VERTEBRAL COMPRESSION FRACTURES, SI JOINT DYSFUNCTION, MYOFASCIAL PAIN SYNDROME

Hamilton Chen, MD

Vertebral Compression FractureGeneral• Compression fracture of the vertebral body• Commonly seen in thoracolumbar junction• Etiology may be from trauma, osteomalacia, medications, neoplasms,

or osteoporosisEpidemiology• 700,000 vertebral body compression fractures occur each year, twice

the rate of hip fractures• Most vertebral compression fractures are secondary to osteoporosis• Osteoporosis is the most common metabolic disorder of bone,

affecting approximately 100 million people worldwide.• In the United States, it is estimated that at least 10 million people

suffer from osteoporosis and an additional 18 million people are at significant risk for development of the disorder.

Vertebral Compression FracturesPathophysiology of Osteoporosis/Compression

Fractures• Osteoporosis is characterized by decreased bone

mass or increased porosity and results in diminished structural support of the osseous spinal column.

• Primary osteoporosis is considered to have two etiologic variants.

• Type I affects postmenopausal women and is related to rapid loss of bone after menopause

• Type II affects individuals over 70 years-old and involves age-related loss of bone or senile osteoporosis.

• Secondary osteoporosis is loss of bone caused by an agent or disease process such as corticosteroids, endocrine disorders, or an inflammatory process

• Diminished bone density leads to compression fractures

• Caused by forces transmitted along the vertebral body. • Ligaments are intact, and compression fractures are

usually stable

Vertebral Compression FracturesPathophysiology• No generally accepted system of severity grading in compression fractures• Denis classification system based on the 3-column theory of spinal instability

is the most often used.• Anterior column: consists of the anterior two-thirds of the annulus and

vertebral body, along with the anterior longitudinal ligament.• Middle column: consists of the posterior one third of the annulus and vertebral

body, along with the posterior longitudinal ligament.• Posterior column: consists of all bony and tissue elements posterior to the

anterior and middle column.

Denis Classification

Mechanisms of Vertebral FracturesFlexion-compression mechanism (wedge or compression fracture)•Compression of anterior column, with variable involvement of middle and posterior column

Axial-compression mechanism•results in an injury called a burst fracture, and the pattern involves failure of both the anterior and middle columns

Flexion-distraction mechanism•Causes chance fracture - This pattern involves failure of the posterior column

Rotational fracture-dislocation mechanism•Mechanism of this fracture is a combination of lateral flexion and rotation•The resultant injury pattern is failure of both the posterior and middle columns with varying degrees of anterior column insult.

Vertebral Compression Fractures

Symptoms• If secondary to trauma, may develop neurologic

symptoms, significant pain, weakness. • Patients presenting with back pain from compression

fractures from osteoporosis typically report the sudden or acute onset of pain with relatively atraumatic activities:

• Bending forward• Standing from a seated position• Vigorous coughing or sneezing.

• Pain may not be localized to the site of the fracture• Many patients with compression fractures are

asymptomatic

Physical Examination• Complete MSK exam of spine, hip, knee• Complete Neurologic Exam• Focal kyphosis or loss of lumbar lordosis.• Loss of height • Localized tenderness over the involved level• If trauma, look for associated injuries!

Vertebral Compression FractureRadiographic evaluation • X-Rays – AP/Lateral

• Classic ‘‘wedge’’ fracture, which shows loss of anterior vertebral body height with relative preservation of posterior vertebral body height.

• Most frequent sites:• thoracolumbar junction• midthoracic spine.

• Increased segmental kyphosis. • Acute injury - well-demarcated fracture

lines or distinct discontinuity of a thin cortical margin.

• Chronic injury - sclerosis of the fracture lines, a dense cortical margin, and osteophytes bordering the fracture site.

Vertebral Compression FractureOther Radiologic Imaging• CT w/ Thin Cuts• MRI – may differentiate

between acute and chronic fractures, or ruling out tumor or infection.

