Sacroiliac (SI) joint dysfunction has tradition-ally been considered a controversial diagnosis (Seidenberg and Bowen 2010) because of the lack of reliable and valid diagnostics (Rupert et al. 2009; Szadek et al. 2009). SI joint dysfunction has been defined as a lack of voluntary move-ment at the joint (Sharma and Sen 2014). Szadek and colleagues (2009) found select orthopedic tests (e.g., thigh thrust test, compression test, and SI joint stress tests) to show “discriminative power” for the diagnosis of sacroiliac joint pain.
However, more work needs to be done to solidify the relationship between these tests and SI joint dysfunction. Sports that require unidirectional repetitive movements such as gymnastics and skating can result in pelvic and rotational shear at the SI joint and may sprain the joint’s ligaments and contract surrounding musculature, resulting in impaired movement and function of the SI joint (Cohen 2005; Seidenberg and Bowen 2010). A direct trauma to the pelvis from a fall, car acci-dent, or sudden violent contraction may also result in tearing the joint’s surrounding ligaments and tissues, but this is less common (Seidenberg and Bowen 2010).
Common Signs and Symptoms
• Point tenderness over the SI joint (sacral sulcus and PSIS)
• Point tenderness at the posterior hip and low back musculature
• Pain radiating into the buttock, posterolat-eral hip, or low back
• Pain with trunk flexion
• Lack of motor, sensory, or deep tendon reflex
• Positive FABER (flexion, abduction, external rotation) test, piriformis test, or Gaenslen’s test
• Positive March test and Gillet test
• Leg length discrepancy
• Innominate upslip or downslip with or with-out rotation
Common Differential Diagnoses
• Lumbar disc pathology
• Piriformis syndrome
• Gluteus medius strain
• Ankylosing spondylitis
• Reiter’s syndrome
• Spondyloarthropathies
• Autoimmune etiologies (if both SI joints are involved)
• Spinal stenosis
• Compression neuropathies Clinician Therapeutic Interventions
• Perform a thorough clinical and biomechan-ical examination to determine the source of the pain.
• Correct any faulty movement and biome-chanical faults overloading the sacroiliac joint. Leg length discrepancy coupled with weak hip rotators is often seen with this condition.
• If a significant leg length discrepancy is identified, a simple heel lift is not advo-cated because the lift may abnormally affect the arthrokinematics of both SI joints and those in the kinetic chain. Therefore, a bilateral custom orthosis correction should be implemented if a leg length discrepancy is modified.
• Release painful contracted tissues first with PRT prior to using direct manipulative tech-niques.
Treatment Points and Sequencing 1. Sacroiliac joint
9. Psoas (Avoid marked posterior pelvic positioning.)
10. Adductor magus (inferior pubis)
> continued
• Apply thermal ultrasound or a like modality prior to using direct manipulative tech-niques.
• Restore normal sacroiliac joint arthrokine-matics using muscle energy, joint mobiliza-tion, or other manual therapy methods.
• Consider having the patient use an SI belt after the acute phase to promote pain relief and joint stabilization.
• Have the patient avoid movements that produce rotational shear and torsion at the SI joint for four to six weeks, progressing slowly back into these movements once pelvic stabilization has been attained.
• Consider using KT Tape or a similar tape product to provide pain relief.
• Implement a progressive spinal stabilization program.
• Educate the patient about proper ADL movement techniques to reduce stress at the lumbosacral tissues.
• Educate the patient about how to self- mobilize and apply muscle energy to the SI joint to nourish the joint and keep it mobile.
Patient Self-Treatment Interventions
• Avoid movements that cause pain, particu-larly trunk flexion and rotation.
• Avoid trunk flexion and sit-ups in the initial rehabilitation phase.
• Perform daily SI joint self-mobilization and muscle energy techniques.
• Apply palliative heat and ice as needed.
• Once the joint has stabilized, stretch the posterior muscles after physical or thera-peutic exercise.
Sacroiliac Joint Dysfunction > continued
Summary
Although pelvic somatic dysfunction may appear to be an enigma to both the novice and sea-soned practitioner, with close consideration of proximal and distal and intrinsic and extrinsic risk factors, the puzzle may be solved. Given the gravity of potential underlying disease and injury conditions that may mimic pelvic pain, PRT practitioners must be steadfast in their attempt to identify its source. If the causative factors or origin of the pelvic dysfunction are not readily determined, treatment of pelvic somatic dysfunction with PRT will tend to be safer than direct therapies and will yield pain relief, improved strength, and optimally, enhanced function.
CHAPTER
CHAPTER OBJECTIVES
After reading this chapter, you should be able to do the following:
Appreciate the factors that may influence the development of somatic dysfunction of spinal tissues.
