Seminars and Continuing Education


Post-traumatic stress disorder (PTSD) is a condition of persistent mental and emotional distress occurring as a result of injury or severe psychological shock, typically involving disturbance of sleep and constant vivid recall of experience, with dulled responses to others and to the outside world.  Symptoms typically include nightmares or flashbacks, avoidance of situations that bring back the trauma, heightened reactivity to stimuli, anxiety or depressed mood.  The condition may last months or years, with triggers that can bring back memories of the trauma accompanied by intense emotional and physical reactions.  PTSD is fairly common in the US; more than 3 million cases are diagnosed per year. 

Of motor vehicle accident survivors, 9% develop PTSD.  Research conducted to identify at-risk individuals disclosed the following:

Pre-existing factors for the likelihood of development of post motor vehicle accident PTSD include:

  • Poor ability to cope in reaction to traumatic events
  • The presence of a mental health problem (most commonly depression)
  • Poor social support

Accident related variables:

  • Seriousness of physical injury
  • Loss of significant others

Post-accident predictors are:

  • The rate of physical recovery from injury
  • Level of social support
  • Level of active re-engagement in work and social activities

The difference between MVA-related PTSD is an increased likelihood of being injured or developing chronic pain syndrome.  As a result, many people rely on their primary care physicians for treatment and do not seek out psychological treatment for some time.  It is important to identify PTSD symptoms early and seek appropriate psychological treatment so symptoms to not become chronic.

Behavior therapy, cognitive therapy and medications have proven effective for treating MVA-related PTSD.  It may also be useful for the claimant to work with a chronic pain specialist to help manage the physical pain caused by injury.  These treatments can be provided in conjunction with one another.

To learn more about Post Traumatic Stress Disorder in Civil Litigation, register for our complimentary luncheon presentations by Terence Young, PsyD, a Board Certified Neuropsychologist scheduled to take place on October 19th at Rare on the Square in Madison, and October 26th at the Capital Grille in Milwaukee.  See our Seminars/Events page for more information and to register.  These presentations will offer CLE credit and space is limited, so register today!

In the UK, the “whiplash capital of Europe,” for every single accident reported, there are 2.7 claims for whiplash damages.  In the United States, whiplash injuries make up for 25% of payments made by insurance companies, with approximately $2.7 billion being paid out annually.  So, it is clear that whiplash is a claim to be reckoned with.

So, what exactly is whiplash?  Whiplash is caused by the head’s jerking action pulling muscles and ligaments beyond their typical range of motion, causing fibers to tear.  Torn fibers in muscle or tendon is termed a “strain.”  If it involves a ligament, it is referred to as a “sprain.”  Whiplash often involves a combined strain and sprain.  A whiplash injury can involve cervical muscles, intervertebral joints, disks, ligaments and/or nerve roots.  Most often it is limited to soft-tissue injury.  However, whiplash injuries can be complex and could include many related problems such as joint dysfunction, disk herniation, nervous system problems, chronic pain, and cognitive dysfunction.

Symptoms of whiplash become apparent usually within the first 24 hours following the accident, but typically appear within the first six to 12 hours.  Symptoms can continue to get worse days after the injury.  Common symptoms often include neck pain and stiffness, and headaches that usually start at the base of the skull.  Other symptoms might include:  dizziness, pain that hurts more with neck movement, fatigue, loss of range of motion in the neck, tingling or numbness in the arms, and/or tenderness or pain in the upper back, shoulder or arms.

Risk factors for whiplash include degenerative disease, pre-existing health problems, vehicle size, headrest position, position of head at impact, and age.  Women and children are more seriously injured then men because they have smaller necks.  Not using the shoulder harness and failure to wear a seatbelt greatly increase the risk of whiplash injury.

So, how is whiplash treated?  Usually, recovery is complete within the first few months, though some people experience ongoing symptoms.  Generally, symptoms that extend beyond six months are considered chronic.  Typically, treatment includes pain medication and special exercises to help increase range of motion in the neck.

