Janda Was Ahead of His Time
Dr. Vladimir Janda was a Czech neurologist and physiatrist. He retired as the director of the physiotherapy school at the Charles University 3rd Faculty of Medicine in 2000. Janda has done extensive clinical research on the pathogenesis and treatment of chronic musculoskeletal pain. He is known around the world for his concepts of muscle imbalance, and continued to be active in clinical practice, research, and lecturing until his death in November, 2002. The purpose of this paper is to review Janda’s approach to the evaluation and management of chronic musculoskeletal pain.
Janda became interested in physical medicine after falling victim to polio in his teens. He spent 3 years in rehabilitation, after which he pursued his medical degree specializing in neurology and physical medicine. He published his first book in Czechoslovakia on muscle testing at the age of 20. Noting the work of Hans Kraus, as well as that of Henry and Florence Kendall, Janda became intrigued by the functional role of muscles. He first observed that both polio and low back pain patients often had a dysfunctional gluteus maximus. His observations led to testing his patients with surface electromyography where he noted patterns of muscle contraction with particular limb movements, leading him to conclude that the timing or recruitment pattern of synergists should be emphasized rather than traditional manual muscle testing for strength. His thesis, “Postural and phasic muscles in the pathogenesis of low back pain” was presented in 1968 (Janda, 1968). In 1979, he identified his specific “crossed syndromes” of muscle imbalance (Janda, 1979) based on his clinical observations and research and theorized that muscle imbalance was predictable and involved the entire motor system.
Structure vs. Function
In musculoskeletal medicine, there are two main schools of thought, that is, a structural or functional approach. In the structural approach, the pathology of specific static structures is emphasized; this is the typical orthopaedic approach that emphasizes diagnosis based on localized evaluation and special tests (X-Ray, MRI, CT Scan, etc). On the other hand, the functional approach recognizes the function of all processes and systems within the body, rather than focusing on a single site of pathology. While the structural approach is necessary and valuable for acute injury or exacerbation, the functional approach is preferable when addressing chronic musculoskeletal pain.
The Sensorimotor System
In chronic pain, special diagnostic tests of localized areas (for example, low back radiographs) are often normal, although the patient complains of pain. The site of pain is often not the cause of the pain. Recent evidence by supports the fact that chronic pain is centrally-mediated (Staud et al. 2001). Similarly, research on the efficacy of different modes of exercise management of chronic pain has shown a central effect of exercise in decreasing chronic low back pain (Mannion et al. 1999). This research supports the basis of Janda’s approach: the interdependence of the musculoskeletal and central nervous system. Janda states that these two anatomical systems cannot be separated functionally. Therefore, the term “sensorimotor” system is used to define the functional system of human movement. In addition, changes within one part of the system will be reflected by compensations or adaptations elsewhere within the system because of the body’s attempt at homeostasis (Panjabi, 1992).
The muscular system often reflects the status of the sensorimotor system, as it receives information from both the musculoskeletal and central nervous systems. Changes in tone within the muscle are the first responses to nociception by the sensorimotor system. This has been supported by various studies demonstrating the effect of joint pathology on muscle tone. For example, the presence of knee effusion causes reflex inhibition of the vastus medialis (Stokes & Young, 1984). The multifidus has been shown to atrophy in patients with chronic low back pain (Hides et al. 1994), and muscles demonstrate increased latency after ankle sprains (Konradsen & Raven, 1990) and ACL tears (Ihara & Nakayama, 1986). The global effect of joint pathology on the sensorimotor system was demonstrated by Bullock-Saxton (1994). She noted a delay in firing patterns of the hip muscles and decreased vibratory sensation in patients with ankle sprains.
Because of the involvement of the CNS in muscle imbalance and pain, Janda emphasizes the importance of the afferent proprioceptive system. A reflex loop from the joint capsular mechanoreceptors and the muscles surrounding the joint is responsible for reflexive joint stabilization (Guanche et al. 1995; Tsuda et al. 2001). In chronic instability, deafferentation (the loss of proper afferent information from a joint) is often responsible for poor joint stabilization (Freeman et al. 1965).