Locate and palpate spinal tissue structures to be treated with positional release therapy (PRT).
Apply PRT techniques to spinal tissues affected by somatic dysfunction.
Identify how common injury conditions such as thoracic outlet syndrome may be treated based on somatic lesion patterns.
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8
Spine
Pain
and disability associated with spinal con-ditions are a common health and economic prob-lem globally. Low back pain is one of the leading causes of disability and work-time loss (Andersson 1999; Hoy et al. 2012; Luo et al. 2004). In 1998 it was estimated that low back pain direct health care expenditures in the United States alone were in excess of $90.7 billion (Luo et al. 2004). Hoy and colleagues (2010) found that low back pain, once thought to be a problem unique to Western countries, is now a global problem that causes a significant burden on all aspects of society.It is generally accepted that 70 to 85% of people will experience pain and disability related to a spinal condition at some point in life (Andersson 1999). Todd (2011) reported that up to two thirds of people present with degenerative cervical spine disorders in their lifetimes, and the prevalence increases with age. The occurrence of low back pain has also been reported to be greatest in the third decade of life and to be prevalent up to the age of 60 to 65, at which point it gradually declines.
The rise and fall of low back pain across the life span has been attributed to a greater work-life demand at middle age, followed by a decrease in the retirement years (Hoy et al. 2010).
Although activity and compressive forces at the spinal tissues are necessary for their nourish-ment and growth, too much demand may lead to accelerated degeneration and disc derangement (Bartynski et al. 2013). Bartynski and colleagues (2013) proposed that competitive athletes may be more susceptible to disc degeneration and subse-quent derangement as a result of increased spinal mechanical compression and strain during the years of competitive activity. Whether athletes are at more risk for spine conditions than nonathletes is still unclear, but Bono (2004) found a greater prevalence of disc degeneration among athletes.
However, whether this places them at an increased risk for back pain is uncertain. To date, discogra-phy studies have not shown a causal relationship between disc degeneration and disc derangement (Bartynski et al. 2013; Endean et al. 2011), but research with athletes in this area is lacking. How-ever, Livshits and colleagues (2011) did find disc degeneration to be a significant risk factor for low back pain among women.
Additional risk factors for low back pain are increased weight (body mass index); obesity (particularly in women; Shiri et al. 2009); low socioeconomic and educational status (Hoy et al. 2010); genetic predisposition (among women;
Livshits et al. 2011); and psychosocial factors such as increased stress, depression, and work dissat-isfaction (Hoy et al. 2010). Although most acute low back pain resolves within three months with little or no intervention irrespective of risk factors, approximately 5% of cases become chronic, which presents unique treatment challenges (Bartynski et al. 2013).
An understanding of the factors that lead to chronicity is lacking at this time, but chronicity may be related to the rate of recurrence. In an examination of low back pain epidemiology between genders and across populations, recur-rence within one year ranged approximately between 60 and 80%. The propensity for recur-rence increases with age and among females (Hoy et al. 2010). Recurrent episodes of chronic low back pain may propagate somatic dysfunction through a host of dysfunctional neurochemical and structural processes, producing pain generators at multiple neuronal levels (Kuchera 2005). As dis-cussed in chapter 2, persistent chronic pain may result in central sensitization at the second order, resulting in the production of a painful stimulus in the absence of tissue damage. Therefore, when assessing a patient with chronic pain, clinicians must consider potential pain generators and whether multiple factors may be affecting their production and persistence.
Kuchera (2008) recommended that clinicians evaluating patients with chronic pain explore psychosocial (e.g., depression), homeostatic (e.g., increased autonomic activity), and structure- function (biomechanics) issues to develop a multimodal treatment plan (see Kuchera for a full review), which may include the use of PRT.
Positional release therapy and strain counterstrain (SCS) have shown promise for reducing acute and chronic spine-related pain (Wong 2012). However, to date, PRT and SCS research has been focused on the cervical area with particular attention on cervicogenic pain, headache, migraine, and tem-poromandibular dysfunction. Although the review of the effectiveness of SCS for these conditions has been well elucidated by Wong (2011), there is not yet robust support for the use of PRT or SCS for the treatment of acute or chronic nonspecific low back pain over traditional therapies. The lack of support may be related to how PRT and osteo-pathic therapies are defined.
