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Assessment and Treatment of Muscle Imbalance
The Janda Approach
by Phillip Page, Clare C. Frank and Robert Lardner
312 Pages
Assessment and Treatment of Muscle Imbalance: The Janda Approach blends postural techniques, neurology, and functional capabilities in order to alleviate chronic musculoskeletal pain and promote greater functionality. Developed by Vladimir Janda, respected neurologist and physiotherapist , the Janda approach presents a unique perspective to rehabilitation. In contrast to a more traditional structural view, the Janda approach is functional—emphasizing the importance of the sensorimotor system in controlling movement and chronic musculoskeletal pain syndromes from sports and general activities. Assessment and Treatment of Muscle Imbalance: The Janda Approach is the only text to offer practical, evidence-based application of Janda’s theories.
Filled with illustrations, photos, and step-by-step instructions, Assessment and Treatment of Muscle Imbalance uses a systematic approach in presenting information that can be used in tandem with other clinical techniques. This resource for practitioners features the following tools:
--A rationale for rehabilitation of the musculoskeletal sytem based on the relationship between the central nervous system and the motor system --A systematic method for the functional examination of the muscular system --Treatment processes focusing on the triad of normalization of peripheral structures, restoration of muscle balance, and facilitation of afferent systems and sensorimotor training --The role of muscle imbalance and functional pathology of sensorimotor systems for specific pain complaints, including cervical pain syndrome, upper- and lower-extremity pain syndromes, and low back pain syndromes
Assessment and Treatment of Muscle Imbalance provides an evidence-based explanation of muscle imbalance. The step-by-step Janda system of evaluation is explained—including analysis of posture, balance, and gait; evaluation of movement patterns; testing of muscle length; and assessment of the soft tissue. The text explores treatment options for muscle imbalance through facilitation and inhibition techniques and sensorimotor training to restore neuromsucular function. It also includes four case studies examining musculoskeletal conditions and showing how the Janda approach compares with other treatments. This text combines theory, evidence, and applications to assist clinicians in implementing the Janda approach into their practice.
Assessment and Treatment of Muscle Imbalance: The Janda Approach focuses on the neurological aspects of muscle imbalance that are common causes of pain and dysfunction in sports and occupational activities. By distilling the scientific works of Vladimir Janda into a practical, systematic approach, this unique resource will assist health care providers in treating patients with musculoskeletal complaints as well as exercise professionals in developing appropriate exercise prescription and training programs.
Part I. The Scientific Basis of Muscle Imbalance
Chapter 1. Structural and Functional Approaches to Muscle Imbalance
Intrinsic Versus Extrinsic Fuction
Muscle Balance in Function and Pathology
Muscle Imbalance Paradigms
Summary
Chapter 2. The Sensorimotor System
Sensorimotor Hardware and Software
Neuromuscular Aspects of Postural Stability and Joint Stabilization
Pathology in Proprioception
Summary
Chapter 3. Chain Reactions
Articular Chains
Muscular Chains
Neurological Chains
Summary
Chapter 4. Pathomechanics of Musculoskeletal Pain and Muscle Imbalance
Pathology of Musculoskeletal Pain
Pathomechanics of Muscular Imbalance
Causes of Muscle Tightness and Weakness
Janda’s Classification of Muscle Imbalance Patterns
Summary
Part II. Functional Evaluation of Muscle Imbalance
Chapter 5. Posture, Balance, and Gait Analysis
Muscle Analysis of Standing Posture
Evaluation of Balance
Evaluation of Gait
Summary
Chapter 6. Evaluation of Movement Patterns
Janda’s Basic Movement Patterns
Additional Movement Tests Complementary to Janda’s Tests
Selected Manual Muscle Tests
Summary
Chapter 7. Muscle Length Testing
Muscle Length Assessment Technique
Lower-Quarter Muscles
Upper-Quarter Muscles
Hypermobility
Summary
Chapter 8. Soft-Tissue Assessment
Characteristics of Trigger Points
Assessment of Trigger Point or Tender Point Chains
Scars
Myofascia
Summary
Part III. Treatment of Muscle Imbalance Syndromes
Chapter 9. Normalization of Peripheral Structures
Central Indirect techniques
Local Direct techniques
Summary
Chapter 10. Restoration of Muscle Balance
Factors Contributing to Muscle Weakness
Additional Treatment Techniques for Muscle Weakness
Factors Contributing to Muscle Tightness
Additional Treatment Techniques for Muscle Tightness
Summary
Chapter 11. Sensorimotor Training
Role of Sensorimotor Training in Janda’s Treatment
Sensorimotor Training Components
Sensorimotor Training Progression
Summary
Part IV. Clinical Syndromes
Chapter 12. Cervical Pain Syndromes
Regional Considerations
Common Pathologies
Case Study
Summary
Chapter 13. Upper-Extremity Pain Syndromes
Regional Considerations
Assessment
Common Pathologies
Case Study
Summary
Chapter 14. Lumbar Pain Syndromes
Regional Considerations
Common Pathologies
Sacroiliac Dysfunction
Assessment
Management of Low Back Pain Syndromes
Case Study
Conclusion
Summary
Chapter 15. Lower-Extremity Pain Syndromes
Regional Considerations
Assessment
Common Pathologies
Case Study
Summary
Phil Page, MS, PT, ATC, CSCS, trained under the guidance of Dr. Vladimir Janda and has taught the Janda approach at national and international workshops. A certified kinesiotaping practitioner, Page is currently working toward his doctorate in kinesiology at Louisiana State University in Baton Rouge, where his research focuses on EMG and muscle imbalance. He is also director of clinical education and research for Thera-Band products.
Page and his wife, Angela, live in Baton Rouge with their four children. In his free time, he enjoys spending time with his family, fishing, and cooking.
Clare C. Frank, DPT, is an orthopedic clinical specialist in private practice in Los Angeles. She serves on the clinical faculty for Kaiser Permanente Movement Science Fellowship in Los Angeles. She also serves as a guest lecturer at the local universities and teaches throughout the United States and internationally.
Frank studied under and taught with Dr. Vladimir Janda. She is a certified instructor of the Janda approach to musculoskeletal pain syndromes, a certified kinesiotaping practitioner, and a certified instructor of Kolar’s approach to dynamic neuromuscular stabilization.
Frank is board certified in orthopedic physical therapy and a fellow of the American Academy of Orthopedic Manual Physical Therapy.
Robert Lardner, PT, was born in Nigeria in 1961. His first career was as a professional ballet and modern dancer after studying at the Rambert Academy outside London, England. He graduated from the department of physical therapy, Lund’s University, Sweden in 1991. He studied with Professors Janda, Lewit and Kolář from the Czech Republic, who are pioneers of functional rehabilitation and manual medicine.
Lardner worked in several inpatient and outpatient rehabilitation facilities in Sweden prior to moving to the United States in 1992. He was a staff physical therapist at McNeal Hospital, Clearing Industrial Clinic, and a physical therapy supervisor at Mercy Hospital. He also was in charge of physical therapy services at a number of private outpatient and sports clinics.
Lardner is currently in private practice in Chicago and teaches various rehabilitation seminars throughout the United States and Europe.
“A practical text for clinicians treating patients with musculoskeletal complaints.”
SciTech Book News (March 2010)
“An excellent book and a fitting tribute to Janda - well done! I attended several of Janda's courses in the UK over a period of many years and his influence on my professional life was significant.”
Christopher Norris, PhD, MSc, MCSP, MBAcC -- Director of Norris Associates
"This would make a useful addition to every clinician’s library—especially physical therapists, chiropractors, osteopaths, and all those using hands-on therapies."
Journal of Bodywork and Movement Therapies
"…a thorough, well-organized, and well-written summary of the Janda approach to muscle imbalance."
Journal of Orthopedic and Sports Physical Therapy
"With its modest price tag and practical insights of both assessment and treatment of muscle imbalance, I would recommend this book to any practitioner or student planning to treat MSK disorders."
Manual Therapy
This book "provides a lot of useful information that is different from the typical treatment approaches taught in most physical therapy schools and it can only help give clinicians insights that may help them treat their patients."
Orthopedic Physical Therapy Practice
Causes of muscle weakness
A look at the causes of muscle weakness as well as Janda’s classification of muscle imbalance patterns.
Muscle tension can decrease as a result of a structural lesion in the CNS such as a spinal cord injury or stroke. A loss of tension leads to flaccidity or weakness. Weak muscles are also described as hypotonic or inhibited. Functionally, muscle can be weak as a result of neuroflexive or adaptive changes and may exhibit delayed activation in movement patterns.
Neuroflexive Factors for Decreased Tension
Many contractile factors can contribute to decreased muscle tension:
- Reciprocal inhibition (Sherrington 1907). Muscle becomes inhibited reflexively when its antagonist is activated. Weakness is often reflex-mediated inhibition secondary to increased tension of the antagonist.
- Arthrogenic weakness (Stokes and Young 1984; DeAndrade, Grant, and Dison. 1965). Muscle becomes inhibited via anterior horn cells due to joint swelling or dysfunction. This weakness also leads to selective atrophy of Type II fibers (Edstrom 1970).
- Deafferentation (Freeman, Dean, and Hanham 1965). Deafferentation is a decrease in afferent information from neuromuscular receptors. Damage to joint mechanoreceptors (as seen with ligamentous injury) with subsequent loss of articular reflexes can cause altered motor programs, often influencing many muscles remote from the injured area (Bullock-Saxton 1994). This loss of afferent information ultimately leads to de-efferentation, or the loss of efferent signals to alpha motor neurons, which results in decreased muscle strength.
- Pseudoparesis (Janda 1986a). Pseudoparesis is a clinical presentation of weakness of neuroflexive origin. Pseudoparesis has three clinical signs: hypotonia upon inspection and palpation, a score of 4 out of 5 on a manual muscle test, and a change in the muscle activation pattern that may include delayed onset with early synergist activation or decreased EMG levels. Facilitatory techniques often restore muscle strength and activation. Normally facilitatory input can be inhibitory to a pseudoparetic muscle (Janda 1986a).
- TrP weakness (Simons, Travell, and Simons 1999). Hyperirritable bands of muscle fiber decrease the stimulation threshold, leading to overuse, early fatigue, and ultimately weakness. Muscles with active TrPs fatigue more rapidly than normal muscles do (Mense and Simons 2001), and they exhibit a decreased number of firing motor units and poor synchronization (Janda 1993).
- Fatigue. Muscle fatigue can be caused by metabolic or neurological factors. Often during exercise muscles are fatigued before pain is experienced. Thus the patient develops compensatory and faulty movement patterns before experiencing pain.
Adaptive Factors for Decreased Tension
Noncontractile factors causing decreased muscle tension are stretch weakness and tightness weakness:
- Stretch weakness (Kendall, McCreary, and Provance 1993; Sahrmann 2002a, 2002b). Stretch weakness is a condition in which a muscle is elongated beyond physiological neutral but not beyond the normal ROM (Janda 1993). Prolonged muscle elongation causes muscle spindle inhibition and the creation of additional sarcomeres. The increased muscle length also changes the length-tension curve. Stretch weakness is also known as positional weakness and is often associated with overuse and postural changes.
- Tightness weakness (Janda 1993). This is the most severe form of muscle tightness. It is often overlooked clinically. Overused muscle shortens over time, changing the muscle's length-tension curve and becoming more readily activated and weaker after time. There is also an increase in the noncontractile tissue and a decrease in elasticity, leading to hypertrophy. Ultimately, overuse leads to ischemia and degeneration of muscle fibers, which further weakens the muscle.
When an inhibited and weak muscle is resisted, as is the aim of strengthening exercises, its activity tends to decrease rather than increase (Janda 1987). It is important to distinguish between neuroflexive weakness and structural weakness. Often, if the tight antagonist is stretched, the weak and inhibited muscle spontaneously increases in strength.
Janda's Classification of Muscle Imbalance Patterns
Through his observations of patients with neurological disorders and chronic musculoskeletal pain, Janda found that the typical muscle response to joint dysfunction is similar to the muscle patterns found in upper motor neuron lesions, concluding that muscle imbalances are controlled by the CNS (Janda 1987). Janda believed that muscle tightness or spasticity is predominant. Often, weakness from muscle imbalance results from reciprocal inhibition of the tight antagonist. The degree of tightness and weakness varies between individuals, but the pattern rarely does. These patterns lead to postural changes and joint dysfunction and degeneration.
Janda identified three stereotypical patterns associated with distinct chronic pain syndromes: the upper-crossed, lower-crossed, and layer syndromes. These syndromes are characterized by specific patterns of muscle weakness and tightness that cross between the dorsal and the ventral sides of the body.
Upper-Crossed Syndrome
Upper-crossed syndrome (UCS) is also referred to as proximal or shoulder girdle crossed syndrome (figure 4.2a; Janda 1988). In UCS, tightness of the upper trapezius and levator scapula on the dorsal side crosses with tightness of the pectoralis major and minor. Weakness of the deep cervical flexors ventrally crosses with weakness of the middle and lower trapezius. This pattern of imbalance creates joint dysfunction, particularly at the atlanto-occipital joint, C4-C5 segment, cervicothoracic joint, glenohumeral joint, and T4-T5 segment. Janda noted that these focal areas of stress within the spine correspond to transitional zones in which neighboring vertebrae change in morphology. Specific postural changes are seen in UCS, including forward head posture, increased cervical lordosis and thoracic kyphosis, elevated and protracted shoulders, and rotation or abduction and winging of the scapulae (figure 4.2b). These postural changes decrease glenohumeral stability as the glenoid fossa becomes more vertical due to serratus anterior weakness leading to abduction, rotation, and winging of the scapulae. This loss of stability requires the levator scapula and upper trapezius to increase activation to maintain glenohumeral centration (Janda 1988).
Lower-Crossed Syndrome
Lower-crossed syndrome (LCS) is also referred to as distal or pelvic crossed syndrome (figure 4.3a; Janda 1987). In LCS, tightness of the thoracolumbar extensors on the dorsal side crosses with tightness of the iliopsoas and rectus femoris. Weakness of the deep abdominal muscles ventrally crosses with weakness of the gluteus maximus and medius. This pattern of imbalance creates joint dysfunction, particularly at the L4-L5 and L5-S1 segments, SI joint, and hip joint. Specific postural changes seen in LCS include anterior pelvic tilt, increased lumbar lordosis, lateral lumbar shift, lateral leg rotation, and knee hyperextension. If the lordosis is deep and short, then imbalance is predominantly in the pelvic muscles; if the lordosis is shallow and extends into the thoracic area, then imbalance predominates in the trunk muscles (Janda 1987).
Janda identified two subtypes of LCS: A and B (see figure 4.3, b-c). Patients with LCS type A use more hip flexion and extension movement for mobility; their standing posture demonstrates an anterior pelvic tilt with slight hip flexion and knee flexion. These individuals compensate with a hyperlordosis limited to the lumbar spine and with a hyperkyphosis in the upper lumbar and thoracolumbar segments.
Learn to assess muscle length
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening.
Muscle Length Assessment Technique
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening. Precise testing requires that one of the bony attachments of the muscle (usually the origin) be in a fixed position while the other bony attachment is moved passively in the direction of lengthening the muscle. In other words, muscle length testing assesses the resistance to passive movement. This is in contrast to typical flexibility or ROM testing. The actual ROM can be measured for documentation purposes, but it gives limited clinical information in muscle imbalance syndromes. The most valuable clinical information is the muscular end feel and the location of the ROM end feel. The elongation of the muscle should be performed slowly to avoid eliciting a quick stretch of the muscle spindle and subsequently inducing a twitch response and muscle contraction. In addition, for the best accuracy and precision, muscle length testing should be performed when the patient is not in acute pain in order to avoid pain inhibition and muscle guarding. In summary, there are four steps to assessing muscle length:
1. Ensure maximal lengthening of the muscle from origin to insertion.
2. Firmly stabilize one end (usually the origin).
3. Slowly elongate the muscle.
4. Assess the end feel.
Following are the procedures for testing key muscles. Clinicians do not have to perform muscle length testing on every muscle listed; instead, they should assess the muscles that the postural and movement pattern analysis indicate as being possibly tight. Once tight muscles have been identified, the clinician can establish a muscle imbalance pattern (if present) and begin to look for causes of the tightness. Table 7.1 provides the normal results of muscle length for flexibility testing.
Table 7.1 Normal Results of Muscles Tested for Length | |
| Muscle | Normal ranges or end feel |
| Iliopsoas | 0° hip extension, 10° with overpressure |
| Rectus femoris | 90° knee extension, 125° with overpressure |
| TFL-IT band | 0° hip abduction (neutral), 15°-20° with overpressure |
| Adductors | 0° hip abduction (neutral), 20°-25° with overpressure in the modified Thomas test position 45° hip abduction in supine position |
| Hamstrings | 80° hip flexion with contralateral leg extended 90° hip flexion with contralateral leg flexed |
| Triceps surae | 0° ankle dorsiflexion |
| Quadratus lumborum | Thoracolumbar curve should be smooth and gradual |
| Piriformis | Gradual soft end feel |
| Upper trapezius | Gradual soft end feel |
| Levator scapulae | Gradual soft end feel |
| SCM | Gradual soft end feel |
| Pectoralis major | Sternal portion (lower fibers): with shoulder abducted at 150°, arm should be horizontal to table and 15°-20° with overpressure Sternal portion (midfibers): with shoulder abducted to 90°, arm should be horizontal to table and 30° with overpressure Clavicular portion: with shoulder abducted to 60°, arm should hang freely over table |
| Paraspinals | Schober's test: excursion of >2.4 in. (6 cm) |
Lower-Quarter Muscles
The muscles of the lower quarter include those of the leg, pelvis, and lower back. The muscles prone to tightness are those involved in maintaining a single-leg stance (Janda 1987). Tightness of the hip flexors and tightness of the thoracolumbar extensors are hallmark signs of Janda's LCS.
Modified Thomas Test for Hip Flexor
The modified Thomas test (figure 7.2, a-e) allows the clinician to assess four different muscles prone to tightness namely, the one-joint hip flexor, iliacus and psoas major, and the two-joint hip flexors, rectus femoris and TFL-ITB. Tightness of the hip flexors limits hip hyperextension in gait and may cause an anterior pelvic tilt. Weakness of the gluteus maximus often is due to facilitation of the hip flexors.
Patient Position
The patient is asked to sit on the edge of the table, with the coccyx and ischial tuberosities touching the table and one foot on the floor. Then, the patient is asked to flex the opposite hip and knee toward the chest and maintain the position with the hands (see figure 7.2a).
Clinician Position
The clinician stands beside the leg not being tested, facing the patient. While supporting the patient by placing one hand on the midthoracic spine and the other on the knee, the clinician passively rolls the patient down to the table to the supine position. The clinician needs to ensure that the patient's knees are flexed, lumbar spine is flexed, and pelvis is in posterior rotation to fix the origin of the hip flexors.
Test
The clinician passively lowers the tested leg until resistance is felt or movement at the pelvis is detected. With the patient's thigh in the final resting position, the clinician observes whether it is in neutral and parallel to the table or abducted. A normal length of the one-joint hip flexors with the lumbar spine and sacrum flat on the table is indicated by the posterior thigh touching the table (0° of hip extension). With slight overpressure, the thigh should reach 10° to 15° of hyperextension (figure 7.2, b-c). Prominence of a superior patellar groove (figure 7.2d) suggests a short rectus femoris, while prominence of a lateral IT groove suggests a short IT band (see figure 7.2e).
Restoration of muscle balance
Treatment of muscle weakness aims at stimulating and increasing the response of the muscle spindle of the pseudoparetic muscle.
Muscle Length Assessment Technique
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening. Precise testing requires that one of the bony attachments of the muscle (usually the origin) be in a fixed position while the other bony attachment is moved passively in the direction of lengthening the muscle. In other words, muscle length testing assesses the resistance to passive movement. This is in contrast to typical flexibility or ROM testing. The actual ROM can be measured for documentation purposes, but it gives limited clinical information in muscle imbalance syndromes. The most valuable clinical information is the muscular end feel and the location of the ROM end feel. The elongation of the muscle should be performed slowly to avoid eliciting a quick stretch of the muscle spindle and subsequently inducing a twitch response and muscle contraction. In addition, for the best accuracy and precision, muscle length testing should be performed when the patient is not in acute pain in order to avoid pain inhibition and muscle guarding. In summary, there are four steps to assessing muscle length:
1. Ensure maximal lengthening of the muscle from origin to insertion.
2. Firmly stabilize one end (usually the origin).
3. Slowly elongate the muscle.
4. Assess the end feel.
Following are the procedures for testing key muscles. Clinicians do not have to perform muscle length testing on every muscle listed; instead, they should assess the muscles that the postural and movement pattern analysis indicate as being possibly tight. Once tight muscles have been identified, the clinician can establish a muscle imbalance pattern (if present) and begin to look for causes of the tightness. Table 7.1 provides the normal results of muscle length for flexibility testing.
Table 7.1 Normal Results of Muscles Tested for Length | |
| Muscle | Normal ranges or end feel |
| Iliopsoas | 0° hip extension, 10° with overpressure |
| Rectus femoris | 90° knee extension, 125° with overpressure |
| TFL-IT band | 0° hip abduction (neutral), 15°-20° with overpressure |
| Adductors | 0° hip abduction (neutral), 20°-25° with overpressure in the modified Thomas test position 45° hip abduction in supine position |
| Hamstrings | 80° hip flexion with contralateral leg extended 90° hip flexion with contralateral leg flexed |
| Triceps surae | 0° ankle dorsiflexion |
| Quadratus lumborum | Thoracolumbar curve should be smooth and gradual |
| Piriformis | Gradual soft end feel |
| Upper trapezius | Gradual soft end feel |
| Levator scapulae | Gradual soft end feel |
| SCM | Gradual soft end feel |
| Pectoralis major | Sternal portion (lower fibers): with shoulder abducted at 150°, arm should be horizontal to table and 15°-20° with overpressure Sternal portion (midfibers): with shoulder abducted to 90°, arm should be horizontal to table and 30° with overpressure Clavicular portion: with shoulder abducted to 60°, arm should hang freely over table |
| Paraspinals | Schober's test: excursion of >2.4 in. (6 cm) |
Lower-Quarter Muscles
The muscles of the lower quarter include those of the leg, pelvis, and lower back. The muscles prone to tightness are those involved in maintaining a single-leg stance (Janda 1987). Tightness of the hip flexors and tightness of the thoracolumbar extensors are hallmark signs of Janda's LCS.
Modified Thomas Test for Hip Flexor
The modified Thomas test (figure 7.2, a-e) allows the clinician to assess four different muscles prone to tightness namely, the one-joint hip flexor, iliacus and psoas major, and the two-joint hip flexors, rectus femoris and TFL-ITB. Tightness of the hip flexors limits hip hyperextension in gait and may cause an anterior pelvic tilt. Weakness of the gluteus maximus often is due to facilitation of the hip flexors.
Patient Position
The patient is asked to sit on the edge of the table, with the coccyx and ischial tuberosities touching the table and one foot on the floor. Then, the patient is asked to flex the opposite hip and knee toward the chest and maintain the position with the hands (see figure 7.2a).
Clinician Position
The clinician stands beside the leg not being tested, facing the patient. While supporting the patient by placing one hand on the midthoracic spine and the other on the knee, the clinician passively rolls the patient down to the table to the supine position. The clinician needs to ensure that the patient's knees are flexed, lumbar spine is flexed, and pelvis is in posterior rotation to fix the origin of the hip flexors.
Test
The clinician passively lowers the tested leg until resistance is felt or movement at the pelvis is detected. With the patient's thigh in the final resting position, the clinician observes whether it is in neutral and parallel to the table or abducted. A normal length of the one-joint hip flexors with the lumbar spine and sacrum flat on the table is indicated by the posterior thigh touching the table (0° of hip extension). With slight overpressure, the thigh should reach 10° to 15° of hyperextension (figure 7.2, b-c). Prominence of a superior patellar groove (figure 7.2d) suggests a short rectus femoris, while prominence of a lateral IT groove suggests a short IT band (see figure 7.2e).
Rehabilitation of impingement
Rehabilitation rather than surgery is recommended for secondary impingement.
Rehabilitation rather than surgery is recommended for secondary impingement (Brox and Brevik 1996; Kronberg, Németh, and Broström 1990; Michener, Walsworth, and Burnet 2004; Morrison, Frogameni, and Woodworth 1997). Patients with primary impingement (type II and III acromion), however, have only a 64% to 68% success rate with conservative treatment (Morrison, Frogameni, and Woodworth 1997). While rehabilitation and arthroscopic surgery improve impingement symptoms equally (Haarh et al. 2005; Haarh and Andersen 2006), rehabilitation is less costly (Brox et al. 1993).