Here are some interesting facts about whiplash:

  • A cervical spine soft tissue injury can occur in a motor vehicle traveling at only 5 miles per hour
  • Most injuries occur at speeds below 12 miles per hour
  • Crashed vehicles can often withstand collision speeds of 10 miles per hour with no damage
  • It is normal for a delay in the onset of whiplash symptoms, which means someone could say they weren’t hurt at the time of accident and then complain of pain later
  • Mild traumatic brain injury can be the result of a whiplash-type injury
  • Up to 10% of whiplash patients become totally disabled
  • Studies since 1956 show that over 60% of whiplash injuries required long-term medical follow-up

Want to learn more about Whiplash?  Register to attend the 2017 Advanced Topics in Civil Litigation.  For more information or to register, click here.


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.  


  1. Can traumatic brain injuries get worse over time?









I do beguile the thing I am by seeming otherwise.

-Iago in Othello, II.2.122-3.

Shakespeare’s Othello, while ostensibly about the titular character and his wife, Desdemona, centers on English literature’s most notorious and effective liar, Iago, a character so perplexingly foul as to cause Samuel Taylor Coleridge to describe him as “motiveless malignity,” evil for only evil’s sake.  Since most of us have long since forgotten our high school and college lit classes, a brief recap:  Othello saves Venice from a Genoan invasion and is elevated to general.  He also wins the heart of the Doge’s daughter, Desdemona, and marries her.  Iago ostensibly hates Othello because he passed him over for a promotion to lieutenant.  He hatches a plan to convince Othello that Desdemona is unfaithful, which he successfully executes through a series of lies and half-truths, manipulating the other characters like a puppeteer.  Iago ultimately convinces Othello that Desdemona is unfaithful, whereupon he kills her and commits suicide (the play being, after all, a tragedy).

To Coleridge, the greatest imaginable horror is not the overtly hostile brute, but rather the deceiver.  The reason is that the challenge of the hostile brute, while perhaps significant, is open and obvious.  We know what to expect and can prepare to deal with it.  The deceptive person is exponentially worse because we often have no idea that we are being deceived or that the person is deceptive.  We have no chance to prepare because we have no expectation of malfeasance or misbehavior.  Hence, in the play Othello unwittingly considers Iago to be his truest friend while Iago leads him to his demise. 

Human biology suggests Coleridge was right to fear liars.  We became spectacularly successful because of our ability to cooperate and trust one another.  It is how we went from hunter-gatherers to denizens of today’s massive and massively complex technological society.  Deceit directly assaults our social nature and causes us to question the motives of everyone with whom we interact.  This is particularly harmful for social beings whose existential success depends on cooperation.  As a result, our inherently social nature makes us particularly poor at detecting deception.

Despite the fact that we are not very good lie detectors, we often think that we are. While liars are popularly depicted as either furtive bundles of nerves and sweat or overconfident and suave psychopaths, in truth all persons lie to varying degrees and there is no one personality type that is particularly adept at being deceitful.  Studies generally find that we are poor lie detectors.  We often think that traits like Machiavellianism, psychopathy, or narcissism make a person a more effective liar; however, research finds that persons having these personality traits are neither particularly effective liars nor particularly effective lie detectors.  About the only things we know for sure about lying are that, “the ability to lie well correlates with an ability to better detect deception in others; and the control of response latency difference when lying may be the key to producing successful lies and detecting those lies in others.”  Contrary to media portrayals, liars cannot be stereotyped.  Also, the popular belief that persons lying give off telltale signs of deception is simply untrue.  If a person wants to lie, chances are no one will notice. 

