This chapter identifies common soft tissue and musculoskeletal conditions that may be encountered in the treatment of patients with traumatic brain injury (TBI). An overview is provided on these topics:
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Background, diagnosis, and treatment strategies for heterotopic ossification
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Fracture implications and healing
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Musculoskeletal injuries of the shoulder and low back
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Use of musculoskeletal imaging
Heterotopic ossification
The formation of mature lamellar bone in ectopic extraskeletal regions is termed heterotopic ossification (HO). This condition can occur in periarticular and soft tissue areas and be further divided into traumatic HO and neurogenic HO (NHO).
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Etiologies of traumatic HO include fracture, joint replacement, and soft tissue injury.
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Etiologies of NHO may include TBI and spinal cord injury (SCI).
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The incidence of HO after TBI is estimated at 4% to 28% and can occur in more than one location, especially in patients with long bone fractures. ,
Pathophysiology and risk factors
The pathophysiology of HO is not well understood and is believed to be the result of a complex interplay between neurohumoral factors that produce differentiation of pluripotent mesenchymal stem cells into osteoblasts. , Patients with severe TBI have demonstrated elevated serum osteogenic factors and neuropeptides that create an optimal environment for bone formation and mineralization. , Bone morphogenetic protein (BMP) and transforming growth factor β1 (TGF-β1) are also implicated in allowing abnormal bone formation. Other factors such as substance P, leptin, platelet-derived growth factor, interleukin-1, and interleukin-6 are felt to be potential mediators in experimental models.
Risk factors for the development of HO include:
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Higher severity TBI, immobility, limb spasticity, and associated fractures
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Military personnel involved in blast-related injuries have an incidence as high as 60% to 64%.
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Coma duration, use of mechanical ventilation, and clinical signs of autonomic dysregulation are also associated with the development of HO in TBI.
Clinical presentation and diagnosis
Heterotopic ossification typically progresses through three stages of development, starting with immature bone matrix formation. This is followed by an intermediate stage of inflammation and progressive calcification that ends with the final stage of maturation. Symptoms of HO are variable throughout these stages and are further outlined in Table 21.1 . HO commonly develops within the first few months of injury but can be difficult to recognize as symptoms appear similar to deep venous thrombosis, septic joint, hematoma, cellulitis, and pressure injury.
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HO may affect upper and lower extremities but most commonly involves the hip and thigh, which can occur in two-thirds of cases. ,
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In these patients, HO can develop inferomedial to the hip and be associated with adductor spasticity.
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Scherbal et al. demonstrated upregulation of BMP in muscle specimens around the hip in rat models exposed to TBI and tibia fracture compared with tibia fracture alone. This may lend support to why HO develops around the hip.
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The elbow is the second most common location for HO in TBI, with the shoulder and knee affected to a lesser extent. ,
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Diagnostic tests
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In the initial stage, HO is primarily a clinical diagnosis.
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Elevated serum alkaline phosphatase may be the earliest laboratory indication but is nonspecific and may be present in other conditions, including fractures and liver dysfunction.
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Serum levels usually increase over the first 6 to 12 weeks after injury and may be helpful in patients unable to provide clinical history or participate in physical examination.
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Alkaline phosphatase levels do not correlate with maturation of HO.
Imaging modalities
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Imaging modalities such as x-rays may not identify HO in the early stages because of a lack of calcium deposition.
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Bone scan may be the most sensitive test for early detection and can identify HO as early as 2 weeks after symptom onset.
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Magnetic resonance imaging (MRI) and ultrasound have also been used for early detection.
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Argyropoulou et al. demonstrated MRI recognized knee HO almost simultaneously with clinical symptom onset.
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Rosteius et al. used ultrasound for screening HO in SCI patients and showed a sensitivity of 88%.
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In comparison, plain x-rays may not recognize HO for 3 to 6 weeks after symptom onset but can be useful in confirming maturity of HO.
Treatment modalities
Prevention
Methods believed to slow progression of HO include range of motion exercises, medications, and radiation therapy.
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Physical therapy can help preserve joint range of motion and mobility.
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Nonsteroidal antiinflammatory drugs (NSAIDs) such as indomethacin significantly reduce development of HO in SCI patients. Comparable results have been seen in patients undergoing total joint replacement.
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Although NSAIDs are believed to decrease HO in TBI patients, their specific effects are not well described in the literature, and some studies have only evaluated them in combination with other treatments. ,
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NSAIDs also may have adverse effects on the gastrointestinal system and potentially inhibit bone healing after fracture.
