These approaches do not work for everybody.
3. Anticholinergic drugs (that block the acetylcholine receptors in the bladder), such as oxybutenone (ditropan) inhibit bladder reflexes . Note, however, drugs that block bladder reflexes also block reflexes that allow voluntary micturition (the act of emptying the bladder) and can cause urinary retention in people with "incomplete" spinal cord injury.
4. Bladder augmentation. A procedure that is frequently coupled with the mitrafanoff is to increase the size of the bladder with a piece of intestine. This increases the bladder capacity and weakens the ability of the bladder to contract as strongly.
Why.....don't I feel like eating?
• Some people complain of loss of appetite after spinal cord injury. Most people who have lower (thoracic or lumbosacral) spinal cord injury will recover their appetites in the months that follow spinal cord injury. However, in people with cervical spinal cord injuries may have reduced appetites for many months or even years. The cause is unclear but several possible causes should be considered.
1. Increased serum levels of calcium. Spinal cord injury is associated with reduced use of muscle and bone. Atrophy (loss of muscle) and bone loss produce high blood levels of protein and calcium that may suppress appetite. If calcium levels are elevated, treatment to reduce calcium may help improve appetite. These include giving parathyroid and other hormones.
2. Spinal cord injury (particularly to the cervical spinal cord) may interrupt signals that go from the gut to the brain and from the brain to the gut. These include some signals that stimulate the release of insulin, growth hormone, and other pituitary hormones that are responsible for turn on metabolic mechanisms to handle food. Many people with spinal cord injury may have slow insulin responses, resulting in slower clearance of glucose (sugar) from the blood. This may suppress appetite or people feeling satiated after eating. At the same time, sympathetic signals that go through the spinal cord to excite the gut to digest food may not be getting through. The vagus nerve which sends parasympathetic from the brainstem to the gut is usually not affected by spinal cord injury. The imbalance of sympathetic and parasympathetic activity may result in slower digestion and a feeling of fullness.
3. Spinal cord reflexes that respond to ingestion of food may be overactive, producing autonomic dysreflexia (AD) which produces elevated blood pressure and headaches. This may further suppress the appetite.
4. Drugs. Some of the drugs that are used to treat complications of spinal cord injury, such as bladders spasticity, pain, and other problems may suppress appetite.
5. Other associated causes. Some people may have loss of smell after cervical spinal cord injury (this may be related to injury to the olfactory nerve, the nerve that carries signals from the nose to the brain).
How.....long will it hurt?
• Not all pain after spinal cord injury is due to neuropathic pain. There may be legitimate causes of nociceptive pain (resulting from pain signals coming from the body), i.e. back pain (associated with the injury or herniated disc), joint pain (from overuse), visceral pain (people with spinal cord injury have a high risk of getting gallstones, constipation, and other causes of intestinal pain), decubiti (skin breakdown), thrombophlebitis (clots in the veins of the legs), and other conditions. These causes of pain can aggravate neuropathic pain and many people have combinations of nociceptive and neuropathic pain. Thus, it is important to identify, prevent, and treat all these causes of pain. Please note also that many analgesic (pain-stopping) may have side-effects that may contribute to pain. For example, opioid drugs tend to paralyze the gut and aggravate constipation. Once established, pain may become self-perpetrating as more drugs are used to treat the pain and the side-effects of the drugs contribute to the pain.
• The appearance and the duration of pain after spinal cord injury is difficult to predict. About half of people with spinal cord injury do not develop pain. It is not clear why this is the case. Some people have pain for several months that goes away as they recover function. Other people may develop pain many months or even years after injury. There is some animal data that suggests that pain is associated with regrowth and sprouting of new connections that occur in the spinal cord after injury. For example, drugs that suppress this sprouting (such an antibodies against growth factors and methylprednisolone) may retard or prevent the development of neuropathic pain. Several drugs have been reported to reduce neuropathic pain.
1. Low-dose amitryptaline (Elavil), an inhibitor of monoamine oxidase (MAO) that is responsible for breaking down catecholamines and other neurotransmitters in the brain and spinal cord. MAO inhibitors have long been used to treat depression and that is why these drugs are called anti-depressants. However, the dose that reduces neuropathic pain is typically lower (i.e. 20 mg per day) than anti-depressant doses of MAO inhibitors. Note that MAO inhibitors are not the same as antidepressants that block serotonin uptake.
