Author: SCIRE Community Team | Reviewer: Shannon Sproule | Published: 18 October 2017 | Updated: ~
Pressure mapping is a clinical technique that is used to help prevent pressure sores after spinal cord injury (SCI). This page outlines how pressure mapping is used after SCI.
Key Points
- Pressure mapping is a technique that involves the use of a pressure-sensitive mat and computer system to measure the amount of pressure between a person’s body and a supporting surface.
- Pressure mapping is used to help identify areas of excess pressure that may contribute to pressure sores. This can be used to help make decisions about surface options (like wheelchair cushions and bedding) and find out how effective a person’s pressure relief techniques are.
- This technique involves the use of a flexible mat containing pressure sensors that is placed on the surface being tested and then the person is positioned on the mat. The mat is connected to a computer system that creates a color-coded diagram showing areas of pressure.
- Pressure mapping is considered to be a useful tool for making decisions about reducing pressure that is used as a decision-making and educational tool. There is a lack of research on whether pressure mapping directly helps to reduce pressure sores after SCI.
Pressure mapping can be used on supporting surfaces such as wheelchairs.1
Pressure mapping is a technique that is used to identify areas of pressure between a person’s body and a supporting surface like a cushion or chair. A thin, pressure-sensitive mat and computer system are used to develop a map showing areas of pressure where the body contacts the surface. This technique is most often used to identify areas of high pressure associated with wheelchair seating that could contribute to the development of pressure sores.
See our article on Pressure Sores to learn more!
Pressure mapping is also used on other such as mattresses, toilet seats, car seats, sports equipment, or any other surface a person sits or lies on for periods of time that may influence their skin health.
People with spinal cord injuries have an increased risk of developing skin lesions called pressure sores. Pressure sores occur for many reasons, including increased pressure on vulnerable areas of the skin. Bony areas that come into contact with support surfaces, like the sit bones and tailbone in sitting, are highly vulnerable to increased pressure.
Learn how proper wheelchair seating can reduce the risk of pressure sores.
Pressure sore on the side of the ankle.2
Pressure mapping is used to determine areas of increased pressure in certain postures on specific surfaces. It may be used to assess areas of pressure on various surfaces, such as chairs, beds, sofas, car seats, and toilet seats. This information can be used to develop strategies to reduce pressure and improve comfort in these situations.
Pressure mapping may be used as a tool to aid decision-making when selecting support surfaces and equipment, such as assessing which wheelchair cushions provide the best pressure relief for you. Pressure mapping is also used to assess the effectiveness of pressure relief techniques like weight-shifting by providing real-time feedback about the pressure during the performance of these techniques.
Pressure map placed on a wheelchair (left), flexible pressure map (center), and diagram of pressure of a person’s buttocks in sitting (right). Areas of pressure are indicated from high pressures in red (around the sit bones) to lower pressures in blue.3
A flexible mat containing pressure sensors is placed on the surface to be tested. The person being assessed then sits on the mat. Information about pressure between their body and the seat is picked up by sensors in the mat and sent to a computer, where it is translated into a color coded diagram.
The diagram displays the pressure recorded at each sensor in the mat by number and displays areas of high and low pressure with different colors. A clinician then determines the corresponding areas on the body through a hands-on physical examination. This technique is used together with other assessments of pressure sore risk to make recommendations for reducing areas of high pressure. There may be variation in the procedures used for pressure mapping in different settings.
Pressure mapping can be influenced by many aspects of how the procedure is done. For example, how the person positions themselves at the time of the reading and how long the person sits on the mat before the readings are taken can change the findings. There are also different types of systems that collect information about pressure differently. These factors and other concerns have led to disagreement among experts about how to best understand and interpret the results of pressure mapping for clinical use.
In addition, pressure is just one factor that contributes to pressure sores. Friction, moisture, age, body composition, time spent sitting, and many other factors also contribute to pressure sores. These factors cannot be detected by pressure mapping, which limits the use of pressure mapping as a stand-alone tool.
Pressure mapping also requires special equipment and trained health providers which may not be available in settings outside of major rehabilitation centers.
Pressure mapping is considered by experts to be a useful tool for understanding pressure and making decisions about pressure relief. At this time, most of the research that has been done on whether pressure mapping is effective for preventing pressure sores has been done in populations outside of SCI. We do not know if pressure mapping is effective for preventing of pressure sores in people with SCI.
Pressure mapping is clinical tool that may be used in rehabilitation centers to help assess the risk of pressure sores. It is considered to be a valuable tool for making decisions about reducing pressure as well as a useful educational tool for understanding pressure in different positions. There is a lack of research on whether pressure mapping directly helps to reduce pressure sores after SCI.
Hsieh J, McIntyre A, Wolfe D, Lala D, Titus L, Campbell K, Teasell R. (2014). Pressure Ulcers Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors. Spinal Cord Injury Rehabilitation Evidence. Version 5.0. 1-90.
Available from: https://scireproject.com/evidence/rehabilitation-evidence/skin-integrity-pressure-injuries/
Barnett RI, Shelton FE. Measurement of support surface efficacy: pressure. Adv Wound Care 1997; 10(7):21-9.
Brienza DM, Karg PE, Geyer MJ, Kelsey S, Trefler E. The relationship between pressure ulcer incidence and buttock-seat cushion interface pressure in at-risk elderly wheelchair users. Arch Phys Med Rehabil 2001; 82(4):529-33.
Eitzen I. Pressure mapping in seating: a frequency analysis approach. Arch Phys Med Rehabil 2004; 85(7):1136-40.
Ferguson-Pell M, Cardi MD. Prototype development and comparative evaluation of wheelchair pressure mapping system. Assist Technol 1993; 5(2):78-91.
Hamanami K, Tokuhiro A, Inoue H. Finding the optimal setting of inflated air pressure for a multi-cell air cushion for wheelchair patients with spinal cord injury. Acta Med Okayama 2004; 58(1):37-44.
Hanson D, Langemo D, Anderson J, Hunter S, Thompson P. Pressure mapping: seeing the invisible. Adv Skin Wound Care 2006; 19(8):432-4.
Henderson JL, Price SH, Brandstater ME, Mandac BR. Efficacy of three measures to relieve pressure in seated persons with spinal cord injury. Arch Phys Med 1994;75:535-9.
Jan YK, Brienza DM. Technology for Pressure Ulcer Prevention. Top Spinal Cord Inj Rehabil; 2006; 11(3):30-41.
Kernozek TW, Lewin JE. Seat interface pressures of individuals with paraplegia: influence of dynamic wheelchair locomotion compared with static seated measurements. Arch Phys Med Rehabil 1998; 79(3):313-6.
Rondorf-Klym LM, Langemo D. Relationship between body weight, body position, support surface, and tissue interface pressure at the sacrum. Decubitus 1993; 6(1):22-30.
Shelton F, Barnett R, Meyer E. Full-body interface pressure testing as a method for performance evaluation of clinical support surfaces. Appl Ergon 1998; 29(6):491-7.
Stinson MD, Porter-Armstrong A. Seating and pressure support needs of people with cancer in the cervix or rectum: a case series on the clinical usefulness of pressure mapping assessment. Euro J Cancer Care 2007; 17:298-305.
Stinson MD, Porter-Armstrong A, Eakin P. Seat-interface pressure: a pilot study of the relationship to gender, body mass index, and seating position. Arch Phys Med Rehabil 2003; 84(3):405-9.
Sonenblum SE, Sprigle SH. The impact of tilting on blood flow and localized tissue loading. J Tissue Variability 2011;20:3-13.
Taule T, Bergfjord EE, Lunde T, Stokke BH, Storlind H, Sorheim MV et al. Factors influencing optimal seating pressure after spinal cord injury. Spinal Cord 2013;51:273-7.
Image credits
- Veterans wheelchair games 2009 ©U.S. Air Force photo/Staff Sgt. Desiree N. Palacios, CC0 1.0
- Reprinted with permission of the copyright holder, Gordian Medical, Inc. dba American Medical Technologies (courtesy of National Pressure Ulcer Advisory Panel).
- Image ©Cho KH, Beom J, Yuk JH, Ahn SC, CC BY-NC 4.0
- Sit ©Rudez Studio, CC BY 3.0 US
Author: SCIRE Community Team | Reviewer: Andrei Krassioukov and Janice Eng | Published: 12 October 2017 | Updated: ~
Autonomic dysreflexia is a medical emergency that can happen after spinal cord injury (SCI). This page provides an overview of what autonomic dysreflexia is and how it is managed.
For information about emergency treatments, see How is autonomic dysreflexia treated?
Key Points
- Autonomic dysreflexia is a potentially life-threatening medical emergency that can affect people with SCI at T6 and above.
- Autonomic dysreflexia involves a sudden rise in blood pressure, which may be accompanied by heart rate changes, headaches, sweating, and other symptoms.
- Autonomic dysreflexia can be triggered by any strong, irritating, or ‘painful’ stimulus below the level of the injury, such as bladder and bowel problems, tight clothing, or pressure ulcers.
- Emergency treatment involves sitting upright, monitoring blood pressure, loosening tight clothing, and searching for and eliminating the cause of the episode (usually problems related to the bladder, bowel, and skin). If the episode does not resolve, emergency medical treatment involves the use of medications to rapidly lower blood pressure.
