Musculoskeletal pain occurs in 50% to 81% of people living with spinal cord injury. Pain can have a significantly limiting impact. Pain can lead to decreased mobility, endurance, social participation, and depression. Additionally, many people living with spinal cord injury (SCI) rely on their upper body for ADLs (activities of daily living) which may result in decreased independence in cases of severe pain. Musculoskeletal impairments associated with spinal cord injury include decreased muscle mass and bone density, spasticity, contractures, as well as overuse injuries in muscles, tendons, and joints. These issues can contribute to pain and morbidity in patients with SCI. However, there is a lack of research on the risk of developing these conditions in the SCI population. This article aims to investigate and outline the common MSK conditions after SCI. Other musculoskeletal impairments that can often be found in patients with SCI include but are not limited to muscle atrophy, osteoporosis, fractures, spasticity, heterotopic ossification, tendinopathies, and mononeuropathies.
Key points
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Musculoskeletal (MSK) disorders in patients with spinal cord injury (SCI) are more common than patients with non-SCI and mainly caused by impairments in motor, sensory, and autonomic functions. These issues can persist throughout the patient’s life.
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The severity of MSK disorders can vary depending on the level and extent of the SCI injury. Common pathologies include muscle weakness, spasticity, contractures, and osteoporosis, which arise due to the lack of mobility and sensory input resulting from the spinal cord injury.
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Physical therapy and rehabilitation are essential to manage these MSK complications post-SCI to maintain muscle strength, flexibility, and bone density. Regular activity, assistive devices, and orthotics may help prevent, support mobility, and prevent further MSK complications.
Introduction
Musculoskeletal (MSK) pain disorders are common among people with spinal cord injury (SCI), affecting 50% to 81% of the SCI population. MSK-related pain can have a severe impact on their mobility, endurance, social participation, and mental health. Depending on the level and severity of the injury, people with SCI may rely on their upper body for activities of daily living (ADLs), making it hard for them to be independent when experiencing severe pain. Repetitive stress to muscles, ligaments, and tendons can also cause pain in the upper and lower extremities for those who can walk.
Musculoskeletal impairments associated with spinal cord injury include decreased muscle mass (sarcopenia) and bone density, spasticity, contractures, fractures, heterotopic ossification, mononeuropathies, overuse injuries in muscles, tendons, and joints, osteoarthritis, and myalgias. These conditions will be discussed in further detail later in discussion, and an overview of their treatment and prevention will be provided.
Muscle Atrophy
Skeletal muscle atrophy is a common issue that affects people with SCI. This atrophy occurs rapidly, typically within 6 weeks of the injury, due to the lack of use of the muscles below the level of the lesion. The phenotype of skeletal muscles can change depending on the type of mechanical loading or lack thereof, which is frequently observed in this patient population. As a result of physiologic changes to skeletal muscle, patients with SCI ultimately experience a loss of muscle volume and mass. It should be noted that age-related muscle loss and cachexia generally result in muscle atrophy through mechanisms that differ from those discussed here.
Preserving skeletal muscle integrity is essential for regulating metabolism and balance. After SCI, communication breakdown between the brain and muscles can cause changes in the structure of the muscle controlled by the motor neurons, leading to atrophy and fibrosis. Moreover, SCI delays the transmission speed of motor neuron axons, converting skeletal muscle fibers from slow-oxidative to fast-fatigue, fast-glycolysis fibers. Consequently, this leads to heightened muscle fibrosis and the accumulation of adipose tissue.
Physical exercise and hormonal therapy, such as testosterone and androgen therapy, are some of the treatments used to preserve muscle mass after SCI. The exercise training mentioned in the literature includes body weight-support treadmill training, robot-assisted mobility training, resistance training, and heavy-load strength training; depending on the severity and SCI level, these approaches might have limited results due to the heterogeneity of the SCI population.
There is evidence that nutrition might help reduce the effects of muscle atrophy after SCI. Antioxidants such as glutathione, glycine, and leucine can help minimize skeletal muscle injury and atrophy.
In some cases, spasticity may help preserve muscle mass in this patient population. Loss of muscle mass and decreased energy expenditure may contribute to a reduced metabolic rate, resulting in increased fat storage, and putting patients with SCI at higher risk of developing metabolic disorders.