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Radiation therapy is thought to prevent differentiation of mesenchymal stem cells into osteoblasts and has demonstrated less HO formation in patients undergoing surgery around the hip. Still, radiation is not commonly used because dosing guidelines aren’t standardized, and the long-term effects are largely unknown.
Medications
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Patients who develop HO typically begin treatment with NSAIDs, which interfere with bone formation.
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Bisphosphonates have also been shown to reduce HO in early and late stages of maturation, with etidronate believed to reduce HO by inhibiting mineralization of organic osteoid.
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Better results are expected if bisphosphonates are started before HO detection on plain film and continued for 6 months.
Surgical treatment
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Surgical resection of HO may be considered if joint mobilization is severely restricted or if functional tasks and self-care are inhibited.
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Excision is traditionally delayed until maturation of the disease, up to 1.5 years after TBI.
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Recent evidence suggests resection of immature HO may not increase the rate of recurrence. , As such, surgery can be an effective treatment to improve range of motion, prevent ankylosis, reduce pain, and prevent impingement of neurovascular structures.
Future considerations
Future research may identify therapeutic targets that aid in the diagnosis and treatment of HO, including neuropeptides and signaling pathways such as substance P, macrophages, BMP, and retinoic acid receptor agonists. ,
Fractures
Traumatic brain injury may be accompanied by skeletal trauma that results in long bone fractures. These fractures may go undetected in the acute setting in brain injury patients who have cognitive impairments, speech dysfunction, absent sensation, or are unable to participate in physical examination. In a prospective study by Sobus et al., bone scans completed before inpatient rehabilitation revealed 25 undetected fractures in 60 children with TBI.
Normal fracture healing is completed through a series of continuous steps including inflammation, repair, and remodeling.
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The inflammatory phase is generally the shortest stage of healing and allows for migration of chemical mediators to the injury site to create an optimal environment.
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During the reparative process, damaged bone is resorbed, and fibroblasts begin to build a new osteoid matrix. This resorption allows for the detection of fracture lines on plain films. A soft callus then begins to form to bridge the fracture gap. Chondrocytes and osteoblasts then begin to mineralize the fracture callus to assist with union.
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The final stage of remodeling can take months and reshapes immature bone to provide strength and stability to the fracture site.
Patients who have sustained TBI often show an alteration in normal fracture healing. This can include enhanced osteogenesis, resulting in increased callus volume, accelerated callus formation, and higher mineral density. , , One study found the time for bone union decreased by almost half in patients with TBI compared with fracture alone. Although not confirmed, this is believed to be related to multiple signaling cascades that allow release of osteogenic factors.
Although there may be enhanced fracture healing and bone formation in the acute stages after TBI, these same pathways may contribute to long-term impairment in bone metabolism. Patients with TBI have been shown to have decreased bone mineral density, resulting in increased risk of osteopenia and osteoporosis, which can increase fracture risk over time. This is thought to be influenced by variations in parathyroid hormone after TBI, which can result in decreased vitamin D levels. Additionally, systemic inflammation in the chronic stages of TBI may promote osteoclastic activity.
Soft tissue and nerve injuries
Musculoskeletal injuries are common in patients with TBI. They may result from the injury itself or develop over time because of overuse. Like fractures, these soft tissue injuries may go undetected after acute TBI, as Sobus et al. noted 24 areas of soft tissue trauma in 60 children with TBI. Over the long term, TBI patients often report musculoskeletal pain causing limited function and quality of life. A study by Brown et al. contacted patients for follow-up approximately 26 years after their initial injury and found 79% reported some type of musculoskeletal complaint.
Falsetti et al. evaluated 163 patients with acquired brain injury and signs or symptoms of musculoskeletal pathology with ultrasound. Patients included had diagnoses of stroke and severe brain injury, which included TBI. Musculoskeletal complications were seen in approximately half of these patients, with shoulder pain found in more than 25%. Diagnoses included shoulder subluxation, rotator cuff pathology, and frozen shoulder. Contractures and spasticity were noted in 18% of the patients.
Musculoskeletal problems of the shoulder
Musculoskeletal injuries to the shoulder commonly include impingement syndrome, rotator cuff injury, adhesive capsulitis, and glenohumeral instability.
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Impingement syndrome is a frequent cause of shoulder pain, with the supraspinatus tendon most commonly involved.
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Poor blood supply in a hypovascular zone along the articular surface of the tendon may be responsible for this phenomenon.
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Anatomical changes such as a hooked acromion, weak scapular stabilizers, or glenohumeral joint capsule tightness also may contribute.