In a systematic review, Michener, Walsworth, and Burnet and colleagues (2004) found strong support in the literature for therapeutic exercise of the rotator cuff and scapular muscles as well as for stretching of the anterior and posterior shoulder. Furthermore, exercise is more effective when combined with joint mobilization (Michener, Walsworth, and Burnet 2004; Senbursa, Baltaci, and Atay 2007). The following are impingement rehabilitation recommendations with evidence-based rationale:
- Integrate the entire upper-extremity chain during exercise. This facilitates the kinetic chain from the hand to the spine (Burkhart, Morgan, and Kibler 2003; Kibler 1998b, 2006; McMullen and Uhl 2000). Figure 13.5 illustrates exercises that integrate the whole kinetic chain.
- Include hip and trunk stabilization exercises. This facilitates force transmission and proximal stabilization between the upper extremity and the trunk (Burkhart, Morgan, and Kibler 2003; Kibler 1998b, 2006; McMullen and Uhl 2000).
- Isolate the rotator cuff and scapular stabilizers first, before performing multijoint movements. Performing multijoint shoulder movements does not increase the strength of smaller single-joint muscles such as the rotator cuff (Giannakopoulos et al. 2004). Strengthening exercises isolating the rotator cuff should be performed first (Jobe and Pink 1993; Malliou et al. 2004).
- Exercise in the scapular plane. The scapular plane offers the most balanced position of the capsule and provides ideal joint centration during elevation (Borsa, Timmons, and Sauers 2003).
- Exercise both shoulders. Abnormal muscle activation often occurs in both the involved and the uninvolved shoulder (Cools et al. 2003; Cools, Declercq et al. 2007; Wadsworth and Bullock-Saxton 1997).
- Include neuromuscular exercises such as closed kinetic chain exercises and PNF. Patients with impingement demonstrate reduced proprioception (Machner et al. 2003) and so require proprioceptive rehabilitation (Ginn and Cohen 2005; Kamkar, Irrgang, and Whitney 1993; Smith and Burnolli 1989). Figure 13.6 illustrates a closed kinetic chain shoulder exercise for improving proprioception (Naughton, Adams, and Maher 2005).
- Stretch the posterior shoulder when internal rotation is limited. The posterior capsule is often tight in athletes with impingement, limiting internal rotation and follow-through (Myers et al. 2006; Tyler et al. 2000). The cross-body stretch (see figure 13.7) improves internal rotation in subjects with posterior shoulder tightness (McClure et al. 2007).
Causes of muscle weakness
A look at the causes of muscle weakness as well as Janda’s classification of muscle imbalance patterns.
Muscle tension can decrease as a result of a structural lesion in the CNS such as a spinal cord injury or stroke. A loss of tension leads to flaccidity or weakness. Weak muscles are also described as hypotonic or inhibited. Functionally, muscle can be weak as a result of neuroflexive or adaptive changes and may exhibit delayed activation in movement patterns.
Neuroflexive Factors for Decreased Tension
Many contractile factors can contribute to decreased muscle tension:
- Reciprocal inhibition (Sherrington 1907). Muscle becomes inhibited reflexively when its antagonist is activated. Weakness is often reflex-mediated inhibition secondary to increased tension of the antagonist.
- Arthrogenic weakness (Stokes and Young 1984; DeAndrade, Grant, and Dison. 1965). Muscle becomes inhibited via anterior horn cells due to joint swelling or dysfunction. This weakness also leads to selective atrophy of Type II fibers (Edstrom 1970).
- Deafferentation (Freeman, Dean, and Hanham 1965). Deafferentation is a decrease in afferent information from neuromuscular receptors. Damage to joint mechanoreceptors (as seen with ligamentous injury) with subsequent loss of articular reflexes can cause altered motor programs, often influencing many muscles remote from the injured area (Bullock-Saxton 1994). This loss of afferent information ultimately leads to de-efferentation, or the loss of efferent signals to alpha motor neurons, which results in decreased muscle strength.
- Pseudoparesis (Janda 1986a). Pseudoparesis is a clinical presentation of weakness of neuroflexive origin. Pseudoparesis has three clinical signs: hypotonia upon inspection and palpation, a score of 4 out of 5 on a manual muscle test, and a change in the muscle activation pattern that may include delayed onset with early synergist activation or decreased EMG levels. Facilitatory techniques often restore muscle strength and activation. Normally facilitatory input can be inhibitory to a pseudoparetic muscle (Janda 1986a).
- TrP weakness (Simons, Travell, and Simons 1999). Hyperirritable bands of muscle fiber decrease the stimulation threshold, leading to overuse, early fatigue, and ultimately weakness. Muscles with active TrPs fatigue more rapidly than normal muscles do (Mense and Simons 2001), and they exhibit a decreased number of firing motor units and poor synchronization (Janda 1993).
- Fatigue. Muscle fatigue can be caused by metabolic or neurological factors. Often during exercise muscles are fatigued before pain is experienced. Thus the patient develops compensatory and faulty movement patterns before experiencing pain.
Adaptive Factors for Decreased Tension
Noncontractile factors causing decreased muscle tension are stretch weakness and tightness weakness:
- Stretch weakness (Kendall, McCreary, and Provance 1993; Sahrmann 2002a, 2002b). Stretch weakness is a condition in which a muscle is elongated beyond physiological neutral but not beyond the normal ROM (Janda 1993). Prolonged muscle elongation causes muscle spindle inhibition and the creation of additional sarcomeres. The increased muscle length also changes the length-tension curve. Stretch weakness is also known as positional weakness and is often associated with overuse and postural changes.
- Tightness weakness (Janda 1993). This is the most severe form of muscle tightness. It is often overlooked clinically. Overused muscle shortens over time, changing the muscle's length-tension curve and becoming more readily activated and weaker after time. There is also an increase in the noncontractile tissue and a decrease in elasticity, leading to hypertrophy. Ultimately, overuse leads to ischemia and degeneration of muscle fibers, which further weakens the muscle.
When an inhibited and weak muscle is resisted, as is the aim of strengthening exercises, its activity tends to decrease rather than increase (Janda 1987). It is important to distinguish between neuroflexive weakness and structural weakness. Often, if the tight antagonist is stretched, the weak and inhibited muscle spontaneously increases in strength.
Janda's Classification of Muscle Imbalance Patterns
Through his observations of patients with neurological disorders and chronic musculoskeletal pain, Janda found that the typical muscle response to joint dysfunction is similar to the muscle patterns found in upper motor neuron lesions, concluding that muscle imbalances are controlled by the CNS (Janda 1987). Janda believed that muscle tightness or spasticity is predominant. Often, weakness from muscle imbalance results from reciprocal inhibition of the tight antagonist. The degree of tightness and weakness varies between individuals, but the pattern rarely does. These patterns lead to postural changes and joint dysfunction and degeneration.
Janda identified three stereotypical patterns associated with distinct chronic pain syndromes: the upper-crossed, lower-crossed, and layer syndromes. These syndromes are characterized by specific patterns of muscle weakness and tightness that cross between the dorsal and the ventral sides of the body.
Upper-Crossed Syndrome
Upper-crossed syndrome (UCS) is also referred to as proximal or shoulder girdle crossed syndrome (figure 4.2a; Janda 1988). In UCS, tightness of the upper trapezius and levator scapula on the dorsal side crosses with tightness of the pectoralis major and minor. Weakness of the deep cervical flexors ventrally crosses with weakness of the middle and lower trapezius. This pattern of imbalance creates joint dysfunction, particularly at the atlanto-occipital joint, C4-C5 segment, cervicothoracic joint, glenohumeral joint, and T4-T5 segment. Janda noted that these focal areas of stress within the spine correspond to transitional zones in which neighboring vertebrae change in morphology. Specific postural changes are seen in UCS, including forward head posture, increased cervical lordosis and thoracic kyphosis, elevated and protracted shoulders, and rotation or abduction and winging of the scapulae (figure 4.2b). These postural changes decrease glenohumeral stability as the glenoid fossa becomes more vertical due to serratus anterior weakness leading to abduction, rotation, and winging of the scapulae. This loss of stability requires the levator scapula and upper trapezius to increase activation to maintain glenohumeral centration (Janda 1988).
Lower-Crossed Syndrome
Lower-crossed syndrome (LCS) is also referred to as distal or pelvic crossed syndrome (figure 4.3a; Janda 1987). In LCS, tightness of the thoracolumbar extensors on the dorsal side crosses with tightness of the iliopsoas and rectus femoris. Weakness of the deep abdominal muscles ventrally crosses with weakness of the gluteus maximus and medius. This pattern of imbalance creates joint dysfunction, particularly at the L4-L5 and L5-S1 segments, SI joint, and hip joint. Specific postural changes seen in LCS include anterior pelvic tilt, increased lumbar lordosis, lateral lumbar shift, lateral leg rotation, and knee hyperextension. If the lordosis is deep and short, then imbalance is predominantly in the pelvic muscles; if the lordosis is shallow and extends into the thoracic area, then imbalance predominates in the trunk muscles (Janda 1987).
Janda identified two subtypes of LCS: A and B (see figure 4.3, b-c). Patients with LCS type A use more hip flexion and extension movement for mobility; their standing posture demonstrates an anterior pelvic tilt with slight hip flexion and knee flexion. These individuals compensate with a hyperlordosis limited to the lumbar spine and with a hyperkyphosis in the upper lumbar and thoracolumbar segments.
Learn to assess muscle length
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening.
Muscle Length Assessment Technique
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening. Precise testing requires that one of the bony attachments of the muscle (usually the origin) be in a fixed position while the other bony attachment is moved passively in the direction of lengthening the muscle. In other words, muscle length testing assesses the resistance to passive movement. This is in contrast to typical flexibility or ROM testing. The actual ROM can be measured for documentation purposes, but it gives limited clinical information in muscle imbalance syndromes. The most valuable clinical information is the muscular end feel and the location of the ROM end feel. The elongation of the muscle should be performed slowly to avoid eliciting a quick stretch of the muscle spindle and subsequently inducing a twitch response and muscle contraction. In addition, for the best accuracy and precision, muscle length testing should be performed when the patient is not in acute pain in order to avoid pain inhibition and muscle guarding. In summary, there are four steps to assessing muscle length:
1. Ensure maximal lengthening of the muscle from origin to insertion.
2. Firmly stabilize one end (usually the origin).
3. Slowly elongate the muscle.
4. Assess the end feel.
Following are the procedures for testing key muscles. Clinicians do not have to perform muscle length testing on every muscle listed; instead, they should assess the muscles that the postural and movement pattern analysis indicate as being possibly tight. Once tight muscles have been identified, the clinician can establish a muscle imbalance pattern (if present) and begin to look for causes of the tightness. Table 7.1 provides the normal results of muscle length for flexibility testing.
Table 7.1 Normal Results of Muscles Tested for Length | |
| Muscle | Normal ranges or end feel |
| Iliopsoas | 0° hip extension, 10° with overpressure |
| Rectus femoris | 90° knee extension, 125° with overpressure |
| TFL-IT band | 0° hip abduction (neutral), 15°-20° with overpressure |
| Adductors | 0° hip abduction (neutral), 20°-25° with overpressure in the modified Thomas test position 45° hip abduction in supine position |
| Hamstrings | 80° hip flexion with contralateral leg extended 90° hip flexion with contralateral leg flexed |
| Triceps surae | 0° ankle dorsiflexion |
| Quadratus lumborum | Thoracolumbar curve should be smooth and gradual |
| Piriformis | Gradual soft end feel |
| Upper trapezius | Gradual soft end feel |
| Levator scapulae | Gradual soft end feel |
| SCM | Gradual soft end feel |
| Pectoralis major | Sternal portion (lower fibers): with shoulder abducted at 150°, arm should be horizontal to table and 15°-20° with overpressure Sternal portion (midfibers): with shoulder abducted to 90°, arm should be horizontal to table and 30° with overpressure Clavicular portion: with shoulder abducted to 60°, arm should hang freely over table |
| Paraspinals | Schober's test: excursion of >2.4 in. (6 cm) |
Lower-Quarter Muscles
The muscles of the lower quarter include those of the leg, pelvis, and lower back. The muscles prone to tightness are those involved in maintaining a single-leg stance (Janda 1987). Tightness of the hip flexors and tightness of the thoracolumbar extensors are hallmark signs of Janda's LCS.
Modified Thomas Test for Hip Flexor
The modified Thomas test (figure 7.2, a-e) allows the clinician to assess four different muscles prone to tightness namely, the one-joint hip flexor, iliacus and psoas major, and the two-joint hip flexors, rectus femoris and TFL-ITB. Tightness of the hip flexors limits hip hyperextension in gait and may cause an anterior pelvic tilt. Weakness of the gluteus maximus often is due to facilitation of the hip flexors.
Patient Position
The patient is asked to sit on the edge of the table, with the coccyx and ischial tuberosities touching the table and one foot on the floor. Then, the patient is asked to flex the opposite hip and knee toward the chest and maintain the position with the hands (see figure 7.2a).
Clinician Position
The clinician stands beside the leg not being tested, facing the patient. While supporting the patient by placing one hand on the midthoracic spine and the other on the knee, the clinician passively rolls the patient down to the table to the supine position. The clinician needs to ensure that the patient's knees are flexed, lumbar spine is flexed, and pelvis is in posterior rotation to fix the origin of the hip flexors.
Test
The clinician passively lowers the tested leg until resistance is felt or movement at the pelvis is detected. With the patient's thigh in the final resting position, the clinician observes whether it is in neutral and parallel to the table or abducted. A normal length of the one-joint hip flexors with the lumbar spine and sacrum flat on the table is indicated by the posterior thigh touching the table (0° of hip extension). With slight overpressure, the thigh should reach 10° to 15° of hyperextension (figure 7.2, b-c). Prominence of a superior patellar groove (figure 7.2d) suggests a short rectus femoris, while prominence of a lateral IT groove suggests a short IT band (see figure 7.2e).
Restoration of muscle balance
Treatment of muscle weakness aims at stimulating and increasing the response of the muscle spindle of the pseudoparetic muscle.
Muscle Length Assessment Technique
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening. Precise testing requires that one of the bony attachments of the muscle (usually the origin) be in a fixed position while the other bony attachment is moved passively in the direction of lengthening the muscle. In other words, muscle length testing assesses the resistance to passive movement. This is in contrast to typical flexibility or ROM testing. The actual ROM can be measured for documentation purposes, but it gives limited clinical information in muscle imbalance syndromes. The most valuable clinical information is the muscular end feel and the location of the ROM end feel. The elongation of the muscle should be performed slowly to avoid eliciting a quick stretch of the muscle spindle and subsequently inducing a twitch response and muscle contraction. In addition, for the best accuracy and precision, muscle length testing should be performed when the patient is not in acute pain in order to avoid pain inhibition and muscle guarding. In summary, there are four steps to assessing muscle length:
1. Ensure maximal lengthening of the muscle from origin to insertion.
2. Firmly stabilize one end (usually the origin).
3. Slowly elongate the muscle.
4. Assess the end feel.
Following are the procedures for testing key muscles. Clinicians do not have to perform muscle length testing on every muscle listed; instead, they should assess the muscles that the postural and movement pattern analysis indicate as being possibly tight. Once tight muscles have been identified, the clinician can establish a muscle imbalance pattern (if present) and begin to look for causes of the tightness. Table 7.1 provides the normal results of muscle length for flexibility testing.
Table 7.1 Normal Results of Muscles Tested for Length | |
| Muscle | Normal ranges or end feel |
| Iliopsoas | 0° hip extension, 10° with overpressure |
| Rectus femoris | 90° knee extension, 125° with overpressure |
| TFL-IT band | 0° hip abduction (neutral), 15°-20° with overpressure |
| Adductors | 0° hip abduction (neutral), 20°-25° with overpressure in the modified Thomas test position 45° hip abduction in supine position |
| Hamstrings | 80° hip flexion with contralateral leg extended 90° hip flexion with contralateral leg flexed |
| Triceps surae | 0° ankle dorsiflexion |
| Quadratus lumborum | Thoracolumbar curve should be smooth and gradual |
| Piriformis | Gradual soft end feel |
| Upper trapezius | Gradual soft end feel |
| Levator scapulae | Gradual soft end feel |
| SCM | Gradual soft end feel |
| Pectoralis major | Sternal portion (lower fibers): with shoulder abducted at 150°, arm should be horizontal to table and 15°-20° with overpressure Sternal portion (midfibers): with shoulder abducted to 90°, arm should be horizontal to table and 30° with overpressure Clavicular portion: with shoulder abducted to 60°, arm should hang freely over table |
| Paraspinals | Schober's test: excursion of >2.4 in. (6 cm) |
Lower-Quarter Muscles
The muscles of the lower quarter include those of the leg, pelvis, and lower back. The muscles prone to tightness are those involved in maintaining a single-leg stance (Janda 1987). Tightness of the hip flexors and tightness of the thoracolumbar extensors are hallmark signs of Janda's LCS.
Modified Thomas Test for Hip Flexor
The modified Thomas test (figure 7.2, a-e) allows the clinician to assess four different muscles prone to tightness namely, the one-joint hip flexor, iliacus and psoas major, and the two-joint hip flexors, rectus femoris and TFL-ITB. Tightness of the hip flexors limits hip hyperextension in gait and may cause an anterior pelvic tilt. Weakness of the gluteus maximus often is due to facilitation of the hip flexors.
Patient Position
The patient is asked to sit on the edge of the table, with the coccyx and ischial tuberosities touching the table and one foot on the floor. Then, the patient is asked to flex the opposite hip and knee toward the chest and maintain the position with the hands (see figure 7.2a).
Clinician Position
The clinician stands beside the leg not being tested, facing the patient. While supporting the patient by placing one hand on the midthoracic spine and the other on the knee, the clinician passively rolls the patient down to the table to the supine position. The clinician needs to ensure that the patient's knees are flexed, lumbar spine is flexed, and pelvis is in posterior rotation to fix the origin of the hip flexors.
Test
The clinician passively lowers the tested leg until resistance is felt or movement at the pelvis is detected. With the patient's thigh in the final resting position, the clinician observes whether it is in neutral and parallel to the table or abducted. A normal length of the one-joint hip flexors with the lumbar spine and sacrum flat on the table is indicated by the posterior thigh touching the table (0° of hip extension). With slight overpressure, the thigh should reach 10° to 15° of hyperextension (figure 7.2, b-c). Prominence of a superior patellar groove (figure 7.2d) suggests a short rectus femoris, while prominence of a lateral IT groove suggests a short IT band (see figure 7.2e).
Rehabilitation of impingement
Rehabilitation rather than surgery is recommended for secondary impingement.
Rehabilitation rather than surgery is recommended for secondary impingement (Brox and Brevik 1996; Kronberg, Németh, and Broström 1990; Michener, Walsworth, and Burnet 2004; Morrison, Frogameni, and Woodworth 1997). Patients with primary impingement (type II and III acromion), however, have only a 64% to 68% success rate with conservative treatment (Morrison, Frogameni, and Woodworth 1997). While rehabilitation and arthroscopic surgery improve impingement symptoms equally (Haarh et al. 2005; Haarh and Andersen 2006), rehabilitation is less costly (Brox et al. 1993).
In a systematic review, Michener, Walsworth, and Burnet and colleagues (2004) found strong support in the literature for therapeutic exercise of the rotator cuff and scapular muscles as well as for stretching of the anterior and posterior shoulder. Furthermore, exercise is more effective when combined with joint mobilization (Michener, Walsworth, and Burnet 2004; Senbursa, Baltaci, and Atay 2007). The following are impingement rehabilitation recommendations with evidence-based rationale:
- Integrate the entire upper-extremity chain during exercise. This facilitates the kinetic chain from the hand to the spine (Burkhart, Morgan, and Kibler 2003; Kibler 1998b, 2006; McMullen and Uhl 2000). Figure 13.5 illustrates exercises that integrate the whole kinetic chain.
- Include hip and trunk stabilization exercises. This facilitates force transmission and proximal stabilization between the upper extremity and the trunk (Burkhart, Morgan, and Kibler 2003; Kibler 1998b, 2006; McMullen and Uhl 2000).
- Isolate the rotator cuff and scapular stabilizers first, before performing multijoint movements. Performing multijoint shoulder movements does not increase the strength of smaller single-joint muscles such as the rotator cuff (Giannakopoulos et al. 2004). Strengthening exercises isolating the rotator cuff should be performed first (Jobe and Pink 1993; Malliou et al. 2004).
- Exercise in the scapular plane. The scapular plane offers the most balanced position of the capsule and provides ideal joint centration during elevation (Borsa, Timmons, and Sauers 2003).
- Exercise both shoulders. Abnormal muscle activation often occurs in both the involved and the uninvolved shoulder (Cools et al. 2003; Cools, Declercq et al. 2007; Wadsworth and Bullock-Saxton 1997).
- Include neuromuscular exercises such as closed kinetic chain exercises and PNF. Patients with impingement demonstrate reduced proprioception (Machner et al. 2003) and so require proprioceptive rehabilitation (Ginn and Cohen 2005; Kamkar, Irrgang, and Whitney 1993; Smith and Burnolli 1989). Figure 13.6 illustrates a closed kinetic chain shoulder exercise for improving proprioception (Naughton, Adams, and Maher 2005).
- Stretch the posterior shoulder when internal rotation is limited. The posterior capsule is often tight in athletes with impingement, limiting internal rotation and follow-through (Myers et al. 2006; Tyler et al. 2000). The cross-body stretch (see figure 13.7) improves internal rotation in subjects with posterior shoulder tightness (McClure et al. 2007).
Causes of muscle weakness
A look at the causes of muscle weakness as well as Janda’s classification of muscle imbalance patterns.
Muscle tension can decrease as a result of a structural lesion in the CNS such as a spinal cord injury or stroke. A loss of tension leads to flaccidity or weakness. Weak muscles are also described as hypotonic or inhibited. Functionally, muscle can be weak as a result of neuroflexive or adaptive changes and may exhibit delayed activation in movement patterns.
Neuroflexive Factors for Decreased Tension
Many contractile factors can contribute to decreased muscle tension:
- Reciprocal inhibition (Sherrington 1907). Muscle becomes inhibited reflexively when its antagonist is activated. Weakness is often reflex-mediated inhibition secondary to increased tension of the antagonist.
- Arthrogenic weakness (Stokes and Young 1984; DeAndrade, Grant, and Dison. 1965). Muscle becomes inhibited via anterior horn cells due to joint swelling or dysfunction. This weakness also leads to selective atrophy of Type II fibers (Edstrom 1970).
- Deafferentation (Freeman, Dean, and Hanham 1965). Deafferentation is a decrease in afferent information from neuromuscular receptors. Damage to joint mechanoreceptors (as seen with ligamentous injury) with subsequent loss of articular reflexes can cause altered motor programs, often influencing many muscles remote from the injured area (Bullock-Saxton 1994). This loss of afferent information ultimately leads to de-efferentation, or the loss of efferent signals to alpha motor neurons, which results in decreased muscle strength.
- Pseudoparesis (Janda 1986a). Pseudoparesis is a clinical presentation of weakness of neuroflexive origin. Pseudoparesis has three clinical signs: hypotonia upon inspection and palpation, a score of 4 out of 5 on a manual muscle test, and a change in the muscle activation pattern that may include delayed onset with early synergist activation or decreased EMG levels. Facilitatory techniques often restore muscle strength and activation. Normally facilitatory input can be inhibitory to a pseudoparetic muscle (Janda 1986a).
- TrP weakness (Simons, Travell, and Simons 1999). Hyperirritable bands of muscle fiber decrease the stimulation threshold, leading to overuse, early fatigue, and ultimately weakness. Muscles with active TrPs fatigue more rapidly than normal muscles do (Mense and Simons 2001), and they exhibit a decreased number of firing motor units and poor synchronization (Janda 1993).
- Fatigue. Muscle fatigue can be caused by metabolic or neurological factors. Often during exercise muscles are fatigued before pain is experienced. Thus the patient develops compensatory and faulty movement patterns before experiencing pain.
Adaptive Factors for Decreased Tension
Noncontractile factors causing decreased muscle tension are stretch weakness and tightness weakness:
- Stretch weakness (Kendall, McCreary, and Provance 1993; Sahrmann 2002a, 2002b). Stretch weakness is a condition in which a muscle is elongated beyond physiological neutral but not beyond the normal ROM (Janda 1993). Prolonged muscle elongation causes muscle spindle inhibition and the creation of additional sarcomeres. The increased muscle length also changes the length-tension curve. Stretch weakness is also known as positional weakness and is often associated with overuse and postural changes.
- Tightness weakness (Janda 1993). This is the most severe form of muscle tightness. It is often overlooked clinically. Overused muscle shortens over time, changing the muscle's length-tension curve and becoming more readily activated and weaker after time. There is also an increase in the noncontractile tissue and a decrease in elasticity, leading to hypertrophy. Ultimately, overuse leads to ischemia and degeneration of muscle fibers, which further weakens the muscle.
When an inhibited and weak muscle is resisted, as is the aim of strengthening exercises, its activity tends to decrease rather than increase (Janda 1987). It is important to distinguish between neuroflexive weakness and structural weakness. Often, if the tight antagonist is stretched, the weak and inhibited muscle spontaneously increases in strength.