Osteoporosis and Fractures
A common injury in spinal cord patients is fractures resulting from low bone mineral density at specific locations. Osteoporosis is a common condition in people with spinal cord injuries, characterized by reduced bone mineral density and the deterioration of bone microarchitecture, which ultimately leads to reduced bone strength. As a result, these individuals are at an increased risk of experiencing fragility fractures at specific load-bearing locations. Fractures in the lower extremities are usually caused by minor trauma, such as turning in bed or during transfers. These fractures can also lead to further clinical complications, including infections, increased spasticity, and autonomic dysreflexia. The typical rate of fractures observed in patients with spinal cord injuries is 2.2% during the first year following their initial injury. Up to 50%-60% of patients with motor complete injury will develop significant bone loss and fracture within the first 5 to 7 years after their initial injury. The anatomic location of these fractures in the lower extremities is typically in the distal femur and the proximal tibial. The spinal cord injury population develops osteoporotic fractures in the knee more frequently than in the help and pelvis, as seen in the general population. Lower extremity bone loss is seen in the tetraplegic and paraplegic population; however, upper extremity bone loss and fracture are only seen in the tetraplegic population due to immobilization. Women with spinal cord injury were reported to have a 1.6 times higher risk of long bone fractures compared with men with spinal cord injury as well, and this is thought to be due to the higher degree of bone loss in women overall.
There is little known about fracture characteristics and applied fracture treatment in the spinal cord injury population. Frotzler and colleagues conducted a study to classify long bone fractures, outline fracture management as well as describe fracture-related complications in individuals with a history of traumatic spinal cord injury. Most of these were simple, extra-articular fractures, and the patient’s AIS score did not significantly influence fracture characteristics. However, most patients enrolled in the study were AIS A or B. No fractures were documented in the upper limbs. Of the individuals enrolled in the study, 86% were found to have their first reported fracture 20 years after their initial injury. This correlates to previous studies showing that individuals with chronic spinal cord injury had reduced bone mineral density by 50% to 70% in lower extremity long bones. Counseling patients who have chronic spinal cord injury about the increased risk of long bone fractures in the lower extremities is imperative for further function and longevity.
Zleik and colleagues performed a systematic scoping review to identify fracture risk in spinal cord injury, treatment of osteoporosis, and management of osteoporotic fractures in this population. Their review found that the DEXA scan was most sensitive to evaluate low bone mineral density, especially if it is targeted at the femoral neck, distal femur, and proximal tibia, the most common fractures in the spinal cord population. DEXA scan is recommended every 2 years for continued surveillance of osteopenia and osteoporosis.
The Paralyzed Veteran’s Association (PVA) has outlined recommendations for patients to prevent complications from osteoporosis in spinal cord injury. Repeated loading of the skeletal system is vital in this population to maintain bone mass. The combination of active standing with or without neuromuscular electrical stimulation can aid in this process while a patient is undergoing physical therapy. Specifically, functional neuromuscular electrical stimulation applied in the lower extremities with cycling or rowing over a 9 to 12-month period was found to slow the process of bone mineral loss in the femur and tibia in patients with chronic spinal cord injury. However, further studies need to be performed to evaluate this therapeutic intervention. There is moderate-level evidence that bone mineral density (BMD) decline can be attenuated when NMES is delivered during passive weight bearing through the lower extremities in an erect posture with a load of approximately 70%-150% of body weight.
A combination of clinical and demographic factors identified a higher risk for osteoporotic fractures in spinal cord injury, such as being of Caucasian race, female sex, prior fracture history, medication use (corticosteroids, opioids, anticonvulsants), longer injury duration, paraplegia, and completeness of injury. Secondary causes of osteoporosis and spinal cord injury need to be ruled out.
The PVA clinical guidelines also outline studies involving multiple bisphosphonates to prevent bone loss. Alendronate was found in a randomized controlled trial to prevent bone loss at the femoral neck, trochanter, and pelvis at 12 and 18 months after treatment compared with placebo. Pamidronate IV has also been found to have attenuated bone loss 12 months after treatment; however, there was significant heterogeneity in the patient population within the randomized control trial. Several small trials evaluate zoledronic acid infusion during the first 90 days after acute spinal cord injury; however, most of these studies did not assess regional bone loss in the distal femur and proximal tibia, whereby bone loss is known to affect these areas the most.
One study has demonstrated improvements in bone mineral density when combining zoledronic acid and rowing exercise with physical therapy. This is clinically correlative to patients with spinal cord injury because increased bone mineral density around the distal femur and proximal tibia will decrease the rate of osteoporotic fracture.
In 2022, the Delphi Consensus Recommendations were published, providing guidelines for fracture management in patients with chronic spinal cord injury. Nonoperative management for lower extremity fractures has been commonly practiced; however, with patients wanting to maintain their independence and with improved therapeutic techniques, patients may be treated operatively. Management of pain following a lower extremity fracture should follow CanPain SCI guidelines. Skilled physical and occupational therapists should assess new needs to improve the function of these patients, such as adaptive strategies for transfers, mobility, and ambulation. Monitoring of complications after fracture should take place in outpatient follow-up, which includes heterotopic ossification, spasticity, autonomic dysreflexia, and neuropathic pain. Deep vein thrombosis prophylaxis should be initiated for a total of 2 to 4 weeks for acute fracture in patients with chronic spinal cord injury; however, this is a low-level recommendation.
