Chronicity Factors

Ligamento-muscular Reflex (See Ligamento-muscular Reflex)
In 2006, Panjabi [1] hypothesized that an injured ligament sends corrupted afferent information and that “the neuromuscular control unit has difficulty in interpreting the corrupted transducer signals” which, in turn, would lead to undesirable changes. However, the word corrupted suggests the presence of errors that have been introduced unintentionally. Rather, research indicates that the muscles are activated in a distinct pattern designed to protect the injured ligament. Instead of corrupted signals from the receptors, the ligamento-muscular reflex ensures that the signals are accurate and result in well-defined contraction/inhibition patterns which consistently alter the strength of contraction and timing sequence of muscles in order to protect the injured ligament.

Nociceptors [2] and mechanoceptors [3] within the sacroiliac ligaments respond selectively to activate or inhibit muscles to counter the stress applied to the injured ligaments[4-12]. It was found that the response from an injured ligament varied markedly from that of a normal ligament, not in which particular muscles were affected, but in the degree and speed of their activation or inhibition.

Adaptive patterns occur over time, through both neural and muscular reprogramming, which can lead to recurrent problems, including joint instability, muscular spasm, apprehension upon certain movements, feelings of heaviness and helplessness, and giving way. Entire muscles, or independent fibers within the muscles, may contract to provide a specific, graded response to the injured ligaments [13].

Two positive feedback loops exist, which intensify and perpetuate muscle imbalance in the affected muscles and, in a chain reaction, spread to surrounding muscles, leading to increased joint stiffness. To limit immediate harm, the reaction may occur through a fast acting monosynaptic reflex directly from the afferent nerve to the motor neuron [4, 14-16]. Or, in an attempt to restore and maintain stability, a relatively slow acting polysynaptic reflex will activate the gamma muscle spindle system to induce muscles to produce joint stiffness and prepare the joint for future destabilizing events [4, 5, 7, 17, 18].

Because the sacroiliac ligaments directly control the tone of all the muscles that attach to the sacrum or innominates, most of our musculoskeletal system is directly regulated by the sacroiliac joint.

Once injured, ligaments heal poorly, if at all; instead, the body adapts in a long term process that slowly spreads throughout the musculoskeletal system. Eventually, neural responses from the ligaments lead to persistent muscle contraction or inhibition patterns.

Chronic stress can lead to continuously distorted muscle firing patterns that can alter joint angles and posture and generate pain in the back, hip, and upper legs. When applied to the sacroiliac joint, and the combined interaction of the vast array of ligaments and muscles involved, it is not difficult to comprehend the debilitation that is possible with a sacroiliac lesion.

All of the counternutation muscles (see Counternutators) throughout the trunk, pelvis, and upper legs, on the side of injury, as well as the nutation muscles (see Nutators) on the opposite side, go into a constant state of contraction, resulting in altered joint function from head to foot. At the same time, the nutation muscles on the side of injury, and the counternutation muscles on the opposite side, become inhibited. In other words, most of the muscular mass of the body directly participates in this reaction, inducing the trunk to rotate and laterally bend toward the side of injury. For example, in a right nutation lesion, the left shoulder will rotate forward and down toward the right side of the pelvis, while the pelvis rotates to the left. At the same time, the righting reflexes, in accordance with the vestibular system, will provide a strong counterrotational force to align the eyes and shoulders with the horizon, resulting in a scoliotic-type twist to the spine. (See SIJ Overcompensation Pattern).

Edema: Effusion – distension – weakness and atrophy
As in any injured joint, even slight tearing of the ligaments will cause some separation of the sacral and iliac surfaces [19]. This opening would allow infusion of fluids into the joint space, causing increased internal pressure and stretch to the interosseous, short posterior, and other ligaments that restrict nutation, resulting in inhibition of the muscles (nutators) that would further damage the ligaments [20, 21]. As in other joints, where increased distension has been shown to occur many times daily, one may experience feelings of heaviness and helplessness at irregular intervals [22] but, with the sacroiliac joint, I suggest that the effect may be felt anywhere in the pelvis, trunk, or upper legs. It has been found that muscular weakness, atrophy, and deformation are directly related to inhibition [20, 22-27], as well as to muscle tightness [28, 29]. Janda referred to it as “tightness weakness.” [30]

Kennedy[25] found that infusion of 60cc of normal saline into the knee joint caused a 30% to 50% inhibition of quadriceps contraction as demonstrated through the Hoffman reflex, which is similar to an electrically elicited deep tendon reflex. They found that inhibition, and antagonist contraction, will be maintained as long as effusion remains in the joint, which implies a long term inhibitory effect of internal joint pressure. The inhibition was eliminated with anesthesia. They suggested that ligament injury may lead to a destructive positive cycle; ie, ligament injury - joint laxity - disrupted proprioceptive feedback - loss of muscular splinting - and repeated ligament injury. They also suggested that joint effusion may be a cause of the joint “giving way” at unpredictable times. I propose that similar studies on the syndesmotic region of the sacroiliac joint be undertaken, as these may provide greater insight into the ligamento-muscular relationships involved in the nutation syndrome.