2. Anti-epileptic drugs, such as gapapentin (neurontin). There is some evidence that neuropathic pain is associated with high-frequency firing of neurons in the brain and spinal cord. Some anti-epileptic drugs have been successfully used to treat neuropathic pain. Initial studies with gabapentin suggested that the drug is effective only for a short period but recent studies suggest that increasing the dose to very high levels (as much as 4-5 grams a day) will produce stable relief of neuropathic pain. Unfortunately, many people cannot tolerate the side-effects of these drugs.
3. Glutamate receptor blockers. There is likewise some evidence both from animal studies and clinical trials that drugs the block glutamate receptors may reduce neuropathic pain, especially when combined with other treatments such as MAO inhibitors or anti-epileptic drugs. Dextromethorphan is a drug that is often used to suppress coughs in children and may be useful when combined with other treatments. Another drug that has long been used to treat neuropathic pain in people with cancer is ketamine. This drug is a tranquilizer and has lots of side-effects at high doses but, when taken orally at relatively low doses, ketamine may take the edge off the pain.
4. Opioids. For many years, traditional opioid analgesics such as morphine, oxycodone, fentanyl, etc. were thought to be ineffective for neuropathic pain. This was usually because people accomodate rapidly to these drugs. Because opioids are addictive and have significant side-effects, most doctors were unwilling to give high doses or people cannot tolerate high doses. However, for some people with intractable neuropathic pain and who can tolerate the side effects, high-dose opioids are often effective.
Will....I ever walk again?
• This is of course the big question that everybody asks. Instead of just saying that I believe that there will be treatments that will restore function even long times after spinal cord injury, let me point out that many people have recovered walking after spinal cord injury. A person who has preservation of function below the injury level during the first days after spinal cord injury, is likely to recover substantial motor and sensory function after injury. The second and third National Acute Spinal Cord Injury Studies (NASCIS 2 and NASCIS 3) which showed the high-dose methylprednisolone is beneficial in spinal cord injury showed that people admitted to hospital with even slight preserved motor or sensory function below the injury site (i.e. "incomplete injury") are likely to recover substantial motor and sensory function over 6-16 months after spinal cord injury. A person who had a so-called "incomplete" spinal cord injury during the first 24 hours after injury will on average recover 75% of the function they had lost. Probably over half of the people will recover ability to walk (albeit not necessarily normally). Many therapies have been reported stimulate regeneration and improve locomotor recovery in animals. Approximately 15% of people with so-called "complete" spinal cord injury will recover substantial motor or sensory function below the injury level. The goal of therapies is of course to convert as many people with "complete" spinal cord injury to "incomplete" injuries, to restore more function to people with "incomplete" spinal cord injuries. My definition of a "cure" of spinal cord injury is to restore sufficient function to a person that another person would not be able to tell that the person had spinal cord injury. This is possible. I know many people who had spinal cord injury who have recovered to the extent that you would not know that they had spinal cord injury. It is useful to think of spinal cord injury therapies in "generations". The first generation of therapies that are currently in clinical trial will restore some function to some people. The second generation of therapies that will be entering clinical trial within 5 years should restore more function to more people. The third generation of therapies will probably include combinations or sequential therapies that will "cure" individuals. This is an achievable goal. The pace of developing such therapies depend on the investment that society makes in research.
Spinal cord injury causes much more than sensory loss and paralysis. In many cases, spinal cord injury causes pain and many other complications of interrupting connections between the brain and body.
Why.....does it hurt so much?
• Most people think that spinal cord injury causes only sensory loss and paralysis. Spinal cord injury causes pain and abnormal movements (spasticity and spasms). Over 50% of people say that they have pain after spinal cord injury. Pain is the sensory counterpart to increased excitability of the motor system or spasticity in the spinal cord. This is because many of the connections in the spinal cord are inhibitory (suppresses activity) and damage to the inhibitory systems and also reorganization of the spinal cord circuitry lead to increased excitability. This increased excitability result not only is spasticity and spasms but also the presence of spontaneous pain and abnormal feelings. See answer below regarding causes of neuropathic pain.
Why.....do my legs feel like they are in water?
• Altered sensations. Our sensory systems are not just conduits for sensations from the periphery to our brains. The brain and the spinal cord are constantly filtering signals. For example, we accomodate rapidly to sensations, so that we can ignore constant sensory input such as those resulting from clothing and shoes. At the same time, we also increase sensitivity. For instance, have you every wondered why people are ticklish, so that slight touch (even imaginary touches) can produce strong sensory responses. Because spinal cord injury damages not only the sensory connections but also the pathways the control sensory threshold, this may lead to a variety of abnormal sensations, such as the legs feeling like they are under water.
Why.....do my legs feel like they are freezing?
• The spinal cord interprets incoming signals and categorizes them into various classes of sensations, such as temperature, touch, position, movement, and pain. When the signals are something that the spinal cord is recognizes, the signals are relayed to the brain. However, some of the signals are absent or the controls of the signals are not functioning, the spinal cord send abnormal signals to the brain that may be recognized as "freezing", "burning", or "pressure" sensations.
Why.....do my hands and feet swell?
• Swelling of the feet. The spinal cord controls blood flow in the legs. Normally, when a person stands up, the blood vessels in the legs constrict to keep all the blood from pooling in the legs. Likewise, muscle activity squeezes the veins so that the blood is pushed up the veins (which have valves that prevent the blood from running backwards). This "pumping" action moves blood back into the body. These vascular reflexes are impaired after spinal cord injury. Blood pools in the legs when a person sits in a wheelchair. Fluid accumulate in the legs. If the person raises his or her legs, the fluid will run back into the body. Support hoses and even alternating expanding air pumps can help move blood and fluids out of the legs.
• Swelling of the hands is more unusual after spinal cord injury. Although it may be due to abnormal sympathic activity that is cause dilation of blood vessels in the hands, I have heard fewer complaints of hand swelling than feet swelling. This may be because the arms and hands are often higher than the heart (the source of blood flow) and there is less opportunity for pooling of blood in the hands.
Why.....do my wrists ache?
• Aching in various joints of the body is common after spinal cord injury. This is because people with spinal cord injury often overuse certain joints of their bodies. Aching of the shoulders, for example, is very common in people who use manual wheelchairs a lot. If the wrists are aching, this may be because of overuse or overexercise of the hands, for example, due to use of the hands to operate a wheelchair. However, these are consequences of use. While spinal cord injury can cause neuropathic pain that may be centered on the wrists, it is important to not blame all aches and pains on spinal cord injury. It is important to rule out causes of such pain before concluding that it is due to spinal cord injury. For example, a person may have carpal tunnel syndrome, i.e. a condition in which the tunnel through which the hand tendons and nerves pass through in the wrist is constricted, and surgery may be able to fix this and other joint problems.
Why.....does my bladder feel so spasmatic?
• Bladder spasticity is very common after spinal cord injury. Spinal cord injury damages spinal tracts from the brain that sense and control the bladder. The spinal cord circuits that control the bladder become abnormally excitable when this happens. For example, one powerful reflex of the bladder is to contract when it is filled with urine. Normally, the bladder will relax the sphincter at the neck of the bladder to allow the urine out. However, the sphincter may not relax on time. When the bladder contracts "spasmodically" but the sphincter does not relax, pressures rise in the bladder, sometimes forcing urine to go into the ureters, the tubes that go from the kidneys to the bladder. If the urine is infected, retrograde reflux (backward movement of urine) may cause kidney infections. Such infections is a leading cause of kidney damage and death after spinal cord injury. Several treatment approaches are used for bladder spasticity.
1. Catheterization. The bladder is catheterized through the uretha (the tube leading from the bladder to the outside, through the penis). Because an indwelling (constantly present) foley catheter placed in the urethra tends to cause infections, sterile intermittent catheterization has the lowest risk of urinary tract infections and is the recommended approach. For people with cervical spinal cord injury who have weak hands and cannot catheterize themselves, an indwelling catheter (that is always left in) is an option. Because an indwelling foley catheter (placed through the urethra) tends to increase the incidence of infections, it is preferable to use a suprapubic catheter (placed into bladder through the abdomenal wall above the pubis). Alternatively, a surgical procedure can use the appendix or a piece of intestine to form a conduit from the umbilicus (belly button) or abdomenal wall to the bladder. The former is called a Mitrafanoff procedure.
2. Treatment and prevention of urinary tract infections, bladder stones, and other causes of bladder irritation . Infections of the bladder (cystitis) and bladder stones increase bladder irritability and spasticity. Treatment and prevention of urinary tract infections will reduce spasticity. Note that bacteria in the urine (bacteriuria) does not necessarily mean urinary tract infection. Doctors use to treat all bacteriuria with antibiotics but this practice is being discouraged because constant or repeated antibiotic therapies encourages the development of antibiotic resistant bacteria. Antibiotics should be used only if there is evidence of infection, i.e. the presence of fever, blood cells in the urine, etc. One of the most effective methods of reducing urinary tract infections is to drink plenty of fluids, increasing urine volume which washes away bacteria and keep them from colonizing the bladder. Other methods include taking vitamin C, cranberry concentrates, mandelamine, and other chemicals that inhibit bacterial growth in the urine. These approaches do not work for everybody.
3. Anticholinergic drugs (that block the acetylcholine receptors in the bladder), such as oxybutenone (ditropan) inhibit bladder reflexes . Note, however, drugs that block bladder reflexes also block reflexes that allow voluntary micturition (the act of emptying the bladder) and can cause urinary retention in people with "incomplete" spinal cord injury.
4. Bladder augmentation. A procedure that is frequently coupled with the mitrafanoff is to increase the size of the bladder with a piece of intestine. This increases the bladder capacity and weakens the ability of the bladder to contract as strongly.
Why.....don't I feel like eating?
• Some people complain of loss of appetite after spinal cord injury. Most people who have lower (thoracic or lumbosacral) spinal cord injury will recover their appetites in the months that follow spinal cord injury. However, in people with cervical spinal cord injuries may have reduced appetites for many months or even years. The cause is unclear but several possible causes should be considered.
1. Increased serum levels of calcium. Spinal cord injury is associated with reduced use of muscle and bone. Atrophy (loss of muscle) and bone loss produce high blood levels of protein and calcium that may suppress appetite. If calcium levels are elevated, treatment to reduce calcium may help improve appetite. These include giving parathyroid and other hormones.
2. Spinal cord injury (particularly to the cervical spinal cord) may interrupt signals that go from the gut to the brain and from the brain to the gut. These include some signals that stimulate the release of insulin, growth hormone, and other pituitary hormones that are responsible for turn on metabolic mechanisms to handle food. Many people with spinal cord injury may have slow insulin responses, resulting in slower clearance of glucose (sugar) from the blood. This may suppress appetite or people feeling satiated after eating. At the same time, sympathetic signals that go through the spinal cord to excite the gut to digest food may not be getting through. The vagus nerve which sends parasympathetic from the brainstem to the gut is usually not affected by spinal cord injury. The imbalance of sympathetic and parasympathetic activity may result in slower digestion and a feeling of fullness.
3. Spinal cord reflexes that respond to ingestion of food may be overactive, producing autonomic dysreflexia (AD) which produces elevated blood pressure and headaches. This may further suppress the appetite.
4. Drugs. Some of the drugs that are used to treat complications of spinal cord injury, such as bladders spasticity, pain, and other problems may suppress appetite.
5. Other associated causes. Some people may have loss of smell after cervical spinal cord injury (this may be related to injury to the olfactory nerve, the nerve that carries signals from the nose to the brain).
How.....long will it hurt?
• Not all pain after spinal cord injury is due to neuropathic pain. There may be legitimate causes of nociceptive pain (resulting from pain signals coming from the body), i.e. back pain (associated with the injury or herniated disc), joint pain (from overuse), visceral pain (people with spinal cord injury have a high risk of getting gallstones, constipation, and other causes of intestinal pain), decubiti (skin breakdown), thrombophlebitis (clots in the veins of the legs), and other conditions. These causes of pain can aggravate neuropathic pain and many people have combinations of nociceptive and neuropathic pain. Thus, it is important to identify, prevent, and treat all these causes of pain. Please note also that many analgesic (pain-stopping) may have side-effects that may contribute to pain. For example, opioid drugs tend to paralyze the gut and aggravate constipation. Once established, pain may become self-perpetrating as more drugs are used to treat the pain and the side-effects of the drugs contribute to the pain.
• The appearance and the duration of pain after spinal cord injury is difficult to predict. About half of people with spinal cord injury do not develop pain. It is not clear why this is the case. Some people have pain for several months that goes away as they recover function. Other people may develop pain many months or even years after injury. There is some animal data that suggests that pain is associated with regrowth and sprouting of new connections that occur in the spinal cord after injury. For example, drugs that suppress this sprouting (such an antibodies against growth factors and methylprednisolone) may retard or prevent the development of neuropathic pain. Several drugs have been reported to reduce neuropathic pain.
1. Low-dose amitryptaline (Elavil), an inhibitor of monoamine oxidase (MAO) that is responsible for breaking down catecholamines and other neurotransmitters in the brain and spinal cord. MAO inhibitors have long been used to treat depression and that is why these drugs are called anti-depressants. However, the dose that reduces neuropathic pain is typically lower (i.e. 20 mg per day) than anti-depressant doses of MAO inhibitors. Note that MAO inhibitors are not the same as antidepressants that block serotonin uptake.
2. Anti-epileptic drugs, such as gapapentin (neurontin). There is some evidence that neuropathic pain is associated with high-frequency firing of neurons in the brain and spinal cord. Some anti-epileptic drugs have been successfully used to treat neuropathic pain. Initial studies with gabapentin suggested that the drug is effective only for a short period but recent studies suggest that increasing the dose to very high levels (as much as 4-5 grams a day) will produce stable relief of neuropathic pain. Unfortunately, many people cannot tolerate the side-effects of these drugs.
3. Glutamate receptor blockers. There is likewise some evidence both from animal studies and clinical trials that drugs the block glutamate receptors may reduce neuropathic pain, especially when combined with other treatments such as MAO inhibitors or anti-epileptic drugs. Dextromethorphan is a drug that is often used to suppress coughs in children and may be useful when combined with other treatments. Another drug that has long been used to treat neuropathic pain in people with cancer is ketamine. This drug is a tranquilizer and has lots of side-effects at high doses but, when taken orally at relatively low doses, ketamine may take the edge off the pain.
4. Opioids. For many years, traditional opioid analgesics such as morphine, oxycodone, fentanyl, etc. were thought to be ineffective for neuropathic pain. This was usually because people accomodate rapidly to these drugs. Because opioids are addictive and have significant side-effects, most doctors were unwilling to give high doses or people cannot tolerate high doses. However, for some people with intractable neuropathic pain and who can tolerate the side effects, high-dose opioids are often effective.
Will....I ever walk again?
• This is of course the big question that everybody asks. Instead of just saying that I believe that there will be treatments that will restore function even long times after spinal cord injury, let me point out that many people have recovered walking after spinal cord injury. A person who has preservation of function below the injury level during the first days after spinal cord injury, is likely to recover substantial motor and sensory function after injury. The second and third National Acute Spinal Cord Injury Studies (NASCIS 2 and NASCIS 3) which showed the high-dose methylprednisolone is beneficial in spinal cord injury showed that people admitted to hospital with even slight preserved motor or sensory function below the injury site (i.e. "incomplete injury") are likely to recover substantial motor and sensory function over 6-16 months after spinal cord injury. A person who had a so-called "incomplete" spinal cord injury during the first 24 hours after injury will on average recover 75% of the function they had lost. Probably over half of the people will recover ability to walk (albeit not necessarily normally). Many therapies have been reported stimulate regeneration and improve locomotor recovery in animals. Approximately 15% of people with so-called "complete" spinal cord injury will recover substantial motor or sensory function below the injury level. The goal of therapies is of course to convert as many people with "complete" spinal cord injury to "incomplete" injuries, to restore more function to people with "incomplete" spinal cord injuries. My definition of a "cure" of spinal cord injury is to restore sufficient function to a person that another person would not be able to tell that the person had spinal cord injury. This is possible. I know many people who had spinal cord injury who have recovered to the extent that you would not know that they had spinal cord injury. It is useful to think of spinal cord injury therapies in "generations". The first generation of therapies that are currently in clinical trial will restore some function to some people. The second generation of therapies that will be entering clinical trial within 5 years should restore more function to more people. The third generation of therapies will probably include combinations or sequential therapies that will "cure" individuals. This is an achievable goal. The pace of developing such therapies depend on the investment that society makes in research.
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