Epidural Stimulation

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Authors: Dominik Zbogar and Sharon Jang | Reviewer: Susan Harkema | Published: 14 February 2022 | Updated: ~

Key Points

  • Epidural stimulation is a treatment that sends electrical signals to the spinal cord.
  • Epidural stimulation requires a surgical procedure to implant electrodes close to the spinal cord.
  • One of the ways epidural stimulation works is by replacing the signals that would normally be sent from the brain to the spinal cord before spinal cord injury (SCI).
  • Epidural stimulation affects numerous systems. Stimulation aimed at activating leg muscles may potentially also affect bowel, bladder, sexual, and cardiovascular function.
  • Studies of epidural stimulation in spinal cord injury (SCI) generally do not include a comparison group without stimulation. The benefits of epidural stimulation that have been reported have been in small numbers of participants. So, while reports thus far are encouraging, more research is necessary.
  • Because it is in the research and development phase, epidural stimulation for spinal cord injury is not part of standard care nor is it a readily available treatment.

Neuromodulation is a general term for any treatment that changes or improves nerve pathways. Different types of neuromodulation can work at different sites along the nervous system (e.g., brain, nerves, spinal cord) and may or may not be invasive (i.e., involve surgery). Epidural stimulation (also known as epidural spinal cord stimulation or direct spinal cord stimulation) is a type of invasive neuromodulation that stimulates the spinal cord using electrical currents. This is done by placing an electrode on the dura (the protective covering around the spinal cord).

To read more about other types of neuromodulation used in SCI, access these SCIRE Community articles: Functional Electrical Stimulation (FES), Transcutaneous Electrical Nerve Stimulation (TENS), sacral nerve stimulation, and intrathecal Baclofen.

Watch our neuromodulation series videos! Our experts explain experimental to more commonplace applications, and individuals with SCI describe how neuromodulation has affected their lives.

 

 

 

What is “an Epidural”?

Epi- is a prefix and means “upon”, and the dura (full name: dura mater) is a protective covering of the spinal cord. So epidural means “upon the dura”, and in the context of epidural stimulation, this is where the electrodes that stimulate the spinal cord are placed. Yes, it is also possible to have sub-dural (under the dura) or endo-dural (within the dura) electrode placement. And, there are more layers between the dura and the spinal cord, not to mention the spinal cord itself where electrodes could be placed in what is called intraspinal microstimulation. The benefit of being beneath the dura and closer to the spinal cord is that there is a more direct stimulation. Having the electrode closer to the spinal cord allows more precision with the signal going more directly to the neurons.

The drawback is that more complications can arise with closer placement because the electrodes are in the spinal cord tissue. Such placement is currently rare, experimental, or non-existent but that will change as the technology advances. Intraspinal microstimulation has been tested in animal models and is in the process of being translated to humans.

You are probably familiar with the term “epidural” already, as it is often mentioned in relation to childbirth. If a new mother says she had an epidural, what she usually means is that she had pain medication injected into the epidural space for the purpose of managing pain during birth.

We specifically discuss epidural spinal cord stimulation in this article. Spinal cord stimulation can also be applied transcutaneously. This type of spinal cord stimulation is non-invasive as the stimulating electrodes are placed on the skin. With transcutaneous stimulation, the signal has to travel a greater distance through muscle, fat, and other tissues, which means the ability to be precise with stimulation is hampered. However, it does allow for more flexibility in electrode placement and does not require surgery. There is research published or underway investigating the impact of transcutaneous stimulation in some of the areas discussed above, including hand, leg, and cardiovascular function.

Normally, input from your senses travels in the form of electrical signals through the nerves, up the spinal cord, and reaches the brain. The brain then tells the muscles or organs what to do by sending electrical signals back down the spinal cord. After a spinal cord injury, this pathway is disrupted, preventing electrical signals from traveling below the level of injury to reach where they need to go. However, the nerves, muscles, and organs can still respond below the injury to electrical signals.

Epidural stimulation works by helping the network of nerves in the spinal cord below the injury function better and take advantage of any leftover signals from the spinal cord. To do so, the stimulation must be fine-tuned to make sure the amount of stimulation is optimal for each person and a specific function, such as moving the legs.

Recent studies of the role of epidural stimulation on standing and walking have noted unexpected beneficial changes in some participants’ bowel, bladder, sexual, and temperature regulation function. This highlights both the potential for epidural stimulation to improve quality of life in multiple ways and that much research remains to be done to understand how epidural stimulation affects the body.


There may still be spared connections in the spinal cord with a complete injury.

How can someone with a complete injury regain movement control with epidural stimulation?

Being assessed with a complete injury implies that there is no spared function below the injury. However, scientists are finding that this may not be the case. Studies have found that even with a complete loss of sensory and motor function, there may be some inactive connections that are still intact across the injury site. These remaining pathways may be important for regaining movement or other functions. Another hypothesis is that epidural stimulation in combination with training may encourage stronger connections across the level of injury. Although these pathways may provide some substitution for the injured ones, they are not as effective as non-injured pathways across the injury level.

When it is decided that an individual will receive epidural stimulation, a health professional, such as a neurosurgeon, will perform an assessment of the spinal cord using magnetic resonance imaging (MRI) to determine the best place to implant the electrodes.

In most of the studies mentioned in this article, the electrodes were placed between the T9-L1 levels, though researchers are investigating the impact of epidural stimulation on hand function.


Xray image of wires connecting power and signal to electrodes (red circle) placed on a spinal cord.

There are two possible procedures. One approach is to have two surgeries. During the initial surgery, a hollow needle is inserted through the skin into the epidural space, guided using fluoroscopy, a type of X-ray that allows the surgeon to see where the needle is in real time. Potential spots on the spinal cord are tested using a stimulator. A clinician will look to see if stimulation over those areas of the spinal cord leads to a desired response. Once found, the electrode array is properly positioned over the dura and the surgery is completed. This begins a trial period where the response to epidural stimulation is monitored. During this time the electrode array is attached to an electrical generator and power supply, which is worn on a belt outside of the body. When it is shown that things are working as desired, the generator is implanted underneath the skin in the abdomen or buttocks. The generator can be rechargeable or non-rechargeable. A remote control allows one to turn the generator on or off and control the frequency and intensity of stimulation.

The second method is to only have one surgery and no trial period. This is possible due to increased knowledge in how to stimulate the spinal cord. Soon after surgery, the individual will be taught how and when to use the epidural stimulation system at home. If needed, the frequency (how often) and intensity (how strong) of the stimulation will be adjusted at follow-up appointments with the physician. In other cases, many practice sessions of learning the right way to stimulate may be needed before a person can stimulate at home.

If the epidural stimulation is used for leg control, movement training, standing, and stepping will be required to learn how to coordinate and control movement during stimulation. This is required for the recovery of voluntary movements, standing and/or walking.

Epidural stimulation can be used in all people with SCI, regardless of the level or completeness of injury. However, certain situations can make it an unsafe treatment in some. It is important to speak to a health professional about your health history before beginning any new treatment.

Epidural stimulation should not be used in the following situations:

  • By people with implanted medical devices like cardiac pacemakers
  • By people who are unable to follow instructions or provide accurate feedback
  • By people with an active infection
  • By people with psychological or psychiatric conditions (e.g., depression, schizophrenia, substance abuse)
  • By people who are unable to form clots (anticoagulopathy)
  • Near areas of spinal stenosis (narrowing of the spinal canal)

Epidural stimulation should be used with caution in the following situations:

  • By children or pregnant women
  • By people who require frequent imaging tests like ultrasound or MRI (some epidural stimulation systems are compatible)
  • By people using anticoagulant medications (blood thinners)

Epidural stimulation is generally well-tolerated, but there is a risk of experiencing negative effects.

The most common risks and side effects of epidural stimulation include:

  • Technical difficulties with equipment, such as malfunction or shifting of the electrodes that may require surgery to fix
  • Unpleasant sensations of jolting, tingling, burning, stinging, etc. (from improper remote settings)

Other less common risks and side effects of epidural stimulation include:

  • Damage to the nervous system
  • Leakage of cerebrospinal fluid
  • Increased pain or discomfort
  • Broken bones
  • Masses/lumps growing around the site of the implanted electrode

Risks specific to the surgery which involves the removal of part of the vertebral bone (laminectomy) include:

  • bleeding and/or infection at the surgical site
  • spinal deformity and instability

Proper training on how to use the equipment and using the stimulation according to the directions of your health provider can help decrease the risks of experiencing these side effects.

Neuromodulation methods to manage bladder function have usually involved stimulation of the sacral nerves (which are outside of the spinal cord), not with epidural spinal cord stimulation. This is reflected in the fact that almost no research exists regarding the effects of epidural stimulation on bowel and bladder function in the previous century.

New information on epidural stimulation relating to bladder function is coming. In the last several years, several studies (weak evidence) from a very small group of participants of participants (who were AIS A or B) have found consistent improvements in bladder function. Participants in these reports were fitted with epidural stimulators for reactivation of paralyzed leg muscles for walking and reported additional benefits of improvements in bladder and/or bowel function. However, other studies have shown small changes to bladder function and no changes to bowel function. Negative changes, such as decreased control over the bladder, have even been noticed by some participants in another study. These findings suggest that epidural stimulation may improve quality of life by safely increasing the required time between catheterizations. Fewer catheterizations and reduced pressure in the bladder would preserve lower and upper urinary tract health. More research is required, especially with respect to bowel function. It must be noted that walk training alone has been shown to improve bladder and bowel function. Epidural stimulation may provide additional improvement to bladder function in comparison to walk training alone. Neuromodulation methods to manage bladder function have usually involved stimulation of the sacral nerves (which are outside of the spinal cord), not with epidural spinal cord stimulation. This is reflected in the fact that almost no research exists regarding the effects of epidural stimulation on bowel and bladder function in the previous century.

For more information, visit our pages on Bowel and Bladder Changes After SCI!

Why does walk/stand training alone have a beneficial effect on bladder, bowel, and sexual function?

Relationships between the leg movement and nerves in the low back regions have been identified.

Some evidence suggests that walk/step training alone can create improvements in bladder/bowel function. Researchers hypothesize that the sensory information created through walking or standing provides stimulation to the nerves in the low back region, which contains the nerves to stimulate bowel, bladder, and sexual function. Research has shown that bending and straightening the legs can be enhanced by how full the bladder is and the voiding of urine.

One of the consequences of SCI is the loss of muscle mass below the injury and a tendency to accumulate fat inside the abdomen (abdominal fat or visceral fat) and under the skin (subcutaneous fat). These changes and lower physical activity after SCI increase the risk for several diseases.

A single (weak-evidence) study measured body composition in four young males with complete injuries. Participants underwent 80 sessions of stand and step training without epidural stimulation, followed by another 160 sessions of stand/step training with epidural stimulation. This involved one hour of standing and one hour of stepping five days a week. After all, training was complete, all four participants had a small reduction in their body fat, and all participants but one experienced an increase in their fat free body mass (i.e., the weight of their bones, muscles, organs, and water in the body) in comparison to their initial values prior to stimulation. While all participants experienced a reduction of fat, the amount of fat loss was minimal, ranging from 0.8 to 2.4 kg over a period of a year.

The first use of epidural stimulation was as a treatment for chronic pain in the 1960s. Since then, it has been widely used for chronic pain management in persons without SCI. However, it is important to recognize that the chronic pain experienced by those without SCI is different from the chronic neuropathic pain experienced after SCI. This may explain, to some extent, why epidural stimulation has not been as successful in pain treatment for SCI. The mechanism by which electrical stimulation of the spinal cord can help with pain relief is unclear. Some research suggests that special nerve cells that block pain signals to the brain may be activated by epidural stimulation.

There are a few studies focused on the role of epidural stimulation in managing pain after SCI. A number of other studies included a mix of different people with and without SCI. Because chronic neuropathic pain after SCI may not be the same as the chronic pain others experience, studies that do not separate mixed groups raise questions about the validity of findings. The number of individuals with SCI in these studies is often small, most were published in the 1980s and 1990s and so are quite dated, and the research is classified as weak evidence.

The results of this body of research show that some people may receive some pain reduction. Those who saw the most reduction in pain were individuals with an incomplete SCI. Also, satisfaction with pain reduction drops off over time. One study showed only 18% were satisfied 3 years after implantation. A different study looking at the long-term use of epidural stimulation for pain reduction found seven of nine individuals stopped using this method.

In the only recent study in this area, one woman with complete paraplegia (weak evidence) experienced a reduction in neuropathic pain frequency and intensity, and a reduction in average pain from 7 to 4 out of 10, with 0 being no pain and 10 being the worst imaginable pain. This improvement remained up to three months later after implantation of the epidural stimulation device.

It should be noted that the studies for pain place electrodes in different parts of the spinal cord compared to the more recent studies for voluntary movement, standing and stepping.

Refer to our article on Pain After SCI for more information!

Using epidural stimulation to improve respiratory function is useful because it contracts the diaphragm and other muscles that help with breathing. Also, these muscles are stimulated in a way that imitates a natural pattern of breathing, reducing muscle fatigue. More common methods of improving respiratory function do not use epidural stimulation, but rather, directly stimulate the nerves that innervate the respiratory muscles. While such methods significantly improve quality of life and function in numerous ways, they are not without issues, including muscle fatigue from directly stimulating the nerves.

To date, most research into using epidural stimulation to improve respiratory function has been done in animals. Recently, research has been done in humans and weak evidence suggests that epidural stimulation may:

  • help produce a cough strong enough to clear secretions independently.
  • reduce frequency of respiratory tract infections.
  • reduce the time required caregiver support.
  • help individuals project their voice better and communicate more effectively.

Long term use of epidural stimulation shows that improvements remain over years and that minimal supervision is needed, making it suitable for use in the community.

Refer to our article on Respiratory Changes After SCI for more information!

The impact of epidural stimulation on sexual function has been a secondary focus in research studies looking at standing and walking. Currently, there are reports from one male and two females.

After a training program of walk training with epidural stimulation, one young adult male reported stronger, more frequent erections and the ability to reach full orgasm occasionally, which was not possible before epidural stimulation. However, this study looked at the effects of walk training and epidural stimulation together, which took place after several months of walk training without stimulation. Because the researchers did not describe what the individual’s sexual function was like after walk training, it is difficult to say how much benefit is attributed to epidural stimulation versus walk training.

In another study with two middle-aged females 5-10 years post-injury, one reported no change in sexual function and the other reported the ability to experience orgasms with epidural stimulation, which was not possible since her injury.

Refer to our article on Sexual Health After SCI for more information!

Botulinum toxin (Botox) injections and surgically implanted intrathecal Baclofen pumps are the most common ways to manage spasticity. Baclofen pumps are not without issues, however. Many individuals do not qualify for this treatment if they have seizures or blood pressure instability, and pumps require regular refilling.

Research in the 80s and 90s on the use of epidural stimulation for spasticity did not report very positive findings. It was noted that greater benefits were found in those with incomplete injury compared to those who were complete. Another paper concluded that (weak evidence) the beneficial effects of epidural stimulation on spasticity may subside for most users over a short period of time. This, combined with the potential for equipment failure and adverse events, suggested that epidural stimulation was not a feasible approach for ongoing management of spasticity.

More recently, positive results with epidural stimulation have been observed (weak evidence). This is likely due to improvements in technology, electrode placement, and stimulation parameters. Positive findings show that participants:

  • reported fewer spasms over 2 years
  • reported a reduction in severe spasms over 2 years
  • reported a reduction in spasticity
  • reported an improvement in spasticity over 1 year
  • were able to stop or reduce the dose of antispastic medication

For more information, visit our page on Botulinum Toxin and Spasticity!

In a study with a single participant (weak evidence) investigating walking, an individual implanted with an epidural stimulator also reported improvement in body temperature control, however details were not provided. More research is required to understand the role of epidural stimulation for temperature regulation.

In severe SCI, individuals may suffer from chronic low blood pressure and orthostatic hypotension (fall in blood pressure when moving to more upright postures). These conditions can have significant effects on health and quality of life. Some recent studies have looked at how epidural stimulation affects cardiovascular function to improve orthostatic hypotension. Overall, they show (weak evidence) that epidural stimulation immediately increases blood pressure in individuals with low blood pressure while not affecting those who have normal blood pressure. They also showed that there is a training effect with repeated stimulation. This means that after consistently using stimulation for a while, normal blood pressure can occur even without stimulation when moving from lying to sitting.

Moreover, researchers are starting to believe that changes in orthostatic hypotension and blood pressure can promote changes in the immune system (Bloom et al., 2020). In the body, the blood helps to circulate immune cells so they are able to fight infections in various areas. One case study found that after 97 sessions of epidural stimulation, the participant had fewer precursors for inflammation and more precursors for immune responses. Although these changes are exciting, researchers are still unsure why this happens, and whether these effects occur with all people who are implanted with an epidural stimulator.

Refer to our article on Orthostatic Hypotension for more information!

For individuals with tetraplegia, even some recovery of hand function can mean a big improvement in quality of life. Research into using epidural stimulation to improve hand function consists of one case study (weak evidence) involving two young adult males who sustained motor complete cervical spinal cord injury over 18 months prior.

The researchers reported improvements in voluntary movement and hand function with training while using epidural stimulation implanted in the neck. Training involved grasping and moving a handgrip while receiving stimulation. For 2 months, one man engaged in weekly sessions while the other trained daily for seven days. One participant was tested for a longer time as a permanent electrode was implanted, while the other participant only received a temporary implant. Both participants increased hand strength over the course of one session. Additional sessions brought additional gradual improvements in hand strength as well as hand control (i.e., the ability to move the hand precisely). These improvements carried over to everyday activities, such as feeding, bathing, dressing, grooming, transferring in and out of bed and moving in bed. Notably, these improvements were maintained when participants were not using epidural stimulation.

Being able to control your trunk (or torso) is important for performing everyday activities such as picking things up or reaching for items. One study found that using epidural stimulation can increase the amount of distance you are able to lean forward. The improvement in forward reach occurred immediately when the stimulation was turned on. The two participants in this study were also able to reach more side to side as well, but the improvement was minor.

Learning to make voluntary movements

Voluntary movements (i.e., being able to move your body when you want to) of affected limbs can occur with the use of epidural stimulation. Researchers are still unsure of the right training regimen to optimize results. For example, one study found that many sessions of step training with epidural stimulation are required for participants to slowly regain voluntary movement of the leg and foot with epidural stimulation when lying down. However, another study found that participants were able to voluntarily move their legs with stimulation and no stand training.

Voluntary movements (i.e., being able to move your body when you want to) of affected limbs can occur with the use of epidural stimulation. Researchers are still unsure of the right training regimen to optimize results. For example, one study found that many sessions of step and stand training with epidural stimulation are required for participants to slowly regain voluntary movement of the leg and foot with epidural stimulation when lying down. However, another study found that participants were able to voluntarily move their legs with stimulation and no stand training though the amount each participant was able to move their legs with epidural stimulation varied greatly. For example, one participant was able to voluntarily move their leg without any stimulation after over 500 hours of stand training with epidural stimulation while another participant from the same study was not able to voluntarily move their leg without stimulation after training. Overall, more than 25 people can move some or all of their leg joints voluntarily from the first time they receive epidural stimulation.

More recently, research shows that some with epidural stimulators can produce voluntary movements without stimulation on and without any intensive training program. In one study, participants did not do a consistent intensive training program, although many of them attended out-patient therapy or did therapy at home. Over the period of a year, 3 of 7 participants were able to voluntarily bend their knee, and bend and straighten their hips. Additionally, of those 3 participants, 2 were able to point their toes up and down. While the number of people able to make voluntary movements without stimulation is small, many more studies are underway.

Recent research indicates that epidural stimulation can influence walking function in individuals with limited or no motor function. While these findings are exciting, researchers are still learning how to use stimulation effectively to produce walking motions. Before being able to walk again, people must be able to make voluntary movements and be able to stand.

Learning to stand

Some studies have also found that with extensive practice (e.g., 80 sessions), independent standing (i.e., standing without the help of another person, but holding onto a bar) may be achieved without epidural stimulation. Gaining the ability to stand may also occur with stand training combined with epidural stimulation. However, the findings with regard to the effect of stand training with epidural stimulation have been mixed. For example, one study showed that stand training for 5 days a week over a 4 month period with epidural stimulation resulted in independent standing for up to 10 minutes in an individual with a complete C7 injury, while another study has suggested that independent standing for 1.5 minutes can be achieved with epidural stimulation and 2 weeks of non-step specific training in an individual with complete T6 injury.

Learning to walk

Earlier research has found that epidural stimulation can help with the development of walking-like movements, but these movements do not resemble “normal” walking. Instead, they resemble slight up and down movements of the leg. Recent studies have shown that with 10 months of practicing activities while lying down on the back and on the side, in addition to standing and stepping training, people are able to take a step without assistance from another person or body weight support. While some individuals in these studies have been able to regain some walking function, they are walking at a very slow pace, ranging from 0.19 meters per second to 0.22 meters per second. This is much slower than the 0.66 meters per second required for community walking. For example, of the 4 participants in one study, two were able to walk on the ground with a walker, one was only able to walk on a treadmill, and one was able to walk on the ground while holding the hands of another person. These differences in walking abilities gained by participants were not expected.

In late 2018, one researcher demonstrated that constant epidural stimulation was interfering with proprioception, or the body’s ability to know where your limbs are in space, which ultimately hinders the walking relearning process. The solution to this problem involves activating the stimulation in a specific sequence, rather than having it continuously on. With this method and a year’s worth of training, participants were able to begin walking with an assistive device (such as a walker or poles) without stimulation. However, these individuals had to intensively practice standing and walking with stimulation for many months to produce these results. In these studies, one case of injury was reported where a participant sustained a hip fracture during walking with a body weight support. Further studies on how to individualize therapy will be necessary as the response to treatment in these studies varied greatly from person to person depending on the frequency and intensity of the stimulation.

Is it the training or the epidural stimulation?

Most of the stand/walk training conducted in the studies is with the use of a body weight support treadmill.


Arm and leg movement and blood pressure have been seen to improve with epidural stimulation, but the role of rehabilitation in these recoveries is unclear. Rehabilitation techniques can have an effect on regaining motor function. For example, step/walk training alone can help improve the ability to make voluntary movements, walking and blood pressure among individuals with incomplete injuries.  In much of the current research, epidural stimulation is paired with extensive training (typically around 80 sessions) before and after the epidural stimulator is implanted. Furthermore, these studies do not compare the effects of epidural stimulation to a control group who receives a fake stimulation (a placebo) which would help to see if stimulation truly has an effect. Without this comparison, we are unable to clearly understand the extent of recovery that is attributable to epidural stimulation versus the effects of training. However, evidence now shows that voluntary movement and cardiovascular function can be improved from the first time epidural stimulation is used, if the stimulation parameters are specific for the function and person, which supports the role of epidural stimulation in improving function.

Access to new medical treatment for those requiring it cannot come soon enough. Experimental therapies are typically expensive and not covered by health care. Rigorous and sufficient testing is required before treatments become standard practice and receive health care coverage. Epidural stimulation for improving function in SCI is a unique example because epidural stimulation technology has been used widely to treat intractable back pain in individuals without SCI. The benefit of this is that, if/when epidural stimulation for individuals with SCI is shown to be safe and effective, the move from experimental clinical practice could happen relatively quickly as a number of hurdles from regulatory bodies have already been overcome. That said, current barriers to accessing epidural stimulation noted in a survey study of doctors include a lack of strong evidence research showing benefits, a lack of guidelines for the right stimulation settings, and an inability to determine who will benefit from it.

In Canada, the cost for an institution to install an epidural stimulation system for back pain in those without spinal cord injury, which is a common procedure, was $21,595 CAD. The cost incurred by a Canadian citizen undergoing implantation in Canada is $0 as it is covered by publicly funded health care.

 

In the United States, the cost for an institution to install an epidural stimulation system for back pain in those without spinal cord injury ranged between $32,882 USD (Medicare) and $57,896 USD (Blue Cross Blue Shield). The cost incurred for American citizens in the US will vary widely depending on their insurance coverage.

In contrast, for individuals with SCI, an epidural stimulation system is reported to cost over $100,000 USD in Thailand, and higher in other countries. Prospective clients should be aware that the epidural stimulation offered by these clinics may not be the same as that in the research reported in this article.

The recommended course for those wishing to try epidural stimulation is to register in a clinical trial. Regardless, persons interested in pursuing surgery at a private clinic or registering for clinical trials will find it useful to refer to the clinical trial guidelines published by ICORD (https://icord.org/research/iccp-clinical-trials-information/) for information on what they should be aware of when considering having an epidural stimulator implanted. Research studies that involve epidural stimulation can be found by searching the clinicaltrials.gov database.

Overall, there is evidence that epidural stimulation can improve function and health after SCI in numerous ways. However, because of the invasive nature of epidural stimulator implantation, research in this area involves few participants, no control groups, and no randomization, so it is classified as weak evidence. It is therefore important to keep in mind that while these recent reports are encouraging, more rigorous studies with more participants are needed to confirm the benefits and risks of this treatment to determine its place in SCI symptom management.

Epidural stimulation is not “plug and play” technology. Each implanted device needs to be tailored to the spine of the recipient. Some individuals respond to certain stimulation settings while others may respond better to other settings. Furthermore, over time, the need to change stimulation settings or even reposition the implant to maintain effectiveness may be required. Extensive physical training appears to be required for epidural stimulation to be most effective in improving standing or walking. The additional benefit of epidural stimulation to walk training is not always clear from the literature.

For a review of how we assess evidence at SCIRE Community and advice on making decisions, please see SCIRE Community Evidence.


Parts of this page have been adapted from the SCIRE Project (Professional) “Spasticity”, “Bladder Management”, and “Pain Management” chapters:

Hsieh JTC, Connolly SJ, McIntyre A, Townson AF, Short C, Mills P, Vu V, Benton B, Wolfe DL (2016). Spasticity Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Curt A, Mehta S, Sakakibara BM, editors. Spinal Cord Injury Rehabilitation Evidence. Version 6.0.

Available from: scireproject.com/evidence/rehabilitation-evidence/spasticity/

Hsieh J, McIntyre A, Iruthayarajah J, Loh E, Ethans K, Mehta S, Wolfe D, Teasell R. (2014). Bladder Management Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors. Spinal Cord Injury Rehabilitation Evidence. Version 5.0: p 1-196.

Available from: scireproject.com/evidence/rehabilitation-evidence/bladder-management/

Mehta S, Teasell RW, Loh E, Short C, Wolfe DL, Benton B, Hsieh JTC (2016). Pain Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Loh E, McIntyre A, Querée M, editors. Spinal Cord Injury Rehabilitation Evidence. Version 6.0: p 1-92.

Available from: scireproject.com/evidence/rehabilitation-evidence/pain-management/


Evidence for “What is epidural stimulation” is based on the following studies:

International Neuromodulation Society. (2010). Neuromodulation: An Emerging Field.

Toossi, A., Everaert, D. G., Azar, A., Dennison, C. R., & Mushahwar, V. K. (2017). Mechanically Stable Intraspinal Microstimulation Implants for Human Translation. Annals of Biomedical Engineering, 45(3), 681–694. Retrieved from http://link.springer.com/10.1007/s10439-016-1709-0

Evidence for “How does epidural stimulation work?” is based on the following studies:

Evidence for “How are epidural stimulation electrodes implanted?” is based on the following studies:

Lu, D. C., Edgerton, V. R., Modaber, M., AuYong, N., Morikawa, E., Zdunowski, S., … Gerasimenko, Y. (2016a). Engaging Cervical Spinal Cord Networks to Reenable Volitional Control of Hand Function in Tetraplegic Patients. Neurorehabilitation & Neural Repair, 30(10), 951–962. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/27198185

Lu, D. C., Edgerton, V. R., Modaber, M., AuYong, N., Morikawa, E., Zdunowski, S., … Gerasimenko, Y. (2016b). Engaging Cervical Spinal Cord Networks to Reenable Volitional Control of Hand Function in Tetraplegic Patients. Neurorehabilitation & Neural Repair, 30(10), 951–962.