- Prevention is an important part of managing autonomic dysreflexia. This typically involves maintaining good bladder, bowel, and skin care, and using medications during procedures that could trigger autonomic dysreflexia.
Autonomic dysreflexia (also called autonomic hyperreflexia) is a potentially life-threatening medical condition that can happen after spinal cord injury. Autonomic dysreflexia involves a sudden rise in blood pressure accompanied by changes in heart rate and other symptoms like headaches and sweating. The blood pressure responses in the body are poorly controlled because of the SCI and can become dangerously high.
Pathophysiology of autonomic dysreflexia.1
Autonomic dysreflexia typically affects people with SCI at T6 and above (although occasionally as low as T8). In general, people with higher level of injury and complete injuries are more likely to experience autonomic dysreflexia. Autonomic dysreflexia can occur at any time after the SCI.
Autonomic dysreflexia involves a sudden rise in blood pressure of 20 to 30 mmHg above your normal systolic blood pressure. Since the normal blood pressure of people with SCI is often 20 to 30 mmHg lower than in those without SCI, blood pressure can be in a range that is commonly considered ‘normal’ or ‘slightly elevated’ and still be high for that person.
This rise in blood pressure is usually accompanied by symptoms. Symptoms will be different for everyone and can range from some mild discomfort to life threatening and severe.
Signs and symptoms of autonomic dysreflexia
- A sudden rise in systolic blood pressure (20 to 30 mmHg above normal)
- Changes in heart rate, usually a slow heart rate which sometimes becomes rapid
- A pounding or throbbing headache
- Sweating, flushing, or blotching of the skin above the SCI
- Goosebumps or hair standing on end above the SCI
- Dry and pale skin below the SCI
- Worsening of muscle spasms
- A metallic taste in the mouth
- Feeling anxious or a feeling of ‘impending doom’
- A stuffy or runny nose
- Blurred vision or seeing spots
- Nausea
- Difficulty breathing
Autonomic dysreflexia can be life threatening when severe. If left untreated, uncontrolled elevated blood pressure can lead to serious conditions like stroke, heart attack, detached retinas, seizures, and even death.
Although these complications are uncommon, it is important that autonomic dysreflexia is recognized and treated immediately. Talk to your health providers about setting up a plan for managing episodes of autonomic dysreflexia as soon as they happen.
Autonomic dysreflexia can be triggered by any strong stimulation below the SCI, including anything that could be considered uncomfortable, irritating, or painful if it could be felt. For example, a wound can trigger autonomic dysreflexia even if it the person does not feel it. Autonomic dysreflexia can also be caused by normal body processes that are strongly stimulating, such as a full bladder or sexual stimulation. The most common triggers are related to the bladder or bowel.
Common causes of autonomic dysreflexia
- A bladder that is full – this may be caused by a blocked or kinked catheter, an overfilled collection bag, or incomplete emptying of urine
- Other bladder causes such as urinary tract infections or bladder procedures (like when putting in a catheter)
- A bowel that is full or impacted (contains a hard mass of stool that is stuck)
- Other bowel causes such as constipation, infections, haemorrhoids, or bowel procedures (such as during digital rectal stimulation)
- Pressure ulcers, wounds, or burns
- Skin irritation from pressure, pinching, ingrown toenails, or tight clothing
- Hot or cold temperatures
- Strong sexual stimulation
- Menstrual cramping
- Labour and delivery
- Broken bones and heterotopic ossification
- Surgery and other medical procedures (including functional electrical stimulation)
- Ulcers and other abdominal conditions
Autonomic dysreflexia is caused by dysfunction of the autonomic nervous system after SCI that leads to poorly controlled blood pressure responses.
The autonomic nervous system
The autonomic nervous system controls largely unconscious bodily processes such as blood pressure, heart rate, breathing rate, body temperature, digestion, bladder, bowel, and sexual function. It has two divisions:
The sympathetic nervous system prepares the body for stressful or emergency situations. It is often called the ‘fight or flight’ system, because it prepares the body for action. For example, it increases heart rate and constricts blood vessels.
The parasympathetic nervous system prepares the body for normal, non-emergency situations. It is often called the ‘rest and digest’ system, because it allows the body to restore itself. For example, it slows heart rate and relaxes blood vessels.
The sympathetic and parasympathetic systems have different (and often opposite) effects on the organs and work together to control bodily functions according to the situation.
Blood pressure is carefully controlled by the autonomic nervous system to ensure that circulation works properly. The body monitors blood pressure and makes adjustments to maintain blood pressure within an optimal range. This is done in part by tightening (constricting) or relaxing (dilating) the blood vessels and changing heart rate.
What happens in autonomic dysreflexia
When the body below the SCI detects strong stimulation, it activates the sympathetic nervous system, causing the constriction of blood vessels in the lower body. This causes blood pressure to rise.
Pressure sensors in the arteries then detect the elevated blood pressure and relay this message to the brain. Under normal circumstances, the brain sends signals through the spinal cord and cranial nerves to relax the blood vessels and slow heart rate. This restores blood pressure to normal.
However, when there is an SCI, the signal to relax the blood vessels is blocked from travelling to the lower body. Because of this, the blood vessels remain constricted and the body cannot restore blood pressure to normal. This causes the uncontrolled elevated blood pressure that happens during autonomic dysreflexia.
Why does autonomic dysreflexia happen at T6 and above?
The level of T6 is important because nerves from this part of the spinal cord constrict a large group of blood vessels in the abdomen called the splanchnic vascular bed. These blood vessels contain a large volume of blood, so when the blood vessels are constricted, it causes the blood pressure to rise significantly. Injuries below T6 do not usually cause enough of a change in blood pressure to cause autonomic dysreflexia.
Autonomic dysreflexia is a medical emergency and needs to be treated immediately. Emergency treatment involves a series of steps to lower blood pressure and remove the cause of the episode. If these steps are unsuccessful, emergency medical treatments are used to try to reduce blood pressure quickly.
Immediate treatment of autonomic dysreflexia
- Get into an upright sitting position (or bring your head up) and if possible, lower your legs
- If possible, check your blood pressure and re-check it every 5 minutes
- Loosen tight clothing or devices (including tape, straps, and equipment)
- Search for and remove the cause of the episode:
- Check for bladder problems
- If your catheter is kinked or blocked, reposition or flush the catheter
- If your bladder or collection bag is full, drain
- If your urine is cloudy or smells bad, it could be a bladder infection – contact a health provider
- Check for bowel problems
- If your bowel is full, use your bowel management routine to empty it (such as digital rectal stimulation)
- Check for other problems like hemorrhoids
- Check for bladder problems
- Check for skin problems and remove them if possible (such as ingrown toenails, skin irritation, pressure ulcers, infections, or wounds)
- Check for other problems (such as broken bones)
- Seek medical attention if blood pressure remains high (150 mmHg or above) after following these steps
If blood pressure returns to normal, continue to monitor your symptoms and blood pressure to make sure they do not return and report the incident to a health provider.
This approach is considered to be the most effective first treatment for autonomic dysreflexia. However, although this procedure is commonly used and recommended by health providers, it is supported primarily by expert opinion rather than evidence from research studies.
Emergency medical treatments
If the steps above do not reduce blood pressure and it remains high (150 mmHg or above), seek emergency medical attention by calling an ambulance or visiting an emergency department. Emergency medical treatments involve the use of medications that rapidly lower blood pressure. The health providers may also run a series of tests to identify the cause of the episode if one has not been found.
The most commonly used drugs for autonomic dysreflexia are:
- Captopril
- Nifedipine (Adalat, Procardia)
- Nitrates (Nitroglycerine, Depo-Nit, Nitrostat, Nitrol, Nitro-Bid)
However, there is little research evidence to suggest which medications work best for treating autonomic dysreflexia. Speak to your health providers for more information about medications used in autonomic dysreflexia emergencies.
The most effective way of managing autonomic dysreflexia is to prevent triggering it in the first place. People who get autonomic dysreflexia may be able to take steps to avoid triggering episodes, especially during procedures that are known to cause autonomic dysreflexia.
Learn to recognize autonomic dysreflexia and your triggers
In order to be able to manage episodes of autonomic dysreflexia, it is important to be able to recognize an episode and know what to do when it happens.
- Learn about and educate family members and friends about what autonomic dysreflexia is, how to recognize it, and what to do if it happens.
- Work with your health providers to identify your risk for autonomic dysreflexia, how to prevent it, and what to do if it happens.
- Carry an autonomic dysreflexia medical emergency card. These wallet-sized cards describes autonomic dysreflexia and its symptoms and treatments for use in an emergency – it can be used to quickly describe the condition and its treatment to your health providers.
Preventing autonomic dysreflexia from bladder problems
Bladder problems are the most common triggers of autonomic dysreflexia. Methods that may be used to prevent bladder problems from triggering autonomic dysreflexia include:
- Maintaining a bladder routine is the most important way to prevent problems like bladder distension and urinary tract infections.
- Preventing irritation during bladder procedures (such as catheterization) using anaesthetic medications (such as capsaicin or lidocaine).