Tonic and Phasic Muscle Systems
Janda identified two groups of muscles based on their phylogenetic development (Janda, 1987). Functionally, muscles can be classified as “tonic” or “phasic”. The tonic system consists of the “flexors”, and is phylogenetically older and dominant. These muscles are involved in repetitive or rhythmic activity (Umphred, 2001), and are activated in flexor synergies. The phasic system consists of the “extensors”, and emerges shortly after birth. These muscles work eccentrically against the force of gravity and emerge in extensor synergies (Umphred, 2001).
|Tonic MusclesProne to Tightness or Shortness||Phasic MusclesProne to Weakness or Inhibition|
Tensor Fascia Lata
Upper limb flexors
|Peroneus Longus, BrevisTibialis Anterior
Vastus Medialis, Lateralis
Gluteus Maximus, Medius, Minimus
Deep neck flexors
Upper limb extensors
Janda noted that the tonic system muscles are prone to tightness or shortness, and the phasic system muscles are prone to weakness or inhibition (Table 1). Based on his clinical observations of orthopedic and neurological patients, Janda found that this response is based on the neurological response of nociception in the muscular system. For example, following structural lesions in the central nervous systems (such cerebral palsy or cerebrovascular accident), the tonic flexor muscles tend to be spastic and the phasic extensor muscles tend to be flaccid. Therefore, patterns of muscle imbalance may be due to CNS influence, rather than structural changes within the muscle itself.
It’s important to note that this classification is not rigid, in that some muscles may exhibit both tonic and phasic characteristics. It should also be noted that in addition to neurological predisposition to tightness or weakness, structural changes within the muscle also contribute to muscle imbalance. However, in chronic pain that is centralized within the CNS, patterns of muscle imbalance are often a result of neurological influence rather than structural changes.
Janda’s Crossed Syndromes
Over time, these imbalances will spread throughout the muscular system in a predictable manner. Janda has classified these patterns as “Upper Crossed Syndrome” (UCS), “Lower Crossed Syndrome” (LCS), and “Layer Syndrome” (LS) (Janda, 1987, 1988). [UCS is also known as “cervical crossed syndrome”; LCS is also known as “pelvic crossed syndrome; and LS is also known as “stratification syndrome.”] Crossed syndromes are characterized by alternating sides of inhibition and facilitation in the upper quarter and lower quarter. Layer syndrome, essentially a combination of UCS and LCS is characterized by alternating patterns of tightness and weakness, indicating long-standing muscle imbalance pathology. Janda’s syndromes are summarized in Figure 1.
Upper crossed syndrome is characterized by facilitation of the upper trapezius, levator, sternocleidomastoid, and pectoralis muscles, as well as inhibition of the deep cervical flexors, lower trapezius, and serratus anterior. Lower crossed syndrome is characterized by facilitation of the thoraco-lumbar extensors, rectus femoris, and iliopsoas, as well as inhibition of the abdominals (particularly transversus abdominus) and the gluteal muscles.
By using Janda’s classification, clinicians can begin to predict patterns of tightness and weakness in the sensorimotor system’s attempt to reach homeostasis. Janda noted that these changes in muscular tone create a muscle imbalance, which leads to movement dysfunction. Muscles prone to tightness generally have a “lowered irritability threshold” and are readily activated with any movement, thus creating abnormal movement patterns. These imbalances and movement dysfunctions may have direct effect on joint surfaces, thus potentially leading to joint degeneration. In some cases, joint degeneration may be a direct source of pain, but the actual cause of pain is often secondary to muscle imbalance. Therefore, clinicians should find and treat the cause of the pain rather than focus on the source of the pain.
Systematic evaluation of muscular imbalance begins with static postural assessment, observing muscles for characteristic signs of hypertonicity or hypotonicity. This is followed by observation of single leg stance and gait. Static posture, gait and balance often give the best indication of the status of the sensorimotor system. Computerized force plate posturography is often valuable in quantifying sensory and motor deficits. Next, characteristic movement patterns are assessed, and specific muscles are tested for tightness or shortness. Surface electromyography is useful in quantifying muscle activation patterns. All the above information collected provides the clinician a system to determine or rule out the presence of muscle imbalance syndromes. Furthermore, identification of specific patterns and syndromes of imbalance also provides the clinician to choose appropriate interventions to address the cause of the dysfunction.
