Friday, December 28, 2012

Crucial Issues

Crucial Issues

In our opinion, the most powerful arguments against the inclusion of PRI in the Guides are that (1) PRI assessments are likely to be unreliable and (2) they might lead to systematic errors in assessment, such that persuasive patients can “game the system” and get inappropriately high impairment awards. Both of these arguments derive from the permise that it is very difficult for examiners to determine the extent to which patients are affected by their pain. These difficulties were succinctly captured by Scarry when she said: “To have great pain is to have certainty; to hear that another person has pain is to have doubt.” The problem of reliability and validity of PRI assessment is much more than an academic problem in measurement theory. The Guides serves the societal role of providing the equitable method of compensation individuals who ability to function has been compromised by a medical condition. For the Guides must employ assessment procedures that are reliable and valid, rather than capricious ones that can be manipulated by persuasive patients. Thus, regardless of how severely pain affects individuals with various medical conditions, a PRI assessment system must have reasonable reliability and validity to accomplish the societal goal of fairly compensating them.

In fact, the key issue separating proponents and opponents of impairment due to pain is the weight they place on ease of measurement of PRI vs. relevance of PRI. Advocates for PRI emphasize that pain has great relevance to the ability to function of individuals who have various medical conditions, but these advocates tend to downplay the problems of measuring PRI. Opponents tend to emphasize problems in measurement but ignore the issue of relevance. In principle, empirical research could be performed to determine the strength of the independent contribution that pain makes to the burden of illness borne by individuals with various medical condition, and whether examiners can reliably and validly assess PRI. Considerable research has been done on the first issue, at least for some common painful conditions such as disorders of the lumbar spine. Unfortunately, though, essentially no research has been done on the issue of determining the reliability and validity of PRI assessments. Construct validation research is greatly needed in this area. At this time, as a practical matter, decisions regarding PRI for purposes of the Guides’ Sixth Edition must be based on judgment rather than empirical data.

Monday, December 24, 2012

Chronic Pain Syndrome

Chronic Pain Syndrome

In both the Fourth and Fifth Editions of the Guides, a definition of chronic pain syndrome (CPS) was included that captured the major biopsychosocial characteristics of chronic pain. Indeed, the biopsychosocial approach to chronic pain and disability is currently viewed as the most heuristic perspective to the understanding, assessment, and treatment of chronic pain disorders, and has replaced the outdated biomedical reductionist perspective. This biopsychosocial approach views chronic pain as a complex and dynamic interaction among biological, psychosocial, and social factors that perpetuates, and may even worsen, the clinical presentation. Each person will experience a chronic pain condition uniquely, this accounting for the great individual difference in how pain is expressed. The complexity of a chronic pain disorder is especially evident when it persists over time, as a range of psychosocial and economic factors can interact with pathophysiology to modulate a patient’s report of discomfort and disability healing occurs, all patients experience some degree of physical deconditioning associated with stiffness and muscle atrophy in the injured area. Risk factors for profound deconditioning with the injured area becoming a “weak link” include extended periods of inactivity, inhibition of function due to pain, and fear avoidance. In striking contrast, the traditional and outdated biomedical approach assumes that all pain symptoms have specific physical causes, and attempts to eradicate the cause directly by identifying and rectifying the presumed pathophysiology. However, chronic pain can rarely be understood by the linear, nociceptive mechanism. As will be discussed later in this chapter, there is often an absence of a document-able relationship between pain and pathophysiology.

With the above biopsychosocial perspective in mind, CPS can be described as pain that continues beyond the normal healing time for the patient’s diagnosis and includes significant psychosocial dysfunction. It should be noted that this definition does not include any specific time frame to use in making the diagnosis of CPS. This omission is intentional and reflects clinical reality, in that some conditions would be expected to resolve in several days and others in several months or even years. The diagnosis of CPS should then be temporally connected to the point at which a given condition or conditions were expected to have resolved, rather than to any arbitrary time period for an injury or event. Regardless of when it occurs, CPS is a condition that ultimately adversely affects the patient’s well being, level of function, and quality of life. The major characteristics associated with CPS include the following with 3 or more required for a diagnosis:

Ÿ  Use of prescription drugs beyond the recommended duration and/or abuse of or dependence on prescription drugs or other substances.
Ÿ  Excessive dependence on health care providers, spouse, or family.
Ÿ  Secondary physical deconditioning due to disuse and/or fear-avoidance of physical activity due to pain.
Ÿ  Withdrawal from social milieu, including work, recreation, or other social contacts.
Ÿ  Failure to restore pre-injury function after a period of disability, such that the physical capacity is insufficient to pursue work, family, or recreational needs.
Ÿ  Development of psychosocial sequelae after that initial incident, including anxiety, fear-avoidance, depression, or nonorganic illness behaviors.