• Nuclear studies

Vertebral Compression FractureTreatment of Compression Fractures• Important to treat osteoporosis, if it is the underlying cause• May necessitate a short period of bed rest for no longer than a few days,

followed by gradual mobilization. • Continuous hyperextension bracing with a spinal orthosis may be beneficial

for up to the first 6 to 8 weeks until the acute pain resolves. • Appropriate analgesic medications should be prescribed to reduce pain

• Acetaminophen• Muscles relaxants• Opiates• Calcitonin

• Silverman and Azria (2002) did a review specifically looking at studies that used calcitonin as an analgesic following an OVCF. Their results found that calcitonin effectively relieves OVCF pain as quickly as 1 week or less. The mechanism of action as an analgesic is unknown but likely is due to central mediation or endorphin mediation.

• Nonsteroidal anti-inflammatory medication – discourage use in acute setting

Osteoporosis Medications

Name the Brace

Vertebral Compression FracturesRehabilitation • Physical Therapy

• Gentle mobilization • Ensure proper body mechanics (avoid flexion, extensor strengthening)• Optimize transfer techniques• Train with gait aids (such as a wheeled walker) to reduce biomechanical

stresses on the spine and to ensure gait safety.• Pain-relieving modalities

• Occupational therapy • Activities of daily living• Reinforce proper spinal ergonomics• Equipment needs• Fall prevention

• Successful rehabilitation is targeted at increasing comfort, decreasing deformity, and decreasing resultant disability

Vertebral Compression FracturesProcedures• Percutaneous vertebroplasty or kyphoplasty

• Use of polymethyl methacrylate (cement) to reduce fracture pain, reinforce thoracic vertebral strength, and improve function

• Complications can include infection, bleeding, fracture, and systemic issues such as embolism, or cement leaks.

• Surgery is rarely necessary for osteoporotic vertebral compression fractures. May be considered in patients with:• Severe pain due to nonunion of the fracture• Spinal instability• Neurologic complications occur

Kyphoplasty

Vertebroplasty

Sacroiliac Joint DysfunctionGeneral• C-shaped articulation between sacrum and ileum• Innervated by L5 dorsal ramus and lateral S1 to S3 dorsal rami• Etiology may be from hyper or hypomobile joint patterns, repetitive overloads,

trauma, and capsular tears/injury• Diagnosis that should be arrived at only after careful consideration of other

diagnoses

Epidemiology• Several attempts have been made to establish the prevalence of SIJ

syndrome; results vary widely.• Schwarzer et al remarked that the prevalence of sacroiliac pain would appear

to be at least 13% and perhaps as high a 30% in patients with low back and buttock pain

• Bernard and Kirkaldy-Willis reported the prevalence rate to be 22.5% in 1293 patients with back pain

Sacroiliac Joint Anatomy

Sacroiliac Joint DysfunctionFunctional Anatomy• The SIJ is a true diarthrodial joint that joins the sacrum to the pelvis.• In this joint, hyaline cartilage on the sacral side moves against

fibrocartilage on the iliac side. The joint is generally C shaped with 2 lever arms that interlock at the second sacral level.

• The joint contains numerous ridges and depressions, indicating its function for stability more than motion. • Stability is provided by the ridges present in the joint and by the presence of

generously sized ligaments. • Ligamentous structures offer resistance to shear and loading.

• Function of the SIJ is to dissipate loads of the torso through the pelvis to the lower extremities and vice versa

• Clinicians vary in their opinions about how much mobility is normal, whether it could result in pain, and whether it can clinically be detected

• SIJ has limited motion that allows it to dissipate and transfer significant loads and stresses. • Studies by Weisel indicate that most movement occurs when rising from the

sitting to the standing position. Amount of motion is small, making assessment of sacroiliac motion during physical examination difficult

Sacroiliac Joint DysfunctionPresentation• Key element in the diagnosis of sacroiliac dysfunction is pain.

• Pain pattern varies• buttocks at or near the posterior superior iliac spine

(PSIS). • pain radiating to the hip, posterior thigh, or even calf

has been described.• Worsens with prolonged sitting or twisting or rotary motions.

• Usually a dull ache or sharp, stabbing, or knifelike.

Sacroiliac Joint DysfunctionPhysical Examination• Perform thorough assessment of the low back, hips, and pelvis• Provocative tests for SI joint dysfunction should be performed to differentiate

sacroiliac joint–derived back pain from other regional pain generators. • Studies show that when these tests are considered separately, the most commonly

used provocative tests have low specificity for sacroiliac dysfunction• One possible explanation for this is interrater unreliability. • Others suggest that both the minimal range of motion around the joints and the

difficulty in simulating physiologic stresses through the joints make it more likely that provocative tests will elicit pain from surrounding structures.