Evidence for “Are there restrictions or precautions for using epidural stimulation?” is based on the following studies:

Moore, D. M., & McCrory, C. (2016). Spinal cord stimulation. BJA Education, 16(8), 258–263. Retrieved from https://linkinghub.elsevier.com/retrieve/pii/S2058534917300975

Wolter, T. (2014). Spinal cord stimulation for neuropathic pain: current perspectives. Journal of Pain Research, 7, 651–663.

Evidence for “Are there risks and side effects of epidural stimulation?” is based on the following studies:

Eldabe, S., Buchser, E., & Duarte, R. V. (2015). Complications of Spinal Cord Stimulation and Peripheral Nerve Stimulation Techniques: A Review of the Literature. Pain Medicine, 17(2), pnv025. Retrieved from https://academic.oup.com/painmedicine/article-lookup/doi/10.1093/pm/pnv025

Taccola, G., Barber, S., Horner, P. J., Bazo, H. A. C., & Sayenko, D. (2020). Complications of epidural spinal stimulation: lessons from the past and alternatives for the future. Spinal Cord, 58(10), 1049–1059. Retrieved from http://dx.doi.org/10.1038/s41393-020-0505-8

Evidence for “Epidural stimulation and bladder and bowel function” is based on the following studies:

Herrity, A. N., Williams, C. S., Angeli, C. A., Harkema, S. J., & Hubscher, C. H. (2018). Lumbosacral spinal cord epidural stimulation improves voiding function after human spinal cord injury. Scientific Reports, 8(1), 1–11. Retrieved from http://dx.doi.org/10.1038/s41598-018-26602-2

Herrity, April N., Aslan, S. C., Ugiliweneza, B., Mohamed, A. Z., Hubscher, C. H., & Harkema, S. J. (2021). Improvements in Bladder Function Following Activity-Based Recovery Training With Epidural Stimulation After Chronic Spinal Cord Injury. Frontiers in Systems Neuroscience, 14(January), 1–14.

Hubscher, C. H., Herrity, A. N., Williams, C. S., Montgomery, L. R., Willhite, A. M., Angeli, C. A., & Harkema, S. J. (2018). Improvements in bladder, bowel and sexual outcomes following task-specific locomotor training in human spinal cord injury. Plos One, 1–26.

Darrow, D., Balser, D., Netoff, T. I., Krassioukov, A., Phillips, A., Parr, A., & Samadani, U. (2019). Epidural Spinal Cord Stimulation Facilitates Immediate Restoration of Dormant Motor and Autonomic Supraspinal Pathways after Chronic Neurologically Complete Spinal Cord Injury. Journal of Neurotrauma, 2336, neu.2018.6006. Retrieved from https://www.liebertpub.com/doi/10.1089/neu.2018.6006

Beck, L., Veith, D., Linde, M., Gill, M., Calvert, J., Grahn, P., … Zhao, K. (2020). Impact of long-term epidural electrical stimulation enabled task-specific training on secondary conditions of chronic paraplegia in two humans. Journal of Spinal Cord Medicine, 0(0), 1–6. Retrieved from https://doi.org/10.1080/10790268.2020.1739894

Evidence for “Epidural stimulation and body composition” is based on the following studies:

Terson de Paleville, D. G. L., Harkema, S. J., & Angeli, C. A. (2019). Epidural stimulation with locomotor training improves body composition in individuals with cervical or upper thoracic motor complete spinal cord injury: A series of case studies. The Journal of Spinal Cord Medicine, 42(1), 32–38.

Evidence for “Epidural stimulation and pain” is based on the following studies:

Guan, Y. (2012). Spinal cord stimulation: neurophysiological and neurochemical mechanisms of action. Current Pain and Headache Reports, 16(3), 217–225.

Marchand, S. (2015). Spinal cord stimulation analgesia. PAIN, 156(3), 364–365.

Tasker, R. R., DeCarvalho, G. T., & Dolan, E. J. (1992). Intractable pain of spinal cord origin: clinical features and implications for surgery. Journal of Neurosurgery.

Cioni, B., Meglio, M., Pentimalli, L., & Visocchi, M. (1995). Spinal cord stimulation in the treatment of paraplegic pain. Journal of Neurosurgery, 82(1), 35–39.

Warms, C. A., Turner, J. A., Marshall, H. M., & Cardenas, D. D. (2002). Treatments for chronic pain associated with spinal cord injuries: many are tried, few are helpful. Clinical Journal of Pain, 18(3), 154–163.

Reck, T. A., & Landmann, G. (2017). Successful spinal cord stimulation for neuropathic below-level spinal cord injury pain following complete paraplegia: a case report. Spinal Cord Series and Cases, 3, 17049.

Evidence for “Epidural stimulation and respiratory function” is based on the following studies:

Hachmann, J. T., Grahn, P. J., Calvert, J. S., Drubach, D. I., Lee, K. H., & Lavrov, I. A. (2017). Electrical Neuromodulation of the Respiratory System After Spinal Cord Injury. Mayo Clinic Proceedings, 92(9), 1401–1414. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/28781176

DiMarco, A. F., Kowalski, K. E., Geertman, R. T., & Hromyak, D. R. (2006). Spinal cord stimulation: a new method to produce an effective cough in patients with spinal cord injury. American Journal of Respiratory and Critical Care Medicine, 173(12), 1386–1389.

DiMarco, A. F., Kowalski, K. E., Geertman, R. T., & Hromyak, D. R. (2009). Lower thoracic spinal cord stimulation to restore cough in patients with spinal cord injury: results of a National Institutes of Health-sponsored clinical trial. Part I: methodology and effectiveness of expiratory muscle activation. Archives of Physical Medicine & Rehabilitation, 90(5), 717–725.

Harkema, S. J., Wang, S., Angeli, C. A., Chen, Y., Boakye, M., Ugiliweneza, B., & Hirsch, G. A. (2018). Normalization of Blood Pressure With Spinal Cord Epidural Stimulation After Severe Spinal Cord Injury. Frontiers in Human Neuroscience, 12, 83.

DiMarco, A. F., Kowalski, K. E., Hromyak, D. R., & Geertman, R. T. (2014). Long-term follow-up of spinal cord stimulation to restore cough in subjects with spinal cord injury. The Journal of Spinal Cord Medicine, 37(4), 380–388.

Evidence for “Epidural stimulation and sexual function” is based on the following studies:

Harkema, S., Gerasimenko, Y., Hodes, J., Burdick, J., Angeli, C., Chen, Y., … Edgerton, V. R. (2011). Effect of epidural stimulation of the lumbosacral spinal cord on voluntary movement, standing, and assisted stepping after motor complete paraplegia: A case study. The Lancet, 377(9781), 1938–1947.

Darrow, D., Balser, D., Netoff, T. I., Krassioukov, A., Phillips, A., Parr, A., & Samadani, U. (2019). Epidural Spinal Cord Stimulation Facilitates Immediate Restoration of Dormant Motor and Autonomic Supraspinal Pathways after Chronic Neurologically Complete Spinal Cord Injury. Journal of Neurotrauma, 2336, neu.2018.6006. Retrieved from https://www.liebertpub.com/doi/10.1089/neu.2018.600

Evidence for “Epidural stimulation and spasticity” is based on the following studies:

Nagel, S. J., Wilson, S., Johnson, M. D., Machado, A., Frizon, L., Chardon, M. K., … Howard, M. A. 3rd. (2017). Spinal Cord Stimulation for Spasticity: Historical Approaches, Current Status, and Future Directions. Neuromodulation: Journal of the International Neuromodulation Society, 20(4), 307–321.

Dekopov, A. V., Shabalov, V. A., Tomsky, A. A., Hit, M. V., & Salova, E. M. (2015). Chronic spinal cord stimulation in the treatment of cerebral and spinal spasticity. Stereotactic and Functional Neurosurgery.

Dimitrijevic, M. R., Illis, L. S., Nakajima, K., Sharkey, P. C., & Sherwood, A. M. (1986). Spinal cord stimulation for the control of spasticity in patients with chronic spinal cord injury: II. Neurophysiologic observations. Central Nervous System Trauma, 3(2), 145–152. Retrieved from http://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&D=med2&AN=3490313

Midha, M., & Schmitt, J. K. (1998). Epidural spinal cord stimulation for the control of spasticity in spinal cord injury patients lacks long-term efficacy and is not cost-effective. Spinal Cord, 36(3), 190–192. Retrieved from https://www.nature.com/articles/3100532

Barolat, G., Singh-Sahni, K., Staas, W. E. J., Shatin, D., Ketcik, B., & Allen, K. (1995). Epidural spinal cord stimulation in the management of spasms in spinal cord injury: a prospective study. Stereotactic & Functional Neurosurgery, 64(3), 153–164.

Dekopov, A. V., Shabalov, V. A., Tomsky, A. A., Hit, M. V., & Salova, E. M. (2015). Chronic spinal cord stimulation in the treatment of cerebral and spinal spasticity. Stereotactic and Functional Neurosurgery.

Pinter, M. M., Gerstenbrand, F., & Dimitrijevic, M. R. (2000). Epidural electrical stimulation of posterior structures of the human lumbosacral cord: 3. Control Of spasticity. Spinal Cord, 38(9), 524–531. Retrieved from https://www.nature.com/articles/3101040

Evidence for “Epidural stimulation and temperature regulation” is based on the following studies:

Edgerton, V. R., & Harkema, S. (2011). Epidural stimulation of the spinal cord in spinal cord injury: current status and future challenges. Expert Review of Neurotherapeutics, 11(10), 1351–1353. Retrieved from http://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&D=med7&AN=21955190

Harkema, S. J., Gerasimenko, Y., Hodes, J., Burdick, J., Angeli, C., Chen, Y., … Edgerton, V. R. (2011). Supplementary index: Effect of epidural stimulation of the lumbosacral spinal cord on voluntary movement, standing, and assisted stepping after motor complete paraplegia: A case study. The Lancet, 377(9781), 1938–1947. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21601270

Evidence for “Epidural stimulation and cardiovascular function” is based on the following studies:

Bloom, O., Wecht, J. M., Legg Ditterline, B. E., Wang, S., Ovechkin, A. V., Angeli, C. A., … Harkema, S. J. (2020). Prolonged Targeted Cardiovascular Epidural Stimulation Improves Immunological Molecular Profile: A Case Report in Chronic Severe Spinal Cord Injury. Frontiers in Systems Neuroscience, 14(October), 1–11.

Evidence for “Epidural stimulation and hand function” is based on the following study:

Lu, D. C., Edgerton, V. R., Modaber, M., AuYong, N., Morikawa, E., Zdunowski, S., … Gerasimenko, Y. (2016a). Engaging Cervical Spinal Cord Networks to Reenable Volitional Control of Hand Function in Tetraplegic Patients. Neurorehabilitation & Neural Repair, 30(10), 951–962. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/27198185

Evidence for “Epidural stimulation and movement: trunk control” is based on the following studies:

Evidence for “Epidural stimulation and movement: voluntary movements” is based on the following studies:

Rejc, E., Angeli, C. A., Bryant, N., & Harkema, S. J. (2017). Effects of Stand and Step Training with Epidural Stimulation on Motor Function for Standing in Chronic Complete Paraplegics. Journal of Neurotrauma, 34, 1787–18023. Retrieved from www.liebertpub.com

Angeli, C. A., Edgerton, V. R., Gerasimenko, Y. P., & Harkema, S. J. (2014). Altering spinal cord excitability enables voluntary movements after chronic complete paralysis in humans. Brain, 137(Pt 5), 1394–1409. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3999714/

Peña Pino, I., Hoover, C., Venkatesh, S., Ahmadi, A., Sturtevant, D., Patrick, N., Freeman, D., Parr, A., Samadani, U., Balser, D., Krassioukov, A., Phillips, A., Netoff, T. I., & Darrow, D. (2020). Long-Term Spinal Cord Stimulation After Chronic Complete Spinal Cord Injury Enables Volitional Movement in the Absence of Stimulation. Frontiers in systems neuroscience14, 35. https://doi.org/10.3389/fnsys.2020.00035

Evidence for “Epidural stimulation and movement: walking and standing” is based on the following studies:

Grahn, P. J., Lavrov, I. A., Sayenko, D. G., Straaten, M. G. Van, Gill, M. L., Strommen, J. A., … Lee, K. H. (2017). Enabling Task-Specific Volitional Motor Functions via Spinal Cord Neuromodulation in a Human with Paraplegia. Mayo Clinic Proceedings, 92(4), 544–554. Retrieved from http://dx.doi.org/10.1016/j.mayocp.2017.02.014

Harkema, S. J., Gerasimenko, Y., Hodes, J., Burdick, J., Angeli, C., Chen, Y., … Edgerton, V. R. (2011). Supplementary index: Effect of epidural stimulation of the lumbosacral spinal cord on voluntary movement, standing, and assisted stepping after motor complete paraplegia: A case study. The Lancet, 377(9781), 1938–1947. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21601270

Rejc, E., Angeli, C. A., Atkinson, D., & Harkema, S. J. (2017). Motor recovery after activity-based training with spinal cord epidural stimulation in a chronic motor complete paraplegic. Scientific Reports, 7(1), 13476. Retrieved from www.nature.com/scientificreports

Rejc, E., Angeli, C., & Harkema, S. (2015). Effects of Lumbosacral Spinal Cord Epidural Stimulation for Standing after Chronic Complete Paralysis in Humans. PLoS ONE [Electronic Resource], 10(7), e0133998. Retrieved from http://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&D=med8&AN=26207623

Grahn, P. J., Lavrov, I. A., Sayenko, D. G., Straaten, M. G. Van, Gill, M. L., Strommen, J. A., … Lee, K. H. (2017). Enabling Task-Specific Volitional Motor Functions via Spinal Cord Neuromodulation in a Human with Paraplegia. Mayo Clinic Proceedings, 92(4), 544–554. Retrieved from http://dx.doi.org/10.1016/j.mayocp.2017.02.014

Gill, M. L., Grahn, P. J., Calvert, J. S., Linde, M. B., Lavrov, I. A., Strommen, J. A., … Zhao, K. D. (2018). Neuromodulation of lumbosacral spinal networks enables independent stepping after complete paraplegia. Nature Medicine, 24(11), 1677–1682. Retrieved from https://doi.org/10.1038/s41591-018-0175-7

Angeli, C. A., Boakye, M., Morton, R. A., Vogt, J., Benton, K., Chen, Y., … Harkema, S. J. (2018). Recovery of Over-Ground Walking after Chronic Motor Complete Spinal Cord Injury. New England Journal of Medicine, 379(13), 1244–1250. Retrieved from http://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&D=medl&AN=30247091

van de Port, I. G., Kwakkel, G., & Lindeman, E. (2008). Community ambulation in patients with chronic stroke: How is it related to gait speed? Journal of Rehabilitation Medicine, 40(1), 23–27.

Wagner, F. B., Mignardot, J.-B., Le Goff-Mignardot, C. G., Demesmaeker, R., Komi, S., Capogrosso, M., … Courtine, G. (2018). Targeted neurotechnology restores walking in humans with spinal cord injury. Nature, 563(7729), 65–71. Retrieved from http://www.nature.com/articles/s41586-018-0649-2

Angeli, C. A., Edgerton, V. R., Gerasimenko, Y. P., & Harkema, S. J. (2014). Altering spinal cord excitability enables voluntary movements after chronic complete paralysis in humans. Brain, 137(Pt 5), 1394–1409. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3999714/

Carhart, M. R., He, J., Herman, R., D’Luzansky, S., & Willis, W. T. (2004). Epidural spinal-cord stimulation facilitates recovery of functional walking following incomplete spinal-cord injury. IEEE Transactions on Neural Systems & Rehabilitation Engineering, 12(1), 32–42. Retrieved from http://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&D=med5&AN=15068185

Harkema, S. J., Wang, S., Angeli, C. A., Chen, Y., Boakye, M., Ugiliweneza, B., & Hirsch, G. A. (2018). Normalization of Blood Pressure With Spinal Cord Epidural Stimulation After Severe Spinal Cord Injury. Frontiers in Human Neuroscience, 12, 83.

Legg Ditterline, B. E., Aslan, S. C., Wang, S., Ugiliweneza, B., Hirsch, G. A., Wecht, J. M., & Harkema, S. (2020). Restoration of autonomic cardiovascular regulation in spinal cord injury with epidural stimulation: a case series. Clinical Autonomic Research, (0123456789), 2–5. Retrieved from https://doi.org/10.1007/s10286-020-00693-2

Evidence for “Costs and availability of epidural stimulation” is based on the following studies:

Solinsky, R., Specker-Sullivan, L., & Wexler, A. (2020). Current barriers and ethical considerations for clinical implementation of epidural stimulation for functional improvement after spinal cord injury. Journal of Spinal Cord Medicine, 43(5), 653–656.

Kumar, K., & Bishop, S. (2009). Financial impact of spinal cord stimulation on the healthcare budget: a comparative analysis of costs in Canada and the United States. Journal of Neurosurgery: Spine.

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  1. Image by SCIRE Community Team
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  5. Adapted from image made by Mysid Inkscape, based on plate 770 from Gray’s Anatomy (1918, public domain).
  6. Pregnant woman holding tummy. [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)] via Google Images.
  7. Edited from Nervous system, Musculature. ©Servier Medical Art. CC BY 3.0.
  8. Neurons ©NIH Image Gallery. CC BY-NC 2.0.
  9. Image by SCIRE Community
  10. bladder by fauzan akbar from the Noun Project
  11. Large Intestine by BomSymbols from the Noun Project
  12. Feet by Matt Brooks from the Noun Project
  13. hip by priyanka from the Noun Project
  14. visceral fat by Olena Panasovska from the Noun Project
  15. Lightning by FLPLF from the Noun Project
  16. Lungs by dDara from the Noun Project
  17. Love by Jake Dunham from the Noun Project
  18. Male by Centis MENANT from the Noun Project
  19. Female by Centis MENANT from the Noun Project
  20. Image by SCIRE Community
  21. Temperature by Adrien Coquet from the Noun Project
  22. Heart by Nick Bluth from the Noun Project
  23. Image by SCIRE Community
  24. Hand by Sergey Demushkin from the Noun Project
  25. Torso by Ronald Vermeijs from the Noun Project
  26. Yoga posture by Gan Khoon Lay from the Noun Project
  27. Standing by Rafo Barbosa from the Noun Project
  28. Walking by Samy Menai from the Noun Project
  29. Image by SCIRE Community
  30. Canada by Yohann Berger from the Noun Project
  31. United States of America by Yohann Berger from the Noun Project

 

Disclaimer: This document does not provide medical advice. This information is provided for educational purposes only. Consult a qualified health professional for further information or specific medical advice. The SCIRE Project, its partners and collaborators disclaim any liability to any party for any loss or damage by errors or omissions in this publication.

Cannabis (Marijuana) and Cannabinoids

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Authors: SCIRE Community Team | Reviewer: Andrea Townson and Janice Eng | Published: 2 April 2019 | Updated: Apr 20, 2020

Cannabis (marijuana) is an alternative treatment option for pain and spasticity after spinal cord injury (SCI). This page outlines basic information about cannabis and its use after SCI.

Key Points

  • “Cannabis” refers to products derived from the cannabis plant, such as marijuana. The natural cannabinoids or compounds found in cannabis can also be made synthetically.
  • Cannabis may be inhaled as a smoke or vapour or taken by mouth as a capsule or spray.
  • Smoking cannabis is not recommended due to the risks associated with inhaling smoke.
  • The safety of cannabis products for use after SCI is not known. Please consult your health providers for detailed safety information.
  • Research on cannabis use after SCI is in its early stages. Studies done so far show that cannabis products may have beneficial effects on pain and are unclear about its effects on spasticity. More research is needed to establish if cannabis is a safe and effective treatment after SCI.
A photograph of leaves of a cannabis plant

Leaves of a cannabis plant.1

Cannabis is a term that refers to the products of cannabis (hemp) plants, a group of plants from central Asia that are now cultivated around the world. Cannabis sativa, Cannabis indica, and Cannabis ruderalis are three well-known types of cannabis, but many strains or varieties exist, both pure and hybrid types. Common preparations of cannabis include marijuana, which is the dried leaves and flowering tops of the plant, and hashish, which is its condensed resin. Cannabis has been used for thousands of years as a medicine and recreational drug.

Currently, cannabis is a controlled substance in most regions because of its psychoactive effects. However, exceptions are made in some places for approved medical or spiritual uses. In addition to medical use, in Canada recreational use of cannabis has also been made legal as of October 2018. Here, the sale of recreational cannabis was originally limited to dried cannabis and oils, but as of October 2019 edibles and concentrates are also legal for sale.

Cannabis has been studied as a treatment for conditions as diverse as nausea associated with cancer chemotherapy, loss of appetite in people with HIV, and spasticity associated with multiple sclerosis.

Cannabis has its unique properties because of naturally-occurring chemical compounds within the plant called cannabinoids. Cannabinoids act on receptors on the surface of cells called cannabinoid receptors, causing effects on body processes like pain, memory, appetite, and immune responses.

Diagram categorizing cannabinoids into endocannabinoids (produced in the body), phytocannabinoids (produced by the cannabis plant), and synthetic cannabinoids (synthesized in a lab)

There are various sources of cannabinoids, both natural and synthetic.2

Cannabinoids occur naturally within the body (endocannabinoids), in cannabis plants (phytocannabinoids), and can also be synthesized in a lab (synthetic cannabinoids). There are more than 60 cannabinoids present in cannabis, with the most well-known being Delta-9-tetrahydrocannabinol (commonly known as THC), which is responsible for many of the psychoactive effects for which cannabis is known such as creating a “high” or sense of euphoria. Other cannabinoids, like Cannabidiol (also known as CBD), are not psychoactive and may have different effects such as improving mental health concerns and preventing oxidative damage although evidence for this is currently not conclusive. Because of these benefits over THC as well as the reduced health risks, CBD is believed to be the component of cannabis that gives rise to its medicinal potential and opposes the negative psychiatric effects associated with THC.

The chemical structures of THC and CBD

The chemical structures of THC and CBD.3

Cannabis/Cannabinoids, whether plant-derived or human-made, may be used for medicinal or recreational purposes in a variety of ways.

Medical cannabinoid products

Medical cannabis

The laws and regulations required to get approval for medical marijuana differ by country and region. In Canada, use of medical cannabis requires authorization for use from a physician.

Prescription synthetic cannabinoids

In some countries, certain synthetic cannabinoids are available for therapeutic use and require a prescription from a physician. Like other medications, these products are registered with a Drug Identification Number (DIN) in Canada or with the Food and Drug Administration (FDA) in the United States. Prescription synthetic cannabinoids are carefully regulated and monitored for their composition and effects on the body and are developed to minimize accompanying intoxication.

Recreational cannabis products

An indoor grow op with rows of cannabis plants in pots.

There are various environmental and health risks associated with unlicensed grow-ops.4

Recreational use of cannabis is legal in Canada, but still subject to provincial or territorial restrictions. Recreational use outside these restrictions is illegal. Like medical cannabis, the production and distribution of recreational cannabis is regulated to ensure safety and quality. There are various concerns with the use of cannabis that is not regulated or produced legally. These cannabis products may include harmful contaminants (e.g., mold, bacteria, and pesticides) or have much greater variation in their chemical composition than cannabis products intended for medical use. It can be difficult to know exactly what dose you are receiving and the risks and side effects for using these products may be unknown. Another issue with cannabis sourced from illegal grow-ops include its negative impact on the environment as these sites may misuse toxic pesticides and may divert water supply away from lakes or rivers, threatening plant, wildlife, and human health. Unregulated cannabis products are not recommended for treating symptoms of SCI.

Illegal synthetic cannabinoids

A hand holding a jar of synthetic cannabinoids mixed with shredded cannabis plant material.

Illegal synthetic cannabinoids may be sold to look like cannabis.5

Even though synthetic cannabinoids act on the same receptors as the phytocannabinoids found in the cannabis plant, they may produce different effects on the body. Some non-prescription synthetic cannabinoids are made to imitate the psychoactive effects of THC, making them potentially dangerous especially since their actions on the body can be unpredictable. Known by names like “Spice” and “K2,” these compounds are often combined with plant-based products and sold as “alternatives” to marijuana. However, all activities associated with non-prescription synthetic cannabinoids (e.g., production, distribution, use) are illegal in Canada. Besides the fact that illegal synthetic cannabinoids have not been tested in humans, their product composition can vary greatly and may be laced with other unknown and potentially deadly substances. Synthetic cannabinoids also more potent than plant-derived THC. This means that they bind more strongly to the cannabinoid receptors, increasing the risk of overdose.

Cartoon image showing different dosage forms of cannabis (vape pen, capsules, cream, and oil).

Photograph of a female smoking a joint.

Smoking is not a recommended method of using cannabis.10

Cannabis products are usually inhaled or taken by mouth. Smoking is the most common method among the general population as well as within the SCI population. However, there are serious concerns about the negative health effects to the user and those nearby associated with inhaling and exhaling smoke, which contains many of the same harmful compounds as tobacco smoke. People with SCI, in particular, should avoid smoking cannabis as respiratory issues including compromised breathing and pneumonia are already prevalent in the SCI population. Vaporization is another method where the cannabis leaves are heated to form a vapour that is then inhaled. While vaping prevents the cannabinoids from burning which decreases the amount of toxic by-products produced compared to smoking, it is not without risks and has recently been associated with vaping-associated pulmonary injury (VAPI). After a sharp increase in VAPI cases in August and September of 2019, emergency department visits continue to decline. This is thought to be due to the removal of vitamin E acetate from most products, increased public awareness of the risks associated with THC containing e-cigarettes or vaping devices, and law enforcement actions related to illicit products in the US. Canadian extracts for vaping that contain THC are not allowed to have any added vitamins, minerals, nicotine, sugars, flavouring or colouring agents.

Cannabis can also be taken by mouth in the form of food items or other products like oils, capsules, and mouth sprays. Other less common methods cannabis may be delivered include through the skin (e.g. creams, lotions, balms, patches, etc.), through the rectum, or into the veins


A bottle of CBD oil with a dropper above.

Cannabis can be prepared by extracting the cannabinoids from the plant and dissolving it in oil.11

Cannabidiol oil

CBD oil is becoming more popular among people who wish to gain the health benefits of cannabis and avoid the psychoactive effects of THC. Although many people use CBD oil for a range of ailments, there is limited safety and efficacy data (and no research in SCI) to support its use for these conditions. Recently, positive results from three clinical trials with strong evidence have led the Food and Drug Administration (FDA) in the United States to approve the use of CBD oil for two rare forms of epilepsy in June 2018.

Prescription synthetic cannabinoids

Prescription synthetic cannabinoids often use isolated cannabinoid compounds or combinations of cannabinoids. This includes products such as:

  • Nabilone (Cesamet), a synthetic cannabinoid similar to THC that is taken by mouth as a capsule.
  • Dronabinol (Marinol), synthetic THC that is taken by mouth as a capsule. Please note that dronabinol is no longer available in Canada.
  • Nabiximols (Sativex), a mix of cannabis plant-derived THC and CBD that is taken as a mouth spray.
A jar of dried marijuana including the flowers and leaves.

Marijuana is the dried flowers and leaves of cannabis.12

There are currently no standard cannabis dosing regimens for SCI-related conditions. Dosing for medical cannabis varies based on factors such as method of delivery, past cannabis use, and the medical condition being treated. Additionally, the amount of THC and CBD in marijuana is not always the same. Thus, the effects of different marijuana products are not always the same. Levels of THC and CBD in a product can change based on the strain of the plant used as well as how the plant was grown and prepared.

