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Trigger points are points of hyperirritability.
A German named Max Langer discovered that spots could appear in the muscles sensitive and that the tissue of these points was more rigid than the surrounding ones.
These points were named in 1948 by Dr. Janet Travell, a White House physician, during the Kennedy presidency.
Dr. Travell called “Trigger Points” and she developed a treatment method using saline injections for their suppression.
She later discovered that it was possible to deactivate the T.P. using only direct pressure on them.
T.P. is a tiny zone (diameter between 0.5 and 1 centimeter) highly irritable located inside the muscle, which appears rigid on palpitation and produces pain, limitation of stretch amplitude, and weakness without atrophy or neurological deficit.
Sometimes it can give rise to autonomous (vegetative) phenomena and distortion of proprioceptive sensitivity.
From the histopathological point of view, it is recognized as a key element of the Trigger Point, the presence of muscle knots, which corresponds to a segment of muscle fiber subjected to a strong contracture of its sarcomeres.
The muscle fibers that contain muscle knots form a taut band. The area or region of muscle fibers that contains muscle knots constitutes the palpable painful muscle nodule.
Only some fibers of the affected muscle present this microscopic alteration. At the level of contraction nodes, sarcomeres present a strong contraction (shorter and wider) differing markedly from the sarcomeres of the normal fibers of the same muscle. At the end of the fibers with contraction knots sarcomeres are elongated and slimmed down.
From the pathophysiological point of view, Trigger Points are intimately associated with neuromuscular junctions that are in a dysfunctional state.
The neuromuscular junction is the structure that links the terminal nerve of a motor neuron with a muscle fiber. It contains the synapse, the neurotransmitter that is the
acetylcholine. The functional alteration occurs in fibers of the muscle causing segmental contraction (shortening) trigger point area and compensatory passive elongation towards
both ends. The fibers in this state can be palpated (tense band).
The dysfunction of the neuromuscular junction would be related, according to a hypothesis to a local energy crisis, caused due to neurovegetative dysregulation. They develop within the reference zone of the original active TP. They do not cause pain during normal activities. They are only painful palpation.
They are activated by cold, heat, atmospheric pressure changes, and repetitive damage.
In normal clinical practice, we can find three types of myofascial Trigger Points:
The distribution and topographic frequency of the Trigger Points are not uniform.
They are preferentially located in the muscles of the head, neck, and shoulder girdle such as the temporalis muscle, masseter muscle, trapezius muscle, supraspinatus muscle, rhomboids muscle, sternocleidomastoid muscle.
In the lumbar region, those most frequently affected by Trigger Points are the erectus of the rachis and the quadratus lumborum.
Curiously the muscles most predisposed to the appearance of Trigger Points are those that also function as muscles accessory respiratory muscles.
Referred pain also appears more frequently when Trigger Points are located in the areas of the neck and shoulders.
Other common muscles where Trigger Points are located are in the leg and hip muscles.
The reason why a Trigger Point is formed in a certain moment and in a certain muscle, is still unknown, despite the many hypotheses issued.
However, multiple pathogenic factors have been found to trigger, predisposing, or favoring Trigger Points, such as:
The diagnosis of Trigger Points is based mainly on clinical assessment through the meticulous manual exploration of the Trigger Points and identification of the zones of reference.
So Trigger Points are identified by palpation, first superficial and later deep. This requires a certain practice, skill, good touch, and great palpatory anatomy.
The T.P. It is palpated as a painful or hyper-painful nodule, hard, very small, with a size ranging between 5 and 10 millimeters in diameter and with a consistency like “crunchy rice”.
The temperature of the affected muscle will be increased by a very localized area in cases of acute dysfunction. Will be decreased in chronic cases (ischemia), which indicates changes in fibrotic tissue and vascular ecstasy with decreased metabolism.
Local edema can be perceived, which is a sign of
waterlogging of the tissues (lymphatic failure). In chronic cases, the initial edema is gradually replaced by fibrotic (connective tissue) changes.
There are no laboratory or radiological objective data that can be correlated with the clinical findings.
However, some theses and works have attempted to demonstrate that electromyography and thermography as tests complementary can provide data in favor of the diagnosis.
Various biochemical abnormalities have been indicated, including:
Furthermore, the accumulation of H2O and fat, mucopolysaccharides, platelets, and mast cells (degranulated) have been shown in nodules fibrotic. Platelets and mast cells release serotonin and histamine, which stimulate the peripherals nerve, contributing in this way to a state of hypersensitivity.
Capillary lysis, myofibrillar lysis, and endothelial cell changes have also been presented.
Although all these abnormalities have been detected in the Trigger Points biopsy is not diagnostic.
To diagnose and quantify trigger Points is necessary to resort to methods that are not always very objective, since the pain when perceived subjectively, has not been able to be quantified with accuracy, despite multiple attempts, and must use measurement systems based on questionnaires and scales.
The most important are the following:
Summarizing the clinical characteristics of the trigger point pain syndrome or myofascial pain syndrome we can identify these findings in the muscle area affected:
In recent years it has been noted that numerous sports injuries, muscle pain, and athletic disorders called in sports jargon “contractures” or “muscle knots”, are nothing more than myofascial pain with the formation of trigger points.
If you carefully explore the muscles involved, it will be observed that there is no such overload globally, it is not the entire muscle that hurts.
We will find that the shortened and weak muscle has a tight band on the inside of which a TP appears. These TPs are located in muscles overstressed by sports practice, which increase your vulnerability to damage, with greater and rapid exhaustion, and an increase in tension and stiffness, which are direct results of the training.
These muscle microtraumas from exercise, favor the accumulation of waste products that originate in the muscle (particularly lactic acid and potassium ions), reduce drastically the oxygenation capacity of the same, and reduce the blood flow.
All this implies a shortening of the muscle fiber that causes tension in the muscle, pain as a response of the nerve to the compression carried out by the spasmodic muscle, and so on until pain becomes chronic.
All these conditions increase muscle vulnerability and the period of muscle recovery, activating a vicious circle predisposing the athlete to get a sports injury.
The development of PGs in specific muscle areas of the athlete is conditioned, commonly by a wide variety of factors, among these we must highlight the:
Many factors can perpetuate Trigger Points in athletes, the most frequent being the following:
Clinically, the athlete manifests dull and heavy pain.
The muscle feels tense, hypertonic, and contracted.
The muscle is exhausted quickly and significantly decreases sports performance.
There are different types of treatments and rehabilitation techniques that can be utilized to treat trigger points.
Depending on the status and entity of the Trigger points, we can perform different rehabilitation techniques to ease trigger points such as: