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Pain in the courtroom: can you prove it?

YOU have been injured in an accident. You have the normal symptoms of a soft tissue or whiplash injury such as pain in the neck and back, inflammation, swelling, muscle spasm, and restriction of movement. These gradually subside but you continue to have chronic pains in the muscles of the neck and back accompanied at times by fatigue, stiffness, and a general aching. This continues for years after the accident. You are seen by a rheumatologist who diagnoses fibromyalgia. Alternatively, you are seen by a pain specialist who diagnoses myofascial pain syndrome. What is the difference? And can you prove in court that either condition arose from that accident years ago?

An illustration of the difficulties faced by the plaintiff is the case of Mackie v. Wolfe, a 1994 Alberta court decision. There, the injured plaintiff was attempting to prove that her fibromyalgia was related to a motor vehicle accident which occurred 8 years earlier. Even the plaintiff's doctor stated "there is no known cause of fibromyalgia". All the court could do was speculate as to the causes.

The only attempt to determine whether the pain was muscular in origin was an examination of the plaintiff by a physiatrist called by the defence. She found trigger points but no tender points in her physical examination of the plaintiff. She found that the plaintiff suffered from "mild myofascial pain". However, she did not perform any surface electromyograph (EMG) studies on the workings of the muscles and, therefore, was unable to discuss the causes of the myofascial pain.

Without evidence to show a relationship to the car crash, the court found no connection between the crash and the plaintiff's fibromyalgia.

In the case of Logozar v. Golder, 1992, in the Alberta Court of Appeal, Justice McClung stated "the plaintiff/appellant claimed that her pain was an outgrowth of a condition known as fibromyalgia (fibrositis) which is a rheumatic soft-tissue syndrome marked by chronic muscle deterioration. All doctors agreed that fibromyalgia and its onset is, medically, of unknown origin."

The court concluded that "the conflicting opinions touching the source of the plaintiff/appellant's current deficits had to be weighed against the evidence that only 18-25% of fibromyalgia sufferers can point to trauma as its precipitating event." That equates to a 1 in 4 or 1 in 3 chance of a causal relationship between the two. No court will or should compensate a person when there are these odds against the car crash and the condition being related.

In the Journal of Arthritis and Rheumatism (33: 2), rheumatologists define fibromyalgia as the existence of "widespread pain in combination with tenderness at eleven or more of 18 specific tender points sites". However, this definition does not provide an explanation as to the initial triggering cause of this pain and its connection to a traumatic event such as a motor vehicle accident. To attempt to prove in court something medical science cannot support is doomed to failure.

A more promising route is to see if there is a provable link between the crash, muscle damage, and pain of a chronic nature. This is the route of proving myofascial pain syndrome -- pain within the body of the muscle.

There are three major types of muscles in the human body. However, we are concerned here only with those muscles which act upon the bones of the skeleton to produce motion of the body parts and locomotion of the body as a whole.

Studies show that these muscles produce movement by contracting not by expanding. They always pull, never push. They work together in groups, however, rather than acting singly. Examples of this are shown in the diagram of rotating the torso. (Figure 1)

The unpleasant feeling we describe as pain is interpreted by our brain as being centred in a particular point of the body. Usually, however, the pain a person experiences in muscles is referred or transmitted from some other part of the muscle system. That explains why so often examination of the painful area reveals no anatomical evidence of pain and why some doctors become skeptical of the injury. Studies have shown that pressure applied in one area of a muscle will cause pain to be referred to another part of the muscle system. The point which causes such pain when pressed is called a trigger point (TP). Examples of trigger point patterns are shown in the attached diagram. (Figure 2)

It is important to consider the definitions of skeletal muscle pain according to current medical knowledge. A paramount medical text is Myofascial Pain and Dysfunction -- The Trigger Point Manual by Drs. Janet Travell and David G. Simons written in 1983. As stated by the authors, "clinical interest in pain of muscular origins (myofascial pain) has ebbed and flowed through the years as new names and new concepts of its cause have come and gone". Is the pain produced from a trigger point in the muscle? "Throughout his series of nearly a dozen papers on `fibrositis' between 1941 and 1963, the Australian Michael Kelly was impressed by both the palpable hardness of the nodule associated with the tender point in the muscle and by the distant referral of pain from the afflicted muscle".