The problem of deceit in traumatic brain injury is particularly vexing since there are limited objective measures available to differentiate between legitimate claims and malingering or symptom magnification.  To give an idea of the scope of the problem, research has demonstrated symptom magnification or malingering likely occurs in about 40% of mild head injury claims.  This presents difficulties for both insurers and legitimately injured claimants.  Insurers are understandably wary of paying claims for which little or no objective evidence exists and high rates of symptom magnification and malingering exist.  Claimants get frustrated when insurers question their claims because they suffered an injury for which limited diagnostic tests are available.  Both insurers and claimants would be served best if there was a reliable way to differentiate legitimate traumatic brain injury from malingering or symptom magnification.  The question is whether there is such a reliable way to do so.

The good news is that advances in neuroimaging are beginning to differentiate how physically injured brains function versus uninjured brains and brains of persons with psychological conditions.  For example, a July 2015 study published at PLoS ONE described differences in single photon emission computed tomography (“SPECT”) scans between persons suffering from traumatic brain injury versus posttraumatic stress disorder.  The study specifically concluded that “hypoperfusion in the orbitofrontal cortex, temporal poles, and anterior cingulum are consistent with the most frequent findings in the TBI literature” while “increases in the limbic structures, cingulum, basal ganglia, insula, thalamus, prefrontal cortex, and temporal lobes” were noted in subjects with PTSD.  The authors report that SPECT scans may be able “to differentiate TBI from PTSD with sufficient sensitivity, specificity and accuracy to incrementally enhance clinical decision-making.” 

The bad news is that we are just at the cusp of the neuroimaging revolution.  This means doctors cannot simply order a SPECT scan (or any other imaging study) and state to a reasonable degree of medical certainty whether a particular patient is suffering from a particular condition based on the results of the scan.  More research will be needed before imaging studies can be relied on to differentiate between the fact of injury and the type of injury being claimed.  Though the news on the neuroimaging front is encouraging, until it becomes medically accepted as a diagnostic tool we will have to rely on clinical examination and testing to assess whether a particular patient is suffering from a TBI, a psychological injury, or is attempting to deceive us.

So can we determine if a claimant is trying to deceive us with clinical examination and testing?  First, it is useful to define exactly what malingering is.  According to the American Psychiatric Association, malingering is “the intentional production of false or grossly exaggerated physical or psychological symptoms motivated by external incentives…”  In the case of malingering in a personal injury claim, the external incentive is to obtain compensation from the tort system.  It is also useful to know that the vast majority of mild traumatic brain injury resolves within 6 months.  Most mild traumatic brain injuries are unremarkable events that are self-limiting and require little active care.  In most cases, a person suffering a mild traumatic brain injury will get better no matter what they do and whether they seek treatment or not.

The symptoms of traumatic brain injury are nonspecific and include memory loss, attention deficits, mood changes, anxiety, and headache.  These symptoms are also present in psychological conditions such as depression and PTSD and are so nonspecific as to be easily feigned.  Fortunately, neuropsychological testing “can identify those who exaggerate or fake with moderately high levels of sensitivity and specificity.”  One of the chief ways of detecting feigners is through the use of tests or indices that measure effort or intentional failure.  These include the Test of Memory Malingering (“TOMM”), the Word Memory Test, the Computerized Assessment of Response Bias, the Portland Digit Recognition Test, and the Victoria Symptom Validity Test.  For example, the TOMM has been found to have a 100% positive predictive power (the likelihood that a person has the condition when a test detects the condition) and a 90% negative predictive power (probability that a person does not have the condition when a test does not detect the condition).  Researchers noted that “these statistics indicate that we can be 90% confident that a person gave good effort when he or she scored above the suggested cutoff value (for suboptimal performance).  On the other hand, when a participant scored below the cutoff, we can have 100% confidence that he or she performed suboptimally.” 

Interested in learning more about traumatic brain injuries and how to tell legitimate claims from illegitimate ones?  Attend Medical Systems’ Advanced Medical Topics in Civil Litigation Symposium where Dr. Marc Novom and Dr. Brad Grunert will tackle traumatic brain injury from medical and psychological perspectives to give you their insights on how they analyze these claims and what you can do to manage them more effectively.