Some authors consider PRT a manipulative tech-nique that involves the direct and indirect manip-ulation of tissues (Lewis, Souvlis, and Sterling
2011) and thus group it with joint mobilization, which may result in classification errors in larger systematic studies. For example, in a systematic review and meta-analysis of complementary alternative medicine (CAM) for neck and low back pain, Furlan and colleagues (2011) examined manipulation and mobilization independently, but also in paired fashion, and did not mention the type of mobilization or manipulation. There-fore, terminology may be a confounding factor in determining the efficacy of PRT for the treatment
of spine-related pain if it is not identified as PRT and also if it is grouped with other manipulative therapies. Additionally, capturing tissue and neuro-logical changes has traditionally been challenging, as previously discussed. Regardless, the strong evidence of pain reduction and improvement in disability for cervical and cranial conditions observed among SCS and PRT researchers provides a base of support and an impetus for further study of its usefulness in treating a myriad of spinal conditions.
TREATMENT
Common Anatomical Areas and Conditions for PRT
Anterior Structures
• Muscle strain
• Ligament sprain
• Osteoarthritis
• Acquired (acute) torticollis
• Thoracic outlet syndrome
• Whiplash
• Cervicogenic headache
• Cervical fusion
• Disc pathology
• Radiculopathy
• Degenerative disc disease
• Scoliosis
Posterior Structures
• Muscle strain
• Ligament sprain
• Osteoarthritis
• Facet joint syndrome
• Sacroiliac joint dysfunction
• Nonspecific low back pain
• Disc pathology
• Radiculopathy
• Lumbar fusion
• Degenerative disc disease
• Coccydynia
• Scoliosis
• Sciatica
• Spondylolisthesis
• Spondylosis
Sternocleidomastoid
The sternocleidomastoid (SCM) is composed of two large muscular heads at the lateral and anterior aspects of the neck. Both heads merge superiorly at the neck to produce the prominent-looking strap when turn-ing the head side to side. Lesions often develop in the SCM when the head and neck are positioned in a compromised flexed and rotated position during sleep, producing an acute torticollis.
Sternocleidomastoid Levator scapulae Trapezius
E6296/Speicher/Fig. 8.01/532173/JG/R1
Origin: Sternal (medial) head: Ventral surface of the manubrium
Clavicular (lateral) head: Superior and anterior surface of the medial third of the clavicle
Insertion: Mastoid process of the temporal bone, lateral half of the superior nuchal line at the occiput
Action: Cervical spine flexion (both heads), cervical spine lateral flexion to the same side, cervical spine rotation to the opposite side, capital extension (posterior fibers), sternum elevation with forced inspiration
Innervation: Accessory (XI) nerve C2-C3 (ventral rami)
Palpation Procedure
• Place the patient in a supine position and sit behind the patient’s head.
• Ask the patient to slightly flex and rotate the head to the opposite side to bring out the SCM.
Note the V appearance distally formed by the clavicular and sternal heads.
• Lightly pince the midbelly of the SCM between your thumb and forefinger and allow it to roll under your fingers while gently pulling upward.
Repeat this procedure moving proximally to the mastoid process and downward along the two heads of the SCM.
• Because the carotid artery passes deep to the SCM, when pincing the tissue, be careful not to impinge the vessel. If you feel a strong rhyth-mic pulse with your palpation, reposition your fingers and repalpate.
• Note the location of any tender points or fas-ciculatory response along the muscle and its attachment sites.
• Once you have determined the most dominant tender point or fasciculation (or both), maintain light pressure with the pad(s) of the finger(s) at the location throughout the PRT treatment procedure until reassessment has occurred.
SCM palpation procedure.
PRT Clinician Procedure
• Place the patient supine.
• While palpating the SCM lesion with your near hand, elevate the shoulder of the involved side until a fasciculation is felt or maximal relaxation of the tissue is attained.
• Slide your far hand and arm under the neck and place the palm of the hand on the shoulder of the involved side.
• Using your far forearm, move the cervical spine into flexion.
• After the flexion position of comfort is attained, with the far forearm, rotate the head toward the lesion, and then apply lateral cervical flexion.
• Apply downward shoulder pressure using your far hand to fine-tune the positioning.
• Typically, distally oriented lesions require more cervical flexion than those that are proximally located.
• Corollary tissues treated: Longus colli, anterior rectus capitis, rectus capitis lateralis, hyoids, anterior and middle scalenes
Patient Self-Treatment Procedure
• Identify with your fingers where the SCM is most tender.
• While keeping the palpation fingers on the area of tenderness, place a pillow or folded towel under your head to encourage cervical flexion. Note the amount of cervical flexion that produces the greatest fasciculatory response or level of tissue relaxation, or both.
• Elevate the shoulder on the involved side.
• Laterally flex and rotate your head toward the shoulder on the involved side, noting again the greatest fasciculatory response or tissue relaxation (or both) at which the position should be held.
• Maintain the treatment position until the fas-ciculatory response abates or for three to five minutes.
SCM PRT clinician procedure.
SCM patient self-treatment procedure.