- Managing reflex spasms of the bladder muscles (detrusor hyperreflexia) through methods including botulinum toxin (Botox) injections or sacral denervation (deafferentation) surgery.
- Bladder surgeries, such as bladder augmentation, may be used for some individuals with bladder dysfunction after an SCI and have been shown to help reduce episodes of autonomic dysreflexia.
See our article on Urinary Tract Infections to learn more!
Preventing autonomic dysreflexia from bowel problems
Bowel problems are another common trigger of autonomic dysreflexia. Methods that may be used to prevent bowel problems from triggering autonomic dysreflexia include:
- Maintaining a bowel routine and management (including fibre and fluid intake) to prevent problems like bowel distension, faecal impaction, and constipation.
- Preventing irritation during invasive bowel procedures or medical procedures (such as digital rectal stimulation) using anesthetics (such as lidocaine gel or lidocaine anal blocks).
- Bowel surgeries, such as colostomy or ileostomy, may be considered for people with chronic bowel problems that cause autonomic dysreflexia and other problems.
See our article on Bowel Changes after Spinal Cord Injury for more information!
Preventing autonomic dysreflexia from skin problems
Pressure ulcers, ingrown toenails, and burns can all be additional causes of autonomic dysreflexia. Methods that may be used to prevent skin problems from triggering autonomic dysreflexia include:
- Maintain an effective skin care routine, which involves regular pressure relief, inspection of skin, and proper cleaning.
- Avoid wearing tight clothing and keep clothing and sheets smooth.
- Maintain regular foot care.
- Treat skin injuries and infections early.
Preventing autonomic dysreflexia from other causes
- Although individuals with SCI do not have sensation in areas where surgeries may occur, anesthesia should be used to avoid triggering autonomic dysreflexia during surgery.
- Anesthesia (spinal or epidural if possible) is needed with vaginal, Caesarean, or instrumental delivery to prevent autonomic dysreflexia during labour.
- Be aware that strong sexual stimulation can cause autonomic dysreflexia. Take precautions and be aware of your responses to stimulation.
The bottom line
Autonomic dysreflexia is a serious medical condition that requires immediate recognition and treatment. First line treatment involves sitting up, removing tight clothing, and removing the cause of episode. This is supported by expert opinion. Emergency medical treatments for episodes of autonomic dysreflexia involve fast acting anti-hypertensive agents such as nifedipine, nitrates, and captopril, although the best treatment to use has not been determined.
It is best to discuss treatment options with your health providers to find out which treatments are suitable for you. For a review of how we assess evidence at SCIRE Community and advice on making decisions, please see SCIRE Community Evidence.
Krassioukov A, Blackmer J, Teasell RW, Eng JJ (2014). Autonomic Dysreflexia Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors.
Spinal Cord Injury Rehabilitation Evidence. Version 5.0. Vancouver: p 1- 35. Available from: http://scireproject.com/evidence/rehabilitation-evidence/autonomic-dysreflexia.
Barton CH, Khonsari F, Vaziri ND, Byrne C, Gordon S, Friis R. T http://scireproject.com/evidence/rehabilitation-evidence/autonomic-dysreflexia The effect of modified transurethral sphincterotomy on autonomic dysreflexia. J Urol 1986;135:83-85.http://scireproject.com/evidence/rehabilitation-evidence/autonomic-dysreflexia-re/
Sidi AA, Becher EF, Reddy PK, Dykstra DD. Augmentation enterocystoplasty for the management of voiding dysfunction in spinal cord injury patients. J Urol 1990;143:83-85.
Perkash I. Transurethral sphincterotomy provides significant relief in autonomic dysreflexia in spinal cord injured male patients: Long-term followup results. J Urol 2007;177:1026-1029.
Ke QS, Kuo HC. Transurethral incision of the bladder neck to treat bladder neck dysfunction and voiding dysfunction in patients with high-level spinal cord injuries. Neuro Uro 2010;29:748-752.
Hohenfellner M, Pannek J, Botel U, Bahms S, Pfitzenmaier J, Fichtner J, et al. Sacral bladder denervation for treatment of detrusor hyperreflexia and autonomic dysreflexia. Urol 2001;58:28-32.
Kutzenberger J. Surgical therapy of neurogenic detrusor overactivity (hyperreflexia) in paraplegic patients by sacral deafferentation and implant driven micturition by sacral anterior root stimulation: methods, indications, results, complications, and future prospects. Acta Neurochir Suppl 2007;97:333-339.
Coggrave MJ, Ingram RM, Gardner BP, Norton CS. The impact of stoma for bowel management after spinal cord injury. Spinal Cord 2012;50:848-852.
Cosman BC, Vu TT. Lidocaine anal block limits autonomic dysreflexia during anorectal procedures in spinal cord injury: a randomized, double-blind, placebo-controlled trial. Dis Colon Rectum 2005;48:1556-1561.
Cosman BC, Vu TT, Plowman BK. Topical lidocaine does not limit autonomic dysreflexia during anorectal procedures in spinal cord injury: a prospective, double-blind study. Int J Colorectal Dis 2002;17:104-108.
Furusawa K, Sugiyama H, Tokuhiro A, Takahashi M, Nakamura T, Tajima F. Topical anesthesia blunts the pressor response induced by bowel manipulation in subjects with cervical spinal cord injury. Spinal Cord 2009;47:144-148.
Cross LL, Meythaler JM, Tuel SM, Cross LA. Pregnancy, labor and delivery post spinal cord injury. Paraplegia 1992;30:890-902.
Hughes SJ, Short DJ, Usherwood MM, Tebbutt H. Management of the pregnant woman with spinal cord injuries. Br J Obstet Gynaecol 1991;98:513-518.
Cross LL, Meythaler JM, Tuel SM, Cross AL. Pregnancy following spinal cord injury. West J Med 1991;154:607-611.
Skowronski E, Hartman K. Obstetric management following traumatic tetraplegia: case series and literature review. Aust N Z J Obstet Gynaecol 2008;48:485-491.
Lambert DH, Deane RS, Mazuzan JE. Anesthesia and the control of blood pressure in patients with spinal cord injury. Anesth Analg 1982;61:344-348.
Eltorai IM, Wong DH, Lacerna M, Comarr, AE, Montroy R. Surgical aspects of autonomic dysreflexia. J Spinal Cord Med 1997;20:361-364.
Matthews JM, Wheeler GD, Burnham RS, Malone LA, Steadward RD. The effects of surface anaesthesia on the autonomic dysreflexia response during functional electrical stimulation. Spinal Cord 1997;35:647-651.
Kim JH, Rivas DA, Shenot PJ, Green B, Kennelly M, Erickson, JR, O’Leary M, Yoshimura N, Chancellor MB. Intravesical resiniferatoxin for refractory detrusor hyperreflexia: a multicenter, blinded, randomized, placebo-controlled trial. J Spinal Cord Med 2003;26:358-363.
Giannantoni A, Di Stasi SM, Stephen RL, Navarra P, Scivoletto G, Mearini E, Porena M. Intravesical capsaicin versus resiniferatoxin in patients with detrusor hyperreflexia: a prospective randomized study. J Urol 2002;167:1710-1714.
Igawa Y, Satoh T, Mizusawa H, Seki S, Kato H, Ishizuka O, Nishizawa O. The role of capsaicin-sensitive afferents in autonomic dysreflexia in patients with spinal cord injury. BJU Int 2003;91:637-641.
Dykstra DD, Sidi AA, Scott AB, Pagel JM, Goldish GD. Effects of botulinum A toxin on detrusor-sphincter dyssynergia in spinal cord injury patients. J Urol 1988;139:919-922.
Schurch B, Stohrer M, Kramer G, Schmid DM, Gaul G, Hauri D. Botulinum-A toxin for treating detrusor hyperreflexia in spinal cord injured patients: a new alternative to anticholinergic drugs? Preliminary results. J Urol 2000;164:692-697.
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Image Credits
- Image by SCIRE Professional Team
- Headache ©8thBox, CC0 1.0
- Doctor1 ©Clker-Free-Vector-Images, CC0 1.0
- Voltage ©Clker-Free-Vector-Images, CC0 1.0
- Highbp ©stevepb, CC0 1.0
- Headshock ©Geralt, CC0 1.0
- Body vessels © Clker-Free-Vector-Images, CC0 1.0
- Stetho ©Clker-Free-Vector-Images, CC0 1.0
- Ambulance ©Pettycon, CC0 1.0
- Excretory system ©Olena Panasovska, CC BY 3.0 US
- Digestive System ©Design Science, CC0 1.0
- Modified from: Man Resting on Long Chair ©Gan Khoon Lay, CC BY 3.0
- Tasklist ©Pettycon, CC0 1.0
Author: SCIRE Community Team | Reviewer: B. Catharine Craven | Published: 11 October 2017 | Updated: 14 March 2019
Osteoporosis is a condition that affects the bones of the hip and knee regions after spinal cord injury (SCI). This page provides information about osteoporosis after SCI and common treatments used for this condition.
Key Points
- SCI may cause declines in hip and knee region bone mineral density that leads to osteoporosis, and a greater risk of fracture over the person’s lifetime.