Janda's Classification of Muscle Imbalance Patterns
Through his observations of patients with neurological disorders and chronic musculoskeletal pain, Janda found that the typical muscle response to joint dysfunction is similar to the muscle patterns found in upper motor neuron lesions, concluding that muscle imbalances are controlled by the CNS (Janda 1987). Janda believed that muscle tightness or spasticity is predominant. Often, weakness from muscle imbalance results from reciprocal inhibition of the tight antagonist. The degree of tightness and weakness varies between individuals, but the pattern rarely does. These patterns lead to postural changes and joint dysfunction and degeneration.
Janda identified three stereotypical patterns associated with distinct chronic pain syndromes: the upper-crossed, lower-crossed, and layer syndromes. These syndromes are characterized by specific patterns of muscle weakness and tightness that cross between the dorsal and the ventral sides of the body.
Upper-Crossed Syndrome
Upper-crossed syndrome (UCS) is also referred to as proximal or shoulder girdle crossed syndrome (figure 4.2a; Janda 1988). In UCS, tightness of the upper trapezius and levator scapula on the dorsal side crosses with tightness of the pectoralis major and minor. Weakness of the deep cervical flexors ventrally crosses with weakness of the middle and lower trapezius. This pattern of imbalance creates joint dysfunction, particularly at the atlanto-occipital joint, C4-C5 segment, cervicothoracic joint, glenohumeral joint, and T4-T5 segment. Janda noted that these focal areas of stress within the spine correspond to transitional zones in which neighboring vertebrae change in morphology. Specific postural changes are seen in UCS, including forward head posture, increased cervical lordosis and thoracic kyphosis, elevated and protracted shoulders, and rotation or abduction and winging of the scapulae (figure 4.2b). These postural changes decrease glenohumeral stability as the glenoid fossa becomes more vertical due to serratus anterior weakness leading to abduction, rotation, and winging of the scapulae. This loss of stability requires the levator scapula and upper trapezius to increase activation to maintain glenohumeral centration (Janda 1988).
Lower-Crossed Syndrome
Lower-crossed syndrome (LCS) is also referred to as distal or pelvic crossed syndrome (figure 4.3a; Janda 1987). In LCS, tightness of the thoracolumbar extensors on the dorsal side crosses with tightness of the iliopsoas and rectus femoris. Weakness of the deep abdominal muscles ventrally crosses with weakness of the gluteus maximus and medius. This pattern of imbalance creates joint dysfunction, particularly at the L4-L5 and L5-S1 segments, SI joint, and hip joint. Specific postural changes seen in LCS include anterior pelvic tilt, increased lumbar lordosis, lateral lumbar shift, lateral leg rotation, and knee hyperextension. If the lordosis is deep and short, then imbalance is predominantly in the pelvic muscles; if the lordosis is shallow and extends into the thoracic area, then imbalance predominates in the trunk muscles (Janda 1987).
Janda identified two subtypes of LCS: A and B (see figure 4.3, b-c). Patients with LCS type A use more hip flexion and extension movement for mobility; their standing posture demonstrates an anterior pelvic tilt with slight hip flexion and knee flexion. These individuals compensate with a hyperlordosis limited to the lumbar spine and with a hyperkyphosis in the upper lumbar and thoracolumbar segments.
Learn to assess muscle length
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening.
Muscle Length Assessment Technique
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening. Precise testing requires that one of the bony attachments of the muscle (usually the origin) be in a fixed position while the other bony attachment is moved passively in the direction of lengthening the muscle. In other words, muscle length testing assesses the resistance to passive movement. This is in contrast to typical flexibility or ROM testing. The actual ROM can be measured for documentation purposes, but it gives limited clinical information in muscle imbalance syndromes. The most valuable clinical information is the muscular end feel and the location of the ROM end feel. The elongation of the muscle should be performed slowly to avoid eliciting a quick stretch of the muscle spindle and subsequently inducing a twitch response and muscle contraction. In addition, for the best accuracy and precision, muscle length testing should be performed when the patient is not in acute pain in order to avoid pain inhibition and muscle guarding. In summary, there are four steps to assessing muscle length:
1. Ensure maximal lengthening of the muscle from origin to insertion.
2. Firmly stabilize one end (usually the origin).
3. Slowly elongate the muscle.
4. Assess the end feel.
Following are the procedures for testing key muscles. Clinicians do not have to perform muscle length testing on every muscle listed; instead, they should assess the muscles that the postural and movement pattern analysis indicate as being possibly tight. Once tight muscles have been identified, the clinician can establish a muscle imbalance pattern (if present) and begin to look for causes of the tightness. Table 7.1 provides the normal results of muscle length for flexibility testing.
Table 7.1 Normal Results of Muscles Tested for Length | |
| Muscle | Normal ranges or end feel |
| Iliopsoas | 0° hip extension, 10° with overpressure |
| Rectus femoris | 90° knee extension, 125° with overpressure |
| TFL-IT band | 0° hip abduction (neutral), 15°-20° with overpressure |
| Adductors | 0° hip abduction (neutral), 20°-25° with overpressure in the modified Thomas test position 45° hip abduction in supine position |
| Hamstrings | 80° hip flexion with contralateral leg extended 90° hip flexion with contralateral leg flexed |
| Triceps surae | 0° ankle dorsiflexion |
| Quadratus lumborum | Thoracolumbar curve should be smooth and gradual |
| Piriformis | Gradual soft end feel |
| Upper trapezius | Gradual soft end feel |
| Levator scapulae | Gradual soft end feel |
| SCM | Gradual soft end feel |
| Pectoralis major | Sternal portion (lower fibers): with shoulder abducted at 150°, arm should be horizontal to table and 15°-20° with overpressure Sternal portion (midfibers): with shoulder abducted to 90°, arm should be horizontal to table and 30° with overpressure Clavicular portion: with shoulder abducted to 60°, arm should hang freely over table |
| Paraspinals | Schober's test: excursion of >2.4 in. (6 cm) |
Lower-Quarter Muscles
The muscles of the lower quarter include those of the leg, pelvis, and lower back. The muscles prone to tightness are those involved in maintaining a single-leg stance (Janda 1987). Tightness of the hip flexors and tightness of the thoracolumbar extensors are hallmark signs of Janda's LCS.
Modified Thomas Test for Hip Flexor
The modified Thomas test (figure 7.2, a-e) allows the clinician to assess four different muscles prone to tightness namely, the one-joint hip flexor, iliacus and psoas major, and the two-joint hip flexors, rectus femoris and TFL-ITB. Tightness of the hip flexors limits hip hyperextension in gait and may cause an anterior pelvic tilt. Weakness of the gluteus maximus often is due to facilitation of the hip flexors.
Patient Position
The patient is asked to sit on the edge of the table, with the coccyx and ischial tuberosities touching the table and one foot on the floor. Then, the patient is asked to flex the opposite hip and knee toward the chest and maintain the position with the hands (see figure 7.2a).
Clinician Position
The clinician stands beside the leg not being tested, facing the patient. While supporting the patient by placing one hand on the midthoracic spine and the other on the knee, the clinician passively rolls the patient down to the table to the supine position. The clinician needs to ensure that the patient's knees are flexed, lumbar spine is flexed, and pelvis is in posterior rotation to fix the origin of the hip flexors.
Test
The clinician passively lowers the tested leg until resistance is felt or movement at the pelvis is detected. With the patient's thigh in the final resting position, the clinician observes whether it is in neutral and parallel to the table or abducted. A normal length of the one-joint hip flexors with the lumbar spine and sacrum flat on the table is indicated by the posterior thigh touching the table (0° of hip extension). With slight overpressure, the thigh should reach 10° to 15° of hyperextension (figure 7.2, b-c). Prominence of a superior patellar groove (figure 7.2d) suggests a short rectus femoris, while prominence of a lateral IT groove suggests a short IT band (see figure 7.2e).
Restoration of muscle balance
Treatment of muscle weakness aims at stimulating and increasing the response of the muscle spindle of the pseudoparetic muscle.
Muscle Length Assessment Technique
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening. Precise testing requires that one of the bony attachments of the muscle (usually the origin) be in a fixed position while the other bony attachment is moved passively in the direction of lengthening the muscle. In other words, muscle length testing assesses the resistance to passive movement. This is in contrast to typical flexibility or ROM testing. The actual ROM can be measured for documentation purposes, but it gives limited clinical information in muscle imbalance syndromes. The most valuable clinical information is the muscular end feel and the location of the ROM end feel. The elongation of the muscle should be performed slowly to avoid eliciting a quick stretch of the muscle spindle and subsequently inducing a twitch response and muscle contraction. In addition, for the best accuracy and precision, muscle length testing should be performed when the patient is not in acute pain in order to avoid pain inhibition and muscle guarding. In summary, there are four steps to assessing muscle length:
1. Ensure maximal lengthening of the muscle from origin to insertion.
2. Firmly stabilize one end (usually the origin).
3. Slowly elongate the muscle.
4. Assess the end feel.
Following are the procedures for testing key muscles. Clinicians do not have to perform muscle length testing on every muscle listed; instead, they should assess the muscles that the postural and movement pattern analysis indicate as being possibly tight. Once tight muscles have been identified, the clinician can establish a muscle imbalance pattern (if present) and begin to look for causes of the tightness. Table 7.1 provides the normal results of muscle length for flexibility testing.
Table 7.1 Normal Results of Muscles Tested for Length | |
| Muscle | Normal ranges or end feel |
| Iliopsoas | 0° hip extension, 10° with overpressure |
| Rectus femoris | 90° knee extension, 125° with overpressure |
| TFL-IT band | 0° hip abduction (neutral), 15°-20° with overpressure |
| Adductors | 0° hip abduction (neutral), 20°-25° with overpressure in the modified Thomas test position 45° hip abduction in supine position |
| Hamstrings | 80° hip flexion with contralateral leg extended 90° hip flexion with contralateral leg flexed |
| Triceps surae | 0° ankle dorsiflexion |
| Quadratus lumborum | Thoracolumbar curve should be smooth and gradual |
| Piriformis | Gradual soft end feel |
| Upper trapezius | Gradual soft end feel |
| Levator scapulae | Gradual soft end feel |
| SCM | Gradual soft end feel |
| Pectoralis major | Sternal portion (lower fibers): with shoulder abducted at 150°, arm should be horizontal to table and 15°-20° with overpressure Sternal portion (midfibers): with shoulder abducted to 90°, arm should be horizontal to table and 30° with overpressure Clavicular portion: with shoulder abducted to 60°, arm should hang freely over table |
| Paraspinals | Schober's test: excursion of >2.4 in. (6 cm) |
Lower-Quarter Muscles
The muscles of the lower quarter include those of the leg, pelvis, and lower back. The muscles prone to tightness are those involved in maintaining a single-leg stance (Janda 1987). Tightness of the hip flexors and tightness of the thoracolumbar extensors are hallmark signs of Janda's LCS.
Modified Thomas Test for Hip Flexor
The modified Thomas test (figure 7.2, a-e) allows the clinician to assess four different muscles prone to tightness namely, the one-joint hip flexor, iliacus and psoas major, and the two-joint hip flexors, rectus femoris and TFL-ITB. Tightness of the hip flexors limits hip hyperextension in gait and may cause an anterior pelvic tilt. Weakness of the gluteus maximus often is due to facilitation of the hip flexors.
Patient Position
The patient is asked to sit on the edge of the table, with the coccyx and ischial tuberosities touching the table and one foot on the floor. Then, the patient is asked to flex the opposite hip and knee toward the chest and maintain the position with the hands (see figure 7.2a).
Clinician Position
The clinician stands beside the leg not being tested, facing the patient. While supporting the patient by placing one hand on the midthoracic spine and the other on the knee, the clinician passively rolls the patient down to the table to the supine position. The clinician needs to ensure that the patient's knees are flexed, lumbar spine is flexed, and pelvis is in posterior rotation to fix the origin of the hip flexors.
Test
The clinician passively lowers the tested leg until resistance is felt or movement at the pelvis is detected. With the patient's thigh in the final resting position, the clinician observes whether it is in neutral and parallel to the table or abducted. A normal length of the one-joint hip flexors with the lumbar spine and sacrum flat on the table is indicated by the posterior thigh touching the table (0° of hip extension). With slight overpressure, the thigh should reach 10° to 15° of hyperextension (figure 7.2, b-c). Prominence of a superior patellar groove (figure 7.2d) suggests a short rectus femoris, while prominence of a lateral IT groove suggests a short IT band (see figure 7.2e).
Rehabilitation of impingement
Rehabilitation rather than surgery is recommended for secondary impingement.
Rehabilitation rather than surgery is recommended for secondary impingement (Brox and Brevik 1996; Kronberg, Németh, and Broström 1990; Michener, Walsworth, and Burnet 2004; Morrison, Frogameni, and Woodworth 1997). Patients with primary impingement (type II and III acromion), however, have only a 64% to 68% success rate with conservative treatment (Morrison, Frogameni, and Woodworth 1997). While rehabilitation and arthroscopic surgery improve impingement symptoms equally (Haarh et al. 2005; Haarh and Andersen 2006), rehabilitation is less costly (Brox et al. 1993).
In a systematic review, Michener, Walsworth, and Burnet and colleagues (2004) found strong support in the literature for therapeutic exercise of the rotator cuff and scapular muscles as well as for stretching of the anterior and posterior shoulder. Furthermore, exercise is more effective when combined with joint mobilization (Michener, Walsworth, and Burnet 2004; Senbursa, Baltaci, and Atay 2007). The following are impingement rehabilitation recommendations with evidence-based rationale:
- Integrate the entire upper-extremity chain during exercise. This facilitates the kinetic chain from the hand to the spine (Burkhart, Morgan, and Kibler 2003; Kibler 1998b, 2006; McMullen and Uhl 2000). Figure 13.5 illustrates exercises that integrate the whole kinetic chain.
- Include hip and trunk stabilization exercises. This facilitates force transmission and proximal stabilization between the upper extremity and the trunk (Burkhart, Morgan, and Kibler 2003; Kibler 1998b, 2006; McMullen and Uhl 2000).
- Isolate the rotator cuff and scapular stabilizers first, before performing multijoint movements. Performing multijoint shoulder movements does not increase the strength of smaller single-joint muscles such as the rotator cuff (Giannakopoulos et al. 2004). Strengthening exercises isolating the rotator cuff should be performed first (Jobe and Pink 1993; Malliou et al. 2004).
- Exercise in the scapular plane. The scapular plane offers the most balanced position of the capsule and provides ideal joint centration during elevation (Borsa, Timmons, and Sauers 2003).
- Exercise both shoulders. Abnormal muscle activation often occurs in both the involved and the uninvolved shoulder (Cools et al. 2003; Cools, Declercq et al. 2007; Wadsworth and Bullock-Saxton 1997).
- Include neuromuscular exercises such as closed kinetic chain exercises and PNF. Patients with impingement demonstrate reduced proprioception (Machner et al. 2003) and so require proprioceptive rehabilitation (Ginn and Cohen 2005; Kamkar, Irrgang, and Whitney 1993; Smith and Burnolli 1989). Figure 13.6 illustrates a closed kinetic chain shoulder exercise for improving proprioception (Naughton, Adams, and Maher 2005).
- Stretch the posterior shoulder when internal rotation is limited. The posterior capsule is often tight in athletes with impingement, limiting internal rotation and follow-through (Myers et al. 2006; Tyler et al. 2000). The cross-body stretch (see figure 13.7) improves internal rotation in subjects with posterior shoulder tightness (McClure et al. 2007).
Causes of muscle weakness
A look at the causes of muscle weakness as well as Janda’s classification of muscle imbalance patterns.
Muscle tension can decrease as a result of a structural lesion in the CNS such as a spinal cord injury or stroke. A loss of tension leads to flaccidity or weakness. Weak muscles are also described as hypotonic or inhibited. Functionally, muscle can be weak as a result of neuroflexive or adaptive changes and may exhibit delayed activation in movement patterns.
Neuroflexive Factors for Decreased Tension
Many contractile factors can contribute to decreased muscle tension:
- Reciprocal inhibition (Sherrington 1907). Muscle becomes inhibited reflexively when its antagonist is activated. Weakness is often reflex-mediated inhibition secondary to increased tension of the antagonist.
- Arthrogenic weakness (Stokes and Young 1984; DeAndrade, Grant, and Dison. 1965). Muscle becomes inhibited via anterior horn cells due to joint swelling or dysfunction. This weakness also leads to selective atrophy of Type II fibers (Edstrom 1970).
- Deafferentation (Freeman, Dean, and Hanham 1965). Deafferentation is a decrease in afferent information from neuromuscular receptors. Damage to joint mechanoreceptors (as seen with ligamentous injury) with subsequent loss of articular reflexes can cause altered motor programs, often influencing many muscles remote from the injured area (Bullock-Saxton 1994). This loss of afferent information ultimately leads to de-efferentation, or the loss of efferent signals to alpha motor neurons, which results in decreased muscle strength.
- Pseudoparesis (Janda 1986a). Pseudoparesis is a clinical presentation of weakness of neuroflexive origin. Pseudoparesis has three clinical signs: hypotonia upon inspection and palpation, a score of 4 out of 5 on a manual muscle test, and a change in the muscle activation pattern that may include delayed onset with early synergist activation or decreased EMG levels. Facilitatory techniques often restore muscle strength and activation. Normally facilitatory input can be inhibitory to a pseudoparetic muscle (Janda 1986a).
- TrP weakness (Simons, Travell, and Simons 1999). Hyperirritable bands of muscle fiber decrease the stimulation threshold, leading to overuse, early fatigue, and ultimately weakness. Muscles with active TrPs fatigue more rapidly than normal muscles do (Mense and Simons 2001), and they exhibit a decreased number of firing motor units and poor synchronization (Janda 1993).
- Fatigue. Muscle fatigue can be caused by metabolic or neurological factors. Often during exercise muscles are fatigued before pain is experienced. Thus the patient develops compensatory and faulty movement patterns before experiencing pain.
Adaptive Factors for Decreased Tension
Noncontractile factors causing decreased muscle tension are stretch weakness and tightness weakness:
- Stretch weakness (Kendall, McCreary, and Provance 1993; Sahrmann 2002a, 2002b). Stretch weakness is a condition in which a muscle is elongated beyond physiological neutral but not beyond the normal ROM (Janda 1993). Prolonged muscle elongation causes muscle spindle inhibition and the creation of additional sarcomeres. The increased muscle length also changes the length-tension curve. Stretch weakness is also known as positional weakness and is often associated with overuse and postural changes.
- Tightness weakness (Janda 1993). This is the most severe form of muscle tightness. It is often overlooked clinically. Overused muscle shortens over time, changing the muscle's length-tension curve and becoming more readily activated and weaker after time. There is also an increase in the noncontractile tissue and a decrease in elasticity, leading to hypertrophy. Ultimately, overuse leads to ischemia and degeneration of muscle fibers, which further weakens the muscle.
When an inhibited and weak muscle is resisted, as is the aim of strengthening exercises, its activity tends to decrease rather than increase (Janda 1987). It is important to distinguish between neuroflexive weakness and structural weakness. Often, if the tight antagonist is stretched, the weak and inhibited muscle spontaneously increases in strength.
Janda's Classification of Muscle Imbalance Patterns
Through his observations of patients with neurological disorders and chronic musculoskeletal pain, Janda found that the typical muscle response to joint dysfunction is similar to the muscle patterns found in upper motor neuron lesions, concluding that muscle imbalances are controlled by the CNS (Janda 1987). Janda believed that muscle tightness or spasticity is predominant. Often, weakness from muscle imbalance results from reciprocal inhibition of the tight antagonist. The degree of tightness and weakness varies between individuals, but the pattern rarely does. These patterns lead to postural changes and joint dysfunction and degeneration.
Janda identified three stereotypical patterns associated with distinct chronic pain syndromes: the upper-crossed, lower-crossed, and layer syndromes. These syndromes are characterized by specific patterns of muscle weakness and tightness that cross between the dorsal and the ventral sides of the body.
Upper-Crossed Syndrome
Upper-crossed syndrome (UCS) is also referred to as proximal or shoulder girdle crossed syndrome (figure 4.2a; Janda 1988). In UCS, tightness of the upper trapezius and levator scapula on the dorsal side crosses with tightness of the pectoralis major and minor. Weakness of the deep cervical flexors ventrally crosses with weakness of the middle and lower trapezius. This pattern of imbalance creates joint dysfunction, particularly at the atlanto-occipital joint, C4-C5 segment, cervicothoracic joint, glenohumeral joint, and T4-T5 segment. Janda noted that these focal areas of stress within the spine correspond to transitional zones in which neighboring vertebrae change in morphology. Specific postural changes are seen in UCS, including forward head posture, increased cervical lordosis and thoracic kyphosis, elevated and protracted shoulders, and rotation or abduction and winging of the scapulae (figure 4.2b). These postural changes decrease glenohumeral stability as the glenoid fossa becomes more vertical due to serratus anterior weakness leading to abduction, rotation, and winging of the scapulae. This loss of stability requires the levator scapula and upper trapezius to increase activation to maintain glenohumeral centration (Janda 1988).
Lower-Crossed Syndrome
Lower-crossed syndrome (LCS) is also referred to as distal or pelvic crossed syndrome (figure 4.3a; Janda 1987). In LCS, tightness of the thoracolumbar extensors on the dorsal side crosses with tightness of the iliopsoas and rectus femoris. Weakness of the deep abdominal muscles ventrally crosses with weakness of the gluteus maximus and medius. This pattern of imbalance creates joint dysfunction, particularly at the L4-L5 and L5-S1 segments, SI joint, and hip joint. Specific postural changes seen in LCS include anterior pelvic tilt, increased lumbar lordosis, lateral lumbar shift, lateral leg rotation, and knee hyperextension. If the lordosis is deep and short, then imbalance is predominantly in the pelvic muscles; if the lordosis is shallow and extends into the thoracic area, then imbalance predominates in the trunk muscles (Janda 1987).
Janda identified two subtypes of LCS: A and B (see figure 4.3, b-c). Patients with LCS type A use more hip flexion and extension movement for mobility; their standing posture demonstrates an anterior pelvic tilt with slight hip flexion and knee flexion. These individuals compensate with a hyperlordosis limited to the lumbar spine and with a hyperkyphosis in the upper lumbar and thoracolumbar segments.
Learn to assess muscle length
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening.
Muscle Length Assessment Technique
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening. Precise testing requires that one of the bony attachments of the muscle (usually the origin) be in a fixed position while the other bony attachment is moved passively in the direction of lengthening the muscle. In other words, muscle length testing assesses the resistance to passive movement. This is in contrast to typical flexibility or ROM testing. The actual ROM can be measured for documentation purposes, but it gives limited clinical information in muscle imbalance syndromes. The most valuable clinical information is the muscular end feel and the location of the ROM end feel. The elongation of the muscle should be performed slowly to avoid eliciting a quick stretch of the muscle spindle and subsequently inducing a twitch response and muscle contraction. In addition, for the best accuracy and precision, muscle length testing should be performed when the patient is not in acute pain in order to avoid pain inhibition and muscle guarding. In summary, there are four steps to assessing muscle length:
1. Ensure maximal lengthening of the muscle from origin to insertion.
2. Firmly stabilize one end (usually the origin).
3. Slowly elongate the muscle.
4. Assess the end feel.
Following are the procedures for testing key muscles. Clinicians do not have to perform muscle length testing on every muscle listed; instead, they should assess the muscles that the postural and movement pattern analysis indicate as being possibly tight. Once tight muscles have been identified, the clinician can establish a muscle imbalance pattern (if present) and begin to look for causes of the tightness. Table 7.1 provides the normal results of muscle length for flexibility testing.
Table 7.1 Normal Results of Muscles Tested for Length | |
| Muscle | Normal ranges or end feel |
| Iliopsoas | 0° hip extension, 10° with overpressure |
| Rectus femoris | 90° knee extension, 125° with overpressure |
| TFL-IT band | 0° hip abduction (neutral), 15°-20° with overpressure |
| Adductors | 0° hip abduction (neutral), 20°-25° with overpressure in the modified Thomas test position 45° hip abduction in supine position |
| Hamstrings | 80° hip flexion with contralateral leg extended 90° hip flexion with contralateral leg flexed |
| Triceps surae | 0° ankle dorsiflexion |
| Quadratus lumborum | Thoracolumbar curve should be smooth and gradual |
| Piriformis | Gradual soft end feel |
| Upper trapezius | Gradual soft end feel |
| Levator scapulae | Gradual soft end feel |
| SCM | Gradual soft end feel |
| Pectoralis major | Sternal portion (lower fibers): with shoulder abducted at 150°, arm should be horizontal to table and 15°-20° with overpressure Sternal portion (midfibers): with shoulder abducted to 90°, arm should be horizontal to table and 30° with overpressure Clavicular portion: with shoulder abducted to 60°, arm should hang freely over table |
| Paraspinals | Schober's test: excursion of >2.4 in. (6 cm) |
Lower-Quarter Muscles
The muscles of the lower quarter include those of the leg, pelvis, and lower back. The muscles prone to tightness are those involved in maintaining a single-leg stance (Janda 1987). Tightness of the hip flexors and tightness of the thoracolumbar extensors are hallmark signs of Janda's LCS.