"A major block to a general understanding of myofascial pain disorders has been the profusion of terms with parallel meanings, overlapping meanings and some with multiple meanings". In attempting to identify myofascial pain disorders (pain originating from within the body of the muscle), the following list of terms has been used by medical specialists. The list is only partial:

* Muscular Rheumatism

* Interstitial Myofibrositis

* Myofascial Pain Syndrome

* Myofascitis

* Trigger Points (Trigger areas, Trigger zones)

* Myofascial Pain - Dysfunction Syndrome

* Fibrositis

An important step was taken, say Travell and Simons, when formal definitions were developed. "A myofascial trigger point is a hyperirritable locus (spot) within a taut band of skeletal muscle, located in the muscular tissue or its associated fascia (sheath enclosing the muscle). The spot is painful on compression and can evoke characteristic referred pain and autonomic phenomena"

As Travell and Simons noted, "Myofascial TPs are classified as either active or latent. An active TP causes the patient pain. A latent TP is clinically silent with respect to pain, but may cause restriction of movement and weakness of the affected muscle. A latent TP may persist for years after apparent recovery from injury; it predisposes to acute attacks of pain, since minor overstretching, overuse, or chilling of the muscle may suffice to reactivate it. Both latent and active TPs cause dysfunction; only active TPs cause pain." This is important to understand especially in the common situation where a person goes for periods of time without pain, then suddenly experiences pain after a change in daily exercise routines. While the initial cause of a TP may be hotly disputed, Travell and Simons point out, "Normal muscles do not contain TPs. Normal muscles have no taut bands of muscle fibres, are not tender to firm palpitation, exhibit no local twitch responses, and do not refer pain in response to applied pressure."

Drs. Travell and Simons use the following definition: "it is important to note that trigger points are activated directly by acute overload, overwork fatigue, direct trauma, and by chilling". Patients implicate an acute traumatic cause when they relate the onset of their myofascial pain to a specific event or movement (acute overload) that often had occurred months or years before. Primary myofascial TPs also develop in muscles subject to excessive repetitive or sustained contractions (overwork fatigue) (Donaldson, Skubick, and Donaldson, Electromyograph--Trigger Point and Myofascial Symptoms, 1991.)

What is being described is not the initial creation of a TP within a previously normal muscle, but the activation of a TP that may have lain latent following periods of apparent recovery after an injury to the muscle.

Secondary TPs are likely to develop in an adjacent muscle that is chronically overloaded by protective spasm maintained to reduce strain on the first muscle that is hypersensitive, shortened, and weakened due to primary TPs. This describes how compensation by using the uninjured muscle produces a trigger point in that uninjured muscle. A person injured on one side compensates by overworking the muscles of the uninjured side causing trigger points of pain to be activated there.

Travell and Simons concluded that "the signs and symptoms of myofascial TP activity long outlast the precipitating event. When injured, most tissues heal, but muscles `learn' to avoid pain. Active TPs develop habits of guarding that limit movement of that muscle. Chronic muscular pain, stiffness, and dysfunction result."

If these TPs are not contained in normal muscles and are activated by acute overload, overwork fatigue, direct trauma or by chilling, is it possible to determine in a particular patient what caused the TP in the first place? From the lawyer's perspective, is it possible to prove causation of this TP and its resulting myofascial pain from an accident for which compensation can be sought from a third party?