Especially for those who have never used cannabis in the past, it is recommended that they start on low doses before slowly increasing the dose until their therapeutic goals are met. To minimize negative side effects related to THC and maximize symptom control, a strain with low THC and high CBD may be used initially. Immediately discontinue use if any intolerable side effects occur.

People who use cannabis for medicinal purposes consume an average of 1-3 g/day or 10-20 g/week. Even with equal grams of the same cannabis strain, the amount of cannabis the body actually absorbs differs depending on the method of delivery. For example, people who wish to switch from inhaling cannabis to taking cannabis by mouth may need to increase in their daily cannabis use by 2.5 times to get an equivalent dose. Each different form and method of cannabis use will change how quickly the drug produces an effect and how long it lasts in the body. For example, inhalation of cannabis will generally lead to a faster onset of action and longer-lasting effect than oral ingestion.

Inhalation Oral ingestion
Onset of action Few minutes 30 minutes (up to 3-4 hours)
Peak of effect 30 minutes 3-4 hours
Duration of effect 2-4 hours (up to 24 hours) 8 hours (up to 12-24 hours)

It is important that you closely follow the directions of your health providers and consult with them before making any changes to your cannabis use. Speak to your health provider for more detailed information.

The safety of medical cannabis use after SCI is not yet known. However, a number of risks and side effects of cannabis use in the general population are known. Many of the short-term side effects of cannabis have been reported to be mild to moderately severe and related to the dose of the drug taken. Uncommon but serious adverse effects may also exist. Furthermore, the risks to long-term users are not well known and some side effects may be related to regular use over time.

This is not a complete list. Speak to your health provider for detailed information about the risks and side effects of cannabis use.

Short-term side effects of cannabis may include:

Diagram of the human body showing the different side effects cannabis can have on the body.

Cannabis can cause many side effects to different body systems.13

  • Dizziness and lightheadedness
  • Dry mouth, throat irritation, and cough
  • Drowsiness
  • Altered judgment and attention
  • Anxiety and agitation
  • Hallucinations
  • Disorientation and confusion
  • Increased heart rate
  • Impaired coordination and balance
  • Impaired short-term memory
  • Headache
  • Paranoia and psychosis
  • Reddening of the eyes
  • Decreased intra-ocular pressure (pressure within the eyes)
  • Muscle relaxation
  • Interactions with other medications

Because cannabis lingers in the body long after use, task performance may be impaired for up to 24 hours. It is recommended to avoid operating heavy machinery or performing dangerous activities for 3-4 hours after inhaling cannabis, 6 hours after oral ingestion of cannabis, and 8 hours if a “high” is experienced. Examples of high-risk activities may include performing transfers and participating in physical therapy sessions.

Long-term cannabis use may be associated with:

  • Addiction and withdrawal
  • Airway problems like chronic bronchitis
  • Possible increased risk of mental disorders like anxiety, depression, schizophrenia, and psychosis in people at risk for these conditions
  • Possible increased cancer risk with long term smoking, although this is not yet clear

An emerging concern is the effects that cannabis use may have on adolescents and young adults. Studies have suggested that cannabis use early in adolescence may alter brain development and could be related to the development of psychotic disorders as adults.

Overdosage of cannabinoids

A cartoon cannabis leaf with an up arrow on the top left and a warning sign on the bottom right.Overdoses of cannabis, although not common, have been reported. The risk increases when both oral and inhaled forms of cannabinoids (prescription or recreational) are combined. The signs and symptoms of overdose are generally tolerable and overlap with the effects of THC such as dizziness, drowsiness, and sensory impairment. More severe complications including psychosis and convulsions occur rarely.

Unlike cannabis, synthetic cannabinoids carry a greater risk of overdose because they are more potent than THC. The clinical presentation of toxicity will depend on the specific synthetic cannabinoid used, but can be severe and even result in death. Since its introduction into the United States in 2008, there have been cases of adverse reactions in all 50 states. There is currently no antidote to synthetic cannabinoids, making the illegal use of these drugs an emerging public health threat. If you or someone you know experiences an overdose, seek medical attention immediately.

A cartoon cannabis leaf with a thumbs up and thumbs down above.

Studies show that cannabis is mostly used by patients with SCI for (chronic) pain and spasm relief, as well as for anxiety, stress and depression, bowel and bladder management, nausea, to increase appetite, to improve sleep, to decrease other medication use and for pleasure, recreation and relaxation. However, research has only studied the use of cannabinoid products in the treatment of pain and spasticity after SCI.

Pain

Early research provides moderate evidence that smoked and vapourized cannabis may help to reduce neuropathic pain. There is also weak evidence that oral plant-derived cannabinoid sprays may help to reduce neuropathic pain. Moderate evidence from two other studies indicates no benefit with synthetic cannabinoids. In one, dronabinol was no different than diphenhydramine (an anti-allergy medication with no pain-relieving properties) for reducing neuropathic pain. In the other, a synthetic cannabinoid called Normast showed no benefit. These last two studies were specific to people with SCI, while the other studies above also included people with other neurological conditions. Further research specific to people with SCI is needed to determine if cannabis and synthetic cannabinoids are safe and effective for pain after SCI.

 

Hear Matt describe his experience with synthetic and non-synthetic marijuana for pain management.

Spasticity

Research on cannabinoid products for spasticity after SCI has been conflicting. Four studies provide moderate evidence that synthetic cannabinoids and vapourized cannabis may help with spasticity after SCI. However, two other studies with moderate evidence have been inconclusive about whether cannabinoid products helped.

Overall, these studies show that cannabinoid-based treatments may have benefits in the treatment of spasticity, but further research through larger and more rigorous studies are needed before conclusions can be drawn about how effective they are.

There is early evidence that cannabinoid products may help to treat neuropathic pain after SCI and conflicting evidence about whether they help to treat spasticity after SCI. More studies are needed to confirm these findings.

It is not known whether cannabis is safe to use after SCI, especially over the long term, since cannabis use is associated with a number of potential risks and side effects. Until more research is done, it is important that you discuss this treatment option with your health providers in detail to find out if it is a suitable and safe treatment option for you.

For a review of how we assess evidence at SCIRE Community and advice on making decisions, please see SCIRE Community Evidence.

Parts of this page has been adapted from SCIRE Project (Professional) “Pain Management” and “Spasticity” Chapters:

Mehta S, Teasell RW, Loh E, Short C, Wolfe DL, Hsieh JTC (2014). Pain Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors. Spinal Cord Injury Rehabilitation Evidence. Version 5.0: p 1-79.

Available from: https://scireproject.com/evidence/rehabilitation-evidence/pain-management/

Hsieh JTC, Wolfe DL, Townson AF, Short C, Connolly SJ, Mehta S, Curt A, Foulon BL (2012). Spasticity Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan V, Mehta S, Sakakibara BM, Boily K, editors. Spinal Cord Injury Rehabilitation Evidence. Version 4.0.

Available from: https://scireproject.com/evidence/rehabilitation-evidence/spasticity/

 

Evidence for “What is cannabis” is based on:

Atakan, Z. (2012). Cannabis, a complex plant: different compounds and different effects on individuals. Therapeutic Advances in Psychopharmacology, 2(6), 241–254. https://doi.org/10.1177/2045125312457586

Baker, D., Pryce, G., Croxford, J. L., Brown, P., Pertwee, R. G., Huffman, J. W., & Layward, L. (2000). Cannabinoids control spasticity and tremor in a multiple sclerosis model. Nature, 404(6773), 84–87. https://doi.org/10.1038/35003583

Ben Amar, M. (2006). Cannabinoids in medicine: A review of their therapeutic potential. Journal of Ethnopharmacology, 105(1–2), 1–25. https://doi.org/10.1016/j.jep.2006.02.001

Birdsall, S. M., Birdsall, T. C., & Tims, L. A. (2016). The Use of Medical Marijuana in Cancer. Current Oncology Reports, 18(7), 40. https://doi.org/10.1007/s11912-016-0530-0

Evidence for “What are cannabinoids?” is based on:

Aizpurua-Olaizola, O., Elezgarai, I., Rico-Barrio, I., Zarandona, I., Etxebarria, N., & Usobiaga, A. (2017). Targeting the endocannabinoid system: future therapeutic strategies. Drug Discovery Today, 22(1), 105–110. https://doi.org/10.1016/j.drudis.2016.08.005

Zerrin 2012

Crippa, J. A., Guimarães, F. S., Campos, A. C., & Zuardi, A. W. (2018). Translational Investigation of the Therapeutic Potential of Cannabidiol (CBD): Toward a New Age. Frontiers in Immunology, 9, 2009. https://doi.org/10.3389/fimmu.2018.02009

National Academies of Sciences, Engineering, and Medicine. 2017. The health effects of cannabis and cannabinoids: The current state of evidence and recommendations for research. Washington, DC: The National Academies Press. doi: 10.17226/24625.

Whiting et al. (2015) Cannabinoids for Medical Use. A Systematic Review and Meta-Analysis. JAMA 313(24): 2456-2473.

Mücke M, Phillips T, Radbruch L, Petzke F, Häuser W.(2018) Cannabis-based Medicine for chronic neurophathic pain in adults. Cochrane Database of Systematic Reviews, Issue 3. Art. No: CD012182 DOI: 10.1002/14651858.CD012182.pub2

Evidence for “How are cannabinoids used?” is based on:

Drossel, C., Forchheimer, M., & Meade, M. A. (2016). Characteristics of Individuals with Spinal Cord Injury Who Use Cannabis for Therapeutic Purposes. Topics in Spinal Cord Injury Rehabilitation, 22(1), 3–12. https://doi.org/10.1310/sci2201-3

Sheel, A. W., Welch, J. F., & Townson, A. (n.d.). Respiratory Management Following Spinal Cord Injury. Retrieved from www.scireproject.com

Health Canada (2018) Information for health care professionals. Cannabis (marihuana, marijuana) and the cannabinoids. Ottawa; Health Canada publications.

Center for Disease Control (2020) Outbreak of Lung Injury Associated with the Use of E-Cigarette, or Vaping, Products. Retrieved on 13-02-2020 from: https://www.cdc.gov/tobacco/basic_information/e-cigarettes/severe-lung-disease.html

Evidence for “Cannabidiol oil” is based on:

Devinsky, O., Cross, J. H., Laux, L., Marsh, E., Miller, I., Nabbout, R., … Wright, S. (2017). Trial of Cannabidiol for Drug-Resistant Seizures in the Dravet Syndrome. New England Journal of Medicine, 376(21), 2011–2020. https://doi.org/10.1056/NEJMoa1611618

Devinsky, O., Patel, A. D., Cross, J. H., Villanueva, V., Wirrell, E. C., Privitera, M., … Zuberi, S. M. (2018). Effect of Cannabidiol on Drop Seizures in the Lennox–Gastaut Syndrome. New England Journal of Medicine, 378(20), 1888–1897. https://doi.org/10.1056/NEJMoa1714631

Thiele, E. A., Marsh, E. D., French, J. A., Mazurkiewicz-Beldzinska, M., Benbadis, S. R., Joshi, C., … Wilfong, A. (2018). Cannabidiol in patients with seizures associated with Lennox-Gastaut syndrome (GWPCARE4): a randomised, double-blind, placebo-controlled phase 3 trial. The Lancet, 391(10125), 1085–1096. https://doi.org/10.1016/S0140-6736(18)30136-3

Shannon, S., & Opila-Lehman, J. (2016). Effectiveness of Cannabidiol Oil for Pediatric Anxiety and Insomnia as Part of Posttraumatic Stress Disorder: A Case Report. The Permanente Journal, 20(4), 16-005. https://doi.org/10.7812/TPP/16-005

Evidence for “What is the suggested dosing of cannabis?” is based on:

Health Canada. (2013). Information for Health Care Professionals Cannabis (marihuana, marijuana) and the cannabinoids. Retrieved from https://www.canada.ca/content/dam/hc-sc/migration/hc-sc/dhp-mps/alt_formats/pdf/marihuana/med/infoprof-eng.pdf

Evidence for “What are the risks and side effets of cannabis? Is based on:

Grant, I., Atkinson, J. H., Gouaux, B., & Wilsey, B. (2012). Medical marijuana: clearing away the smoke. The Open Neurology Journal, 6, 18–25. https://doi.org/10.2174/1874205X01206010018

Volkow, N. D., Baler, R. D., Compton, W. M., & Weiss, S. R. B. (2014). Adverse health effects of marijuana use. The New England Journal of Medicine, 370(23), 2219–2227. https://doi.org/10.1056/NEJMra1402309

Zhang, M. W., & Ho, R. C. M. (2015). The Cannabis Dilemma: A Review of Its Associated Risks and Clinical Efficacy. Journal of Addiction, 2015, 1–6. https://doi.org/10.1155/2015/707596

Health Canada. (2013). Information for Health Care Professionals Cannabis (marihuana, marijuana) and the cannabinoids. Retrieved from https://www.canada.ca/content/dam/hc-sc/migration/hc-sc/dhp-mps/alt_formats/pdf/marihuana/med/infoprof-eng.pdf

Evidence for “What are cannabinoids used for after spinal cord injury?” is based on:

Cardenas DD, Jensen MP. (2006) Treatments for chronic pain in persons with spinal cord injury: A survey study. The journal of spinal cord medicine 29:109-117.

Shroff FM. (2015) Experiences with Holistic Health Practices among Adults with Spinal Cord Injury. Rehabilitation Process and Outcome 4:27-34.

Drossel C, Forchheimer M, Meade MA. (2016) Characteristics of Individuals with Spinal Cord Injury Who Use Cannabis for Therapeutic Purposes. Top Spinal Cord Inj Rehabil;22:3-12.

Government of Canada (2019) Final regulations: Edible cannabis, cannabis extracts, cannabis topicals. Retrieved on 13-02-2020 from: https://www.canada.ca/en/health-canada/services/drugs-medication/cannabis/resources/regulations-edible-cannabis-extracts-topicals.html

Andresen SR, Biering-Sorensen F, Hagen EM, Nielsen JF, Bach FW, Finnerup NB. (2017) Cannabis use in persons with traumatic spinal cord injury in Denmark. J Rehabil Med 49:152-160.

Bruce D, Brady JP, Foster E, Shattell M. (2018) Preferences for Medical Marijuana over Prescription Medications Among Persons Living with Chronic Conditions: Alternative, Complementary, and Tapering Uses. Journal of alternative and complementary medicine (New York, NY) 24:146-153.

Hawley LA, Ketchum JM, Morey C, Collins K, Charlifue S. (2018) Cannabis Use in Individuals With Spinal Cord Injury or Moderate to Severe Traumatic Brain Injury in Colorado. Archives of physical medicine and rehabilitation 99:1584-1590.

Evidence for “Pain” is based on:

[1] Wilsey, B., Marcotte, T., Tsodikov, A., Millman, J., Bentley, H., Gouaux, B., & Fishman, S. (2008). A Randomized, Placebo-Controlled, Crossover Trial of Cannabis Cigarettes in Neuropathic Pain. The Journal of Pain, 9(6), 506–521. https://doi.org/10.1016/j.jpain.2007.12.010

[2] Wilsey, B., Marcotte, T. D., Deutsch, R., Zhao, H., Prasad, H., & Phan, A. (2016). An Exploratory Human Laboratory Experiment Evaluating Vaporized Cannabis in the Treatment of Neuropathic Pain From Spinal Cord Injury and Disease. The Journal of Pain, 17(9), 982–1000. https://doi.org/10.1016/j.jpain.2016.05.010

[3] Wade, D. T., Robson, P., House, H., Makela, P., & Aram, J. (2003). A preliminary controlled study to determine whether whole-plant cannabis extracts can improve intractable neurogenic symptoms. Clinical Rehabilitation, 17(1), 21–29. https://doi.org/10.1191/0269215503cr581oa

[4] Rintala, D. H., Fiess, R. N., Tan, G., Holmes, S. A., & Bruel, B. M. (2010). Effect of Dronabinol on Central Neuropathic Pain After Spinal Cord Injury. American Journal of Physical Medicine & Rehabilitation, 89(10), 840–848. https://doi.org/10.1097/PHM.0b013e3181f1c4ec

Andresen, S.R., Bing, J., Hansen, R.M., Biering-Sørenson, F., Hagen, E.M., Rice, A.S., Nielsen, J.F., Bach, F.W., Finnerup, N.B., (2016) Ultramicronized palmitoylethanolamide in Spinal Cord Injury Neuropathic Pain: A Randomized, Double-blind, Placebo-controlled Trial. Pain. 157(9): 2097-103.

Evidence for “Spasticity” is based on:

[1] Pooyania, S., Ethans, K., Szturm, T., Casey, A., & Perry, D. (2010). A Randomized, Double-Blinded, Crossover Pilot Study Assessing the Effect of Nabilone on Spasticity in Persons With Spinal Cord Injury. Archives of Physical Medicine and Rehabilitation, 91(5), 703–707. https://doi.org/10.1016/j.apmr.2009.12.025

[3] Maurer, M., Henn, V., Dittrich, A., & Hofmann, A. (1990). Delta-9-tetrahydrocannabinol shows antispastic and analgesic effects in a single case double-blind trial. European Archives of Psychiatry and Clinical Neuroscience, 240(1), 1–4. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/2175265

[4] Hagenbach, U., Luz, S., Ghafoor, N., Berger, J. M., Grotenhermen, F., Brenneisen, R., & Mäder, M. (2007). The treatment of spasticity with Δ9-tetrahydrocannabinol in persons with spinal cord injury. Spinal Cord, 45(8), 551–562. https://doi.org/10.1038/sj.sc.3101982

[6] Grao-Castellote, C., Torralba-Collados, F., Gonzalez, L. M., & Giner-Pascual, M. (2017). [Delta-9-tetrahydrocannabinol-cannabidiol in the treatment of spasticity in chronic spinal cord injury: a clinical experience]. Revista de Neurologia, 65(7), 295–302. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/28929471

[2] Wilsey, B., Marcotte, T. D., Deutsch, R., Zhao, H., Prasad, H., & Phan, A. (2016). An Exploratory Human Laboratory Experiment Evaluating Vaporized Cannabis in the Treatment of Neuropathic Pain From Spinal Cord Injury and Disease. The Journal of Pain, 17(9), 982–1000. https://doi.org/10.1016/j.jpain.2016.05.010

[5] Kogel, R. W., Johnson, P. B., Chintam, R., Robinson, C. J., & Nemchausky, B. A. (1995). Treatment of Spasticity in Spinal Cord Injury with Dronabinol, a Tetrahydrocannabinol Derivative. American Journal of Therapeutics, 2(10), 799–805. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/11854790

Other references

Allan, G. M., Ramji, J., Perry, D., Ton, J., Beahm, N. P., Crisp, N., … Lindblad, A. J. (2018). Simplified guideline for prescribing medical cannabinoids in primary care. Canadian Family Physician, 64(2).

National Center for Environmental Health. (n.d.). Synthetic cannabinoids: What are they? What are their effects? | HSB | NCEH. Retrieved March 29, 2019, from https://www.cdc.gov/nceh/hsb/chemicals/sc/default.html

Villan, S. (2008). Use of Δ9-tetrahydrocannabinol in the treatment of spasticity in spinal cord injury patients. Spinal Cord, 46(6), 460–460. https://doi.org/10.1038/sj.sc.3102149

Image credits

  1. Marijuana ©United States Fish and Wildlife Service, CC0 1.0
  2. Image by SCIRE Community Team
  3. Cannabidiol and THC Biosynthesis ©Madkamin, CC BY-SA 4.0
  4. Weeds ©The Other Dan, CC BY-NC 2.0
  5. ‘Spice’ — a designer synthetic cannabinoid ©G.W. Pomeroy, CC0 1.0
  6. Vape Pen ©Aly Dodds, CC BY 3.0 US
  7. Cannabis Pills ©Mooms, CC BY 3.0 US
  8. CBD Oil ©Mooms, CC BY 3.0 US
  9. Cannabis Cream ©Mooms, CC BY 3.0 US
  10. When in Amsterdam… ©ashton, CC BY 2.0
  11. CBDistillery-OIL-benefits ©Robert Fischer, CC BY-NC 2.0
  12. Hmmmm cannabis ©Steven Schwartz, CC BY 2.0
  13. Bodily effects of cannabis ©Mikael Häggström, CC0 1.0
  14. Marijuana side effect ©dDara, CC BY 3.0 US
  15. Marijuana side effect ©dDara, CC BY 3.0 US


Disclaimer: This document does not provide medical advice. This information is provided for educational purposes only. Consult a qualified health professional for further information or specific medical advice. The SCIRE Project, its partners and collaborators disclaim any liability to any party for any loss or damage by errors or omissions in this publication.

Spasticity

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Author: SCIRE Community Team | Reviewer: Holly Timms, Felicia Wong | Published: 21 November 2017 | Updated: ~

Spasticity is a common symptom of spinal cord injury (SCI) that causes movement problems and other symptoms. This page outlines basic information about spasticity and how it is treated after SCI.

Key Points

  • Spasticity is a disorder of movement control that causes muscle spasms, increased muscle tone, and overactive reflexes. It can happen when the brain or spinal cord are damaged.
  • Spasticity may cause problems with movement and posture, pain, fatigue, and many other symptoms. However, spasticity can also have benefits for movement and health.
  • It is important to work together with your health team to decide whether your spasticity is problematic and worth treating.
  • Treatment for spasticity usually begins with identifying specific triggers that make it worse. Management of these spasticity triggers along with other conservative treatments may alleviate these symptoms. Many of these treatments provide short-term relief of spasticity.
  • Oral medications and botulinum toxin injections are also commonly used and effective for treating spasticity after SCI.

Cartoon muscle fibre with zigzags to symbolize pain

Spasticity is a movement control disorder that happens when the brain and spinal cord are damaged or do not develop properly. It is usually experienced as involuntary muscle spasms, increased muscle tone, and overactive reflexes.

Spasticity is a common symptom of SCI that can affect as many as three-quarters of people with SCI. It is more common among people with cervical and incomplete SCI. Spasticity can also be a symptom of other conditions like brain injury, stroke, and multiple sclerosis.

Spasticity can be experienced in many different ways depending on the person and the characteristics of their SCI.

Signs and symptoms of spasticity:

  • Muscles that are constantly and involuntarily tensed (increased muscle tone)
  • Stiff muscles that resist movement
  • Muscle pain and fatigue
  • Muscle spasms or jerky movements
  • Uncontrolled movements or difficulty coordinating movements
  • Exaggerated reflexes
  • Altered posture or positioning

Spasticity is different from normal muscle tension because the amount of tension depends on the speed that the muscle is stretched. Faster movement speeds cause greater tension and resistance to movement.

Clonus

Picture of a foot flexing and pointing at the ankle with arrows showing the directions of motion up and down

Clonus is often seen as rhythmic tapping or beating motion of the foot at the ankle.2

Clonus is a series of involuntary, rhythmic muscle contractions and relaxations, which often accompanies spasticity.

Clonus is most often seen in the ankle as a rhythmic tapping or beating motion of the foot that is triggered when there is stimulus to the ball of the foot. This can happen when putting weight onto the foot during transfers, standing, or walking. Clonus can also be experienced in other joints. Clonus can last for anywhere from a few seconds to several minutes.

Clonus is not the same as spasticity, but a related symptom that happens for similar reasons.

 

Spasticity may be constant or triggered by something

Picture showing a man transferring from his wheelchair onto a bed

Transfers are a common trigger of spasticity.3

The symptoms of spasticity may be constant or come and go. They may also change over time. Some people will have muscle tension that is always present, while others will have spasticity that comes on or gets worse when it is triggered by something. Common spasticity triggers include:

  • Movement of the arms or legs, especially quick movements
  • Position changes, such as transfers, walking, or moving in bed
  • Stretching
  • Tight clothing or other discomfort below the level of injury
  • Pressure sores, skin irritation, or wounds
  • Bladder problems
  • Bowel problems
  • Cold temperatures
  • Menstrual cycle or pregnancy
  • Emotional or psychological stress
  • Poor positioning in the wheelchair or bed
  • Any other illnesses

A change in spasticity can be a sign of other health problems

Sudden or unexplained changes in spasticity can sometimes signal a health problem that needs attention – most commonly a bladder infection or skin breakdown. If you are not sure why your spasticity has changed, speak to your health providers for further testing.

Spasticity is related to several changes to the body that happen after SCI. The main reason for spasticity after SCI is a reduced ability of the brain to ‘calm down’ overactive reflexes. Over time, the muscles and tendons may also change, becoming more tense and stiff, which also contributes to the symptoms of spasticity.

The stretch reflex

The stretch reflex is an automatic movement response that happens when a muscle is stretched quickly, causing the muscle to tense. It is commonly tested as the ‘tendon tap’ below the kneecap.

Image of a man touching the flame of a candle. A red line connects to a muscle in the arm and up to the spinal cord. From there, a blue line travels from the spinal cord and back down the arm.

Pain signals from touching something hot travels to the spinal cord and back to the muscles without going to the brain first.4

When a muscle is quickly stretched, it activates special stretch sensors called muscle spindles. They send a signal through sensory neurons to the spinal cord. In the spinal cord, the message is passed along to motor neurons, which send a movement command back to the muscle, causing it to contract. This reflex happens in the spinal cord without travelling to the brain first.

Like muscle stretch, pain can also trigger spinal cord reflexes that use the same nerve pathway as the stretch reflex. For example, stepping on something sharp or touching a hot burner activates spinal cord reflexes.

The brain normally dampens spinal cord reflexes

Although the stretch reflex happens in the spinal cord, the brain influences how sensitive the reflex is. The brain normally sends signals down the spinal cord, which dampens the sensitivity of reflexes.

This is called descending inhibition. ‘Descending’ means ‘coming down from the brain’, and ‘inhibition’ means ‘reducing the activity of’ the stretch reflex. Descending inhibition is important because it tells the stretch reflex to ‘calm down’ so it doesn’t get in the way of normal movements.

Spinal cord injury prevents the brain from dampening spinal cord reflexes

When the spinal cord is injured, descending inhibition from the brain is cut off. Without its calming effects,
the stretch reflex becomes overactive. This can lead to a constant level of muscle tension (called muscle tone) and excessive reflexes which cause the muscles to tighten uncontrollably or unexpectedly and the other symptoms of spasticity.

Watch SCIRE’s YouTube video explaining why spasticity happens after SCI.5

The main way that spasticity is diagnosed and monitored is through a physical examination. Your health providers will talk to you about your symptoms, functional abilities, and current treatment plan, look at your muscles and posture, and test the muscles in various ways. This may include:

  • Hands-on tests where the joints are moved slowly and quickly
  • Active tests of strength and movement
    A man lying down on a bed with a healthcare provider performing a physical assessment beside him

    Your health provider may perform a physical exam to help determine your need for spasticity treatment.6

  • Testing your reflexes

Your health providers may also observe tasks like walking, transferring, and eating – this can help them understand how spasticity affects you in your everyday life.

Health providers often use special collections of questions and tests called outcome measures, which help them accurately keep track of changes in spasticity. Spasticity may change over time so regular check-ins with your health team, especially while figuring out what works best for you, are often an important part of managing your spasticity.

Spasticity can negatively affect the health and wellness of some people, but it can sometimes have benefits as well. It is important to determine whether your spasticity is a problem for you. Treating spasticity unnecessarily can have drawbacks, such as unwanted side effects, costs, and time. It is important that you discuss your treatment options and weigh the pros and cons of treating spasticity together with your health team to determine the best course of action for you.