Modified Thomas Test for Hip Flexor
The modified Thomas test (figure 7.2, a-e) allows the clinician to assess four different muscles prone to tightness namely, the one-joint hip flexor, iliacus and psoas major, and the two-joint hip flexors, rectus femoris and TFL-ITB. Tightness of the hip flexors limits hip hyperextension in gait and may cause an anterior pelvic tilt. Weakness of the gluteus maximus often is due to facilitation of the hip flexors.
Patient Position
The patient is asked to sit on the edge of the table, with the coccyx and ischial tuberosities touching the table and one foot on the floor. Then, the patient is asked to flex the opposite hip and knee toward the chest and maintain the position with the hands (see figure 7.2a).
Clinician Position
The clinician stands beside the leg not being tested, facing the patient. While supporting the patient by placing one hand on the midthoracic spine and the other on the knee, the clinician passively rolls the patient down to the table to the supine position. The clinician needs to ensure that the patient's knees are flexed, lumbar spine is flexed, and pelvis is in posterior rotation to fix the origin of the hip flexors.
Test
The clinician passively lowers the tested leg until resistance is felt or movement at the pelvis is detected. With the patient's thigh in the final resting position, the clinician observes whether it is in neutral and parallel to the table or abducted. A normal length of the one-joint hip flexors with the lumbar spine and sacrum flat on the table is indicated by the posterior thigh touching the table (0° of hip extension). With slight overpressure, the thigh should reach 10° to 15° of hyperextension (figure 7.2, b-c). Prominence of a superior patellar groove (figure 7.2d) suggests a short rectus femoris, while prominence of a lateral IT groove suggests a short IT band (see figure 7.2e).
Restoration of muscle balance
Treatment of muscle weakness aims at stimulating and increasing the response of the muscle spindle of the pseudoparetic muscle.
Muscle Length Assessment Technique
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening. Precise testing requires that one of the bony attachments of the muscle (usually the origin) be in a fixed position while the other bony attachment is moved passively in the direction of lengthening the muscle. In other words, muscle length testing assesses the resistance to passive movement. This is in contrast to typical flexibility or ROM testing. The actual ROM can be measured for documentation purposes, but it gives limited clinical information in muscle imbalance syndromes. The most valuable clinical information is the muscular end feel and the location of the ROM end feel. The elongation of the muscle should be performed slowly to avoid eliciting a quick stretch of the muscle spindle and subsequently inducing a twitch response and muscle contraction. In addition, for the best accuracy and precision, muscle length testing should be performed when the patient is not in acute pain in order to avoid pain inhibition and muscle guarding. In summary, there are four steps to assessing muscle length:
1. Ensure maximal lengthening of the muscle from origin to insertion.
2. Firmly stabilize one end (usually the origin).
3. Slowly elongate the muscle.
4. Assess the end feel.
Following are the procedures for testing key muscles. Clinicians do not have to perform muscle length testing on every muscle listed; instead, they should assess the muscles that the postural and movement pattern analysis indicate as being possibly tight. Once tight muscles have been identified, the clinician can establish a muscle imbalance pattern (if present) and begin to look for causes of the tightness. Table 7.1 provides the normal results of muscle length for flexibility testing.
Table 7.1 Normal Results of Muscles Tested for Length | |
| Muscle | Normal ranges or end feel |
| Iliopsoas | 0° hip extension, 10° with overpressure |
| Rectus femoris | 90° knee extension, 125° with overpressure |
| TFL-IT band | 0° hip abduction (neutral), 15°-20° with overpressure |
| Adductors | 0° hip abduction (neutral), 20°-25° with overpressure in the modified Thomas test position 45° hip abduction in supine position |
| Hamstrings | 80° hip flexion with contralateral leg extended 90° hip flexion with contralateral leg flexed |
| Triceps surae | 0° ankle dorsiflexion |
| Quadratus lumborum | Thoracolumbar curve should be smooth and gradual |
| Piriformis | Gradual soft end feel |
| Upper trapezius | Gradual soft end feel |
| Levator scapulae | Gradual soft end feel |
| SCM | Gradual soft end feel |
| Pectoralis major | Sternal portion (lower fibers): with shoulder abducted at 150°, arm should be horizontal to table and 15°-20° with overpressure Sternal portion (midfibers): with shoulder abducted to 90°, arm should be horizontal to table and 30° with overpressure Clavicular portion: with shoulder abducted to 60°, arm should hang freely over table |
| Paraspinals | Schober's test: excursion of >2.4 in. (6 cm) |
Lower-Quarter Muscles
The muscles of the lower quarter include those of the leg, pelvis, and lower back. The muscles prone to tightness are those involved in maintaining a single-leg stance (Janda 1987). Tightness of the hip flexors and tightness of the thoracolumbar extensors are hallmark signs of Janda's LCS.
Modified Thomas Test for Hip Flexor
The modified Thomas test (figure 7.2, a-e) allows the clinician to assess four different muscles prone to tightness namely, the one-joint hip flexor, iliacus and psoas major, and the two-joint hip flexors, rectus femoris and TFL-ITB. Tightness of the hip flexors limits hip hyperextension in gait and may cause an anterior pelvic tilt. Weakness of the gluteus maximus often is due to facilitation of the hip flexors.
Patient Position
The patient is asked to sit on the edge of the table, with the coccyx and ischial tuberosities touching the table and one foot on the floor. Then, the patient is asked to flex the opposite hip and knee toward the chest and maintain the position with the hands (see figure 7.2a).
Clinician Position
The clinician stands beside the leg not being tested, facing the patient. While supporting the patient by placing one hand on the midthoracic spine and the other on the knee, the clinician passively rolls the patient down to the table to the supine position. The clinician needs to ensure that the patient's knees are flexed, lumbar spine is flexed, and pelvis is in posterior rotation to fix the origin of the hip flexors.
Test
The clinician passively lowers the tested leg until resistance is felt or movement at the pelvis is detected. With the patient's thigh in the final resting position, the clinician observes whether it is in neutral and parallel to the table or abducted. A normal length of the one-joint hip flexors with the lumbar spine and sacrum flat on the table is indicated by the posterior thigh touching the table (0° of hip extension). With slight overpressure, the thigh should reach 10° to 15° of hyperextension (figure 7.2, b-c). Prominence of a superior patellar groove (figure 7.2d) suggests a short rectus femoris, while prominence of a lateral IT groove suggests a short IT band (see figure 7.2e).
Rehabilitation of impingement
Rehabilitation rather than surgery is recommended for secondary impingement.
Rehabilitation rather than surgery is recommended for secondary impingement (Brox and Brevik 1996; Kronberg, Németh, and Broström 1990; Michener, Walsworth, and Burnet 2004; Morrison, Frogameni, and Woodworth 1997). Patients with primary impingement (type II and III acromion), however, have only a 64% to 68% success rate with conservative treatment (Morrison, Frogameni, and Woodworth 1997). While rehabilitation and arthroscopic surgery improve impingement symptoms equally (Haarh et al. 2005; Haarh and Andersen 2006), rehabilitation is less costly (Brox et al. 1993).
In a systematic review, Michener, Walsworth, and Burnet and colleagues (2004) found strong support in the literature for therapeutic exercise of the rotator cuff and scapular muscles as well as for stretching of the anterior and posterior shoulder. Furthermore, exercise is more effective when combined with joint mobilization (Michener, Walsworth, and Burnet 2004; Senbursa, Baltaci, and Atay 2007). The following are impingement rehabilitation recommendations with evidence-based rationale:
- Integrate the entire upper-extremity chain during exercise. This facilitates the kinetic chain from the hand to the spine (Burkhart, Morgan, and Kibler 2003; Kibler 1998b, 2006; McMullen and Uhl 2000). Figure 13.5 illustrates exercises that integrate the whole kinetic chain.
- Include hip and trunk stabilization exercises. This facilitates force transmission and proximal stabilization between the upper extremity and the trunk (Burkhart, Morgan, and Kibler 2003; Kibler 1998b, 2006; McMullen and Uhl 2000).
- Isolate the rotator cuff and scapular stabilizers first, before performing multijoint movements. Performing multijoint shoulder movements does not increase the strength of smaller single-joint muscles such as the rotator cuff (Giannakopoulos et al. 2004). Strengthening exercises isolating the rotator cuff should be performed first (Jobe and Pink 1993; Malliou et al. 2004).
- Exercise in the scapular plane. The scapular plane offers the most balanced position of the capsule and provides ideal joint centration during elevation (Borsa, Timmons, and Sauers 2003).
- Exercise both shoulders. Abnormal muscle activation often occurs in both the involved and the uninvolved shoulder (Cools et al. 2003; Cools, Declercq et al. 2007; Wadsworth and Bullock-Saxton 1997).
- Include neuromuscular exercises such as closed kinetic chain exercises and PNF. Patients with impingement demonstrate reduced proprioception (Machner et al. 2003) and so require proprioceptive rehabilitation (Ginn and Cohen 2005; Kamkar, Irrgang, and Whitney 1993; Smith and Burnolli 1989). Figure 13.6 illustrates a closed kinetic chain shoulder exercise for improving proprioception (Naughton, Adams, and Maher 2005).
- Stretch the posterior shoulder when internal rotation is limited. The posterior capsule is often tight in athletes with impingement, limiting internal rotation and follow-through (Myers et al. 2006; Tyler et al. 2000). The cross-body stretch (see figure 13.7) improves internal rotation in subjects with posterior shoulder tightness (McClure et al. 2007).
Causes of muscle weakness
A look at the causes of muscle weakness as well as Janda’s classification of muscle imbalance patterns.
Muscle tension can decrease as a result of a structural lesion in the CNS such as a spinal cord injury or stroke. A loss of tension leads to flaccidity or weakness. Weak muscles are also described as hypotonic or inhibited. Functionally, muscle can be weak as a result of neuroflexive or adaptive changes and may exhibit delayed activation in movement patterns.
Neuroflexive Factors for Decreased Tension
Many contractile factors can contribute to decreased muscle tension:
- Reciprocal inhibition (Sherrington 1907). Muscle becomes inhibited reflexively when its antagonist is activated. Weakness is often reflex-mediated inhibition secondary to increased tension of the antagonist.
- Arthrogenic weakness (Stokes and Young 1984; DeAndrade, Grant, and Dison. 1965). Muscle becomes inhibited via anterior horn cells due to joint swelling or dysfunction. This weakness also leads to selective atrophy of Type II fibers (Edstrom 1970).
- Deafferentation (Freeman, Dean, and Hanham 1965). Deafferentation is a decrease in afferent information from neuromuscular receptors. Damage to joint mechanoreceptors (as seen with ligamentous injury) with subsequent loss of articular reflexes can cause altered motor programs, often influencing many muscles remote from the injured area (Bullock-Saxton 1994). This loss of afferent information ultimately leads to de-efferentation, or the loss of efferent signals to alpha motor neurons, which results in decreased muscle strength.
- Pseudoparesis (Janda 1986a). Pseudoparesis is a clinical presentation of weakness of neuroflexive origin. Pseudoparesis has three clinical signs: hypotonia upon inspection and palpation, a score of 4 out of 5 on a manual muscle test, and a change in the muscle activation pattern that may include delayed onset with early synergist activation or decreased EMG levels. Facilitatory techniques often restore muscle strength and activation. Normally facilitatory input can be inhibitory to a pseudoparetic muscle (Janda 1986a).
- TrP weakness (Simons, Travell, and Simons 1999). Hyperirritable bands of muscle fiber decrease the stimulation threshold, leading to overuse, early fatigue, and ultimately weakness. Muscles with active TrPs fatigue more rapidly than normal muscles do (Mense and Simons 2001), and they exhibit a decreased number of firing motor units and poor synchronization (Janda 1993).
- Fatigue. Muscle fatigue can be caused by metabolic or neurological factors. Often during exercise muscles are fatigued before pain is experienced. Thus the patient develops compensatory and faulty movement patterns before experiencing pain.
Adaptive Factors for Decreased Tension
Noncontractile factors causing decreased muscle tension are stretch weakness and tightness weakness:
- Stretch weakness (Kendall, McCreary, and Provance 1993; Sahrmann 2002a, 2002b). Stretch weakness is a condition in which a muscle is elongated beyond physiological neutral but not beyond the normal ROM (Janda 1993). Prolonged muscle elongation causes muscle spindle inhibition and the creation of additional sarcomeres. The increased muscle length also changes the length-tension curve. Stretch weakness is also known as positional weakness and is often associated with overuse and postural changes.
- Tightness weakness (Janda 1993). This is the most severe form of muscle tightness. It is often overlooked clinically. Overused muscle shortens over time, changing the muscle's length-tension curve and becoming more readily activated and weaker after time. There is also an increase in the noncontractile tissue and a decrease in elasticity, leading to hypertrophy. Ultimately, overuse leads to ischemia and degeneration of muscle fibers, which further weakens the muscle.
When an inhibited and weak muscle is resisted, as is the aim of strengthening exercises, its activity tends to decrease rather than increase (Janda 1987). It is important to distinguish between neuroflexive weakness and structural weakness. Often, if the tight antagonist is stretched, the weak and inhibited muscle spontaneously increases in strength.
Janda's Classification of Muscle Imbalance Patterns
Through his observations of patients with neurological disorders and chronic musculoskeletal pain, Janda found that the typical muscle response to joint dysfunction is similar to the muscle patterns found in upper motor neuron lesions, concluding that muscle imbalances are controlled by the CNS (Janda 1987). Janda believed that muscle tightness or spasticity is predominant. Often, weakness from muscle imbalance results from reciprocal inhibition of the tight antagonist. The degree of tightness and weakness varies between individuals, but the pattern rarely does. These patterns lead to postural changes and joint dysfunction and degeneration.
Janda identified three stereotypical patterns associated with distinct chronic pain syndromes: the upper-crossed, lower-crossed, and layer syndromes. These syndromes are characterized by specific patterns of muscle weakness and tightness that cross between the dorsal and the ventral sides of the body.
Upper-Crossed Syndrome
Upper-crossed syndrome (UCS) is also referred to as proximal or shoulder girdle crossed syndrome (figure 4.2a; Janda 1988). In UCS, tightness of the upper trapezius and levator scapula on the dorsal side crosses with tightness of the pectoralis major and minor. Weakness of the deep cervical flexors ventrally crosses with weakness of the middle and lower trapezius. This pattern of imbalance creates joint dysfunction, particularly at the atlanto-occipital joint, C4-C5 segment, cervicothoracic joint, glenohumeral joint, and T4-T5 segment. Janda noted that these focal areas of stress within the spine correspond to transitional zones in which neighboring vertebrae change in morphology. Specific postural changes are seen in UCS, including forward head posture, increased cervical lordosis and thoracic kyphosis, elevated and protracted shoulders, and rotation or abduction and winging of the scapulae (figure 4.2b). These postural changes decrease glenohumeral stability as the glenoid fossa becomes more vertical due to serratus anterior weakness leading to abduction, rotation, and winging of the scapulae. This loss of stability requires the levator scapula and upper trapezius to increase activation to maintain glenohumeral centration (Janda 1988).
Lower-Crossed Syndrome
Lower-crossed syndrome (LCS) is also referred to as distal or pelvic crossed syndrome (figure 4.3a; Janda 1987). In LCS, tightness of the thoracolumbar extensors on the dorsal side crosses with tightness of the iliopsoas and rectus femoris. Weakness of the deep abdominal muscles ventrally crosses with weakness of the gluteus maximus and medius. This pattern of imbalance creates joint dysfunction, particularly at the L4-L5 and L5-S1 segments, SI joint, and hip joint. Specific postural changes seen in LCS include anterior pelvic tilt, increased lumbar lordosis, lateral lumbar shift, lateral leg rotation, and knee hyperextension. If the lordosis is deep and short, then imbalance is predominantly in the pelvic muscles; if the lordosis is shallow and extends into the thoracic area, then imbalance predominates in the trunk muscles (Janda 1987).
Janda identified two subtypes of LCS: A and B (see figure 4.3, b-c). Patients with LCS type A use more hip flexion and extension movement for mobility; their standing posture demonstrates an anterior pelvic tilt with slight hip flexion and knee flexion. These individuals compensate with a hyperlordosis limited to the lumbar spine and with a hyperkyphosis in the upper lumbar and thoracolumbar segments.
Learn to assess muscle length
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening.
Muscle Length Assessment Technique
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening. Precise testing requires that one of the bony attachments of the muscle (usually the origin) be in a fixed position while the other bony attachment is moved passively in the direction of lengthening the muscle. In other words, muscle length testing assesses the resistance to passive movement. This is in contrast to typical flexibility or ROM testing. The actual ROM can be measured for documentation purposes, but it gives limited clinical information in muscle imbalance syndromes. The most valuable clinical information is the muscular end feel and the location of the ROM end feel. The elongation of the muscle should be performed slowly to avoid eliciting a quick stretch of the muscle spindle and subsequently inducing a twitch response and muscle contraction. In addition, for the best accuracy and precision, muscle length testing should be performed when the patient is not in acute pain in order to avoid pain inhibition and muscle guarding. In summary, there are four steps to assessing muscle length:
1. Ensure maximal lengthening of the muscle from origin to insertion.
2. Firmly stabilize one end (usually the origin).
3. Slowly elongate the muscle.
4. Assess the end feel.
Following are the procedures for testing key muscles. Clinicians do not have to perform muscle length testing on every muscle listed; instead, they should assess the muscles that the postural and movement pattern analysis indicate as being possibly tight. Once tight muscles have been identified, the clinician can establish a muscle imbalance pattern (if present) and begin to look for causes of the tightness. Table 7.1 provides the normal results of muscle length for flexibility testing.
Table 7.1 Normal Results of Muscles Tested for Length | |
| Muscle | Normal ranges or end feel |
| Iliopsoas | 0° hip extension, 10° with overpressure |
| Rectus femoris | 90° knee extension, 125° with overpressure |
| TFL-IT band | 0° hip abduction (neutral), 15°-20° with overpressure |
| Adductors | 0° hip abduction (neutral), 20°-25° with overpressure in the modified Thomas test position 45° hip abduction in supine position |
| Hamstrings | 80° hip flexion with contralateral leg extended 90° hip flexion with contralateral leg flexed |
| Triceps surae | 0° ankle dorsiflexion |
| Quadratus lumborum | Thoracolumbar curve should be smooth and gradual |
| Piriformis | Gradual soft end feel |
| Upper trapezius | Gradual soft end feel |
| Levator scapulae | Gradual soft end feel |
| SCM | Gradual soft end feel |
| Pectoralis major | Sternal portion (lower fibers): with shoulder abducted at 150°, arm should be horizontal to table and 15°-20° with overpressure Sternal portion (midfibers): with shoulder abducted to 90°, arm should be horizontal to table and 30° with overpressure Clavicular portion: with shoulder abducted to 60°, arm should hang freely over table |
| Paraspinals | Schober's test: excursion of >2.4 in. (6 cm) |
Lower-Quarter Muscles
The muscles of the lower quarter include those of the leg, pelvis, and lower back. The muscles prone to tightness are those involved in maintaining a single-leg stance (Janda 1987). Tightness of the hip flexors and tightness of the thoracolumbar extensors are hallmark signs of Janda's LCS.
Modified Thomas Test for Hip Flexor
The modified Thomas test (figure 7.2, a-e) allows the clinician to assess four different muscles prone to tightness namely, the one-joint hip flexor, iliacus and psoas major, and the two-joint hip flexors, rectus femoris and TFL-ITB. Tightness of the hip flexors limits hip hyperextension in gait and may cause an anterior pelvic tilt. Weakness of the gluteus maximus often is due to facilitation of the hip flexors.
Patient Position
The patient is asked to sit on the edge of the table, with the coccyx and ischial tuberosities touching the table and one foot on the floor. Then, the patient is asked to flex the opposite hip and knee toward the chest and maintain the position with the hands (see figure 7.2a).
Clinician Position
The clinician stands beside the leg not being tested, facing the patient. While supporting the patient by placing one hand on the midthoracic spine and the other on the knee, the clinician passively rolls the patient down to the table to the supine position. The clinician needs to ensure that the patient's knees are flexed, lumbar spine is flexed, and pelvis is in posterior rotation to fix the origin of the hip flexors.
Test
The clinician passively lowers the tested leg until resistance is felt or movement at the pelvis is detected. With the patient's thigh in the final resting position, the clinician observes whether it is in neutral and parallel to the table or abducted. A normal length of the one-joint hip flexors with the lumbar spine and sacrum flat on the table is indicated by the posterior thigh touching the table (0° of hip extension). With slight overpressure, the thigh should reach 10° to 15° of hyperextension (figure 7.2, b-c). Prominence of a superior patellar groove (figure 7.2d) suggests a short rectus femoris, while prominence of a lateral IT groove suggests a short IT band (see figure 7.2e).
Restoration of muscle balance
Treatment of muscle weakness aims at stimulating and increasing the response of the muscle spindle of the pseudoparetic muscle.
Muscle Length Assessment Technique
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening. Precise testing requires that one of the bony attachments of the muscle (usually the origin) be in a fixed position while the other bony attachment is moved passively in the direction of lengthening the muscle. In other words, muscle length testing assesses the resistance to passive movement. This is in contrast to typical flexibility or ROM testing. The actual ROM can be measured for documentation purposes, but it gives limited clinical information in muscle imbalance syndromes. The most valuable clinical information is the muscular end feel and the location of the ROM end feel. The elongation of the muscle should be performed slowly to avoid eliciting a quick stretch of the muscle spindle and subsequently inducing a twitch response and muscle contraction. In addition, for the best accuracy and precision, muscle length testing should be performed when the patient is not in acute pain in order to avoid pain inhibition and muscle guarding. In summary, there are four steps to assessing muscle length:
1. Ensure maximal lengthening of the muscle from origin to insertion.
2. Firmly stabilize one end (usually the origin).
3. Slowly elongate the muscle.
4. Assess the end feel.
Following are the procedures for testing key muscles. Clinicians do not have to perform muscle length testing on every muscle listed; instead, they should assess the muscles that the postural and movement pattern analysis indicate as being possibly tight. Once tight muscles have been identified, the clinician can establish a muscle imbalance pattern (if present) and begin to look for causes of the tightness. Table 7.1 provides the normal results of muscle length for flexibility testing.
Table 7.1 Normal Results of Muscles Tested for Length | |
| Muscle | Normal ranges or end feel |
| Iliopsoas | 0° hip extension, 10° with overpressure |
| Rectus femoris | 90° knee extension, 125° with overpressure |
| TFL-IT band | 0° hip abduction (neutral), 15°-20° with overpressure |
| Adductors | 0° hip abduction (neutral), 20°-25° with overpressure in the modified Thomas test position 45° hip abduction in supine position |
| Hamstrings | 80° hip flexion with contralateral leg extended 90° hip flexion with contralateral leg flexed |
| Triceps surae | 0° ankle dorsiflexion |
| Quadratus lumborum | Thoracolumbar curve should be smooth and gradual |
| Piriformis | Gradual soft end feel |
| Upper trapezius | Gradual soft end feel |
| Levator scapulae | Gradual soft end feel |
| SCM | Gradual soft end feel |
| Pectoralis major | Sternal portion (lower fibers): with shoulder abducted at 150°, arm should be horizontal to table and 15°-20° with overpressure Sternal portion (midfibers): with shoulder abducted to 90°, arm should be horizontal to table and 30° with overpressure Clavicular portion: with shoulder abducted to 60°, arm should hang freely over table |
| Paraspinals | Schober's test: excursion of >2.4 in. (6 cm) |
Lower-Quarter Muscles
The muscles of the lower quarter include those of the leg, pelvis, and lower back. The muscles prone to tightness are those involved in maintaining a single-leg stance (Janda 1987). Tightness of the hip flexors and tightness of the thoracolumbar extensors are hallmark signs of Janda's LCS.
Modified Thomas Test for Hip Flexor
The modified Thomas test (figure 7.2, a-e) allows the clinician to assess four different muscles prone to tightness namely, the one-joint hip flexor, iliacus and psoas major, and the two-joint hip flexors, rectus femoris and TFL-ITB. Tightness of the hip flexors limits hip hyperextension in gait and may cause an anterior pelvic tilt. Weakness of the gluteus maximus often is due to facilitation of the hip flexors.
Patient Position
The patient is asked to sit on the edge of the table, with the coccyx and ischial tuberosities touching the table and one foot on the floor. Then, the patient is asked to flex the opposite hip and knee toward the chest and maintain the position with the hands (see figure 7.2a).
Clinician Position
The clinician stands beside the leg not being tested, facing the patient. While supporting the patient by placing one hand on the midthoracic spine and the other on the knee, the clinician passively rolls the patient down to the table to the supine position. The clinician needs to ensure that the patient's knees are flexed, lumbar spine is flexed, and pelvis is in posterior rotation to fix the origin of the hip flexors.
Test
The clinician passively lowers the tested leg until resistance is felt or movement at the pelvis is detected. With the patient's thigh in the final resting position, the clinician observes whether it is in neutral and parallel to the table or abducted. A normal length of the one-joint hip flexors with the lumbar spine and sacrum flat on the table is indicated by the posterior thigh touching the table (0° of hip extension). With slight overpressure, the thigh should reach 10° to 15° of hyperextension (figure 7.2, b-c). Prominence of a superior patellar groove (figure 7.2d) suggests a short rectus femoris, while prominence of a lateral IT groove suggests a short IT band (see figure 7.2e).
Rehabilitation of impingement
Rehabilitation rather than surgery is recommended for secondary impingement.
Rehabilitation rather than surgery is recommended for secondary impingement (Brox and Brevik 1996; Kronberg, Németh, and Broström 1990; Michener, Walsworth, and Burnet 2004; Morrison, Frogameni, and Woodworth 1997). Patients with primary impingement (type II and III acromion), however, have only a 64% to 68% success rate with conservative treatment (Morrison, Frogameni, and Woodworth 1997). While rehabilitation and arthroscopic surgery improve impingement symptoms equally (Haarh et al. 2005; Haarh and Andersen 2006), rehabilitation is less costly (Brox et al. 1993).
In a systematic review, Michener, Walsworth, and Burnet and colleagues (2004) found strong support in the literature for therapeutic exercise of the rotator cuff and scapular muscles as well as for stretching of the anterior and posterior shoulder. Furthermore, exercise is more effective when combined with joint mobilization (Michener, Walsworth, and Burnet 2004; Senbursa, Baltaci, and Atay 2007). The following are impingement rehabilitation recommendations with evidence-based rationale:
- Integrate the entire upper-extremity chain during exercise. This facilitates the kinetic chain from the hand to the spine (Burkhart, Morgan, and Kibler 2003; Kibler 1998b, 2006; McMullen and Uhl 2000). Figure 13.5 illustrates exercises that integrate the whole kinetic chain.
- Include hip and trunk stabilization exercises. This facilitates force transmission and proximal stabilization between the upper extremity and the trunk (Burkhart, Morgan, and Kibler 2003; Kibler 1998b, 2006; McMullen and Uhl 2000).
- Isolate the rotator cuff and scapular stabilizers first, before performing multijoint movements. Performing multijoint shoulder movements does not increase the strength of smaller single-joint muscles such as the rotator cuff (Giannakopoulos et al. 2004). Strengthening exercises isolating the rotator cuff should be performed first (Jobe and Pink 1993; Malliou et al. 2004).
- Exercise in the scapular plane. The scapular plane offers the most balanced position of the capsule and provides ideal joint centration during elevation (Borsa, Timmons, and Sauers 2003).
- Exercise both shoulders. Abnormal muscle activation often occurs in both the involved and the uninvolved shoulder (Cools et al. 2003; Cools, Declercq et al. 2007; Wadsworth and Bullock-Saxton 1997).
- Include neuromuscular exercises such as closed kinetic chain exercises and PNF. Patients with impingement demonstrate reduced proprioception (Machner et al. 2003) and so require proprioceptive rehabilitation (Ginn and Cohen 2005; Kamkar, Irrgang, and Whitney 1993; Smith and Burnolli 1989). Figure 13.6 illustrates a closed kinetic chain shoulder exercise for improving proprioception (Naughton, Adams, and Maher 2005).
- Stretch the posterior shoulder when internal rotation is limited. The posterior capsule is often tight in athletes with impingement, limiting internal rotation and follow-through (Myers et al. 2006; Tyler et al. 2000). The cross-body stretch (see figure 13.7) improves internal rotation in subjects with posterior shoulder tightness (McClure et al. 2007).
Causes of muscle weakness
A look at the causes of muscle weakness as well as Janda’s classification of muscle imbalance patterns.
Muscle tension can decrease as a result of a structural lesion in the CNS such as a spinal cord injury or stroke. A loss of tension leads to flaccidity or weakness. Weak muscles are also described as hypotonic or inhibited. Functionally, muscle can be weak as a result of neuroflexive or adaptive changes and may exhibit delayed activation in movement patterns.
Neuroflexive Factors for Decreased Tension
Many contractile factors can contribute to decreased muscle tension:
- Reciprocal inhibition (Sherrington 1907). Muscle becomes inhibited reflexively when its antagonist is activated. Weakness is often reflex-mediated inhibition secondary to increased tension of the antagonist.
- Arthrogenic weakness (Stokes and Young 1984; DeAndrade, Grant, and Dison. 1965). Muscle becomes inhibited via anterior horn cells due to joint swelling or dysfunction. This weakness also leads to selective atrophy of Type II fibers (Edstrom 1970).
- Deafferentation (Freeman, Dean, and Hanham 1965). Deafferentation is a decrease in afferent information from neuromuscular receptors. Damage to joint mechanoreceptors (as seen with ligamentous injury) with subsequent loss of articular reflexes can cause altered motor programs, often influencing many muscles remote from the injured area (Bullock-Saxton 1994). This loss of afferent information ultimately leads to de-efferentation, or the loss of efferent signals to alpha motor neurons, which results in decreased muscle strength.
- Pseudoparesis (Janda 1986a). Pseudoparesis is a clinical presentation of weakness of neuroflexive origin. Pseudoparesis has three clinical signs: hypotonia upon inspection and palpation, a score of 4 out of 5 on a manual muscle test, and a change in the muscle activation pattern that may include delayed onset with early synergist activation or decreased EMG levels. Facilitatory techniques often restore muscle strength and activation. Normally facilitatory input can be inhibitory to a pseudoparetic muscle (Janda 1986a).
- TrP weakness (Simons, Travell, and Simons 1999). Hyperirritable bands of muscle fiber decrease the stimulation threshold, leading to overuse, early fatigue, and ultimately weakness. Muscles with active TrPs fatigue more rapidly than normal muscles do (Mense and Simons 2001), and they exhibit a decreased number of firing motor units and poor synchronization (Janda 1993).
- Fatigue. Muscle fatigue can be caused by metabolic or neurological factors. Often during exercise muscles are fatigued before pain is experienced. Thus the patient develops compensatory and faulty movement patterns before experiencing pain.
Adaptive Factors for Decreased Tension
Noncontractile factors causing decreased muscle tension are stretch weakness and tightness weakness:
- Stretch weakness (Kendall, McCreary, and Provance 1993; Sahrmann 2002a, 2002b). Stretch weakness is a condition in which a muscle is elongated beyond physiological neutral but not beyond the normal ROM (Janda 1993). Prolonged muscle elongation causes muscle spindle inhibition and the creation of additional sarcomeres. The increased muscle length also changes the length-tension curve. Stretch weakness is also known as positional weakness and is often associated with overuse and postural changes.
- Tightness weakness (Janda 1993). This is the most severe form of muscle tightness. It is often overlooked clinically. Overused muscle shortens over time, changing the muscle's length-tension curve and becoming more readily activated and weaker after time. There is also an increase in the noncontractile tissue and a decrease in elasticity, leading to hypertrophy. Ultimately, overuse leads to ischemia and degeneration of muscle fibers, which further weakens the muscle.
When an inhibited and weak muscle is resisted, as is the aim of strengthening exercises, its activity tends to decrease rather than increase (Janda 1987). It is important to distinguish between neuroflexive weakness and structural weakness. Often, if the tight antagonist is stretched, the weak and inhibited muscle spontaneously increases in strength.
Janda's Classification of Muscle Imbalance Patterns
Through his observations of patients with neurological disorders and chronic musculoskeletal pain, Janda found that the typical muscle response to joint dysfunction is similar to the muscle patterns found in upper motor neuron lesions, concluding that muscle imbalances are controlled by the CNS (Janda 1987). Janda believed that muscle tightness or spasticity is predominant. Often, weakness from muscle imbalance results from reciprocal inhibition of the tight antagonist. The degree of tightness and weakness varies between individuals, but the pattern rarely does. These patterns lead to postural changes and joint dysfunction and degeneration.
Janda identified three stereotypical patterns associated with distinct chronic pain syndromes: the upper-crossed, lower-crossed, and layer syndromes. These syndromes are characterized by specific patterns of muscle weakness and tightness that cross between the dorsal and the ventral sides of the body.
Upper-Crossed Syndrome
Upper-crossed syndrome (UCS) is also referred to as proximal or shoulder girdle crossed syndrome (figure 4.2a; Janda 1988). In UCS, tightness of the upper trapezius and levator scapula on the dorsal side crosses with tightness of the pectoralis major and minor. Weakness of the deep cervical flexors ventrally crosses with weakness of the middle and lower trapezius. This pattern of imbalance creates joint dysfunction, particularly at the atlanto-occipital joint, C4-C5 segment, cervicothoracic joint, glenohumeral joint, and T4-T5 segment. Janda noted that these focal areas of stress within the spine correspond to transitional zones in which neighboring vertebrae change in morphology. Specific postural changes are seen in UCS, including forward head posture, increased cervical lordosis and thoracic kyphosis, elevated and protracted shoulders, and rotation or abduction and winging of the scapulae (figure 4.2b). These postural changes decrease glenohumeral stability as the glenoid fossa becomes more vertical due to serratus anterior weakness leading to abduction, rotation, and winging of the scapulae. This loss of stability requires the levator scapula and upper trapezius to increase activation to maintain glenohumeral centration (Janda 1988).
Lower-Crossed Syndrome
Lower-crossed syndrome (LCS) is also referred to as distal or pelvic crossed syndrome (figure 4.3a; Janda 1987). In LCS, tightness of the thoracolumbar extensors on the dorsal side crosses with tightness of the iliopsoas and rectus femoris. Weakness of the deep abdominal muscles ventrally crosses with weakness of the gluteus maximus and medius. This pattern of imbalance creates joint dysfunction, particularly at the L4-L5 and L5-S1 segments, SI joint, and hip joint. Specific postural changes seen in LCS include anterior pelvic tilt, increased lumbar lordosis, lateral lumbar shift, lateral leg rotation, and knee hyperextension. If the lordosis is deep and short, then imbalance is predominantly in the pelvic muscles; if the lordosis is shallow and extends into the thoracic area, then imbalance predominates in the trunk muscles (Janda 1987).
Janda identified two subtypes of LCS: A and B (see figure 4.3, b-c). Patients with LCS type A use more hip flexion and extension movement for mobility; their standing posture demonstrates an anterior pelvic tilt with slight hip flexion and knee flexion. These individuals compensate with a hyperlordosis limited to the lumbar spine and with a hyperkyphosis in the upper lumbar and thoracolumbar segments.
Learn to assess muscle length
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening.
Muscle Length Assessment Technique
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening. Precise testing requires that one of the bony attachments of the muscle (usually the origin) be in a fixed position while the other bony attachment is moved passively in the direction of lengthening the muscle. In other words, muscle length testing assesses the resistance to passive movement. This is in contrast to typical flexibility or ROM testing. The actual ROM can be measured for documentation purposes, but it gives limited clinical information in muscle imbalance syndromes. The most valuable clinical information is the muscular end feel and the location of the ROM end feel. The elongation of the muscle should be performed slowly to avoid eliciting a quick stretch of the muscle spindle and subsequently inducing a twitch response and muscle contraction. In addition, for the best accuracy and precision, muscle length testing should be performed when the patient is not in acute pain in order to avoid pain inhibition and muscle guarding. In summary, there are four steps to assessing muscle length:
1. Ensure maximal lengthening of the muscle from origin to insertion.
2. Firmly stabilize one end (usually the origin).
3. Slowly elongate the muscle.
4. Assess the end feel.
Following are the procedures for testing key muscles. Clinicians do not have to perform muscle length testing on every muscle listed; instead, they should assess the muscles that the postural and movement pattern analysis indicate as being possibly tight. Once tight muscles have been identified, the clinician can establish a muscle imbalance pattern (if present) and begin to look for causes of the tightness. Table 7.1 provides the normal results of muscle length for flexibility testing.
Table 7.1 Normal Results of Muscles Tested for Length | |
| Muscle | Normal ranges or end feel |
| Iliopsoas | 0° hip extension, 10° with overpressure |
| Rectus femoris | 90° knee extension, 125° with overpressure |
| TFL-IT band | 0° hip abduction (neutral), 15°-20° with overpressure |
| Adductors | 0° hip abduction (neutral), 20°-25° with overpressure in the modified Thomas test position 45° hip abduction in supine position |
| Hamstrings | 80° hip flexion with contralateral leg extended 90° hip flexion with contralateral leg flexed |
| Triceps surae | 0° ankle dorsiflexion |
| Quadratus lumborum | Thoracolumbar curve should be smooth and gradual |
| Piriformis | Gradual soft end feel |
| Upper trapezius | Gradual soft end feel |
| Levator scapulae | Gradual soft end feel |
| SCM | Gradual soft end feel |
| Pectoralis major | Sternal portion (lower fibers): with shoulder abducted at 150°, arm should be horizontal to table and 15°-20° with overpressure Sternal portion (midfibers): with shoulder abducted to 90°, arm should be horizontal to table and 30° with overpressure Clavicular portion: with shoulder abducted to 60°, arm should hang freely over table |
| Paraspinals | Schober's test: excursion of >2.4 in. (6 cm) |
Lower-Quarter Muscles
The muscles of the lower quarter include those of the leg, pelvis, and lower back. The muscles prone to tightness are those involved in maintaining a single-leg stance (Janda 1987). Tightness of the hip flexors and tightness of the thoracolumbar extensors are hallmark signs of Janda's LCS.
Modified Thomas Test for Hip Flexor
The modified Thomas test (figure 7.2, a-e) allows the clinician to assess four different muscles prone to tightness namely, the one-joint hip flexor, iliacus and psoas major, and the two-joint hip flexors, rectus femoris and TFL-ITB. Tightness of the hip flexors limits hip hyperextension in gait and may cause an anterior pelvic tilt. Weakness of the gluteus maximus often is due to facilitation of the hip flexors.
Patient Position
The patient is asked to sit on the edge of the table, with the coccyx and ischial tuberosities touching the table and one foot on the floor. Then, the patient is asked to flex the opposite hip and knee toward the chest and maintain the position with the hands (see figure 7.2a).
Clinician Position
The clinician stands beside the leg not being tested, facing the patient. While supporting the patient by placing one hand on the midthoracic spine and the other on the knee, the clinician passively rolls the patient down to the table to the supine position. The clinician needs to ensure that the patient's knees are flexed, lumbar spine is flexed, and pelvis is in posterior rotation to fix the origin of the hip flexors.
Test
The clinician passively lowers the tested leg until resistance is felt or movement at the pelvis is detected. With the patient's thigh in the final resting position, the clinician observes whether it is in neutral and parallel to the table or abducted. A normal length of the one-joint hip flexors with the lumbar spine and sacrum flat on the table is indicated by the posterior thigh touching the table (0° of hip extension). With slight overpressure, the thigh should reach 10° to 15° of hyperextension (figure 7.2, b-c). Prominence of a superior patellar groove (figure 7.2d) suggests a short rectus femoris, while prominence of a lateral IT groove suggests a short IT band (see figure 7.2e).
Restoration of muscle balance
Treatment of muscle weakness aims at stimulating and increasing the response of the muscle spindle of the pseudoparetic muscle.
Muscle Length Assessment Technique
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening. Precise testing requires that one of the bony attachments of the muscle (usually the origin) be in a fixed position while the other bony attachment is moved passively in the direction of lengthening the muscle. In other words, muscle length testing assesses the resistance to passive movement. This is in contrast to typical flexibility or ROM testing. The actual ROM can be measured for documentation purposes, but it gives limited clinical information in muscle imbalance syndromes. The most valuable clinical information is the muscular end feel and the location of the ROM end feel. The elongation of the muscle should be performed slowly to avoid eliciting a quick stretch of the muscle spindle and subsequently inducing a twitch response and muscle contraction. In addition, for the best accuracy and precision, muscle length testing should be performed when the patient is not in acute pain in order to avoid pain inhibition and muscle guarding. In summary, there are four steps to assessing muscle length:
1. Ensure maximal lengthening of the muscle from origin to insertion.
2. Firmly stabilize one end (usually the origin).
3. Slowly elongate the muscle.
4. Assess the end feel.
Following are the procedures for testing key muscles. Clinicians do not have to perform muscle length testing on every muscle listed; instead, they should assess the muscles that the postural and movement pattern analysis indicate as being possibly tight. Once tight muscles have been identified, the clinician can establish a muscle imbalance pattern (if present) and begin to look for causes of the tightness. Table 7.1 provides the normal results of muscle length for flexibility testing.
Table 7.1 Normal Results of Muscles Tested for Length | |
| Muscle | Normal ranges or end feel |
| Iliopsoas | 0° hip extension, 10° with overpressure |
| Rectus femoris | 90° knee extension, 125° with overpressure |
| TFL-IT band | 0° hip abduction (neutral), 15°-20° with overpressure |
| Adductors | 0° hip abduction (neutral), 20°-25° with overpressure in the modified Thomas test position 45° hip abduction in supine position |
| Hamstrings | 80° hip flexion with contralateral leg extended 90° hip flexion with contralateral leg flexed |
| Triceps surae | 0° ankle dorsiflexion |
| Quadratus lumborum | Thoracolumbar curve should be smooth and gradual |
| Piriformis | Gradual soft end feel |
| Upper trapezius | Gradual soft end feel |
| Levator scapulae | Gradual soft end feel |
| SCM | Gradual soft end feel |
| Pectoralis major | Sternal portion (lower fibers): with shoulder abducted at 150°, arm should be horizontal to table and 15°-20° with overpressure Sternal portion (midfibers): with shoulder abducted to 90°, arm should be horizontal to table and 30° with overpressure Clavicular portion: with shoulder abducted to 60°, arm should hang freely over table |
| Paraspinals | Schober's test: excursion of >2.4 in. (6 cm) |
Lower-Quarter Muscles
The muscles of the lower quarter include those of the leg, pelvis, and lower back. The muscles prone to tightness are those involved in maintaining a single-leg stance (Janda 1987). Tightness of the hip flexors and tightness of the thoracolumbar extensors are hallmark signs of Janda's LCS.
Modified Thomas Test for Hip Flexor
The modified Thomas test (figure 7.2, a-e) allows the clinician to assess four different muscles prone to tightness namely, the one-joint hip flexor, iliacus and psoas major, and the two-joint hip flexors, rectus femoris and TFL-ITB. Tightness of the hip flexors limits hip hyperextension in gait and may cause an anterior pelvic tilt. Weakness of the gluteus maximus often is due to facilitation of the hip flexors.
Patient Position
The patient is asked to sit on the edge of the table, with the coccyx and ischial tuberosities touching the table and one foot on the floor. Then, the patient is asked to flex the opposite hip and knee toward the chest and maintain the position with the hands (see figure 7.2a).
Clinician Position
The clinician stands beside the leg not being tested, facing the patient. While supporting the patient by placing one hand on the midthoracic spine and the other on the knee, the clinician passively rolls the patient down to the table to the supine position. The clinician needs to ensure that the patient's knees are flexed, lumbar spine is flexed, and pelvis is in posterior rotation to fix the origin of the hip flexors.
Test
The clinician passively lowers the tested leg until resistance is felt or movement at the pelvis is detected. With the patient's thigh in the final resting position, the clinician observes whether it is in neutral and parallel to the table or abducted. A normal length of the one-joint hip flexors with the lumbar spine and sacrum flat on the table is indicated by the posterior thigh touching the table (0° of hip extension). With slight overpressure, the thigh should reach 10° to 15° of hyperextension (figure 7.2, b-c). Prominence of a superior patellar groove (figure 7.2d) suggests a short rectus femoris, while prominence of a lateral IT groove suggests a short IT band (see figure 7.2e).
Rehabilitation of impingement
Rehabilitation rather than surgery is recommended for secondary impingement.
Rehabilitation rather than surgery is recommended for secondary impingement (Brox and Brevik 1996; Kronberg, Németh, and Broström 1990; Michener, Walsworth, and Burnet 2004; Morrison, Frogameni, and Woodworth 1997). Patients with primary impingement (type II and III acromion), however, have only a 64% to 68% success rate with conservative treatment (Morrison, Frogameni, and Woodworth 1997). While rehabilitation and arthroscopic surgery improve impingement symptoms equally (Haarh et al. 2005; Haarh and Andersen 2006), rehabilitation is less costly (Brox et al. 1993).
In a systematic review, Michener, Walsworth, and Burnet and colleagues (2004) found strong support in the literature for therapeutic exercise of the rotator cuff and scapular muscles as well as for stretching of the anterior and posterior shoulder. Furthermore, exercise is more effective when combined with joint mobilization (Michener, Walsworth, and Burnet 2004; Senbursa, Baltaci, and Atay 2007). The following are impingement rehabilitation recommendations with evidence-based rationale:
- Integrate the entire upper-extremity chain during exercise. This facilitates the kinetic chain from the hand to the spine (Burkhart, Morgan, and Kibler 2003; Kibler 1998b, 2006; McMullen and Uhl 2000). Figure 13.5 illustrates exercises that integrate the whole kinetic chain.
- Include hip and trunk stabilization exercises. This facilitates force transmission and proximal stabilization between the upper extremity and the trunk (Burkhart, Morgan, and Kibler 2003; Kibler 1998b, 2006; McMullen and Uhl 2000).
- Isolate the rotator cuff and scapular stabilizers first, before performing multijoint movements. Performing multijoint shoulder movements does not increase the strength of smaller single-joint muscles such as the rotator cuff (Giannakopoulos et al. 2004). Strengthening exercises isolating the rotator cuff should be performed first (Jobe and Pink 1993; Malliou et al. 2004).
- Exercise in the scapular plane. The scapular plane offers the most balanced position of the capsule and provides ideal joint centration during elevation (Borsa, Timmons, and Sauers 2003).
- Exercise both shoulders. Abnormal muscle activation often occurs in both the involved and the uninvolved shoulder (Cools et al. 2003; Cools, Declercq et al. 2007; Wadsworth and Bullock-Saxton 1997).
- Include neuromuscular exercises such as closed kinetic chain exercises and PNF. Patients with impingement demonstrate reduced proprioception (Machner et al. 2003) and so require proprioceptive rehabilitation (Ginn and Cohen 2005; Kamkar, Irrgang, and Whitney 1993; Smith and Burnolli 1989). Figure 13.6 illustrates a closed kinetic chain shoulder exercise for improving proprioception (Naughton, Adams, and Maher 2005).
- Stretch the posterior shoulder when internal rotation is limited. The posterior capsule is often tight in athletes with impingement, limiting internal rotation and follow-through (Myers et al. 2006; Tyler et al. 2000). The cross-body stretch (see figure 13.7) improves internal rotation in subjects with posterior shoulder tightness (McClure et al. 2007).
Causes of muscle weakness
A look at the causes of muscle weakness as well as Janda’s classification of muscle imbalance patterns.
Muscle tension can decrease as a result of a structural lesion in the CNS such as a spinal cord injury or stroke. A loss of tension leads to flaccidity or weakness. Weak muscles are also described as hypotonic or inhibited. Functionally, muscle can be weak as a result of neuroflexive or adaptive changes and may exhibit delayed activation in movement patterns.
Neuroflexive Factors for Decreased Tension
Many contractile factors can contribute to decreased muscle tension:
- Reciprocal inhibition (Sherrington 1907). Muscle becomes inhibited reflexively when its antagonist is activated. Weakness is often reflex-mediated inhibition secondary to increased tension of the antagonist.
- Arthrogenic weakness (Stokes and Young 1984; DeAndrade, Grant, and Dison. 1965). Muscle becomes inhibited via anterior horn cells due to joint swelling or dysfunction. This weakness also leads to selective atrophy of Type II fibers (Edstrom 1970).
- Deafferentation (Freeman, Dean, and Hanham 1965). Deafferentation is a decrease in afferent information from neuromuscular receptors. Damage to joint mechanoreceptors (as seen with ligamentous injury) with subsequent loss of articular reflexes can cause altered motor programs, often influencing many muscles remote from the injured area (Bullock-Saxton 1994). This loss of afferent information ultimately leads to de-efferentation, or the loss of efferent signals to alpha motor neurons, which results in decreased muscle strength.
- Pseudoparesis (Janda 1986a). Pseudoparesis is a clinical presentation of weakness of neuroflexive origin. Pseudoparesis has three clinical signs: hypotonia upon inspection and palpation, a score of 4 out of 5 on a manual muscle test, and a change in the muscle activation pattern that may include delayed onset with early synergist activation or decreased EMG levels. Facilitatory techniques often restore muscle strength and activation. Normally facilitatory input can be inhibitory to a pseudoparetic muscle (Janda 1986a).
- TrP weakness (Simons, Travell, and Simons 1999). Hyperirritable bands of muscle fiber decrease the stimulation threshold, leading to overuse, early fatigue, and ultimately weakness. Muscles with active TrPs fatigue more rapidly than normal muscles do (Mense and Simons 2001), and they exhibit a decreased number of firing motor units and poor synchronization (Janda 1993).
- Fatigue. Muscle fatigue can be caused by metabolic or neurological factors. Often during exercise muscles are fatigued before pain is experienced. Thus the patient develops compensatory and faulty movement patterns before experiencing pain.
Adaptive Factors for Decreased Tension
Noncontractile factors causing decreased muscle tension are stretch weakness and tightness weakness:
- Stretch weakness (Kendall, McCreary, and Provance 1993; Sahrmann 2002a, 2002b). Stretch weakness is a condition in which a muscle is elongated beyond physiological neutral but not beyond the normal ROM (Janda 1993). Prolonged muscle elongation causes muscle spindle inhibition and the creation of additional sarcomeres. The increased muscle length also changes the length-tension curve. Stretch weakness is also known as positional weakness and is often associated with overuse and postural changes.
- Tightness weakness (Janda 1993). This is the most severe form of muscle tightness. It is often overlooked clinically. Overused muscle shortens over time, changing the muscle's length-tension curve and becoming more readily activated and weaker after time. There is also an increase in the noncontractile tissue and a decrease in elasticity, leading to hypertrophy. Ultimately, overuse leads to ischemia and degeneration of muscle fibers, which further weakens the muscle.
When an inhibited and weak muscle is resisted, as is the aim of strengthening exercises, its activity tends to decrease rather than increase (Janda 1987). It is important to distinguish between neuroflexive weakness and structural weakness. Often, if the tight antagonist is stretched, the weak and inhibited muscle spontaneously increases in strength.
Janda's Classification of Muscle Imbalance Patterns
Through his observations of patients with neurological disorders and chronic musculoskeletal pain, Janda found that the typical muscle response to joint dysfunction is similar to the muscle patterns found in upper motor neuron lesions, concluding that muscle imbalances are controlled by the CNS (Janda 1987). Janda believed that muscle tightness or spasticity is predominant. Often, weakness from muscle imbalance results from reciprocal inhibition of the tight antagonist. The degree of tightness and weakness varies between individuals, but the pattern rarely does. These patterns lead to postural changes and joint dysfunction and degeneration.
Janda identified three stereotypical patterns associated with distinct chronic pain syndromes: the upper-crossed, lower-crossed, and layer syndromes. These syndromes are characterized by specific patterns of muscle weakness and tightness that cross between the dorsal and the ventral sides of the body.
Upper-Crossed Syndrome
Upper-crossed syndrome (UCS) is also referred to as proximal or shoulder girdle crossed syndrome (figure 4.2a; Janda 1988). In UCS, tightness of the upper trapezius and levator scapula on the dorsal side crosses with tightness of the pectoralis major and minor. Weakness of the deep cervical flexors ventrally crosses with weakness of the middle and lower trapezius. This pattern of imbalance creates joint dysfunction, particularly at the atlanto-occipital joint, C4-C5 segment, cervicothoracic joint, glenohumeral joint, and T4-T5 segment. Janda noted that these focal areas of stress within the spine correspond to transitional zones in which neighboring vertebrae change in morphology. Specific postural changes are seen in UCS, including forward head posture, increased cervical lordosis and thoracic kyphosis, elevated and protracted shoulders, and rotation or abduction and winging of the scapulae (figure 4.2b). These postural changes decrease glenohumeral stability as the glenoid fossa becomes more vertical due to serratus anterior weakness leading to abduction, rotation, and winging of the scapulae. This loss of stability requires the levator scapula and upper trapezius to increase activation to maintain glenohumeral centration (Janda 1988).
Lower-Crossed Syndrome
Lower-crossed syndrome (LCS) is also referred to as distal or pelvic crossed syndrome (figure 4.3a; Janda 1987). In LCS, tightness of the thoracolumbar extensors on the dorsal side crosses with tightness of the iliopsoas and rectus femoris. Weakness of the deep abdominal muscles ventrally crosses with weakness of the gluteus maximus and medius. This pattern of imbalance creates joint dysfunction, particularly at the L4-L5 and L5-S1 segments, SI joint, and hip joint. Specific postural changes seen in LCS include anterior pelvic tilt, increased lumbar lordosis, lateral lumbar shift, lateral leg rotation, and knee hyperextension. If the lordosis is deep and short, then imbalance is predominantly in the pelvic muscles; if the lordosis is shallow and extends into the thoracic area, then imbalance predominates in the trunk muscles (Janda 1987).
Janda identified two subtypes of LCS: A and B (see figure 4.3, b-c). Patients with LCS type A use more hip flexion and extension movement for mobility; their standing posture demonstrates an anterior pelvic tilt with slight hip flexion and knee flexion. These individuals compensate with a hyperlordosis limited to the lumbar spine and with a hyperkyphosis in the upper lumbar and thoracolumbar segments.
Learn to assess muscle length
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening.
Muscle Length Assessment Technique
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening. Precise testing requires that one of the bony attachments of the muscle (usually the origin) be in a fixed position while the other bony attachment is moved passively in the direction of lengthening the muscle. In other words, muscle length testing assesses the resistance to passive movement. This is in contrast to typical flexibility or ROM testing. The actual ROM can be measured for documentation purposes, but it gives limited clinical information in muscle imbalance syndromes. The most valuable clinical information is the muscular end feel and the location of the ROM end feel. The elongation of the muscle should be performed slowly to avoid eliciting a quick stretch of the muscle spindle and subsequently inducing a twitch response and muscle contraction. In addition, for the best accuracy and precision, muscle length testing should be performed when the patient is not in acute pain in order to avoid pain inhibition and muscle guarding. In summary, there are four steps to assessing muscle length:
1. Ensure maximal lengthening of the muscle from origin to insertion.
2. Firmly stabilize one end (usually the origin).
3. Slowly elongate the muscle.
4. Assess the end feel.
Following are the procedures for testing key muscles. Clinicians do not have to perform muscle length testing on every muscle listed; instead, they should assess the muscles that the postural and movement pattern analysis indicate as being possibly tight. Once tight muscles have been identified, the clinician can establish a muscle imbalance pattern (if present) and begin to look for causes of the tightness. Table 7.1 provides the normal results of muscle length for flexibility testing.
Table 7.1 Normal Results of Muscles Tested for Length | |
| Muscle | Normal ranges or end feel |
| Iliopsoas | 0° hip extension, 10° with overpressure |
| Rectus femoris | 90° knee extension, 125° with overpressure |
| TFL-IT band | 0° hip abduction (neutral), 15°-20° with overpressure |
| Adductors | 0° hip abduction (neutral), 20°-25° with overpressure in the modified Thomas test position 45° hip abduction in supine position |
| Hamstrings | 80° hip flexion with contralateral leg extended 90° hip flexion with contralateral leg flexed |
| Triceps surae | 0° ankle dorsiflexion |
| Quadratus lumborum | Thoracolumbar curve should be smooth and gradual |
| Piriformis | Gradual soft end feel |
| Upper trapezius | Gradual soft end feel |
| Levator scapulae | Gradual soft end feel |
| SCM | Gradual soft end feel |
| Pectoralis major | Sternal portion (lower fibers): with shoulder abducted at 150°, arm should be horizontal to table and 15°-20° with overpressure Sternal portion (midfibers): with shoulder abducted to 90°, arm should be horizontal to table and 30° with overpressure Clavicular portion: with shoulder abducted to 60°, arm should hang freely over table |
| Paraspinals | Schober's test: excursion of >2.4 in. (6 cm) |
Lower-Quarter Muscles
The muscles of the lower quarter include those of the leg, pelvis, and lower back. The muscles prone to tightness are those involved in maintaining a single-leg stance (Janda 1987). Tightness of the hip flexors and tightness of the thoracolumbar extensors are hallmark signs of Janda's LCS.
Modified Thomas Test for Hip Flexor
The modified Thomas test (figure 7.2, a-e) allows the clinician to assess four different muscles prone to tightness namely, the one-joint hip flexor, iliacus and psoas major, and the two-joint hip flexors, rectus femoris and TFL-ITB. Tightness of the hip flexors limits hip hyperextension in gait and may cause an anterior pelvic tilt. Weakness of the gluteus maximus often is due to facilitation of the hip flexors.
Patient Position
The patient is asked to sit on the edge of the table, with the coccyx and ischial tuberosities touching the table and one foot on the floor. Then, the patient is asked to flex the opposite hip and knee toward the chest and maintain the position with the hands (see figure 7.2a).
Clinician Position
The clinician stands beside the leg not being tested, facing the patient. While supporting the patient by placing one hand on the midthoracic spine and the other on the knee, the clinician passively rolls the patient down to the table to the supine position. The clinician needs to ensure that the patient's knees are flexed, lumbar spine is flexed, and pelvis is in posterior rotation to fix the origin of the hip flexors.
Test
The clinician passively lowers the tested leg until resistance is felt or movement at the pelvis is detected. With the patient's thigh in the final resting position, the clinician observes whether it is in neutral and parallel to the table or abducted. A normal length of the one-joint hip flexors with the lumbar spine and sacrum flat on the table is indicated by the posterior thigh touching the table (0° of hip extension). With slight overpressure, the thigh should reach 10° to 15° of hyperextension (figure 7.2, b-c). Prominence of a superior patellar groove (figure 7.2d) suggests a short rectus femoris, while prominence of a lateral IT groove suggests a short IT band (see figure 7.2e).
Restoration of muscle balance
Treatment of muscle weakness aims at stimulating and increasing the response of the muscle spindle of the pseudoparetic muscle.
Muscle Length Assessment Technique
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening. Precise testing requires that one of the bony attachments of the muscle (usually the origin) be in a fixed position while the other bony attachment is moved passively in the direction of lengthening the muscle. In other words, muscle length testing assesses the resistance to passive movement. This is in contrast to typical flexibility or ROM testing. The actual ROM can be measured for documentation purposes, but it gives limited clinical information in muscle imbalance syndromes. The most valuable clinical information is the muscular end feel and the location of the ROM end feel. The elongation of the muscle should be performed slowly to avoid eliciting a quick stretch of the muscle spindle and subsequently inducing a twitch response and muscle contraction. In addition, for the best accuracy and precision, muscle length testing should be performed when the patient is not in acute pain in order to avoid pain inhibition and muscle guarding. In summary, there are four steps to assessing muscle length:
1. Ensure maximal lengthening of the muscle from origin to insertion.
2. Firmly stabilize one end (usually the origin).
3. Slowly elongate the muscle.
4. Assess the end feel.
Following are the procedures for testing key muscles. Clinicians do not have to perform muscle length testing on every muscle listed; instead, they should assess the muscles that the postural and movement pattern analysis indicate as being possibly tight. Once tight muscles have been identified, the clinician can establish a muscle imbalance pattern (if present) and begin to look for causes of the tightness. Table 7.1 provides the normal results of muscle length for flexibility testing.
Table 7.1 Normal Results of Muscles Tested for Length | |
| Muscle | Normal ranges or end feel |
| Iliopsoas | 0° hip extension, 10° with overpressure |
| Rectus femoris | 90° knee extension, 125° with overpressure |
| TFL-IT band | 0° hip abduction (neutral), 15°-20° with overpressure |
| Adductors | 0° hip abduction (neutral), 20°-25° with overpressure in the modified Thomas test position 45° hip abduction in supine position |
| Hamstrings | 80° hip flexion with contralateral leg extended 90° hip flexion with contralateral leg flexed |
| Triceps surae | 0° ankle dorsiflexion |
| Quadratus lumborum | Thoracolumbar curve should be smooth and gradual |
| Piriformis | Gradual soft end feel |
| Upper trapezius | Gradual soft end feel |
| Levator scapulae | Gradual soft end feel |
| SCM | Gradual soft end feel |
| Pectoralis major | Sternal portion (lower fibers): with shoulder abducted at 150°, arm should be horizontal to table and 15°-20° with overpressure Sternal portion (midfibers): with shoulder abducted to 90°, arm should be horizontal to table and 30° with overpressure Clavicular portion: with shoulder abducted to 60°, arm should hang freely over table |
| Paraspinals | Schober's test: excursion of >2.4 in. (6 cm) |
Lower-Quarter Muscles
The muscles of the lower quarter include those of the leg, pelvis, and lower back. The muscles prone to tightness are those involved in maintaining a single-leg stance (Janda 1987). Tightness of the hip flexors and tightness of the thoracolumbar extensors are hallmark signs of Janda's LCS.
Modified Thomas Test for Hip Flexor
The modified Thomas test (figure 7.2, a-e) allows the clinician to assess four different muscles prone to tightness namely, the one-joint hip flexor, iliacus and psoas major, and the two-joint hip flexors, rectus femoris and TFL-ITB. Tightness of the hip flexors limits hip hyperextension in gait and may cause an anterior pelvic tilt. Weakness of the gluteus maximus often is due to facilitation of the hip flexors.
Patient Position
The patient is asked to sit on the edge of the table, with the coccyx and ischial tuberosities touching the table and one foot on the floor. Then, the patient is asked to flex the opposite hip and knee toward the chest and maintain the position with the hands (see figure 7.2a).
Clinician Position
The clinician stands beside the leg not being tested, facing the patient. While supporting the patient by placing one hand on the midthoracic spine and the other on the knee, the clinician passively rolls the patient down to the table to the supine position. The clinician needs to ensure that the patient's knees are flexed, lumbar spine is flexed, and pelvis is in posterior rotation to fix the origin of the hip flexors.
Test
The clinician passively lowers the tested leg until resistance is felt or movement at the pelvis is detected. With the patient's thigh in the final resting position, the clinician observes whether it is in neutral and parallel to the table or abducted. A normal length of the one-joint hip flexors with the lumbar spine and sacrum flat on the table is indicated by the posterior thigh touching the table (0° of hip extension). With slight overpressure, the thigh should reach 10° to 15° of hyperextension (figure 7.2, b-c). Prominence of a superior patellar groove (figure 7.2d) suggests a short rectus femoris, while prominence of a lateral IT groove suggests a short IT band (see figure 7.2e).
Rehabilitation of impingement
Rehabilitation rather than surgery is recommended for secondary impingement.
Rehabilitation rather than surgery is recommended for secondary impingement (Brox and Brevik 1996; Kronberg, Németh, and Broström 1990; Michener, Walsworth, and Burnet 2004; Morrison, Frogameni, and Woodworth 1997). Patients with primary impingement (type II and III acromion), however, have only a 64% to 68% success rate with conservative treatment (Morrison, Frogameni, and Woodworth 1997). While rehabilitation and arthroscopic surgery improve impingement symptoms equally (Haarh et al. 2005; Haarh and Andersen 2006), rehabilitation is less costly (Brox et al. 1993).
In a systematic review, Michener, Walsworth, and Burnet and colleagues (2004) found strong support in the literature for therapeutic exercise of the rotator cuff and scapular muscles as well as for stretching of the anterior and posterior shoulder. Furthermore, exercise is more effective when combined with joint mobilization (Michener, Walsworth, and Burnet 2004; Senbursa, Baltaci, and Atay 2007). The following are impingement rehabilitation recommendations with evidence-based rationale:
- Integrate the entire upper-extremity chain during exercise. This facilitates the kinetic chain from the hand to the spine (Burkhart, Morgan, and Kibler 2003; Kibler 1998b, 2006; McMullen and Uhl 2000). Figure 13.5 illustrates exercises that integrate the whole kinetic chain.
- Include hip and trunk stabilization exercises. This facilitates force transmission and proximal stabilization between the upper extremity and the trunk (Burkhart, Morgan, and Kibler 2003; Kibler 1998b, 2006; McMullen and Uhl 2000).
- Isolate the rotator cuff and scapular stabilizers first, before performing multijoint movements. Performing multijoint shoulder movements does not increase the strength of smaller single-joint muscles such as the rotator cuff (Giannakopoulos et al. 2004). Strengthening exercises isolating the rotator cuff should be performed first (Jobe and Pink 1993; Malliou et al. 2004).
- Exercise in the scapular plane. The scapular plane offers the most balanced position of the capsule and provides ideal joint centration during elevation (Borsa, Timmons, and Sauers 2003).
- Exercise both shoulders. Abnormal muscle activation often occurs in both the involved and the uninvolved shoulder (Cools et al. 2003; Cools, Declercq et al. 2007; Wadsworth and Bullock-Saxton 1997).
- Include neuromuscular exercises such as closed kinetic chain exercises and PNF. Patients with impingement demonstrate reduced proprioception (Machner et al. 2003) and so require proprioceptive rehabilitation (Ginn and Cohen 2005; Kamkar, Irrgang, and Whitney 1993; Smith and Burnolli 1989). Figure 13.6 illustrates a closed kinetic chain shoulder exercise for improving proprioception (Naughton, Adams, and Maher 2005).
- Stretch the posterior shoulder when internal rotation is limited. The posterior capsule is often tight in athletes with impingement, limiting internal rotation and follow-through (Myers et al. 2006; Tyler et al. 2000). The cross-body stretch (see figure 13.7) improves internal rotation in subjects with posterior shoulder tightness (McClure et al. 2007).
Causes of muscle weakness
A look at the causes of muscle weakness as well as Janda’s classification of muscle imbalance patterns.
Muscle tension can decrease as a result of a structural lesion in the CNS such as a spinal cord injury or stroke. A loss of tension leads to flaccidity or weakness. Weak muscles are also described as hypotonic or inhibited. Functionally, muscle can be weak as a result of neuroflexive or adaptive changes and may exhibit delayed activation in movement patterns.
Neuroflexive Factors for Decreased Tension
Many contractile factors can contribute to decreased muscle tension:
- Reciprocal inhibition (Sherrington 1907). Muscle becomes inhibited reflexively when its antagonist is activated. Weakness is often reflex-mediated inhibition secondary to increased tension of the antagonist.
- Arthrogenic weakness (Stokes and Young 1984; DeAndrade, Grant, and Dison. 1965). Muscle becomes inhibited via anterior horn cells due to joint swelling or dysfunction. This weakness also leads to selective atrophy of Type II fibers (Edstrom 1970).
- Deafferentation (Freeman, Dean, and Hanham 1965). Deafferentation is a decrease in afferent information from neuromuscular receptors. Damage to joint mechanoreceptors (as seen with ligamentous injury) with subsequent loss of articular reflexes can cause altered motor programs, often influencing many muscles remote from the injured area (Bullock-Saxton 1994). This loss of afferent information ultimately leads to de-efferentation, or the loss of efferent signals to alpha motor neurons, which results in decreased muscle strength.
- Pseudoparesis (Janda 1986a). Pseudoparesis is a clinical presentation of weakness of neuroflexive origin. Pseudoparesis has three clinical signs: hypotonia upon inspection and palpation, a score of 4 out of 5 on a manual muscle test, and a change in the muscle activation pattern that may include delayed onset with early synergist activation or decreased EMG levels. Facilitatory techniques often restore muscle strength and activation. Normally facilitatory input can be inhibitory to a pseudoparetic muscle (Janda 1986a).
- TrP weakness (Simons, Travell, and Simons 1999). Hyperirritable bands of muscle fiber decrease the stimulation threshold, leading to overuse, early fatigue, and ultimately weakness. Muscles with active TrPs fatigue more rapidly than normal muscles do (Mense and Simons 2001), and they exhibit a decreased number of firing motor units and poor synchronization (Janda 1993).
- Fatigue. Muscle fatigue can be caused by metabolic or neurological factors. Often during exercise muscles are fatigued before pain is experienced. Thus the patient develops compensatory and faulty movement patterns before experiencing pain.
Adaptive Factors for Decreased Tension
Noncontractile factors causing decreased muscle tension are stretch weakness and tightness weakness:
- Stretch weakness (Kendall, McCreary, and Provance 1993; Sahrmann 2002a, 2002b). Stretch weakness is a condition in which a muscle is elongated beyond physiological neutral but not beyond the normal ROM (Janda 1993). Prolonged muscle elongation causes muscle spindle inhibition and the creation of additional sarcomeres. The increased muscle length also changes the length-tension curve. Stretch weakness is also known as positional weakness and is often associated with overuse and postural changes.
- Tightness weakness (Janda 1993). This is the most severe form of muscle tightness. It is often overlooked clinically. Overused muscle shortens over time, changing the muscle's length-tension curve and becoming more readily activated and weaker after time. There is also an increase in the noncontractile tissue and a decrease in elasticity, leading to hypertrophy. Ultimately, overuse leads to ischemia and degeneration of muscle fibers, which further weakens the muscle.
When an inhibited and weak muscle is resisted, as is the aim of strengthening exercises, its activity tends to decrease rather than increase (Janda 1987). It is important to distinguish between neuroflexive weakness and structural weakness. Often, if the tight antagonist is stretched, the weak and inhibited muscle spontaneously increases in strength.
Janda's Classification of Muscle Imbalance Patterns
Through his observations of patients with neurological disorders and chronic musculoskeletal pain, Janda found that the typical muscle response to joint dysfunction is similar to the muscle patterns found in upper motor neuron lesions, concluding that muscle imbalances are controlled by the CNS (Janda 1987). Janda believed that muscle tightness or spasticity is predominant. Often, weakness from muscle imbalance results from reciprocal inhibition of the tight antagonist. The degree of tightness and weakness varies between individuals, but the pattern rarely does. These patterns lead to postural changes and joint dysfunction and degeneration.
Janda identified three stereotypical patterns associated with distinct chronic pain syndromes: the upper-crossed, lower-crossed, and layer syndromes. These syndromes are characterized by specific patterns of muscle weakness and tightness that cross between the dorsal and the ventral sides of the body.
Upper-Crossed Syndrome
Upper-crossed syndrome (UCS) is also referred to as proximal or shoulder girdle crossed syndrome (figure 4.2a; Janda 1988). In UCS, tightness of the upper trapezius and levator scapula on the dorsal side crosses with tightness of the pectoralis major and minor. Weakness of the deep cervical flexors ventrally crosses with weakness of the middle and lower trapezius. This pattern of imbalance creates joint dysfunction, particularly at the atlanto-occipital joint, C4-C5 segment, cervicothoracic joint, glenohumeral joint, and T4-T5 segment. Janda noted that these focal areas of stress within the spine correspond to transitional zones in which neighboring vertebrae change in morphology. Specific postural changes are seen in UCS, including forward head posture, increased cervical lordosis and thoracic kyphosis, elevated and protracted shoulders, and rotation or abduction and winging of the scapulae (figure 4.2b). These postural changes decrease glenohumeral stability as the glenoid fossa becomes more vertical due to serratus anterior weakness leading to abduction, rotation, and winging of the scapulae. This loss of stability requires the levator scapula and upper trapezius to increase activation to maintain glenohumeral centration (Janda 1988).
Lower-Crossed Syndrome
Lower-crossed syndrome (LCS) is also referred to as distal or pelvic crossed syndrome (figure 4.3a; Janda 1987). In LCS, tightness of the thoracolumbar extensors on the dorsal side crosses with tightness of the iliopsoas and rectus femoris. Weakness of the deep abdominal muscles ventrally crosses with weakness of the gluteus maximus and medius. This pattern of imbalance creates joint dysfunction, particularly at the L4-L5 and L5-S1 segments, SI joint, and hip joint. Specific postural changes seen in LCS include anterior pelvic tilt, increased lumbar lordosis, lateral lumbar shift, lateral leg rotation, and knee hyperextension. If the lordosis is deep and short, then imbalance is predominantly in the pelvic muscles; if the lordosis is shallow and extends into the thoracic area, then imbalance predominates in the trunk muscles (Janda 1987).
Janda identified two subtypes of LCS: A and B (see figure 4.3, b-c). Patients with LCS type A use more hip flexion and extension movement for mobility; their standing posture demonstrates an anterior pelvic tilt with slight hip flexion and knee flexion. These individuals compensate with a hyperlordosis limited to the lumbar spine and with a hyperkyphosis in the upper lumbar and thoracolumbar segments.
Learn to assess muscle length
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening.
Muscle Length Assessment Technique
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening. Precise testing requires that one of the bony attachments of the muscle (usually the origin) be in a fixed position while the other bony attachment is moved passively in the direction of lengthening the muscle. In other words, muscle length testing assesses the resistance to passive movement. This is in contrast to typical flexibility or ROM testing. The actual ROM can be measured for documentation purposes, but it gives limited clinical information in muscle imbalance syndromes. The most valuable clinical information is the muscular end feel and the location of the ROM end feel. The elongation of the muscle should be performed slowly to avoid eliciting a quick stretch of the muscle spindle and subsequently inducing a twitch response and muscle contraction. In addition, for the best accuracy and precision, muscle length testing should be performed when the patient is not in acute pain in order to avoid pain inhibition and muscle guarding. In summary, there are four steps to assessing muscle length:
1. Ensure maximal lengthening of the muscle from origin to insertion.
2. Firmly stabilize one end (usually the origin).
3. Slowly elongate the muscle.
4. Assess the end feel.
Following are the procedures for testing key muscles. Clinicians do not have to perform muscle length testing on every muscle listed; instead, they should assess the muscles that the postural and movement pattern analysis indicate as being possibly tight. Once tight muscles have been identified, the clinician can establish a muscle imbalance pattern (if present) and begin to look for causes of the tightness. Table 7.1 provides the normal results of muscle length for flexibility testing.
