Medical Systems recently held a lunch and learn at Lombardi’s Steakhouse in Appleton, Wisconsin at which hand surgery expert Jan Bax, M.D. discussed common hand injuries. During his presentation, Dr. Bax alerted attendees to a recent white paper from the American Academy of Orthopaedic Surgeons (“AAOS”) that reports a moderate level of medical evidence links computer use to the development of carpal tunnel syndrome (see p. 222). As Dr. Bax pointed out, the paper was published in the last couple of months so its ultimate effect in the worker’s compensation arena is undetermined. Nevertheless, Dr. Bax expressed concern that the paper will lead to renewed carpal tunnel syndrome claims based on repetitive computer use (keyboarding and mouse use). He noted this is especially troublesome because the hand surgery section of the AAOS considers it a settled issue that computer use does not cause carpal tunnel syndrome.
The white paper assigns levels of evidence supporting the various factors that are sometimes alleged to cause carpal tunnel syndrome. The highest level of evidence is “strong,” which requires consistent evidence from two or more high quality studies. The second highest level of evidence is “moderate,” which requires consistent evidence from two or more moderate quality studies or evidence from a single high quality study. This is the level of evidence the AAOS finds for the position that computer use causes carpal tunnel syndrome. The second lowest level of evidence is “limited,” which requires consistent evidence from two or more low quality studies, one moderate study, or insufficient/inconsistent evidence recommending for or against the diagnosis. The lowest level of evidence is “consensus,” which requires that there is no reliable evidence but rather is based on unsupported clinical opinion.
As Dr. Bax noted, finding that moderate evidence supports the link between computer use and carpal tunnel syndrome is troubling because it is actually is a high level of evidence and may sway triers of fact despite the nearly uniform position of actual hand surgery specialists that there is no such causal link. This is especially true given the findings in some of the research cited. Coggon, et al., specifically stated that there was an “absence of association with the use of computer keyboards” and noted this “is also consistent with the findings overally from other research.” The researchers concluded that “obesity and diabetes, and the physical stresses to tissues from the use of hand-held vibratory tools and repeated forceful movements of the wrist and hand, all cause impaired function of the median nerve” but that computer keyboard probably only focuses attention on symptoms without being injurious to the tissues of the wrist. Coggon, et al. seem to support a more nuanced relationship between computer keyboard use and carpal tunnel syndrome than is portrayed in the AAOS white paper. Likewise, Eleftheriou, et al. studied the link between computer keyboard use and carpal tunnel syndrome but related the following disclaimer:
One limitation is related to [the study’s] cross-sectional design which does not allow us to conclude if the association between cumulative exposure to key-board use is of causative nature. The study included workers present when the study was formed, which implies a possible selection bias as is the case in all cross-sectional studies, especially if the study population was affected by high turn-over. It’s a limitation of our study that we don’t have data on actual turn-over of the staff…Further, we didn’t control for possible confounding factors like anthropometric characteristics of the wrist…
Eleftheriou, et al. reported only “a possible association between cumulative exposure to keyboard strokes and the development of [carpal tunnel syndrome]…” They specifically noted that additional studies need to be done to verify their results and to address causality.
The AAOS white paper is a troubling development in carpal tunnel syndrome worker’s compensation cases since it potentially throws into question the settled opinion among hand surgery specialists that keyboard use does not cause carpal tunnel syndrome. As Dr. Bax noted at the recent Medical Systems lunch and learn, it is too early to tell exactly what the effects of the paper will be, though they are not likely to be positive. In the event that the AAOS white paper is cited to support work-related carpal tunnel syndrome cases among keyboard users, it will be critical to choose experts who understand and can explain the limitations of the evidence on which the paper relies. Without an expert who will vigorously question and thoroughly refute the evidence, the AAOS white paper is likely to carry more weight in keyboard-related carpal tunnel syndrome claims than it otherwise should.
It hurts. Yes it does. But what does that mean? Does it mean that I shouldn’t do it? Perhaps not. In fact, the inhibitory effects of pain can actually be deleterious to our health. Ordinarily, pain is a mechanism that helps us avoid injury, i.e. the classic nociceptive response to touching something that is hot. However, there are many cases in which pain can prevent us from doing things that are actually good for us. One such example is leg pain in peripheral artery disease.