Problems with spasticity

A cartoon person sitting on the side of the bed holding his head with zigzags above the head and a clock on the wallMuscle spasms and reflexes can contribute to a number of potential problems, such as:

  • Pain
  • Sleep problems
  • Reduced mobility and function
  • Difficulties maintaining posture and positioning
  • Skin breakdown and hygiene concerns
  • Bladder and bowel accidents
  • Joint contractures
  • Sexual and reproductive health issues
  • Difficulties with care

Benefits of spasticity

Spasticity can also have some benefits for people with SCI, which may include:

  • Better mobility, standing, and walking
  • Assistance with transfers (such as supporting the body weight while transferring from a wheelchair to a bed or chair)
  • Preventing muscle wasting or weakening due to inactivity
  • Improved circulation
  • Intentionally triggered spasms can help to empty the bowel and bladder in people with certain types of bowel or bladder problems
  • Reflex erections during sexual activity
  • It may serve as a warning sign of infections or other health issues

YouTube video about the downfalls of treating non-problematic spasticity.8

There are many different treatments for spasticity. Every person’s spasticity is different, so finding the best treatment or combination of treatments often involves trial and error.

Spasticity treatment usually starts with conservative treatments such as positioning and maintaining good muscle length. If these do not provide enough relief, spasticity medications and injections may be recommended. Surgical treatments are considered as a last option for severe spasticity.

Avoiding spasticity triggers

An important part of managing spasticity is learning how to manage your spasticity triggers. Spasticity is often triggered by bladder, bowel, skin, or other health issues, so maintaining good overall health and taking care of these issues is an important part of managing spasticity. Speak to your health providers about optimizing your self-care routines to prevent spasticity.

Movement and therapeutic treatment options

There are a number of different movement, hands-on, and electrical treatments that may be done on your own, with a caregiver, or in conjunction with a therapist. These treatments generally produce fewer side effects than medications or surgeries; however, they also tend to have short-term effects.

Posture and positioning

Good posture and positioning may help to keep the muscles at an appropriate length and help prevent contractures. You may need to work with your health providers to determine the best positions and equipment to manage your spasticity.

Stretching and range of motion

Stretching and range of motion exercises are commonly used treatments to reduce spasticity and minimize complications like contractures after SCI. Stretching is often achieved through prolonged positioning, such as placing a wedge between the knees to stretch the hips.

Bracing and casting

Photograph of a person using a standing frame with cushions behind and in front of the legs to help align them. The person is resting their arms on a small desk that is attached to the frame.Various braces, orthoses, and casts may be used to maintain proper positioning of the arms and legs to help reduce spasticity, improve function, and prevent complications.

Standing

Standing can provide a prolonged stretch to certain muscles, such as the calf and hamstring muscles, which may help with spasticity. For some people, standing may be done using specialized equipment such as tilt tables, standing frames, and standing wheelchairs.

Neurodevelopmental therapy (NDT)

Neurodevelopmental therapy (NDT, sometimes called Bobath therapy) is a type of physiotherapy and occupational therapy treatment where a therapist uses hands-on techniques to guide a person through movements. It is used to help practice quality functional movements.

Walking

Illustration showing a person walking on a treadmill supported by a harness around their pelvis and waste attached to an overhead suspension system by straps. Suspension system is behind the treadmill and on the other side has an off-weighting system labelled 'weight' and a height adjustable winch.Walking may be done by some people (typically with incomplete SCI) with or without gait aids or assistance from health providers or with the use of specialized equipment such as body weight supported treadmill training or robotic exoskeletons.

Functional electrical stimulation (FES) exercise

Functional electrical stimulation (FES) involves the use of electrical stimulation to activate specific muscles of the arms or legs during an activity such as stationary cycling, arm exercises or walking.

See our article on FES for more information! 

Massage

Massaging muscles may help to stimulate the sensory nerves, which are part of the reflex spasticity response.

Transcutaneous electrical nerve stimulation (TENS)

Transcutaneous electrical nerve stimulation (TENS) involves the use of electrodes placed on the skin to stimulate the sensory nerves without producing muscle tension.

See our article on TENS for more information!

Do movement and therapeutic treatment options work?

Although many of these treatments are commonly used in the treatment of spasticity, the research is unclear about whether a number of these therapies, including stretching and range of motion, standing, neurodevelopmental therapy, and massage; are actually effective for reducing spasticity after SCI. However, many of these treatments often have several therapeutic purposes after SCI (such as reducing pain or preventing contractures), which may explain their widespread use. Further research is needed to better understand the effects of these treatments on spasticity.

However, there is evidence that body weight supported treadmill training, robotic exoskeleton walking, functional electrical stimulation (FES) exercise, and TENS are effective treatments for reducing spasticity after SCI.

Medications

Oral medications are typically prescribed for the treatment of widespread spasticity. Finding the right medication may involve trial and error and involves working closely with your doctor to find the best fit for you.

Baclofen (tablets and baclofen pumps)

Baclofen (Lioresal) is a muscle relaxant that is commonly used to treat spasticity. It can be taken as tablets by mouth or administered into the sac surrounding the spinal cord (called intrathecal baclofen) through a surgically implanted baclofen pump. Baclofen is effective for treating spasticity after SCI.  However, it can have several side effects such as dizziness, drowsiness, anxiety, confusion, and weakness. Extra care is also needed when discontinuing therapy to avoid withdrawal symptoms. Baclofen is the most common medication prescribed for spasticity after SCI.

See our article on Baclofen for more information.

Baclofen is commonly used for controlling spasticity after a spinal cord injury. This can be achieved by surgically implementing a pump that connects directly to the spinal cord.11

Watch “Intrathecal Baclofen for Reducing Spasticity After Spinal Cord Injury” from our SCIRE video series on Neuromodulation!

Other spasticity medications

A number of other medications are used clinically or have been studied for their effects on spasticity after SCI. Speak to your doctor or pharmacist for more information about these medications.

Medications that are effective for spasticity after SCI:
  • TizanidineA cartoon bottle and capsules beside it
  • Clonidine
  • Cyproheptadine
Medications that may be effective for spasticity after SCI:
  • Cannabinoid medications (Dronabinol and Nabilone)
  • Gabapentin
  • Orphenadrine Citrate
  • Diazepam
  • Dantrolene
Medications that are not supported for treating spasticity after SCI:
  • Fampridine (4-Aminopyridine)
  • Levetiracetam

Injections

Injections into the nerves and muscles may be used to help manage localized areas of spasticity.

Botulinum toxin (Botox) injections

Silhouette of a syringe and injection bottleBotulinum toxin is a toxin that can cause muscle paralysis. Very small doses of certain strains of botulinum toxin can be injected into muscles to treat spasticity. It is commonly known for its cosmetic use by its trade names Botox, Dysport, and Xeomin. Botulinum toxin injections are temporary, with effects that wear off over time (usually around 3 to 6 months). Research evidence supports that botulinum toxin is effective in reducing focal spasticity after SCI.

See our article on Botulinum Toxin for more information

Phenol injections

Phenol injections involve injecting a type of alcohol into nerves which supply the spastic muscle. Phenol damages the nerve axons, so the nerves cannot send signals to the muscles that cause spasticity. This procedure is also sometimes used with another alcohol, ethanol. Phenol injections may be effective for reducing spasticity after SCI.

Surgical treatments

A silhouette of surgeon performing surgery on a person.Surgery is typically reserved for and joint contractures are impacting care, function and quality of life

Tendon releases or transfers

Tendon releases are surgeries that lengthen shortened tendons (the part of the muscle that attaches to a bone) affected by spasticity. Tendon transfers involve surgically moving tendons that attach to muscles. These techniques can assist with better positioning of the feet or arms when excessive spasticity interferes with safe or appropriate positioning. However, there is limited research investigating the specific effects with SCI.

Myelotomy and Rhizotomy

Myelotomy and rhizotomy are surgical procedures that involve intentionally damaging part of the spinal cord (myelotomy) or nerve (rhizotomy) to reduce spasticity. Damaging the nerve fibers related to spasticity can prevent them from communicating and causing unwanted muscle spasms. These techniques are not common because they are permanent and invasive. They are only used for severe and intolerable spasticity that does not respond to other treatments. Myelotomy is effective for reducing spasticity after SCI.

Other treatments

A woman with a magnetic coil placed above the head.

Alternative treatments like TMS are being explored as a potential treatment for SCI spasticity.15

A number of other medical, alternative, and self-management treatments may be used to manage spasticity. There is some limited evidence that other treatments, such as transcranial magnetic stimulation (TMS), hippotherapy (therapeutic horseback riding), and others may help to treat spasticity after SCI. However, these treatments are not typically used or available in standard practice at this time. Speak with your health providers about any treatments you are considering trying as a treatment for your spasticity.

The research evidence suggests that conservative treatments that involve active movement and electrical stimulation help to reduce spasticity short-term after SCI. It is not clear whether passive movement therapies like stretching help treat spasticity.

Medications and injections may include baclofen and botulinum toxin injections, which are effective for treating spasticity but may have additional side effects. There are many other drugs and treatments that may require further research. Surgery may be considered as a last resort if other treatments fail.

It is important to discuss any questions of concerns that you have about your treatment options in detail with your health providers to find the best management options for you.

For a review of how we assess evidence at SCIRE Community and advice on making decisions, please see SCIRE Community Evidence.

Parts of this page have been adapted from the SCIRE Professional “Spasticity” Module:

Hsieh JTC, Connolly SJ, McIntyre A, Townson AF, Short C, Mills P, Vu V, Benton B, Wolfe DL (2016). Spasticity Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Curt A, Mehta S, Sakakibara BM, editors. Spinal Cord Injury Rehabilitation Evidence. Version 6.0.

Available from: https://scireproject.com/evidence/spasticity/

 

Evidence for “Movement and physical therapies” is based on the following studies:

Stretching and range of motion

[1] Skold C. Spasticity in spinal cord injury: self-and clinically rated intrinsic fluctuations and intervention-induced changes. Arch Phys Med Rehabil 2000;81:144-9.

[2] Kakebeeke T, Lechner H, Knapp P. The effect of passive cycling movements on spasticity after spinal cord injury: preliminary results. Spinal Cord 2005;43:483-8.

Standing

[1] Odeen I & Knutsson E. Evaluation of the effects of muscle stretch and weight load in patients with spastic paraplegia. Scand J Rehabil Med 1981;13:117-21.

[2] Short-term effects of surface electrical stimulation. Arch Phys Med Rehabil 1988b;69:598-604.

[3] Adams M, Hicks A. Comparison of the effects of body-weight-supported treadmill training and tilt-table standing on spasticity in individuals with chronic spinal cord injury. J Spinal Cord Med 2011;34:488-94.

Neurodevelopmental Therapy

[1] Li S, Xue S, Li Z, Liu X. Effect of baclofen combined with neural facilitation technique on the reduction of muscular spasm in patients with spinal cord injury. Neur Regen Res 2007;2:510-2.

Walking

[1] Fang C, Hsu M, Chen C, Cheng H, Chou C, Chang Y. Robot-assisted passive exercise for ankle hypertonia in individuals with chronic spinal cord injury. J Med Biol Eng 2015;35:464-72.

[2] Mirbagheri M, Kindig M, Niu X. Effects of robotic-locomotor training on stretch reflex function and muscular properties in individuals with spinal cord injury. Clinical Neurophysiol 2015;126:997-1006.

[3] Manella K & Field-Fote E. Modulatory effects of locomotor training on extensor spasticity in individuals with motor-incomplete spinal cord injury. Restor Neurol Neurosci 2013;31:633-46.

Functional Electrical Stimulation

[1] Kapadia N, Masani K, Craven B, et al. A randomized trial of functional electrical stimulation for walking in incomplete spinal cord injury: Effects on walking competency. J Spinal Cord Med 2014;37:511-24.

[2] Manella K & Field-Fote E. Modulatory effects of locomotor training on extensor spasticity in individuals with motor-incomplete spinal cord injury. Restor Neurol Neurosci 2013;31:633-46.

[3] Ralston K, Harvey L, Batty J, et al. Functional electrical stimulation cycling has no clear effect on urine output, lower limb swelling, and spasticity in people with spinal cord injury: A randomised cross-over trial. J Physiother 2013;59:237-43.

[4] Kuhn D, Leichtfried V, Schobersberger W. Four weeks of functional electrical stimulated cycling after spinal cord injury: a clinical cohort study. Inter J Rehabil Res 2014;37:243-50.

[5] Sadowsky C, Hammond E, Strohl A, et al. Lower extremity functional electrical stimulation cycling promotes physical and functional recovery in chronic spinal cord injury. J Spinal Cord Med 2013;36:623-31.

[6] Reichenfelser W, Hackl H, Hufgard J, Kastner J, Gstaltner K, Gföhler M. Monitoring of spasticity and functional ability in individuals with incomplete spinal cord injury with a functional electrical stimulation cycling system. J Rehabil Med 2012;44:444-9.

[7] Krause P, Szecsi J, Straube A. Changes in spastic muscle tone increase in patients with spinal cord injury using functional electrical stimulation and passive leg movements. Clin Rehabil 2008;22:627-34

[8] Mirbagheri M, Ladouceur M, Barbeau H, Kearney R. The effects of long-term FES-assisted walking on intrinsic and reflex dynamic stiffness in spastic spinal-cord-injured subjects. Trans Neural Syst Rehabil Eng 2002;10:280-9.

[9] Granat M, Ferguson A, Andrews B, Delargy M. The role of functional electrical stimulation in the rehabilitation of patients with incomplete spinal cord injury–observed benefits during gait studies. Paraplegia 1993;31:207-15.

[10] Thoumie P, Le C, Beillot J, Dassonville J, Chevalier T, Perrouin-Verbe B et al. Restoration of functional gait in paraplegic patients with the RGO-II hybrid orthosis. A multicenter controlled study. II: Physiological evaluation. Paraplegia 1995;33:654-9.

Transcutaneous Electrical Nerve Stimulation

[1] Oo W. Efficacy of addition of transcutaneous electrical nerve stimulation to standardized physical therapy in subacute spinal spasticity: a randomized controlled trial. Arch Phys Med Rehabil 2014;95:2013-20.

[2] Chung B & Cheng, B. Immediate effect of transcutaneous electrical nerve stimulation on spasticity in patients with spinal cord injury. Clinical Rehabilitation 2010;24:202-210.

[3] Aydin G, Tomruk S, Keleş I, Demir SO, Orkun S. Transcutaneous electrical nerve stimulation versus baclofen in spasticity: clinical and electrophysiologic comparison. Am J Phys Med Rehabil. 2005 Aug;84(8):584-92.

Massage

[1] Goldberg J, Seaborne D, Sullivan S, Leduc B. The effect of therapeutic massage on H-reflex amplitude in persons with a spinal cord injury. Phys Ther 1994;74:728-37.

Evidence for “Medications” is based on the following studies:

Baclofen

[1] Chu V, Hornby T, Schmit B. Effect of antispastic drugs on motor reflexes and voluntary muscle contraction in incomplete spinal cord injury. Arch Phys Med Rehabil 2014;95:622-32.

[2] Nance P, Huff F, Martinez-Arizala A, Ayyoub Z, Chen D, Bian A, Stamler D. Efficacy and safety study of arbaclofen placarbil in patients with spasticity due to spinal cord injury. Spinal Cord 2011;49:974-80.

[3] Aydin G, Tomruk S, Keles I, Demir S, Orkun S. Transcutaneous electrical nerve stimulation versus baclofen in spasticity: clinical and electrophysiologic comparison. Am J Phys Med Rehabil 2005;84:584-92.

[4] Duncan G, Shahani B, Young R. An evaluation of baclofen treatment for certain symptoms in patients with spinal cord lesions. A double-blind, cross-over study. Neurology 1976;26:441-6.

[5] Burke D, Gillies J, Lance J. An objective assessment of a gamma aminobutyric acid derivative in the control of spasticity. Proc Aust Assoc Neurol 1971;8:131-4.

[6] Dicpinigaitis P, Allusson V, Baldanti A, and Nalamati J. Ethnic and gender differences in cough reflex sensitivity. Respiration 2001;68:480-2.

[7] Veerakumar A, Cheng J, Sunshine A, Ye X, Zorowitz R, Anderson W. Baclofen dosage after traumatic spinal cord injury: a multi-decade retrospective analysis. Clin Neurol Neurosurg 2015;129:50-6.

[8] Nance P. A comparison of clonidine, cyproheptadine and baclofen in spastic spinal cord injured patients. J Am Paraplegia Soc 1994;17:150-6.

Intrathecal Baclofen

[1] Ordia J, Fischer E, Adamski E, Spatz E. Chronic intrathecal delivery of baclofen by a programmable pump for the treatment of severe spasticity. J Neurosurg 1996;85:452-7.

[2] Nance P, Schryvers O, Schmidt B, Dubo H, Loveridge B, Fewer D. Intrathecal baclofen therapy for adults with spinal spasticity: therapeutic efficacy and effect on hospital admissions. Can J Neurol Sci 1995;22:22-9.

[3] Coffey J, Cahill D, Steers W, Park T, Ordia J, Meythaler J, et al. Intrathecal baclofen for intractable spasticity of spinal origin: results of a long-term multicenter study. J Neurosurg 1993;78:226-32.

[4] Hugenholtz H, Nelson R, Dehoux E, Bickerton R. Intrathecal baclofen for intractable spinal spasticity-a double-blind cross-over comparison with placebo in 6 patients. Can J Neurol Sci 1992;19:188-95.

[5] Loubser P, Narayan R, Sandin K, Donovan W, Russell K. Continuous infusion of intrathecal baclofen: long-term effects on spasticity in spinal cord injury. Paraplegia 1991;29:48-64.

[6] Penn R, Savoy S, Corcos D, Latash M, Gottlieb G, Parke B et al. Intrathecal baclofen for severe spinal spasticity. N Engl J Med 1989;320:1517-21.

[7] Boviatsis E, Kouyialis A, Korfias S, Sakas D. Functional outcome of intrathecal baclofen administration for severe spasticity. Clin Neurol Neurosurg 2005;107:289-95.

[8] Azouvi P, Mane M, Thiebaut J, Denys P, Remy-Neris O, Bussel B. Intrathecal baclofen administration for control of severe spinal spasticity: functional improvement and long-term follow-up. Arch Phys Med Rehabil 1996;77:35-9.

[9] Plassat R, Perrouin Verbe B, Menei P, Menegalli D, Mathe J, Richard I. Treatment of spasticity with intrathecal baclofen administration: Long-term follow-up review of 40 patients. Spinal Cord 2004;42:686-93.

[10] Zahavi A, Geertzen J, Middel B, Staal M, Rietman J. Long term effect (more than five years) of intrathecal baclofen on impairment, disability, and quality of life in patients with severe spasticity of spinal origin. J Neurol Neurosurg Psychi 2004;75:1553-7.

[11] Korenkov A, Niendorf W, Darwish N, Glaeser E, Gaab M. Continuous intrathecal infusion of baclofen in patients with spasticity caused by spinal cord injuries. Neurosurg Rev 2002;25:228-30.

[12] Broseta J, Garcia-March G, Sanchez-Ledesma M, Anaya J, Silva I. Chronic intrathecal baclofen administration in severe spasticity. Stereotact Funct Neurosurg 1990;54-55:147-53.

[13] Parke B, Penn R, Savoy S, Corcos D. Functional outcome after delivery of intrathecal baclofen. Arch Phys Med Rehabil 1989;70:30-2.

Tizanidine

[1] Chu et al. 2014.

[2] Nance P, Bugaresti J, Shellenberger K, Sheremata W, Martinez-Arizala A. Efficacy and safety of tizanidine in the treatment of spasticity in patients with spinal cord injury. Neurol 1994;44:S44-51.

[3] Mirbagheri M, Kindig M, Niu X, Varoqui D. Therapeutic effects of anti-spastic medication on neuromuscular abnormalities in SCI: A system identification approach. IEEE EMBS 2013;6203-6.

Clonidine

[1] Stewart J, Barbeau H, Gauthier S. Modulation of locomotor patterns and spasticity with clonidine in spinal cord injured patients. Can J Neurol Sci 1991;18:321-32.

[2] Malinovsky J, Malinge M, Lepage J, Pinaud M. Sedation caused by clonidine in patients with spinal cord injury. Bri J Anaesthesia 2003;90:742-5.

[3] Remy-Neris O, Barbeau H, Daniel O, Boiteau F, Bussel B. Effects of intrathecal clonidine injection on spinal reflexes and human locomotion in incomplete paraplegic subjects. Exp Brain Res 1999;129:433-40.

4-Aminopyridine

[1] Cardenas D, Ditunno J, Graziani V, Jackson A, Lammertse D, Potter P, et al. Phase 2 trial of sustained-release fampridine in chronic spinal cord injury. Spinal Cord 2007;45:158-68.

[2] Cardenas D, Ditunno JF, Graziani V, et al. Two phase 3, multicenter, randomized, placebo-controlled clinical trials of fampridine-SR for treatment of spasticity in chronic spinal cord injury. Spinal Cord 2014;52:70-76.

[3] Potter P, Hayes K, Segal J, Hsieh J, Brunnemann S, Delaney G, et al. Randomized double-blind crossover trial of fampridine-SR (sustained release 4-aminopyridine) in patients with incomplete spinal cord injury. J Neurotrauma 1998a;15:837-49.

[4] Potter P, Hayes K, Hsieh J, Delaney G, Segal J. Sustained improvements in neurological function in spinal cord injured patients treated with oral 4-aminopyridine: Three cases. Spinal Cord 1998b;36:147-55.

[5] Donovan W, Halter J, Graves D, Blight A, Calvillo O, McCann M, et al. Intravenous infusion of 4-AP in chronic spinal cord injured subjects. Spinal Cord 2000;38:7-15.

[6] Hayes K, Potter P, Wolfe D, Hsieh J, Delaney G, Blight AR. 4-Aminopyridine-sensitive neurologic deficits in patients with spinal cord injury. J Neurotrauma 1994;11:433-46.

Cyproheptadine

[1] Thompson C, Hornby T. Divergent modulation of clinical measures of volitional and reflexive motor behaviors following serotonergic medications in human incomplete spinal cord injury. J Neurotrauma. 2013;30:498-502.

[2] Nance et al. 1994.

[3] Meythaler J, Roper J, Brunner R. Cyproheptadine for intrathecal baclofen withdrawal. Arch Phys Med Rehabil 2003;84:638-42.

Gabapentin

[1] Gruenthal M, Mueller M, Olson W, Priebe M, Sherwood A, Olson W. Gabapentin for the treatment of spasticity in patients with spinal cord injury. Spinal Cord 1997;35:686-9.

Orphenadrine Citrate

[1] Casale R, Glynn C, Buonocore M. Reduction of spastic hypertonia in patients with spinal cord injury: a double-blind comparison of intravenous orphenadrine citrate and placebo. Arch Phys Med Rehabil 1995;76:660-5.

Cannabinoids

[1] Pooyania S, Ethans K, Szturm T, Casey A, Perry D. A randomized, double-blinded, crossover pilot study assessing the effect of nabilone on spasticity in persons with spinal cord injury. Arch Phys Med Rehabil 2010;91:703-7.

[2] Hagenbach U, Luz S, Ghafoor N, Berger J, Grotenhermen F, Brenneisen R, et al. The treatment of spasticity with Delta9-tetrahydrocannabinol in persons with spinal cord injury. Spinal Cord 2007;45:551-62.

[3] Kogel R, Johnson P, Chintam R, Robinson C, Nemchausky B. Treatment of spasticity in spinal cord injury with dronabinol, a tetrahydrocannabinol derivative. Am J Ther 1995;2:799-805.

Evidence for “Injections” is based on the following studies:

[1] Richardson D, Sheean G, Werring D, Desai M, Edwards S, Greenwood R et al. Evaluating the role of botulinum toxin in the management of focal hypertonia in adults. J Neurol Neurosurg Psychi 2000;69:499-506.

[2] Spiegl U, Maier D, Gonschorek O, Heyde C, Buhren V. Antispastic therapy with botulinum toxin type A in patients with traumatic spinal cord lesion. GMS Interdiscip Plast Reconstr Surg 2014;3:1-5.

[3] Bernuz B, Genet F, Terrat P, et al. Botulinum toxin effect on voluntary and stretch reflex-related torque produced by the quadriceps: An isokinetic pilot study. Neurorehabil Neural Repair 2012;26:542-7.

[4] Hecht M, Stolze H, uf dem B, Giess R, Treig T, Winterholler M et al. Botulinum neurotoxin type A injections reduce spasticity in mild to moderate hereditary spastic paraplegia–report of 19 cases. Mov Disord 2008;23:228-33.

[5] Uchikawa K, Toikawa H, Liu M. Subscapularis motor point block for spastic shoulders in patients with cervical cord injury. Spinal Cord 2009;47:249-51.

[6] Ghai A, Sangwan S, Hooda S, Garg N, Kundu Z, Gupta T. Evaluation of interadductor approach in neurolytic blockade of obturator nerve in spastic patients. Saudi J Anaesth 2013;7:420-6.

[7] Ghai A, Sangwan S, Hooda S, Kiran S, Garg N. Obturator neurolysis using 65% alcohol for adductor muscle spasticity. Saudi J Anaesth 2012;6:282-4.

[8] Yasar E, Tok F, Taskaynatan M, Yilmaz B, Balaban B, Alaca R. The effects of phenol neurolysis of the obturator nerve on the distribution of buttock-seat interface pressure in spinal cord injury patients with hip adductor spasticity. Spinal Cord 2010;48:828-31.

Evidence for “Surgeries” is based on the following studies:

[1] Livshits A, Rappaport Z, Livshits V, Gepstein R. Surgical treatment of painful spasticity after spinal cord injury. Spinal Cord 2002;40:161-6.

[2] Putty T & Shapiro S. Efficacy of dorsal longitudinal myelotomy in treating spinal spasticity: a review of 20 cases. J Neurosurg 1991;75:397-401.

Other references:

Abel NA, Smith RA. Intrathecal baclofen for treatment of intractable spinal spasticity. Arch Phys Med Rehabil 1994; 75:54-58.

Adams MM, Hicks AL. Spasticity after spinal cord injury. Spinal Cord 2005;43(10):577-586.

Al-Khodairy AT, Gobelet C, Rossier AB. Has botulinum toxin type A a place in the treatment of spasticity in spinal cord injury patients? Spinal Cord 1998; 36(12):854-858.

Avellino AM, Loeser JD. Intrathecal baclofen for the treatment of intractable spasticity of spine or brain etiology. Neuromodulation 2000; 3(2):75-81.

Bajd T, Gregoric M, Vodovnik L, Benko H. Electrical stimulation in treating spasticity resulting from spinal cord injury. Arch Phys Med Rehabil 1985; 66(8):515-517.

Bakheit AM, Pittock S, Moore AP, Wurker M, Otto S, Erbguth F et al. A randomized, double-blind, placebo-controlled study of the efficacy and safety of botulinum toxin type A in upper limb spasticity in patients with stroke. Eur J Neurol 2001; 8(6):559-565.

Bohannon RW. Tilt table standing for reducing spasticity after spinal cord injury. Arch Phys Med Rehabil 1993; 74(10):1121-1122.

Burchiel KJ, Hsu FP. Pain and spasticity after spinal cord injury: mechanisms and treatment. Spine 2001; 26(24 Suppl):S146-S160.

Canadian Paraplegic Association. Workplace participation national survey of Canadians with SCI. Canadian Paraplegic Association http://www.canparaplegic.org/en/Employment_and_Education_24/EMPLOYMENT_6/14.html. 1996; Last accessed: 9-15-2008.

Corry IS, Cosgrove AP, Walsh EG, McClean D, Graham HK. Botulinum toxin A in the hemiplegic upper limb: a double-blind trial. Dev Med Child Neurol 1997; 39(3):185-193.

Elbasiouny, S. M., Moroz, D., Bakr, M. M., & Mushahwar, V. K. (2010). Management of spasticity after spinal cord injury: current techniques and future directions. Neurorehabilitation and neural repair24(1), 23-33.

Gorgey AS, Dudley GA. Spasticity may defend skeletal muscle size and composition after incomplete spinal cord injury. Spinal Cord 2008; 46(2):96-102.

Goulet C, Arsenault AB, Bourbonnais D, Laramee MT, Lepage Y. Effects of transcutaneous electrical nerve stimulation on H-reflex and spinal spasticity. Scand J Rehabil Med 1996; 28(3):169-176.