Table 7.1 Normal Results of Muscles Tested for Length | |
| Muscle | Normal ranges or end feel |
| Iliopsoas | 0° hip extension, 10° with overpressure |
| Rectus femoris | 90° knee extension, 125° with overpressure |
| TFL-IT band | 0° hip abduction (neutral), 15°-20° with overpressure |
| Adductors | 0° hip abduction (neutral), 20°-25° with overpressure in the modified Thomas test position 45° hip abduction in supine position |
| Hamstrings | 80° hip flexion with contralateral leg extended 90° hip flexion with contralateral leg flexed |
| Triceps surae | 0° ankle dorsiflexion |
| Quadratus lumborum | Thoracolumbar curve should be smooth and gradual |
| Piriformis | Gradual soft end feel |
| Upper trapezius | Gradual soft end feel |
| Levator scapulae | Gradual soft end feel |
| SCM | Gradual soft end feel |
| Pectoralis major | Sternal portion (lower fibers): with shoulder abducted at 150°, arm should be horizontal to table and 15°-20° with overpressure Sternal portion (midfibers): with shoulder abducted to 90°, arm should be horizontal to table and 30° with overpressure Clavicular portion: with shoulder abducted to 60°, arm should hang freely over table |
| Paraspinals | Schober's test: excursion of >2.4 in. (6 cm) |
Lower-Quarter Muscles
The muscles of the lower quarter include those of the leg, pelvis, and lower back. The muscles prone to tightness are those involved in maintaining a single-leg stance (Janda 1987). Tightness of the hip flexors and tightness of the thoracolumbar extensors are hallmark signs of Janda's LCS.
Modified Thomas Test for Hip Flexor
The modified Thomas test (figure 7.2, a-e) allows the clinician to assess four different muscles prone to tightness namely, the one-joint hip flexor, iliacus and psoas major, and the two-joint hip flexors, rectus femoris and TFL-ITB. Tightness of the hip flexors limits hip hyperextension in gait and may cause an anterior pelvic tilt. Weakness of the gluteus maximus often is due to facilitation of the hip flexors.
Patient Position
The patient is asked to sit on the edge of the table, with the coccyx and ischial tuberosities touching the table and one foot on the floor. Then, the patient is asked to flex the opposite hip and knee toward the chest and maintain the position with the hands (see figure 7.2a).
Clinician Position
The clinician stands beside the leg not being tested, facing the patient. While supporting the patient by placing one hand on the midthoracic spine and the other on the knee, the clinician passively rolls the patient down to the table to the supine position. The clinician needs to ensure that the patient's knees are flexed, lumbar spine is flexed, and pelvis is in posterior rotation to fix the origin of the hip flexors.
Test
The clinician passively lowers the tested leg until resistance is felt or movement at the pelvis is detected. With the patient's thigh in the final resting position, the clinician observes whether it is in neutral and parallel to the table or abducted. A normal length of the one-joint hip flexors with the lumbar spine and sacrum flat on the table is indicated by the posterior thigh touching the table (0° of hip extension). With slight overpressure, the thigh should reach 10° to 15° of hyperextension (figure 7.2, b-c). Prominence of a superior patellar groove (figure 7.2d) suggests a short rectus femoris, while prominence of a lateral IT groove suggests a short IT band (see figure 7.2e).
Restoration of muscle balance
Treatment of muscle weakness aims at stimulating and increasing the response of the muscle spindle of the pseudoparetic muscle.
Muscle Length Assessment Technique
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening. Precise testing requires that one of the bony attachments of the muscle (usually the origin) be in a fixed position while the other bony attachment is moved passively in the direction of lengthening the muscle. In other words, muscle length testing assesses the resistance to passive movement. This is in contrast to typical flexibility or ROM testing. The actual ROM can be measured for documentation purposes, but it gives limited clinical information in muscle imbalance syndromes. The most valuable clinical information is the muscular end feel and the location of the ROM end feel. The elongation of the muscle should be performed slowly to avoid eliciting a quick stretch of the muscle spindle and subsequently inducing a twitch response and muscle contraction. In addition, for the best accuracy and precision, muscle length testing should be performed when the patient is not in acute pain in order to avoid pain inhibition and muscle guarding. In summary, there are four steps to assessing muscle length:
1. Ensure maximal lengthening of the muscle from origin to insertion.
2. Firmly stabilize one end (usually the origin).
3. Slowly elongate the muscle.
4. Assess the end feel.
Following are the procedures for testing key muscles. Clinicians do not have to perform muscle length testing on every muscle listed; instead, they should assess the muscles that the postural and movement pattern analysis indicate as being possibly tight. Once tight muscles have been identified, the clinician can establish a muscle imbalance pattern (if present) and begin to look for causes of the tightness. Table 7.1 provides the normal results of muscle length for flexibility testing.
Table 7.1 Normal Results of Muscles Tested for Length | |
| Muscle | Normal ranges or end feel |
| Iliopsoas | 0° hip extension, 10° with overpressure |
| Rectus femoris | 90° knee extension, 125° with overpressure |
| TFL-IT band | 0° hip abduction (neutral), 15°-20° with overpressure |
| Adductors | 0° hip abduction (neutral), 20°-25° with overpressure in the modified Thomas test position 45° hip abduction in supine position |
| Hamstrings | 80° hip flexion with contralateral leg extended 90° hip flexion with contralateral leg flexed |
| Triceps surae | 0° ankle dorsiflexion |
| Quadratus lumborum | Thoracolumbar curve should be smooth and gradual |
| Piriformis | Gradual soft end feel |
| Upper trapezius | Gradual soft end feel |
| Levator scapulae | Gradual soft end feel |
| SCM | Gradual soft end feel |
| Pectoralis major | Sternal portion (lower fibers): with shoulder abducted at 150°, arm should be horizontal to table and 15°-20° with overpressure Sternal portion (midfibers): with shoulder abducted to 90°, arm should be horizontal to table and 30° with overpressure Clavicular portion: with shoulder abducted to 60°, arm should hang freely over table |
| Paraspinals | Schober's test: excursion of >2.4 in. (6 cm) |
Lower-Quarter Muscles
The muscles of the lower quarter include those of the leg, pelvis, and lower back. The muscles prone to tightness are those involved in maintaining a single-leg stance (Janda 1987). Tightness of the hip flexors and tightness of the thoracolumbar extensors are hallmark signs of Janda's LCS.
Modified Thomas Test for Hip Flexor
The modified Thomas test (figure 7.2, a-e) allows the clinician to assess four different muscles prone to tightness namely, the one-joint hip flexor, iliacus and psoas major, and the two-joint hip flexors, rectus femoris and TFL-ITB. Tightness of the hip flexors limits hip hyperextension in gait and may cause an anterior pelvic tilt. Weakness of the gluteus maximus often is due to facilitation of the hip flexors.
Patient Position
The patient is asked to sit on the edge of the table, with the coccyx and ischial tuberosities touching the table and one foot on the floor. Then, the patient is asked to flex the opposite hip and knee toward the chest and maintain the position with the hands (see figure 7.2a).
Clinician Position
The clinician stands beside the leg not being tested, facing the patient. While supporting the patient by placing one hand on the midthoracic spine and the other on the knee, the clinician passively rolls the patient down to the table to the supine position. The clinician needs to ensure that the patient's knees are flexed, lumbar spine is flexed, and pelvis is in posterior rotation to fix the origin of the hip flexors.
Test
The clinician passively lowers the tested leg until resistance is felt or movement at the pelvis is detected. With the patient's thigh in the final resting position, the clinician observes whether it is in neutral and parallel to the table or abducted. A normal length of the one-joint hip flexors with the lumbar spine and sacrum flat on the table is indicated by the posterior thigh touching the table (0° of hip extension). With slight overpressure, the thigh should reach 10° to 15° of hyperextension (figure 7.2, b-c). Prominence of a superior patellar groove (figure 7.2d) suggests a short rectus femoris, while prominence of a lateral IT groove suggests a short IT band (see figure 7.2e).
Rehabilitation of impingement
Rehabilitation rather than surgery is recommended for secondary impingement.
Rehabilitation rather than surgery is recommended for secondary impingement (Brox and Brevik 1996; Kronberg, Németh, and Broström 1990; Michener, Walsworth, and Burnet 2004; Morrison, Frogameni, and Woodworth 1997). Patients with primary impingement (type II and III acromion), however, have only a 64% to 68% success rate with conservative treatment (Morrison, Frogameni, and Woodworth 1997). While rehabilitation and arthroscopic surgery improve impingement symptoms equally (Haarh et al. 2005; Haarh and Andersen 2006), rehabilitation is less costly (Brox et al. 1993).
In a systematic review, Michener, Walsworth, and Burnet and colleagues (2004) found strong support in the literature for therapeutic exercise of the rotator cuff and scapular muscles as well as for stretching of the anterior and posterior shoulder. Furthermore, exercise is more effective when combined with joint mobilization (Michener, Walsworth, and Burnet 2004; Senbursa, Baltaci, and Atay 2007). The following are impingement rehabilitation recommendations with evidence-based rationale:
- Integrate the entire upper-extremity chain during exercise. This facilitates the kinetic chain from the hand to the spine (Burkhart, Morgan, and Kibler 2003; Kibler 1998b, 2006; McMullen and Uhl 2000). Figure 13.5 illustrates exercises that integrate the whole kinetic chain.
- Include hip and trunk stabilization exercises. This facilitates force transmission and proximal stabilization between the upper extremity and the trunk (Burkhart, Morgan, and Kibler 2003; Kibler 1998b, 2006; McMullen and Uhl 2000).
- Isolate the rotator cuff and scapular stabilizers first, before performing multijoint movements. Performing multijoint shoulder movements does not increase the strength of smaller single-joint muscles such as the rotator cuff (Giannakopoulos et al. 2004). Strengthening exercises isolating the rotator cuff should be performed first (Jobe and Pink 1993; Malliou et al. 2004).
- Exercise in the scapular plane. The scapular plane offers the most balanced position of the capsule and provides ideal joint centration during elevation (Borsa, Timmons, and Sauers 2003).
- Exercise both shoulders. Abnormal muscle activation often occurs in both the involved and the uninvolved shoulder (Cools et al. 2003; Cools, Declercq et al. 2007; Wadsworth and Bullock-Saxton 1997).
- Include neuromuscular exercises such as closed kinetic chain exercises and PNF. Patients with impingement demonstrate reduced proprioception (Machner et al. 2003) and so require proprioceptive rehabilitation (Ginn and Cohen 2005; Kamkar, Irrgang, and Whitney 1993; Smith and Burnolli 1989). Figure 13.6 illustrates a closed kinetic chain shoulder exercise for improving proprioception (Naughton, Adams, and Maher 2005).
- Stretch the posterior shoulder when internal rotation is limited. The posterior capsule is often tight in athletes with impingement, limiting internal rotation and follow-through (Myers et al. 2006; Tyler et al. 2000). The cross-body stretch (see figure 13.7) improves internal rotation in subjects with posterior shoulder tightness (McClure et al. 2007).
Causes of muscle weakness
A look at the causes of muscle weakness as well as Janda’s classification of muscle imbalance patterns.
Muscle tension can decrease as a result of a structural lesion in the CNS such as a spinal cord injury or stroke. A loss of tension leads to flaccidity or weakness. Weak muscles are also described as hypotonic or inhibited. Functionally, muscle can be weak as a result of neuroflexive or adaptive changes and may exhibit delayed activation in movement patterns.
Neuroflexive Factors for Decreased Tension
Many contractile factors can contribute to decreased muscle tension:
- Reciprocal inhibition (Sherrington 1907). Muscle becomes inhibited reflexively when its antagonist is activated. Weakness is often reflex-mediated inhibition secondary to increased tension of the antagonist.
- Arthrogenic weakness (Stokes and Young 1984; DeAndrade, Grant, and Dison. 1965). Muscle becomes inhibited via anterior horn cells due to joint swelling or dysfunction. This weakness also leads to selective atrophy of Type II fibers (Edstrom 1970).
- Deafferentation (Freeman, Dean, and Hanham 1965). Deafferentation is a decrease in afferent information from neuromuscular receptors. Damage to joint mechanoreceptors (as seen with ligamentous injury) with subsequent loss of articular reflexes can cause altered motor programs, often influencing many muscles remote from the injured area (Bullock-Saxton 1994). This loss of afferent information ultimately leads to de-efferentation, or the loss of efferent signals to alpha motor neurons, which results in decreased muscle strength.
- Pseudoparesis (Janda 1986a). Pseudoparesis is a clinical presentation of weakness of neuroflexive origin. Pseudoparesis has three clinical signs: hypotonia upon inspection and palpation, a score of 4 out of 5 on a manual muscle test, and a change in the muscle activation pattern that may include delayed onset with early synergist activation or decreased EMG levels. Facilitatory techniques often restore muscle strength and activation. Normally facilitatory input can be inhibitory to a pseudoparetic muscle (Janda 1986a).
- TrP weakness (Simons, Travell, and Simons 1999). Hyperirritable bands of muscle fiber decrease the stimulation threshold, leading to overuse, early fatigue, and ultimately weakness. Muscles with active TrPs fatigue more rapidly than normal muscles do (Mense and Simons 2001), and they exhibit a decreased number of firing motor units and poor synchronization (Janda 1993).
- Fatigue. Muscle fatigue can be caused by metabolic or neurological factors. Often during exercise muscles are fatigued before pain is experienced. Thus the patient develops compensatory and faulty movement patterns before experiencing pain.
Adaptive Factors for Decreased Tension
Noncontractile factors causing decreased muscle tension are stretch weakness and tightness weakness:
- Stretch weakness (Kendall, McCreary, and Provance 1993; Sahrmann 2002a, 2002b). Stretch weakness is a condition in which a muscle is elongated beyond physiological neutral but not beyond the normal ROM (Janda 1993). Prolonged muscle elongation causes muscle spindle inhibition and the creation of additional sarcomeres. The increased muscle length also changes the length-tension curve. Stretch weakness is also known as positional weakness and is often associated with overuse and postural changes.
- Tightness weakness (Janda 1993). This is the most severe form of muscle tightness. It is often overlooked clinically. Overused muscle shortens over time, changing the muscle's length-tension curve and becoming more readily activated and weaker after time. There is also an increase in the noncontractile tissue and a decrease in elasticity, leading to hypertrophy. Ultimately, overuse leads to ischemia and degeneration of muscle fibers, which further weakens the muscle.
When an inhibited and weak muscle is resisted, as is the aim of strengthening exercises, its activity tends to decrease rather than increase (Janda 1987). It is important to distinguish between neuroflexive weakness and structural weakness. Often, if the tight antagonist is stretched, the weak and inhibited muscle spontaneously increases in strength.
Janda's Classification of Muscle Imbalance Patterns
Through his observations of patients with neurological disorders and chronic musculoskeletal pain, Janda found that the typical muscle response to joint dysfunction is similar to the muscle patterns found in upper motor neuron lesions, concluding that muscle imbalances are controlled by the CNS (Janda 1987). Janda believed that muscle tightness or spasticity is predominant. Often, weakness from muscle imbalance results from reciprocal inhibition of the tight antagonist. The degree of tightness and weakness varies between individuals, but the pattern rarely does. These patterns lead to postural changes and joint dysfunction and degeneration.
Janda identified three stereotypical patterns associated with distinct chronic pain syndromes: the upper-crossed, lower-crossed, and layer syndromes. These syndromes are characterized by specific patterns of muscle weakness and tightness that cross between the dorsal and the ventral sides of the body.
Upper-Crossed Syndrome
Upper-crossed syndrome (UCS) is also referred to as proximal or shoulder girdle crossed syndrome (figure 4.2a; Janda 1988). In UCS, tightness of the upper trapezius and levator scapula on the dorsal side crosses with tightness of the pectoralis major and minor. Weakness of the deep cervical flexors ventrally crosses with weakness of the middle and lower trapezius. This pattern of imbalance creates joint dysfunction, particularly at the atlanto-occipital joint, C4-C5 segment, cervicothoracic joint, glenohumeral joint, and T4-T5 segment. Janda noted that these focal areas of stress within the spine correspond to transitional zones in which neighboring vertebrae change in morphology. Specific postural changes are seen in UCS, including forward head posture, increased cervical lordosis and thoracic kyphosis, elevated and protracted shoulders, and rotation or abduction and winging of the scapulae (figure 4.2b). These postural changes decrease glenohumeral stability as the glenoid fossa becomes more vertical due to serratus anterior weakness leading to abduction, rotation, and winging of the scapulae. This loss of stability requires the levator scapula and upper trapezius to increase activation to maintain glenohumeral centration (Janda 1988).
Lower-Crossed Syndrome
Lower-crossed syndrome (LCS) is also referred to as distal or pelvic crossed syndrome (figure 4.3a; Janda 1987). In LCS, tightness of the thoracolumbar extensors on the dorsal side crosses with tightness of the iliopsoas and rectus femoris. Weakness of the deep abdominal muscles ventrally crosses with weakness of the gluteus maximus and medius. This pattern of imbalance creates joint dysfunction, particularly at the L4-L5 and L5-S1 segments, SI joint, and hip joint. Specific postural changes seen in LCS include anterior pelvic tilt, increased lumbar lordosis, lateral lumbar shift, lateral leg rotation, and knee hyperextension. If the lordosis is deep and short, then imbalance is predominantly in the pelvic muscles; if the lordosis is shallow and extends into the thoracic area, then imbalance predominates in the trunk muscles (Janda 1987).
Janda identified two subtypes of LCS: A and B (see figure 4.3, b-c). Patients with LCS type A use more hip flexion and extension movement for mobility; their standing posture demonstrates an anterior pelvic tilt with slight hip flexion and knee flexion. These individuals compensate with a hyperlordosis limited to the lumbar spine and with a hyperkyphosis in the upper lumbar and thoracolumbar segments.
Learn to assess muscle length
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening.
Muscle Length Assessment Technique
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening. Precise testing requires that one of the bony attachments of the muscle (usually the origin) be in a fixed position while the other bony attachment is moved passively in the direction of lengthening the muscle. In other words, muscle length testing assesses the resistance to passive movement. This is in contrast to typical flexibility or ROM testing. The actual ROM can be measured for documentation purposes, but it gives limited clinical information in muscle imbalance syndromes. The most valuable clinical information is the muscular end feel and the location of the ROM end feel. The elongation of the muscle should be performed slowly to avoid eliciting a quick stretch of the muscle spindle and subsequently inducing a twitch response and muscle contraction. In addition, for the best accuracy and precision, muscle length testing should be performed when the patient is not in acute pain in order to avoid pain inhibition and muscle guarding. In summary, there are four steps to assessing muscle length:
1. Ensure maximal lengthening of the muscle from origin to insertion.
2. Firmly stabilize one end (usually the origin).
3. Slowly elongate the muscle.
4. Assess the end feel.
Following are the procedures for testing key muscles. Clinicians do not have to perform muscle length testing on every muscle listed; instead, they should assess the muscles that the postural and movement pattern analysis indicate as being possibly tight. Once tight muscles have been identified, the clinician can establish a muscle imbalance pattern (if present) and begin to look for causes of the tightness. Table 7.1 provides the normal results of muscle length for flexibility testing.
Table 7.1 Normal Results of Muscles Tested for Length | |
| Muscle | Normal ranges or end feel |
| Iliopsoas | 0° hip extension, 10° with overpressure |
| Rectus femoris | 90° knee extension, 125° with overpressure |
| TFL-IT band | 0° hip abduction (neutral), 15°-20° with overpressure |
| Adductors | 0° hip abduction (neutral), 20°-25° with overpressure in the modified Thomas test position 45° hip abduction in supine position |
| Hamstrings | 80° hip flexion with contralateral leg extended 90° hip flexion with contralateral leg flexed |
| Triceps surae | 0° ankle dorsiflexion |
| Quadratus lumborum | Thoracolumbar curve should be smooth and gradual |
| Piriformis | Gradual soft end feel |
| Upper trapezius | Gradual soft end feel |
| Levator scapulae | Gradual soft end feel |
| SCM | Gradual soft end feel |
| Pectoralis major | Sternal portion (lower fibers): with shoulder abducted at 150°, arm should be horizontal to table and 15°-20° with overpressure Sternal portion (midfibers): with shoulder abducted to 90°, arm should be horizontal to table and 30° with overpressure Clavicular portion: with shoulder abducted to 60°, arm should hang freely over table |
| Paraspinals | Schober's test: excursion of >2.4 in. (6 cm) |
Lower-Quarter Muscles
The muscles of the lower quarter include those of the leg, pelvis, and lower back. The muscles prone to tightness are those involved in maintaining a single-leg stance (Janda 1987). Tightness of the hip flexors and tightness of the thoracolumbar extensors are hallmark signs of Janda's LCS.
Modified Thomas Test for Hip Flexor
The modified Thomas test (figure 7.2, a-e) allows the clinician to assess four different muscles prone to tightness namely, the one-joint hip flexor, iliacus and psoas major, and the two-joint hip flexors, rectus femoris and TFL-ITB. Tightness of the hip flexors limits hip hyperextension in gait and may cause an anterior pelvic tilt. Weakness of the gluteus maximus often is due to facilitation of the hip flexors.
Patient Position
The patient is asked to sit on the edge of the table, with the coccyx and ischial tuberosities touching the table and one foot on the floor. Then, the patient is asked to flex the opposite hip and knee toward the chest and maintain the position with the hands (see figure 7.2a).
Clinician Position
The clinician stands beside the leg not being tested, facing the patient. While supporting the patient by placing one hand on the midthoracic spine and the other on the knee, the clinician passively rolls the patient down to the table to the supine position. The clinician needs to ensure that the patient's knees are flexed, lumbar spine is flexed, and pelvis is in posterior rotation to fix the origin of the hip flexors.
Test
The clinician passively lowers the tested leg until resistance is felt or movement at the pelvis is detected. With the patient's thigh in the final resting position, the clinician observes whether it is in neutral and parallel to the table or abducted. A normal length of the one-joint hip flexors with the lumbar spine and sacrum flat on the table is indicated by the posterior thigh touching the table (0° of hip extension). With slight overpressure, the thigh should reach 10° to 15° of hyperextension (figure 7.2, b-c). Prominence of a superior patellar groove (figure 7.2d) suggests a short rectus femoris, while prominence of a lateral IT groove suggests a short IT band (see figure 7.2e).
Restoration of muscle balance
Treatment of muscle weakness aims at stimulating and increasing the response of the muscle spindle of the pseudoparetic muscle.
Muscle Length Assessment Technique
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening. Precise testing requires that one of the bony attachments of the muscle (usually the origin) be in a fixed position while the other bony attachment is moved passively in the direction of lengthening the muscle. In other words, muscle length testing assesses the resistance to passive movement. This is in contrast to typical flexibility or ROM testing. The actual ROM can be measured for documentation purposes, but it gives limited clinical information in muscle imbalance syndromes. The most valuable clinical information is the muscular end feel and the location of the ROM end feel. The elongation of the muscle should be performed slowly to avoid eliciting a quick stretch of the muscle spindle and subsequently inducing a twitch response and muscle contraction. In addition, for the best accuracy and precision, muscle length testing should be performed when the patient is not in acute pain in order to avoid pain inhibition and muscle guarding. In summary, there are four steps to assessing muscle length:
1. Ensure maximal lengthening of the muscle from origin to insertion.
2. Firmly stabilize one end (usually the origin).
3. Slowly elongate the muscle.
4. Assess the end feel.
Following are the procedures for testing key muscles. Clinicians do not have to perform muscle length testing on every muscle listed; instead, they should assess the muscles that the postural and movement pattern analysis indicate as being possibly tight. Once tight muscles have been identified, the clinician can establish a muscle imbalance pattern (if present) and begin to look for causes of the tightness. Table 7.1 provides the normal results of muscle length for flexibility testing.