• Several investigators have shown that in the diagnosis of sacroiliac joint disease, a multitest regimen is more clinically useful than any individual test finding.

• Recent research suggests that three or more positive findings on provocative tests are 85% sensitive and 79% specific for sacroiliac joint disease.

Palpation, Fortin Finger Test

Ganslens Test

FABER Test

Compression Test

Yeoman’s Test

Sacroiliac Joint DysfunctionDiagnostic Studies• X-ray • Bone scan • Computed tomography • Magnetic resonance imaging• Fluoroscopically guided diagnostic

anesthetic injectionLabs• Complete blood cell (CBC) count• Erythrocyte sedimentation rate

(ESR)• C-reactive protein (CRP) level• Antinuclear antibody (ANA) profile• Human leukocyte antigen (HLA)-

B27 status• Rheumatoid factor (RF)

MRI Sacroilitis

Sacroiliac Joint DysfunctionTreatment• Rest, avoid provocative activities• Local modalities such as ice and heat or topical analgesics • Manipulative therapy can alleviate pain and help with muscle

spasms but does not change joint alignment significantly. No significant muscle groups cross the sacroiliac joint.

• Acetaminophen, nonsteroidal anti-inflammatory medications, and muscle relaxants.

• True sacroilitis related to a seronegative spondyloarthropathy may be candidates for the use of disease-modifying antirheumatic drugs.

• Physical therapy • Lumbar core muscle strengthening and lower extremity flexibility• Modalities - ice massage, heat, electrical stimulation, ultrasound

• Sacroiliac joint belts• Manual Therapy

Sacroiliac Joint DysfunctionTreatments• Ultrasound/fluoroscopically

guided intra-articular steroid injection

• Radiofrequency denervation• Surgical fusion is very rarely

performed

Myofascial Pain SyndromeGeneral• Regional pain disorder, characterized by hypersensitive areas called

myofascial trigger pointsEpidemiology• Extremely common, and almost everyone develops a trigger point

(TrP) at some time. • In the US, 14.4% of the general population suffers from chronic

musculoskeletal pain.• Approximately 21-93% of patients with regional pain complaints have

myofascial pain. • No gender or racial differences in the incidence of myofascial pain

have been described in the literature.• Sedentary individuals are more prone to develop active TrPs than are

individuals who exercise vigorously on a daily basis.

Myofascial Pain SyndromePathophysiology• Myofascial trigger point is defined as hyperirritable spot in taut band of skeletal

muscle fibers• Clinical Characteristics:

• Painful or Tender Spot• Taut Band• Referred Tenderness and Referred Pain• Local Twitch Responses• Motor Dysfunction• Autonomic Phenomena (temperature, sweating, dryness, dizziness)

Myofascial Pain SyndromePresentation• Dull or achy pain, sometimes poorly localized, particularly during repetitive

activities or activities requiring sustained postures. • Symptoms exacerbated with digital pressure over tender areas of muscle with

reproduction of the patient's usual pain• Symptoms are relieved with rest or cessation of repetitive activities

Physical Exam• Palpates a localized tender spot in a nodular portion of a taut rope-like band

of muscle fibers.• Manual pressure over a trigger point should elicit pain at that area and may

also elicit pain at a distant site (referred pain) from the point under the fingertip.

• Applied pressure often earns the response “That's my pain!” • Insertion of a needle, abrupt palpation, or even a brisk tap with the fingertip

directly over the trigger point may induce a brief muscle contraction (twitch response).

Myofascial Pain SyndromeDiagnostic Tests• No definitive laboratory test or imaging method is diagnostic of MPS. • Diagnosis is made primarily by history and physical examination• Needle electromyography (EMG) examination of trigger points (TrPs)

in humans and rabbits has shown high-voltage spike activity and spontaneous, low-voltage endplate noise

Treatment• Wide variety of therapy is available to patients with MPS. • Much of the variation in forms of treatment (and diagnoses) of this

disorder results from differences in culture, training, and recognition of an often undiagnosed syndrome of pain, dysfunction, and autonomic dysregulation.