What is it about shoulders?  They seem to cause an inordinate amount of problems, especially when the rotator cuff is involved.  And invariably, there is a question as to whether a shoulder claim involves an acute injury, an acute aggravation of a preexisting condition, an occupational injury, or the mere manifestation of a preexisting condition.  One of the biggest challenges in claims is determining whether and to what extent a shoulder condition is work-related.  Unfortunately, this task is often difficult for physicians too.

The hallmark of an acute rotator cuff injury is an asymptomatic shoulder, a discernible traumatic event, and immediate pain and weakness.  Unfortunately, this type of presentation accounts for less than 10% of all rotator cuff tears according to some literature.  In addition, the medical literature suggests that acute rotator cuff tears are underdiagnosed in emergency departments and often attributed to tendonitis, bursitis, arthritis, or some combination of all three.  To further complicate matters, many other conditions of the shoulder, cervical spine, and peripheral nerve system can produce symptoms that are similar to symptoms occurring in rotator cuff tears.  And finally, a somewhat sizable percentage of the population has asymptomatic rotator cuff tears which makes the determination of the etiology of the cuff defect difficult to determine.

The best way to assess whether a rotator cuff tear is acute or traumatic is with diagnostic imaging.  Numerous studies have found that mid-substance tears are more likely to be acute than insertional tears.  The presence of swelling and joint fluid or a hematoma also suggest that a tear is acute.  To the contrary, the absence of joint and bursal fluid suggests a chronic tear.  The presence of fatty infiltration and the degree of rotator cuff atrophy are also useful findings to assess the chronicity of the tear.  Interestingly, at least one study found that the “injury mechanism and the activity at the moment of injury did not correlate with the presence of a rotator cuff lesion,” but also found “a strong age correlation, with a prevalence of RCTs above 50% in patients aged over 50 years…” This study suggests a shockingly high rate of rotator cuff injury resulting from shoulder trauma in persons over 50. 

The strong correlation between age and rotator cuff tear caused one study’s authors to postulate that “it is even likely that there [is] no such thing as an acute cuff tear without some previous tendon degeneration.”  The authors of another study address the complicated relationship between the chronicity and symptomatic nature of rotator cuff tears and note that the “duration of symptoms does not necessarily reflect the duration a patient has had a rotator cuff tear…  It is not understood why full-thickness tears become symptomatic in some individuals and not others.”  How then, can any physician determine to a reasonable degree of medical certainty if a particular rotator cuff tear relates to the patient’s employment in the absence of diagnostic imaging that suggests a tear is acute?

In truth, the answer is that any physician who attributes a symptomatic rotator cuff tear to a workplace injury is most likely engaging in speculation if there is no acute traumatic event and no diagnostic imaging evidence demonstrating that the tear is acute.  This doesn’t mean that the tear can’t be acute and work-related, simply that there is no reasonable basis for a physician to determine the exact etiology of the tear to a reasonable degree of medical certainty.  In handling claims, it is important to recognize these situations and pose the question to the IME doctor directly as to there is any way, given the current state of evidence-based medicine, to determine what caused a rotator cuff tear (or caused it to become symptomatic) to a reasonable degree of medical certainty in the absence of an acute traumatic event, diagnostic imaging evidence that a tear is acute, or occupational risk factors such as repetitive overhead work.  If there are no specific risk factors, no precipitating injury, and no diagnostic imaging evidence of an acute tear, the answer should always be “no.”

From a claims perspective, there are several useful things that can be gleaned from the medical literature addressing rotator cuff conditions.  First, a definitive assessment of causation in the absence of a discrete, acute precipitating event with imaging evidence demonstrating the presence of an acute tear or an occupational risk factor should be considered impossible.  Of course treating surgeons will attempt to relate rotator cuff conditions to workplace injuries that do not meet the above criteria, but it is incumbent from a claims perspective that the IME physician points to the relevant medical literature and explains why it is not possible, to a reasonable degree of medical certainty, to determine the etiology of a rotator cuff tear in the absence of the above criteria. 