The New York Times recently ran an article about leg pain and peripheral artery disease (“PAD”). PAD is essentially atherosclerosis in the extremities as opposed to the cardiac arteries. It causes many problems, including leg pain. Ironically, exercise is one of the recommended treatments for PAD (and the leg pain it causes), but many never pursue exercise because when a person with PAD starts exercising it causes more leg pain. Eventually, the leg pain diminishes, but the start of exercise precipitates an increase in pain. As the Times article reports, those who work through the pain generally experience both a decrease in pain and an increase in function. This is instructive for those of us involved in medico-legal claims, where complaints of pain often thwart a return to normal function.
Pain is often an intractable part of medico-legal claims. A person is involved in an accident or alleges an occupation-related condition, receives treatment (often surgery), and recovers physiologically from the injury. Unfortunately, this is not the end of the story. Instead of returning to full functionality, the person remains impaired and cites “pain” to explain the ongoing loss of function. For everyone involved in medico-legal claims, the problem of “pain” causing ongoing loss of function is incredibly frustrating. Pain does not, however, have to be an intractable problem.
The biggest hurdle to overcoming residual pain in the context of an injury claim is overcoming the normal response to nociceptive pain, which is the nervous system’s way of limiting physical harm. Think of the proverbial hand on a hot stove: the nerves send a pain message to the brain, you move your hand to avoid getting burned. Although the nociceptive response is marvelous for such acute tissue insults, it is not particularly useful for dealing with pain related to atrophy, deconditioning, or surgical changes to tissues. Nociception is not useful in this circumstances because pain is not a signal of the tissue-yielding associate with injury, but rather with the tissue-yielding necessary to rebuild strength and function that is lost with atrophy, deconditioning, and surgical changes to tissues. As everyone knows, increasing one’s activity level after periods of deconditioning results in soreness; however, everyone also knows that being sore should not prevent further workouts. If every person who lost fitness and wanted to regain it allowed pain to dictate their activity levels, few if any would ever become fit again. The same process obtains after the atrophy, deconditioning, and surgical changes that occur following injury and convalescence. Hence, it is perfectly normal for a person with an injury to experience pain with the rehabilitation that occurs after the injured or repaired tissues have healed. This pain is not injurious but instead is a normal part of the rehabilitation process.
Convincing persons with injury claims that the pain associated with atrophy, deconditioning, and surgical changes is normal during rehabilitation can be challenging but it is not impossible. A large part of the challenge lies in overcoming the natural human tendency to conserve energy. Put simply, basic survival requires that all living organisms (including humans) expend less energy than they take in. For contemporary Americans this is problematic because we do not have to expend much energy to meet our basic survival needs and we have access to a surfeit of relatively cheap calories. In other words, the contemporary American economy makes it easy for most Americans to be sedentary. If a person is accustomed to being sedentary, she already exists in a deconditioned state. Whether or not she intentionally avoids activity-related soreness matters little because she doesn’t experience it either way. Absent injury, she can maintain an inactive lifestyle and will, as we normally do, avoid doing things that cause pain. This state of deconditioning and pain avoidance, which are normal consequences of being human in much of America today, predisposes persons to have problems when rehabilitating an injury.
As noted above, the problem can be solved. First, treating practitioners should explain from the earliest opportunity that recovery requires effort and the effort itself with hurt. It is absolutely critical that injured persons understand recovery requires hard work and is almost always painful. Fair or not, this is normal and injured persons should expect it. Second, treating practitioners ought to have frank discussions about the role deconditioning will play in their injured patients’ recoveries. Doing so is not paternalistic, it is instead being honest. It is also critical in an era in which healthcare practitioners are increasingly being judged by patient outcomes. For example, being 50 pounds overweight will make recovery from an ACL tear harder because the rehabilitation will be physically taxing to many uninjured parts of the injured person’s body. Rehabilitation will tax the person’s cardiovascular system and the uninjured joints of the person’s back, hips, opposite knee, and ankles. Being deconditioned means rehabilitation will hurt more and be more difficult. Injured persons need to understand this going into rehabilitation.
Merely knowing pain will be part of rehabilitation is necessary but not sufficient to overcome the inhibitory effects of pain. Healthcare providers should demand that injured persons who undergo treatment demonstrate the ability to differentiate between pain associated with acute injury or harm and pain associated with rehabilitation, i.e. pain associated with increasing fitness. Surely knowledgeable physical therapists and other rehabilitation specialists should be able to demonstrate the difference in addition to explaining it. Healthcare providers should also demand that patients acknowledge that recovery from injury requires determination and that patients pledge to give full effort, even when experiencing the normal pain or discomfort associated with rehabilitation. Obviously there are limits to the binding effects of such a pledge, but it would help to put injured patients into the right mindset to tackle rehabilitation effectively and with full effort. Patients could also be told that their ability to receive rehabilitation services will depend on the effort level they give in therapy and in performing all recommended home exercises. This could easily be measured with periodic functional testing such as range of motion measurement, strength testing, and endurance testing. This would be no different than a spine surgeon refusing to perform a fusion on patients with a history of smoking until the patients can demonstrate that they have stopped smoking.
Obviously there are other issues that impact a medico-legal claimant’s ability to deal with residual pain from the claimed accident or occupational exposure. Dealing with all of these aspects would require more space and time than this blog allows. For example, everyone acknowledges that psychosocial factors play a large role in many claimants’ recoveries. In addition, motivation to return to work or full functionality plays a similarly large role. Nevertheless, the healthcare profession can do much to educate claimants on the difference between pain that signals injury and pain that signals recovery. As in peripheral artery disease patients who start to exercise, patients rehabilitating from an injury are almost certain to experience pain during rehabilitation. It is critical that the therapists and other healthcare providers involved in the rehabilitation process do everything in their power to prevent patients from giving anything less than full effort due to non-injurious and amorphous complaints of “pain.” Doing so will set claimant-patients on the right track to recovery and will help get them out of the mindset that pain justifies inactivity. Like the peripheral artery disease patients, claimants who get past the initial pain will find their condition to be much improved. And that is what everyone in medico-legal claims really wants.
Last week psychiatrist Jeffrey Zigun, M.D. and psychologist Brad Grunert, Ph.D. spoke at Medical Systems’ 2016 Advanced Medical Topics in Civil Litigation Symposium on mild traumatic brain injury. Three topics came up repeatedly during the individual experts’ presentations and in the follow-up panel discussion:
The answers to the first two of the three issues are surprisingly simple, while the answer to the third is, or at least can be, much more complicated.
With respect to the question of whether mild traumatic brain injuries can get worse over time, the simple answer according to the experts is “no.” Both Dr. Zigun and Dr. Grunert were clear in their statement that recovery from mild traumatic brain injury follows a predictable recovery. The physical injury to the brain itself reaches maximum medical improvement within a year and all expected improvements in functioning occur within two years of the injury. This is significant because a number of participants in the seminar reported scenarios in which a claimant/plaintiff experienced a precipitous decrease in functioning 12, 18, or even 24+ months after the initial injury. In at least some cases, the decrease in functioning was measured on neuropsychiatric testing and was deemed not to be malingering. Both Dr. Zigun and Dr. Grunert were clear in their presentations and in the panel discussions that such a decrease in functioning would not be due to an underlying mild traumatic brain injury, even if the injury were permanent. Brain injuries get better over time; they don’t yo-yo up and down or suddenly get worse after a period of improvement. Unfortunately, a decrease in functioning after a period of improvement can still be related to the accident. More on this later.