- Osteoporosis is a condition in which the bones become less dense, changing the bone structure and making the bones more likely to break (fracture) following simple activities.
- A bone density test is needed to detect osteoporosis and help you to estimate your fracture risk.
- People living with SCI, low bone density, and high fracture risk need treatment to reduce fractures.
- Common treatments for osteoporosis after SCI include bisphosphonate medications, supplements, and physical treatments (such as standing and functional electrical stimulation).
- The research evidence suggests that bisphosphonate medications are effective for preventing and treating bone loss after SCI and are usually started early after SCI. Physical treatments are not supported by current evidence for treating bone loss after SCI.
Osteoporosis is a condition in which the bones become less dense, changing the bone structure and making the bones more likely to break.
Bone mineral density is low in osteoporosis, making bones porous and brittle.1
A bone mineral density test helps you and your doctor to measure the density of your bones and estimate how likely you are to get a fracture (broken bone) in the next ten years. Centres with expertise in SCI will ask you to have the density measured of your spine, hip and knee regions.
Healthy bone is constantly being broken down and reformed by the body’s cells in a process called bone remodeling. As a part of this process, the cells that breakdown bone tissue and the cells that create new bone, work to keep or increase the bone’s strength. Bones can adapt and change to the demands placed on them
After SCI, the cells that breakdown bone (osteoclasts) work over time, and the cells which build bone (osteoblasts) cannot keep pace, this results in thinning of the bone cortex and a lower number of bone cross struts and trabeculae. These changes in the bone decrease bone mineral density, usually areas rich in trabelcular bone are affected first and then the bone cortex.
Osteoporosis often affects people with SCI in a unique pattern called sublesional osteoporosis (‘sublesional’ means ‘below the level of injury’). Sublesional osteoporosis is a condition which involves:
-
X-ray image of a hip fracture.2
Excessive bone resorption below the level of injury
- Low bone mineral density of the hip and or knee regions
- An increased risk of fracture
Bone tissues start to breakdown as early as the first few days after SCI. Among people with motor complete SCI, bone tissue resorption is highest between 3 and 6 months after injury and may continue for years. The rate of decline in bone density is less predictable in people with incomplete or non-traumatic SCI.
Osteoporosis is very common in people living with SCI long-term and increases the risk for fragility fractures.
Fragility fractures are fractures caused by minimal force such as twisting during a transfer or a low speed fall from your wheelchair. Fragility fractures typically happen at the lower part of the femur (thigh bone) just above the knee and the top of the tibia (shin bone) just below the knee. A red or swollen leg should prompt you to have an x-ray to rule out a fracture. Fractures can cause serious medical problems such as blood clots, skin infections, and pressure sores. Fractures above the knee are usually fixed by a surgeon, whereas fractures below the knee are usually casted. After SCI, fractures can be slow or hard to heal. Fragility fractures
Spinal cord injury can affect the body in a number of different ways that contribute to osteoporosis. These changes may include:
Changes to Body systems
Spinal cord injury affects many different systems in the body. Changes in the immune, hormone, circulatory, and nervous systems after SCI contribute to weaker bones after SCI. The role of these factors is not fully understood.
Fewer weight-bearing activities
Weight-bearing activities, like standing and walking, place forces through the bones of the legs and hips that stimulate the bones to become stronger. When a person spends less time standing and more time sitting, the bones experience fewer forces and adapt by becoming less dense and weaker.
Foods containing calcium and vitamin D help maintain bone strength.3-6
Reduced muscle activity
Because muscles are connected to bones by tendons, the repeated pulling of muscles on bones during movement stimulates the bones to become stronger. When muscles become weak or paralyzed, the muscles atrophy and the muscles and bones nearby have fat deposited in them and there are not as many forces applied to the bones.
Lifestyle changes
Physical activity and nutritional habits can also influence the bones. After SCI, rates of physical activity, which can help to strengthen bone, are often lower than in people without SCI. In addition, changes in nutritional habits, such as reduced calcium and vitamin D intake can also contribute to low bone density after SCI.
Fragility fractures are very common after SCI. Individuals with these risk factors are more likely to experience a fracture after SCI. if you have more than 3 of the following fracture risk factors, please discuss them with your health care team.
Risk factors for fractures after SCI:
Women- Have a motor complete SCI (AIS A or AIS B, no movement of the legs)
- Paraplegia
- SCI for more than 10 years
- People less than 16 years of age at the time of the SCI onset
- People who consume more than 5 servings of alcohol per day
- Long term use of medications; specifically, anticonvulsants, heparin, or opioid medications
- Low weight for one’s height (a Body Mass Index (BMI) of less than 19)
- Low knee region bone mineral density
- Prior fragility fracture
- Family history of fracture
A DXA test is a non-invasive way to measure bone mineral density.8
Measuring and monitoring bone mineral density after SCI is an important part of managing bone health. These measurements allow health providers to diagnose osteoporosis, estimate your fracture risk and monitor changes in your bone density over time. There are several methods that are commonly used to measure different aspects of bone health.
A bone density test or DXA (Dual-Energy X-ray Absorptiometry) Test is an imaging modality that uses non-invasive x-ray technology to scan and measure bone mineral density. DXA is the most widely used tool for measuring bone mineral density and diagnosing osteoporosis.
Peripheral Quantitative Computed Tomography is another non-invasive imaging method that can be used to diagnose osteoporosis of the shin region. This type of scan measures cortical thickness and trabecular volumetric bone mineral density. However, it is most often used in research.
Diagnosing osteoporosis
Health care providers will review your medical history, measure your blood chemistry and bone density, and ask you about your risk factors for fracture before diagnosing osteoporosis or estimating your future risk of fracture. After a fracture, you should undergo screening for osteoporosis.
Vitamin D supplementation may have a role in osteoporosis prevention post-SCI.9
1. Adequate, but not too much Vitamin D intake
Vitamin D is a vitamin that has an essential role in maintaining bone health by increasing the absorption of calcium. After SCI, there are a number of different factors that may contribute to a vitamin D deficiency, including reduced exposure to sunlight, inadequate diet, and side effects from medications metabolized by the liver. Research evidence suggests that vitamin D supplements can help to maintain bone mineral density in the legs after SCI. Your health care team should measure and monitor your vitamin D serum level to ensure it remains in the optimal range.
There are currently no SCI guidelines on vitamin D intake. In Canada, the general recommendation for adults is to consume 600 IU of vitamin D each day or 800 IU each day for those older than 70 years. Osteoporosis Canada recommends that people with osteoporosis, multiple fractures, or conditions affecting vitamin D absorption should aim for 800-2000 IU each day. Intakes greater than 4000 IU per day are not recommended to prevent adverse effects associated with excessive levels of calcium due to its increased absorption by vitamin D.
2. Adequate, but not too much Calcium intake
Calcium is the main mineral in bone and is a common supplement used to treat women with osteoporosis after menopause. Current evidence suggests that calcium supplements alone do not reduce bone loss after SCI. However, calcium and vitamin D are used together to maintain bone density. Additionally, research suggests that high calcium intake achieved by using supplements may be linked to the development of coronary artery calcification (hardening of the heart arteries due to calcium build-up). Increasing calcium intake through food sources instead appeared to decrease this risk. As a result, dietary sources of calcium should be optimized first before considering supplementation.
There are currently no SCI guidelines on calcium intake. In Canada, the general recommendation for adults is to consume 1000-1200 mg of calcium each day or 1200 mg each day for those older than 70 years. Intakes greater than 2000-2500 mg per day are not recommended to prevent adverse effects such as bone pain and kidney stones. If you have stones in your bladder or kidney, calcium intake will need to be lower than that of your peers.
3. Drug Therapy
There are two main treatment approaches that can be taken to osteoporosis after SCI, depending on the length of time since the injury:
Early approaches
Bone loss happens at a faster rate during the first year after SCI, so treatments during this time focus on preventing the loss of bone mineral density by slowing the rate of bone loss. Early treatment may involve oral bisphosphonate medications, which are often started within the first 3 months after injury.
Later approaches
If sublesional osteoporosis occurs of the hip and knee regions (usually after the first year), later treatment seeks to keep or increase hip or knee region bone mineral density. Treatments during this period may include bisphosphonate medications, Denosumab, or Recombinant Parathyroid Hormone (PTH), supplements, and physical treatments. These treatments are based on the assumption that regional increases in bone density will result in a lower fracture risk.
Bisphosphonate medications are a family of drugs used to prevent the loss of bone mineral density. These drugs work by slowing the breakdown of bone or bone resorption. There are several drugs within this group, including Etidronate (Didrocal), Alendronate (Fosamax), Risedronate (Actonel), Clodronate (Bonefos, Clastion), and Tiludronate (Skelid). These drugs may be taken by mouth or through an intravenous (IV) line.
Bisphosphonate medications are often prescribed early after SCI to prevent declines in bone density during the first year. Research evidence has mostly supported that bisphosphonate medications help to reduce bone mineral density loss in the hip and knee regions during the first year after SCI. These medications appear to be more effective when given earlier after SCI.
Bisphosphonates are also used to treat existing bone loss after SCI. One research study has shown that Alendronate is effective for maintaining or increasing bone mineral density later after SCI.
