Technically speaking a “sprain” and a “strain” are two different types of injuries. A sprain refers to damage of a ligament, while a strain implies damage to a muscle and its tendon. An easy way to remember this is that a strain, has the letter “t” in the word, as does “tendon”. And tendons attach to muscles, not ligaments. Regardless, I’m going to lump the two together because most injuries involve damage, or result in dysfunction, in both a muscle (and its tendon) and a ligament.
Very often a patient will ask whether their pain is stemming from a muscle, tendon, ligament, nerve, disc, or joint. And my answer is often, “all of the above”. Because the body is so interconnected, an injury often does involve all of the above. That said, identifying the “pain generator” or primary tissue involved in causing the pain is something that can (and should) be done by the treating doctor. However, in order to fully resolve a patient’s pain, and return them to optimal function, it’s not uncommon to have to “fix” all of the above. The reason for this is because muscles (and their attached tendons) move bones, ligaments stabilize joints (as they attach bone-to-bone), and joints affect nerve function. When these structures are directly (or indirectly) affecting the spine, spinal discs may become involved. That said, I’ll now discuss the triad of a sprain/strain injury as it relates to muscle dysfunction. I’m going to speak of muscle dysfunction in particular, because if the muscles are not “fixed”, none of the other structures will get “fixed”.
With any injury, or even chronic pain (which may result from an old imperceivable injury) there is always muscle dysfunction. One muscle will become inhibited (or “weak” in lay terms), its antagonist (or muscle and with the opposing action) will become dysfunctional due to shortening of its overlying connective tissue or fascia, and its synergist (or muscle with the same or similar function) will become hypertonic or over-contracted. This is why I use the word “triad”.
First, I’ll discuss the inhibited muscle which is also the one I look to identify first in the triad. This is the muscle that can’t properly perform its function due to an injury (or micro-trauma) to the muscle or its tendon’s attachment to the bone. This is typically due to overstretching or over-contracting from a force that it can’t withstand. The result of this is that it cannot properly contract in its everyday function, which results in subsequent compensations. Those compensations have to do with the other two major muscle dysfunctions.
Next, the antagonist to the inhibited muscle will typically become shortened. The entire muscle can become shortened, but very often it’s the fascia (or overlying connective tissue) that shortens or becomes “knotted” and becomes the major problem. This is the typical “knot”, or more appropriately termed “trigger point” in a muscle that we often feel compelled to stretch or (hopefully) have someone else knead or massage. The eventual result of this type of muscle dysfunction is that after it becomes stretched through normal movement or deliberate stretching, it then becomes inhibited for a brief period of time. This will eventually lead to more joint instability.
Lastly, the synergist to the inhibited muscle becomes hypertonic or overcontracted. That is, the nervous system “directs” the muscle to overcontract or work harder, as it now has to take on the job of the inhibited (synergist) muscle in addition to performing its own function. This will also typically result in a “knot”or trigger point. However, this trigger point doesn’t usually respond (from a functional standpoint, though perhaps it may provide the person temporary pain relief) to stretching. It will need to be shortened (usually with pressure applied to the trigger point) in order to return to normal function. This type of muscle dysfunction will cause the muscle to become inhibited after it is contracted, leading to joint instability.
So, to rehash; a sprain/strain injury almost always involves a triad of muscle dysfunction. That is, one primary muscle is inhibited, while its antagonist becomes (“fascially”) shortened, and its synergist becomes hypertonic or over-contracted. Additionally, the adept practitioner will realize that the patient usually experiences pain in the synergist or over-contracted muscle. Or, the patient will complain of a tight muscle that will not relent to continued stretching. The reason for this is that the primary problem is the injured/inhibited muscle, which creates the subsequent compensations in the antagonist and synergist muscles. Thus, stretching (or focusing on) the compensatory muscles is usually futile or only provides transient relief. Specific muscle tests by the practitioner will uncover the primary cause of the problem and resulting pain and dysfunction.
This is not to say that only the primary (inhibited) muscle needs to be addressed. Often, the compensatory muscle dysfunction needs treatment, and there will almost always be a spinal and/or extremity joint that needs to be adjusted to allow for proper range of motion and continued muscle balance. Ligament and spinal discs (which are composed of ligamentous tissue) may also need specific attention.
As with any condition, each patient needs to be evaluated and treated as the individual they are, which yields the best results in resolving a patient’s pain and restoring them to optimal function.
Dr. Robert D’Aquila – NYC Chiropractor – Applied Kinesiology
[…] That said, they would typically be high just following an acute injury and not necessarily with a chronic sprain/strain injury. Aside from an acute injury though; it may be prudent to search for sources of chronic cell damage […]