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Patients typically report pain along the anterior and lateral shoulder that is worsened with overhead activity. Examination of the shoulder with maneuvers compressing the region between the acromion and humeral head can reproduce symptoms.
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Cervical spine pathology may also refer pain to the shoulder and is often included in workup of shoulder pain.
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Nonoperative treatment of this condition focuses on rehabilitation therapies that emphasize scapular stabilization exercises, including strengthening agonists and stretching antagonistic muscles.
General principles of rehabilitation after injury follow three broad stages that include acute, recovery, and functional phases.
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During the acute phase, emphasis is placed on reducing symptoms, core strengthening, and maintenance of aerobic conditioning. When the patient has pain-free range of motion and can participate in strengthening exercises, they may advance to the recovery phase.
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The recovery phase involves restoration of flexibility, strength, and proprioception of the injured limb. Once full strength is regained, the patient can then progress to the functional phase.
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The functional phase works on task-specific activities and emphasizes return to normal activity.
Radiculopathies
Radiculopathy is caused by mechanical compression of a nerve root that results in a variety of symptoms, including pain, paresthesia, numbness, tingling, or weakness. Mechanical compression is commonly caused by disk herniation but may also result from spinal stenosis, facet joint arthropathy, synovial cyst, or neoplasm.
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In the lumbar region, the most common disk herniations are at L4–L5 and L5–S1, with the L5 and S1 nerve roots most commonly involved.
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In the cervical region, the C7 and C6 nerve roots are most commonly implicated.
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Radiculitis can occur in the absence of mechanical compression and is felt to be a result of chemically induced inflammation of the nerve.
Clinically, patients may report symptoms within a dermatomal distribution. Weakness or atrophy may also be present in a given myotome.
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For example, an L4–L5 disk herniation causing mechanical compression of the L5 nerve root may produce radiating pain along the posterolateral thigh and anterolateral leg. Numbness in the lateral leg and first web space may be appreciated in classic presentations.
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Diminished reflexes may also be found, such as a depressed patellar reflex in patients with L4 nerve root compression.
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Red flag symptoms may alert clinicians to conditions that require further diagnostic workup and may include the presence of constitutional symptoms, systemic illness, gait disturbance, and bowel or bladder dysfunction.
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Clinicians should also be aware of signs and symptoms of myelopathy, such as the presence of upper motor neuron signs, which may warrant urgent evaluation and possible intervention.
The natural history of radiculopathy tends to favor resolution of symptoms over time. If symptoms are causing functional impairments and limiting quality of life, then conservative treatments may include NSAIDs, therapy, and epidural steroid injections.
Musculoskeletal imaging
Imaging modalities are commonly used to assist in the diagnosis of various musculoskeletal injuries. Advancements in these technologies have allowed for improved anatomical visualization and in some instances dynamic and functional evaluation.
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Traditional plain radiography allows for evaluation of bony anatomy, which can assist in diagnosing fractures, bony deformities, ossification, and arthritic changes.
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Computed tomography (CT) generates overlapping contiguous images of the scanned area and offers better visualization of fractures and organs.
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MRI doesn’t use radiation but instead uses a magnetic field to create images that are a few body layers thick at a time. This allows for improved visualization of soft tissue structures and organs.
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Many consider MRI the gold standard in spinal imaging and for soft tissue pathology.
The use of ultrasound has also increased because of advances in technology that have improved image resolution, accessibility, and portability. Musculoskeletal ultrasound has assisted in the diagnosis of soft tissue and nerve injuries and is commonly used for needle guidance in procedures. Musculoskeletal ultrasound has many advantages compared with other imaging modalities.
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For example, it does not use radiation and provides improved patient comfort.
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It also allows for dynamic evaluation of ligaments and tendons during examination.
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Warden et al. found ultrasound to have a higher sensitivity and equivalent specificity to MRI in confirming clinically diagnosed patellar tendinopathy.
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During ultrasound-guided procedures, real-time visualization of vascular structures and nerves also allows for improved safety.
Musculoskeletal structures have characteristic features when visualized with ultrasound :
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Normal tendons have a hyperechoic appearance with a fibrillar echotexture and organized linear strands.
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Muscle and cartilage both appear hypoechoic, and cartilage may appear anechoic at times.
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Ligaments have a hyperechoic and striated appearance that is usually more compact compared with tendons.
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Nerves have a fascicular appearance with a hyperechoic rim that is described as a honeycomb pattern.