Despite support from research, there are still many things about the use of bisphosphonates after SCI that we do not know, such as their long-term effects and what the best length of treatment is. Bisphosphonate medications may also have side effects (such as heartburn, stomach upset, racing heart, jaw or thigh pain), drug interactions, and specific instructions for use that should be discussed in detail with your health providers before taking the medications.
For more detailed information about bisphosphonate medications, see SCIRE Professional’s module on Bone Heath.
There are a number of physical treatment options that have been proposed for preventing and treating bone loss after SCI, however, the evidence does not support their regular use in treating bone loss after SCI.
FES can be applied to the leg muscles during assisted walking.11
Functional electrical stimulation
Functional electrical stimulation (FES) is a treatment that applies electrical stimulation to the muscles during activities like standing, walking, or cycling. This treatment involves repeated pulling of the muscles on bones, which could help to strengthen the bones.
There is evidence suggesting that functional electrical stimulation cycling does not prevent bone loss in the lower leg early after SCI but may help to increase bone mineral density in stimulated areas of the leg during the later period after SCI. However, the stimulation needs to be ongoing or the benefits will be lost.
SCIRE Community provides additional detailed information about FES following SCI.
Electrical stimulation
Electrical stimulation to the muscles without functional activities may also be used. There is evidence suggesting that electrical stimulation can maintain or increase bone density over the stimulated areas. However, other studies have shown that the effects of electrical stimulation may return to baseline density within a few months after the treatment has ended.
Weight-bearing activities (standing and walking)
More research is needed to support weight-bearing activities for osteoporosis prevention.12
Weight-bearing activities are activities where the weight of the body is supported through the bones. Weight-bearing has long been considered to have an important role in bone health because it causes compression of the bones that may stimulate bone strengthening.
Weight-bearing treatments after SCI may include a variety of standing and walking activities, such as standing frames, braces, standing with functional electrical stimulation, and treadmill training.
Current evidence for weight-bearing activities for maintaining or improving bone health after SCI is inconclusive and needs further study.
Physical Activity
Physical activity is thought to improve bone health through a variety of processes that cause an increase in bone density. However, there is currently no evidence to support physical activity as a treatment for low bone density after SCI.
Therapies have been found to be ineffective:
Therapeutic ultrasound
Therapeutic ultrasound is a treatment that uses ultrasonic waves to provide energy to tissues deep within the body. Scientists have studied whether this treatment could provide stimulation to the bones to help prevent bone loss after SCI. However, current evidence suggests that therapeutic ultrasound is not effective for preventing bone loss after SCI.
Vibration exercise
Vibration exercise is a treatment that involves mechanical vibration of the body during resistance exercises. Current evidence suggests that vibration training is not effective for treating bone loss in the arms after SCI.
After SCI, low bone density implies an increased fracture risk. All of the current therapies are aimed at increasing bone mass and reducing your future risk of fracture.
Bisphosphonate medications are effective for preventing and treating bone loss after SCI and are usually started early after SCI onset. Non-drug physical treatments are not supported by current evidence for treating bone loss after SCI.
It is important to discuss any questions of concerns that you have about your treatment options in detail with your health providers to find the best management options for you. For a review of how we assess evidence at SCIRE Community and advice on making decisions, please see SCIRE Community Evidence.
Parts of this page have been adapted from the SCIRE Professional “Bone Health” Module:
Craven C, Lynch CL, Eng JJ (2014). Bone Health Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors. Spinal Cord Injury Rehabilitation Evidence. Version 5.0. Vancouver: p 1- 37.
Available from: https://scireproject.com/evidence/bone-health/
Astorino TA, Harness ET and Witzke KA. Effect of chronic activity-based therapy on bone mineral density and bone turnover in persons with spinal cord injury. Eur J Appl Physiol 2013; 113: 3027- 3037.
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Bauman WA, Spungen AM. Coronary heart disease in individuals with spinal cord injury. Spinal Cord 2008;46:466-76.
Bauman WA, Morrison NG, Spungen AM. Vitamin D replacement therapy in persons with spinal cord injury. J Spinal Cord Med 2005;28:203-7.
Bauman WA, Spungen AM, Adkins RH, Kemp BJ. Metabolic and endocrine changes in persons aging with spinal cord injury. Assist Technol 1999c;11(2):88-96.
Bauman WA, Spungen AM, Zhong YG, Mobbs CV. Plasma leptin is directly related to body adiposity in subjects with spinal cord injury. Horm Metab Res 1997;28:732-6.
Bauman WA, Zhong YG, Schwartz E. Vitamin D deficiency in veterans with chronic spinal cord injury. Metabolism 1995;44:1612-6.
Bauman WA, Spungen AM, Raza M, Tothstein J, Zhang RL, Zhong YG, et al. Coronary artery disease: metabolic risk factors and latent disease in individuals with paraplegia. Mt Sinai J Med 1992;59:163-8.
Belanger M, Stein RB, Wheeler GD, Gordon T, Leduc B. Electrical stimulation: can it increase muscle strength and reverse osteopenia in spinal cord injured individuals? Arch Phys Med Rehabil 2000;8:1090-1098.
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Chain A, Koury JC, and Bezerra FF. Physical activity benefits bone density and bone-related hormones in adult men with cervical spinal cord injury. Eur J Appl Physiol 2012; 112: 3179-3186
Chen SC, Lai CH, Chan WP, Huang MH, Tsai HW, Chen JJ. Increases in bone mineral density after functional electrical stimulation cycling exercises in spinal cord injured patients. Disabil Rehabil 2005;27:1337-1341.
Cherniak EP, Levis S, Troen BR. Hypovitaminosis D: A stealthy epidemic that requires treatment. Geriatrics 2008;63:24-30.
Craven BC Robertson LA, McGillivray CF , and Adachi JD . Detection and treatment of sublesional osteoporosis after people with spinal cord injury Topics in SCI Rehabil 2009: 14(4):1-22.
Dudley-Javoroski S, Saha PK, Liang G, Li C, Gao Z, and Shields RK. High dose compressive loads attenuate bone mineral loss in humans with spinal cord injury. Osteoporos Int 2012; 23:2335- 2346.
Dudley-Javoroski S, and Shields RK. Active-resisted stance modulates regional bone mineral density in humans with spinal cord injury. Journal of Spinal Cord Medicine 2013; 36: 191-199.
Dudley-Javoroski S, and Shields RK. Asymmetric bone adaptations to soleus mechanical loading after spinal cord injury. J Musculoskelet Neuronal Interact. 2008;8:227-38.
Dudley-Javoroski S, and Shields RK. Does estimation and surveillance of mechanical loading interventions for bone loss after spinal cord injury. Phys Ther 2008; 88: 387-96.
Eser P, de Bruin ED, Telley I, Lechner HE, Knecht H, Stussi E. Effect of electrical stimulation-induced cycling on bone mineral density in spinal cord-injured patients. Eur J Clin Invest 2003;33:412-419.
Eser P, Frotzler A, Zehnder Y, Denoth J. Fracture threshold in the femur and tibia of people with spinal cord injury as determined by peripheral quantitative computed tomography. Arch Phys Med Rehabil. 2005;86:498-504.
Eser P, Schiessl H, Willnecker J. Bone loss and steady state after spinal cord injury: a cross-sectional study using pQCT. Journal of Musculoskeletal Neuronal Interactions 2004;4:197-198
Ford ES, Ajani UA, McGuire LC, Liu S. Concentrations of serum vitamin D and the metabolic syndrome among U.S. adults. Diabetes Care 2005;28:1228-30.
Frotzler A, Coupaud S, Perret C, Kakebeeke TH, Hunt KJ, Eser P. Effect of detraining on bone and muscle tissue in subjects with chronic spinal cord injury after a period of electrically-stimulated cycling: A small cohort study. Journal of Rehabilitation Medicine 2009; 41: 282-285.
Giangregorio LM, Hicks AL, Webber CE, Phillips SM, Craven BC, Bugaresti JM, et al. Body weight supported treadmill training in acute spinal cord injury: impact on muscle and bone. Spinal Cord 2005;43:649-657.
Giangregorio LM, Webber CE, Phillips SM, Hicks AL, Craven BC, Bugaresti JM, et al. Can body weight supported treadmill training increase bone mass and reverse muscle atrophy in individuals with chronic incomplete spinal cord injury? Appl Physiol Nutr Metab. 2006;31:283-291.
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Image credits:
- Osteoparoz by Aisha Huseynova. CC BY-SA 4.0, via Wikimedia Commons.
- Cdm hip fracture 343 by Booyabazooka. CC BY-SA 3.0, via Wikimedia Commons.
- Soy Beans by Jessica and Lon Binder. CC BY-NC-ND 2.0, via Flickr.
- Steamed Kale by Laurel F. CC BY-SA 2.0, via Flickr.
- Broccoli by Steffen Zahn. CC BY 2.0, via Flickr.
- Shiitake Chinese Mushrooms by Artizone. CC BY-NC-ND 2.0, via Flickr.
- Fracture by fahmionline, ID. CC BY 3.0 US, via The Noun Project.
- Bone density machine by bwaters23. CC BY-NC-SA 2.0, via Flickr.