Janda Approach to Treatment
1. Normalize the periphery. The Janda approach to treatment of musculoskeletal pain follows several steps. Treatment of muscle imbalance and movement impairment begins with normalizing afferent information entering the sensorimotor system. This includes providing an optimal environment for healing (by reducing effusion and protection of healing tissues, restoring proper postural alignment (through postural and ergonomic education), and correcting the biomechanics of a peripheral joint (through manual therapy techniques).
2. Restore Muscle Balance. Once peripheral structures are normalized, muscle balance is restored. Normal muscle tone surrounding joints must be restored. Sherrington’s law of reciprocal inhibition (Sherrington, 1907) states that a hypertonic antagonist muscle may be reflexively inhibiting their agonist. Therefore, in the presence of tight and/or short antagonistic muscles, restoring normal muscle tone and/or length must first be addressed before attempting to strengthen a weakened or inhibited muscle. Techniques to decrease tone must be specific to the cause of the hypertonicity. These include post-isometric relaxation (PIR) (Lewit, 1994) and post-facilitation stretch (PFS) (Janda, 1988). Muscles that have been reflexively inhibited by tight antagonists often recover spontaneously after addressing the tightness. In the Janda approach, the coordinated firing patterns of muscle are more important than the absolute strength of muscles. The strongest muscle is not functional if it cannot contract quickly and in coordination with other muscles; therefore, isolated muscle strengthening is not emphasized in the Janda approach. Instead, muscles are facilitated to contract at the proper time during coordinated movement patterns to provide reflexive joint stabilization.
3. Increase afferent input to facilitate reflexive stabilization. Once muscle balance has been addressed, Janda stresses increasing proprioceptive input into the CNS with a specific exercise program, “Sensorimotor Training” (SMT) (Janda & Vavrova, 1996). This program increases afferent information entering the subcortical pathways (including spinocerebellar, spinothalamic, and vestibulocerebellar pathways) to facilitate automatic coordinated movements. SMT involves progressive stimulation through specific exercises with increasing level of challenge to the sensorimotor system. SMT has been proven to improve proprioception, strength, and postural stability in ankle instability (Freeman et al. 1965), knee instability (Ihara & Nakayam, 1996), and after ACL reconstruction (Pavlu & Novosadova, 2001).
4. Increase endurance in coordinated movement patterns. Finally, endurance is increased through repetitive, coordinated movement patterns. Since fatigue is a predisposing factor to compensated movement patterns, endurance is also more important than absolute strength. Exercises are performed at low intensities and high volumes to simulate activities of daily living.
The Janda approach is valuable in today’s managed care environment. Once these patterns and syndromes are identified, specific treatment can be implemented without expensive equipment. Early detection of these causes of chronic pain allows the clinician to treat the patient with fewer visits and less expensive equipment compared to traditional interventions that emphasize modalities and passive treatments. The key to the Janda approach is in the home exercise program. Inexpensive home exercise equipment such as wobble boards, elastic bands, and foam pads are used with a specific progression of exercises as the patient improves in function.
In summary, the Janda approach emphasizes the importance of the CNS in the sensorimotor system, and its role in the pathogenesis in musculoskeletal pain. In particular: the neurological pre-disposition of muscles to exhibit predictable changes in tone, and the importance of proprioception and afferent information in the regulation of muscle tone and movement. Therefore, assessment and treatment focus on the sensorimotor system, rather than the musculoskeletal system itself. Using a functional, rather than a structural approach, the cause of musculoskeletal pain can be quickly identified and addressed. The Janda approach can be a valuable tool for the clinician in the evaluation and treatment of chronic musculoskeletal pain.
About The Author
Phil Page, PhD, MS, PT, ATC, CSCS
Director of Clinical Education and Research for Performance Health products, Dr. Phil Page directs the Thera-Band Academy. He is a licensed physical therapist and certified athletic trainer. His clinical and research interests include the role of muscle imbalance in musculoskeletal pain, and in promoting physical activity in older adults. He has presented internationally on exercise and rehabilitation topics, and has numerous publications. He has a master’s degree in Exercise Physiology, and a PhD in Kinesiology. He is also a certified strength and conditioning specialist. He has worked with the athletic programs at LSU, Tulane, the New Orleans Saints and Seattle Seahawks, as well as the United States Olympic Track and Field Trials.