One of the more interesting aspects of the symposium was the discussions about the role of intelligence in recovery from a mild traumatic brain injury. The experts both stressed that intelligence is enormously important in assessing how individuals will recover from permanent mild traumatic brain injury. The reason is that those with more intelligence have more to lose before the loss of function becomes a significant impairment. The example Dr. Grunert used was an academic researcher: she may have some memory impairment following a mild traumatic brain injury, but it may only mean that she has to look up citations she previously had memorized. This will obviously add some time to her research, but it will not impair the quality of the research itself or her ability to write. On the other hand, a factory worker who has to follow a specific procedure when operating a dangerous machine will have no margin for error. If her memory was on the lower end of average to begin with, losing any amount of memory function could cause her to be unable to follow the specific procedure when operating machinery. Since there is no margin of error, the factory worker’s memory impairment would cost her the ability to do her job. Hence, one point both Dr. Zigun and Dr. Grunert made was that impairment following mild traumatic brain injury is often different for persons of high intelligence than it is for persons of lower intelligence.
The trickiest question the experts dealt with is how to determine the fact of a traumatic brain injury. In many cases a person hits their head and the symptoms of concussion are obvious. These might include brief loss of consciousness, dizziness, retrograde and/or anterograde amnesia, headache, wooziness, etc. In other cases the fact of injury might be less obvious. Perhaps the person did not strike their head in a motor vehicle crash, but reported some symptoms consistent with mild traumatic brain injury. Further complicating matters are cases where there is a preexisting history of psychological problems such as depression, anxiety, or other psychological diagnoses. In all cases, Dr. Zigun and Dr. Grunert stressed the importance of early neuropsychological testing. Dr. Grunert noted that neuropsychological testing has a high degree of reliability and specificity. In addition, neuropsychological testing is good at ferreting out malingering from legitimate claims. Early testing also establishes a baseline from which test results should not decline in mild traumatic brain injury.
As the experts and the audience discussed, often the fact of injury is not an issue at the beginning of a claim, though. Instead, the fact of injury becomes an issue after a year or more. Usually, this seems to occur as a result of a decline in functioning, whether supported through neuropsychiatric testing or not. As the experts agreed, simply because a person declines in functioning after a mild traumatic brain injury should have stabilized does not mean that they are not continuing to suffer from a permanent brain injury or that the decline in function is not legitimate or related to the accident. Both Dr. Zigun and Dr. Grunert agreed that a decline in functioning a year or more after a mild traumatic brain injury only means that the brain injury itself is probably not responsible for the decline in functioning. Instead, they pointed to psychological conditions as often being the culprit.
When the audience heard this, many persons wanted to know if the psychological conditions would be related to the accident, especially if there was a preexisting history. As Dr. Zigun noted numerous times, it depends. For example, Dr. Zigun addressed the simple fact that many of the drugs used to treat psychological conditions also have positive effects on the sequelae from traumatic brain injury. Take SSRIs, commonly used to treat depression. Dr. Zigun pointed out that one symptom of depression is memory impairment, which is also a symptom of mild traumatic brain injury. SSRIs help alleviate memory impairment in both depression and mild traumatic brain injury. Dr. Zigun noted that if a person is diagnosed with mild traumatic brain injury, they may very well end up on an SSRI. Once the brain injury stabilizes, the person may be weaned off the SSRI. However, if the person has simultaneously developed depression, weaning her from the SSRI may cause a decrease in functioning related to the depression, including worsening memory impairment. Both experts agreed that the decrease in functioning in such a case could be legitimate but that it would not be related to the mild traumatic brain injury.
How, then, can we determine if a decline in functioning relates to the accident? The answer, unfortunately, is not clear cut. The experts stressed that to evaluate whether a decline in functioning, once determined to be legitimate and not malingering, relates to an accident, the analysis essentially looks to the totality of the circumstances to attempt to parse out the causal factors. The case a number of audience members brought up was the situation in which there is a preexisting history of a psychological condition such as depression which is determined to be the reason for the post-accident decline in functioning. Dr. Zigun and Dr. Grunert agreed that it is exceptionally difficult to determine whether the development of a psychological condition is accident-related. They noted that many factors could cause the onset of depression episode that would be related to the accident. For example, if the mild traumatic brain injury caused a memory impairment that prevents the injured person from returning to work, it would not be unusual for the person to develop depression. The depression would not be caused by the brain injury itself, but rather would be the result of the job loss, which resulted from the brain injury. On the other hand, if the injured person has recovered well and is coping with any residual impairments from the brain injury, the depression is likely to be independent of the brain injury. The bottom line is that declines in psychological functioning in the context of a permanent mild traumatic brain injuries present challenging cases for experts in which causation can only be determined by assessing the totality of the circumstances.