Abnormal features visualized with ultrasound may include tendons with hypoechoic areas and a loss of the normal fibrillar echotexture. Neovascularity may also be seen within injured tendons and can be assessed with color Doppler. Nerve compression syndromes may cause nerve swelling with increased circumference appreciated on ultrasound.
Review questions
- 1.
You are consulted to evaluate a 25-year-old male patient with a history of seizure disorder who was involved in a motor vehicle accident resulting in a severe traumatic brain injury (TBI) and facial fracture. The patient is currently in a coma and receiving total parenteral nutrition. Which of these patient characteristics is a risk factor for the development of heterotopic ossification (HO)?
- a.
History of seizure disorder
- b.
Prolonged coma duration
- c.
Male gender
- d.
Presence of facial fracture
- a.
- 2.
Which of these is the most common location for the development of HO in patients with TBI?
- a.
Knee
- b.
Wrist
- c.
Hip
- d.
Shoulder
- a.
- 3.
A 50-year-old woman with a recent history of TBI is currently admitted in the acute rehabilitation unit. She has developed HO of the left hip with severely restricted range of motion that is limiting her self-care and functional tasks. The patient is being considered for surgical excision of the HO. Which of these is the best tool to evaluate for maturity of the HO?
- a.
Bone scan
- b.
Plain x-ray
- c.
Dual-energy x-ray absorptiometry (DEXA)
- d.
Alkaline phosphatase level
- a.
Answers on page 391.
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- 4.
A 45-year-old man with a TBI 2 months ago reports pain in his left hip and difficulty bending over to tie his shoe for approximately 1 week. On physical examination, you notice decreased range of motion, warmth at the hip, and mild edema in the left thigh down to the knee. What is the best next step?
- a.
Evaluate with plain x-ray.
- b.
Start aggressive range of motion exercises.
- c.
Start treatment with indomethacin.
- d.
Evaluate with Doppler ultrasonography.
- a.
- 5.
A 35-year-old patient with a history of TBI presents with a 4-week history of low back pain with radiating symptoms down the right lower extremity. The patient reports the pain started after lifting a heavy box during a recent move. On physical examination, you notice decreased light touch sensation along the medial malleolus and a slightly depressed right patellar reflex. You suspect that the patient may have a disk herniation at which of these levels?
- a.
L3
- b.
L4
- c.
L5
- d.
S1
- a.
- 6.
You are evaluating a 42-year-old man with a 3-month history of low back pain radiating into the left leg. He has tried conservative management with physical therapy without improvement in symptoms. In the past few days, he has noticed decreased sensation in his buttocks and reports two episodes of bladder incontinence. He tells you his family member had a similar pain that was relieved with an epidural steroid injection. What is the next best step in management?
- a.
Obtain L-spine magnetic resonance imaging (MRI)
- b.
Trial of opiate therapy
- c.
Obtain a bone scan
- d.
Refer for epidural steroid injection
- a.
- 7.
Which of the following describes the sonographic appearance of a normal tendon?
- a.
Hypoechoic with a fibrillar echotexture
- b.
Hyperechoic with a compact striated appearance
- c.
Hyperechoic with a fibrillar echotexture
- d.
Hypoechoic with a compact striated appearance
- a.
- 8.
Which of these statements regarding ultrasound is true?
- a.
Ultrasound has superior visualization of fractures compared with computed tomography.
- b.
Ultrasound has an advantage over MRI because it does not use radiation.
- c.
Both ultrasound and plain radiography allow for dynamic evaluation of tendons on examination.
- d.
Ultrasound can allow for real-time visualization of vascular structures during ultrasound-guided procedures.
- a.
- 9.
A 33-year-old man with a history of TBI presents to your clinic with pain along the anterior and lateral aspects of his left shoulder. He recently started a new job as a painter. Passive internal rotation and forward flexion of the shoulder through full range of motion reproduces his symptoms. He is otherwise neurologically intact. Which of these is the most likely cause of this patient’s shoulder pain?
- a.
Impingement syndrome
- b.
Adhesive capsulitis
- c.
Bicipital tendinopathy
- d.
Shoulder–hand syndrome
- a.
- 10.
A 28-year-old patient is currently admitted to your rehabilitation unit after sustaining a TBI from a motor vehicle accident. She reports right shoulder pain since the accident. An MRI of the right shoulder reveals a partial thickness supraspinatus tear. Which of these describes the acute phase of rehabilitation the patient should begin?
- a.
Concentric strengthening exercises
- b.
Focus on reduction of symptoms and pain-free range of motion
- c.
Isometric strengthening exercises
- d.
Task-specific activities
- a.
References
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