We now have available highly sophisticated techniques to show that a muscle is functioning abnormally and thus are able to link it to an injury. One proven scientific technique is through the use of surface EMG. As stated by Drs. Donaldson and Skubick, "electromyography studies the activity of the striated muscles using electronic techniques. Electrodes are placed over the belly of a muscle allowing for the study of the electrical activity of that muscle." Research indicates that the amount of electrical activity in a muscle correlates highly with the amount of force a muscle generates. In healthy muscles, this relationship is linear and predictable. The muscle evaluation sites are shown in the attached diagram. (Figure 3)

When lengthened or shortened, during movement, a muscle produces an electrical signal which correlates with the amount of force the muscle is generating. This is measured in microvolts. An example of measuring of muscle activity is shown in the attached diagram. (Figure 4)

Through computer analysis, Drs. Donaldson and Skubick found that the activities of several muscles may be compared simultaneously, thus revealing those muscles which are functioning in normal and in abnormal manners. Deviance from a linear pattern and differences in the amount of force generated between muscles are of diagnostic significance.

Their studies concluded that dynamic surface EMG analysis allows for documentation as to biochemical imbalances between muscle partners. In this situation, a healthy or stronger muscle will develop trigger points due to biochemical overloading. Simply put, the injury to one group of muscles puts added strain and stress on the same group of muscles on the other side of the body, causing trigger points to develop in turn.

Drs. Donaldson and Skubick found that in the evaluation of myofascial pain, surface EMG allows for an accurate assessment of the biomechanical properties of the appropriate muscles. Surface EMG not only identifies overactive muscles which have trigger points but also allows for a broad comprehension of why the trigger points develop so effective treatment can follow. An example of the assessment technique is shown in the attached diagram. (Figure 5)

In plain language, the assessment by surface EMGs show that an injured muscle is functioning abnormally. The next step is proving how the muscle was injured. Armed with the use of surface EMG and given the history of how the patient/client moved within a motor vehicle at the time of collision, the results of the surface EMG study can be directly illustrative of how the person's skeletal muscles were injured.

As stated by Donaldson in "Testing for the Existence of Muscular Injury in Motor Vehicle Accident Victims using Surface Electromyography", 1995, "there is a relationship between the position a person was in at the moment of impact and the surface EMG assessments. If a person was in a rotated position at time of impact this can be clearly demonstrated. Rotation of the body is achieved by the muscles exerting an unequal force about a joint with one muscle lengthening while the muscle on the other side is shortening.

If severe force in another direction is then applied to these muscles, the muscle in the lengthened position later shows decreased electrical activity. Conversely the muscle in the shortened position shows increased electrical activity afterwards. The muscle showing the increased electrical activity over a period of time develops the trigger point. This trigger point over time causes other trigger points to develop by affecting the interaction amongst muscles," say Donaldson and Skubick.

Courts in Alberta since 1991 have accepted such evidence in cases involving victims of car crashes claiming for damages for chronic pain. In 1991, the Alberta Court of Queen's Bench accepted evidence of surface EMG studies to show evidence of injury to the muscles of the neck and back of two car occupants, driver and passenger. This is reported in the case of Josue v. Pedersen, Court of Queen's Bench, December 1991.

The writer has presented similar evidence in court in more recent cases, and the court has accepted this evidence and the expert opinion of physicians working in the field.

In summary, the light at the end of the tunnel in proving the link between a car crash and a person's chronic muscle pain is through the use of trigger point assessment coupled with a complete physical examination including a detailed history of how the person's body moved in the vehicle at the time of the car crash. The injury and its relationship to current pain is, then, corroborated by the use of surface EMGs. The result is an expert opinion to use in court to prove on a balance of probabilities that the car crash injured the particular muscles which, in turn, continue to cause the referral pain of a chronic nature.

It is folly to proceed to court without these steps. It is even more foolhardy to proceed to court having to persuade a judge to decide what medical science has not detailed; i.e., the cause of fibromyalgia.
COPYRIGHT 1996 Legal Resource Centre of Alberta Ltd.
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Author:John Sutherland
Date:Jun 1, 1996
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