Saturday, December 22, 2012

Definition of Pain

Definition of Pain

The International Association Study of Pain defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.” Pain is a prominent symptom in many acute injuries and illnesses, and often subsides as the medical condition resolves. Since such acute pain is usually short lived, it is not a problem that is considered in an impairment rating system. However, chronic pain is a problem that potentially could be the cause for an impairment rating. The definition of chronic pain is imprecise but, in a general way, it refers to pain that persists over time. For the purposes of the Guides, chronic pain is defined as pain that persists beyond the expected healing time of the medical disorder thought to have initiated the pain. For many sections inthe Guides, chronic pain will be pain that persists beyond 3 months, as most common conditions affecting the musculoskeletal and other organ and systems will substantially heal in this time frame. The nervous system is a notable exception. Although any time point is arbitrary, 3 months should encompass the expected healing time in most situations where there is tissue injury but will allow for situations in which there is no expected healing time. 

Wednesday, December 12, 2012


Medical causality is imputed when the association between a medical condition and a given exposure (physical, biologic, or chemical) is such as to lead one to believe that the condition would not have occurred in the absence of the exposure. The temporal relationship between the exposure or injury and the medical condition (or symptoms suggestive of the condition) is the first factor that must be assessed. The illness or disease should occur after the exposure (referred to as “temporal ordering”) and within a time period that is reasonable given the nature of the exposure (temporalcontiguity). In certain situations (such as asbestos, lead, and benzene exposure) there is a long latency between the time of exposure and the appearance of disease. Hence, regardless of whether a temporal relationship appears to be present, determining causality also requires one to assess whether a causal relationship is biologically plausible.
               A causal relationship is biologically plausible when:

               1. The relationship between the medical condition and the exposure or injury can be explained anatomically or physiologically.
               2. The duration, intensity, or mechanism of exposure or injury was sufficient to cause the illness or injury in question.
               3. There is evidence suggesting that the exposure is consistently or reliably associated with the process under investigation in the population under investigation or in peer-reviewed literature.
               4. Cause and effect are contiguous--ie, there is a readily understandable relationship between the two, in which an increase in the magnitude of the exposure reliably leads to an increase in the severity of its alleged effect upon the injured or exposed person, and vice versa.
               5. There is literature providing biologic or statistical evidence indicating that the symptoms or disorder could develop as a result of the exposure (coherence).
               6. There is specificity of the association for the injury (ie, the absence of other factors, especially pre-existing disease, that could have caused or contributed to the problem).

               The independent examiner is obligated to evaluate the validity and strength of all postulated causal mechanism. Mechanisms that appear weak, or are clearly flawed, must be identified as such and accepted as likely only when at least two other criteria for biologic plausibility have been met. Optimally one would wish to satisfy all criteria. There are, however, circumstances when contiguity cannot be demonstrated, as some exposures lead to disease in a noncontiguous fashion. Specificity of association is also difficult to illustrate definitively given the multifactor nature of many disease processes. Literature supportive of causality is generally available, but must be closely scrutinized before relying upon it as it is often poor quality.

Monday, December 10, 2012

Muscle Strains

Muscle Strains
Muscle strains are probably the most common type of injury to the myotendinous unit (MTU). A muscle strain is an acute stretch-induced injury secondary to excessive indirect force generated by eccentric muscular contraction. Muscle strains may occur anywhere in the body, but the most frequent muscles involved are the quadriceps femoris, biceps femoris, semimembranosus, semitendinosis, and gastronomies-soleus complex. Muscles that cross two joints and have a high proportion of fast twitch fibers are more prone to muscles stabilizing the hip, shoulder, and elbow joints. The pain elicited from an acute muscle strain is typically experienced during an athletic activity or immediately at its termination. The pathologic changes in an acutely strained muscle include disruption of the muscle fibers near the myotendinous junction along with edema and hemorrhage. The grade of a muscle strain depends on the degree of fiber disruption and the clinical findings.
               The appearance of a grade 1 muscle strain on MRI is similar to the findings of a grade 1 muscle contusion. There may be enlargement of the muscle due to interstitial edema and hemorrhage and, on a spin-echo T2-weighted or STIR sequence, there will be increased signal intensity within the muscle. Muscle strains are frequently located near the muscle’s myotendinous junction. The tendon of a multipennate muscle extends into the muscle belly; therefore, the symptoms elicited by a strain may be located anywhere within a muscle and not merely at its ends. MRI has provided excellent documentation of the extent and position of these injuries. Fleckenstein et al reported on the MRI appearance of the natural history of acute muscle strains. Acutely, the abnormal signal intensity was identified throughout the muscle, but on follow-up studies the abnormal signal intensity was most prominent in the periphery of the muscle. In one patient there was persistent abnormal signal intensity within the muscle after complete resolution of symptoms.
               A grade2 muscle strain manifests clinically as muscle pain associated with a loss of strength. Pathologically there is a macroscopic partial tear of the MTU. On an MRI study, there will be a partial tear of the muscle fibers associated with edema and/or hemorrhage. With a grade 3 strain there is a complete disruption of the MTU. Plain films provide little useful information in the evaluation of most muscle strains. Only if there is a grade 3 strain that results in gross instability or malalignment (e.g., a quadriceps rupture) will plain films be helpful. CT has also been used to evaluate muscular strain injuries, but it provides less useful clinical information compared to an MRI examination.
               In addition to the evaluation of acute or delayed muscle injuries, MRI is an ideal imaging modality to follow the evolution of the inflammatory and reparative processes within a muscle. With MRI it is possible to detect any sequelae from a MTU injury (e.g., muscle atrophy or fibrosis). Clinically it can be extremely difficult to determine when a muscle has completely healed, and if an athlete or worker returns to his or her athletic activity or job too soon after injury, he or she may be predisposed to repeat injury. MRI has detected acute MTU injuries that were superimposed on sub acute or chronic injuries that may be predisposed the muscle to reinjury.