Gracies JM, Nance P, Elovic E, McGuire J, Simpson DM. Traditional pharmacological treatments for spasticity. Part II: General and regional treatments. Muscle Nerve Suppl 1997; 6:S92-120.

Granat MH, Ferguson AC, Andrews BJ, Delargy M. The role of functional electrical stimulation in the rehabilitation of patients with incomplete spinal cord injury–observed benefits during gait studies. Paraplegia 1993; 31(4):207-215.

Gruenthal M, Mueller M, Olson WL, Priebe MM, Sherwood AM, Olson WH. Gabapentin for the treatment of spasticity in patients with spinal cord injury. Spinal Cord 1997; 35(10):686-689.

Hayes KC. Fampridine-SR for multiple sclerosis and spinal cord injury. Expert Rev Neurother 2007; 7(5):453-461.

Heetla HW, Staal MJ, Kliphuis C, van Laar T. The incidence and management of tolerance in intrathecal baclofen therapy. Spinal Cord, 2009; 47:751-756.

Heetla HW, Staal MJ, Kliphuis C, van Laar T. Tolerance to continuous intrathecal baclofen infusion can be reversed by pulsatile bolus infusion. Spinal Cord, 2010; 48: 483-486.

Hidler, J. M., & Rymer, W. Z. (1999). A simulation study of reflex instability in spasticity: origins of clonus. IEEE Transactions on Rehabilitation Engineering, 7(3), 327-340.

Hinderer SR, Lehmann JF, Price R, White O, deLateur BJ, Deitz J. Spasticity in spinal cord injured persons: quantitative effects of baclofen and placebo treatments. Am J Phys Med Rehabil 1990; 69(6):311-317.

Hinderer SR. The supraspinal anxiolytic effect of baclofen for spasticity reduction. Am J Phys Med Rehabil 1990; 69(5):254-258.

Hyman N, Barnes M, Bhakta B, Cozens A, Bakheit M, Kreczy-Kleedorfer B et al. Botulinum toxin (Dysport) treatment of hip adductor spasticity in multiple sclerosis: a prospective, randomised, double blind, placebo controlled, dose ranging study. J Neurol Neurosurg Psychiatry 2000; 68(6):707-712.

Kesiktas N, Paker N, Erdogan N, Gulsen G, Bicki D, Yilmaz H. The use of hydrotherapy for the management of spasticity. Neurorehabil Neural Repair 2004; 18(4):268-273.

Kirshblum S. Treatment alternatives for spinal cord injury related spasticity. J Spinal Cord Med 1999; 22(3):199-217.

Kiser TS, Reese NB, Maresh T, Hearn S, Yates C, Skinner RD et al. Use of a motorized bicycle exercise trainer to normalize frequency-dependent habituation of the H-reflex in spinal cord injury. J Spinal Cord Med 2005; 28(3):241-245.

Krause P, Szecsi J, Straube A. Changes in spastic muscle tone increase in patients with spinal cord injury using functional electrical stimulation and passive leg movements. Clinical Rehabilitation 2008; 22(7):627-634.

Kunkel CF, Scremin AM, Eisenberg B, Garcia JF, Roberts S, Martinez S. Effect of “standing” on spasticity, contracture, and osteoporosis in paralyzed males. Arch Phys Med Rehabil 1993; 74:73-78.

Lechner HE, Feldhaus S, Gudmundsen L, Hegemann D, Michel D, Zach GA et al. The short-term effect of hippotherapy on spasticity in patients with spinal cord injury. Spinal Cord 2003; 41(9):502-505.

Levi R, Hultling C, Nash MS, Seiger A. The Stockholm spinal cord injury study: 1. medical problems in a regional SCI population. Paraplegia 1995; 33:308-315.

Maurer M, Henn V, Dittrich A, Hofmann A. Delta-9-tetrahydrocannabinol shows antispastic and analgesic effects in a single case double-blind trial. Eur Arch Psychiatry Clin Neurosci 1990; 240(1):1-4.

Maynard FM, Karunas RS, Waring WP, III. Epidemiology of spasticity following traumatic spinal cord injury. Arch Phys Med Rehabil 1990; 71(8):566-569.

Midha M, Schmitt JK. Epidural spinal cord stimulation for the control of spasticity in spinal cord injury patients lacks long-term efficacy and is not cost-effective. Spinal Cord 1998; 36(3):190-192.

Mirbagheri MM, Ladouceur M, Barbeau H, Kearney RE. The effects of long-term FES-assisted walking on intrinsic and reflex dynamic stiffness in spastic spinal-cord-injured subjects. IEEE Trans Neural Syst Rehabil Eng 2002; 10(4):280-289.

Nance PW, Shears AH, Nance DM. Reflex changes induced by clonidine in spinal cord injured patients. Paraplegia 1989; 27(4):296-301.

Ochs G, Struppler A, Meyerson BA, Linderoth B, Gybels J, Gardner BP et al. Intrathecal baclofen for long-term treatment of spasticity: a multi-centre study. J Neurol Neurosurg Psychiatry 1989; 52:933-939.

Penn RD. Intrathecal baclofen for spasticity of spinal origin: seven years of experience. J Neurosurg 1992 ;77:236-240.

Possover M, Schurch B, Henle KP. New strategies of pelvic nerves stimulation for recovery of pelvic visceral functions and locomotion in paraplegics. Neurourol Urodyn 2010 Nov; 29(8).

Rayegani, S. M., Shojaee, H., Sedighipour, L., Soroush, M. R., Baghbani, M., & Amirani, O. B. (2011). The effect of electrical passive cycling on spasticity in war veterans with spinal cord injury. Frontiers in Neurology; 2(39):1-7.

Richardson D, Edwards S, Sheean GL, Greenwood RJ, Thompson AJ. The effect of botulinum toxin on hand function after incomplete spinal cord injury at the level of C5/6: a case report. Clin Rehabil 1997; 11(4):288-292.

Shields RK, Dudley-Javoroski S. Monitoring standing wheelchair use after spinal cord injury: a case report. Disabil Rehabil 2005; 27:142-146.

Simpson DM, Alexander DN, O’Brien CF, Tagliati M, Aswad AS, Leon JM et al. Botulinum toxin type A in the treatment of upper extremity spasticity: a randomized, double-blind, placebo-controlled trial. Neurology 1996; 46(5):1306-1310.

Simpson DM. Clinical trials of botulinum toxin in the treatment of spasticity. Muscle Nerve Suppl 1997; 6:S169-S175.

Smith SJ, Ellis E, White S, Moore AP. A double-blind placebo-controlled study of botulinum toxin in upper limb spasticity after stroke or head injury. Clin Rehabil 2000; 14(1):5-13.

Snow BJ, Tsui JK, Bhatt MH, Varelas M, Hashimoto SA, Calne DB. Treatment of spasticity with botulinum toxin: a double-blind study. Ann Neurol 1990; 28(4):512-515.

Thoumie P, Le CG, Beillot J, Dassonville J, Chevalier T, Perrouin-Verbe B et al. Restoration of functional gait in paraplegic patients with the RGO-II hybrid orthosis. A multicenter controlled study. II: Physiological evaluation. Paraplegia 1995; 33(11):654-659.

Wainberg M, Barbeau H, Gauthier S. The effects of cyproheptadine on locomotion and on spasticity in patients with spinal cord injuries. J Neurol Neurosurg Psychiatry 1990; 53(9):754-763.

Walter JS, Sacks J, Othman R, Rankin AZ, Nemchausky B, Chintam R et al. A database of self-reported secondary medical problems among VA spinal cord injury patients: its role in clinical care and management. J Rehabil Res Dev 2002; 39:53-61.

Wasiak J, Hoare B, Wallen M. Botulinum toxin A as an adjunct to treatment in the management of the upper limb in children with spastic cerebral palsy. Cochrane Database Syst Rev 2004; (4):CD003469.

Lechner H, Kakebeeke T, Hegemann D, Baumberger M. The effect of hippotherapy on spasticity and on mental well-being of persons with spinal cord injury. Arch Phys Med Rehabil 2007;88:1241-8.

Nardone R, Holler Y, Thomschewski A, et al. rTMS modulates reciprocal inhibition in patients with traumatic spinal cord injury. Spinal Cord 2014;52:831-5.

Benito J, Kumru H, Murillo N, et al. Motor and gait improvement in patients with incomplete spinal cord injury induced by high-frequency repetitive transcranial magnetic stimulation. Top Spin Cord Injury Rehabil 2012;18:106-12.

Kumru H, Vidal J, Kofler M, Portell E, Valls-Sole J. Alterations in excitatory and inhibitory brainstem interneuronal circuits after severe spinal cord injury. Journal of Neurotrauma, 2010;27:721-8.

Image credits:

  1. Muscle strain ©Kylie Mhai, CC BY 3.0 US
  2. Modified from: Dorsiplantar ©Connexions, CC BY 3.0
  3. Image by SCIRE Community Team
  4. Imgnotraçat arc reflex eng ©MartaAguayo, CC BY-SA 3.0
  5. Image by SCIRE Community Team
  6. Image by SCIRE Community Team
  7. Insomnia ©Gan Khoon Lay, CC BY 3.0 US
  8. Image by SCIRE Community Team
  9. Standing frame ©Memasa, CC BY-SA 3.0
  10. Image by SCIRE Community Team
  11. Intrathecal-pump-cartoon ©Anand Swaminathan, CC BY-SA 3.0
  12. Pills ©Nikita Kozin, CC BY 3.0 US
  13. Treatment ©Royal@design, CC BY 3.0 US
  14. Surgery ©Healthcare Symbols, CC0 1.0
  15. Neuro-ms ©Baburov, CC BY-SA 4.0

 

Disclaimer: This document does not provide medical advice. This information is provided for educational purposes only. Consult a qualified health professional for further information or specific medical advice. The SCIRE Project, its partners and collaborators disclaim any liability to any party for any loss or damage by errors or omissions in this publication.

Baclofen

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Author: SCIRE Community Team | Reviewer: Patricia Mills | Published: 21 November 2017 | Updated: ~

Baclofen is a medication that is used to treat spasticity. This page provides basic information about baclofen and its use after spinal cord injury (SCI).

Key Points

  • Baclofen (Lioresal) is a medication that is used to relax muscles affected by spasticity.
  • Baclofen is derived from gamma aminobutyric acid (GABA), a chemical in the body that helps to reduce reflexes that are responsible for spasticity.
  • Baclofen can be taken by mouth as a tablet or injected into the spinal canal in a liquid form through an implanted pump (an intrathecal baclofen pump).
  • Research evidence supports that both baclofen tablets and baclofen pumps are effective to reduce spasticity after SCI.
Ball and stick model of baclofen.

Ball and stick model of baclofen.1

Baclofen is a medication that is used to treat spasticity. It is also known by the trade name Lioresal. Baclofen is a muscle relaxant medication that helps to reduce muscle tension and spasms caused by nervous system disorders like spinal cord injury and multiple sclerosis.

Baclofen is derived from a chemical called gamma aminobutyric acid (GABA), which reduces muscle activity. It can enter into the brain and spinal cord, where it helps to reduce reflexes responsible for spasticity. Baclofen can be taken by mouth as a tablet or injected into the spinal canal as a fluid using an implanted baclofen pump.

Baclofen in tablet form is usually the first type of medication used to treat spasticity after SCI. There is strong evidence that oral baclofen improves the symptoms of spasticity

Baclofen administered by intrathecal pump is usually a last option that is explored because of the surgery that is required to implant the pump. However, when it is used, there is strong evidence that intrathecal baclofen is effective to treat the symptoms of spasticity in people with SCI.

Baclofen is a prescription medication that is given with specific instructions from your health providers on how to take it. It is important to follow their instructions closely when taking this medication and discuss any questions you have about your use of the medication directly with your team.

Baclofen tablets

Two round white 20mg baclofen tablets with "DAN" and "5731" inscribed on one side, and "20" inscribed on the other side.

Baclofen tablet 20 mg. 2

Baclofen is usually taken by mouth as a tablet. Baclofen is prescribed at a unique dose for you and then carefully monitored. Treatment is usually started with a trial of a low dose of the drug to find out if it works and then slowly increased to determine the optimal dose. This dose will then be maintained while continuing to take the drug.

You can expect some side effects when starting Baclofen (and any other anti-spasticity drug), so do not be surprised if that should happen. As your body gets used to the new drug, the side effects can improve and in some cases completely resolve. Side effects, if they occur, usually are experienced before the drug starts to work on the spasticity therefore it is important to stay on the drug as long as the side effects are tolerable. If the side effects have not improved or are not tolerable by the end of 2 weeks of starting the new drug, and you don’t feel that the benefit of the drug is worth the side effects that you are experiencing, then notify your physician as you will likely have to either decrease the dose or consider trying another drug instead.

Cartoon diagram of a man's body with a disc-shaped intrathecal pump implanted under the skin with a red wire catheter inserted into the spinal column

Diagram showing an intrathecal pump inside the spinal column.3

Baclofen pumps (Intrathecal baclofen)

Baclofen may also be injected directly into the sac that surrounds the spinal cord. This is called intrathecal baclofen. ‘Intrathecal’ means ‘within the spinal sac’ (also called the thecal sac).

Intrathecal baclofen is usually administered using a surgically implanted pump that is placed under the skin near the abdomen called a baclofen pump. The pump is then connected to the spinal cord fluid through a thin tube (catheter) that travels through your soft tissue underneath the skin. The pump provides a dose of the medication through the catheter at regular intervals according to its settings.

Baclofen pumps are first managed by a health provider in a hospital setting in the early days following surgical implantation. Then, the device can be programmed to release a programmed dose of baclofen throughout the day for use at home.

Regular visits to the intrathecal baclofen pump doctor are required to refill the pump and monitor for any problems. Therefore, in order for you to be a candidate for getting the pump, you need to be able to travel from where you live to where the pump can be serviced. The pump can be removed if you decide you no longer would like to receive the treatment.

Increasing oral baclofen dosage may result in a number of side effects like sleepiness. The solution is a pump implanted under the skin that administers baclofen directly to the spinal cord, aka “intrathecally”.

When are baclofen pumps used?

Typically, intrathecal baclofen is recommended when spasticity is severe and widespread throughout the body, and other approaches to manage your spasticity, such as medications by mouth, have not worked. Much lower doses of baclofen are used when given as an intrathecal injection. This may help people with severe spasticity to manage spasticity more effectively, and usually results in no side effects.

However, it is important to know that complications with the pump can occur, potentially causing episodes of too much baclofen (baclofen overdose) or too little baclofen (baclofen withdrawal) to be delivered. Therefore, it is important to consult with an intrathecal baclofen pump expert in order to determine if the pump is a good option for you.

Baclofen is not appropriate for everyone. There are certain situations in which it may not be safe to use. This is not a complete list; please consult a health provider for detailed safety information before using this treatment.

Baclofen should not be used in the following situations:

  • By people with health conditions such as epilepsy, kidney problems, diabetes, or breathing problems
  • By people with conditions that cause confusion or depression
  • By people with abnormal blood circulation in the brain
  • By people experiencing pain in the stomach or intestine
  • By individuals with a baclofen allergy
  • By pregnant and nursing women
  • Oral baclofen may be unsafe in individuals with liver disease or difficulty urinating
  • Intrathecal baclofen may be unsafe for people with a history of heart problems, infections, or by those who are prone to autonomic dysreflexia

Even for those who are not restricted from using baclofen (see above), there may be risks and side effects with the use of this treatment. It is important to discuss these possibilities in detail with your health provider before using this treatment.

Risks and side effects of baclofen may include:

  • Drowsiness, tiredness, or dizziness
  • Muscle weakness
  • Confusion
  • Difficulty sleeping (insomnia)
  • Interactions with other drugs such as antidepressants, sleeping pills, alcohol, and other medications
  • Baclofen pumps are implanted surgically, which carries a risk of infection and other surgical risks

Because baclofen helps to relax the muscles, it may also have unintended effects on other medical problems that benefit from increased muscle tone. For example:

  • It may further reduce the cough reflex in people who already have trouble coughing
  • It may make it more difficult to walk, stand, or do other tasks requiring muscle strength and movement
  • Baclofen pumps may make it more difficult for men to have erections, although this may be regained when reducing the dose or stopping treatment

In addition, stopping baclofen therapy abruptly can cause withdrawal. This can cause a variety of symptoms, including seizures, hallucinations, confusion, and fever. When baclofen is stopped, the dose of the medication should be gradually lowered over time before it can be stopped. It is important to follow the routine recommended by your health providers when stopping use of this medication.

Important considerations when treating spasticity

Although we often focus on the negative effects of spasticity, it can also have benefits. For example, spasticity in the legs can sometimes help people transfer more effectively or stand and walk. For this reason, when treatments like baclofen work the way they are supposed to, they can sometimes have negative effects, such as:

  • Reduced functional abilities, such as the ability to transfer, stand, or walk
  • Loss of health benefits of spasticity, such as better circulation and muscle strength
  • Loss of spasticity as a warning sign of other health problems (such as infections or injuries below the level of injury)

The decision to treat spasticity needs to be made by you and your health team on a personal basis, taking into consideration function, symptoms, and the benefits and drawbacks of treatment.

Baclofen is a common treatment for spasticity after SCI. Both baclofen tablets and baclofen pumps are effective for reducing spasticity in people with SCI. As baclofen therapy requires careful dosing and monitoring, it is important to discuss with your health provider about whether this treatment option is suitable for you and how to use it appropriately.

For a review of how we assess evidence at SCIRE Community and advice on making decisions, refer to SCIRE Community Evidence.

Parts of this page have been adapted from the SCIRE Professional “Spasticity” Module:

Hsieh JTC, Connolly SJ, McIntyre A, Townson AF, Short C, Mills P, Vu V, Benton B, Wolfe DL (2016). Spasticity Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Loh E, McIntyre A, Querée M, editors. Spinal Cord Injury Rehabilitation Evidence. Version 6.0: p 1-135.

Available from: https://scireproject.com/evidence/spasticity/

Evidence for “What is baclofen?” is based on the following studies:

Oral baclofen:

[1] Chu V, Hornby T, Schmit B. Effect of antispastic drugs on motor reflexes and voluntary muscle contraction in incomplete spinal cord injury. Arch Phys Med Rehabil 2014;95:622-32.

[2] Nance P, Huff F, Martinez-Arizala A, Ayyoub Z, Chen D, Bian A, Stamler D. Efficacy and safety study of arbaclofen placarbil in patients with spasticity due to spinal cord injury. Spinal Cord 2011;49:974-80.

[3] Aydin G, Tomruk S, Keles I, Demir S, Orkun S. Transcutaneous electrical nerve stimulation versus baclofen in spasticity: clinical and electrophysiologic comparison. Am J Phys Med Rehabil 2005;84:584-92.

[4] Duncan G, Shahani B, Young R. An evaluation of baclofen treatment for certain symptoms in patients with spinal cord lesions. A double-blind, cross-over study. Neurology 1976;26:441-6.

[5] Burke D, Gillies J, Lance J. An objective assessment of a gamma aminobutyric acid derivative in the control of spasticity. Proc Aust Assoc Neurol 1971;8:131-4.

[6] Dicpinigaitis P, Allusson V, Baldanti A, and Nalamati J. Ethnic and gender differences in cough reflex sensitivity. Respiration 2001;68:480-2.Dicpinigaitis P, Allusson V, Baldanti A, and Nalamati J. Ethnic and gender differences in cough reflex sensitivity. Respiration 2001;68:480-2.

[7] Veerakumar A, Cheng J, Sunshine A, Ye X, Zorowitz R, Anderson W. Baclofen dosage after traumatic spinal cord injury: a multi-decade retrospective analysis. Clin Neurol Neurosurg 2015;129:50-6.

[8] Nance P. A comparison of clonidine, cyproheptadine and baclofen in spastic spinal cord injured patients. J Am Paraplegia Soc 1994;17:150-6.

Intrathecal baclofen:

[1] Ordia J, Fischer E, Adamski E, Spatz E. Chronic intrathecal delivery of baclofen by a programmable pump for the treatment of severe spasticity. J Neurosurg 1996;85:452-7.

[2] Nance P, Schryvers O, Schmidt B, Dubo H, Loveridge B, Fewer D. Intrathecal baclofen therapy for adults with spinal spasticity: therapeutic efficacy and effect on hospital admissions. Can J Neurol Sci 1995;22:22-9.

[3] Coffey J, Cahill D, Steers W, Park T, Ordia J, Meythaler J, et al. Intrathecal baclofen for intractable spasticity of spinal origin: results of a long-term multicenter study. J Neurosurg 1993;78:226-32.

[4] Hugenholtz H, Nelson R, Dehoux E, Bickerton R. Intrathecal baclofen for intractable spinal spasticity-a double-blind cross-over comparison with placebo in 6 patients. Can J Neurol Sci 1992;19:188-95.

[5] Loubser P, Narayan R, Sandin K, Donovan W, Russell K. Continuous infusion of intrathecal baclofen: long-term effects on spasticity in spinal cord injury. Paraplegia 1991;29:48-64.

[6] Penn R, Savoy S, Corcos D, Latash M, Gottlieb G, Parke B et al. Intrathecal baclofen for severe spinal spasticity. N Engl J Med 1989;320:1517-21.

[7] Boviatsis E, Kouyialis A, Korfias S, Sakas D. Functional outcome of intrathecal baclofen administration for severe spasticity. Clin Neurol Neurosurg 2005;107:289-95.

[8] Azouvi P, Mane M, Thiebaut J, Denys P, Remy-Neris O, Bussel B. Intrathecal baclofen administration for control of severe spinal spasticity: functional improvement and long-term follow-up. Arch Phys Med Rehabil 1996;77:35-9.

[9] Plassat R, Perrouin Verbe B, Menei P, Menegalli D, Mathe J, Richard I. Treatment of spasticity with intrathecal baclofen administration: Long-term follow-up review of 40 patients. Spinal Cord 2004;42:686-93.

[10] Zahavi A, Geertzen J, Middel B, Staal M, Rietman J. Long term effect (more than five years) of intrathecal baclofen on impairment, disability, and quality of life in patients with severe spasticity of spinal origin. J Neurol Neurosurg Psychi 2004;75:1553-7.

[11] Korenkov A, Niendorf W, Darwish N, Glaeser E, Gaab M. Continuous intrathecal infusion of baclofen in patients with spasticity caused by spinal cord injuries. Neurosurg Rev 2002;25:228-30.

[12] Broseta J, Garcia-March G, Sanchez-Ledesma M, Anaya J, Silva I. Chronic intrathecal baclofen administration in severe spasticity. Stereotact Funct Neurosurg 1990;54-55:147-53.

[13] Parke B, Penn R, Savoy S, Corcos D. Functional outcome after delivery of intrathecal baclofen. Arch Phys Med Rehabil 1989;70:30-2.

Other references:

Burchiel KJ, Hsu FP. Pain and spasticity after spinal cord injury: mechanisms and treatment. Spine 2001; 26(24 Suppl):S146-S160.

Denys P, Mane M, Azouvi P, Chartier-Kastler E, Thiebaut JB, Bussel B. Side effects of chronic intrathecal baclofen on erection and ejaculation in patients with spinal cord lesions. Arch Phys Med Rehabil 1998; 79(5):494-496.

Dicpinigaitis PV, Dobkin JB, Reichel J. Typical versus cough-variant of asthma: differentiation by cough reflex sensitivity and the antitussive effect of zafirlukast. Eur Respir J. 2000; 16:525s.

Gracies JM, Nance P, Elovic E, McGuire J, Simpson DM. Traditional pharmacological treatments for spasticity. Part II: General and regional treatments. Muscle Nerve Suppl 1997; 6:S92-120.

Hinderer SR. The supraspinal anxiolytic effect of baclofen for spasticity reduction. Am J Phys Med Rehabil 1990; 69(5):254-258.

Jones ML, Leslie DP, Bilsky G, Bowman B. Effects of intrathecal baclofen on perceived sexual functioning in men with spinal cord injury. J Spinal Cord Med 2008; 31:97-102.

Kirshblum S. Treatment alternatives for spinal cord injury related spasticity. J Spinal Cord Med 1999; 22(3):199-217.

Knutsson E, Lindblom U, Martensson A. Plasma and cerebrospinal fluid levels of baclofen (Lioresal) at optimal therapeutic responses in spastic paresis. J Neurol Sci 1974; 23(3):473-484.

Nance PW, Schryvers O, Schmidt B, Dubo H, Loveridge B, Fewer D. Intrathecal baclofen therapy for adults with spinal spasticity: therapeutic efficacy and effect on hospital admissions. Can J Neurol Sci 1995; 22:22-29.

Nance PW. A comparison of clonidine, cyproheptadine and baclofen in spastic spinal cord injured patients. J Am Paraplegia Soc 1994; 17(3):150-156.

Postma TJBM, Oenema D, Terpstra S et al. Cost analysis of the treatment of severe spinal spasticity with a continuous intrathecal baclofen infusion system. PharmacoEconomics 1999; 15(4):395-404.

CPS [Internet]. Ottawa (ON): Canadian Pharmacists Association; c2016 [cited 2017 Oct 10]. Available from: https://www.pharmacists.ca/products-services/ or http://www.myrxtx.ca. Also available in paper copy from the publisher.

Image credits

  1. Baclofen ball-and-stick model, ©Vaccinationist, CC BY-SA 4.0,
  2. National Institutes of Health, part of the United States Department of Health and Human ServicesBaclofen 20 mg oral tablet, CC0 1.0
  3. Intrathecal-pump-cartoon, ©R.E.B.E.L EM, CC BY-NC-ND 3.0.

 

Disclaimer: This document does not provide medical advice. This information is provided for educational purposes only. Consult a qualified health professional for further information or specific medical advice. The SCIRE Project, its partners and collaborators disclaim any liability to any party for any loss or damage by errors or omissions in this publication.

Botulinum Toxin

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Author: SCIRE Community Team | Reviewer: Patricia Mills | Published: 10 November 2017 | Updated: ~

Botulinum toxin injections may be used as a treatment after spinal cord injury (SCI). This page provides an overview of the use of botulinum toxin after SCI.

Key Points

  • Botulinum toxin is a protein made by bacteria that can cause muscle weakness or paralysis.
  • Very small doses of certain strains of botulinum toxin may be injected into muscles as a treatment for various medical conditions.
  • Botulinum toxin injections are currently used to treat muscle spasticity and certain types of bladder problems after SCI.
  • Research evidence supports that botulinum toxin is effective to reduce spasticity in muscles and to manage certain types of bladder problems after SCI.
A structure of a botulinum toxin molecule

A structure of a botulinum toxin molecule.1

Botulinum toxin is a protein produced by bacteria. Although this protein can be toxic to humans, injections of very small amounts of certain strains of botulinum toxin are used in medicine. Botulinum toxin is well-known by the trade names Botox, Dysport, and Xeomin as a cosmetic procedure for reducing wrinkles. However, it is also used as a treatment for various other medical conditions.

Botulinum toxin injections may be used after SCI to treat:

  • Problematic spasticity that is located in specific muscles (widespread spasticity is usually treated with an oral medication instead)
  • Overactive (reflex) bladder problems after SCI

Botulinum toxin injections into the bladder may also help to prevent autonomic dysreflexia that is triggered by bladder problems after SCI.

Monochrome cartoon logo of bottle and injection needleBotulinum toxin is given with an injection into the affected spastic muscle or bladder. 

The exact procedures and dose provided will be different for each person. Consult your health provider for further information about how botulinum toxin procedures may be done.

Multiple injections may be given in one session to ensure enough of the toxin reaches the muscle. After the injections, it may take up to a week for you to notice an effect. Exercise and stretching are usually recommended after the injection to enhance the effects of botulinum toxin.

Botulinum toxin injections are not permanent, and their effects wear off in usually around 3 months (in the case of muscle injections) to 6 months (in the case of bladder injections). Sessions are scheduled on an ongoing basis to maintain the effects of the treatment.