Table 7.1 Normal Results of Muscles Tested for Length | |
| Muscle | Normal ranges or end feel |
| Iliopsoas | 0° hip extension, 10° with overpressure |
| Rectus femoris | 90° knee extension, 125° with overpressure |
| TFL-IT band | 0° hip abduction (neutral), 15°-20° with overpressure |
| Adductors | 0° hip abduction (neutral), 20°-25° with overpressure in the modified Thomas test position 45° hip abduction in supine position |
| Hamstrings | 80° hip flexion with contralateral leg extended 90° hip flexion with contralateral leg flexed |
| Triceps surae | 0° ankle dorsiflexion |
| Quadratus lumborum | Thoracolumbar curve should be smooth and gradual |
| Piriformis | Gradual soft end feel |
| Upper trapezius | Gradual soft end feel |
| Levator scapulae | Gradual soft end feel |
| SCM | Gradual soft end feel |
| Pectoralis major | Sternal portion (lower fibers): with shoulder abducted at 150°, arm should be horizontal to table and 15°-20° with overpressure Sternal portion (midfibers): with shoulder abducted to 90°, arm should be horizontal to table and 30° with overpressure Clavicular portion: with shoulder abducted to 60°, arm should hang freely over table |
| Paraspinals | Schober's test: excursion of >2.4 in. (6 cm) |
Lower-Quarter Muscles
The muscles of the lower quarter include those of the leg, pelvis, and lower back. The muscles prone to tightness are those involved in maintaining a single-leg stance (Janda 1987). Tightness of the hip flexors and tightness of the thoracolumbar extensors are hallmark signs of Janda's LCS.
Modified Thomas Test for Hip Flexor
The modified Thomas test (figure 7.2, a-e) allows the clinician to assess four different muscles prone to tightness namely, the one-joint hip flexor, iliacus and psoas major, and the two-joint hip flexors, rectus femoris and TFL-ITB. Tightness of the hip flexors limits hip hyperextension in gait and may cause an anterior pelvic tilt. Weakness of the gluteus maximus often is due to facilitation of the hip flexors.
Patient Position
The patient is asked to sit on the edge of the table, with the coccyx and ischial tuberosities touching the table and one foot on the floor. Then, the patient is asked to flex the opposite hip and knee toward the chest and maintain the position with the hands (see figure 7.2a).
Clinician Position
The clinician stands beside the leg not being tested, facing the patient. While supporting the patient by placing one hand on the midthoracic spine and the other on the knee, the clinician passively rolls the patient down to the table to the supine position. The clinician needs to ensure that the patient's knees are flexed, lumbar spine is flexed, and pelvis is in posterior rotation to fix the origin of the hip flexors.
Test
The clinician passively lowers the tested leg until resistance is felt or movement at the pelvis is detected. With the patient's thigh in the final resting position, the clinician observes whether it is in neutral and parallel to the table or abducted. A normal length of the one-joint hip flexors with the lumbar spine and sacrum flat on the table is indicated by the posterior thigh touching the table (0° of hip extension). With slight overpressure, the thigh should reach 10° to 15° of hyperextension (figure 7.2, b-c). Prominence of a superior patellar groove (figure 7.2d) suggests a short rectus femoris, while prominence of a lateral IT groove suggests a short IT band (see figure 7.2e).
Rehabilitation of impingement
Rehabilitation rather than surgery is recommended for secondary impingement.
Rehabilitation rather than surgery is recommended for secondary impingement (Brox and Brevik 1996; Kronberg, Németh, and Broström 1990; Michener, Walsworth, and Burnet 2004; Morrison, Frogameni, and Woodworth 1997). Patients with primary impingement (type II and III acromion), however, have only a 64% to 68% success rate with conservative treatment (Morrison, Frogameni, and Woodworth 1997). While rehabilitation and arthroscopic surgery improve impingement symptoms equally (Haarh et al. 2005; Haarh and Andersen 2006), rehabilitation is less costly (Brox et al. 1993).
In a systematic review, Michener, Walsworth, and Burnet and colleagues (2004) found strong support in the literature for therapeutic exercise of the rotator cuff and scapular muscles as well as for stretching of the anterior and posterior shoulder. Furthermore, exercise is more effective when combined with joint mobilization (Michener, Walsworth, and Burnet 2004; Senbursa, Baltaci, and Atay 2007). The following are impingement rehabilitation recommendations with evidence-based rationale:
- Integrate the entire upper-extremity chain during exercise. This facilitates the kinetic chain from the hand to the spine (Burkhart, Morgan, and Kibler 2003; Kibler 1998b, 2006; McMullen and Uhl 2000). Figure 13.5 illustrates exercises that integrate the whole kinetic chain.
- Include hip and trunk stabilization exercises. This facilitates force transmission and proximal stabilization between the upper extremity and the trunk (Burkhart, Morgan, and Kibler 2003; Kibler 1998b, 2006; McMullen and Uhl 2000).
- Isolate the rotator cuff and scapular stabilizers first, before performing multijoint movements. Performing multijoint shoulder movements does not increase the strength of smaller single-joint muscles such as the rotator cuff (Giannakopoulos et al. 2004). Strengthening exercises isolating the rotator cuff should be performed first (Jobe and Pink 1993; Malliou et al. 2004).
- Exercise in the scapular plane. The scapular plane offers the most balanced position of the capsule and provides ideal joint centration during elevation (Borsa, Timmons, and Sauers 2003).
- Exercise both shoulders. Abnormal muscle activation often occurs in both the involved and the uninvolved shoulder (Cools et al. 2003; Cools, Declercq et al. 2007; Wadsworth and Bullock-Saxton 1997).
- Include neuromuscular exercises such as closed kinetic chain exercises and PNF. Patients with impingement demonstrate reduced proprioception (Machner et al. 2003) and so require proprioceptive rehabilitation (Ginn and Cohen 2005; Kamkar, Irrgang, and Whitney 1993; Smith and Burnolli 1989). Figure 13.6 illustrates a closed kinetic chain shoulder exercise for improving proprioception (Naughton, Adams, and Maher 2005).
- Stretch the posterior shoulder when internal rotation is limited. The posterior capsule is often tight in athletes with impingement, limiting internal rotation and follow-through (Myers et al. 2006; Tyler et al. 2000). The cross-body stretch (see figure 13.7) improves internal rotation in subjects with posterior shoulder tightness (McClure et al. 2007).
Causes of muscle weakness
A look at the causes of muscle weakness as well as Janda’s classification of muscle imbalance patterns.
Muscle tension can decrease as a result of a structural lesion in the CNS such as a spinal cord injury or stroke. A loss of tension leads to flaccidity or weakness. Weak muscles are also described as hypotonic or inhibited. Functionally, muscle can be weak as a result of neuroflexive or adaptive changes and may exhibit delayed activation in movement patterns.
Neuroflexive Factors for Decreased Tension
Many contractile factors can contribute to decreased muscle tension:
- Reciprocal inhibition (Sherrington 1907). Muscle becomes inhibited reflexively when its antagonist is activated. Weakness is often reflex-mediated inhibition secondary to increased tension of the antagonist.
- Arthrogenic weakness (Stokes and Young 1984; DeAndrade, Grant, and Dison. 1965). Muscle becomes inhibited via anterior horn cells due to joint swelling or dysfunction. This weakness also leads to selective atrophy of Type II fibers (Edstrom 1970).
- Deafferentation (Freeman, Dean, and Hanham 1965). Deafferentation is a decrease in afferent information from neuromuscular receptors. Damage to joint mechanoreceptors (as seen with ligamentous injury) with subsequent loss of articular reflexes can cause altered motor programs, often influencing many muscles remote from the injured area (Bullock-Saxton 1994). This loss of afferent information ultimately leads to de-efferentation, or the loss of efferent signals to alpha motor neurons, which results in decreased muscle strength.
- Pseudoparesis (Janda 1986a). Pseudoparesis is a clinical presentation of weakness of neuroflexive origin. Pseudoparesis has three clinical signs: hypotonia upon inspection and palpation, a score of 4 out of 5 on a manual muscle test, and a change in the muscle activation pattern that may include delayed onset with early synergist activation or decreased EMG levels. Facilitatory techniques often restore muscle strength and activation. Normally facilitatory input can be inhibitory to a pseudoparetic muscle (Janda 1986a).
- TrP weakness (Simons, Travell, and Simons 1999). Hyperirritable bands of muscle fiber decrease the stimulation threshold, leading to overuse, early fatigue, and ultimately weakness. Muscles with active TrPs fatigue more rapidly than normal muscles do (Mense and Simons 2001), and they exhibit a decreased number of firing motor units and poor synchronization (Janda 1993).
- Fatigue. Muscle fatigue can be caused by metabolic or neurological factors. Often during exercise muscles are fatigued before pain is experienced. Thus the patient develops compensatory and faulty movement patterns before experiencing pain.
Adaptive Factors for Decreased Tension
Noncontractile factors causing decreased muscle tension are stretch weakness and tightness weakness:
- Stretch weakness (Kendall, McCreary, and Provance 1993; Sahrmann 2002a, 2002b). Stretch weakness is a condition in which a muscle is elongated beyond physiological neutral but not beyond the normal ROM (Janda 1993). Prolonged muscle elongation causes muscle spindle inhibition and the creation of additional sarcomeres. The increased muscle length also changes the length-tension curve. Stretch weakness is also known as positional weakness and is often associated with overuse and postural changes.
- Tightness weakness (Janda 1993). This is the most severe form of muscle tightness. It is often overlooked clinically. Overused muscle shortens over time, changing the muscle's length-tension curve and becoming more readily activated and weaker after time. There is also an increase in the noncontractile tissue and a decrease in elasticity, leading to hypertrophy. Ultimately, overuse leads to ischemia and degeneration of muscle fibers, which further weakens the muscle.
When an inhibited and weak muscle is resisted, as is the aim of strengthening exercises, its activity tends to decrease rather than increase (Janda 1987). It is important to distinguish between neuroflexive weakness and structural weakness. Often, if the tight antagonist is stretched, the weak and inhibited muscle spontaneously increases in strength.
Janda's Classification of Muscle Imbalance Patterns
Through his observations of patients with neurological disorders and chronic musculoskeletal pain, Janda found that the typical muscle response to joint dysfunction is similar to the muscle patterns found in upper motor neuron lesions, concluding that muscle imbalances are controlled by the CNS (Janda 1987). Janda believed that muscle tightness or spasticity is predominant. Often, weakness from muscle imbalance results from reciprocal inhibition of the tight antagonist. The degree of tightness and weakness varies between individuals, but the pattern rarely does. These patterns lead to postural changes and joint dysfunction and degeneration.
Janda identified three stereotypical patterns associated with distinct chronic pain syndromes: the upper-crossed, lower-crossed, and layer syndromes. These syndromes are characterized by specific patterns of muscle weakness and tightness that cross between the dorsal and the ventral sides of the body.
Upper-Crossed Syndrome
Upper-crossed syndrome (UCS) is also referred to as proximal or shoulder girdle crossed syndrome (figure 4.2a; Janda 1988). In UCS, tightness of the upper trapezius and levator scapula on the dorsal side crosses with tightness of the pectoralis major and minor. Weakness of the deep cervical flexors ventrally crosses with weakness of the middle and lower trapezius. This pattern of imbalance creates joint dysfunction, particularly at the atlanto-occipital joint, C4-C5 segment, cervicothoracic joint, glenohumeral joint, and T4-T5 segment. Janda noted that these focal areas of stress within the spine correspond to transitional zones in which neighboring vertebrae change in morphology. Specific postural changes are seen in UCS, including forward head posture, increased cervical lordosis and thoracic kyphosis, elevated and protracted shoulders, and rotation or abduction and winging of the scapulae (figure 4.2b). These postural changes decrease glenohumeral stability as the glenoid fossa becomes more vertical due to serratus anterior weakness leading to abduction, rotation, and winging of the scapulae. This loss of stability requires the levator scapula and upper trapezius to increase activation to maintain glenohumeral centration (Janda 1988).
Lower-Crossed Syndrome
Lower-crossed syndrome (LCS) is also referred to as distal or pelvic crossed syndrome (figure 4.3a; Janda 1987). In LCS, tightness of the thoracolumbar extensors on the dorsal side crosses with tightness of the iliopsoas and rectus femoris. Weakness of the deep abdominal muscles ventrally crosses with weakness of the gluteus maximus and medius. This pattern of imbalance creates joint dysfunction, particularly at the L4-L5 and L5-S1 segments, SI joint, and hip joint. Specific postural changes seen in LCS include anterior pelvic tilt, increased lumbar lordosis, lateral lumbar shift, lateral leg rotation, and knee hyperextension. If the lordosis is deep and short, then imbalance is predominantly in the pelvic muscles; if the lordosis is shallow and extends into the thoracic area, then imbalance predominates in the trunk muscles (Janda 1987).
Janda identified two subtypes of LCS: A and B (see figure 4.3, b-c). Patients with LCS type A use more hip flexion and extension movement for mobility; their standing posture demonstrates an anterior pelvic tilt with slight hip flexion and knee flexion. These individuals compensate with a hyperlordosis limited to the lumbar spine and with a hyperkyphosis in the upper lumbar and thoracolumbar segments.
Learn to assess muscle length
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening.
Muscle Length Assessment Technique
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening. Precise testing requires that one of the bony attachments of the muscle (usually the origin) be in a fixed position while the other bony attachment is moved passively in the direction of lengthening the muscle. In other words, muscle length testing assesses the resistance to passive movement. This is in contrast to typical flexibility or ROM testing. The actual ROM can be measured for documentation purposes, but it gives limited clinical information in muscle imbalance syndromes. The most valuable clinical information is the muscular end feel and the location of the ROM end feel. The elongation of the muscle should be performed slowly to avoid eliciting a quick stretch of the muscle spindle and subsequently inducing a twitch response and muscle contraction. In addition, for the best accuracy and precision, muscle length testing should be performed when the patient is not in acute pain in order to avoid pain inhibition and muscle guarding. In summary, there are four steps to assessing muscle length:
1. Ensure maximal lengthening of the muscle from origin to insertion.
2. Firmly stabilize one end (usually the origin).
3. Slowly elongate the muscle.
4. Assess the end feel.
Following are the procedures for testing key muscles. Clinicians do not have to perform muscle length testing on every muscle listed; instead, they should assess the muscles that the postural and movement pattern analysis indicate as being possibly tight. Once tight muscles have been identified, the clinician can establish a muscle imbalance pattern (if present) and begin to look for causes of the tightness. Table 7.1 provides the normal results of muscle length for flexibility testing.
Table 7.1 Normal Results of Muscles Tested for Length | |
| Muscle | Normal ranges or end feel |
| Iliopsoas | 0° hip extension, 10° with overpressure |
| Rectus femoris | 90° knee extension, 125° with overpressure |
| TFL-IT band | 0° hip abduction (neutral), 15°-20° with overpressure |
| Adductors | 0° hip abduction (neutral), 20°-25° with overpressure in the modified Thomas test position 45° hip abduction in supine position |
| Hamstrings | 80° hip flexion with contralateral leg extended 90° hip flexion with contralateral leg flexed |
| Triceps surae | 0° ankle dorsiflexion |
| Quadratus lumborum | Thoracolumbar curve should be smooth and gradual |
| Piriformis | Gradual soft end feel |
| Upper trapezius | Gradual soft end feel |
| Levator scapulae | Gradual soft end feel |
| SCM | Gradual soft end feel |
| Pectoralis major | Sternal portion (lower fibers): with shoulder abducted at 150°, arm should be horizontal to table and 15°-20° with overpressure Sternal portion (midfibers): with shoulder abducted to 90°, arm should be horizontal to table and 30° with overpressure Clavicular portion: with shoulder abducted to 60°, arm should hang freely over table |
| Paraspinals | Schober's test: excursion of >2.4 in. (6 cm) |
Lower-Quarter Muscles
The muscles of the lower quarter include those of the leg, pelvis, and lower back. The muscles prone to tightness are those involved in maintaining a single-leg stance (Janda 1987). Tightness of the hip flexors and tightness of the thoracolumbar extensors are hallmark signs of Janda's LCS.
Modified Thomas Test for Hip Flexor
The modified Thomas test (figure 7.2, a-e) allows the clinician to assess four different muscles prone to tightness namely, the one-joint hip flexor, iliacus and psoas major, and the two-joint hip flexors, rectus femoris and TFL-ITB. Tightness of the hip flexors limits hip hyperextension in gait and may cause an anterior pelvic tilt. Weakness of the gluteus maximus often is due to facilitation of the hip flexors.
Patient Position
The patient is asked to sit on the edge of the table, with the coccyx and ischial tuberosities touching the table and one foot on the floor. Then, the patient is asked to flex the opposite hip and knee toward the chest and maintain the position with the hands (see figure 7.2a).
Clinician Position
The clinician stands beside the leg not being tested, facing the patient. While supporting the patient by placing one hand on the midthoracic spine and the other on the knee, the clinician passively rolls the patient down to the table to the supine position. The clinician needs to ensure that the patient's knees are flexed, lumbar spine is flexed, and pelvis is in posterior rotation to fix the origin of the hip flexors.
Test
The clinician passively lowers the tested leg until resistance is felt or movement at the pelvis is detected. With the patient's thigh in the final resting position, the clinician observes whether it is in neutral and parallel to the table or abducted. A normal length of the one-joint hip flexors with the lumbar spine and sacrum flat on the table is indicated by the posterior thigh touching the table (0° of hip extension). With slight overpressure, the thigh should reach 10° to 15° of hyperextension (figure 7.2, b-c). Prominence of a superior patellar groove (figure 7.2d) suggests a short rectus femoris, while prominence of a lateral IT groove suggests a short IT band (see figure 7.2e).
Restoration of muscle balance
Treatment of muscle weakness aims at stimulating and increasing the response of the muscle spindle of the pseudoparetic muscle.
Muscle Length Assessment Technique
Muscle length testing involves elongating the muscle in the direction opposite of its action while assessing its resistance to passive lengthening. Precise testing requires that one of the bony attachments of the muscle (usually the origin) be in a fixed position while the other bony attachment is moved passively in the direction of lengthening the muscle. In other words, muscle length testing assesses the resistance to passive movement. This is in contrast to typical flexibility or ROM testing. The actual ROM can be measured for documentation purposes, but it gives limited clinical information in muscle imbalance syndromes. The most valuable clinical information is the muscular end feel and the location of the ROM end feel. The elongation of the muscle should be performed slowly to avoid eliciting a quick stretch of the muscle spindle and subsequently inducing a twitch response and muscle contraction. In addition, for the best accuracy and precision, muscle length testing should be performed when the patient is not in acute pain in order to avoid pain inhibition and muscle guarding. In summary, there are four steps to assessing muscle length:
1. Ensure maximal lengthening of the muscle from origin to insertion.
2. Firmly stabilize one end (usually the origin).
3. Slowly elongate the muscle.
4. Assess the end feel.
Following are the procedures for testing key muscles. Clinicians do not have to perform muscle length testing on every muscle listed; instead, they should assess the muscles that the postural and movement pattern analysis indicate as being possibly tight. Once tight muscles have been identified, the clinician can establish a muscle imbalance pattern (if present) and begin to look for causes of the tightness. Table 7.1 provides the normal results of muscle length for flexibility testing.
Table 7.1 Normal Results of Muscles Tested for Length | |
| Muscle | Normal ranges or end feel |
| Iliopsoas | 0° hip extension, 10° with overpressure |
| Rectus femoris | 90° knee extension, 125° with overpressure |
| TFL-IT band | 0° hip abduction (neutral), 15°-20° with overpressure |
| Adductors | 0° hip abduction (neutral), 20°-25° with overpressure in the modified Thomas test position 45° hip abduction in supine position |
| Hamstrings | 80° hip flexion with contralateral leg extended 90° hip flexion with contralateral leg flexed |
| Triceps surae | 0° ankle dorsiflexion |
| Quadratus lumborum | Thoracolumbar curve should be smooth and gradual |
| Piriformis | Gradual soft end feel |
| Upper trapezius | Gradual soft end feel |
| Levator scapulae | Gradual soft end feel |
| SCM | Gradual soft end feel |
| Pectoralis major | Sternal portion (lower fibers): with shoulder abducted at 150°, arm should be horizontal to table and 15°-20° with overpressure Sternal portion (midfibers): with shoulder abducted to 90°, arm should be horizontal to table and 30° with overpressure Clavicular portion: with shoulder abducted to 60°, arm should hang freely over table |
| Paraspinals | Schober's test: excursion of >2.4 in. (6 cm) |
Lower-Quarter Muscles
The muscles of the lower quarter include those of the leg, pelvis, and lower back. The muscles prone to tightness are those involved in maintaining a single-leg stance (Janda 1987). Tightness of the hip flexors and tightness of the thoracolumbar extensors are hallmark signs of Janda's LCS.
Modified Thomas Test for Hip Flexor
The modified Thomas test (figure 7.2, a-e) allows the clinician to assess four different muscles prone to tightness namely, the one-joint hip flexor, iliacus and psoas major, and the two-joint hip flexors, rectus femoris and TFL-ITB. Tightness of the hip flexors limits hip hyperextension in gait and may cause an anterior pelvic tilt. Weakness of the gluteus maximus often is due to facilitation of the hip flexors.
Patient Position
The patient is asked to sit on the edge of the table, with the coccyx and ischial tuberosities touching the table and one foot on the floor. Then, the patient is asked to flex the opposite hip and knee toward the chest and maintain the position with the hands (see figure 7.2a).
Clinician Position
The clinician stands beside the leg not being tested, facing the patient. While supporting the patient by placing one hand on the midthoracic spine and the other on the knee, the clinician passively rolls the patient down to the table to the supine position. The clinician needs to ensure that the patient's knees are flexed, lumbar spine is flexed, and pelvis is in posterior rotation to fix the origin of the hip flexors.
Test
The clinician passively lowers the tested leg until resistance is felt or movement at the pelvis is detected. With the patient's thigh in the final resting position, the clinician observes whether it is in neutral and parallel to the table or abducted. A normal length of the one-joint hip flexors with the lumbar spine and sacrum flat on the table is indicated by the posterior thigh touching the table (0° of hip extension). With slight overpressure, the thigh should reach 10° to 15° of hyperextension (figure 7.2, b-c). Prominence of a superior patellar groove (figure 7.2d) suggests a short rectus femoris, while prominence of a lateral IT groove suggests a short IT band (see figure 7.2e).
Rehabilitation of impingement
Rehabilitation rather than surgery is recommended for secondary impingement.
Rehabilitation rather than surgery is recommended for secondary impingement (Brox and Brevik 1996; Kronberg, Németh, and Broström 1990; Michener, Walsworth, and Burnet 2004; Morrison, Frogameni, and Woodworth 1997). Patients with primary impingement (type II and III acromion), however, have only a 64% to 68% success rate with conservative treatment (Morrison, Frogameni, and Woodworth 1997). While rehabilitation and arthroscopic surgery improve impingement symptoms equally (Haarh et al. 2005; Haarh and Andersen 2006), rehabilitation is less costly (Brox et al. 1993).
In a systematic review, Michener, Walsworth, and Burnet and colleagues (2004) found strong support in the literature for therapeutic exercise of the rotator cuff and scapular muscles as well as for stretching of the anterior and posterior shoulder. Furthermore, exercise is more effective when combined with joint mobilization (Michener, Walsworth, and Burnet 2004; Senbursa, Baltaci, and Atay 2007). The following are impingement rehabilitation recommendations with evidence-based rationale:
- Integrate the entire upper-extremity chain during exercise. This facilitates the kinetic chain from the hand to the spine (Burkhart, Morgan, and Kibler 2003; Kibler 1998b, 2006; McMullen and Uhl 2000). Figure 13.5 illustrates exercises that integrate the whole kinetic chain.
- Include hip and trunk stabilization exercises. This facilitates force transmission and proximal stabilization between the upper extremity and the trunk (Burkhart, Morgan, and Kibler 2003; Kibler 1998b, 2006; McMullen and Uhl 2000).
- Isolate the rotator cuff and scapular stabilizers first, before performing multijoint movements. Performing multijoint shoulder movements does not increase the strength of smaller single-joint muscles such as the rotator cuff (Giannakopoulos et al. 2004). Strengthening exercises isolating the rotator cuff should be performed first (Jobe and Pink 1993; Malliou et al. 2004).
- Exercise in the scapular plane. The scapular plane offers the most balanced position of the capsule and provides ideal joint centration during elevation (Borsa, Timmons, and Sauers 2003).
- Exercise both shoulders. Abnormal muscle activation often occurs in both the involved and the uninvolved shoulder (Cools et al. 2003; Cools, Declercq et al. 2007; Wadsworth and Bullock-Saxton 1997).
- Include neuromuscular exercises such as closed kinetic chain exercises and PNF. Patients with impingement demonstrate reduced proprioception (Machner et al. 2003) and so require proprioceptive rehabilitation (Ginn and Cohen 2005; Kamkar, Irrgang, and Whitney 1993; Smith and Burnolli 1989). Figure 13.6 illustrates a closed kinetic chain shoulder exercise for improving proprioception (Naughton, Adams, and Maher 2005).
- Stretch the posterior shoulder when internal rotation is limited. The posterior capsule is often tight in athletes with impingement, limiting internal rotation and follow-through (Myers et al. 2006; Tyler et al. 2000). The cross-body stretch (see figure 13.7) improves internal rotation in subjects with posterior shoulder tightness (McClure et al. 2007).
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