Myofascial Pain SyndromeTreatment• Physical therapy

• Techniques that focus on correction of muscle shortening by targeted stretching, strengthening of affected muscles, and correction of aggravating postural and biomechanical factors

• Therapeutic modalities such as biofeedback, ultrasound, lasers, heat, and massage• Oral Medications

• Nonsteroidal anti-inflammatory drugs (NSAIDs) • Muscle relaxants

• Procedures• interventional techniques can be an effective adjunct in the multidisciplinary

management of patients • Myofascial trigger point injections should be individualized for both the patient and

the clinician. • The diagnostic skill required to find active myofascial trigger points depends on

considerable innate palpation ability, authoritative training, and extensive clinical experience.

Levator ScapulaGeneral• Frequently the culprit for “stiff

neck”

Anatomy• Origin - transverse process of C1-

C4• Insertion - below to superior angle

of scapula

Action• Scapula rotation, elevation• Neck Extension, Flexion, Rotation

Levator Scapula Referral Pattern

Levator Scapula TrP

Exam•Lie patient on uninvolved side•Press on free border of upper trapezius aside with index finger to straddle tense levator scapulae•Straddle other trigger point just cephalad to superior angle of scapula

Levator Scapula Spray and Stretch

•Spray vapocoolant in slow repeated sweeps while having patient reach downward with right arm•Release trigger point after spray while elongating muscle while patient exhales•Use heel of hand to stretch longest fibers•Other hand stabilizes patient’s head

Levator Scapula TrP Injection

SternocleidomastoidGeneral• Two divisions of muscle, both

clavicular divisions and sternal divisions can have TrPs

Anatomy• Origin

• Sternal division – Manubrium• Clavicular division – Medial

clavicle• Insertion - Mastoid process of

temporal bone Action• Rotate face to contralateral

side • Neck flexion• Auxiliary muscles of inhalation

Sternocleidomastoid Referral Pattern

Sternocleidomastoid Exam

• Use pincer palpation • Examine sternal division

with patient seated• Examine deeper clavicular

division with patient spine and head tilted ipsilaterally to permit examiners fingers to reach it

Sternocleidomastoid Spray and Stretch

• A - Clavicular division• B – Sternal division• C – Completion of sternal

division • Cover eyes with gauze• Apply spray when patient

breathes out to avoid inhalation of spray vapors

Sternocleidomastoid TrP

TrapeziusGeneral•Tripartate muscle, each has different fiber directions

Anatomy•Origin – Midline occiput to T12•Insertion – Lateral clavicle, acromion, spine and scapula

Actions•Neck rotation•Neck lateral flexion•Scapula rotation, adduction, depression, elevation

Trapezius Trigger Points

Trapezius Trigger Points

Trapezius – Exam• Use pincer palpation for

TrP1 and have patient supine

• For rest of TrP, have patient sitting

Trapezius – Spray and Stretch• Right upper trapezius

muscle• Place right arm on pillow for

support• After spray, press laterally

and downward on scapula while stabilizing head with other hand

Spray and Stretch

Middle Trapezius• Spray with patient in lateral

decubitus position. • Release by stabilizing

scapula and back. Ask patient to look to the right and breath in, then look to left and breathes out. Then let arm drop to floor.

Lower Trapezius• Spray with patient in lateral

decubitus• Release with same technique

as middle trapezius

TrP Injections

Quadratus LumborumOrigin•Originates on the Internal surface of the Posterior portion of the Anterior Lip of the Iliac Crest.

Insertion•Transverse processes L1-L4 via ilio lumbar ligament.•Interno-Inferior surface of the 12th rib.

Action•Lateral flexion of vertebral column, with ipsilateral contraction•Extension of lumbar vertebral column, with bilateral contraction•Fixes the 12th rib during forced expiration•elevates ilium, with ipsilateral contraction

Quadratus Lumborum

PiriformisOrigin•Anterior and Internal surface of the Sacrum.•Through the sciatic notch and attaches on the anterior sacrum

Insertion•Upper border of the greater trochanter

Action•Lateral rotation of the femur and hip joint•laterally rotates the extended thigh and abducts the flexed thigh

Piriformis Referral Pattern