A black and white cartoon diagram of a neural synapse

When botulinum toxin is injected into a muscle, it blocks the nerves to the muscles from releasing a chemical called acetylcholine. Acetylcholine makes muscles contract (tense). When its release is blocked, the muscles are unable to contract, causing weakness or paralysis. In a muscle with spasticity, botulinum toxin can help to decrease muscle spasms.

Botulinum toxin can be used to treat overactive (reflex) bladder problems for similar reasons. These bladder problems happen when the bladder muscle or the bladder sphincters spasm, preventing emptying or causing random emptying of urine (detrusor hyperreflexia). The injection of botulinum toxin into these muscles reduces muscle spasms, which may help to treat these problems.

Botulinum toxin is not suitable for everyone for medical reasons. It is also important to know that botulinum toxin treatments can be expensive depending on how your medications are funded. Consult your doctor for detailed information about whether this treatment is safe and appropriate for you.

Botulinum toxin should not be used in the following situations:

Silhouette cartoon of pregnant woman

  • By people with other neuromuscular disorders, such as myasthenia gravis
  • By people who have an allergy to any of the injection ingredients
  • By pregnant or nursing women
  • In areas of infection

Botulinum toxin should be used with caution in the following situations:

  • By people taking anticoagulants (blood thinners)

Additional precautions when botulinum toxin is used in the bladder:

  • By people who have a current or multiple recent bladder or kidney infections (urinary tract infections)
  • By people who are not willing or able to do clean intermittent catheterization or have a Foley catheter inserted. This is because there is a potential short term side effect of too much bladder muscle relaxation leading to an inability to fully empty the bladder (urinary retention) without a catheter.

Botulinum toxin injections are generally considered to have low risk of serious medical complications with their use. However, there are side effects and risks of this treatment that are important to discuss with your doctor. Side effects usually happen within the first few days after injection, but sometimes last longer. This is not a complete list; speak to your doctor for detailed information about botulinum toxin injections.

Risks and side effects of botulinum toxin injections may include:Stock image of figure experiencing knee pain

  • Muscle weakness – usually in the muscles that receive the injection, but may be generalized to other muscles, although this is a rare occurrence
  • Long-term use may lead to loss of muscle size and bulk that happens when the muscles are not used (muscle atrophy)

Risks and side effects of botulinum toxin used for bladder problems include:

  • Bladder and kidney infections (urinary tract infections)
  • Blood in the urine
  • An inability to fully empty the bladder (urinary retention)

For more information on urinary tract infections, check out our article here!

Risks and side effects related to injections of any kind:

In addition to the risks of botulinum toxin itself, injections of any kind may cause pain or tenderness, inflammation, changes to sensation, redness, infections, bleeding, bruising, light-headedness and fainting.

Important considerations when treating spasticity

Although we often focus on the negative effects of spasticity, it can also have benefits. For example, spasticity in the legs can sometimes help people transfer more effectively or stand and walk. For this reason, when treatments like botulinum toxin work the way they are supposed to, they can sometimes have negative effects, such as:

  • Reduced functional abilities, such as the ability to transfer, stand, or walk
  • Loss of health benefits of spasticity, such as better circulation, and muscle strength
  • Loss of spasticity as a warning sign of other health problems (such as infections or injuries below the level of injury)

The decision to treat spasticity needs to be made by you and your health team on a personal basis, taking into consideration function, symptoms, and the benefits and drawbacks of treatment.

Botulinum toxin has been studied thoroughly as a treatment for spasticity in other conditions like stroke and brain injury. There is strong evidence to support that it is effective for treating spasticity in these conditions. Fewer studies have looked at how effective botulinum toxin injections are after SCI.

Spasticity

There is moderate evidence that botulinum toxin injections can be used to improve muscle spasticity in the injected muscle after SCI. It may also help to improve problems related to spasticity, such as pain, sleep disturbances, and walking problems.

Overactive (reflex) bladder problems

There is strong evidence that botulinum toxin injections are an effective treatment option for reducing the symptoms of overactive (reflex) bladder problems after SCI. This includes both:

  • Injections into the bladder muscle to prevent leaking or incontinence
  • Injections into the sphincter muscles to improve bladder emptying
    Image showing the urinary system. Bottom right image shows a person's abdomen with two bean-shaped kidneys connecting by tubes labelled 'ureters' to the bladder (just above the pubic bone). Enlargement top left shows the bladder surrounded by a smooth muscle labelled 'bladder wall muscle'. Urine is contained in the bladder. The bladder connect downward to a tube labelled 'urethra'. The exit of the bladder to the urethra has muscles surrounding it labelled 'bladder sphincter muscles'.

    The components of the urinary system.7

Autonomic dysreflexia and the spastic bladder

Some of the studies that have looked at treating bladder problems after SCI have also found that some participants also had fewer episodes of autonomic dysreflexia after treatment. This was thought to be because bladder problems triggered autonomic dysreflexia in these individuals. However, there is not enough evidence to use botulinum toxin as a direct treatment for preventing autonomic dysreflexia at this time.

See our article on Autonomic Dysreflexia for more information!

Botulinum toxin injections are a treatment option for spasticity and overactive (reflex) bladder problems after SCI. Botulinum toxin can be effective for reducing the symptoms related to these problems after SCI. It is important to discuss with your health provider about whether this treatment option is suitable for you.

For a review of how we assess evidence at SCIRE Community and advice on making decisions, please see SCIRE Community Evidence.

Parts of this page have been adapted from the SCIRE Project (Professional) “Bladder Management”, “Autonomic Dysreflexia”, and “Spasticity” chapters:

Hsieh JTC, Connolly SJ, McIntyre A, Townson AF, Short C, Mills P, Vu V, Benton B, Wolfe DL (2016). Spasticity Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Loh E, McIntyre A, Querée M, editors. Spinal Cord Injury Rehabilitation Evidence. Version 6.0: p 1-135.

Available from: https://scireproject.com/evidence/rehabilitation-evidence/spasticity/

Hsieh J, McIntyre A, Iruthayarajah J, Loh E, Ethans K, Mehta S, Wolfe D, Teasell R. (2014). Bladder Management Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors. Spinal Cord Injury Rehabilitation Evidence. Version 5.0: p 1-196.

Available from: https://scireproject.com/evidence/rehabilitation-evidence/bladder-management/

Krassioukov A, Blackmer J, Teasell RW, Eng JJ (2014). Autonomic Dysreflexia Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors. Spinal Cord Injury Rehabilitation Evidence. Version 5.0. Vancouver: p 1- 35.

Available from: https://scireproject.com/evidence/rehabilitation-evidence/autonomic-dysreflexia/

 

Evidence for “Is botulinum toxin effective?” is based on the following studies:

Spasticity:

[1] Richardson D, Sheean G, Werring D, Desai M, Edwards S, Greenwood R et al. Evaluating the role of botulinum toxin in the management of focal hypertonia in adults. J Neurol Neurosurg Psychi 2000;69:499-506.

[2] Spiegl U, Maier D, Gonschorek O, Heyde C, Buhren V. Antispastic therapy with botulinum toxin type A in patients with traumatic spinal cord lesion. GMS Interdiscip Plast Reconstr Surg 2014;3:1-5.

[3] Bernuz B, Genet F, Terrat P, et al. Botulinum toxin effect on voluntary and stretch reflex-related torque produced by the quadriceps: An isokinetic pilot study. Neurorehabil Neural Repair 2012;26:542-7.

[4] Hecht M, Stolze H, uf dem B, Giess R, Treig T, Winterholler M et al. Botulinum neurotoxin type A injections reduce spasticity in mild to moderate hereditary spastic paraplegia–report of 19 cases. Mov Disord 2008;23:228-33.

[5] Al-Khodairy A, Gobelet C, Rossier A. Has botulinum toxin type A a place in the treatment of spasticity in spinal cord injury patients? Spinal Cord 1998;36:854-8.

Bladder problems:

Detrusor overactivity

[1] Mehta S, Hill D, McIntyre A, Foley N, Hsieh J, Ethans K et al. Meta-analysis of botulinum toxin A detrusor injections in the treatment of neurogenic detrusor overactivity after spinal cord injury. Arch Phys Med Rehabil 2013;94(8):1473-1481.

[2] Schurch B, de SM, Denys P, Chartier-Kastler E, Haab F, Everaert K et al. Botulinum toxin type is a safe and effective treatment for neurogenic urinary incontinence: Results of a single treatment, randomized, placebo controlled 6-month study. J Urol 2005;174(1):196-200.

[3] Grosse J, Kramer G, Jakse G. Comparing two types of botulinum-A toxin detrusor injections in patients with severe neurogenic detrusor overactivity: A case-control study. BJU International 2009;104:651-656.

[4] Schurch B, Denys Pierre, Kozma CM, Reese PR, Slaton T, Barron RL. Botulinum toxin A improves the quality of life of patients with neurogenic urinary incontinence. European urology 2007:52(3):850-859.

[5] Del Popolo G, Filocamo MT, Li Marzi V, Macchiarella A, Cecconi F, Lombardi G, Nicita G. Neurogenic detrusor overactivity treated with english botulinum toxin a: 8-year experience of one single centre. Eur Urol. 2008 May;53(5):1013-19.

[6] Giannantoni A, Meatini E, Del Zingaro M, Porena M. Six-year follow-up of Botulinum Toxin A intradetrosrial injections in patients with refractory neurogenic detrusor overactivity: Clinical and urodynamic results. European Urology 2009;55:705-712.

[7] Klaphajone J, Kitisomprayoonkul W, Sriplakit S. Botulinum toxin type A injections for treating neurogenic detrusor overactivity combined with low-compliance bladder in patients with spinal cord lesions. Arch Phys Med Rehabil 2005;86:2114-2118.

[8] Kuo H. Therapeutic effects of suburothelial injection of botulinum a toxin for neurogenic detrusor overactivity due to chronic cerebrovascular accident and spinal cord lesions. Urology 2006;67:232-236.

[9] Kuo H. Satisfaction with urethral injection of botulinum toxin A for detrusor sphincter dyssynergia in patients with spinal cord lesion. Neurourol Urodyn 2008;27:793-796.

[10] Pannek J, Gocking K, Bersch U. Long-term effects of repeated intradetrusor botulinum neurotoxin A injections on detrusor function in patients with neurogenic bladder dysfunction. BJU International 2009;104:1246-1250.

[11] Tow AM, Toh KL, Chan SP, Consigliere D. Botulinum toxin type A for refractory neurogenic detrusor overactivity in spinal cord injured patients in Singapore. Ann Acad Med Singapore 2007;36(1):11-17.

[12] Wefer B, Ehlken B, Bremer J, Burgdörfer H, Domurath B, Hampel C. Treatment outcomes and resource use of patients with neurogenic detrusor overactivity receiving botulinum toxin A (BOTOX®) therapy in Germany. World J Urol 2010;28(3):385-390.

[13] Akbar M, Abel R, Seyler TM, Bedke J, Haferkamp A, Gerner HJ et al. Repeated botulinum-A toxin injections in the treatment of myelodysplastic children and patients with spinal cord injuries with neurogenic bladder dysfunction. BJU Int 2007;100(3):639-645.

[14] Patki P, Hamid R, Shah PJ, Craggs M. Long-term efficacy of AMS 800 artificial urinary sphincter in male patients with urodynamic stress incontinence due to spinal cord lesion. Spinal Cord 2006;44(5):297-300.

[15] Herschorn S, Gajewski J, Ethans K, Corcos J, Carlson K, Bailly G et al. Efficacy of botulinum toxin A injection for neurogenic detrusor overactivity and urinary incontinence: A randomized, double-blind trial. J urology 2011;185(6):2229-2235.

[16] Abdel-Meguid T. Botulinum toxin-A injections into neurogenic overactive bladder—to include or exclude the trigone? A prospective, randomized, controlled trial. J urology 2010;184(6):2423-2428.

[17] Krhut J, Samal V, Nemec D, Zvara P. Intradetrusor versus suburothelial onabotulinumtoxinA injections for neurogenic detrusor overactivity: A pilot study. Spinal cord 2012;50(12):904-907.

Sphincter overactivity

[1] Kuo H. Therapeutic outcome and quality of life between urethral and detrusor botulinum toxin treatment for patients with spinal cord lesions and detrusor sphincter dyssynergia. Inter J Clin Prac 2013;67(10):1044-1049.

[2] Kuo H. Satisfaction with urethral injection of botulinum toxin A for detrusor sphincter dyssynergia in patients with spinal cord lesion. Neurourol Urodyn 2008;27:793-796.

[3] Tsai SJ, Ying TH, Huang YH, Cheng JW, Bih LI, Lew HL. Transperineal injection of botulinum toxin A for treatment of detrusor sphincter dyssynergia: Localization with combined fluoroscopic and electromyographic guidance. Arch Phys Med Rehabil 2009;90:832-836

[4] DeSeze M, Petit H, Gallien P, de Seze MP, Joseph PA, Mazaux JM et al. Botulinum a toxin and detrusor sphincter dyssynergia: A double-blind lidocaine-controlled study in 13 patients with spinal cord disease. Eur Urol 2002;42(1):56-62.

[5] Chen SL, Bih LI, Chen GD, Huang YH, You YH, Lew HL. Transrectal ultrasound-guided transperineal botulinum toxin A injection to the external urethral sphincter for treatment of detrusor external sphincter dyssynergia in patients with spinal cord injury. Arch Phys Med Rehabil 2010;91:340-344.

[6] Schurch B, Hauri D, Rodic B, Curt A, Meyer M, Rossier AB. Botulinum-A toxin as a treatment of detrusor-sphincter dyssynergia: A prospective study in 24 spinal cord injury patients. J Urol 1996;155(3):1023-1029.

[7] Phelan MW, Franks M, Somogyi GT, Yokoyama T, Fraser MO, Lavelle JP et al. Botulinum toxin urethral sphincter injection to restore bladder emptying in men and women with voiding dysfunction. J Urol 2001;165(4):1107-1110.

Other references:

Alvares R, Silva,J, Barboza A, Monteiro R. Botulinum toxin A in the treatment of spinal cord injury patients with refractory neurogenic detrusor overactivity. International braz j urol 2010;36(6):732-737.

Bagi P, Biering-Sørensen F. Botulinum toxin A for treatment of neurogenic detrusor overactivity and incontinence in patients with spinal cord lesions. Scandinavian J Urol and nephrology 2004;38(6):495-498.

Caremel R, Courtois F, Charvier K, Ruffion A, Journel N. Side effects of intradetrusor botulinum toxin injections on ejaculation and fertility in men with spinal cord injury: Preliminary findings. BJU international 2012;109(11):1698-1702.

Chang E, Ghosh N, Yanni D, Lee S, Alexandru D, Mozaffar T. A Review of Spasticity Treatments: Pharmacological and Interventional Approaches. Crit Rev Phys Rehabil Med. 2013;25(1-2):11-22.

Chen G, Liao L. Injections of botulinum toxin A into the detrusor to treat neurogenic detrusor overactivity secondary to spinal cord injury. Intern Urol Nephrol 2011;43(3):655-662.

Chen S, Kuo H. Therapeutic outcome and patient adherence to repeated onabotulinumtoxinA detrusor injections in chronic spinal cord-injured patients and neurogenic detrusor overactivity. Journal of the Formosan Medical Association 2013.

Cho YS, Kim KH. Botulinum toxin in spinal cord injury patients with neurogenic detrusor overactivity. J Exerc Rehabil. 2016 Dec 31;12(6):624-631.

CPS [Internet]. Ottawa (ON): Canadian Pharmacists Association; c2016 [cited 2017 Nov 2]. Available from: https://www.pharmacists.ca/products-services/ or http://www.myrxtx.ca. Also available in paper copy from the publisher.

Del Popolo G, Filocamo M, Li Marzi V, Macchiarella A, Cecconi F, Lombardi G, et al. Intermittent self-catheterization habits and opinion on aspetic VaPro catheter in French neurogenic bladder population. Spinal Cord 2012;50(11):853-858.

Dykstra DD, Sidi AA, Scott AB, Pagel JM, Goldish GD. Effects of botulinum A toxin on detrusor-sphincter dyssynergia in spinal cord injury patients. J Urol 1988;139(5):919-922.

Dykstra DD, Sidi AA. Treatment of detrusor-sphincter dyssynergia with botulinum A toxin: A double-blind study. Arch Phys Med Rehabil 1990;71(1):24-26.

Ehren I, Volz D, Farrelly E, Berglund L, Brundin L, Hultling C et al. Efficacy and impact of botulinum toxin A on quality of life in patients with neurogenic detrusor overactivity: A randomised, placebo-controlled, double-blind study. Scand J Urol Nephrol 2007;41(4):335-340.

Fried G & Fried K. Spinal cord injury and use of botulinum toxin in reducing spasticity. Phys Med Rehabil Clin N Am 2003;14:901-10.

Fried GW, Fried KM. Spinal cord injury and use of botulinum toxin in reducing spasticity. Phys Med Rehabil Clin N Am. 2003 Nov;14(4):901-10. Review.

Game X, Chartier-Kastler E, Ayoub N, Even-Schneider A, Richard F, Denys P. Outcome after treatment of detrusor-sphincter dyssynergia by temporary stent. Spinal Cord 2008; 46:74-77.

Grosse J, Kramer G, Jakse G. Comparing two types of botulinum-A toxin detrusor injections in patients with severe neurogenic detrusor overactivity: A case-control study. BJU International 2009; 104:651-656.

Haar GT, Dyson M, Oakley EM. The use of ultrasound by physiotherapists in Britain, 1985. Ultrasound in Med & Biol 1987. 13(10): 659-663.

Haferkamp A, Schurch B, Reitz A, Krengel U, Grosse J, Kramer G. Lack of ultrastructural detrusor changes following endoscopic injection of botulinum toxin type A in overactive neurogenic bladder. European urology 2004;46(6):784-791.

Hajebrahimi S, Altaweel W, Cadoret J, Cohen E, Corcos J. Efficacy of botulinum-A toxin in adults with neurogenic overactive bladder: Initial results. Canadian J Urol 2005;12:2543-2546.

Hikita K, Honda M, Kawamoto B, Panagiota T, Inoue S, Hinata N. Botulinum toxin type A injection for neurogenic detrusor overactivity: Clinical outcome in Japanese patients. International J Urol 2013;20(1):94-99.

Hori S, Patki P, Attar K, Ismail S, Vasconcelos J, Shah P. Patients’ perspective of botulinum toxin-A as a long-term treatment option for neurogenic detrusor overactivity secondary to spinal cord injury. BJU International 2009;104,:216-220.

Karsenty G, Chartier-Kastler E, Mozer P, Even-Schneider A, Denys P, Richard F. A novel technique to achieve cutaneous continent urinary diversion in spinal cord-injured patients unable to catheterize through native urethra. Spinal Cord 2008;46(4):305-310.

Karsenty G, Reitz A, Lindemann G, Boy S, Schurch B. Persistence of therapeutic effect after repeated injections of botulinum toxin type A to treat incontinence due to neurogenic detrusor overactivity. Urology 2006;68(6):1193-1197.

Kaviani A, Khavari R. Disease-Specific Outcomes of Botulinum Toxin Injections for Neurogenic Detrusor Overactivity. Urol Clin North Am. 2017 Aug;44(3):463-474.

Kuo H. Satisfaction with urethral injection of botulinum toxin A for detrusor sphincter dyssynergia in patients with spinal cord lesion. Neurourol Urodyn 2008;27:793-796.

Kuo H. Therapeutic outcome and quality of life between urethral and detrusor botulinum toxin treatment for patients with spinal cord lesions and detrusor sphincter dyssynergia. Inter J Clin Prac 2013;67(10):1044-1049.

Kuo HC, Liu SH. Effect of repeated detrusor onabotulinumtoxinA injections on bladder and renal function in patients with chronic spinal cord injuries. Neurourol Urodyn 2011;30:1541–1545.

Lui J, Sarai M, Mills PB. Chemodenervation for treatment of limb spasticity following spinal cord injury: a systematic review. Spinal Cord. 2015 Apr;53(4):252-64. doi: 10.1038/sc.2014.241. Epub 2015 Jan 13. Review.

Lui J, Sarai M, Mills PB. Chemodenervation for treatment of limb spasticity following spinal cord injury: a systematic review. Spinal Cord. 2015 Apr;53(4):252-64. doi: 10.1038/sc.2014.241. Epub 2015 Jan 13. Review.

Marciniak C, Rader L, Gagnon C. The use of botulinum toxin for spasticity after spinal cord injury. Am J Phys Med Rehabil. 2008 Apr;87(4):312-7; quiz 318-20, 329.

Mascarenhas F, Cocuzza M, Gomes C, Leão N. Trigonal injection of botulinum toxin‐A does not cause vesicoureteral reflux in neurogenic patients. Neurourol Urodyn 2008;27(4):311-314.

Ni J, Wang X, Cao N, Si J, Gu B. Is repeat Botulinum Toxin A injection valuable for neurogenic detrusor overactivity-A systematic review and meta-analysis. Neurourol Urodyn. 2017 Jul 26. doi: 10.1002/nau.23354. [Epub ahead of print]

Nigam PK, Nigam A. Botulinum toxin. Indian J Dermatol 2010; 55(1):8-14.

Petit H, Wiart L, Gaujard E, Le BF, Ferriere JM, Lagueny A et al. Botulinum A toxin treatment for detrusor-sphincter dyssynergia in spinal cord disease. Spinal Cord 1998;36(2):91-94.

Reitz A, Denys P, Fermanian C, Schurch B, Comperat E, Chartier-Kastler E. Do repeat intradetrusor botulinum toxin type a injections yield valuable results? Clinical and urodynamic results after five injections in patients with neurogenic detrusor overactivity. Euro Urol 2007;52(6):1729-1735.

Reitz A, Stohrer M, Kramer G, Del Popolo G, Chartier-Kastler E, Pannek J et al. European experience of 200 cases treated with Botulinum-A Toxin injections into the detrusor muscle for urinary incontinence due to neurogenic detrusor overactivity. European Urology 2004;45:510-515.

Richardson D, Edwards S, Sheean GL, Greenwood RJ, Thompson AJ. The effect of botulinum toxin on hand function after incomplete spinal cord injury at the level of C5/6: a case report. Clin Rehabil 1997; 11(4):288-292.

Schurch B, Stohrer M, Kramer G, Schmid DM, Gaul G, Hauri D. Botulinum-A toxin for treating detrusor hyperreflexia in spinal cord injured patients: A new alternative to anticholinergic drugs? Preliminary results. J Urol 2000;164(3 Pt 1):692-697.

Image credits

  1. Botulinum toxin 3BTA ©Clr324, CC0 1.0
  2. Injection ©priyanka, CC BY 3.0 US
  3. Synapse ©Clker-Free-Vector-Images, CC0 1.0
  4. Injection ©Vectors Point, CC BY 3.0 US
  5. Pregnancy botox risk ©waldryano, CC0 1.0
  6. Pain botox ©3dman_eu, CC0 1.0
  7. Modified from: Urinary Sphincter ©BruceBlaus, CC BY-SA 4.0

 

Disclaimer: This document does not provide medical advice. This information is provided for educational purposes only. Consult a qualified health professional for further information or specific medical advice. The SCIRE Project, its partners and collaborators disclaim any liability to any party for any loss or damage by errors or omissions in this publication.

Autonomic Dysreflexia

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Author: SCIRE Community Team | Reviewer: Andrei Krassioukov and Janice Eng | Published: 12 October 2017 | Updated: ~

Autonomic dysreflexia is a medical emergency that can happen after spinal cord injury (SCI). This page provides an overview of what autonomic dysreflexia is and how it is managed.

For information about emergency treatments, see How is autonomic dysreflexia treated?

Key Points

  • Autonomic dysreflexia is a potentially life-threatening medical emergency that can affect people with SCI at T6 and above.
  • Autonomic dysreflexia involves a sudden rise in blood pressure, which may be accompanied by heart rate changes, headaches, sweating, and other symptoms.
  • Autonomic dysreflexia can be triggered by any strong, irritating, or ‘painful’ stimulus below the level of the injury, such as bladder and bowel problems, tight clothing, or pressure ulcers.
  • Emergency treatment involves sitting upright, monitoring blood pressure, loosening tight clothing, and searching for and eliminating the cause of the episode (usually problems related to the bladder, bowel, and skin). If the episode does not resolve, emergency medical treatment involves the use of medications to rapidly lower blood pressure.
  • Prevention is an important part of managing autonomic dysreflexia. This typically involves maintaining good bladder, bowel, and skin care, and using medications during procedures that could trigger autonomic dysreflexia.

Autonomic dysreflexia (also called autonomic hyperreflexia) is a potentially life-threatening medical condition that can happen after spinal cord injury. Autonomic dysreflexia involves a sudden rise in blood pressure accompanied by changes in heart rate and other symptoms like headaches and sweating. The blood pressure responses in the body are poorly controlled because of the SCI and can become dangerously high.

Flowchart showing the pathophysiology of AD

Pathophysiology of autonomic dysreflexia.1


Autonomic dysreflexia typically affects people with SCI at T6 and above (although occasionally as low as T8). In general, people with higher level of injury and complete injuries are more likely to experience autonomic dysreflexia. Autonomic dysreflexia can occur at any time after the SCI.

Autonomic dysreflexia involves a sudden rise in blood pressure of 20 to 30 mmHg above your normal systolic blood pressure. Since the normal blood pressure of people with SCI is often 20 to 30 mmHg lower than in those without SCI, blood pressure can be in a range that is commonly  considered ‘normal’ or ‘slightly elevated’ and still be high for that person.

This rise in blood pressure is usually accompanied by symptoms. Symptoms will be different for everyone and can range from some mild discomfort to life threatening and severe.

Signs and symptoms of autonomic dysreflexia

  • A sudden rise in systolic blood pressure (20 to 30 mmHg above normal)
  • Changes in heart rate, usually a slow heart rate which sometimes becomes rapid
  • A pounding or throbbing headache
  • Sweating, flushing, or blotching of the skin above the SCI
  • Goosebumps or hair standing on end above the SCI
  • Dry and pale skin below the SCI
  • Worsening of muscle spasms
  • A metallic taste in the mouth
  • Feeling anxious or a feeling of ‘impending doom’
  • A stuffy or runny nose
  • Blurred vision or seeing spots
  • Nausea
  • Difficulty breathing

Cartoon female doctorAutonomic dysreflexia can be life threatening when severe. If left untreated, uncontrolled elevated blood pressure can lead to serious conditions like stroke, heart attack, detached retinas, seizures, and even death.

Although these complications are uncommon, it is important that autonomic dysreflexia is recognized and treated immediately. Talk to your health providers about setting up a plan for managing episodes of autonomic dysreflexia as soon as they happen.

high voltage sign with electric arrow bolt

Autonomic dysreflexia can be triggered by any strong stimulation below the SCI, including anything that could be considered uncomfortable, irritating, or painful if it could be felt. For example, a wound can trigger autonomic dysreflexia even if it the person does not feel it. Autonomic dysreflexia can also be caused by normal body processes that are strongly stimulating, such as a full bladder or sexual stimulation. The most common triggers are related to the bladder or bowel.

Common causes of autonomic dysreflexia

  • A bladder that is full – this may be caused by a blocked or kinked catheter, an overfilled collection bag, or incomplete emptying of urine
  • Other bladder causes such as urinary tract infections or bladder procedures (like when putting in a catheter)
  • A bowel that is full or impacted (contains a hard mass of stool that is stuck)
  • Other bowel causes such as constipation, infections, haemorrhoids, or bowel procedures (such as during digital rectal stimulation)
  • Pressure ulcers, wounds, or burns
  • Skin irritation from pressure, pinching, ingrown toenails, or tight clothing
  • Hot or cold temperatures
  • Strong sexual stimulation
  • Menstrual cramping
  • Labour and delivery
  • Broken bones and heterotopic ossification
  • Surgery and other medical procedures (including functional electrical stimulation)
  • Ulcers and other abdominal conditions

Autonomic dysreflexia is caused by dysfunction of the autonomic nervous system after SCI that leads to poorly controlled blood pressure responses.