- Vitamin D pills by Laura Dahl. CC BY-NC-ND 2.0, via Flickr.
- Bone density by Eucalyp. [CC BY 3.0 US.
- Functional Electrical Stimulation Therapy for walking ©MilosRPopovic, CC BY-SA 4.0.
- Body weight-supported treadmill training with HAL Robot Suit exoskeleton by Oliver Jansen. CC BY-NC-ND 4.0.
Author: SCIRE Community Team | Reviewer: Shannon Sproule | Published: 10 October 2017 | Updated: ~
Functional electrical stimulation is a treatment that activates muscles below the spinal cord injury (SCI) during exercise and activity. This page outlines basic information about functional electrical stimulation and its use for movement and strength after SCI.
Key Points
- Electrical stimulation can be used to activate muscles that are weak or paralyzed after an SCI.
- Functional electrical stimulation (FES) involves stimulating the muscles during an activity like exercise or movement.
- FES is relatively safe and widely available treatment option for improving muscle strength and fitness after SCI.
- Overall, the research evidence suggests that FES is most likely effective for improving muscle strength after SCI. It may also improve fitness, walking skills, bone density and other symptoms, although more high quality research is needed to confirm.
Functional electrical stimulation (FES) is a type of neuromodulation where electrical stimulation is applied to the nerves located outside the spinal cord and brain. This stimulation causes the muscles to contract and can assist with purposeful or functional movement in weak or paralyzed muscles.
FES is delivered using a variety of handheld or specialized commercial electrical therapy machines connected to electrodes that are placed on the skin’s surface. Systems are also available with implanted electrodes in the muscles, although this is very specialized and not widely available.
FES electrodes are placed on the leg muscles to be used during stationary cycling.1
Muscle stimulation is used for several reasons after SCI:
To promote movement and strength in weak or paralyzed muscles: Muscle stimulation is used early in rehabilitation to promote movement in muscles that are not moving or only producing a flicker of movement. It may promote recovery of movement function by assisting with normal movements and with repetition of movements.
To improve fitness and health: When FES is used as part of a rhythmic exercise like cycling, walking, or rowing, it can help to maintain health of the heart, lungs, and circulation. It may also help to maintain healthy bones.
To assist with functional movement activities like stepping, getting up to standing, and grasping: FES can be used to assist with purposeful movements by improving muscle contractions (for weakened muscles), mobility or range of movement as well as possibly decreasing spasticity.
To maintain muscle mass below the SCI: Regular use of FES may help to prevent muscle loss that happens when the muscles that are paralyzed are not used. Unless neurological return occurs this improvement will stop if the FES is discontinued.
To control the muscles of breathing and bladder function: This includes the use of surgically implanted diaphragmatic pacers (FES systems that create muscle contractions in the diaphragm to stimulate regular breaths) and bladder control systems (FES systems that stimulate the muscles of urination). However, this page will focus on FES used for movement and strength after SCI.
Watch our YouTube video about FES!
Other names for FES of muscles
You may hear other names for FES such as “neuromuscular electrical stimulation” (NMES) or simply “electrical stimulation” (ES). These terms are often used to refer to electrical stimulation of the muscles during more passive activities (like lying down or sitting), while ”FES” usually describes stimulation during purposeful activities like cycling or walking. However, in practice these terms are often used interchangeably to describe similar or related treatments and the goals of all are to promote strength, movement and function and decrease pain and spasticity.
There are a number of other neuromodulation techniques that are used for various purposes in SCI, including transcutaneous electrical nerve stimulation, sacral nerve stimulation, and intrathecal Baclofen, described in other SCIRE Community articles.
It is important to speak with a health provider about using FES to make sure it is safe and suitable for you and to learn how to use the equipment correctly.
FES is usually applied through electrodes that are placed on the surface of the skin, although electrodes can also be implanted into the muscles. Electrodes are placed over nerves or part of the muscles below the SCI that respond well to electrical stimulation. The electrodes are then attached to an adjustable machine that generates the stimulation. Your health provider will determine the settings that are used for the treatment and how long it will last.
The electrical stimulation is then gradually turned up until the muscles begin to tense or contract. Depending on your sensation, as the machine is turned up, you may feel pins and needles or other unusual sensations, which may take some time to get used to. The aim is to create a forceful but tolerable muscle contraction.
FES is applied through electrodes on the leg muscles during assisted walking.2
If the electrical stimulation goes well, it is then combined with a movement task. This may be as simple as lifting a wrist or ankle or more complex such as cycling on a stationary bike, rowing on a rowing machine, grasping, or stepping in parallel bars or a body weight support treadmill system.
The length of each session will vary depending on the goals of the treatment. Time may be required to enable your muscles to tolerate longer sessions as the muscles may fatigue quickly. Sessions are usually done several times per week for several weeks to gain training benefits.
Your health provider will monitor your response to the treatment and inspect the skin for any redness or irritation after the treatment has ended. Once you have learned to use FES safely, you may be able to use it on your own.
Our bodies naturally use electrical signals as part of the nervous system. When we move, the brain generates and sends electrical impulses along the spinal cord and nerves to tell the muscles to move.
Spinal cord injury can interrupt this pathway, preventing electrical impulses from passing through the spinal cord to reach the muscles. However, if the nerves and muscles below the injury are not damaged, they can still respond to electrical signals.
FES electrodes are placed over nerves or over electrically-sensitive parts of the muscles below the SCI. The specific type of electrical stimulation used with FES can trigger the nerve cells of movement (motor neurons) to send signals that cause muscle movement. An intact peripheral nerve and healthy muscle tissue are required to enable the external source of electricity to facilitate muscle contraction.
FES does not work for nerve injuries outside the spinal cord
FES can only be used for muscle weakness or paralysis caused by injuries to the spinal cord, but not injuries to the conus medullaris, cauda equina, or the nerves outside of the spinal cord. The nerve cells in these structures (called lower motor neurons) must to be intact for FES to work.
Like exercise, regular treatment with FES is usually needed to maintain the effects of the treatment. For people with complete injuries, when FES treatments are stopped, the treatment effects will usually go away over time. For people with incomplete injuries, the goal is for some carryover of strength and movement be retained after the treatment is stopped.
There are some situations in which FES may be unsafe to use. This not a complete list, speak to a health provider about your health history and whether FES is safe for you.
FES should not be used in the following situations:
- Near implanted medical devices like heart pacemakers
- On areas of active cancer, or by people with bleeding disorders or other major medical conditions
- On areas with blood clots, bleeding, damaged skin, infection, or poor circulation
- By pregnant women
- Electrodes should not be placed over the eyes, through the head, through the chest or abdomen, or on the front of the neck or genitals
- By people with recent broken bones
- By people with damage to the nerves or muscles near the area where FES is used
FES should be used with caution in the following situations:
FES is often used with the following conditions after SCI but should be monitored closely. Speak to your health provider for more information.
- By people who have had seizures
- By people prone to severe autonomic dysreflexia (people with cervical and thoracic injuries)
- By people with uncontrolled spasticity
- By people with severe osteoporosis
- In areas where heterotopic ossification causes restricted movement
- In areas with reduced or absent sensation (below the level of injury)
- By people who are unable to follow instructions or provide accurate feedback
FES is generally well tolerated by people who can use it safely (see above for when FES may be unsafe). Serious medical complications from FES are rare. However, there are risks and side effects that should be discussed with a health provider before using FES.
More common risks and side effects of FES include:
- Discomfort or pain
- Skin redness or irritation
- Nausea, light-headedness, or autonomic dysreflexia
Other less common risks and side effects of FES include:
- Mild electrical burns near the electrodes
- Skin breakdown near the electrodes
- Fainting
- Worsening of muscle spasms (spasticity)
- Muscle and joint injuries, such as joint swelling or muscle strains
- Broken bones
- Mild electrical shocks (from improper use or faulty equipment)
In some cases, risks and side effects may be caused by improper use of the equipment. It is essential to learn to use the equipment from a health provider and to only use FES according to their direction and with the settings that they recommend.
For some people, side effects of FES may be stronger at first, but as their body gets used to FES with repeated treatments, their physical reactions may reduce over time.
Several studies have shown that FES helps to improve strength and fitness after SCI.
Strength
Studies have shown that both FES arm exercise and FES cycling helps to maintain or improve strength after SCI. However, FES cycling may be more effective for maintaining strength after injury than improving strength that has already been lost. This is supported by moderate evidence from five studies.
Cardiovascular fitness
Fifteen studies have looked at FES for improving many different aspects of fitness after SCI. Taken altogether, these studies provide weak evidence that FES training done at least 3 days per week for 2 months helps to improve many aspects of cardiovascular fitness after SCI.
Walking
Studies show that FES improves walking speed and distance in people with both incomplete and complete SCI. Some of these studies also showed that regular use of FES carried over to improve walking even without FES. This is supported by weak evidence from eight studies.
The effects of FES treatment may also help to prevent complications of SCI like pressure sores, bone loss, spasticity, and orthostatic hypotension. These benefits may accompany gains in strength or fitness related to FES treatment.