In addition, metabolites from muscle contraction may be augmented by ischemia to activate group III and IV muscle afferents, which stimulate gamma motor neurons and increase spindle sensitivity to stretch. In turn, the spindles increase the activation level of alpha motor neurons, causing increased reflex mediated stiffness in the primary muscle in a cycle of “increased metabolites - muscle stiffness - increased metabolites”. This vicious cycle may spread to surrounding muscles “Such a distribution of the increased muscle stiffness to secondary muscles will further aggravate the vicious circle…[and] may constitute a mechanism or series of events by which several muscles, via positive feedback, will influence each other to increase the reflex mediated stiffness [5].”

Muscle Spindle Interaction
Gamma muscle spindle systems of different muscles can interact and influence each other. At certain thresholds, positive feedback loops involving the primary muscles can spread to nearby secondary muscles to create an independent, self-perpetuating, secondary positive feedback loop, which may project back to the primary muscle spindle [5], “secondary spindle afferents – fusimotor neurons – muscle spindles.” This independent positive cycle greatly amplifies the effects of the aberrant input and may create persistently abnormal muscle stiffness and inhibition patterns, which may induce errors in muscular coordination and joint stability. This “potentially vicious cycle” could greatly amplify and spread the effects of the aberrant input.

Importantly, these reflexes were significantly increased, generating a 79% larger muscle response when loading was done during movement, emphasizing the enhanced susceptibility of ligaments to damage during strenuous activity [7, 14].

Joint Laxity
Holm & Indahl [21] stated that “Changes in loading on the sacroiliac joints may result in altered activation of the stabilizing muscles, and thus play an important regulatory function in stabilization and movement of the upper body during postural changes. Instability of a spinal motion segment…is believed to be manifested as a ‘slipping’ as a result of laxity in the motion segment”. They suggested that “…this kind of hypermobility does not seem to occur but the motion pattern is greatly altered… [and] may rather result in altered firing patterns and changes in the coordination pattern of the muscles.” Because they are in a continuous state of contraction, the counternutation muscles become tight and painful[9, 20, 21]. Conversely, because the muscles that promote ipsilateral nutation are inhibited, over time, they become flaccid, atrophic and painful [30]p5-6[31].

Gravitational Line Anteriority
Body weight alone can create significant stress by forcing the sacral base to move anteriorly and inferiorly, bringing the gravitational weight line farther anterior and increasing instability at the sacroiliac joint. In response, the counternutation muscles would contract to pull the sacral base superior and posterior, towards the ilia, in an attempt to straighten the lumbar spine. However, other counternutation muscles rotate the iliac crest anteriorly, towards the sacrum. Being more numerous and significantly larger, the muscles attaching to the innominates have more force than those attaching to the sacrum, so they rotate the entire pelvis anteriorly. As the pelvis rotates anteriorly, the sacral base is brought still farther from the gravitational line, increasing leveraged force on the sacroiliac ligaments in a positive degenerative cycle; i.e., sacral nutation - anterior pelvic rotation – sacral nutation.

Delayed reaction times
Injured ligaments have also led to significantly slower reaction times in their associated muscles [7, 32, 33] and may be the cause of a joint suddenly giving out [34]. A delayed reaction time indicates altered proprioception. It follows that increased activity, such as sports or work involving bending, lifting, or twisting, increases susceptibility to further damage, since the stress may be transferred to ligaments in other joints which may be unprepared to handle the load.

Poor timing sequences and imbalanced contraction patterns may be a significant part of chronic musculoskeletal pain syndromes and, in a chain reaction, spread to surrounding muscles, leading to increased joint stiffness. A sacroiliac sprain can change coordination patterns in many muscles which, by their attachments to the sacrum and innominates, can act through various vectors to alter posture and joint angles throughout the musculoskeletal system [9].These distortions can occur whether the muscles directly cross the sacroiliac joint, as in the knee, or do not directly cross the sacroiliac joint, or in the ankle [12, 35] or the temporal mandibular joint [36].

Tensegrity – Maintenance of Joint Tension
In keeping with the principles of tensegrity [37], the sacrum is suspended in a web of tension such that stress applied at one point is distributed uniformly, and instantly, throughout the structure [38-40]. The Serola Theory adds that, during the reciprocating phases of nutation and counternutation, the sacrum is alternately suspended by ligaments and muscles as they share responsibility for maintaining tension in the joints. During nutation in a normal joint, ligaments that restrict nutation become tight and those that restrict counternutation become lax; during counternutation, the opposite reaction occurs. When nutation limiting ligaments sprain, a ligamento-muscular response would activate, continuously contracting the ipsilateral counternutation muscles in order to reduce or prevent further stress on those ligaments. Because they will be in a continuous state of contraction as long as the ligament is insufficient, they will become tight and painful [9, 20, 21]. Conversely, because the muscles that promote ipsilateral nutation are inhibited, over time, they become flaccid, atrophic and painful [31] [30]p5-6 (See Muscle-Ligament Role in Joint Tension).

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