The autonomic nervous system

The autonomic nervous system controls largely unconscious bodily processes such as blood pressure, heart rate, breathing rate, body temperature, digestion, bladder, bowel, and sexual function. It has two divisions:

The sympathetic nervous system prepares the body for stressful or emergency situations. It is often called the ‘fight or flight’ system, because it prepares the body for action. For example, it increases heart rate and constricts blood vessels.

The parasympathetic nervous system prepares the body for normal, non-emergency situations. It is often called the ‘rest and digest’ system, because it allows the body to restore itself. For example, it slows heart rate and relaxes blood vessels.

The sympathetic and parasympathetic systems have different (and often opposite) effects on the organs and work together to control bodily functions according to the situation.

 

Blood pressure cuff and pillbox

Blood pressure is carefully controlled by the autonomic nervous system to ensure that circulation works properly. The body monitors blood pressure and makes adjustments to maintain blood pressure within an optimal range. This is done in part by tightening (constricting) or relaxing (dilating) the blood vessels and changing heart rate.

What happens in autonomic dysreflexia

Transparent body showing circulatory systemWhen the body below the SCI detects strong stimulation, it activates the sympathetic nervous system, causing the constriction of blood vessels in the lower body. This causes blood pressure to rise.

Pressure sensors in the arteries then detect the elevated blood pressure and relay this message to the brain. Under normal circumstances, the brain sends signals through the spinal cord and cranial nerves to relax the blood vessels and slow heart rate. This restores blood pressure to normal.

However, when there is an SCI, the signal to relax the blood vessels is blocked from travelling to the lower body. Because of this, the blood vessels remain constricted and the body cannot restore blood pressure to normal. This causes the uncontrolled elevated blood pressure that happens during autonomic dysreflexia.

Why does autonomic dysreflexia happen at T6 and above?

The level of T6 is important because nerves from this part of the spinal cord constrict a large group of blood vessels in the abdomen called the splanchnic vascular bed. These blood vessels contain a large volume of blood, so when the blood vessels are constricted, it causes the blood pressure to rise significantly. Injuries below T6 do not usually cause enough of a change in blood pressure to cause autonomic dysreflexia.

Autonomic dysreflexia is a medical emergency and needs to be treated immediately. Emergency treatment involves a series of steps to lower blood pressure and remove the cause of the episode. If these steps are unsuccessful, emergency medical treatments are used to try to reduce blood pressure quickly.

Immediate treatment of autonomic dysreflexia

  • Get into an upright sitting position (or bring your head up) and if possible, lower your legs
  • If possible, check your blood pressure and re-check it every 5 minutes
  • Loosen tight clothing or devices (including tape, straps, and equipment)
  • Search for and remove the cause of the episode:
    • Check for bladder problems
      • If your catheter is kinked or blocked, reposition or flush the catheter
      • If your bladder or collection bag is full, drain
      • If your urine is cloudy or smells bad, it could be a bladder infection – contact a health provider
    • Check for bowel problems
      • If your bowel is full, use your bowel management routine to empty it (such as digital rectal stimulation)
      • Check for other problems like hemorrhoids
  • Check for skin problems and remove them if possible (such as ingrown toenails, skin irritation, pressure ulcers, infections, or wounds)
  • Check for other problems (such as broken bones)
  • Seek medical attention if blood pressure remains high (150 mmHg or above) after following these steps

If blood pressure returns to normal, continue to monitor your symptoms and blood pressure to make sure they do not return and report the incident to a health provider.

This approach is considered to be the most effective first treatment for autonomic dysreflexia. However, although this procedure is commonly used and recommended by health providers, it is supported primarily by expert opinion rather than evidence from research studies.

Emergency medical treatments

Cartoon teal ambulanceIf the steps above do not reduce blood pressure and it remains high (150 mmHg or above), seek emergency medical attention by calling an ambulance or visiting an emergency department. Emergency medical treatments involve the use of medications that rapidly lower blood pressure. The health providers may also run a series of tests to identify the cause of the episode if one has not been found.

The most commonly used drugs for autonomic dysreflexia are:

  • Captopril
  • Nifedipine (Adalat, Procardia)
  • Nitrates (Nitroglycerine, Depo-Nit, Nitrostat, Nitrol, Nitro-Bid)

However, there is little research evidence to suggest which medications work best for treating autonomic dysreflexia. Speak to your health providers for more information about medications used in autonomic dysreflexia emergencies.

The most effective way of managing autonomic dysreflexia is to prevent triggering it in the first place. People who get autonomic dysreflexia may be able to take steps to avoid triggering episodes, especially during procedures that are known to cause autonomic dysreflexia.

Learn to recognize autonomic dysreflexia and your triggers

In order to be able to manage episodes of autonomic dysreflexia, it is important to be able to recognize an episode and know what to do when it happens.

  • Learn about and educate family members and friends about what autonomic dysreflexia is, how to recognize it, and what to do if it happens.
  • Work with your health providers to identify your risk for autonomic dysreflexia, how to prevent it, and what to do if it happens.
  • Carry an autonomic dysreflexia medical emergency card. These wallet-sized cards describes autonomic dysreflexia and its symptoms and treatments for use in an emergency – it can be used to quickly describe the condition and its treatment to your health providers.

 

Preventing autonomic dysreflexia from bladder problems

Cartoon of the kidneys and bladderBladder problems are the most common triggers of autonomic dysreflexia. Methods that may be used to prevent bladder problems from triggering autonomic dysreflexia include:

  • Maintaining a bladder routine is the most important way to prevent problems like bladder distension and urinary tract infections.
  • Preventing irritation during bladder procedures (such as catheterization) using anaesthetic medications (such as capsaicin or lidocaine).
  • Managing reflex spasms of the bladder muscles (detrusor hyperreflexia) through methods including botulinum toxin (Botox) injections or sacral denervation (deafferentation) surgery.
  • Bladder surgeries, such as bladder augmentation, may be used for some individuals with bladder dysfunction after an SCI and have been shown to help reduce episodes of autonomic dysreflexia.

See our article on Urinary Tract Infections to learn more!

Preventing autonomic dysreflexia from bowel problems

Cartoon of the stomach and intestinesBowel problems are another common trigger of autonomic dysreflexia. Methods that may be used to prevent bowel problems from triggering autonomic dysreflexia include:

  • Maintaining a bowel routine and management (including fibre and fluid intake) to prevent problems like bowel distension, faecal impaction, and constipation.
  • Preventing irritation during invasive bowel procedures or medical procedures (such as digital rectal stimulation) using anesthetics (such as lidocaine gel or lidocaine anal blocks).
  • Bowel surgeries, such as colostomy or ileostomy, may be considered for people with chronic bowel problems that cause autonomic dysreflexia and other problems.

See our article on Bowel Changes after Spinal Cord Injury for more information!

Preventing autonomic dysreflexia from skin problems

A silhouette of a person lying on a recliner chair with red circles highlighting common areas where pressure ulcers developPressure ulcers, ingrown toenails, and burns can all be additional causes of autonomic dysreflexia. Methods that may be used to prevent skin problems from triggering autonomic dysreflexia include:

  • Maintain an effective skin care routine, which involves regular pressure relief, inspection of skin, and proper cleaning.
  • Avoid wearing tight clothing and keep clothing and sheets smooth.
  • Maintain regular foot care.
  • Treat skin injuries and infections early.

Preventing autonomic dysreflexia from other causesCartoon graphic of task list

  • Although individuals with SCI do not have sensation in areas where surgeries may occur, anesthesia should be used to avoid triggering autonomic dysreflexia during surgery.
  • Anesthesia (spinal or epidural if possible) is needed with vaginal, Caesarean, or instrumental delivery to prevent autonomic dysreflexia during labour.
  • Be aware that strong sexual stimulation can cause autonomic dysreflexia. Take precautions and be aware of your responses to stimulation.

See our article on Pressure Injuries for more information! 

The bottom line

Autonomic dysreflexia is a serious medical condition that requires immediate recognition and treatment. First line treatment involves sitting up, removing tight clothing, and removing the cause of episode. This is supported by expert opinion. Emergency medical treatments for episodes of autonomic dysreflexia involve fast acting anti-hypertensive agents such as nifedipine, nitrates, and captopril, although the best treatment to use has not been determined.

It is best to discuss treatment options with your health providers to find out which treatments are suitable for you. For a review of how we assess evidence at SCIRE Community and advice on making decisions, please see SCIRE Community Evidence.

Parts of this page have been adapted from the SCIRE Project (Professional) “Autonomic Dysreflexia” Chapter:

Krassioukov A, Blackmer J, Teasell RW, Eng JJ (2014). Autonomic Dysreflexia Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors.

Spinal Cord Injury Rehabilitation Evidence. Version 5.0. Vancouver: p 1- 35. Available from: http://scireproject.com/evidence/rehabilitation-evidence/autonomic-dysreflexia.

 

Barton CH, Khonsari F, Vaziri ND, Byrne C, Gordon S, Friis R. T http://scireproject.com/evidence/rehabilitation-evidence/autonomic-dysreflexia The effect of modified transurethral sphincterotomy on autonomic dysreflexia. J Urol 1986;135:83-85.http://scireproject.com/evidence/rehabilitation-evidence/autonomic-dysreflexia-re/

Sidi AA, Becher EF, Reddy PK, Dykstra DD. Augmentation enterocystoplasty for the management of voiding dysfunction in spinal cord injury patients. J Urol 1990;143:83-85.

Perkash I. Transurethral sphincterotomy provides significant relief in autonomic dysreflexia in spinal cord injured male patients: Long-term followup results. J Urol 2007;177:1026-1029.

Ke QS, Kuo HC. Transurethral incision of the bladder neck to treat bladder neck dysfunction and voiding dysfunction in patients with high-level spinal cord injuries. Neuro Uro 2010;29:748-752.

Hohenfellner M, Pannek J, Botel U, Bahms S, Pfitzenmaier J, Fichtner J, et al. Sacral bladder denervation for treatment of detrusor hyperreflexia and autonomic dysreflexia. Urol 2001;58:28-32.

Kutzenberger J. Surgical therapy of neurogenic detrusor overactivity (hyperreflexia) in paraplegic patients by sacral deafferentation and implant driven micturition by sacral anterior root stimulation: methods, indications, results, complications, and future prospects. Acta Neurochir Suppl 2007;97:333-339.

Coggrave MJ, Ingram RM, Gardner BP, Norton CS. The impact of stoma for bowel management after spinal cord injury. Spinal Cord 2012;50:848-852.

Cosman BC, Vu TT. Lidocaine anal block limits autonomic dysreflexia during anorectal procedures in spinal cord injury: a randomized, double-blind, placebo-controlled trial. Dis Colon Rectum 2005;48:1556-1561.

Cosman BC, Vu TT, Plowman BK. Topical lidocaine does not limit autonomic dysreflexia during anorectal procedures in spinal cord injury: a prospective, double-blind study. Int J Colorectal Dis 2002;17:104-108.

Furusawa K, Sugiyama H, Tokuhiro A, Takahashi M, Nakamura T, Tajima F. Topical anesthesia blunts the pressor response induced by bowel manipulation in subjects with cervical spinal cord injury. Spinal Cord 2009;47:144-148.

Cross LL, Meythaler JM, Tuel SM, Cross LA. Pregnancy, labor and delivery post spinal cord injury. Paraplegia 1992;30:890-902.

Hughes SJ, Short DJ, Usherwood MM, Tebbutt H. Management of the pregnant woman with spinal cord injuries. Br J Obstet Gynaecol 1991;98:513-518.

Cross LL, Meythaler JM, Tuel SM, Cross AL. Pregnancy following spinal cord injury. West J Med 1991;154:607-611.

Skowronski E, Hartman K. Obstetric management following traumatic tetraplegia: case series and literature review. Aust N Z J Obstet Gynaecol 2008;48:485-491.

Lambert DH, Deane RS, Mazuzan JE. Anesthesia and the control of blood pressure in patients with spinal cord injury. Anesth Analg 1982;61:344-348.

Eltorai IM, Wong DH, Lacerna M, Comarr, AE, Montroy R. Surgical aspects of autonomic dysreflexia. J Spinal Cord Med 1997;20:361-364.

Matthews JM, Wheeler GD, Burnham RS, Malone LA, Steadward RD. The effects of surface anaesthesia on the autonomic dysreflexia response during functional electrical stimulation. Spinal Cord 1997;35:647-651.

Kim JH, Rivas DA, Shenot PJ, Green B, Kennelly M, Erickson, JR, O’Leary M, Yoshimura N, Chancellor MB. Intravesical resiniferatoxin for refractory detrusor hyperreflexia: a multicenter, blinded, randomized, placebo-controlled trial. J Spinal Cord Med 2003;26:358-363.

Giannantoni A, Di Stasi SM, Stephen RL, Navarra P, Scivoletto G, Mearini E, Porena M. Intravesical capsaicin versus resiniferatoxin in patients with detrusor hyperreflexia: a prospective randomized study. J Urol 2002;167:1710-1714.

Igawa Y, Satoh T, Mizusawa H, Seki S, Kato H, Ishizuka O, Nishizawa O. The role of capsaicin-sensitive afferents in autonomic dysreflexia in patients with spinal cord injury. BJU Int 2003;91:637-641.

Dykstra DD, Sidi AA, Scott AB, Pagel JM, Goldish GD. Effects of botulinum A toxin on detrusor-sphincter dyssynergia in spinal cord injury patients. J Urol 1988;139:919-922.

Schurch B, Stohrer M, Kramer G, Schmid DM, Gaul G, Hauri D. Botulinum-A toxin for treating detrusor hyperreflexia in spinal cord injured patients: a new alternative to anticholinergic drugs? Preliminary results. J Urol 2000;164:692-697.

Chen SL, Bih LI, Huang YH, Tsai SJ, Lin TB, Kao YL. Effect of single botulinum toxin A injection to the external urethral sphincter for treating detrusor external sphincter dyssynergia in spinal cord injury. J Rehabil Med 2008;40:744-748.

Kuo HC. Satisfaction with urethral injection of botulinum toxin A for detrusor sphincter dyssynergia in patients with spinal cord lesion. Neurourol Urodyn 2008; 27: 793-796.

Chen SF, Kuo HC. Improvement in autonomic dysreflexia after detrusor onabotulinumtoxinA injections in patients with chronic spinal cord injuries. Tzu Chi Medical Journal 2012;24:201-204.

Giannantoni A, Di Stasi SM, Scivoletto G, Mollo A, Silecchia A, Fuoco U, Vespasiani G. Autonomic dysreflexia during urodynamics. Spinal Cord 1998;36:756-860.

Bycroft J, Shergill I, Choong E, Arya N, Shah P. Autonomic dysreflexia: a medical emergency. Postgraduate Medical Journal. 2005;81(954):232-235.

 

Image Credits

  1. Image by SCIRE Professional Team
  2. Headache ©8thBox, CC0 1.0
  3. Doctor1 ©Clker-Free-Vector-Images, CC0 1.0
  4. Voltage ©Clker-Free-Vector-Images, CC0 1.0
  5. Highbp ©stevepb, CC0 1.0
  6. Headshock ©Geralt, CC0 1.0
  7. Body vessels © Clker-Free-Vector-Images, CC0 1.0
  8. Stetho ©Clker-Free-Vector-Images, CC0 1.0
  9. Ambulance ©Pettycon, CC0 1.0
  10. Excretory system ©Olena Panasovska, CC BY 3.0 US
  11. Digestive System ©Design Science, CC0 1.0
  12. Modified from: Man Resting on Long Chair ©Gan Khoon Lay, CC BY 3.0
  13. Tasklist ©Pettycon, CC0 1.0

 

 

Disclaimer: This document does not provide medical advice. This information is provided for educational purposes only. Consult a qualified health professional for further information or specific medical advice. The SCIRE Project, its partners and collaborators disclaim any liability to any party for any loss or damage by errors or omissions in this publication.

Functional Electrical Stimulation (FES)

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Author: SCIRE Community Team | Reviewer: Shannon Sproule | Published: 10 October 2017 | Updated: ~

Functional electrical stimulation is a treatment that activates muscles below the spinal cord injury (SCI) during exercise and activity. This page outlines basic information about functional electrical stimulation and its use for movement and strength after SCI.

Key Points

  • Electrical stimulation can be used to activate muscles that are weak or paralyzed after an SCI.
  • Functional electrical stimulation (FES) involves stimulating the muscles during an activity like exercise or movement.
  • FES is relatively safe and widely available treatment option for improving muscle strength and fitness after SCI.
  • Overall, the research evidence suggests that FES is most likely effective for improving muscle strength after SCI. It may also improve fitness, walking skills, bone density and other symptoms, although more high quality research is needed to confirm.

Functional electrical stimulation (FES) is a type of neuromodulation where electrical stimulation is applied to the nerves located outside the spinal cord and brain. This stimulation causes the muscles to contract and can assist with purposeful or functional movement in weak or paralyzed muscles.

FES is delivered using a variety of handheld or specialized commercial electrical therapy machines connected to electrodes that are placed on the skin’s surface. Systems are also available with implanted electrodes in the muscles, although this is very specialized and not widely available.

FES electrodes are placed on the leg muscles to be used during stationary cycling.1

Muscle stimulation is used for several reasons after SCI:

To promote movement and strength in weak or paralyzed muscles: Muscle stimulation is used early in rehabilitation to promote movement in muscles that are not moving or only producing a flicker of movement. It may promote recovery of movement function by assisting with normal movements and with repetition of movements.

To improve fitness and health: When FES is used as part of a rhythmic exercise like cycling, walking, or rowing, it can help to maintain health of the heart, lungs, and circulation. It may also help to maintain healthy bones.

To assist with functional movement activities like stepping, getting up to standing, and grasping: FES can be used to assist with purposeful movements by improving muscle contractions (for weakened muscles), mobility or range of movement as well as possibly decreasing spasticity.

To maintain muscle mass below the SCI: Regular use of FES may help to prevent muscle loss that happens when the muscles that are paralyzed are not used. Unless neurological return occurs this improvement will stop if the FES is discontinued.

To control the muscles of breathing and bladder function: This includes the use of surgically implanted diaphragmatic pacers (FES systems that create muscle contractions in the diaphragm to stimulate regular breaths) and bladder control systems (FES systems that stimulate the muscles of urination). However, this page will focus on FES used for movement and strength after SCI.

Watch our YouTube video about FES!

Other names for FES of muscles

You may hear other names for FES such as “neuromuscular electrical stimulation” (NMES) or simply “electrical stimulation” (ES). These terms are often used to refer to electrical stimulation of the muscles during more passive activities (like lying down or sitting), while ”FES” usually describes stimulation during purposeful activities like cycling or walking. However, in practice these terms are often used interchangeably to describe similar or related treatments and the goals of all are to promote strength, movement and function and decrease pain and spasticity.

There are a number of other neuromodulation techniques that are used for various purposes in SCI, including transcutaneous electrical nerve stimulation, sacral nerve stimulation, and intrathecal Baclofen, described in other SCIRE Community articles.

It is important to speak with a health provider about using FES to make sure it is safe and suitable for you and to learn how to use the equipment correctly.

FES is usually applied through electrodes that are placed on the surface of the skin, although electrodes can also be implanted into the muscles. Electrodes are placed over nerves or part of the muscles below the SCI that respond well to electrical stimulation. The electrodes are then attached to an adjustable machine that generates the stimulation. Your health provider will determine the settings that are used for the treatment and how long it will last.

The electrical stimulation is then gradually turned up until the muscles begin to tense or contract. Depending on your sensation, as the machine is turned up, you may feel pins and needles or other unusual sensations, which may take some time to get used to. The aim is to create a forceful but tolerable muscle contraction.

FES is applied through electrodes on the leg muscles during assisted walking.2

If the electrical stimulation goes well, it is then combined with a movement task. This may be as simple as lifting a wrist or ankle or more complex such as cycling on a stationary bike, rowing on a rowing machine, grasping, or stepping in parallel bars or a body weight support treadmill system.

The length of each session will vary depending on the goals of the treatment. Time may be required to enable your muscles to tolerate longer sessions as the muscles may fatigue quickly. Sessions are usually done several times per week for several weeks to gain training benefits.

Your health provider will monitor your response to the treatment and inspect the skin for any redness or irritation after the treatment has ended. Once you have learned to use FES safely, you may be able to use it on your own.

Our bodies naturally use electrical signals as part of the nervous system. When we move, the brain generates and sends electrical impulses along the spinal cord and nerves to tell the muscles to move.

Spinal cord injury can interrupt this pathway, preventing electrical impulses from passing through the spinal cord to reach the muscles. However, if the nerves and muscles below the injury are not damaged, they can still respond to electrical signals.

A leg with two electrodes on the thigh for functional electrical stimulation execise therapy

FES electrodes are placed over nerves or over electrically-sensitive parts of the muscles below the SCI. The specific type of electrical stimulation used with FES can trigger the nerve cells of movement (motor neurons) to send signals that cause muscle movement. An intact peripheral nerve and healthy muscle tissue are required to enable the external source of electricity to facilitate muscle contraction.

FES does not work for nerve injuries outside the spinal cord

FES can only be used for muscle weakness or paralysis caused by injuries to the spinal cord, but not injuries to the conus medullaris, cauda equina, or the nerves outside of the spinal cord. The nerve cells in these structures (called lower motor neurons) must to be intact for FES to work.

Like exercise, regular treatment with FES is usually needed to maintain the effects of the treatment. For people with complete injuries, when FES treatments are stopped, the treatment effects will usually go away over time. For people with incomplete injuries, the goal is for some carryover of strength and movement be retained after the treatment is stopped.

A cartoon pen and clipboard with check marks and x marksThere are some situations in which FES may be unsafe to use. This not a complete list, speak to a health provider about your health history and whether FES is safe for you.

FES should not be used in the following situations:

  • Near implanted medical devices like heart pacemakers
  • On areas of active cancer, or by people with bleeding disorders or other major medical conditions
  • On areas with blood clots, bleeding, damaged skin, infection, or poor circulation
  • By pregnant women
  • Electrodes should not be placed over the eyes, through the head, through the chest or abdomen, or on the front of the neck or genitals
  • By people with recent broken bones
  • By people with damage to the nerves or muscles near the area where FES is used

FES should be used with caution in the following situations:

FES is often used with the following conditions after SCI but should be monitored closely. Speak to your health provider for more information.

FES is generally well tolerated by people who can use it safely (see above for when FES may be unsafe). Serious medical complications from FES are rare. However, there are risks and side effects that should be discussed with a health provider before using FES.

More common risks and side effects of FES include:

Other less common risks and side effects of FES include:

  • Mild electrical burns near the electrodes
  • Skin breakdown near the electrodes
  • Fainting
  • Worsening of muscle spasms (spasticity)
  • Muscle and joint injuries, such as joint swelling or muscle strains
  • Broken bones
  • Mild electrical shocks (from improper use or faulty equipment)

In some cases, risks and side effects may be caused by improper use of the equipment. It is essential to learn to use the equipment from a health provider and to only use FES according to their direction and with the settings that they recommend.

For some people, side effects of FES may be stronger at first, but as their body gets used to FES with repeated treatments, their physical reactions may reduce over time.

Several studies have shown that FES helps to improve strength and fitness after SCI.

Strength

Cartoon of a flexed armStudies have shown that both FES arm exercise and FES cycling helps to maintain or improve strength after SCI. However, FES cycling may be more effective for maintaining strength after injury than improving strength that has already been lost. This is supported by moderate evidence from five studies.

Cardiovascular fitness

Heart with a barbellFifteen studies have looked at FES for improving many different aspects of fitness after SCI. Taken altogether, these studies provide weak evidence that FES training done at least 3 days per week for 2 months helps to improve many aspects of cardiovascular fitness after SCI.

Walking

A person walking between parallel bars with his wheelchair behind him. A heathcare provider on the side watches him.Studies show that FES improves walking speed and distance in people with both incomplete and complete SCI. Some of these studies also showed that regular use of FES carried over to improve walking even without FES. This is supported by weak evidence from eight studies.

The effects of FES treatment may also help to prevent complications of SCI like pressure sores, bone loss, spasticity, and orthostatic hypotension. These benefits may accompany gains in strength or fitness related to FES treatment.

Pressure sores

A woman lifting up her buttocks off her wheelchair by straightening her armsAlthough it is commonly thought that increased muscle bulk from FES will reduce the risk of pressure sores, there are not very many studies which have looked at whether this actually happens. One study provides weak evidence that FES cycling for 2 years reduced the number of pressure ulcers that occurred after SCI. Another study showed that regular FES cycling showed a trend toward reducing seat pressures.

Bone health

Silhouette of a fractured boneResearch studies show that FES cycling does not prevent bone loss after SCI (moderate evidence from two studies). However, it may help to increase bone density that has already been lost, although the evidence for this is conflicting (based on six studies). It is not clear whether any gains in bone density last long-term or if continued FES treatment is needed for them to be maintained.

For more information on bone density, read our article about Osteoporosis.

Spasticity

It is not clear what effects FES has on spasticity after SCI. There is conflicting evidence from three studies about whether FES cycling can help to reduce spasticity after SCI.

Click here for our article on Spasticity.

Orthostatic hypotension

Three studies provide moderate evidence that FES of the legs during a single change in position reduced orthostatic hypotension. However, this only shows that FES prevents orthostatic hypotension while it is applied, and further research is needed to look at what benefits this could have to people living with SCI.

Click here for our article on Orthostatic Hypotension.

Overall, the research evidence suggests that FES is most likely effective for improving muscle strength after SCI. It may also have effects on fitness, walking skills, bone density, skin health, spasticity, and orthostatic hypotension, although more high quality research is needed to confirm. FES appears to be safe when used appropriately and is widely available in most rehabilitation settings. Discuss this treatment with your health providers to find out if it is a suitable treatment option for you.

For a review of how we assess evidence at SCIRE Community and advice on making decisions, please see SCIRE Community Evidence.

Parts of this page have been adapted from the SCIRE Professional “Lower Limb”, “Upper Limb”, “Bone Health”, “Cardiovascular Health and Exercise”, “Orthostatic Hypotension”, “Pressure Ulcers”, and “Spasticity” chapters:

Lam T, Wolfe DL, Domingo A, Eng JJ, Sproule S (2014). Lower Limb Rehabilitation Following Spinal Cord Injury. In: Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors. Spinal Cord Injury Rehabilitation Evidence. Version 5.0. Vancouver: p 1-74.
Available from: http://scireproject.com/evidence/lower-limb/

Connolly SJ, McIntyre A, Mehta, S, Foulon BL, Teasell RW. (2014). Upper Limb Rehabilitation Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors. Spinal Cord Injury Rehabilitation Evidence. Version 5.0: p 1-77.
Available from: http://scireproject.com/evidence/upper-limb/

Craven C, Lynch CL, Eng JJ (2014). Bone Health Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors. Spinal Cord Injury Rehabilitation Evidence. Version 5.0. Vancouver: p 1- 37.
Available from: https://scireproject.com/evidence/bone-health/

Warburton DER, Krassioukov A, Sproule S, Eng JJ (2014). Cardiovascular Health and Exercise Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors. Spinal Cord Injury Rehabilitation Evidence. Version 5.0. Vancouver: p. 1-48.
Available from: https://scireproject.com/evidence/cardiovascular-health-and-exercise/

Krassioukov A, Wecht JM, Teasell RW, Eng JJ (2014). Orthostatic Hypotension Following Spinal Cord Injury. In: Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors. Spinal Cord Injury Rehabilitation Evidence. Version 5.0. Vancouver: p. 1-26.
Available from: https://scireproject.com/evidence/orthostatic-hypotension/

Hsieh J, McIntyre A, Wolfe D, Lala D, Titus L, Campbell K, Teasell R. (2014). Pressure Ulcers Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors. Spinal Cord Injury Rehabilitation Evidence. Version 5.0. 1-90.
Available from: https://scireproject.com/evidence/skin-integrity-and-pressure-injuries/

Hsieh JTC, Connolly SJ, McIntyre A, Townson AF, Short C, Mills P, Vu V, Benton B, Wolfe DL (2016). Spasticity Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Curt A, Mehta S, Sakakibara BM, editors. Spinal Cord Injury Rehabilitation Evidence. Version 6.0.
Available from: https://scireproject.com/evidence/spasticity/

 

Evidence for “Strength” is based on the following studies:

[1] Baldi JC, Jackson RD, Moraille R, and Mysiw WJ. Muscle atrophy is prevented in patients with acute spinal cord injury using functional electrical stimulation. Spinal Cord 1998;36:463-469.