Mild traumatic brain injuries can present vexing cases for claims professionals. As Dr. Zigun and Dr. Grunert discussed, mild traumatic brain injuries can be diagnosed and treated effectively, even in the case of concomitant psychological conditions. We are grateful for their participation in Medical Systems’ 2016 Advanced Medical Topics in Civil Litigation Symposium and for the many insights they shared with our audience.
Osteoarthritis of the knee is the bane of many worker’s compensation claims. Frequently, an injured worker demonstrates evidence of arthritis but claims an acute event aggravated the condition to the point that it was symptomatic. What can be frustrating for the employer or insurance carrier is the fact that in most cases the arthritis itself was not caused by the employment. Thus, the employer or insurance carrier laments the fact that they are being held responsible for 100% of a condition that would have almost certainly become symptomatic regardless of the acute work-related event. Unfortunately, to date there has been no reliable method to measure whether this is accurate or, if so, when the arthritis would have become symptomatic. However, a recent study suggest we may have technology to do just that.
A group of Finnish and Swedish researchers released “A Novel Method to Simulate the Progression of Collagen Degeneration of Cartilage in the Knee” in which they developed a “degeneration algorithm … combined with computational modeling” that accurately predicted the rate at which knee cartilage would deteriorate based on the weight of patients. The study was conducted on 429 patients under 65 years of age who initially had no radiographic evidence of osteoarthritis (cartilage thinning) in their knees. The subjects were divided into a study group, consisting of patients with a BMI of 35 or higher, considered to be at high risk of developing weight-related osteoarthritis of the knee, and a control group, consisting of patients with a BMI lower than 25, considered to be of low risk for developing weight-related osteoarthritis of the knee. As noted, neither group demonstrated radiographic evidence of osteoarthritis at the beginning of the study nor had any member of either group sustained a knee injury that either prevented them from walking for more than 2 days or required surgical intervention. The 2 groups were then followed for 4 years.
The researchers developed an algorithm to predict the rate at which cartilage loss associated with osteoarthritis would occur based on BMI and other physiological characteristics. In their words, “[t]he algorithm was based on cartilage overloading so that cumulatively accumulated excessive stresses (above failure limit) caused alterations in tissue properties with time.” The researchers then developed a computational program to simulate the expected cartilage loss over four years based on the baseline status of knee cartilage from MRI readings. The accuracy of the algorithm and computational modeling was measured against x-rays taken at the beginning of the study and after 4 years. The results demonstrated the ability of the algorithm and modeling to accurately predict which subjects would experience loss of cartilage associate with osteoarthritis and how much loss each subject would experience. According the study, “[t]he simulated onset and development of osteoarthritis agreed with experimental baseline and 4-year follow-up data.” This lead researchers to conclude that, “[t]he present work provides…an important and groundbreaking step toward developing a rapid and subject-specific diagnostic tool for the simulations of the onset and development of knee osteoarthritis and cartilage degeneration related to excessive chronic overloading due to overweight [sic].”
The implications of this individualized ability to predict the onset of knee arthritis could be significant for worker’s compensation. If the method proves to be accurate and reliable in subsequent studies, it could be used in the same manner as occupational hearing tests to measure a baseline condition and determine if the subsequent condition is related to the normal progression of the disease versus an occupational aggravation. Likewise, the method would offer the potential to calculate, based on an employee’s physical condition on the date of injury, the likelihood that the alleged employment-related event aggravated the underlying arthritis and if so how much the employment-related event is responsible for. This would finally allow for an accurate accounting of what portion of a preexisting degenerative condition is related to an industrial event and what portion is due to the natural progression of the condition. While this would admittedly be at best a distant possibility, it is nevertheless a possibility. Hence, the study and its future applications are worth following.
