Excerpted from: (Page, Frank, Lardner. Assessment and Treatment of Muscle Imbalance, The Janda Approach. 2010, Human Kinetics, Champagne IL.)
Patients with chronic musculoskeletal pain continue to experience pain after a period of time that a peripheral pathology would normally resolve. This persistent pain suggests a persistent peripheral input.
These patients also exhibit altered pain processing in the CNS, as seen in the phenomenon of pain centralization. Pain stimuli can alter sensitivity to central perception of pain and can alter the afferent signal at multiple levels, lowering pain thresholds in healthy regions throughout the body. Thus clinicians should evaluate and treat chronic muscle imbalance and chronic musculoskeletal pain as a global sensorimotor dysfunction.
Janda believed that muscles, as opposed to bones, joints, and ligaments, are most often the cause of chronic pain.
Direct causes of muscle pain include muscle and connective tissue damage, muscle spasm and ischemia, and tender points or trigger points. Most pain is associated with muscle spasm but is not the result of the spasm itself; rather the pain is caused by ischemia.
Indirect causes of muscle pain include altered joint forces due to muscle imbalance influencing movement patterns. Joint dysfunction without spasm is typically painless. Muscle imbalance can develop as a result of both acute and chronic pain. Acute pain leads to a localized muscle response that changes the movement pattern to protect or compensate for an injured area. Over time, this altered movement pattern becomes centralized in the CNS. The viscious cycle pain and spasm has been questionable, but the viscious cycle of chronic pain involving the CNS and PNS seems plausible.
Components of the Chronic Musculoskeletal Pain Cycle:
Chronic pain is associated protective adaptive response in muscle in which agonists decrease in tone while antagonists increase in tone. The pattern of neurological imbalance is based on neurodevelopment of the tonic and phasic muscle systems. Muscle imbalance presenting with facilitation of an agonist inhibits the antagonist, possibly increasing the risk of injury.
Impaired Movement Patterns and Postural Changes
Postural responses to pain are common, facilitating the flexor response to protect the injured area. The protective adaptation to pain through compensatory movement results in decreased range of motion and altered movement patterns. Tightness of antagonists subsequently inhibits agonists based on Sherrington’s law of reciprocal inhibition. This imbalance leads to further alterations in normal movement patterns.
Faulty Motor Programming and Motor Learning
Repetitive dysfunctional movement patterns eventually supersede the normal functional motor program because of the effect of motor learning. The dysfunctional movement pattern becomes ingrained in the motor cortex as the new normal program for a specific movement pattern, thus reinforcing the dysfunctional pattern.
Altered Joint Forces and Altered Perception
Altered movement patterns change the normal patterns of joint stress. Muscle imbalance alters joint position, changing the distribution of joint stresses on the joint capsule and surfaces. Afferent input is essential in the modification of muscle activation to make movement well-coordinated and functional. Altered proprioception may be the actual cause of inhibition or spasm, not pain.
Poor proprioception ultimately may be responsible for joint degeneration. Muscle imbalance presents a much greater danger for joints than muscular weakness alone presents. Therefore, functional pathology may in fact cause structural pathology.
Inflammatory mediators such as histamine and bradykinins are known to cause pain. Joint pain and inflammation sensitize musculoskeletal afferent receptors. Pain causes an adaptive response of muscle imbalance and altered posture and movement patterns and thus facilitates the vicious cycle.