Pressure sores
Although it is commonly thought that increased muscle bulk from FES will reduce the risk of pressure sores, there are not very many studies which have looked at whether this actually happens. One study provides weak evidence that FES cycling for 2 years reduced the number of pressure ulcers that occurred after SCI. Another study showed that regular FES cycling showed a trend toward reducing seat pressures.
Bone health
Research studies show that FES cycling does not prevent bone loss after SCI (moderate evidence from two studies). However, it may help to increase bone density that has already been lost, although the evidence for this is conflicting (based on six studies). It is not clear whether any gains in bone density last long-term or if continued FES treatment is needed for them to be maintained.
For more information on bone density, read our article about Osteoporosis.
Spasticity
It is not clear what effects FES has on spasticity after SCI. There is conflicting evidence from three studies about whether FES cycling can help to reduce spasticity after SCI.
Click here for our article on Spasticity.
Orthostatic hypotension
Three studies provide moderate evidence that FES of the legs during a single change in position reduced orthostatic hypotension. However, this only shows that FES prevents orthostatic hypotension while it is applied, and further research is needed to look at what benefits this could have to people living with SCI.
Overall, the research evidence suggests that FES is most likely effective for improving muscle strength after SCI. It may also have effects on fitness, walking skills, bone density, skin health, spasticity, and orthostatic hypotension, although more high quality research is needed to confirm. FES appears to be safe when used appropriately and is widely available in most rehabilitation settings. Discuss this treatment with your health providers to find out if it is a suitable treatment option for you.
For a review of how we assess evidence at SCIRE Community and advice on making decisions, please see SCIRE Community Evidence.
Parts of this page have been adapted from the SCIRE Professional “Lower Limb”, “Upper Limb”, “Bone Health”, “Cardiovascular Health and Exercise”, “Orthostatic Hypotension”, “Pressure Ulcers”, and “Spasticity” chapters:
Lam T, Wolfe DL, Domingo A, Eng JJ, Sproule S (2014). Lower Limb Rehabilitation Following Spinal Cord Injury. In: Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors. Spinal Cord Injury Rehabilitation Evidence. Version 5.0. Vancouver: p 1-74.
Available from: http://scireproject.com/evidence/lower-limb/
Connolly SJ, McIntyre A, Mehta, S, Foulon BL, Teasell RW. (2014). Upper Limb Rehabilitation Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors. Spinal Cord Injury Rehabilitation Evidence. Version 5.0: p 1-77.
Available from: http://scireproject.com/evidence/upper-limb/
Craven C, Lynch CL, Eng JJ (2014). Bone Health Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors. Spinal Cord Injury Rehabilitation Evidence. Version 5.0. Vancouver: p 1- 37.
Available from: https://scireproject.com/evidence/bone-health/
Warburton DER, Krassioukov A, Sproule S, Eng JJ (2014). Cardiovascular Health and Exercise Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors. Spinal Cord Injury Rehabilitation Evidence. Version 5.0. Vancouver: p. 1-48.
Available from: https://scireproject.com/evidence/cardiovascular-health-and-exercise/
Krassioukov A, Wecht JM, Teasell RW, Eng JJ (2014). Orthostatic Hypotension Following Spinal Cord Injury. In: Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors. Spinal Cord Injury Rehabilitation Evidence. Version 5.0. Vancouver: p. 1-26.
Available from: https://scireproject.com/evidence/orthostatic-hypotension/
Hsieh J, McIntyre A, Wolfe D, Lala D, Titus L, Campbell K, Teasell R. (2014). Pressure Ulcers Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Noonan VK, Loh E, McIntyre A, editors. Spinal Cord Injury Rehabilitation Evidence. Version 5.0. 1-90.
Available from: https://scireproject.com/evidence/skin-integrity-and-pressure-injuries/
Hsieh JTC, Connolly SJ, McIntyre A, Townson AF, Short C, Mills P, Vu V, Benton B, Wolfe DL (2016). Spasticity Following Spinal Cord Injury. In Eng JJ, Teasell RW, Miller WC, Wolfe DL, Townson AF, Hsieh JTC, Connolly SJ, Curt A, Mehta S, Sakakibara BM, editors. Spinal Cord Injury Rehabilitation Evidence. Version 6.0.
Available from: https://scireproject.com/evidence/spasticity/
Evidence for “Strength” is based on the following studies:
[1] Baldi JC, Jackson RD, Moraille R, and Mysiw WJ. Muscle atrophy is prevented in patients with acute spinal cord injury using functional electrical stimulation. Spinal Cord 1998;36:463-469.
[2] Scremin AM, Kurta L, Gentili A, Wiseman B, Perell K, Kunkel C, and Scremin OU. Increasing muscle mass in spinal cord injured persons with a functional electrical stimulation exercise program. Arch Phys Med Rehabil 1999;80:1531-1536.
[3] Crameri RM, Weston A, Climstein M, Davis GM, and Sutton JR. Effects of electrical stimulation-induced leg training on skeletal muscle adaptability in spinal cord injury. Scand J Med Sci Sports 2002;12:316-322.
[4] Gerrits HL, de Haan A, Sargeant AJ, Dallmeijer A, and Hopman MT. Altered contractile properties of the quadriceps muscle in people with spinal cord injury following functional electrical stimulated cycle training. Spinal Cord 2000;38:214-223.
[5] Needham-Shropshire BM, Broton JG, Cameron TL, Klose J. Improved motor function in tetraplegics following neuromuscular stimulation-assisted arm ergometry. J Spinal Cord Med 1997;20:49-55.
[6] Cameron T, Broton JG, Needham-Shropshire B, Klose KJ. An upper body exercise system incorporating resistive exercise and neuromuscular electrical stimulation (nms). J Spinal Cord Med 1998;21:1-6.
Evidence for “Cardiovascular Fitness” based on:
[1] Berry HR, Kakebeeke TH, Donaldson N, Perret C, Hunt KJ. Energetics of paraplegic cycling: adaptation to 12 months of high volume training. Technology and Health Care 2012; 20: 73-84.
[2] Griffin L, Decker MJ, Hwang JY, Wang B, Kitchen K, Ding Z, et al. Functional electrical stimulation cycling improves body composition, metabolic and neural factors in persons with spinal cord injury. J Electromyogr Kinesiol 2009;19(4):614-22.
[3] Zbogar D, Eng JJ, Krassioukov AV, Scott JM, Esch BT, Warburton DE. The effects of functional electrical stimulation leg cycle ergometry training on arterial compliance in individuals with spinal cord injury. Spinal Cord 2008;46(11):722-6.
[4] Crameri RM, Cooper P, Sinclair PJ, Bryant G, Weston A. Effect of load during electrical stimulation training in spinal cord injury. Muscle Nerve 2004;29(1):104-11.
[5] Hjeltnes N, Aksnes AK, Birkeland KI, Johansen J, Lannem A, Wallberg-Henriksson H. Improved body composition after 8 wk of electrically stimulated leg cycling in tetraplegic patients. Am J Physiol 1997;273(3 Pt 2):R1072-9.
[6] Mohr T, Andersen JL, Biering-Sorensen F, Galbo H, Bangsbo J, Wagner A, et al. Long-term adaptation to electrically induced cycle training in severe spinal cord injured individuals. Spinal Cord 1997;35(1):1-16.
[7] Barstow TJ, Scremin AM, Mutton DL, Kunkel CF, Cagle TG, Whipp BJ. Changes in gas exchange kinetics with training in patients with spinal cord injury. Med Sci Sports Exerc 1996;28(10):1221-8.
[8] Faghri PD, Glaser RM, Figoni SF. Functional electrical stimulation leg cycle ergometer exercise: training effects on cardiorespiratory responses of spinal cord injured subjects at rest and during submaximal exercise. Arch Phys Med Rehabil 1992;73(11):1085-93.
[9] Hooker SP, Figoni SF, Rodgers MM, Glaser RM, Mathews T, Suryaprasad AG, et al. Physiologic effects of electrical stimulation leg cycle exercise training in spinal cord injured persons. Arch Phys Med Rehabil 1992;73(5):470-6.
[10] Gerrits HL, de Haan A, Sargeant AJ, van Langen H, Hopman MT. Peripheral vascular changes after electrically stimulated cycle training in people with spinal cord injury. Arch Phys Med Rehabil 2001;82(6):832-9.
[11] Ragnarsson KT, Pollack S, O’Daniel W, Jr., Edgar R, Petrofsky J, Nash MS. Clinical evaluation of computerized functional electrical stimulation after spinal cord injury: a multicenter pilot study. Arch Phys Med Rehabil 1988;69(9):672-7.
[12] Taylor JA, Picard G, Widrick JJ. Aerobic capacity with hybrid FES rowing in spinal cord injury: comparison with arms-only exercise and preliminary findings with regular training. PM R 2011;3(9):817-24.
[13] Kahn NN, Feldman SP, Bauman WA. Lower-extremity functional electrical stimulation decreases platelet aggregation and blood coagulation in persons with chronic spinal cord injury: a pilot study. J Spinal Cord Med 2010;33(2): 150-8.
[14] Hakansson NA, Hull ML. Can the efficacy of electrically stimulating pedaling using a commercially available ergometer be improved by minimizing the muscle stress-time integral? Muscle Nerve 2012; 45:393-402.