As our readers are no doubt aware, Governor Walker recently signed Act 180, Wisconsin’s agreed upon worker’s compensation bill. Included in the bill is the newly created Wis. Stat. §102.175(3), which mandates that health care providers apportion permanent disability in accidental injury cases between disability caused by the injury and disability caused by other factors, both pre- and post-injury.
Medical Systems is taking a number of steps to ensure our reports comply with the new apportionment rule. First, we have notified all of our Wisconsin experts of the new requirement and explained the specific circumstances in which it applies. As a part of this process we have also had conversations with experts who have begun encountering apportionment questions to ensure that they understand the process. Second, we are reviewing all IME reports to determine if the expert has addressed apportionment when the expert has found permanent disability arose in an accidental injury case. Finally, we are communicating with our clients on accidental injury cases to ensure that our reports meet the new apportionment requirements.
At Medical Systems, we know that an independent medical examination has the potential to make or break a claim. That’s why we are doing everything in our power to produce reports that are not only well-reasoned, but also are up-to-date with applicable legal standards. Addressing apportionment in Wisconsin accidental injury worker’s compensation cases is a prime example of our continuous efforts to work with our clients to provide the best possible report.
On February 29, 2016 Governor Walker signed the agreed upon worker’s compensation bill. Of particular importance to the IME process is a provision (Wis. Stats. §102.175(3)) that requires all healthcare providers, whether treating providers or independent evaluators, to apportion permanency in accidental injury cases between permanent disability that the injury caused and permanent disability caused by other factors, whether pre- or post-injury. Wis. Stats. §102.175(3)(b) states:
A physician, podiatrist, surgeon, psychologist, or chiropractor who prepares a certified report under s. 102.17(1)(d). relating to a claim for compensation for an accidental injury causing permanent disability that was sustained in the course of employment with the employer against who compensation is claimed SHALL address in the report the issue of causation of the disability and SHALL include in the report an opinion as to the percentage of disability that was caused by other factors, including occupational exposure with the same employer, whether occurring before or after the time of injury. (Emphasis added)
The statute does not apply to occupational injuries and specifically holds the employer responsible for “previous permanent disability… attributable to occupational exposure with the same employer.” Wis. Stats. §102.175(3)(a). The statute does, however, require injured workers, at the request of the employer, to “disclose all previous findings of disability or other impairments that are relevant to that injury.” Wis. Stats. §102.175(3)(c). This should help make the implementation of the provision more effective.
The new statutory provision requires all independent medical examiners to apportion permanent disability (when the expert concludes the injury resulted in permanent disability) in accidental injury claims. The effective date of the statute is March 2, 2016. Medical Systems is working with our experts to ensure that their opinions comply with the new statutory provision and apportion permanency when applicable starting March 2, 2016.
Pain. We all experience it, but what is pain? Certainly pain has a nociceptive component, meaning when we experience injury our nerves send a message to our brain that results in the state of awareness that may be best characterized by the word “ouch.” This is the type of pain that seems best controlled with traditional analgesics such as prescription opioids. Pain may also be neuropathic, meaning it is not the resulted of an injured tissue sending a classic pain signal to the brain but rather is the result of a damaged nerve that is sending abnormal signals to the brain due to the injured state of the nerve itself. This is why persons with neuropathic pain experience paresthesia and hyperesthesia rather than the typical stabbing or aching pain that would associated with physical injury to a muscle, bone, or joint. Chronic pain also differs from neuropathic and nociceptive pain in that it appears to be a learned cognitive response to a patho-anatomic abnormality that may or may not be causing actual nociceptive pain. Further complicating the range of pain that we experience is psychological pain; that is the somatization of psychological distress.
A new Psychological Science study (subscription required) throws a new wrench into the pain picture: persons in financial distress who are also in pain feel higher levels of pain than those are not experiencing economic distress. According to the study,
The link between economic insecurity and physical pain emerged when people experienced the insecurity personally (unemployment), when they were in an insecure context (they were informed that their state had a relatively high level of unemployment), and when they contemplated past and future economic insecurity.
Interestingly, the authors concluded that “the psychological experience of lacking control helped generate the causal link from economic insecurity to physical pain.” This offers some hope that addressing the feeling of lacking control could help to lower the perceived experience of pain.
