Joint Stability

01 Jan
Joint Stability

Happy New Year; wishing you a healthy and prosperous 2019!

Hilton’s Law – “The same trunks of nerves whose branches supply the groups of muscles moving a joint furnish also a distribution of nerves to the skin over the insertion of the same muscles; and the interior of the joint receives its nerves from the same source.”
Hilton also stated “Every fascia of the body has a muscle attached to it, and that every fascia throughout the body must be considered as a muscle.”
So many things to take into consideration when studying the joints ROM and limitation of movement. Look at the disorganization of the foot and ankle complex in Charcot arthropathy or even joint instability in flaccid paralysis. Think of how the ligaments are not limiting the ROM to prevent dislocation. A healthy, well-innervated joint/limb will not have excessive ROM, even in a relaxed state. It is only by reciprocal innervation and inhibition of muscles, whereby the agonist contracts sending an impulse to the antagonist to relax, that movement is even possible.
Knee extension is not stopped by the PCL or ACL, but by tension in these ligaments causing a reflex signal to the knee flexors to contract. This is how the joint capsule and associated ligaments work along with tendons to protect the joints.

Myotatic reflex, or stretch reflex, is a muscle contraction in response to a sudden stretch. When a muscle elongates, the muscle spindle is stretched which results in a monosynaptic reflex. This action helps keep our joints stable. As bones and tendons do not typically pull muscles, the rapid stretch stimulates muscle spindle activity to protect the joint from being distracted.

Noxious stimuli can also increase muscle spindle activity. This is thought to be what drives the pain-spasm-pain cycle in those who suffer from many chronic pain syndromes.  Likewise, this can also lead to a reduction of joint ROM. Joints love movement as it helps stimulate the production of synovial fluid and intraarticular nutrition and waste removal. Movement is necessary for hyaline cartilage health.

Reciprocal inhibition can be altered by having a hypertonic agonist, which will decrease neural input to the antagonist. This alters the force-couple relationship creating synergistic dominance, which leads to faulty movement patterns, poor neuromuscular coordination and proprioception, and arthrokinetic dysfunction. This altered joint motion leads to more pain which can further alter muscle recruitment and motor control, eventually causing joint damage.

Are the ligaments really responsible for joint stability in otherwise healthy joints, or is it altered proprioception and neuromuscular control?

Let’s briefly discuss the specialized neurons called mechanoreceptors. – StretchReflx

Two afferent receptors of muscles and tendons (tenomuscular mechanoreceptors) are: Golgi Tendon Organs, embedded  within the musculotendinous junction, stimulates muscle relaxation after prolonged tension. Muscle Spindles, located within the skeletal muscles, respond to sudden stretch, thus stimulating muscle contraction.

There are two primary joint receptors located within the joint and surrounding ligaments: Ruffini Endings, located on flexion side of joint capsule, respond to extreme joint motion into extension with rotation – they protect joint stability. Pacinian Corpuscles are located throughout the joint capsule, joint, and periarticular tissue; they respond to compressive forces across the joint during movement. Another less discussed articular mechanoreceptor is Golgi-Mazzoni Corpsucles; located within the joint capsule and is activated by compression.

Ligamentous receptors are myelinated and can transmit sensory information regarding joint position to the CNS, they inhibit continued agonist contraction to decrease tension on the ligament. They have been classified into four types. Type II are thickly encapsulated, medium diameter, conical corpuscles believed to provide joint sensation and proprioception, particularly at the beginning of movement; they have a low threshold, rapid adaption and are dynamic. Type III are larger in diameter, thinly encapsulated fusiform corpuscles with high threshold activated by extreme dynamic ROM, slow adapting.  Type I  are thinly encapsulated globular corpuscles with a small diameter and a low threshold, slow adapting both static and dynamic – they are constantly firing to provide proprioception, even at rest . Type IV contain plexuses and free nerve endings, they are very small in diameter, have a high threshold and are responsible for nociception.

My 17 year old autistic son has proprioception dysfunction – which is common in children with ASD and other forms of sensory processing disorders. As a result he holds himself in awkward postures and finds it difficult to follow along with a Pilate’s exercise routine as he is unaware of whether or not his legs are straight or pelvis is aligned with his shoulders, etc.  If you’ve seen kids with ASD constantly kick their feet or flap their hands, that’s just a method they are using to stimulate proprioceptive feedback. They may have difficulty isolating body parts and movements for coordinated tasks. Neuromuscular control is a struggle, as their internal feedback is lacking. Our internal feedback is what allows us to modify movements to achieve joint stability.

Now that you understand how important proprioception is for neuromuscular control, you can imagine how standing or sitting in awkward, unbalanced, misaligned postures can damage the kinetic chain. Foot and ankle complex disorders such as pronation distortion are very common, as is an uneven lumbosacral junction, then there’s scoliosis accompanied by the classic rib hump and uneven shoulder girdle with head tilt. This example is a proprioceptive disorder with origins in the CNS. So what about peripheral neuropathic disorders? As mentioned earlier, in cases of Charcot arthropathy, or neuropathic arthropathy, which is a progressive denervation induced degeneration of the foot and ankle joints that leads to eventual deformity. Without the proper proprioceptive feedback the ligaments fail to withstand abnormal arthrokinematics. This is why it is so important to perform regular exams of diabetic patient’s feet. sensory-examination Diabetes is the most common cause of neuropathic arthropathy leading to this type of foot and ankle joint disorder, but peripheral nerve (lower motor neuron) injury or even brain or spinal cord (upper motor neuron) injuries may be a causal factor. There are even congenital disorders that cause analgesia (CIP). Heavy metal poisoning can also destroy afferent proprioceptive fibers.

Transarticular ligaments provide more than just support for the joint, they also send sensory output which improves arthrokinematics to prevent joint damage. Proprioception is important for kinesthesia, dynamic stabilization of the joints and neuromuscular control to prevent musculoskeletal injury, especially of the joints. Neuromuscular and sensory testing should be part of our routine evaluation. Neuromuscular and proprioceptive retraining should be incorporated into treatment plans to help restore joint stability.




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Posted by on January 1, 2019 in Uncategorized


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