Second, it should not come as a surprise if an employee over 40 who says they hurt their shoulder and is told that it is just a strain or tendinitis when they go the ER later discovers she has a rotator cuff tear.  The medical literature suggests that clinical examination in the emergency setting underestimate the presence of rotator cuff tears.  The relevant study found that in the patient population complaining of an acute shoulder injury who have an inability to perform active abduction above 90° and normal radiographs, more than 50% will have rotator cuff tears.  In establishing reserves, if the medical records show normal radiographs coupled with an inability to actively abduct the shoulder above 90°, it may be wise to consider the likelihood of a rotator cuff tear requiring surgical intervention to be 50%. 

Finally, knowing the different shoulder, neck, and peripheral nerve conditions that have similar symptom constellations to rotator cuff tear will help to assess what the likely diagnosis will be based on the clinical history, examination, and positive findings.  Thus, a shoulder complaint that can be localized to the acromioclavicular joint, is more likely to be a shoulder separation or acromioclavicular arthritis than a rotator cuff tear.  In another example, a complaint of gradual onset of shoulder pain with weakness that is especially noticeable during sleeping hours is likely to be a chronic rotator cuff tear or advanced impingement syndrome than an acute rotator cuff injury.

The bottom line is that shoulder injuries are often difficult claims, especially when they involve rotator cuffs.  Knowing the medical literature about how rotator cuff tears occur and what suggests acute versus chronic tears can help guide the claims analysis.  To learn more about the diagnosis, management, and prognosis of rotator cuff tears, join us on February 26, 2015 for the Medical Systems Advanced Medical Topics in Worker’s Compensation in Brookfield, Wisconsin at which Dr. Bartlett will give an in-depth presentation on acute shoulder injuries.  Claim handlers and legal professionals alike will gain valuable information on what claims will likely be compensable and what medical information can be used to defend against those which should not be compensable.

The employee is a delivery driver and is in a rollover accident.  Miraculously she suffers only minor injuries in the crash.  However, she hits the inside part of her right leg near her knee in the rollover and now, 18 months after the rollover, she still can’t go back to regular duty because she has a permanent foot drop.  Another employee gets his hand stuck in the machine he works on.  The broken bones heal and the tendons are repaired.  Unfortunately, it has been difficult returning him to work because he complains of burning pain every time he touches anything with the injured hand and his doctor has permanently restricted him to one-handed work.

What do these claims have in common?  Peripheral nerve injuries.  Peripheral nerve injuries are complicated, slow-healing, and often result in permanency.  Why are they so complicated and what you can do to make peripheral nerve injury claims go as smoothly as possible?  In this short primer, we hope to answer some of these questions.

To understand why nerve injuries are so challenging, it helps to know some basic nerve physiology.  Nerve cells (neurons) are essentially made up of little factories (axons) that produce chemicals (neurotransmitters) which mediate the electrical signals each nerve cell sends (axon) and receives (dendrite).  Nerve cells are not physically connected to each other and must send the electrical signals across a gap (synapse) to the next nerve cell (dendrite).  The axon of each nerve cell is encased in fatty cells (myelin) that increase the rate at which electrical signals are transmitted between nerve cells.  Branching extensions of the nerve cells (dendrites) receive the electrical signal from the axon of an adjacent nerve cell and transmit the signal to the axon for further transmission.  A failure of any part of this process will disrupt the nerve cell’s functioning and cause sensory or motor problems or both.