Spasticity
Patients who suffer from spinal cord injury will likely experience hypertonicity changes depending on the severity and neurologic level of the lesion. Increased tone below the level of the spinal cord injury is thought to be caused by the disinhibited reflex arc preventing the relaxation of musculature. It affects about 80% of patients with spinal cord injury, especially those who suffer from cervical lesions and incomplete injuries. , These changes in tone can inhibit a patient from performing transfers, daily living, or ambulating. However, there are scenarios whereby patients are required to use their tone to perform specific tasks. An example of this may include quadriceps and hip flexor tone to aid in standing for transfers. Pain, increased body temperature, stress, or infection can influence breakthrough spasticity changes. As clinicians, it is important to understand the patient’s individual goal to use their increased tone to maximize their function.
Management of spasticity is a paradigm that goes from conservative to invasive. Therapy services have used muscle stretching since spasticity has been identified. Stretch is used daily to allow increased range of motion and joint mobility to improve function, and early stretching after the acute phase of spinal cord injury may help prevent joint contracture. The current recommendation for stretching protocol is indeterminate; however, given the severe consequences of contractures and threats of losing mobility with increased spastic changes, daily stretching is recommended for as long as practically possible for these patients. Stretching techniques may include bracing, casting, or splinting and should be used while the patient still maintains adequate mobility and extensibility of soft tissues.
There is inconclusive evidence that physical therapy interventions or types of therapeutic techniques are helpful for spasticity in spinal cord injury. Barbosa and colleagues conducted a systematic review to evaluate the efficacy of physical therapy for spasticity in spinal cord injury and found that 16 of the 17 trials included were inconclusive when compared with sham or differing physical therapy techniques. This raises awareness that physiotherapy may need to be further studied and identified in terms of its role in spasticity development and treatment.
Other nonpharmacologic interventions to manage spasticity include electro-neuromuscular stimulation with acupuncture, induced movement therapy, extracorporeal shock wave therapy, transcranial direct current stimulation in stroke, transcranial magnetic stimulation, and transcutaneous electrical nerve stimulation. Of these interventions, only electro-neuromuscular stimulation with acupuncture was shown to have moderate level evidence for spasticity management, while the remaining had low-quality evidence. Further high-quality evidence studies are required to evaluate these interventions’ role in spasticity for spinal cord patients.
Baclofen has been heavily used in the spinal cord population for spasticity. Dietz and colleagues conducted a systematic review evaluating the efficacy of baclofen on spasticity outcomes. Their review found that baclofen effectively improved spasticity outcome measures with increased efficacy through intrathecal administration. However, adverse oral and intrathecal baclofen events that affected the subject’s quality of life were reported. There is a lack of comparative trials between baclofen and alternative options. Further studies are warranted to help reduce the adverse effects of intrathecal baclofen or identify other intrathecal options to control spasticity. Baclofen has also been hypothesized to be influential in modulating spasticity and providing neuroprotection for patients with spinal cord injury.
Other pharmacologic options for spasticity management include tizanidine, dantrolene, and diazepam. According to a Cochrane Review conducted to assess the effectiveness of drugs used to treat long-term spasticity in patients with spinal cord injury, there were no superiority studies or head-to-head clinical trials to evaluate which medication is more efficacious than the other. Further trials comparing the efficacy of these medications in a randomized control trial are needed to determine the superiority of spasticity in the spinal cord injury population.
Injections of phenol or botulinum toxin have a role in treating spasticity in the spinal cord injury population. It may be indicated for patients who suffer from focal tone changes or whose tone may not be controlled with oral medications alone. Palazon-Garcia and colleagues conducted a retrospective study to evaluate the efficacy of botulinum toxin for focal spasticity in patients with spinal cord injury. Their results found that administering botulinum toxin injection improved tone and pain scores. Earlier administration of the toxin within 6 months of the patient’s initial injury showed greater improvements in goniometric performance than patients outside this window. Also, incomplete injuries were found to have greater improvements in tone than those with complete injuries. This serves as a clinical guidance for providers to consider botulinum toxin administration earlier in the clinical course for improved pain, range of motion, and tone.
Surgical management for spasticity should be reserved for patients whose range of motion is not maximized through conservative treatment. These procedures include but are not limited to tendon lengthening, tenotomy, tendon releases, and/or aponeurotomy to allow an increased range of motion in a desired joint. Clinicians should evaluate the rehabilitation goals of individual patients and determine if their goals could be achieved with surgical intervention in conjunction with oral and injection treatment to control overall spastic tone ( Fig. 1 ).
