Advances and instrumentation in diagnosis and treatment of trigger points in human myofascial pain: veterinary implications

A.1. TRIGGER POINTS (TPs) AND MYOFASCIAL SYNDROMES IN HUMANS

Types of TPs: There are different types: active and passive, primary and secondary. All TPs are associated with dysfunction but only active TPs are associated with pain. Primary and secondary TPs may be active or passive.

Active TPs are very tender on palpation and associated with existing pain or other dysfunction. They may vary in irritability (associated with variation in symptoms) from hour to hour and day to day. The severity and extent of the referred pain depends on the irritability of the TP, not on its size or the size of the affected muscle. Active TPs can become passive after alleviation of the precipitating factors, rest or inadequate therapy (Verhaert 1985).

Passive (latent) TPs are less tender on palpation. They may be found in clinically normal patients and are associated with restricted movement (guarding) and weakness/fatigue of the affected muscles. (Muscles "learn" to avoid movements which cause pain). Passive TPs can be activated easily by many factors, especially overstretching/overuse, and can then trigger clinical pain or dysfunction. The fitter the muscle, the more difficult it is to activate its passive TPs (Verhaert 1985).

Primary TPs are those which arise as a direct result of physical injury, local irritation in virus diseases or direct environmental effects on myofascial tissue. Active primaryTPs, causing pain, "guarding" and increased muscle stress elsewhere, may recruit secondary TPs in the same or other muscles.

Secondary TPs are those which arise due to foci of irritation elsewhere, such as in visceral disease or as recruits to very active primary TPs elsewhere.

Aetiology of TPs: Normal muscle, connective tissue, skin and fully healed scars are not painful on palpation and should contain no TPs. When they arise, TPs are usually located in muscle but foci of irritation in the skin, ligaments, fascia, subcutaneous connective tissue and periosteum can also act as TPs (Janssens 1984; Verhaert 1985). Scar tissue, especially that with keloid formation or areas of local tenderness, may also act a TP (Fox 1975; Khoe 1979; Rogers 1982; Verhaert 1985). Tender scars may arise after surgical incision (especially transverse), haematoma or tissue bruising, burns, local infection, abscesses, vaccination, needle-track infection and in infected tooth-sockets.

TPs are usually initiated (or latent ones activated) by acute or chronic overload or direct injury to the affected muscles (hyper-extension, strain, trauma, a fall, being cast etc). Fatigued or unfit muscles are very prone to injury and, therefore, TPs can easily arise in them (Cain and Rogers 1987).

TPs can also arise during periods of rapid growth (growing pains due to slight muscle, joint and tendon stress/strain) or as a sequel to systemic infection or fever, especially virus infection (Fox 1975; Janssens 1984).

Irritation of the thoracic or abdominal organs, of vertebral nerve-roots, joints, muscles or periosteum may refer pain to related skin and muscle and may establish TPs in the same and nearby spinal segments. Arthritis, subluxation of vertebrae, overriding of vertebral spines or facet joints, vertebral disc lesions or spinal nerve pressure (entrapment) are often associated with TPs. Over-exertion of muscle (hyper-contraction, tearing some of the weaker fibres) and chills/draughts on exposed parts of the body, especially after exercise, or if the part is hot or sweating can also activate TPs (Moss 1972; TP Therapy Symposium 1981; Janssens 1984; Verhaert 1985).

Detection/elimination of active TPs are important in the treatment of clinical pain and other disorders. Regular examination for and elimination of passive TPs (by massage and physical exercise) can restore full muscular function and can prevent many problems. This is the basis of Chinese acupressure, Shiatsu (Japanese AP massage) and Tai Chi (Chinese body exercises).

Clinical detection of TPs: TPs are located by careful palpation of the body, searching for points of exquisite tenderness. As each point is pressed, the human patient is asked: "What do you feel now ?". Unless the TPs are very active, the patient is unaware of their existence or location until they are palpated. TPs persist under general anaesthesia and post-mortem (Schade 1919).

To the palpating hand, TPs feel like nodules surrounded by a taut band of otherwise normal muscle. Occasionally the affected muscle may be hypertonic or in spasm. If the examiner pinches an active TP or snaps a finger across it, the patient may give a local or general jerk (positive "jump sign"). Pressing, pinching or needling the active TP triggers pain to the problem area (referred pain area, joint, other muscles or viscus) unless the referred area is in severe pain beforehand.Local TP tenderness can last for hours afterwards (Verhaert 1985). Passive TPs have similar characteristics but are not as painful and do not refer pain elsewhere to the same degree as active TPs.

The anatomical relationships between TPs and their area of referred pain are quite specific and a detailed knowledge of these relationships can help to predict the location of TPs in pain of specific organs or areas (Anon 1980; Travell and Simons 1984, 1985).

Histologically, TPs can show fat dusting. Severe forms may show fibrosis and dystrophic changes (swollen mitochondria, destruction of myofilaments, ruptured sarcomeres and collagen accumulation) in replacement connective tissue (Michlke et al 1960, Fassbender 1975).

Chronic myofascial syndromes typically present as an acute episode (active TPs present) but with a history of recurrent episodes over months or years. This is due to alternation of the TPs between the active and passive states with rest, time and various therapies which failed to find or eliminate the TPs (Verhaert 1985). TPs, especially those entrapping spinal nerves, may induce related sensory disorders (paraesthesia, hyperaesthesia, tinnitus, disturbed vestibular function (vision, space perception, ataxia)) and autonomic signs (Chung 1983; Travell and Simons 1984, 1985; Janssens 1984). In the early stages signs include: localised vasodilation (thermographic hot-spots) with localised muscle spasm, secretion (saliva, sweat, tears etc) and pilomotor activity. Chronic TPs may show vasoconstriction (thermographic cold-spots), hyper-irritability of motor neurons (Verhaert 1985). The are often fibrotic and quite difficult to penetrate with a needle.

Affected muscles have a restricted range of movement and resist passive or active stretching, as this causes pain. Muscle contraction against a fixed resistance is also painful. They are easily fatigued and can do less work. Muscle atrophy or neurological deficit is seldom present unless the TP or local muscle spasm entraps a nerve (Verhaert 1985).

Although TPs may arise in association with spondylosis, arthritis, disc disease in humans and animals and in canine hip dysplasia, radiography in the more common myofascial disorders is usually negative. Blood tests for muscle enzymes are usually negative unless there is extensive muscle damage, as in equine azoturia.