Unfortunately, nerve injuries take a long time to heal and often heal poorly because of the complex, compound, and disconnected nature of nerve cells.  Nerve injuries are categorized according to the degree to which the nerve cells are compromised. There are two classification systems – one use three categories and one using six categories.  This post will use the simpler, three part system because it is more concise (the six part system breaks second degree injuries into four subcategories based on the seriousness of the injury).  In first degree injuries, or neurapraxia, the nerve remains intact but its signaling ability is damaged.    Ordinarily persons suffering first degree injuries recover completely without residual sensory or motor impairment.  In second degree injuries, or axonotmesis, the axon is damaged but the surrounding connective tissues remain intact.  Recovery takes longer than in first degree injuries, but complete recovery without residual sensory or motor impairment is still the general rule.  In third degree injuries, or neurotmesis, both the axon and the surrounding connective tissue are damaged.  Recovery is exceptionally long in third degree injuries and typically results in some residual sensory or motor impairment.  In addition, surgery is often necessary to restore function in third degree injuries.  The alternate classification system essentially divides the axonotmesis category into four parts based on the severity of the insult to the axon. 

We will focus on third degree injuries because they are the most difficult to treat and usually result in permanency.  In a third degree nerve injury both the axon and supporting connective tissue are injured.  This means that the nerve cell must regenerate both the axon and its supporting structure.  The regeneration is complicated by a post-injury process called Wallerian degeneration.  Approximately 24-36 hours after the initial injury, the axonal injury disintegrates, the myelin sheath degrades, and macrophages and Schwann cells remove the cellular debris from the injury.  In third degree injuries, the supporting connective tissue (endoneurium), which is a tubular structure containing individual axonal fibers, is severed.  This causes problems because regenerating axonal fibers may meander into surrounding tissue or inappropriate neural tubes, thus failing to reinnervate their proper end organs.  The resulting loss of function is analogous to what would happen in a marionette show if the strings to the marionette controllers are cut and then randomly reattached, sometimes to the correct controller, sometimes to the incorrect controller.  Nothing really works right.

When nerve cells start regenerating after Wallerian degeneration, the process is slow.  Within four days of the injury, the injured axons start sending sprouts toward the neurolemma (tube comprised of Schwann cells surrounding the axon).  Schwann cells produce growth factors that attract the sprouts.  If a sprout reaches a neurolemma, it grows into the tube and advances approximately 1 mm per day until it reaches and reinnervates the target tissue.  Surgery may be necessary to guide the sprouts into the neurolemma when the gap is too wide or scar tissue has formed.  This regeneration and repair phase can last many months.  Human peripheral neurons are capable of initiating a regenerative response for at least 12 months after an injury.  Hence, it can be well after a year from the date of injury before a treating physician or an IME doctor will be able to place a patient who sustained a peripheral nerve injury at maximum medical improvement.

Further complicating matters, third degree injuries do not usually heal completely.  Several factors can contribute to an incomplete recovery.  First, intramuscular fibrosis (scarring) may hinder the muscle contraction a nerve impulse produces.  Erroneous cross-reinnervation may result in impaired functioning (the marionettes with crossed strings).  The imperfect regeneration also results in sensory deficits, especially in proprioception (how the body perceives itself in space), that rarely go away completely.  Even in first and second degree nerve injuries, sensory recovery often takes 6-12 months, so determining whether and to what degree permanent sensory impairment has resulted can take a year or more post-injury. 

The site of the injury itself and the regeneration process can result in the development of neuromas or gliomas, which can increase pain and disability.  If surgical realignment or stump approximation does not occur, the migration of axoplasm may form a neuroma, which is an errant scaffolding (structure) for axonal migration.  Essentially, the strands of axonal fibers get tangled as they seek the distal nerve stump, forming a ball of connective tissue and axonal fibers.  While some neuromas cause no problems, many are painful and impair functioning. 

Treatment and rehabilitation following peripheral nerve injury present their own challenges.  For example, in nerve injuries with extensive damage a graft may be needed to connect the two ends of viable nerve.  Using a graft will leave the patient with a large area of numbness that the donor nerve previously innervated.  The size of this area of numbness will shrink over time, but will not go completely away resulting in residual permanency for loss of sensation at a site remote from the injury.  In addition, nerve regeneration itself can be uncomfortable and accompanied by paresthesia (pins and needles) as the target tissue is reinnervated. 