Saturday, December 8, 2012

Muscle Injuries

Muscle Injuries
Muscle Contusions and Tears

Muscle injuries may result from a direct or indirect application of force to the muscle. A direct blow to a muscle may cause a muscle contusion with disruption of muscle fibers. Acute disruption of muscle fibers and capillaries may precipitate soft tissue hemorrhage and a hematoma along with a secondary inflammatory response. With the acute pain associated with muscle injury, it may be difficult on a physical examination to determine the precise location, extent, and severity of an injury. Prior to the implementation of MRI, radiologic imaging studies were of little value in the evaluation of acute muscle injuries. On plain films there may be obscuration of the fat planes surrounding an injured muscle secondary to the perimuscular edema. With CT there may be an alteration of the size or contour of a muscle but detection of intramuscular hemorrhage, edema, or a hematoma is difficult. With the excellent soft tissue contrast resolution provided by MRI, it is now possible to obtain the following important clinical information related to a muscle injury: (1) the extent of muscle edema and/or hemorrhage; (2) is a focal hematoma is present, including its size and location; (3) the degree and extent of muscle fiber disruption; (4) if there is complete disruption of the muscle, whether there is associated muscle retraction; (5) whether there is interruption of the overlying fascia and if there is a muscle herniation; (6) the degree of muscle swelling and the detection of a possible concomitant compartment syndrome; and (7) whether single or multiple muscles are injured. Muscle contusions occur most frequently in the lower extremities, particularly involving the quadriceps mechanism.

               On an MRI examination, a muscle contusion is detected by abnormal signal intensity and morphology of the muscle. On spin-echo sequences, normal muscle demonstrates intermediate signal intensity on T1-weighted sequences and intermediate to low signal intensity on T20weighted sequences. Because hemorrhage infiltrates through the muscle, and mixes with the interstitial edema, it is not possible to separate it from the edematous muscle tissue. With a grade 1 contusion (i.e., microstructural fiber failure) there may be a slight increase in the size of the muscle and the margins of the muscle may have a feathery appearance due to the extension of interstitial edema into the perimuscular tissue. Edematous changes in the adjacent subcutaneous fat are also frequently detected. With a grade 2 muscle contusion (ie, partial tear) there will be a focus of disrupted muscle fibers in addition to the altered signal intensity from the interstitial edema and hemorrhage. A grade 3 muscle contusion will appear similar to a grade 2 contusion, except there will be complete disruption of the muscle fibers. With a muscle hematoma, there will be a focal accumulation of blood within a muscle. A hematoma demonstrates intermediate or high signal intensity on a T1-weighted sequence, depending on the chemical composition of the hematoma, and high signal intensity on a T2-weighted sequence. The sequelae of a muscle contusion may include muscle atrophy, fibrosis, calcification, or ossification.

Wednesday, December 5, 2012

Causality Assessment

Causality Assessment
Before making any impairment or disability determination, the physician is obligated to understand how an organ system (or body part under study) normally functions in the absence of disease. This is then coupled with a thorough understanding of the mechanism of the disease process under investigation. Causality is possible--ie, biologically plausible--if the nature of the adverse effects produced by a given physical, chemical, biologic, or psychological stressor is sufficient to alter the anatomy or physiology of the system or body part involved in a fashion that results in the disease under investigation. There also must be an appropriate temporal relationship between the alleged causal event and the disease manifestations. Furthermore, in situations where there is trauma, the mechanical forces involved must be sufficient to cause the alleged physiologic or anatomic stress.