Evidence for “Walking” is based on the following studies:
[1] Thrasher TA, Flett HM, and Popovic MR. Gait training regimen for incomplete spinal cord injury using functional electrical stimulation. Spinal Cord 2006;44:357-361.
[2] Ladouceur M, and Barbeau H. Functional electrical stimulation-assisted walking for persons with incomplete spinal injuries: changes in the kinematics and physiological cost of overground walking. Scand J Rehabil Med 2000a;32:72-79.
[3] Ladouceur M, and Barbeau H. Functional electrical stimulation-assisted walking for persons with incomplete spinal injuries: longitudinal changes in maximal overground walking speed. Scand J Rehabil Med 2000b;32:28-36.
[4] Wieler M, Stein RB, Ladouceur M, Whittaker M, Smith AW, Naaman S, Barbeau H, Bugaresti J, and Aimone E. Multicenter evaluation of electrical stimulation systems for walking. Arch Phys Med Rehabil 1999;80:495-500.
[5] Klose KJ, Jacobs PL, Broton JG, Guest RS, Needham-Shropshire BM, Lebwohl N, Nash MS, and Green BA. Evaluation of a training program for persons with SCI paraplegia using the Parastep 1 ambulation system: part 1. Ambulation performance and anthropometric measures. Arch Phys Med Rehabil 1997;78:789-793.
[6] Granat MH, Ferguson AC, Andrews BJ, and Delargy M. The role of functional electrical stimulation in the rehabilitation of patients with incomplete spinal cord injury–observed benefits during gait studies. Paraplegia 1993;31:207-215.
[7] Stein RB, Belanger M, Wheeler G, Wieler M, Popovic DB, Prochazka A, and Davis LA. Electrical systems for improving locomotion after incomplete spinal cord injury: an assessment. Arch Phys Med Rehabil 1993;74:954-959.
[8] Granat M, Keating JF, Smith AC, Delargy M, and Andrews BJ. The use of functional electrical stimulation to assist gait in patients with incomplete spinal cord injury. Disabil Rehabil 1992;14:93-97.
Evidence for “Bone health” is based on the following studies:
[1] Eser P, de Bruin ED, Telley I, Lechner HE, Knecht H, Stussi E. Effect of electrical stimulation-induced cycling on bone mineral density in spinal cord-injured patients. Eur J Clin Invest 2003;33:412-419.
[2] Lai CH, Chang WHS, Chan WP, Peng CW, Shen LK, Chen JJJ, Chen SC. Effects of Functional Electrical Stimulation Cycling Exercise on Bone Mineral Density Loss in the Early Stages of Spinal Cord Injury. J Rehabil Med 2010; 42:150-154.
[3] Mohr T, Podenphant J, Biering-Sorensen F, Galbo H, Thamsborg G, Kjaer M. Increased bone mineral density after prolonged electrically induced cycle training of paralyzed limbs in spinal cord injured man. Calcif Tissue Int 1997;61:22-25.
[4] Chen SC, Lai CH, Chan WP, Huang MH, Tsai HW, Chen JJ. Increases in bone mineral density after functional electrical stimulation cycling exercises in spinal cord injured patients. Disabil Rehabil 2005;27:1337-1341.
[5] Frotzler A, Coupaud S, Perret C, Kakebeeke TH, Hunt KJ, Donaldson Nde N, Eser P. High-volume FES-cycling partially reverses bone loss in people with chronic spinal cord injury. Bone. 2008 Jul;43(1):169-76. Epub 2008 Mar 20.
[6] Pacy PJ, Hesp R, Halliday DA, Katz D, Cameron G, Reeve J. Muscle and bone in paraplegic patients, and the effect of functional electrical stimulation. Clin Sci (Lond) 1988;75:481-487.
[7] Leeds EM, Klose J, Ganz W, Serafini A, Green BA. Bone mineral density after bicycle ergometry training. Archives of Physical Medicine and Rehabilitation 1990;71:207-9.
[8] BeDell KK, Scremin AM, Perell KL, Kunkel CF. Effects of functional electrical stimulation-induced lower extremity cycling on bone density of spinal cord-injured patients. Am J Phys Med Rehabil 1996;75:29-34.
Evidence for “Pressure Ulcers” is based on the following studies:
[1] Dolbow DR, Gorgey AS, Dolbow JD, Gater DR. Seat pressure changes after eight weeks of functional electrical stimulation cycling: a pilot study. Top Spinal Cord Inj Rehabil. 2013 Summer;19(3):222-8.
[2] Petrofsky JS. Functional electrical stimulation, a two year study. J Rehabil. 1992;58(3):29–34
Evidence for “Spasticity” is based on the following studies:
[1] Kapadia N, Masani K, Craven B, et al. A randomized trial of functional electrical stimulation for walking in incomplete spinal cord injury: Effects on walking competency. J Spinal Cord Med 2014;37:511-24.
[2] Manella K & Field-Fote E. Modulatory effects of locomotor training on extensor spasticity in individuals with motor-incomplete spinal cord injury. Restor Neurol Neurosci 2013;31:633-46.
[3] Ralston K, Harvey L, Batty J, et al. Functional electrical stimulation cycling has no clear effect on urine output, lower limb swelling, and spasticity in people with spinal cord injury: A randomised cross-over trial. J Physiother 2013;59:237-43.
[4] Kuhn D, Leichtfried V, Schobersberger W. Four weeks of functional electrical stimulated cycling after spinal cord injury: a clinical cohort study. Inter J Rehabil Res 2014;37:243-50.
[5] Mazzoleni S, Stampacchia G, Gerini A, Tombini T, Carrozza M. FES-cycling training in spinal cord injured patients. Eng Med Biol Soc 2013:5339-41.
[6] Sadowsky C, Hammond E, Strohl A, et al. Lower extremity functional electrical stimulation cycling promotes physical and functional recovery in chronic spinal cord injury. J Spinal Cord Med 2013;36:623-31.
[7] Reichenfelser W, Hackl H, Hufgard J, Kastner J, Gstaltner K, Gföhler M. Monitoring of spasticity and functional ability in individuals with incomplete spinal cord injury with a functional electrical stimulation cycling system. J Rehabil Med 2012;44:444-9.
[8] Krause P, Szecsi J, Straube A. Changes in spastic muscle tone increase in patients with spinal cord injury using functional electrical stimulation and passive leg movements. Clin Rehabil 2008;22:627-34.
[9] Mirbagheri M, Ladouceur M, Barbeau H, Kearney R. The effects of long-term FES-assisted walking on intrinsic and reflex dynamic stiffness in spastic spinal-cord-injured
[10] Granat M, Ferguson A, Andrews B, Delargy M. The role of functional electrical stimulation in the rehabilitation of patients with incomplete spinal cord injury–observed benefits during gait studies. Paraplegia 1993;31:207-15.
[11] Thoumie P, Le C, Beillot J, Dassonville J, Chevalier T, Perrouin-Verbe B et al. Restoration of functional gait in paraplegic patients with the RGO-II hybrid orthosis. A multicenter controlled study. II: Physiological evaluation. Paraplegia 1995;33:654-9.
Evidence for “Orthostatic Hypotension” is based on the following studies:
[1] Faghri PD, Yount J. Electrically induced and voluntary activation of physiologic muscle pump: a comparison between spinal cord-injured and able-bodied individuals. Clin Rehabil 2002;16:878-885.
[2] Elokda AS, Nielsen DH, Shields RK. Effect of functional neuromuscular stimulation on postural related orthostatic stress in individuals with acute spinal cord injury. J Rehabil Res Dev 2000;37:535-542.
[3] Sampson EE, Burnham RS, Andrews BJ. Functional electrical stimulation effect on orthostatic hypotension after spinal cord injury. Arch Phys Med Rehabil 2000; 81: 139-143.
Other references:
Electrophysical Agents – Contraindications And Precautions: An Evidence-Based Approach To Clinical Decision Making In Physical Therapy. Physiother Can. 2010 Fall;62(5):1-80.
Gibbons RS, Shave RE, Gall A, Andrews BJ. FES-rowing in tetraplegia: a preliminary report. Spinal Cord. 2014 Dec;52(12):880-6.
Martin R, Sadowsky C, Obst K, Meyer B, McDonald J. Functional electrical stimulation in spinal cord injury: from theory to practice. Top Spinal Cord Inj Rehabil. 2012 Winter;18(1):28-33.
Warms CA, Backus D, Rajan S, Bombardier CH, Schomer KG, Burns SP. Adverse events in cardiovascular-related training programs in people with spinal cord injury: a systematic review. J Spinal Cord Med. 2014 Nov;37(6):672-92.
Image credits
- E-Stim Therapy ©Rankn Jordan, CC BY-NC-SA 2.0
- Functional electrical stimulation ©MilosRPopovic, CC BY-SA 4.0
- Image by SCIRE Community Team
- Checklist ©lastspark,CC BY 3.0 US
- Muscle © Smalllike, CC BY 3.0 US
- cardio ©emma Mitchell, CC BY 3.0 US
- Image by SCIRE Team.
- Image by SCIRE Team.
- fracture ©fahmionline, CC BY 3.0 US
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