Some of the direct consequences of peripheral nerve injury included:

  • Pain (ranging from tingling to intense, burning pain)
  • Numbness and altered sensation
  • Muscle weakness
  • Loss of function
  • Loss of active motion
  • Joint stiffness
  • Emotional distress

Unfortunately neuropathic pain is not well-understood and is difficult to treat.  Anticonvulsants and tricyclic antidepressants are the most popular drugs for neuropathic pain.  “Complete relief is very difficult and only 40-60% of patients achieve partial relief.”  The persistence and refractory nature of neuropathic pain causes psychological distress and is difficult to understand for persons who are accustomed to the way more typical musculoskeletal pain responds to conventional analgesic medications.  From a claims standpoint, neuropathic pain presents great impediments to returning claimants to work because claimants are conditioned to equate pain with physical disability and loss of function, but neuropathic pain frequently does not impair function and is only disabling from a psychological perspective (not to diminish the psychological distress that neuropathic pain causes).  It is critical for return to work efforts that the treating physicians and occupational/physical therapists convey the distinction between neuropathic and musculoskeletal pain to the claimant to avoid protracted disability beyond the period of actual physical impairment caused by the injury.

Weakness and loss of function are common complications of third degree nerve injuries because even in the best case scenario nerve regeneration is imperfect.  As noted above, weakness and loss of function result from many complicating factors including slow regrowth causing irreparable muscle atrophy, imperfect regrowth resulting in loss of function, and the presence of scar tissue in the muscle preventing normal contracture.  This presents challenges to the claim handler who must attempt to gauge return to work, appropriate rehabilitation, and permanent partial disability.  EMG can determine the rate at which nerves are growing and muscles are reinnervating, but functional use/restoration will lag behind reinnervation.  The reinnervated muscles have been without innervation for a time, so the body must relearn how to use the muscles again which takes time.  In addition, the muscles are usually reinnervated imperfectly, so the body is not only relearning how to use the newly innervated muscles, but it is also learning a new neural pattern of action.  The body cannot rely on muscle memory to speed the relearning process because the newly configured reinnervation is different than it was before, meaning muscle memory itself is altered or lost. 

Some studies have found that conservative therapies can be used alone or in conjunction with surgery to help restore function in peripheral nerve injuries.  Laser phototherapy “maintains functional activity of the injured nerve for a long period, decreases scar tissue formation at the injury site, decreases degeneration in corresponding motor neurons of the spinal cord and significantly increases axonal growth and myelinization.”  In addition, acupuncture has been found to be an effective treatment modality in improving the rate of recovery.  In managing nerve injury claims, it is important to know what therapies work and what do not.  Effective claim handlers should be conversant in treatment modalities that can hasten recovery and improve ultimate function so they can ensure patients with peripheral nerve injuries receive the treatment that will get them to an end of healing the fastest and will minimize the inevitable permanent partial disability rating.

Even with effective conservative treatment modalities such as laser phototherapy or acupuncture, recovering function and building strength in peripheral nerve injuries are long and arduous processes that require skilled therapy and a motivated patient.  If either variable is lacking, recovery is likely to be compromised.  A supreme difficulty for claim handlers is managing the nerve injury case where either the employee lacks motivation or their choice of treating therapist appears to be wanting in some fashion.  Early engagement in the claim can help foster a “can do” attitude in the injured worker and a positive relationship with the therapist so that he or she pushes the worker and provides the highest and best evidence-supported rehabilitative care.

The Medical Systems, Inc. “Advanced Topics in Worker’s Compensation Symposium” will address these and other issues related to severe, acute industrial injuries to the hand and wrist with Dr. Jan Bax.  Join us to learn why severe hand and wrist injuries present such difficult challenges, what the best medical and surgical treatments of these injuries are, and what strategies you can utilize to help claimants get the best physical recovery and (in the process) lower your costs. 

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