In the claims context, the experience of pain is a major cost-driver. Persons who experience pain will continue to seek treatment for injuries that have otherwise resolved or stabilized. In addition, persons who experience pain often miss time from work and have other disability-related costs. What complicates the apparent relationship of economic insecurity and pain in the claims context is that persons with claims often experience economic insecurity related to the claimed injuries. For example, an employee suffers a work-related knee injury and has to miss time from work. Even a conceded claim can cause financial distress as compensation benefits are paid out at 2/3 of average weekly wage and the injury may force the employee to miss overtime they expected to work. Matters get worse when a claimant is cut off from benefits but claims ongoing injury and an inability to return to work. In many such cases, claimants lack the savings or other sources of income replacement to weather the economic storm.
The problem from a claims perspective is that the economic situation of the claimant is outside the purview of the claim. For example, if a claimant alleges a work-related low back injury and the insurer questions whether the condition is in fact related to the employment, the insurer will have the claimant undergo an independent medical examination. If the independent medical expert concludes that the claimant’s condition is not related to her employment, the insurer will stop paying benefits to the claimant. At the same time, if the claimant is under work restrictions from her treating physician, she will not be able to return to work. As a result, she will lose her temporary total disability benefits while simultaneously having no recourse to income from her employment. If the Psychological Science study tells us anything, it is that losing temporary total disability benefits without other sources of income or income replacement will likely make the claimant’s physical condition worse. This can be a particularly fraught situation if the claimant is suffering from a degenerative condition that would wax and wane in severity even without economic distress. The study suggests that such a condition could be appreciated as being significantly worse in a claimant who is in economic distress. From a cost perspective, this is a problem because it will almost certainly lead the treating physician to conclude that conservative therapy failed to treat the condition. Concluding that conservative therapy failed often leads to a referral to a surgeon or the recommendation of surgery. All of a sudden, a condition that should be manageable with periodic noninvasive treatment and over-the-counter analgesics, becomes an intractable problem for which surgery is seen as the only option. And surgery is expensive.
If a claim reaches this point, it may be fairly stated that the reason conservative therapy failed and that surgery is being proposes is not due to the condition itself, but rather to the claimant’s financial distress which renders a normally tolerable condition into an intolerable one. The claimant’s financial distress is obviously related to the claim, but is not something over which the claims professional has control. The claims professional is not obliged to follow the recommendations of the IME doctor, but it would be highly unusual for a claims professional to continue to award benefits when she does not have to. The claims professional is not responsible for the claimant beyond the four corners of the claim. Except the decisions of the claims professional within the claim can have, as the study shows, consequences outside the four corners of the claim that can seep back into the claim. As such, it seems prudent for claims handlers to be aware, even if they have little control or choice, that the decision to deny benefits to a claimant can have the perverse effect of making the claim worse (from a cost perspective) than it would otherwise have been. At least then it will not be a surprise when the person with ordinary degenerative disc disease ends up with a fusion, failed back syndrome, and a claim for permanent total disability benefits.
When we think of traumatic brain injury, we typically think of symptoms primarily related to cognition and executive function. Hence, we expect to see memory deficits, difficulty concentrating, and difficulty regulating emotions. We associate the brain with thinking so we often focus on the symptoms related to thinking despite the fact that traumatic brain injury can cause a host of physical symptoms as well.
One of the most troubling physical symptoms is the potential for traumatic brain injury to disrupt the body’s circadian rhythm, or its normal sleeping/waking cycle. According to a 2012 Public Library of Science study, traumatic brain injury, “disrupts the oscillatory expression pattern of several circadian clock and clock-associated genes” in the areas of the brain primarily responsible for regulating the sleep/wake cycle (the suprachiasmic nuclie, or SCN, and hippocampus). In short, traumatic brain injury interferes with our ability to sleep normally. Interestingly, this sleep-impairing aspect of traumatic brain injury has effects on our cognition:
Since the hippocampus mediates learning, memory and cognition, and diurnal regulation by the SCN is essential for proper hippocampal function, disruption of the oscillatory gene expression patterns in these two brain areas seems likely to play a role in the long-term cognitive effects of TBI.