[2] Scremin AM, Kurta L, Gentili A, Wiseman B, Perell K, Kunkel C, and Scremin OU. Increasing muscle mass in spinal cord injured persons with a functional electrical stimulation exercise program. Arch Phys Med Rehabil 1999;80:1531-1536.

[3] Crameri RM, Weston A, Climstein M, Davis GM, and Sutton JR. Effects of electrical stimulation-induced leg training on skeletal muscle adaptability in spinal cord injury. Scand J Med Sci Sports 2002;12:316-322.

[4] Gerrits HL, de Haan A, Sargeant AJ, Dallmeijer A, and Hopman MT. Altered contractile properties of the quadriceps muscle in people with spinal cord injury following functional electrical stimulated cycle training. Spinal Cord 2000;38:214-223.

[5] Needham-Shropshire BM, Broton JG, Cameron TL, Klose J. Improved motor function in tetraplegics following neuromuscular stimulation-assisted arm ergometry. J Spinal Cord Med 1997;20:49-55.

[6] Cameron T, Broton JG, Needham-Shropshire B, Klose KJ. An upper body exercise system incorporating resistive exercise and neuromuscular electrical stimulation (nms). J Spinal Cord Med 1998;21:1-6.

Evidence for “Cardiovascular Fitness” based on:

[1] Berry HR, Kakebeeke TH, Donaldson N, Perret C, Hunt KJ. Energetics of paraplegic cycling: adaptation to 12 months of high volume training. Technology and Health Care 2012; 20: 73-84.

[2] Griffin L, Decker MJ, Hwang JY, Wang B, Kitchen K, Ding Z, et al. Functional electrical stimulation cycling improves body composition, metabolic and neural factors in persons with spinal cord injury. J Electromyogr Kinesiol 2009;19(4):614-22.

[3] Zbogar D, Eng JJ, Krassioukov AV, Scott JM, Esch BT, Warburton DE. The effects of functional electrical stimulation leg cycle ergometry training on arterial compliance in individuals with spinal cord injury. Spinal Cord 2008;46(11):722-6.

[4] Crameri RM, Cooper P, Sinclair PJ, Bryant G, Weston A. Effect of load during electrical stimulation training in spinal cord injury. Muscle Nerve 2004;29(1):104-11.

[5] Hjeltnes N, Aksnes AK, Birkeland KI, Johansen J, Lannem A, Wallberg-Henriksson H. Improved body composition after 8 wk of electrically stimulated leg cycling in tetraplegic patients. Am J Physiol 1997;273(3 Pt 2):R1072-9.

[6] Mohr T, Andersen JL, Biering-Sorensen F, Galbo H, Bangsbo J, Wagner A, et al. Long-term adaptation to electrically induced cycle training in severe spinal cord injured individuals. Spinal Cord 1997;35(1):1-16.

[7] Barstow TJ, Scremin AM, Mutton DL, Kunkel CF, Cagle TG, Whipp BJ. Changes in gas exchange kinetics with training in patients with spinal cord injury. Med Sci Sports Exerc 1996;28(10):1221-8.

[8] Faghri PD, Glaser RM, Figoni SF. Functional electrical stimulation leg cycle ergometer exercise: training effects on cardiorespiratory responses of spinal cord injured subjects at rest and during submaximal exercise. Arch Phys Med Rehabil 1992;73(11):1085-93.

[9] Hooker SP, Figoni SF, Rodgers MM, Glaser RM, Mathews T, Suryaprasad AG, et al. Physiologic effects of electrical stimulation leg cycle exercise training in spinal cord injured persons. Arch Phys Med Rehabil 1992;73(5):470-6.

[10] Gerrits HL, de Haan A, Sargeant AJ, van Langen H, Hopman MT. Peripheral vascular changes after electrically stimulated cycle training in people with spinal cord injury. Arch Phys Med Rehabil 2001;82(6):832-9.

[11] Ragnarsson KT, Pollack S, O’Daniel W, Jr., Edgar R, Petrofsky J, Nash MS. Clinical evaluation of computerized functional electrical stimulation after spinal cord injury: a multicenter pilot study. Arch Phys Med Rehabil 1988;69(9):672-7.

[12] Taylor JA, Picard G, Widrick JJ. Aerobic capacity with hybrid FES rowing in spinal cord injury: comparison with arms-only exercise and preliminary findings with regular training. PM R 2011;3(9):817-24.

[13] Kahn NN, Feldman SP, Bauman WA. Lower-extremity functional electrical stimulation decreases platelet aggregation and blood coagulation in persons with chronic spinal cord injury: a pilot study. J Spinal Cord Med 2010;33(2): 150-8.

[14] Hakansson NA, Hull ML. Can the efficacy of electrically stimulating pedaling using a commercially available ergometer be improved by minimizing the muscle stress-time integral? Muscle Nerve 2012; 45:393-402.

Evidence for “Walking” is based on the following studies:

[1] Thrasher TA, Flett HM, and Popovic MR. Gait training regimen for incomplete spinal cord injury using functional electrical stimulation. Spinal Cord 2006;44:357-361.

[2] Ladouceur M, and Barbeau H. Functional electrical stimulation-assisted walking for persons with incomplete spinal injuries: changes in the kinematics and physiological cost of overground walking. Scand J Rehabil Med 2000a;32:72-79.

[3] Ladouceur M, and Barbeau H. Functional electrical stimulation-assisted walking for persons with incomplete spinal injuries: longitudinal changes in maximal overground walking speed. Scand J Rehabil Med 2000b;32:28-36.

[4] Wieler M, Stein RB, Ladouceur M, Whittaker M, Smith AW, Naaman S, Barbeau H, Bugaresti J, and Aimone E. Multicenter evaluation of electrical stimulation systems for walking. Arch Phys Med Rehabil 1999;80:495-500.

[5] Klose KJ, Jacobs PL, Broton JG, Guest RS, Needham-Shropshire BM, Lebwohl N, Nash MS, and Green BA. Evaluation of a training program for persons with SCI paraplegia using the Parastep 1 ambulation system: part 1. Ambulation performance and anthropometric measures. Arch Phys Med Rehabil 1997;78:789-793.

[6] Granat MH, Ferguson AC, Andrews BJ, and Delargy M. The role of functional electrical stimulation in the rehabilitation of patients with incomplete spinal cord injury–observed benefits during gait studies. Paraplegia 1993;31:207-215.

[7] Stein RB, Belanger M, Wheeler G, Wieler M, Popovic DB, Prochazka A, and Davis LA. Electrical systems for improving locomotion after incomplete spinal cord injury: an assessment. Arch Phys Med Rehabil 1993;74:954-959.

[8] Granat M, Keating JF, Smith AC, Delargy M, and Andrews BJ. The use of functional electrical stimulation to assist gait in patients with incomplete spinal cord injury. Disabil Rehabil 1992;14:93-97.

Evidence for “Bone health” is based on the following studies:

[1] Eser P, de Bruin ED, Telley I, Lechner HE, Knecht H, Stussi E. Effect of electrical stimulation-induced cycling on bone mineral density in spinal cord-injured patients. Eur J Clin Invest 2003;33:412-419.

[2] Lai CH, Chang WHS, Chan WP, Peng CW, Shen LK, Chen JJJ, Chen SC. Effects of Functional Electrical Stimulation Cycling Exercise on Bone Mineral Density Loss in the Early Stages of Spinal Cord Injury. J Rehabil Med 2010; 42:150-154.

[3] Mohr T, Podenphant J, Biering-Sorensen F, Galbo H, Thamsborg G, Kjaer M. Increased bone mineral density after prolonged electrically induced cycle training of paralyzed limbs in spinal cord injured man. Calcif Tissue Int 1997;61:22-25.

[4] Chen SC, Lai CH, Chan WP, Huang MH, Tsai HW, Chen JJ. Increases in bone mineral density after functional electrical stimulation cycling exercises in spinal cord injured patients. Disabil Rehabil 2005;27:1337-1341.

[5] Frotzler A, Coupaud S, Perret C, Kakebeeke TH, Hunt KJ, Donaldson Nde N, Eser P. High-volume FES-cycling partially reverses bone loss in people with chronic spinal cord injury. Bone. 2008 Jul;43(1):169-76. Epub 2008 Mar 20.

[6] Pacy PJ, Hesp R, Halliday DA, Katz D, Cameron G, Reeve J. Muscle and bone in paraplegic patients, and the effect of functional electrical stimulation. Clin Sci (Lond) 1988;75:481-487.

[7]  Leeds EM, Klose J, Ganz W, Serafini A, Green BA. Bone mineral density after bicycle ergometry training. Archives of Physical Medicine and Rehabilitation 1990;71:207-9.

[8] BeDell KK, Scremin AM, Perell KL, Kunkel CF. Effects of functional electrical stimulation-induced lower extremity cycling on bone density of spinal cord-injured patients. Am J Phys Med Rehabil 1996;75:29-34.

Evidence for “Pressure Ulcers” is based on the following studies:

[1] Dolbow DR, Gorgey AS, Dolbow JD, Gater DR. Seat pressure changes after eight weeks of functional electrical stimulation cycling: a pilot study. Top Spinal Cord Inj Rehabil. 2013 Summer;19(3):222-8.

[2] Petrofsky JS. Functional electrical stimulation, a two year study. J Rehabil. 1992;58(3):29–34

Evidence for “Spasticity” is based on the following studies:

[1] Kapadia N, Masani K, Craven B, et al. A randomized trial of functional electrical stimulation for walking in incomplete spinal cord injury: Effects on walking competency. J Spinal Cord Med 2014;37:511-24.

[2] Manella K & Field-Fote E. Modulatory effects of locomotor training on extensor spasticity in individuals with motor-incomplete spinal cord injury. Restor Neurol Neurosci 2013;31:633-46.

[3] Ralston K, Harvey L, Batty J, et al. Functional electrical stimulation cycling has no clear effect on urine output, lower limb swelling, and spasticity in people with spinal cord injury: A randomised cross-over trial. J Physiother 2013;59:237-43.

[4] Kuhn D, Leichtfried V, Schobersberger W. Four weeks of functional electrical stimulated cycling after spinal cord injury: a clinical cohort study. Inter J Rehabil Res 2014;37:243-50.

[5] Mazzoleni S, Stampacchia G, Gerini A, Tombini T, Carrozza M. FES-cycling training in spinal cord injured patients. Eng Med Biol Soc 2013:5339-41.

[6] Sadowsky C, Hammond E, Strohl A, et al. Lower extremity functional electrical stimulation cycling promotes physical and functional recovery in chronic spinal cord injury. J Spinal Cord Med 2013;36:623-31.

[7] Reichenfelser W, Hackl H, Hufgard J, Kastner J, Gstaltner K, Gföhler M. Monitoring of spasticity and functional ability in individuals with incomplete spinal cord injury with a functional electrical stimulation cycling system. J Rehabil Med 2012;44:444-9.

[8] Krause P, Szecsi J, Straube A. Changes in spastic muscle tone increase in patients with spinal cord injury using functional electrical stimulation and passive leg movements. Clin Rehabil 2008;22:627-34.

[9] Mirbagheri M, Ladouceur M, Barbeau H, Kearney R. The effects of long-term FES-assisted walking on intrinsic and reflex dynamic stiffness in spastic spinal-cord-injured

[10] Granat M, Ferguson A, Andrews B, Delargy M. The role of functional electrical stimulation in the rehabilitation of patients with incomplete spinal cord injury–observed benefits during gait studies. Paraplegia 1993;31:207-15.

[11] Thoumie P, Le C, Beillot J, Dassonville J, Chevalier T, Perrouin-Verbe B et al. Restoration of functional gait in paraplegic patients with the RGO-II hybrid orthosis. A multicenter controlled study. II: Physiological evaluation. Paraplegia 1995;33:654-9.

Evidence for “Orthostatic Hypotension” is based on the following studies:

[1] Faghri PD, Yount J. Electrically induced and voluntary activation of physiologic muscle pump: a comparison between spinal cord-injured and able-bodied individuals. Clin Rehabil 2002;16:878-885.

[2] Elokda AS, Nielsen DH, Shields RK. Effect of functional neuromuscular stimulation on postural related orthostatic stress in individuals with acute spinal cord injury. J Rehabil Res Dev 2000;37:535-542.

[3] Sampson EE, Burnham RS, Andrews BJ. Functional electrical stimulation effect on orthostatic hypotension after spinal cord injury. Arch Phys Med Rehabil 2000; 81: 139-143.

Other references:

Electrophysical Agents – Contraindications And Precautions: An Evidence-Based Approach To Clinical Decision Making In Physical Therapy. Physiother Can. 2010 Fall;62(5):1-80.

Gibbons RS, Shave RE, Gall A, Andrews BJ. FES-rowing in tetraplegia: a preliminary report. Spinal Cord. 2014 Dec;52(12):880-6.

Martin R, Sadowsky C, Obst K, Meyer B, McDonald J. Functional electrical stimulation in spinal cord injury: from theory to practice. Top Spinal Cord Inj Rehabil. 2012 Winter;18(1):28-33.

Warms CA, Backus D, Rajan S, Bombardier CH, Schomer KG, Burns SP. Adverse events in cardiovascular-related training programs in people with spinal cord injury: a systematic review. J Spinal Cord Med. 2014 Nov;37(6):672-92.

Image credits

  1. E-Stim Therapy ©Rankn Jordan, CC BY-NC-SA 2.0
  2. Functional electrical stimulation ©MilosRPopovic, CC BY-SA 4.0
  3. Image by SCIRE Community Team
  4. Checklist ©lastspark,CC BY 3.0 US
  5. Muscle © Smalllike, CC BY 3.0 US
  6. cardio ©emma Mitchell, CC BY 3.0 US
  7. Image by SCIRE Team.
  8. Image by SCIRE Team.
  9. fracture ©fahmionline, CC BY 3.0 US

 

Disclaimer: This document does not provide medical advice. This information is provided for educational purposes only. Consult a qualified health professional for further information or specific medical advice. The SCIRE Project, its partners and collaborators disclaim any liability to any party for any loss or damage by errors or omissions in this publication.

Transcutaneous Electrical Nerve Stimulation (TENS)

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Author: SCIRE Community Team | Reviewer: Amrit Dhaliwal | Published: 27 July 2017 | Updated: ~

Transcutaneous electrical nerve stimulation (TENS) is a non-drug treatment option for pain and spasticity. This page outlines basic information about TENS and its use after spinal cord injury (SCI).

Key Points

  • Transcutaneous electrical nerve stimulation (TENS) is a common form of electrotherapy typically used to treat pain.
  • TENS is delivered using electrotherapy machines that send pulsed electrical currents to the body through electrodes placed on the skin’s surface.
  • TENS is a relatively safe, non-invasive, and well-tolerated treatment option for pain and spasticity after SCI.
  • There is moderate evidence that TENS works for neuropathic pain after SCI and strong evidence that TENS works for spasticity after SCI. TENS has not been studied for musculoskeletal pain after SCI, but appears to work for this type of pain in other populations.
Handheld TENS unit attached by electrical wires to four self-adhesive electrodes

TENS machine and electrodes.1

Transcutaneous electrical nerve stimulation (TENS, pronounced ‘tens’) is a common electrotherapy primarily used to treat pain. TENS is a type of electrical stimulation that is delivered using electrical therapy machines connected to electrodes placed on the skin’s surface.

For people with SCI, TENS is used as a treatment option for musculoskeletal pain, neuropathic pain, and spasticity.

It is important to speak with a health provider before using TENS to make sure it is safe and suitable for you and to learn how to use the equipment correctly.

Most machines used for TENS are portable battery-powered devices with adjustable settings like intensity, frequency, and pulse duration. Changing the settings can provide different types of stimulation. The most common types of stimulation are:

  • Conventional TENS uses high frequency stimulation to produce sensations of ‘tingling’ or ‘pins and needles’ in areas with normal sensation.
  • Acupuncture-like TENS uses low frequency stimulation which may or may not cause muscle twitches in the area.
Electrodes placed in pairs along the lower back of a person

Electrodes placed on the skin.2

The machine is connected to a set of electrodes by electrical wires (leads). The electrodes may be self-adhesive or applied with conductive gel onto clean, intact skin. Electrodes may be placed near the area of your symptoms or in other areas directed by your health provider.

Once the electrodes and machine have been set up and connected, the intensity is then slowly turned up until it feels ‘strong, but comfortable’ or reaches a set intensity. It should not cause any pain or discomfort.

Your health provider will determine how long the stimulation is used based on the goals of the treatment. After the TENS machine has been safely turned off and the electrodes have been removed, the skin is inspected for any redness or irritation.

Using TENS below the level of injury

TENS should be used cautiously in areas with reduced or absent sensation because it can cause electrical burns, skin irritation, or autonomic reactions if the person cannot feel that the intensity is too strong.

However, TENS can be used below the level of injury if certain precautions are taken. It should be tried only under the supervision of a health provider. It should be tested in an area of sensation to ensure that there are no harmful reactions and monitored carefully during use.

Cartoon lightning boltsElectrical signals are a natural part of how the nervous system works. Signals that are sent along the nerves are relayed in part as electrical impulses. Because the nerves are naturally susceptible to electrical signals, they can be stimulated by electrical therapies like TENS.

TENS stimulates nerve fibres involved in touch. This might work to treat pain and spasticity in several ways:

  • TENS may reduce pain by blocking pain signals, so you can feel other sensations instead. This works in the same way as when you rub the skin over a sore area of your body. The unusual ‘tingling’ feeling of the TENS stimulation is sent to the brain instead of pain signals.
  • TENS may cause the release of endorphins within the nervous system that may help to reduce pain.
  • TENS may affect spasticity by making it less likely that the nerve cells to the muscles (motor neurons) will fire.
A pacemaker

TENS can interfere with the function of cardiac pacemakers.4

Although there are few reported medical complications caused by using TENS devices, there are many situations in which it could be unsafe to use. The following conditions are some possible restrictions on the use of TENS. Consult a health provider for further safety information.

TENS should not be used in the following situations:

  • Near the neck or head of people who have had seizures
  • Near implanted medical devices like cardiac pacemakers
  • On the abdomen or low back of pregnant women (except during labor and delivery)
  • On areas of active cancer (except under medical supervision in palliative care)
  • On areas with blood clots, bleeding, or infection
  • On the chest of people with major heart problems
  • By people who are unable to follow instructions or provide accurate feedback
  • Electrodes should not be placed over the eyes, through the head, through the chest, on the front of the neck or genitals, or over damaged skin or open wounds

TENS should be used with caution in the following situations:

Learn more in our article on Autonomic Dysreflexia. 

TENS is considered to be a relatively safe and well-tolerated treatment for people who can use it safely (see above for restrictions on using TENS). Serious medical complications from using TENS are rare. However, there are risks and side effects that should be discussed with a health provider before using TENS.

The most common risks and side effects of TENS include:

  • Skin discomfort, irritation, or redness near the electrodes
  • Allergy to the conductive gel
  • Mild electrical burns near the electrodes
  • An increase in pain or discomfort
  • Mild electrical shocks (from improper use or faulty equipment)

Other less common risks and side effects of TENS include:

In some cases, risks and side effects may be caused by improper use of the equipment. For this reason, it is essential to learn to use the equipment from a health provider and to only use TENS according to their direction.

TENS for nerve pain after SCI

Five studies have tested TENS as a treatment for neuropathic pain after SCI, although only three of these studies were suitable to draw conclusions from. These studies provide moderate evidence that TENS is effective for treating neuropathic pain after SCI.

TENS for muscle, bone, and joint pain after SCI

Research has not explored whether TENS is effective for treating musculoskeletal pain after SCI. However, because this type of pain is experienced in areas of normal sensation (above the level of injury), studies done outside of SCI might help provide some guidance about how well this treatment works.

A health provider using TENS on a leg of a person who is lying down on a bed

A health provider using TENS on a person’s leg.5

Reviews of research studies done in conditions like knee arthritis, general acute pain, and chronic low back pain have shown that TENS may be effective for treating musculoskeletal pain from these conditions. However, much of the research included in these reviews (and for TENS generally) is low quality, making it hard to make strong conclusions about whether TENS works for musculoskeletal pain.

Read more in our article, Pain After Spinal Cord Injury.

TENS for spasticity after SCI

Based on six studies that have tested TENS as a treatment for spasticity after SCI, there is strong evidence that an ongoing program of TENS reduces spasticity after SCI. These studies also show that TENS reduces spasticity even after a single session; although the effects are greater when TENS is used as part of an ongoing program.

Overall, there is moderate evidence that TENS works for neuropathic pain after SCI and strong evidence that TENS works for spasticity after SCI. TENS has not been studied for musculoskeletal pain after SCI, but appears to work for this type of pain in other populations.

TENS appears to be safe to use for most people and is widely available as a low cost treatment option. Until more research is done, it is best to discuss this treatment with your health providers to find out more about if it is a suitable treatment option for you.

For a review of how we assess evidence at SCIRE Community and advice on making decisions, please see SCIRE Community Evidence.

This page has been adapted from SCIRE Project (Professional) “Pain Management” and “Spasticity” chapters:

Mehta S, Teasell RW, Loh E, Short C, Wolfe DL, Hsieh JTC (2014). Pain Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors. Spinal Cord Injury Rehabilitation Evidence. Version 5.0: p 1-79.

Available from: https://scireproject.com/evidence/rehabilitation-evidence/pain-management/

Hsieh JTC, Wolfe DL, Townson AF, Short C, Connolly SJ, Mehta S, Curt A, Foulon BL, (2012). Spasticity Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan V, Mehta S, Sakakibara BM, Boily K, editors. Spinal Cord Injury Rehabilitation Evidence. Version 4.0.

Available from: https://scireproject.com/evidence/rehabilitation-evidence/spasticity/

 

Evidence for “TENS for nerve pain after SCI” is based on the following studies:

[1] Davis R, Lentini R. Transcutaneous nerve stimulation for treatment of pain in patients with spinal cord injury. Surg Neurol 1975;4:100-101.

[2] Bi X, Lv H, Chen BL, Li X, Wang XQ. Effects of transcutaneous electrical nerve stimulation on pain in patients with spinal cord injury: a randomized controlled trial. J Phys Ther Sci 2015;27(1):23-5.

[3] Celik EC, Erhan B, Gunduz B, Lakse E. The effect of low-frequency TENS in the treatment of neuropathic pain in patients with spinal cord injury. Spinal Cord. 2013 Apr;51(4):334-7.

[4] Norrbrink C. Transcutaneous electrical nerve stimulation for treatment of spinal cord injury neuropathic pain. J Rehab Res Dev 2009;46:85-93.

[5] Ozkul C, Kilinc M, Yildirim SA, Topcuoglu EY, Akyuz M. Effects of visual illusion and transcutaneous electrical nerve stimulation on neuropathic pain in patients with spinal cord injury: A randomised controlled cross-over trial. J Back Musculoskelet Rehabil 2015;28:709–19.

Evidence for “TENS for muscle, bone, and joint pain after SCI” is based on the following studies:

[1] Osiri M, Welch V, Brosseau L, Shea B, McGowan J, Tugwell P, Wells G. Transcutaneous electrical nerve stimulation for knee osteoarthritis. Cochrane Database Syst Rev. 2000;(4):CD002823.

[2] Johnson MI, Paley CA, Howe TE, Sluka KA. Transcutaneous electrical nerve stimulation for acute pain. Cochrane Database Syst Rev. 2015 Jun 15;(6):CD006142.

[3] Jauregui JJ, Cherian JJ, Gwam CU, Chughtai M, Mistry JB, Elmallah RK, Harwin SF, Bhave A, Mont MA. A Meta-Analysis of Transcutaneous Electrical Nerve Stimulation for Chronic Low Back Pain. Surg Technol Int. 2016 Apr;28:296-302.

Evidence for “TENS for spasticity after SCI” is based on the following studies:

[1] Oo W. Efficacy of addition of transcutaneous electrical nerve stimulation to standardized physical therapy in subacute spinal spasticity: a randomized controlled trial. Arch Phys Med Rehabil 2014;95:2013-20.

[2] Aydin G, Tomruk S, Keles I, Demir SO, Orkun S. Transcutaneous electrical nerve stimulation versus baclofen in spasticity: clinical and electrophysiologic comparison. Am J Phys Med Rehabil 2005;84(8):584-592.

[3] Possover M, Schurch B, Henle KP. New strategies of pelvic nerves stimulation for recovery of pelvic visceral functions and locomotion in paraplegics. Neurourol Urodyn. 2010 Nov;29(8).

[4] Goulet C, Arsenault AB, Bourbonnais D, Laramee MT, Lepage Y. Effects of transcutaneous electrical nerve stimulation on H-reflex and spinal spasticity. Scand J Rehabil Med 1996;28(3):169-176.

[5] Chung BP, Cheng, BK. Immediate effect of transcutaneous electrical nerve stimulation on spasticity in patients with spinal cord injury. Clinical Rehabilitation, 2010;24:202-210.

[6] van der Salm A, Veltink PH, Ijzerman MJ, Groothuis-Oudshoorn KC, Nene AV, Hermens HJ. Comparison of electric stimulation methods for reduction of triceps surae spasticity in spinal cord injury. Arch Phys Med Rehabil 2006;87(2):222-228.

Other references:

Johnson M. Transcutaneous electrical nerve stimulations (TENS). In: Watson T (Ed). Electrotherapy: Evidence-based Practice Twelfth edition. Edinburgh:Churchill Livingstone; 2008:253-296.

Electrophysical Agents – Contraindications And Precautions: An Evidence-Based Approach To Clinical Decision Making In Physical Therapy. Physiother Can. 2010 Fall;62(5):1-80.*

Cheing GL, Hui-Chan CW. Transcutaneous electrical nerve stimulation: Nonparallel antinociceptive effects on chronic clinical pain and acute experimental pain. Arch Phys Med Rehab 1999;80:305-12.

Jones I, Johnson MI. Transcutaneous electrical nerve stimulation. Contin Educ Anaesth Crit Care Pain 2009; 9(4):130-135.

Somers DL, Clemente FR. The relationship between dorsal horn neurotransmitter content and allodynia in neuropathic rats treated with high-frequency transcutaneous electrical nerve stimulation. Arch Phys Med Rehabil 2003; 84(11):1575-1583.

Johnson M. Transcutaneous Electrical Nerve Stimulation: Mechanisms, Clinical Application and Evidence. Rev Pain. 2007 Aug;1(1):7-11.

Image credits:

  1. Tens ©Yeza, CC BY-SA 4.0
  2. Electrical Muscle stimulation ©Wisser68, CC BY-SA 3.0
  3. Electricity ©Artnadhifa, CC BY 3.0 US
  4. St Jude Medical pacemaker with ruler ©Steven Fruitsmaak, CC BY 3.0
  5. Day 2 Outpatient PT 013 ©Roger Mommaerts, CC BY-SA 2.0

 

Disclaimer: This document does not provide medical advice. This information is provided for educational purposes only. Consult a qualified health professional for further information or specific medical advice. The SCIRE Project, its partners and collaborators disclaim any liability to any party for any loss or damage by errors or omissions in this publication.