Bullock-Saxton JE. 1994. Local sensation changes and altered hip muscle function following severe ankle sprain. Phys Ther. 74(1):17-28.
Bullock-Saxton J, Janda V, Bullock M. 1993. Reflex activation of gluteal muscles in walking with balance shoes: an approach to restoration of function for chronic low back pain patients. Spine. 18(6):704-708.
Freeman MA, Dean MR, Hanham IW. 1965. The etiology and prevention of functional instability of the foot. J Bone Joint Surg Br 47(4):678-85.
Guanche C, Knatt T, Solomonow M, Lu Y, Baratta R.1995. The synergistic action of the capsule and the shoulder muscles. Am J Sports Med. 23(3):301-6.
Hides JA, Stokes MJ, Saide M, Jull GA, Cooper DH. 1994. Evidence of lumbar multifidus muscle wasting ipsilateral to symptoms in patients with acute/subacute low back pain. Spine. 19:165-172.
Ihara H, Nakayama A. 1986. Dynamic joint control training for knee ligament injuries. Am J Sports Med. 14:309.
Janda V. 1968. Postural and phasic muscles in the pathogenesis of low back pain. Proceedings of the 11th Congress of International Society of Rehabilitation of the Disabled”, Dublin, Ireland. Pp 553-54.
Janda V. 1979. Die muskularen hauptsyndrome bei vertebragen en beschwerden, theroetische fortschritte und pracktishe erfahrungen der manuellen medizin. International Congress of FIMM. Baden-Baden. pp. 61-65.
Janda V. 1987. Muscles and motor control in low back pain: Assessment and management. In Twomey LT (Ed.) Physical therapy of the low back. Churchill Livingstone: New York. Pp. 253-278.
Janda, V. 1988. Muscles and Cervicogenic Pain Syndromes. In Physical Therapy of the Cervical and Thoracic Spine, ed. R. Grand. New York: Churchill Livingstone.
Janda V, Va’Vrova’. 1996. Sensory motor stimulation. In Liebenson C (ed). Rehabilitation of the Spine. Williams & Wilkins: Baltimore. pp. 319-328.
Konradsen L, Ravn JB. 1990. Ankle instability caused by prolonged peroneal reaction time. Acta Orthop Scand. 1990 Oct;61(5):388-90.
Lewit, K., Simons DG. 1984. Myofascial Pain: Relief by Post-Isometric Relaxation. Arch Phys Med Rehabil 65(8): 452-6.
Mannion AF, Nuntener M, Taimela S, Dvorak J. 1999. A randomized clinical trial of three active therapies for chronic low back pain. Spine. 24(23):2435-48.
Panjabi MM. 1992. The stabilizing system of the spine. Part I. Function, dysfunction, adaptation, and enhancement. J Spinal Disord. 5(4):383-9
Pavlu D, Novosadova K. 2001. [Contribution to the objectivization of the method of sensorimotor training stimulation according to Janda and Vavrova with regard to evidence-based-practice.] Rehabil Phys Med. 8(4):178-181.
Sherrington CS. 1907. On reciprocal innervation of antagonistic muscles. Proc R Soc Lond [Biol] 79B:337.
Staud R, Vierck CJ, Cannon RL, Mauderli AP, Price DD. 2001. Abnormal sensitization and temporal summation of second pain (wind up) in patients with fibromyalgia syndrome. Pain. 91(1-2):165-75.
Stokes M, Young A. 1984. The contribution of reflex inhibition of arthrogenenous muscle weakness. Clin Sci. 67:7-14.
Tsuda E, Okamura Y, Otsuka H, Komatsu T, Tokuya S. 2001. Direct evidence of anterior cruciate ligament-hamstring reflex arc in humans. Am J Sports Med. 29(1):83-87.
Umphred DA, Byl N, Lazaro RT, Roller M. 2001. Interventions for neurological disabilities. In Neurological Rehabilitation (Umphred DA, ed). 4th ed. Mosby: St. Louis. pp. 56-134.