               One should then look for studies supporting the causal relationship between the type of exposure or injury the claimant sustained and the disease process or injury under investigation in the medical literature. If they exist, the next step is to assess whether the epidemiologic and statistical principles used in these studies suggest that the causal association is real, or whether these studies are merely anecdotal or otherwise without scientific basis or validity. If the association between an exposure or injury and the postulated “effect” meets epidemiologic, physiological, and mechanistic criteria for imputing causality, or the injury is a clear sequela of direct trauma, it is then reasonable to assume that a causal relationship between an alleged exposure or injury and the disease process actually exists.

               These types of determinations must not be made solely on the basis of the claimant’s history. The medical records provide a more accurate and defensible history and must support the occurrence of the injury and the appearance of symptoms orsigns of pathology within a time frame that is consistent with the disease process under investigation. Those records from immediately after the injury are best for this purpose, as they are regarding the claimant’s status both before and after a trauma, and often provide the most accurate description of what actually occurred. Emergency room records, police and accident reports, and the employer’s report of occupational injury or disease (for workers’ compensation claims) are examples of documents that are particularly useful in this regard. If these records are not available or are ambiguous, it is best to describe the assessment of causality as provisional rather than definitive, even if the mechanism of injury, the physical examination, and the literature review indicate that a causal relationship may indeed be present.

               Combinations of direct trauma and a preexisting disease process are more difficult to assess for causality and apportionment. One must determine, again, if the requirements of temporal relationship, biologic plausibility, literature support, and sufficient injury have been met. This includes an assessment of whether the trauma would have caused the disease in the absence of the preexisting process or whether the injuries caused by the trauma or whether the injuries caused by the trauma or exposure would ordinarily decrease over time, because these answers provide grounds for apportionment. It is equally important to assess whether the trauma would have progressed on its own accord to a point where the claimant would have has the same clinical presentation; if so, one can argue that the accident only caused an acceleration of an inevitable process.

               When dealing with preexisting conditions, it is mandatory to examine all the records carefully, paying particular attention to the records of those providers who treated the claimant immediately after the accident. These are often the most accurate rendition of the incident and treatment that can be found. Records prior to the accident are even more critical, as they may be the only source of information regarding preexisting conditions. When there are no medical records from before and immediately after an accident, one cannot definitely establish that a causal relationship between current complaints and the accident exists--only that the claimant’s history supports the causal relationship. If the examiner believes that additional information, records, or tests are needed to support conclusions regarding relatedness, then it is necessary to state this and to describe exactly what information or testing is required.
               In conclusion, the examiner can only provide an accurate determination of causality if he or she applies accurate determination of causality assessment, within an objective framework, in which the claimant’s statements have validity only to the extent that they are supported by the medical records. In those instances where the medical records in inadequate, the examiner can make preliminary conclusions regarding causality, especially if the elements of temporal relationship and biologic plausibility have been met, but should reserve final judgment until the entire relevant medical record is available for review.

Monday, December 3, 2012



Little is known about the individual and societal economic burden of WAD. For instance, little is known about the prevalence of long-lasting work disability due to WAD, which probably the most costly part. This burden is probably largely dependent on the legislation in different countries. In 2002, an independent and temporary Commission on whiplash-related injuries was informed in Sweden, initiated by the four largest motor vehicle insurers. The mandate of the 3-year commission was an examination of the problems of WAD from road safety, medical care, insurance and societal aspects. One of the conclusions of the final report was that the yearly cost for society and for the insurance industry was approximately SEK 1.5 billion (US$201 million), while projected costs (i.e. what new cases of WAD arising in a particular year will cost society and insurers by the time the person reaches retirement age) amounted to SEK 4.6 billion (US$648 million). These calculations were based on an annual incidence of 30,000 WAD cases (324 per 100,000 inhabitants) in the year 2002. Since the report’s publication, the number of WAD cases have decreased dramatically to about 16,000 claims in 2008 (173 per 100,000 inhabitants), which, of course, has an impact on the overall costs.
Comparable data has not been found, but there is some evidence from a study that addressed the incidence of WAD in 10 European countries. The administrative data suggests that the total claims cost in Switzerland was 500 million Swiss francs (US$467 million). Switzerland’s population is 80% that of Sweden. Expenditures in addition to the claims cost was not reported in that study.

In summary, as in almost all other diseases and injuries, factors that are involved in the risk or prognosis of WAD are multifactorial and constitute a web of biological, psychological and social components.

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