Medications Archives - SCIRE Community

Apr 02

Cannabis (Marijuana) and Cannabinoids

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.

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What is cannabis?

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.

What are cannabinoids?

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.³

What is the difference between medical and recreational cannabinoids?

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.

What are the ways cannabinoids can be used?

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

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.

What is the suggested dosing of cannabis?

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.

What are the risks and side effects of cannabis?

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

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.

What are cannabinoids used for after spinal cord injury?

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.

The bottom line

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.

Reference list

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://web.archive.org/web/20200213002533/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

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

[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

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

Nov 21

Spasticity

By Scire Admin | | No Comments

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.

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What is spasticity?

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.

What does spasticity feel or look like?

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.

Why does spasticity happen?

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

How is spasticity diagnosed?

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
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.

Should spasticity be treated?

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

Muscle 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

How is spasticity treated?

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

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

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:

Tizanidine
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

Botulinum 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

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 bottom line

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.

Reference list

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 repair, 24(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:

Muscle strain ©Kylie Mhai, CC BY 3.0 US
Modified from: Dorsiplantar ©Connexions, CC BY 3.0
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Nov 21

Baclofen

By Scire Admin | | No Comments

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.

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What is 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.

How is baclofen used?

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

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.

Are there restrictions or precautions for using baclofen?

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

What are the risks and side effects of using baclofen?

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.

The bottom line

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.

Reference list

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.

[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.

[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.

[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

National Institutes of Health, part of the United States Department of Health and Human ServicesBaclofen 20 mg oral tablet, CC0 1.0

Nov 10

Botulinum Toxin

By Scire Admin | | No Comments

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.

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What is botulinum toxin?

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.

How is botulinum toxin treatment done?

Monochrome cartoon logo of bottle and injection needle Botulinum 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.

How does botulinum toxin work?

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.

Are there restrictions or precautions for using botulinum toxin?

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.

What are the risks and side effects of botulinum toxin?

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:

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.

Is botulinum toxin effective?

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
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!

The bottom line

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.

Reference list

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:

[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.

[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.

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.

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.

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