In short, if you don’t sleep normally you don’t think normally. This is problematic for other reasons also since sleep disruption is known to increase the likelihood of developing depression, bipolar disorder, diabetes, hypertension, and metabolic disorders.
The wide-ranging and myriad effects of traumatic brain injury make it essential to obtain an accurate diagnosis early in the process to ensure that the best available treatment is offered. While at least 80% of persons with mild traumatic brain injury will experience a complete recovery, there is small but nontrivial subset of patients whose symptoms will persist as chronic problems. If we are going to administer traumatic brain injury claims effectively, it is imperative that we understand many of the effects from traumatic brain injury are not primarily cognitive in nature but rather are physical.
To learn more about how the physical, cognitive, and psychological aspects of traumatic brain injury relate, check out Medical Systems’ 2016 Advanced Medical Topics in Civil Litigation Symposium on April 7, 2016.
There are certain medical procedures that are so common in worker’s compensation that we don’t give them a second thought. Partial meniscectomy is among them. Most people assume that an employee with a torn meniscus who is experiencing catching and locking in their knee should have a partial meniscectomy to treat the symptoms, regardless of whether we think the meniscus tear is work-related. Turns out that our assumption might be wrong.
The Annals of Internal Medicine published results from a study (subscription required) which found that arthroscopic partial meniscectomy is ineffective for relieving catching and locking symptoms in the knee. The study was conducted on a group of patients with medial knee pain who had confirmed meniscus tears without evidence of arthritis. The participants in the study were randomly assigned to either the treatment group, which received the partial meniscectomy, or a control group, who received a sham arthroscopy. Participants were not aware of which group they were in to control possible bias.
The results of the study were surprising because in every reported measure, the patients undergoing the sham procedure reported fewer mechanical symptoms post-surgery. The most impressive results were among those patients reporting that they were symptom free following the procedure. Among this group, only 28% of the participants undergoing the actual partial meniscectomy reported being symptom-free while 41% of the participants who underwent the sham procedure reported being symptom-free. The study’s authors were quick to note, however, that trauma-related meniscus tears causing mechanical symptoms in persons under 35 do respond well to partial meniscectomy. On the other hand, they pointed out that “in a degenerative knee, seemingly similar symptoms may not even be caused by the meniscal tear - more likely they are a reflection of the overall deterioration of the knee and prone to increase as arthritis develops further.”
In the worker’s compensation context, the dispute is typically whether a meniscus tear is traumatic or degenerative. Regardless, the ineffectiveness and the possibility that the symptoms might be “a reflection of the overall deterioration of the knee and prone to increase as arthritis develops further” is a good reason to tread cautiously when an employee is diagnosed with a meniscus tear. If the employee’s meniscus tear is degenerative in nature, there is a strong likelihood that a partial meniscectomy will have a temporary benefit at best and in the long run will not ameliorate or slow the progression of degenerative arthritis. Hence, a meniscus tear in an older worker that is deemed to be work-related is highly likely to become an arthritic knee that will need to be replaced. And despite the fact that it is bad medicine and bad science, the arthritis is likely to be blamed on the meniscus tear even though the arthritis was probably the problem in the first place. Hence, it behooves every claims professional to take a serious look at meniscus claims and to defend them vigorously now that we know the proposed surgery may very well not work and may very well lead to additional (more costly) claims.
A Journal of the Royal Society of Medicine article analyzed paintings of Michelangelo and concluded that the famous artist suffered from degenerative arthritis. In related news, Michelangelo’s estate filed a claim against the Vatican in Wisconsin for TTD and PPD benefits, alleging the arthritis was due to repetitive trauma from the many painting and sculpture commissions the artist received from the Roman Catholic Church during his life. Regarding the reason for filing in Wisconsin, lawyers for the estate said “We’re pretty sure the Wisconsin statute of limitations on this one hasn’t expired yet.” As to whether Wisconsin is an appropriate venue, the lawyers noted “We’ll figure out a way to keep it here. The Milwaukee Art Museum holds a Michelangelo sketch, Studies of the Medici Madonna. We think that will be enough.”